Author: chad reilly

  • Free-Weight Lifting helps a LOT for Low Back Pain

    The effects of a free-weight-based resistance training intervention on pain, squat biomechanics and MRI-defined lumbar fat infiltration and functional cross-sectional area in those with chronic low back. Welch N, Moran K, Antony J, Richter C, Marshall B, Coyle J, Falvey E, Franklyn-Miller A. BMJ Open Sport Exerc Med. 2015 Nov 9;1(1) [FREE FULL TEXT]

    QUOTES:

    Results: Postintervention pain, disability and quality of life were all significantly improved. In addition, there was a significant reduction in fat infiltration at the L3L4 and L4L5 levels and increase in lumbar extension time to exhaustion of 18%.

    Conclusions: A free-weight-based resistance training intervention can be successfully utilised to improve pain, disability and quality of life in those with low back pain.

    The evidence for RT in musculoskeletal rehabilitation demonstrates greater effectiveness than aerobic, coordination, mobilisation or Pilates training.

    This study demonstrates significant reductions in pain and disability (72% and 76% respectively) in patients with comorbidities presenting with LBP following a 16-week RT programme.

    My comments:

    This study was interesting to me for a lot of reasons. Not the least of which being the exercise program used wasn’t all that different than my typical program for low back pain. The paper doesn’t describe the program in detail but I emailed the primary author and he was kind enough to share it. How cool is that? The program was as follows:

    It’s worth pointing out that before commencing in the exercises, the subjects warmed up and spent a fair amount of time teaching and learning good exercise technique and the ability to maintain a neutral spine during the exercises. If a person with back pain went to the gym and started doing squats and deadlifts with a flexed spine, that would be pretty close to a worst case scenario. However, when performed correctly free-weight resistance training not only increases strength and muscle but good spine motor control (the ability to maneuver loads with motion through your hips preserving a neutral spine) that you don’t get from machine training, or Pilates type exercises. In fact I thought it was really interesting that the authors mentioned Pilates by name because I just read Joseph Pilates books. I’ll have (more to say later) but for back pain Pilates should moderately strengthen abdominal muscle, but 20 out of his 34 exercises included instructions that flex the lumbar spine and 3 more flexed the cervical spine. Today we know that spine flexion is especially harmful to vertebral discs.

    Of the 30 participants in the study, prior MRI reports described 44 disc herniations and 20 incidents of facet joint degeneration, yet with proper coaching they were able to tolerate fairly heavy lifting.

    Interesting to me was the 18% increase in back extensor endurance as measured by the Biering-Sorensen test. Anyone reading my blog knows I’m a BIG FAN of Stuart McGill’s research and he frequently notes that low back pain is more often associated with lesser spine muscle endurance than spine muscle strength. While I don’t disagree, I’ve always thought that bodybuilding type exercises do pretty fair job of increasing local muscle endurance, so why not train for both. I expect higher rep range exercises to work better in this regard, but it’s cool to see sets of 5 work too.

    Also interesting was depending on where measured, spine extensor cross sectional area increased 1.8 to 2.9% while fat infiltrate 8-22%, in spite of the fact that while the exercises were dynamic (with movement) about the hips, legs and shoulders, they were largely isometric (holding still) in the spine extensors.

    Last I’d like to point out that this is not an isolated study, but rather part of a growing body of research showing that progressive resistance exercise to include free weight training helps considerably with chronic low back pain:

    However, I think much of the reason Welch’s group got their exceptional effect sizes was that they also explicitly taught lumbopelvic control and postural adjustment to go along with their exercises. Chronic low back pain being a multifactorial problem, to be cured needs a multi-factorial solution.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Chad’s Continued Electric Stimulation Notes 2015-17 and Onward

    This is a continuation of the “Notes From My Year Year of Electric Muscle Stimulation” which is becoming one of my more popular blog posts. Those notes were what I wrote down as I did EMS (electric muscle stimulation) for all major muscle groups instead of weight training for an entire year (October 2013 thru October 2014). I still think I’m the only person to ever do that and I learned a ton about how to make the most out of EMS for strengthening muscle, and while applying those same parameters to my patients I was happy to find out that the EMS parameters did a great job of decreasing pain (better than TENS in my observation, which turns out to be backed up by research as well.)

    Since that year ended I have continued to use EMS on myself for abdominal training, most frequently with my “core 2” electrode pattern, and I continue to use EMS for neck strength and hypertrophy, and I think somewhere below in the notes I did finally reach my goal of a 17” circumference neck (starting from 15 ⅞) and losing neck fat in the process per my next self experiment of intermittent fasting, which I have stuck with and been doing for over two years now. The neck stim is experimental, supposedly unsafe per every TENS and EMS manual ever written since 1970ish (however based on NO RESEARCH whatsoever that I have been able to locate). So I’m not telling anyone to do it, and I would even tell my readers not to do it. That said, I’m continuing to do it myself, and I don’t think it would be right not to talk about something that if shown safe for others, might be of considerable benefit. So these notes are about what I learned for myself, some of which info I use on my patients to optimize EMS and TENS treatments. For myself I’m not exclusively using EMS anymore for strengthening. I’ve returned to weight training for the bulk of my strengthening, but for abdominals and neck, EMS with Core-1 or Core-2 is just better, for abs I still think WAY better than any exercise ever created.

    So in the last few years I think I have learned a few things with regards to strengthening electrode placements, but I’m not trying out new things almost every day like I did in year one. However, I’ve continue to read research, especially on TENS (transcutaneous electric nerve stimulation) for applications where I might not want to use my go to EMS. So the results of all that is as follows.

    Also the format of my last set of notes was from oldest at the top to newer at the bottom, but on this one I’m just pasting in as I wrote it, new at the top. The other way only delays my sharing of the information for what’s been a couple years. New on top and I think it will be easy to just add things in a day at a time as I think I learn something important enough to write down with no planned schedule. The following is also just my raw notes, so if you chose to read them, don’t expect literary genius.The notes were 27 pages long when copied from my google documents, so if you are looking for something in particular “control-f” is your friend “command-f” if you are on a Mac.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.


    [4-11-17]

    Just tried “trans cerebral” EMS, with the electrodes over the parietal/sphenopalatine ganglion region, which I just read about in a paper on surgically implanted electrodes for cluster headache. I’ve always been a bit afraid to try it, but I’m also thinking that if I start recommending EMS for headaches, with the advisement to keep the electrodes right next to each other, it’s only a matter of time until someone messes that up. I would think the big risk would be could you cause a seizure as with electroconvulsive therapy (ECT) at which point you might be less depressed, but maybe have some memory loss. I’ll have to look in ECT book to see exactly what parameters they used but my recollection was that the amount of stimulation used was WAY more than you get from a TENS/EMS machine.

    I did my 10-10-10 headache program and started with 13/14 mA and only worked up to 15/15 mA. My thoughts are that the farther away electrodes made the stim feel way stronger and the EMS was definitely hitting my masseter muscle. Contrast to supraorbital stimulation with the electrodes side by side, I can get to 30 mA. 15 mA was plenty uncomfortable at first and if my headache patient data holds true for transcerebral stimulation, nobody is going to go that high, nor do they need to go that high to eliminate a headache.

    I didn’t notice any brain stimulation effects, just muscular and tingling outside the head so maybe it’s no big deal. Afterwards I felt fine and I’m able to write this. I felt “alert” afterwards if that means anything. I still wouldn’t recommend it because keeping the electrodes closer together is supposed to keep the stimulation more superficial and superficial stimulation is what is supposed to best target the nerves and blood vessels involved in a migraine, though I’m not sure how this would relate to a cluster headache.


    [4-2-17]

    Sacral stim attempt. Criss cross with posterior electrodes just to the side of the sacrum and brother electrodes on opposite side femoral triangle. 5-15-10 with 35/40 mA to start. Moved up to 45/60 and stim felt pretty strong. No pelvic floor stimulation but paresthesias and twitching in quads. Posterior stimulation doesn’t feel as strong probably because any nerves are way deeper. I couldn’t tell you if there is any detrusor muscle inhibition or not but I imagine the stimulation is going considerably deeper than if you just put one channel electrodes side by side the sacrum. That’s what I would do if I wanted to prevent deep stimulation, like in headaches. At 45/66 during the blast, quad contractions started to cause my knee to extend, but it was easy to overcome by flexing hamstring. 55/66 both knees extended uncontrollably. Not able to overcome with hamstrings. Feels like it might work, and the advantage being electrode placement is easy, uses one thick strap and non-”invasive.”

    Another try. One channel side by side of sacrum. No idea if there is any detrusor inhibition but I do feel glutes contracting without anything else getting in the way. Went to 55/70 within a couple blasts then 65/75, which I would have to think is more than just superficial stimulation, but don’t notice any stim or paresthesias going down legs.

    Did another just like above but moved the single channel of electrodes outward and down a little, right over where I think the sciatic nerve is and went to 55/70 mA and just notice glute flexion with just a hint of a paresthesia in my left ankle that might be my imagination. So I think that makes me think sciatic nerve stimulation is impractical. The nerve is probably too deep to reach in most people. I think my first choice for stim for my upcoming patent with overactive bladder/urge incontinence will be a criss cross pairing of the tibial nerve at the medial ankle with the brother electrodes on the opposite side of the sacrum. Though I’m thinking it might be tough to outdo my criss cross “hips-2” pattern I was using for general hip muscle strengthening. And core 2 I expect would really increase “reflexive” contractions of the pelvic floor. So far I’m not getting much in the way of direct EMS contractions of the pelvic floor without invasive electrodes that I expect most people are loath to do.

    One more idea, criss cross hip out with other side hip in (abductor-adductor). 40/45 to 45/45. Feels like adductors and abductors are working really hard but criss cross stim does feel like it’s hitting pelvic floor muscles much at all.

    Running core-2 now, just to work my abs as usual with 10-50-10. 45 mA first blast the stim does feel like my waist is being squeezed by a snake and I think my pelvic floor muscles do tense up significantly during the EMS blast, but it’s nothing near as hard as my core muscles are contracting with the direct stimulation. Still the pelvic floor contractions feel higher than with any of the leg stim patterns, but probably just in the range of doing kegel exercises.

    Giant 5-8” electrode, single channel, front and back, quickly to 80/100hz, put “rest” stim at 8 hz because of paper I am reading right now indicating that’s probably ideal for detrusor muscle inhibition. Still non-invasive, easy to set up, comfortable, maybe worth a try. To 90/110, you can comfortably get a lot of mA with the giant electrodes.


    [4-1-17]

    Working on stim pattern for what might work for incoming patient diagnosed with overactive bladder / and urge incontinence.

    First try: Criss cross back of knees (tibial n) with parasacral stim. 5-15-10 program, 30/45 mA to start. Went to 33 mA on blast and had unbearable calf cramp so went back to 30 mA. Feels like a lot of deep tingling & but not much in the way of pelvic floor action. Moved distal electrodes to feet, 20/34 mA and it felt stronger but no floor action even up to 23/40 mA. Then did just soles of feet like my neuropathy stim at 25/40 mA and felt almost as good as combined with parasacral stimulation but don’t feel it at all in the hamstrings. Criss cross with single channel over tibial nerve 25/50 mA up to 36/55 mA and it felt like it might work, slightly more proximal stim feeling than with feet stim but no noticeable floor action. Tried tibial nerve stim with 2 electrodes (1 channel) per leg and not criss crossed and 30/45 mA up to 35/45 mA and I didn’t feel it would be as effective as criss crossed with a single channel as all tingling was distal, no proximal feeling at all. The ankle placement seemed to have the benefit of not cramping the calves, but afterwards my calves felt pretty pumped, with some DOMS the next day, particularly the calf that cramped.


    [3-25-17]

    I’m preparing a review blog on RSD and TENS, and I’m reading about the various electrode placements and how they were putting the electrode on the femoral triangle, either with or without the paired electrode being on the dorsum of the foot. I had noticed really good and deep stimulation (that I expect would work better for TENS than EMS) by putting the distal electrode on the sole of the foot, and in theory the sole should feel better because it’s meatier and research as shown that electrode placement over muscle (for pain and certainly for EMS) works better because you can comfortably handle more current. However, even though the top of the foot is  bunch of bones, the dorsum placement felt just as good, probably because when combined with the other electrode being so far away at the hip, the current is running so deep through the leg that it doesn’t matter. Placing the proximal electrode over the sciatic nerve at the glute felt slightly less tingly than over the femoral triangle, but I bet if you have a fatter bottom then then it would work less still as the nerve would be further away from the electrode. Just having the electrode proximal (at the femoral triangle and sciatic notch) didn’t feel like it simulated very far distally either front or rear, so I think having the other electrode placed on the foot (top or bottom) is important if you want deep stim throughout the leg and foot.

    Then I tested a single channel, with one electrode over the sciatic notch on the left and femoral triangle on the right. At 50 mA, left side all I got were glute contractions and right side a mild quad contraction and tingling over the thigh only, maybe very slight in the ankle.


    [3-20-17]

    All that pain, 120 mA with sticky electrodes and I didn’t get a stitch of DOMS. Pec stimulation sucks and I’m at a loss as to why. I still wonder if I can max out the TwinStim4 like I did the Globus. In theory it should be easier since both pulse width and maximum mA are less. So I tried it, got 81 mA on first blast, up to 100 on third blast and riding it out. Using the ___ sticky electrodes. Felt intense as hell, getting that high up with my muscles still that fresh. With the Globus last time I hit 120 mA, but only at the end and on my 2nd run of 10-50-10. Moderate pump after, felt better than worthless. So why is my tolerance to stim so much higher? Probably part is a manned up, and with the Globus it was a lot easier to move up the intensity to feel what I could take. Part is the research is clear that people get used to stim, and can take more over time. So I expect it’s some combination of those two factors.


    [3-17-17]

    Going to try pec stimulation with my Globus Genesy 1100 cause the TwinStim4 is at work, so this won’t be an apples to apples comparison but pretty close. Those sticky electrodes in past weeks did give me a muscle contraction that’s marginally good, but man they hurt. So I just dug out my larger sticky electrodes that came with my Globus machines to give them a try. I’ve never used them before because by the time I upgraded to a Globus machine (still my favorite by far) I was already sold on the merits of rubber carbon electrodes over that of sticky. So if pecs are the only muscle group where sticky works better, I want to find the best sticky electrodes. So let’s start:

    First blast on 10-50-10 program went right to 50 mA, not too bad! Only minor stinging from on electrode at 35 mA on up. 55mA on 2nd blast and maybe spoke too soon, that electrode stings bad. Other 3 don’t. I’ll mark it and see if it’s the pad or placement next time I stim. 60 mA on the 3rd blast, 60 again (definitely getting higher than with the TwinStim4 & ____ combo). 70 mA next, only the one electrode hurts. Pushed left pec up higher independently since that side not stinging so bad, so at 80 and 75 mA with 2 min to go. 80 and 75. Finished with 92 and 85 mA. That was a lot higher, than I got with the TwinStim4 _____ combo. Come to think of it, those other electrodes are here. I’ll try them out with the Globus and see how high I get right now that I’m warmed up. Went right to 65 mA, these electrodes sting more, right from the start but still started higher with Globus than I finished with TwinStim4. 70 mA 2nd, then 75, 80mA (at 80 the stim is intense enough it’s starting to counter the sting with these electrodes) 85mA hurts again. 6 min to go and I’ll see if I can break the 92 I got on the left side with the other electrodes. 90 with 5 to go, if I don’t reach 100 now then I’m not a man. 95 (I have to say that the contraction doesn’t feel exceedingly hard, like my pecs have atrophied some from a decade of no bench press, post 3rd shoulder surgery) and after you get a smaller muscle to contract as hard as you can more stim doesn’t hit it harder. 100, 105, stings pretty bad, one to go. 120 mA MAXED IT! Booyaaah. More than double what I got with the TwinStim4 with the same pads. Will try to max the TwinStim4 and see if the extra 50 mA of the Globus makes that much difference, or if I just toughened up. If I don’t get some good DOMS after that, I don’t know what to say because I just maxed out a Globus Genesy with what are some smallish sticky electrodes. I definitely notice the ease of operation of the Globus and being able to push up the intensity of all the channels at once rather than down once followed by up, up, up one channel at a time with the TWINSTIM4.

    It’s got me thinking about something, those smallish sticky electrodes hurt real bad so I’m probably eliciting a fair number of _________ neurons, so maybe the reason why the larger rubber electrodes work so much better for pain is that with the better conductance and lesser current density, you are only activating the _________ fibers pushing the gait control wheel purely in the opposite direction as the chronic pain central sensitization wheel (the wheel is how I’m conceptualizing it and want to write up a complete description later). If you stim with a lot of pain you would activate both the _____ and _______ and might then jam the wheel. In theory you would want to reverse it I would think.


    [3-4-17]

    Pec stim with TwinStim4 hurts like hell. Not because of the machine but those sticky electrodes just don’t cut it like the rubber ones do. Got to 50 mA, which I think is my highest and it felt effective with my muscles feeling pumped after, but it sure wasn’t a joy. Larger sticky electrodes than the 2×4” ovals will likely be more comfortable.

    I’m going to try core EMS today with two channels and of the TwinStim4 and the super large (5×8”) electrodes and see if the machine is strong enough to drive the giant pads. Was able to turn the machine up immediately to 100 mA (maxing it out) on the first blast. It’s not light and in fact seems pretty strong, but not as strong as the where for core I use twice the channels and smaller electrodes to get more current into my core. And not as strong as when I used the Globus, three channels, and the big pads and got to 120 mA, which evidently raised my blood pressure so much that I had petechiae the following day. As I’m going, I think the trick to not having your blood pressure elevate when the stim hits your core, is to breath out and empty your lungs so there isn’t much for the muscles to push against. I’m not sure if I can get a BP reading that fast to test but it sure feels like my BP is higher when the contraction comes and I’m full of air.

    The other downside of the giant pads is you have to be a bit of a contortionist to apply them around your core. I stopped doing so in my office as the smaller (3.5” circles) were faster and a lot less awkward to put on for both patent and employee.


    [2-22-17]

    Three things:
    One: My pecs are mildly sore from last night’s EMS so maybe there are applications for sticky electrodes, though of all muscle groups tested, only pecs is the first place I have thought so and I still had to shave my chest to get it too work. For strength and hypertrophy I’m sure bench press would be better, but since I have had three shoulder surgeries, bench press is out.
    Two: I was able to get up to 80 mA on neck EMS with my TwinStim4. It felt strong and good with my 3.5” rubber carbon electrodes and my normal criss cross neck EMS electrode placement. It felt hella strong so I think it’s a legit stimulator.

    Three: I have a guy with severe sciatic hypersensitivity secondary to two herniated lumbar discs. So I’m stimming his core to increase core strength and decrease back pain, though his back isn’t bothering him near as much as his leg. So I have been doing FMTENS (my new name for Frequency Modulated TENS) with on pad on his femoral triangle and the other on the sole of his foot with an effort to decrease leg sensitivity per gate control theory. It’s hard to tell if it’s working, because I’m doing a lot of other things too, but anyway his pain is way down. But I was thinking. I’m doing the femoral triangle/foot pad placement for deep leg stimulation as tested once before in my notes after reading about it in some study (I’ll have to see if I cited it) and being duly impressed in real life when I tried it. However I was thinking, putting another channel over the piriformis muscle region to specifically target the sciatic nerve and its brother electrode on the top of the foot might be better. So I did just the femoral triangle/foot bottom on one leg and the same plus a piriformis/foot top placement on the other leg and to be honest I didn’t feel a lot of difference. So the two channels on one leg might be a little better, but not enough to write home about. However, if you have unused channels on your machine, they why not, as the strap use is the same. So next time I think I’ll try femoral nerve/foot bottom with one channel and sciatic nerve/foot bottom with the other and see if one feels better worse, or different.

    Update a couple hours later. My soleus on the right (the two channel leg) is sore like I worked it out real hard, while the left leg (single channel) feels pretty much normal. So I would say the two channels even if it didn’t feel that different during the TENS did get worked harder. Which is interesting because it was FMTENS at 30 mA rather than EMS. I think that’s the benefit of having the electrodes so far apart (hip to foot), the ES just goes real deep.


    [2-21-17]

    Finally figuring out how to train pecs with EMS (maybe). The trick, use Uni-Patch (apparently from Medtronic now) sticky electrodes and you have to shave your chest. Yes I know I always say I hate sticky electrodes, but of the one’s I have tried the Uni-Patch brand are by far the best I have used to long term stick, conductivity and lasting ability (per my experience using them on an EMS bike for TBI and SCI patients. I still like rubber carbon better almost all the time, for all these reasons, but I think for pecs, trying to strap rubber carbon in place, the elastic just won’t hold them tight enough against your skin, so I was always using both hands to hold them in place in addition to some fairly high tension elastic straps. So today was day two using 2” x 4” oval electrodes, one over the upper inner pec and the other on the lower outer pec with channel 1 and the mirror image used on the other pec with channel two. It felt like a good hard contraction, not epic like core or neck, but hopefully better than a waste of time, so I’ll try it for a while and see if it’s worth the effort. I got to 45 mA today, starting at 30 mA, and I forget what I did two days ago but probably not that different. No DOMS on pecs from two days ago though, while my abs were plenty sore from the last time.

    My Uni-Patch electrodes have been in a box for years (maybe 10?) and seem to work just fine, but now I see are on the medtronic website, and I see they have several versions, so when I wear these out I’ll have to do some comparison testing. I should probably give the stock Globus electrodes a shot too.

    I do notice the sticky electrodes sting more even with low intensity (~15 mA) EMS, but if I just keep turning the machine up, the tingling outdoes the stinging. So I’ll see how that lasts if I work up to higher intensities.


    [2-2-17]

    Trying out the two channel Twin Stim 4 machine. It’s actually pretty good. There are a few annoyances with it, like I can only turn up one channel at a time, I can’t upload my presets to it, I can’t rapidly increase the EMS like I can on the Globus or even EV, and it has pictures of body parts to coincide with EMS treatment protocols that defy logical sense. However, it’s an inexpensive ($70) biphasic symmetrical square wave two channel machine that’s programmable and I can save 6 different EMS programs (one for each picture) and 6 different TENS programs, though the TENS programmability seems limited to just changes in length of treatment, rate of impulse and width of impulse, but no individualization of frequency or _____ modulation. Pulse width is 400 uS is pretty stout, and almost as strong as my Globus. For an inexpensive two channel machine, it’s my current recommended machine as best for the money. I expect it work great for headaches, and other applications where one or two channels are all you need, and power needs are not extreme (for example advanced neuropathy). The battery is rechargeable, and I’m not sure how long it will last.


    [8-11-16]

    Playing around with some foot intrinsic pad placements and parameters. What I would do if I were targeting/treating bunions. Pad placement on forefoot top and bottom, not criss crossed, seems the best. Criss cross makes the contractions not feel local enough.

    Did 10-50-10,5hz and started with 40 mA and 50 mA. Did about the same yesterday with 5-10-10,5hz and mA kept going up up up cause muscles fatigued so fast. So maybe Kotz is right.
    Also I’m changing over all my EMS machines to have a 5 hz pulse during the EMS rest period. My reasoning being that if you don’t like it (like I don’t like the 1 hz pulse anyway) you can turn it down to zero during your session, while if you do like it, you can turn it up during your session. Yesterday I did 10-50-10,5hz and both core and neck, didn’t like the 5hz twitch at all, but just turned it down to where I barely felt it, so it was no consequence. I still haven’t tried it on any patients yet to get much feedback.


    [8-3-16]

    Some headache experiments. New employee has chronic headaches, tried my new freq mod TENS program that I was testing, with supraorbital and suboccipital stimulation, and she said her pain was more temporal (which had me a little worried it might not work, but I didn’t verbalize my doubts because I didn’t want to ruin any placebo effects, and because the combination of =SONS and ONS almost always works. She said pain went up a point (3/10 to 4/10) which is the first time in all my my tests that pain increased.

    So I was thinking about that, about how my Freq-Mod TENS program only went up to 80 hz, and if my idea was right about high frequency fatigue, the 120 hz I get with the 5-15-10 and 10-50-10 EMS programs. So the next headache she had on 7-26-16 was combined right side temporal and supraorbital stimulation. So my idea was to do one channel (2 electrodes) one over her supraorbital nerves and the other over her temporal region, which was close so I figured the two channels would target the EMS exactly where we wanted it, and since the electrodes were directly adjacent to each other there would be lower risk of “brain stimulation.” Initially I put FRQ-MOD TENS, and she didn’t like it, so I immediately switched it to my most proven program 5-15-10. The result, 6/10 pain of 3 hour duration was gone about 5 minutes into the 10 minute treatment, with 0/10 pain afterwards, with only 1 headache when at home since the 7-28-16 treatment (on in 9 days so far, not bad!).

    Yesterday we did some additional experiments, cause she said she had bilateral SON region headache. We weren’t sure if it was the different electrode placement or the different parameters that made the difference. I suspect it’s both. She also asked about the Cefaly device, so I wrote up another program using Cefaly parameters, so I programmed them (60 hz, 250 uS, up to 16 mA) but with otherwise equal parameters to what she did last (5-15-10 at 120 hz, 450 us, and mA as tolerated. She got to 6 mA on with the Cefaly parameters, and 4 mA on my preferred settings. She didn’t have a headache at the time, but I wanted to know what she thought of the differences. Also to better simulate the cefaly we used 1.25” square sticky electrodes both ways.
    She said with a headache she’d want my settings but maybe for prevention she would like the Cefaly ones since it felt less intense.

    So I decided to try it myself with the same sticky electrodes and with Cefaly vs my parameters. I got to 16 mA within the first minute the Cefaly parameters, which felt intense but not that intense, but I’m pretty EMS tolerant at this point. I was able to get to 16 mA, immediately and it felt more intense but not much less comfortable, and by the end of the 10 minute treatment I matched my prior record of 30 mA and could have gone higher, but it is my brain were talking about. It’s my second favorite organ.

    Today as a follow up experiment headache she says her headaches are typically temporal or supraorbital (never suboccipital) but the side is inconsistent. So I think for prevention, where you don’t know where the stim is going to go, and you still want the pads very close to each other we tried. Channel 1 on the right SON and TN, and channel 2 on the left SON and TN, SUCH THAT THE PADS OF EACH CHANNEL WERE DIRECTLY ADJACENT TO EACH OTHER NOT CRISS CROSSED WHICH WOULD PROBABLY CAUSE DEEP BRAIN STIMULATION. Deep brain stimulation might be great, or might make you forget your address and phone number, and near as I can tell isn’t at all necessary for the treatment of headaches. That’s just a warning, because, these are just my experimental notes and if I share them online, they are not prescriptions.


    [7-13-16]

    Have a CVA patient who on her 3rd visit is making spectacular progress, drop foot when walking gone, and this seems better than we think she was prior to her first stroke in 2014, TIA in 2010, and her recent stroke 5-13-16. So in addition to exercise, I’m having her do 2-2-10 program which she is working up pretty high. She had neuropathy in her right foot so I tried the combined glove and sock on the right side, thinking that would be a fast and easy way to get real deep stimulation for someone with hemiparesis. The depth of stimulation being so deep because the electrodes were so far away. It didn’t go that well because her foot with the neuropathy was very sensitive to the stim, such that she could only get to 6 mA, while the hand stimulation was easy.

    I hooked it up to myself (left side sock and glove) and worked up to 40 mA in 3 minutes of 2-2-10 program. I stood up to prevent the foot cramping and once standing it was my left arm that was limiting me from going higher. I thought it maybe wasn’t the best combination because my arm felt like it was working a lot more than my leg. However, afterwards (just 3-4 min of stim) my calf muscle felt pumped for a few minutes and “worked” for at least an hour (thus far) and my left forearm feels worked, even into my triceps. So not bad for just one channel of EMS and the mesh gloves.

    Since my CVA patient didn’t anywhere as high as I did, I had her do stim again with the 4” rubber carbon electrodes strapped to her biceps/triceps, forearm (top and bottom) and calf/TA and she worked up the stim to ~25 to 35 mA, so in her case, this time, I think the latter was a better workout. I think continuing with the foot stim with the sock will have merit for the neuropathy going forward, so will likely try it again. Plus I want to see how long those electrodes last with frequent machine washing.
    Interestingly, my soleus (lower calf) had DOMS for 2 days after the experiment with the sock and glove. At the time I did it, I felt like my foot and calf muscles weren’t working nearly has hard as my arm. And it’s not like my muscle are untrained as I’m currently doing single leg DB calf raises for 3 sets of 20 reps (definite “T”) holding a 50 lb dumbbell.


    [5-24-16]

    Did EMS to neck today, a couple days behind schedule and only got to 90 mA, so maybe the secret to getting high mA levels is hitting it more regular to build up a tolerance. Or maybe you don’t want that tolerance because a tolerance may or may not lead to harder muscle contractions. Today felt pretty hard!


    [5-19-16]

    Got to 115 mA at 450 uS on neck this morning and it wasn’t that bad. I figure I might as well go for 120 mA coursing right through my carotid sinus. If that doesn’t kill me, nothing will. Did core 2 and just got to 85 mA. So neck EMS is now my highest tolerance, not counting the calf EMS I did a year ago at 120 mA braced into a leg press machine to prevent cramping.


    [5-17-16]

    I GOT AN IDEA!

    What about aerobic (5 hz) EMS/TENS to the neck. The idea that it would improve aerobic conditioning of the swallowing/breathing muscles to treat sleep apnea. I think 5 hz for 10-30 minutes prior to or following 10-50-10 for muscle strengthening would improve the strength and fitness of the throat muscles for people with sleep apnea, and might also improve the brain/muscle link in those with central sleep apnea. I got the idea from a patient who had sleep apnea return and was going back on the C-Pap in spite of the fact that she had lost 40 lb with intermittent fasting. Also I thought the aerobic TENS would be a good test of the effects of stimulation to the carotid sinus because it’s continuous and thus I can repeatedly monitor my BP with my Omron cuff and fitbit. I predict, HR and BP to go up a bit not down just because of the exercise aspect. Not sure how tolerable it will be because the last time I tried aggressive aerobic EMS I didn’t like it too much, but maybe it won’t be so bad if I don’t do it too hard. I’ll know in a few minutes.
    So 30 min program

    HR at start

    • 136/86 & 47 (dig that resting heart rate!)
    • 1 min, 150/88&78 started at 80 mA and too bumpy so went down to 60, still hella bumpy.
    • 5 min 154/100&80
    • 10 min 140/90&75
    • Went up to 65 and couldn’t get cuff to read, came down to 60 and still had trouble
    • 18 min 114/69&120 fitbit HR 68 (I think the OMRON was wrong on this one)
    • 20 min 143/87&63
    • 25 min 124/85&85 fitbit HR 60
    • 29 min 127/78& 61 fitbit HR 58
    • Right after 127/80&53 fitbit HR 53
    • 5 min later 124/79&51 fitbit HR 51

    How about that? Vitals performed about as I expected they would. As for the experience it was hella bouncy. Shoulders shrugging up and down so I couldn’t read hardly at all, gave up on the idea of reading a paper during the stim. Could barely type out the above responses. Otherwise it wasn’t really uncomfortable, EMS didn’t sting or hurt a log, just bouncy/bumpy the whole time and I think if you had neck pain or a headache it could either get irritating or cure both. I think I could have worked up higher where it would have been painful, but then the BP cuff wouldn’t work, and it was iffy as is, having to take a few different measurements. Most people probably won’t bounce as much as me just because they don’t have as much neck muscle. Fitbit seemed reliable throughout. Borderline hypertension at the start of treatment cured!

    Does make me wonder if what’s better for combined stim, strength or cardio first? Or does it matter.


    [5-10-16]

    Last night I did 10-50-10 EMS on my neck and got to 85 mA on the last blast, which was just 5 mA shy of my prior record. I was pushing it up each time but not really trying for a record but maybe next time I’ll try for a record.

    I also tested out a “guts” program, where I had a 3 second ramp up, _____________

    The ramp felt hella comfortable and I worked up to 60-70 mA as I recall and my abs are sore today, but no idea about viscera, but sure felt like it should work. I felt like I was about to start sweating by the end, like a real workout, and with the short rests it was fairly unpleasant, just because it was on so much, I couldn’t read during, it unlike 10-50-10, where you just have 10 blasts that take your attention, but during the rest periods you can actually read a paragraph.


    [4-9-16]

    Experimented 100 hz instead of 120 hz on neck EMS with my typical 10-50-10 protocol. This was spurred by a email conversation I had with Giovanni probably over a year ago, when I said I had couldn’t find where Charlie Francis said he liked 120 hz with his EMS protocols and Giovanni confirmed that was the case per conversations he had with Charlie, but I still can’t find my cite. Giovanni said he still programmed his Globus machines at 100 hz and Charlie liked the programs and felt I was overkilling it with 120. I think I tried it at the time and stayed with 120 hz anyway, but thought I’d try again. 100 hz felt just fine, activated the muscles great, but I think 120 hz just feels slightly creamier, slightly less grainy a stim than 100. Not near as big a difference as I noticed when testing the 60 hz used with the Cefaly machines, but I put my machine back at 120 anyway.

    This was more spurred by my friend Grant’s professors saying my use of 120 hz was “non-standard”, well I guess if you want standard results, go to Baylor’s school of physical therapy and sign up to be in their dry needling experiment.


    [3-6-16]

    Pecs not sore at all.


    [3-5-16]

    Tried giant pads on pecs, one channel, one pad per pec (portrait) with new wetsuit vest. Started at 75 mA and got to 120 mA and it seemed to work pretty well. Even with the wetsuit though I had to use my hands to press the pads against my pecs for good enough contact to prevent stinging pain above 65 mA or so. Sticking out my chest and retracting my shoulders helped too but not as good as direct pressure with hands, so I had to grab the machine and hold it too my chest before the stim began so I could increase the intensity. Felt like a moderately intense workout, maybe it will get better if pecs hypertrophy, but machine already maxed. Will try other patterns. Will see if I get DOMS tomorrow. Pecs looked and felt a little pumped after.


    [3-1-16]

    Abs pretty sore today, anterior, obliques not so much after core 6. Petechia going away but not gone.


    [2-29-16]

    Haha, looked in the mirror today around lunch and had petechia in forehead, around eyes etc. Not extreme but definitely noticeable. The only time I’ve had it before was


    [2-28-16]

    Weekend EMS. Did neck today cause I’m going to up neck EMS frequency to twice a week. Neck circumference has dropped down ¼ to ½ inch to 17.00, which might be due to fat loss from fasting and my no meals Mondays, or because I decreased my EMS frequency from twice a week to once a week. So neck by itself I got to 85 mA today, which was pretty close to my all time record of 90 mA.

    Also tried Core 6 Big Pads (6 big electrodes all criss cross diagonal, all portrait which fully encircled my core, even overlapping a smidge. I really wanted to test it so I started at 60 mA and worked up to 70, 80, 90, 100, 110, 120, 120, 120 and it was pretty immense. Felt like the valsalva you would get doing 20 rep squats all holding your breath. Like your heads about to pop. Just an immense squeeze. So it definitely works, likely is pushing the bounds of safety. Though I feel fine now. Makes me think with all that EMS coursing transabdominal that it might be ideal for functional abdominal pain/IBS, but you would definitely want to go to the bathroom first, and probably wouldn’t need to go near so high of intensity and my Freq-Mod TENS program might be better, or might not. But for a fact the big pads let you tolerate way more EMS without discomfort. While the stim felt immense it was the muscle contraction causing it. The tingling wasn’t that bad, with no real stinging/prickling that I recall. Also those big pads are a PITA to self apply if you are wearing a shirt and coming up from underneath. Shirtless with just the big strap they went on easy dropped in from on top.

    For core strengthening it might be overkill though and using 6 pads negates the advantage of having two free channels to train neck (or something else) with. Also my waist being 34” is probably the lower limit for how it would work, cause because smaller wasted people would run out of real estate. The electrodes being 5.25” wide when placed in “portrait” would allow another pair (4 channels 8 pads) if waist size were 42” or bigger, if they were so inclined.


    [2-24-16]

    Did Core 4 big pads, all portrait except lumbar which was landscape as I think portrait on the lumbar spine will stim as much bone as muscle, combined with my neck EMS with regular pads.  Started at 50 mA neck and 70 mA core and worked up to 65 and 85 by the end of 10 minutes. As before it’s almost overwhelming. This mornings combined neck and back pain patient I treated got to 56 mA core and 11 mA neck and reported it brought her low back pain and neck pain that were both 3/10 to 0/10 immediately after. She thinks it feels great but isn’t going near as high on the neck, so I’m sure it’s more comfortable. The overwhelming feeling however, hitting both core and neck circumferentially I have to think would really power pain down via gait control theory and might be just the ticket for those with widespread central sensitization with conditions like fibromyalgia.


    [2-19-16]

    My abs are pretty sore from two days ago. Even my lower ribs are sore, probably from large pads overlapping my intercostals.

    Becky tried “Core 4 Big Pads” all portrait today and wasn’t impressed. Said Core 2 feels like a better workout, plus getting Big Pads in place and keeping them wet was a PITA she says.


    [2-16-16]

    Tried core 5 big pads diagonal, all portrait and combined it with neck stim since I had the two extra channels. Worked up to 65 mA on neck and 85 mA on core. Felt like one hell of a workout with all that stim going on at once. Almost overwhelming and with the neck stim going I don’t think I can give a fair assessment of how Core 5 diagonal vs Core 4 felt. I guess I’ll see if I’m sore tomorrow. Seemed hard to get either neck or abs as high as usual at first due to the overwhelming stimmage, but got reasonably high near the end of the 10 minutes. It was cool to get EMS workout done in 10 minutes instead of two times 10 minutes, however with all that EMS going on at once, the 10 minutes feels longer. To be continued.


    [2-12-16]

    Courtney tried Core 5 Big Pads (60-80 mA, all portrait)

    “Not impressed” Says it wasn’t any better than before but there was more paresthesias going down her leg from one of the diagonal anterior electrodes. Says her back was maybe worked a little better but still likes Core 4 Big Pads more. Says Core 5 Big Pads, still feels better than 10 cm electrodes for both comfort (for sure) and workout intensity (maybe) but she says it’s hard to differentiate.


    [2-11-16]

    DOMS in abs from yesterday and interestingly hip abductor muscles getting DOMS too, with portrait placement of large stim pads just barely going down below iliac crest, but seems to have hit hip abductors relatively hard anyway. Want to try with combined targeted hip abductor and adductor stimulation using all four channels.


    [2-10-16]

    First EMS thing I learned this year.

    Core 4 Big Pads

    Trained core just using 2 channels but 4 electrodes that are huge 5”x8” putting one electrode sideways across low back and it’s pain sideways across abdominals while channel two was placed vertically on obliques (I put them vertical so they wouldn’t overlap but it might fit better horizontal so I’m not stimming my iliac crest, which didn’t feel that great. Otherwise it felt like a good workout and only used two channels. I’ll play around with vertical vs horizontal placement of the pads, which I expect will be something that should be mixed and matched in accordance with a person’s girth. Vertical for skinny folks and horizontal for fatter.

    Felt like a good workout. Started out with 75 mA and worked up to 90 mA, and I expect I’ll be able to do more. Also thought of a new idea to try, which would be the same 4 electrodes but instead of placed front back and side side, they would be placed diagonally on quadrants so will try that next time and have the girls all try both in the office to get their feedback. The big pads did seem a little more difficult to get placed well on my core by feel.

    One downside is if I got up to 105 once with the small pads doing core 2, if I keep with the big pads I might max out the Globus, buy maybe not as my stim tolerance seems to have decreased, this year, for which my guess as to shy is increased autophagy of my nervous system from the >9 months of intermittent fasting I have been doing.

    Definitely this is a Globus thing since I started at 75 mA and worked to 90 on first try, there is no way the EV-906 will be powerful enough to drive those big pads.

    I don’t think it’s better than using the smaller 4” circular electrodes, but it frees two additional channels so they could be placed on hip glute medius or maximus or quad/hams just so you can hit more muscle at once if so desired. I got the idea because I did so desire, for my patient who had both low back pain and trochanteric bursitis. So I tried it on her last week and she liked it, so I wanted to see what it felt like. Also tried it on a patient with sports hernia where his abdominal pain was more central so we wanted to use one pad over his central lower abdominal region paired with another big pad on the spine extensors and he said that felt pretty good.

    So anyway, not a lot of new comments on EMS pad placements and experiments in the last year because my treatments are more set and a lot less experimenting, at least on myself. I’m lifting weights now for general fitness, and doing EMS once a week for abs and neck (because that’s better than weights for those) for neck. I was doing twice a week on both but it seemed like overkill and my neck circumference increased substantially by eating more protein with my intermittent fasting, and exceeded my neck circumference goal of 17” hitting 17.25. Girls say any bigger and I’ll look freakish, so I figured I’d lessen my EMS frequency to once a week for maintenance.

    So the big pads seem cool for strength, something new to try out.

    I guess another thing I learned is people love the Frequency Modulated TENS program I wrote up on the Globus Genesy last year. Posterior neck, upper trap and middle trap placement done supine with 4” circle pads is something my neck pain patient LOVE, so I think it’s going to be my go to program for neck pain. I still think EMS to the neck (front and back) is going to be the best thing for pain and strength, but since I test everyone’s heart rate and blood pressure when trying it, I think that increases anxiety, which is something neck pain patients have too much of anyway. So I think I’ll keep up the freq mod TENS for the time being going forward, until I get my safety study completed and published so I can stop increasing people’s anxiety about EMS over the carotid sinus “maybe” being dangerous.

    About Core 4, Courtney said:

    Awesome, got it up way high and was way sore (DOMS). Says the velcro needs to be tighter. Says she noticed with the pads in “landscape” if felt like the charge was stronger on the side of the electrode where the wire was in and less so distal to it. Better than the small pads. She likes it in portrait all the way around and the current felt even. She says started on maybe 50 mA and worked up to 80 mA.


    [9-30-15] EMS tolerance decreasing with increased use, or fasting?

    Just noticing lately that I have been doing EMS to neck and core on the reg, 2-3 days per week, but the mA I am working up to is way less than it was last year or earlier this year. So on neck I’m starting at ~40 mA lately and working to 50 mA, maybe 60 mA, but certainly not the 90 mA I got to several months ago. On core 2 I have been starting around 30-40 mA and working up to 50-70mA, which feels strong as hell- such that I have no idea how I ever got to 105 mA last year. If anything, I’m more fit, muscular and leaner now because I have been doing the intermittent fasting, combined with 4 scoops of whey protein per day over the last couple months. So I think the higher sensitivity to the current is because I’m leaner by a couple percent of body fat while my overall muscle mass has increased with my combination of weights and EMS (right now to different body parts). Charlie Francis talked about that in his book, how the leanest athletes with the most type II muscle fibers often required the least EMS because fat is an insulator and type II nerves and muscles contract with EMS particularly well. At this point it’s the only thing I can think of that would explain it


    [7-30-15] TENS frequency vs amplitude modulation

    Thoughts on TENS modulation: I don’t like amplitude modulation, it feels boring just like stim getting stronger and lighter at a given frequency. It feels like EMS ramping up and down. If I’m going to do that, I would rather just do EMS. Frequency modulation feels novel however, and I think might be psychologically more interesting, distracting, and might thus decrease pain levels more so than regular TENS or intensity modulation. I think it feels better so I might have my employees try both and see which they subjectively like better. When playing around with different programming parameters on my Globus Genesy, I settled on the following as my favorite:

    • Name: tens fr mod
    • Type of stimulation: TENS
    • Number of phases: 1
    • Phase duration: 30’
    • Program name: Symmetric TENS
    • Type of modulation: Frequency Modulation
    • Start workout frequency: 2Hz
    • End workout frequency: 80Hz
    • Workout pulse width: 450 uS
    • Workout duration: 15s

    Comparison amplitude modulation settings

    • Name: tens amp mod
    • Type of stimulation: TENS
    • Number of phases: 1
    • Phase duration: 30’
    • Program name: Symmetric TENS
    • Type of modulation: Amplitude Modulation
    • Workout frequency: 120Hz
    • Start workout amplitude: 100uS
    • End workout amplitude: 450 uS
    • Workout duration: 15s

    [7-29-15] Plantar fasciitis and posterior tibial tendinopathy pad placements

    I tried out a slight adjustment for EMS pad placements for plantar fasciitis. I had been putting my posterior electrode on kind of medial attempting to target the tibialis posterior, but looking at the anatomy I think the muscle belly is more central-posterior than I thought so I’m moving that electrode more central, just below the gastrocnemius. I think I should be getting a lot flexor digitorum longus and flexor hallucis longus, for which I would bet money they both help support the foot arch, though as of yet I am unaware of any references saying as much. I was worried that a more central posterior pad placement might hit the soleus hard enough to raise me up on my toes during the EMS like what happens when I put the pads on my gastrocnemius, but in trying it on myself just now, that wasn’t a problem. So for plantar fasciitis, posterior tibial tendinopathy, or acquired flat foot deformity (for which I expect prevention is a lot better than treatment) my current go to pad placements is standing on the pads with channel one split between the heel and ball of the foot, and channel 2 split between tibialis anterior and tibialis posterior (pad placed centrally, just inferior to the heads of the of the gastrocnemius.)

    Also, today I only got to 70 mA on core 2, compared to Monday when I worked up to 90 mA. I was hoping today to advance higher, thinking that if I keep my frequency of EMS up I could max out the machine and hit 120 mA. So perhaps the lesser tolerance could be due to the fact that I only had 48 hours of rest between Monday and today, while, last time I had 72 hours as I rested over the weekend. So maybe EMS tolerance is greatest if you have that longer rest period. Or maybe I used a different machine and there is some variability in output. I’ll pay attention to both going forward.


    [7-14-15] Core stim in prone position, continuous headache stimulation

    I’m doing neck and core stim (core 2-3) after working out on MWF pretty regularly. My neck circumference is up to 16.75” pretty solid now. Yesterday I tried core 2 laying prone, and my abs felt real strong on lower stim levels pushing me into a bridge. I think I started at 25 mA and working up to 60 mA, but at the higher mA ranges I got a lot more back extension. I’m not sure I liked that, as it was almost painful. I’ll think about it. My abs and low back muscles are pretty sore with DOMS today though from what was otherwise a typical core 2 workout, so there might be something to it.

    I just tried EMS, 120 Hz continuous to supraorbital region, working up to 25 mA. I’m curious if it affects my mood. I have been super high energy lately due to intermittent fasting and my testosterone levels are feeling higher from fasting combined with weightlifting being added back onto it.


    [6-28-15] Forearm/hand stimulation with gloves vs rubber carbon electrodes

    It’s difficult to type because I just finished unilateral forearm workouts with glove electrodes 10-50-10. My left hand did glove and paired CR (carbon-rubber) electrode on my left forearm extensors. On the right I did glove and right forearm flexors. Both felt very effective and both got to ~40 mA. The flexor combination, for some reason, made my hand intrinsic muscles feel palpably harder contracted. Neither was particularly uncomfortable on my wrist and hands even without bracing or holding anything. Neither felt like they worked my forearms much harder than a glove on each hand with a split RL channel, but with split RL can’t palpate my hand intrinsics during stim, and it’s hard to control machine with both hands being stimmed. I think ideal forearm hand workout might be channel 1 (glove/flexors) channel 2 (both forearm extensors). Maybe I will try vice versa with my trigger finger brace to maybe hit the forearm flexors harder. I will try both to see what I like better.

    I read a case study about RSD in a 6 year old and they put one electrode on the bottom of the affected foot and the other on the femoral triangle and they ran 90 and 50 Hz continuous with 2.5 and 3.5 mA. I don’t feel anything until 8 mA, and it starts feeling strong around 19 mA. I did a frequency mod over 30 seconds of 5-120 Hz at 450 us and it felt pretty good. I thought the electrode placement was pretty clever as it got the electrodes pretty far apart and I felt the stim throughout my anterior thigh and everywhere from the knee down. 30 seconds to do the mod over felt boring so I changed it to 15 seconds, then 10. Ten felt most interesting, but was still maybe too long. I certainly feel biased towards the higher rates, which is maybe good since higher rates appear (per the research) to work better for chronic pain. I changed the rate to 1-120 Hz but settled on 2-120 Hz as feeling best. I’m still biased to the high rate it seems. I stretched out modulation over 15 seconds 2-20 Hz and liked it better. Still biased high but more interesting than continuous high.


    [6-26-15] New core electrode placements, core 3

    While doing core 3, I tried 4 pads on front and 4 on spine extensors, criss crossed, I thought it worked by back harder and my obliques less hard (because that’s where I got the extra back electrodes from) so it all stood to reason. I had a number of my employees try it, most liked it though maybe not as much as core 2. I missed the oblique contractions with core 2, so I would therefore still say core 2 is my favorite. However, the following day my abs had decent DOMS, which I didn’t expect, perhaps because the additional spine extension better braced my back so I could work my anterior abdominal better against it, while with core 2 recently I felt my abs were winning the war of cocontraction.  It could also just be the different electrode placements getting the electric currents moving through the nerve and muscle fibers in a different direction, thus activating and training different fibers, so as I have commented before, I think there is merit mixing it up sometimes with regard to electrode placement and/or joint positions to hit the muscles differently. The other thing I noticed was when the stim went off, it really felt like an anterior to posterior squeeze, like I was being squished front to back with a vice. With core 2, I felt the squeeze as well, (much more than core 1) but the squeeze with core 2 felt more circumferential. What it really makes me wish is that Globus came out with a 5 channel machine so I wouldn’t have to compromise obliques for extra pads on the back. In the meantime, I’m thinking a good compromise would be to alternate between core 1 and core 2 for my workouts.

    My abs are still pretty sore even 2 days after. So it’s weird that an extra channel on the back made abs more sore, but unlike last year where I wasn’t weight training at all, just doing EMS, this year I’m lifting again, and I had just done (earlier that day) front squats up to 110 kg for 6 and RDLs 130 kg for 10 reps. The latter worked my back pretty hard and I have been doing so for weeks, so my spine extensors may be pretty DOMS proof. Plus, historically with the EMS I think my abs get more sore than my back. I had been doing EMS (core 2) after my squats and RDLs for weeks also, so I would have thought abs were getting DOMS proof as well. So core 3 might be for real.

    I had 2 people with back pain try it and both said it eliminated their pain immediately after a 10-50-10 workout. One of them, before trying it said her pain was too high up for core 2 to work, and I said perfect because core 3 has 2 electrodes going higher, showed her my diagram and she said cool, with her pain of 3-4/10 immediately reduced to 0/10. Everyone agrees it’s WAY better than any abdominal exercise.

    I also did my neck again in supine and I think that is the ideal position. I usually do it in sitting, but supine takes the load off the head if the person has a weaker neck, and puts their neck in neutral. For a stronger neck like myself, where I worked up to 85-90 mA, the supine position lets me brace my neck better in that safer, more neutral position.


    [6-21-15] Electric stimulation for menstrual cramps

    Reading some papers on EMS for dysmenorrhea and, imagining that I had it, I think 2 pads on the lower abs and 2 pads on the low low back feels like it would be ideal, but I think girls should adjust for comfort. Also, I thought criss-crossing the pads from front to rear felt like it might work a little better because it felt like the stimulation would be deeper and might actually get the uterus. Normal, non-criss-cross placement felt almost as good. I will test that on my people (female people) and see what they think.

    High frequency TENS >100 Hz seems to be what’s most supported in the literature, but I think the low rate TENS groups >10 Hz is getting a bad wrap by researchers sometimes putting the pads on ridiculous acupuncture points on the lower legs or whatever rather than on the source of pain. I think the low rate TENS might work well with better pad placement. If it were me, I would probably want to use some frequency modulated current, with as wide as possible a pulse rate (300-450 uS) since high is necessary to eliminate pain. I expect more to be better than less up to a point although you might not want to go too high, with such a long treatment time. Maybe an hour+ would be an ordeal and an EMS parameters might over fatigue the muscles.  I’ll test it out on some of my girls with dysmenorrhea as they seem pretty willing volunteers.

    JD, reported 6/10 pain was eliminated during Chad’s TENS for 10 minutes, but she said pain returned to 3-4 a few minutes after she stopped. She then did 5-15-10 and reported that it also eliminated pain, but that it still returned to 3-4/10 afterwards, so I want her to try a 2 channel machine belt clipped on to her with a 60 minute treatment time and gel electrodes, which I hope will fully eliminate pain and still be wearable while she works.


    [5-29-15] Glove and sock mesh electrodes, pretty cool!

    I tried out my new sample gloves and socks yesterday, filmed it, and those things are no joke. I started with the gloves, one channel split, and just trying it a few times my forearms felt strained immediately. I did a 10-50-10 workout working up to 40 mA, and my forearms have DOMS today. It felt really good for just the gloves, I didn’t need anything to grip, I just put my hands into fists to brace myself. I felt really strong stim up to my elbows and lesser up to my shoulders. The experience was maybe not as intense as 2 pads on the forearms, but maybe it was because I stopped moving up due to mild wrist strain/pain. Gloves are certainly easier to apply.

    The socks got my legs twitching, which I would expect to pump blood and improve neuropathy. They felt a lot like the flip flop electrodes, but are easier to apply because you didn’t have to be weight bearing. I didn’t feel like foot intrinsic muscles were getting as intense a contraction, much like the flip flops, in comparison to standing on a single channel with 2 pads on ball and heel of foot.


    [5-8-15] 5hz aerobic TENS/EMS still feels best

    I tried 4-5&6 Hz TENS/EMS on calves to see what felt like the best for circulation. I think 5 Hz was best, but probably my experience is colored by the results of my HR tests where 5 Hz won. On my left calf I put the 2, 4” pads on my gastroc in lateral position, and on my right up put one on my TA and the other on my center gastroc to see if it felt like it would squeeze my muscles better against my tibia and fibula for more of a blood pumping effect. I couldn’t tell that it did, and my left was more comfortable and probably got more, while the TA felt like it was working more on my right. I’m sure it was, but overall muscle activation vs 2 pads on the gastrocs felt maybe less. Also, the TA stim hurt more, I think because the anterior electrode was real close to my tibia bone, so it maybe handled 10 mA 65 vs 75 on the calves at about equal comfort. So in theory ,I like the calf/TA placement better but the 2 on the calves felt better so I could work higher. Verdict = a push. Try both, keep what you like. Unless there is a drop foot then probably you want that pad on the TA.


    [5-6-15] More wetsuit trials for electrode placement

    I’m all motivated to stim again for two reasons. First being that I want to see how much muscle mass I can maintain, since I noticed I was losing weight on my Fast 5 diet. Second, I’m doing tests on my “Muscle-Stim-Power Suit” So here goes, first try on hips, the setup was easy without any cuts, but some cuts might made it easier still, particularly for hip adductors, but I was able to reach the pads in without much difficulty. Electrode contact is good without any velcro straps. Doing a regular stim pattern rather than criss-cross since I did criss-cross last time and I figured I’d mix it up. Doing 10-50-10. Verdict, it worked great.

    Even an unmodified wetsuit for legs seems better than straps but reaching pads down from the top was not as convenient as it should be. All of the pads work and the contact feels good. When standing ,upper hamstrings don’t seem that tight to the skin, but since I’m doing the treatment in sitting it’s not a problem. The distal vastus lateralis doesn’t seem that tight but works fine. Maybe I need a tighter wetsuit for pants. I already ordered a smaller jacket to try out. Verdict on thighs, wetsuit worked, but slits will make pad placement easier, hopefully without destroying the integrity of the suit.


    [5-5-15] Wetsuit idea for holding EMS pads in place

    I’m trying out my wetsuit for the first time. 2 blasts with 6 pads on my left side is working great. Maybe next time I’ll buy a tighter one as it might hold the pads better. I wasn’t sure where to make cuts so I just stuck the pads in through the chest area and zipped it up. The only thing I felt like I couldn’t get is the forearms. I might play around with my spandex shirts to put cuts so I can test positioning before I cut my wetsuit since it’s more expensive. Contractions feel good though, even on the chest (well no, chest could be tighter, all else is good). No burning so chest contact not that bad, but EMS to pecs always lackluster. Put channel one on biceps and triceps, 2 criss-crossed on posterior RTC and anterior delt, with channel 3 criss-crossed on pec and posterior delt. Channel 4 was not used but would go well on the forearm/hand. The suit works though, pads staying in place and not sliding around. Next time, I’m going to skip putting the electrode on the front delt because it’s already hypertrophied and it looks like the pec thing might finally be worth doing. Some cuts I think will make it better but it’s already a lot easier and cleaner than trying to strap your own arms.


    [5-3-15] Maybe hard EMS should be right before a meal

    I stimmed neck, abs, core, hips, right and left thighs today. And I’m sitting here thinking it might be good to carbo load afterwards (post workout nutrition and all that) but I missed my window because I’m doing IF and can’t eat for several more hours. So that got me thinking I really ought to be doing my EMS workouts right before I eat at night, or after, or between eating, but after 5-6 pm. Or maybe it don’t matter much, as I feel fine but I’m curious if I gain weight when I weigh myself tomorrow at work.
    My mood today, after stimming my forehead, better than average.


    [5-3-15] Continuous stim for headaches

    Tried EMS continuous just to my supraorbital region but used 150 Hz and was only able to work up to 20 mA.  I forget what I started at but I think it was only 8-10 mA
    A few minutes later I’m doing it again but returning my rate to my normal 120 Hz to see what I get, since I got 30 mA with a different machine at my office 2 days ago.  Started right at 16 mA but only worked to 21 mA, so maybe the difference isn’t the rate, maybe it’s a difference between my Genesy 300 and 1100, or maybe the extra electrodes on the neck made me tolerate more on my head. 120 Hz felt better though, it felt like the frequency was more “in tune” with my body. That might be something to test with others to see what they say. I’m curious how my mood is today. Also I noticed if I pushed my fingers on the pads, that portion of the pad felt like it was delivering more current to my body than the rest. I imagine that might be because I am improving the connection there between pad and skin (but it was already tight) so maybe I’m flattening out my skin and sub-q region getting that electrode portion closer to the sensory nerves under the skin. I’m not sure there is much practical importance here, but I noticed it.


    [5-2-15] Aerobic EMS/TENS 4 hz worse than 5 hz, 5 hz seems the sweet spot

    4 hz cardio test, otherwise same as last time

    • t=0 mA 60 HR and BP 52 116/77
    • t=5 mA= HR=86
    • t=10 75, 98
    • t=15 80, 108 turned on fan
    • t=20 80, 105
    • t=25 85, 116
    • t=30 85, 119

    4 hz felt a little more pleasant than 5 hz, but HR didn’t get quite as high even with 5 extra mA, so it’s probably a push. It felt like the muscles were just barely, but fully relaxed before the next pulse, while at 6 hz it felt like they weren’t, so probably 4-5 hz is the sweet spot and I would guess 5 hz is best for cardio/blood flow. I’m sure it could stand a lot more tests on more people to be sure. It is cool having the Globus Genesy where I can just program and test whatever I want.


    [5-1-15] Globus Genesy vs EV-906 for HAs, better but way more than necessary

    I did HA test of EMS (or you could call it high intensity high rate TENS), basically my favorite EMS program without the rest periods to see how that affects headaches compared to the 10 on 50 off (for 12 minutes with the EV-906) and 5 on 15 off for 12 minutes with the EV-906 I had tried before. Also since the Globus Genesy is now my go to EMS unit in my office I wanted to start testing its use. The differences in parameters are that I generally use a 10 minute treatment time (as developed by Yakov Kots and used by Charlie Francis) with the Globus because with the single button to control all channels at once I don’t need the extra 2 minutes of fiddle time used with the individual channels with the EV-906. Other differences are that the Globus is a symmetrical biphasic square wave, which for practical purposes means both electrodes on a channel are and feel of identical strength. With the EV-906, the black wires feel full strength, while the electrode attached to the red end is noticeably weaker. Is the difference a big deal? I would say no. Do I prefer the symmetrical wave of the Globus? Yes. Is it worth the cost differential between units? I would say that depends on your needs and your discretionary income. Regarding headaches, nobody (thus far) turns the machine up high enough to max out the EV-906 and my pretty amazing results thus far have all been with that machine. So I want to see if the Globus works as well or better. I suspect it will work as well, and with the more even current perhaps marginally better.

    Also, I program in a pulse duration of 450 uS on the Globus (its highest setting) as opposed to the 300 us on the EV-906 (its highest setting), so I’m curious if this has any effect on outcomes. I expect that it won’t with regards to headache intensities, but I expect the max mA level (height of the wave) worked up to by patients will be proportionally lower with the Globus to offset the greater intensity imparted by the longer pulse duration (width of the wave).
    What I noticed afterwards was that I was in a particularly good mood. The best in months. I know there is a fair amount of research on TCDCS and depression, so I wonder if I got a bit of that.


    [4-2-15] Aerobic EMS/TENS 5 hz worked even better than 6 hz
    5 hz cardio test, otherwise same as last time

    • t=0, mA =0 HR 55
    • t=5 70, 105
    • t=10 70, 100
    • t=15 75, 116, turned on fan
    • t=20 80, hard to read, hurts a lot 7.5/10, 121
    • t=25 turned glutes down to 77, 120, thirsty
    • t=30 126

    That was unpleasant! I had to turn glutes down 3 mA because it was intolerable for that many minutes on end. My calves are really sore from plantarflexing so hard due to EMS on calves but all of the joints felt fine. Just the stim at 80 mA, which I got to sooner this time made it sore. 5 hz felt better than 6 hz at the start and it felt like muscles relaxed a little more between each hit, while at 6 hz it felt like only partial relaxation before the next impulse. I already wrote a 4 hz workout to try next time and see how that is for comfort, and will then try the 3 hz pulsed TENS program to compare on heart rate, pain/comfort before changing any other variable, like electrode size or electrode position on the lower leg. I think maybe putting a real big pad over the TA would activate the TA better while still getting co-contraction of the calves so it might be more balanced forces across the ankle.

    126/177 (my calculated max HR) is 71% so not bad for watching TV. Respiration was way up but I’m not sure how to calculate that, but I expect it correlates with HR much as it would on a treadmill. Felt about the same.


    [3-28-15] Aerobic TENS/EMS, bingo, it worked

    Giving aerobic training another try. 6 Hz, Criss cross lateral on all channels, calves, quads, and hamstrings but only 1 BIG rectangle pad on each muscle so this might have a good chance. HR 51 at start, BP 132/88. Started off at 59 mA.

    • 2 min HR 80 BP 157/99
    • 5 min HR 75 BP 150/98
    • 7 min increased to 65 mA (hard to type)
    • 10 min HR 82 BP 157/97 (not exactly comfortable or pleasant feeling and I notice I’m breathing deeper so it seems to be working.
    • 11 min increased to 70 mA, twitches almost violent feeling, 6.5/10 pain
    • 17 min HR 87 BP 148/91 increased to 75 mA right after
    • 20 min HR 103, BP 151/89, feeling warm and starting to sweat, moved to 80 mA
    • 25 min HR 114 BP 163/96 definitely starting to breathe hard
    • 27 min HR 113 BP 171/94
    • 30 min HR 116…

    my max HR at 43 is 177 BPM, 50% is low end of moderate aerobic workout,

    • 89 is 50%
    • 116 is 65%
    • 100 is 56%

    So the last 10 min were getting to be a mild aerobic workout, at/near 65% of max HR.

    I think it worked. I had trouble getting blue dot on BP wrist cuff towards end but was able to with a few tries. I had to put a fan on myself after. I will have to check out the my % HR. It felt like a pretty good workout but wasn’t at all comfortable. It was probably not as bad as the step mill, and I think certainly a worthwhile option, maybe as good as the EMS bike for SCI, and a whole lot cheaper. Maybe lower HZ or pulsed HZ would work as good and feel better. 6 Hz felt really fast. Large and criss crossed electrodes certainly made it better. I think even larger electrodes might work better still since I only got to 80 mA, and the muscles not under the pads didn’t feel like they were contracting. I wasn’t dripping sweat or anything but the couch was damp where I sat. Kind of gross. I will have the fan on next time during the running of the program.

    TENS burst at 5 Hz, when turned up past 30 mA, just melded into a continuous/constant on. 3 Hz stayed separate and I programmed it in and it felt like it might work ,but the contractions felt harder. I’m not sure if that’s good or bad. I may try it for 30 minutes next time and see how it affects HR.

    I have neck and throat DOMS today from 90 mA yesterday. I actually feel some DOMS in my anterior throat when swallowing. Probably hitting the right muscle and then some for dysphagia.


    [3-27-15] Brief detraining with time off from EMS, core and neck

    I did EMS on Monday for the first time in over a month and started stim on core 2 to only 30 mA or so, but today (Friday) I was able to start at 50 mA and work up to maybe 80 or so. With time off, you definitely need to work up again. The neck went easier on Monday getting me to 60 mA I think, and today I worked up to neck 90 mA, a new record. I didn’t even try to breath during the “on” phase because beyond 60-70, I knew I couldn’t. This isn’t such a big deal if you are just holding your breath and bracing yourself anyway, and not alarming if you know what to expect. I felt great afterwards. 60-70 mA on abs started to feel some stinging and I was thinking I was overwhelming my pad area, but neck went to 90 mA with no stinging discomfort so go figure. I felt tingling in my lower left molars above 55 or so mA.


    [1-19-15] Criss-cross thigh placements with giant electrodes

    I tried criss-cross thighs with big pink and new grey pads and started right off at 65 mA with thighs extended. The contraction felt reasonably immense but comfortable. 70, 75, (real strong, contraction feels and looks complete in thighs), 80, 80 (it’s a lot of stim to take all at once), 80 (criss cross I feel like quads are too much and I need more hams but can’t individually add more hams because I have quads and hams criss crossed together. Maybe next time I will criss-cross but keep quads and hams separate) 80, (at 80 mA with the big pads it’s the forceful knee extension that’s stopping me from going higher, EMS under pads is fairly comfortable) 80, 85, 90. Breathing real deep and hard after. Will have to use my BP/HR cuff next time. Thighs feel super fatigued after. Contractions felt very deep.  I’ll bet I’m sore tomorrow. ~20 minutes later my legs still felt fatigued and I felt like I could take a nap.

    10 minutes gave me 10 contractions even with time prolonged due to moving stim up so that’s cool. I wonder if the extra seconds are just taken out of final rest or if time is added onto the program, will have to time it in the future.

    It did take a long time to set up with changing the pads and all. Before I went, I thought the time change might not be worth it because training one leg only takes 10 minutes. The setup with pad changes felt near to 10 minutes. I should have timed it. I’m breathing really hard between sets. This might be getting aerobic with this much muscle going at once. If quads and hams are getting equal stim (and they are with my criss-cross pattern), it seems that the weaker muscle ,hams, needs more stim to help balance out the stronger quads and that in time might help lessen muscle imbalance


    [12-30-14] Four mode TENS program, just to try everything out

    • Chad’s TENS
    • Type:TENS
    • Number of phases: 4
    • Phase 1 duration: 3’
    • Phase 1 Program Name: Symmetric TENS
    • Type of Modulation: Amplitude Modul.
    • Workout Frequency: 120 Hz
    • Start workout amplit.: 180 uS
    • End workout amplit: 450 uS
    • Workout duration: 3s
    • Phase 2 duration: 2’
    • Program Name: Symmetric TENS
    • Type of modulation: Frequency Modul
    • Start workout freq.: 10 Hz
    • End workout freq.: 120 Hz
    • Workout pulse width: 450 uS
    • Workout duration: 6s
    • Phase 3 duration: 3’
    • Program Name: Symmetric TENS
    • Type of Modulation: Continuous
    • Workout frequency: 10Hz
    • Workout pulse width: 450 uS
    • Phase 4 Phase duration: 2’
    • Program Name Symmetric TENS
    • Type of modulation: TENS Burst
    • Burst Frequency: 1 Hz
    • Workout pulse width: 450 uS
  • Electric Stimulation for RSD / CRPS (Chad’s Review)

    Complex Regional Pain Syndrome (CRPS) also known as reflex sympathetic dystrophy  (RSD), causalgia, and a host of other names is kind of like headaches and neuropathy were for me. In that I didn’t initially have any particular interest in the condition but I have a tremendous interests in electric stimulation, particularly electrical muscle stimulation (EMS) and its application to various diagnosis. And my results with using EMS and TENS currents with both headaches and neuropathy have been fantastic and I think the lessons I learned in my “year of EMS” self experiment about various machines, parameters, and electrodes leads me to think I can improve upon what’s already been shown to be positive outcomes in a number of studies. Reading those studies, it gives me some ideas to try with my patients in what I hope is a positive spinning cycle that can reverse the negative spin of chronic pain. So what I intend to do with this review, is link and list comments from relevant papers I was able to acquire, and comment on how I might synthesize that knowledge together for an optimum outcome of maximum recovery, in minimal time, expense and discomfort.

    It also happens that CRPS is tremendously difficult to treat, but seems as though it should get better without drugs or surgery if we can just figure out what may be more than one factor to help it get better. Since learning how to successfully treat other multifactorial problems, like chronic back pain and tendinopathy, I have this confidence (hopefully not false) that I can do the same with other conditions, and on paper CRSP seems like the perfect candidate, where you want to decrease pain, restore blood flow, and eventually restore strength and function and do so in a way that’s going to keep you from freaking out. I’ve had a file on electric stimulation and CRPS and it just had papers from the 70s and early 80s in it with no recent follow up. In rehab it seems electric stimulation was forgotten for a few decades all while the technology became better, machines became a LOT less expensive. While all the TENS and EMS research has been going on, with CRPS most of the papers coming out have been with the use of surgically implanted spinal cord stimulators. While that research has been positive it sounds hella invasive, and I really do think that if you really know what you are doing with electrical stimulation (to leverage up all the variables of TENS and EMS) I think it should work better better than the surgery at a fraction of the cost. So I’m going to start writing about how I would leverage those variables, what researchers from each study figured out that was or wasn’t followed, and what I think they all missed that might help.

    I’ll start off with a paper I just read, a new 2016 study that confirmed in a double blind study that TENS, when added to a physical therapy program substantially improved outcomes, and was the impetus for this blog.

    The effectiveness of transcutaneous electrical nerve stimulation in the management of patients with complex regional pain syndrome: A randomized, double-blinded, placebo-controlled prospective study. Bilgili A, Çakır T, Doğan ŞK, Erçalık T, Filiz MB, Toraman F. J Back Musculoskelet Rehabil. 2016 Nov 21;29(4):661-671.

    MATERIAL AND METHOD:
    The study included 30 patients with stage 1 and 2 CRPS Type I in the upper extremities. The patients were randomly assigned into 2 groups, group 1 (n= 15) received conventional TENS therapy for 20 minutes, and group 2 (n= 15) received sham TENS therapy. The standard physical therapy program, which included contrast bath for 20 minutes; whirlpool bath for 15 minutes; assisted active and passive range of motion, and static stretching exercises up to the pain threshold, was also conducted in both groups. Therapy was scheduled for 15 sessions. A visual analogue scale (VAS) was used to assess spontaneous pain. The Leeds Assessment of Neuropathic Signs and Symptoms (LANSS) scale and the Douleur Neuropathique en 4 Questions (DN-4) were used to assess neuropathic pain. In addition, range of motion (ROM) was measured using a goniometer and volumetric measurements were taken to assess edema. Functional capacity was assessed using a hand dynamometer and the Duruöz Hand Index (DHI). All measurements were performed at baseline and after therapy.

    RESULTS:
    Significant improvements were achieved in spontaneous and neuropathic pain scores, edema, ROM, and functional capacity in both groups (p< 0.05). However, improvement was found to be significantly greater in group 1 regarding pain intensity, neuropathic pain assessed using LANNS, edema, and in the 2nd-3rd finger ROM measurements (p< 0.05). No significant difference was detected between groups regarding improvements in 4th-5th finger and wrist ROM measurements, grip strength, and DN4 and DHI scores (p> 0.05).

    CONCLUSION:
    The addition of TENS to the physical therapy program was seen to make a significant contribution to clinical recovery in CRPS Type 1.

    My comments:

    This paper cost me 27 Euros! The abstract says the TENS worked, but the absolute results indicate the TENS worked better in almost all the parameters tested, just failing to achieve statistical significance in some, and often that improvement was several fold better than the rest of the therapy combined. The physical therapy program included 15 sessions (sessions per week not given) including:

    • real or sham TENS for 20 minutes, if real “Conventional TENS” with a Chattanooga Mobile Stim 2777, 100 hz, 50-100 uS, “amplitude that did not cause discomfort” with two 6×8 cm carbon electrodes with one place on the dorsal forearm and dorsal hand.
    • hot whirlpool bath for 15 min
    • hot and cold contrast baths 20 min
    • exercise (daily active, active assistive, and passive ROM of wrist and finger joints 3 sets of 10 reps each)
    • up to 4 grams paracetamol per day

    Pain decreased 70% in the TENS group compared to 34% in the placebo group. Edema (swelling) in the hand decreased 12.33 mL with TENS more than four times better than the 3.0 reduction with SHAM and all the rest of the physical therapy. Range of motion of every finger digit was better with TENS from 70 to 133% over sham, though for some reason wrist ROM trailed slightly (16 to 43%). Grip strength improved 6.87 kg in the TENS group, more than double the 3.4 kg improvement in the sham group.

    Overall I think this is a great paper. I would have liked to know over how many the weeks the 15 treatments were spread and how high of mA the patients worked up to over that time period and if higher electric stimulation intensities were related to greater outcomes. Also I was glad to see they used rubber carbon electrodes instead of the sticky versions as rubber carbon allows for greater stimulation with less pain, which I expect would be extra important in the RSD patient group. It sounds like with the varied pulse width of 50 to 100 uS they were using amplitude modulation of the TENS, which I expect helped over just a flat constant pulse width TENS, though I prefer frequency modulation, where the rate (Hz) is varied over time rather than varying the pulse with.

    My thoughts on improving outcomes further would be to extend the TENS treatment time to at least 30 minutes as I recently read a paper that found pain sensitivity decreases more at 30 minutes than at 10 or 20 minutes in normal subjects at least. Also I would wonder (as was noted in some older research) if doing the TENS three or even four times per day would work better than once a day, or once three times per week. I would expect more to be better, which is often the case with electric stimulation and pain reduction. Also it seems they were using the TENS specifically to reduce pain in hopes that the exercise program would improve function. I would think that as the patient’s tolerance to the electrical currents improves they could start adding in EMS currents (with a wider pulse width of 300-450 uS) keeping the on period frequency high (100-120 hz) with a 5 second on, 15 second off, or a 10 second on, 50 second off period. During the “off” period a 5 hz pulse could be programmed in (if using a Globus Genesy machine) which I expect would substantially improve blood flow to the affected extremity. Conversely, if using a budget machine, EMS at 5-15-10 or 10-50-10 could be to improve muscle strength, followed by a wide pulse width 5 hz “aerobic EMS” program for 20 or 30 minutes. All of the above “optimization” ideas run into practical, or at least financial, problems in the office where insurance usually reimburses for electrical stimulation for only 15 minutes of electrical stimulation per day. However on the very bright side, top of the line electric stimulators like the Globus Genesy can be owned for $500, and inexpensive two channel stimulators like the TwinStim4 work great for as $69. I’d think you’d still want to pair either with rubber carbon electrodes and good straps to hold them into place. Though the above study used rubber carbon electrodes, I expect larger ones (my favorite universal size is ~10 cm circular) would work better still. Also I would think that adding a second channel applied to the opposite (anterior or palmar) aspect of the hand and forearm would help. I would expect for CRPS in particular that larger electrodes and more channels for a longer time period, more often per day would be especially good, as it would allow more stimulation over a greater area with lesser discomfort, and combined with longer more frequent treatments would allow the person to decrease pain faster, so as to work up to higher TENS intensities, to where they could then make one of the daily sessions an EMS session to better improve muscle strength, endurance and circulation.

    After the above 2016 study I have to go back to 1988 to find another paper describing the use of TENS on humans with CRPS.

    Reflex sympathetic dystrophy in children: treatment with transcutaneous electric nerve stimulation. Kesler RW, Saulsbury FT, Miller LT, Rowlingson JC. Pediatrics. 1988 Nov;82(5):728-32.

    Abstract
    During the past 6 years, ten children with reflex sympathetic dystrophy were treated. Pain in an extremity was the initial complaint in all patients. The pain was unilateral in 90% of the patients; upper and lower extremities were affected with equal frequency. Tenderness to palpation, extreme hyperesthesia, and dysesthesia were other dominant features. All patients had some evidence of autonomic nervous system dysfunction in the affected extremity (swelling, color change, decreased temperature, and/or hyperhidrosis). The median duration of symptoms prior to referral and diagnosis was 5 months. All children were treated as outpatients with a transcutaneous electric nerve stimulator and home-based physical therapy. With this regimen, seven patients had complete remission within 2 months. Two other patients improved with transcutaneous electric nerve stimulation therapy, and one patient had no response to transcutaneous electric nerve stimulation. Reflex sympathetic dystrophy is frequently underdiagnosed in children. Increased awareness of this syndrome is important because accurate diagnosis is crucial and transcutaneous electric nerve stimulation offers a safe, simple, and effective outpatient therapy for reflex sympathetic dystrophy in children.
    Quotes

    “The initial treatment for our patients after our evaluation was the use of trancutaneous electric nerve stimulator for one hour four times daily. The pateints were instructed to place the electrodes over the vascular supply to the extremity and to adjust the voltage to the level of comfort. Physiotherapy was taught to the patients, and they were encouraged to exercise the affected extremity.”

    “The signs and symptoms of reflex sympathetic dystrophy improved in nine of the ten patients. In fact, seven patients experienced complete remission within 2 months of treatment.”
    “Following the introduction of the “gate control theory” of pain by Melzack and Wall, there was great interest in the use of electrical stimulation for the relief of pain. The Gate theory states that nonpainful stimulation of the peripheral nervous system can interfere with the relay of pain sensations in the CNS. This theory may explain why transcutaneous electric nerve stimulation appears to be effective in reducing pain.”

    My comments:

    The results from above are amazing but seem credible to me. My only fault with the paper is that they didn’t describe the parameters (pulse width, rate, duty cycle, etc.) of the TENS used, however perhaps what parameters they used isn’t as important as the fact that they used those parameters four hours a day (60 minutes, four times). That’s 12 times as much as the above mentioned study, plus they were doing the TENS daily instead of a few times per week. That might be enough to explain why they are talking about how 7/10 were cured, instead of “significant improvements” over a control group.
    That does seem one of the common themes as I read about TENS for pain control is that regardless of parameters used, TENS works in a dose response relationship, and four hours a day is a pretty good dose. I would caution that for that long of treatment, I’d think you would want to be using a reasonably light current. My 10-50-10 EMS or even 5 hz aerobic EMS would maybe only be best done once per day, though that still would depend on the intensity of muscle contractions given.
    Also I thought their description of gate control theory was both concise and accurate, and I believe is the primary reason that TENS (and EMS too) work to decrease pain.

    Beyond the above paper I had to go back to the 70s to find research on people.

    Reflex sympathetic dystrophy: successful treatment by transcutaneous nerve stimulation. Richlin DM, Carron H, Rowlingson JC, Sussman MD, Baugher WH, Goldner RD. J Pediatr. 1978 Jul;93(1):84-6.

    Quotes

    “This is a report of a 3 ½-year-old boy with this syndrome successfully treated…”

    “This previously healthy child suffered a right sciatic nerve injury following an intragluteal injection of an antibiotic.”

    “The patient was begun on intermittent transcutaneous nerve stimulation… …set at 40 Hz, pulse width 80 microseconds, and voltage just below the point of discomfort. The proximal electrode was placed over the right femoral triangle and the distal electrode over the dorsum of the right foot. Stimulation was applied for 30 minutes, three times a day, for ten days by the physical therapist.”

    “The patient was re-evaluated five days after starting treatment when a notable decrease in hyperalgesia and an increase in the ability to actively extend the right leg at the knee were noted.”

    “Two days later the patient was free of all pain on both manipulation and palpation of the right leg and foot.”

    “Four weeks following institution of stimulation, the patient was pain free and walking with a drop foot brace. Active plantar flexion of the toes indicated returning S1 function.”

    My comments:

    If it were me, 30 minutes, three times a day, is probably where I would start. I’ve tried and sometimes use a similar electrode placement with an electrode over the femoral triangle, however I put the other on the bottom of the foot rather than the dorsum (top). I expect each would work but the sole of the foot being meatier should be more comfortable. In each case having the electrodes so far apart gives very deep stimulation, which I think would be ideal for CRPS. I would add that given that the child still had drop foot, four weeks later it would have been interesting to know what would have happened if EMS currents were applied to the tibialis anterior muscle after the ten days of TENS had eliminated pain.

    Transcutaneous electrical nerve stimulation in chronic pain after peripheral nerve injury. Bohm E. Acta Neurochir (Wien). 1978;40(3-4):277-83.

    Abstract
    Transcutaneous electrical stimulation was tested in 24 patients with chronic pain following a peripheral nerve injury in an extremity, in 10 patients with a good effect. All of these 10 patients displayed signs of increased sympathetic activity in addition to hyperalgesia. Sympathetic block gave complete freedom from pain. In 14 patients with the same symptomatology but without an increased or with only very slightly increased sympathetic activity, no or an insignificant effect was obtained. Sympathetic block did not relieve the pain in this group. Transcutaneous electrical stimulation should be tried as an alternative to sympathectomy in causalgia major or minor.
    Quotes

    “Commercially available simulators were employed. The electrodes were placed over the nerve central to the lesion at the site where the stimulation caused paraesthesiae radiating into the painful area. As a rule the patients themselves arrived at the most suitable frequency and intensity of the stimulation.”

    “In this series of patients with chronic pain after peripheral nerve injuries transcutaneous electrical stimulation was found to be of great value. The presence of increased sympathetic activity and complete elimination of pain by sympathetic block seems to be prerequisites for successful therapy with this method.”

    My comments:

    Of the 24 patients they report 3 had “permanent freedom of pain”, 7 had “good/excellent effect”, and 14 had “no or transient effect.”

    In this study the results seem good but not as great as noted above. Reasons for the differences are plenty. First they all had peripheral nerve injury which today would make them classify as CRPS (type II) which is less common and generally more severe than the type I variant, without obvious nerve injury. They also noted the patients had already “undergone repeated operations on peripheral nerves” indicating they were likely some of the toughest of cases, putting generally good results in some perspective.
    Unfortunately these researcher didn’t give even basic information about the type of stimulation used, and while they say frequency and intensity were varied by the patient, they didn’t say how long or often the stimulation was applied. It sounds like the TENS was applied in single doses to see what would happen in combination with other treatments to include nerve blocks or surgical procedures. Interestingly they placed the electrodes proximal (above or closer to the body) to the nerve injury, which I think might be a good option if the site of injury and below is too sensitive to be touched, perhaps at least early on. Later I think there are advantages, including the delivery of more current with the electrodes placed both above and below (or on) the painful area. Also I wonder if could have been improved, particularly in the 7 who had “good/excellent effect” and the 14 with “no or transient effect” if the stimulation was provided longer or more frequent.

    Case History Number 96: Reflex Sympathetic Dystrophy In a 6-Year-Old: Successful Treatment by Transcutaneous Nerve Stimulation. STILZ, R. J. MD; CARRON, H. MD; SANDERS, D. B. MD, Anesthesia & Analgesia: May/June 1977 – Volume 56 – Issue 3 – ppg 438-442

    Quotes

    “This otherwise healthy child suffered a traction injury to her right sciatic nerve.”

    “The condition persisted unchanged to the time of admission, 3 months after her initial injury.”

    “Electrodes were arbitrarily placed over the right femoral triangle and the dorsum of the right foot. The frequency of stimulation was set at 90 Hz and the current at 2.5 ma, at which point a tingling but not painful sensation was noted by the patient. Later, these settings were changed to 50 Hz and 3.5 ma, which produced better pain relief.”

    “Within 24 hours after initiation of the stimulation, definite improvement in color and reduced hyperesthesia [pain sensitivity] were noted…”

    “The patient was then discharged from the hospital and was instructed to use the stimulator continuously at home; she was also strongly urged to bear weight on the foot.”

    “There was little subjective change in symptoms over the next 3 days, but late on the 4th day, the patient began to experience significant relief of pain. On awakening on the 5th day following institution of stimulation, she was pain free and able to walk on the foot without discomfort.”

    My comments:

    This is just a case study, but I find a lot of clinical wisdom in some of the older electric stimulation case studies. Again they used the femoral triangle/top of foot electrode placement. Stimulation frequency was reduced from 90 Hz to 50 Hz but I doubt that had much to do with the better pain relief. Rather I would think that due to the increase of current amplitude from 2.5 to 3.5 mA, which is still really low so I would guess they were using a machine with a wide pulse width (uS) though that information wasn’t given. But such low stimulation would explain why they were able to just turn the machine on, and leave it on. And perhaps the long duration of stimulation led to the remarkable short term recovery. The authors go quote Meyer and Field’s 1972 paper, but since I have that paper myself I’ll do it like I want right now.

    Causalgia treated by selective large fibre stimulation of peripheral nerve. Meyer GA, Fields HL. Brain. 1972;95(1):163-8.

    “An accessible site, central to the point of injury was then selected for stimulation. The
    stimulation parameters were 01 msec duration, unidirectional square pulses of variable voltage,
    delivered at a rate 100 Hz. Electrodes consisted of insulated stiff copper wires, tipped with stainless steel balls of 3 mm diameter and 2 cm separation moistened with electrolyte paste and applied directly over the course of the nerve trunk being stimulated. If the electrodes were properly placed, paraesthesiae were elicited in the distribution of the nerve stimulated (Wall and Sweet, 1967). Although we did not monitor stimulus current, the voltage was adjusted so that no motor activity was produced and the sensation perceived was not reported as painful. This ensured that only larger diameter, more rapidly conducting fibres were activated (Collins et ah, 1960).”

    “In order to produce satisfactory paraesthesiae it was necessary to stimulate a section of nerve proximal to the point of injury. Stimulation of affected nerves distal to the lesion usually exacerbated the pain, while stimulation of intact, near-by nerves was ineffectual. We were not able consistently to stimulate the sciatic or tibial nerve by the transcutaneous technique. In all cases, the upper extremity nerves were stimulated at the anterior axillary fold and the common peroneal was stimulated at the knee.”

    “After paraesthesia; had been elicited in an area supplied by the nerve being stimulated for at least two but no more than three minutes, the stimulator was removed and the patients were asked if there had been any change in their condition.”

    “If the electrodes were properly placed, the effect of stimulation was immediate dramatic relief of pain during stimulation for six of the eight cases. After stimulation, pain relief persisted for periods varying from five minutes to ten hours. Although the degree of pain relief varied from patient to patient, it was consistent for a given patient from trial to trial.”

    “Two patients… …were able to begin physical therapy following their first trial of stimulation. Both patients were free of severe pain within one weak.”

    “In general, the earlier treatment is instituted, the more likely it is to be successful.”

    My comments:

    I think this is the 2nd oldest paper on TENS and causalgia, Wall and Sweet 1967 is cited by them as having performed the same procedures with similar results. There are all kinds of insights in this paper, such as making sure the nerve you stimulate is proximal (above) the area injured but that it must include the nerve that covers the affected area. That was a similar finding as what was talked about in the percutaneous (surgically implanted) electrodes for chronic migraine headaches and my own use of transcutaneous electric stimulation agrees with this. They report that placing the electrodes distal (below) the site of injury was generally irritating. However, my own experience with neuropathy (another kind of nerve pain) is that distal placement works well, however I will criss cross the electrodes placing one electrode on the right foot and the other from that same channel on the left such that the simulation runs very deep, up one leg and back down the other. Also in several of the settings described above in the more recent papers they were putting the electrodes both proximal and distal to the painful area, which I think also makes sense and seemed to work really well. With the above and below method, I would expect the proximal electrode to lessen any discomfort imparted by the distal electrode and the amount of stimulation coursing through the injured area to be greater, hopefully leading to better results. So I think in treating a person with CRPS you just don’t want to be dogmatic, you want to have a number of ideas (regarding where to put the electrodes, how many electrodes to use, how to program your machine, and how often and how long to apply the stimulation) to try and experiment with several before deciding on what’s best in general and for a particular person. Also these guys noted that the electric stimulation sometimes gave the pain relief necessary so that the people could begin physical therapy immediately afterwards. So I would think that’s the way to go, TENS or EMS first, with exercise afterwards in the pain reduced afterglow of electric stim, or perhaps sandwich physical therapy exercises between EMS and TENS sections, such that the electric stimulation could again be used to bring down pain that might have been increased with exercise. For most orthopedic conditions I do both EMS or TENS afterwards, but I did have a stroke patient with terrible neuropathic pain in her leg that put her in a wheelchair. This was early on as I was really starting to learn the ins and outs of EMS. I said to her we could try EMS (I did a 10-50-10 program on her) first and I think you’ll either really love it or really hate it. It turned out she loved it, and was able to walk with a cane immediately afterwards. She got a stimulator for home off ebay and fully recovered her ability to walk within 2-3 weeks. After that I thought, maybe I need to have these things on hand.

    Anyways, that’s my comments for now. I’ll add to this review as I find new papers or have more first hand observations to add.

    As always, thanks for reading my blog. While not all my blogs are about electric stimulation a good number of them are, with low back pain being another favorite topic of mine, and for which in my office I almost always use EMS as part of the treatment. So I get a lot of questions about what EMS/TENS machines are best. I haven’t tried them all, but the sweet spot for both performance, price, custom programmability is the Globus Genesy 300. On a budget the EV-906 is good, programmable and what I started with but not as powerful or user friendly as the Globus. If a two channel stimulator is all you need (and for CRSP it might be) I’m really liking the TwinStim4. I’m sure it’s a little self serving that I promote the one I sell, but if you read my notes from my year of EMS you’ll see I’m selling the one’s I think are best. Since there was no one stop shop that sells the machines I like, with the the pads and straps I like, I started my own. In fact I had to get my straps custom made and order 1000 of them to get any kind of discount. So I hope they sell, haha. So check out my shop.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Pain in the Butt, Sacroiliac Pain as Tendinopathy?

    I recently finished the 3rd edition Stuart McGill’s “Low Back Disorders.” I’ve followed his work since reading edition 2 and bulk of my back pain treatments are based on, or consistent with it and his more recent research. For those who don’t know, McGill is a Professor of Spine Biomechanics at the University of Waterloo in Canada, for which he focuses entirely on low back pain. Subsequently, more of my back pain blogs reference his research than any other source.

    I was wondering what was new in the 3rd and if it were worth buying and reading through. In short, it was both. The basic gist of his treatment hasn’t changed (but there was a lot of additional detail and ideas). Said gist to eliminate back pain is to lessen the injury causing stress from daily activities, while working on exercises (to make the person fit enough) and motor skills (to make them coordinated enough) to better tolerate the rigors of life without reinjury. I 100% endorse those principles.

    All the above is all filler, and sets up what I wanted to get too, which was one of the more interesting sections new to the 3rd edition of Low Back Disorders which I have never seen mentioned anywhere else. The observation appears to be anecdotal, but it’s Stuart McGill’s anecdote, which means something, and I also happen to think this observation is often correct. On page 142 he talks about sacroiliac pain (literally pain in the butt) with the following being a few of his quotes:

    “Boguk and colleagues (1996) proved that some low back pain is from the sacroiliac joint itself. The following discussion offers other considerations.”

    “One possibility worth considering is that the high muscular forces may damage the bony attachments of the corresponding muscle tendons. Such damage has perhaps been wrongfully attributed to alternate mechanisms.”

    “It is known that a large portion of the extensor musculature obtains its origin in the SI and posterior superior iliac spine (PSIS) region (Bogduk, 1980). The area of tendon-periosteum attachment area for connective tissue places the connective tissue at high risk of sustaining microfailure, resulting in pain (McGill, 1987).”

    “This mechanical explanation may account for local tenderness on palpation associated with many SI syndrome cases.”

    My comments:

    McGill didn’t use the the word tendinitis, or more accurately the words tendinosis and tendinopathy. However, when he uses the words “microfailure” of the “tendon-periosteum attachment area” of the spine “extensor musculature” at it’s point of “origin in the SI and posterior superior iliac spine” it sure sounds like he’s describing tendinosis, with the resulting pain being tendinopathy of the spine extensor tendons. So far there is zero research describing tendinopathy in this region, but there is no reason I can think of why it couldn’t be. Also thinking about it, gluteus maximus also attaches right there, along the SI joint region as well, so it’s tendinous region could be involved as well, while all this time it’s been blamed on the SI joint or the piriformis muscle (which I have never seen get better stretches either).

    The SI joint as a source of motion or pain has long been a source of debate in physical therapy, with studies and arguments pointing for and against for decades. I’ve never been passionately drawn to either side of the argument. However, I have stress tested a lot of SI joints and rarely do I find those tests positive for pain, and if the tests are painful, I think it’s still hard to tell if the SI joint itself is the source. Also I’m skeptical treatments directed at the SI joint reliably decrease that pain. I wouldn’t go so far as to say they never do, but just not often enough to make such treatments worth routinely doing. I’ll add that sometimes when there is debate and no clear answer, it’s because there’s something amiss and it wouldn’t be the first time that tendinopathy reared it’s head in an unbenounced place. Another reason I don’t usually give SI pain special attention is my SI pain patients generally get all the way better with my somewhat standard low back treatment protocol. So thinking about what McGill wrote above, how I treat back pain and how I treat tendinopathy, I have a idea as to the reason why.

    That reason is that my treatment protocol for back pain, bares more than a passing resemblance to my treatment for tendinopathy. In short, I’m basically treating for both already. Besides biomechanical and postural counseling, teaching the person with back pain how to better maintain a neutral spine during the day, I have them work to increase basically total body strength and endurance emphasising spine stability and hip mobility, with an exercise program that is generally 3 sets of 15 reps, with easy-medium-hard resistance levels. I have them progressing the weights on the next visit if the person is able to get all three sets without pain and with good technique on the prior treatment. That’s almost identical to how I treat tendinopathy, with an example being tennis elbow (aka shooter’s elbow described here) or coracoidopathy described here. In both cases I try to increase strength and endurance of all the muscles stabilizing the affected area, followed by focused strengthening of the affected muscle/tendon with 3 sets of 15 reps ( also easy-medium-hard resistance levels).

    So if a person has tendinopathy of their spine extensor muscles (or gluteus maximus) where they attach on or near the SI joint, that would explain why my back pain type sets and reps, has hitherto resolved those symptoms without me even considering tendinopathy of the area being a possible cause.

    Some considerations I’ll be thinking about going forward is that with back pain I endeavor to never have my patients train through pain, however with tendinopathy I try to use a resistance level that causes some pain, noting that pain almost always stays the same/or lessens in spite of increasing weights from set to set. With back pain, for which I might suspect a bulged (nearly bulged) or herniated disc, training through pain usually results in a worsening the person’s condition from one set to the next. Also with tendinopathy I notice people get better faster if they do the exercises every day rather than three times a week and my observation does have empirical support.

    So if there is SI region tendinopathy I think it’s probably better to error on the site of caution and not increase resistance levels if there is any pain, which thus far seems to be working well enough. However, if the person has SI region pain, no lumbar or radicular symptoms (leg pain and tingling) I might consider a slightly more aggressive (slightly more specific tendinopathy) type approach. However, I imagine there is a lot of overlap between both conditions, such that if someone has spine extensor tendinopathy, they very likely have some spine disc or ligament issues as well even if they don’t have pain yet, so daily pain free resistance exercise of the spine and hip extensor muscles (with the spine kept neutral throughout) is maybe the safest and best approach.

    For the record, I suspect upper back pain and tenderness where the levator scapula muscle attaches to the scapula is sometimes and maybe often be tendinopathy too. Which seems to resolve with my basic neck pain protocol, which like my back pain treatments includes (your guessed it) progressive resistance training with 3 sets of 15 reps (easy-medium-hard).

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Mental & Physical Effects of Drumming (Chad’s Review)

    About a year ago I got the idea I was going to buy a djembe. I can’t even remember for sure why but I think I was reading Eliade’s book on Shamanism, which round about came after reading neuroscientist Sam Harris’ book Waking Up. I banged on the drum a few times, thought it was moderately cool, but not enough to continue regularly. Then circumstances conspired to send me to Burning Man in August/September of 2016. At Burning Man I made a lot of new friends who were into dance, bass beats, and eventually drum circles. I joined in and found it an overall enjoyable experience; more so than drumming by myself.

    Later, looking up papers on something I came across the following paper on drumming and mental health (depression, anxiety, overall mental state, and more just as interesting inflammatory biomarkers). Doing additional pubmed searching on group drumming, drum circles, etc. led to a number of papers I want to read, which I think will make for a good review blog adding papers as I go. I’m not sure how this relates to physical therapy yet but my experience in treating low back pain leads me to believe that a lot of health issues do not improve from fixing one thing, but rather a number of factors. Such that you don’t take steps to curb enough unhealthy factors then you aren’t going to cure the problem. So maybe drumming, dancing and singing or lack thereof, relates to both physical and mental health along with diet, exercise, sleep patterns, and circadian rhythms that overall make people healthier and happier. Since integrative medicine is (according to critics) just a mixture of real medicine and placebo, I’m hoping to science it up a bit as “real medicine” often seems to miss a lot, and “alternative medicine” does have a lot of flaws.

    Anyway, here’s data from the first two studies I read, updates will be added below.

    Study 1
    Synchronized drumming enhances activity in the caudate and facilitates prosocial commitment–if the rhythm comes easily. Kokal I, Engel A, Kirschner S, Keysers C. PLoS One. 2011;6(11):e27272. [FREE FULL TEXT]

    Quotes from study:

    “One hypothesis claims that music and dance are culturally evolved tools for fostering group cohesion and commitment, thereby increasing prosocial in-group behavior and cooperation…”

    “…participants who drummed with a ‘synchronous’ drum partner in the last part of the experiment showed more prosocial commitment towards this drum partner than those who drummed with an ‘asynchronous’ drum partner. These effects were stronger in participants that acquired the rhythm more easily.”

    “These results are consistent with behavioral studies that demonstrate a link between synchronized musical activity and prosocial behavior…”

    “…our results suggest that this may be true only for activities a particular individual masters easily…”

    “…the ease of rhythm imitation was significantly positively correlated with brain activity in the right caudate, which in turn predicted the number of pencils the participants picked up.”

    “By showing an overlap in activated areas during synchronized drumming and monetary reward, our findings suggest that interpersonal synchrony is related to the brain’s reward system.

    My comments:

    This was the first paper I read and they had 18 healthy volunteers without any music training finger drum on bongos while they observed brain activity with functional magnetic resonance imaging (fMRI). While doing so, subjects were rated on how easily they picked up the rhythm, and later with someone playing either in sync with them or out of sync. They found that if the rhythm was easier to pick up, activity in the brain linked with cooperation (the caudate) was increased and that if their co-drummer played in sync with them it improved cooperation. This was tested behaviorally by having the experimenter “accidentally” drop 8 pencils and seeing how many the subject helped pick them up. The increase in cooperation with drumming in sync drumming resulted in subjects to pick up ~5.5 pencils, while out of sync drumming resulted in them picking up just pick up ~1.5 pencils on average. Having been in a few drum circles as of late, the above definitely sounds plausible.

    Study 2
    PLoS One. 2016 Mar 14;11(3):e0151136.Effects of Group Drumming Interventions on Anxiety, Depression, Social Resilience and Inflammatory Immune Response among Mental Health Service Users. Fancourt D, Perkins R, Ascenso S, Carvalho LA, Steptoe A, Williamon A. [FREE FULL TEXT]

    Quotes from study:

    “Growing numbers of mental health organizations are developing community music-making interventions for service users; however, to date there has been little research into their efficacy or mechanisms of effect. This study was an exploratory examination of whether 10
    weeks of group drumming could improve depression, anxiety and social resilience among service users compared with a non-music control group…”

    “Furthermore, it is now recognised that many mental health conditions are characterised by underlying inflammatory immune responses.”

    “A much less researched area is whether general music making within community settings, not led by therapists…”

    “One of the community music interventions growing in popularity for mental health is group drumming, perhaps due to the inclusiveness of drumming circles, lack of fine motor skill requirements and strong steadying rhythms.”

    “Furthermore, research over the past two decades has demonstrated that many mental health conditions are characterized by an underlying imbalance between pro- and anti-inflammatory cytokines (proteins within the immune system), weighted towards a pro-inflammatory response.

    “Unlike music therapy, the professional drummer was not told details of participants’ backgrounds or psychological profiles and did not have specific psychological or therapeutic aims.”

    “…to reduce the bias of having control subjects who were merely more socially isolated than the experimental group, all control subjects were already regular participants in community group social activities (e.g. quiz nights, women’s institute meetings and book clubs) and continued with these activities for the duration of the study.”

    “The overall decrease in anxiety from baseline in the drumming group averaged 9% by week 6 and 20% by week 10.”

    “The overall decrease in depression from baseline in the drumming group averaged 24% by week 6 and 38% by week 10.

    “The overall improvement in social resilience in the drumming group averaged 16% by week 6 and 23% by week 10.

    “…wellbeing scores… …improvement in the drumming group averaged 8% by week 6 and 16% by week 10.

    “When levels of TNFα and IL4 were assessed, there was a shift away from a pro-inflammatory profile towards an anti-inflammatory response. The changes noted in these cytokines are relatively small so future research remains to be carried out as to their biological significance.”

    My comments:

    This paper is interesting for a number of reasons. Unlike the above paper, the subjects were not otherwise healthy but were a diverse group undergoing concurrent mental health services with an average mild depression, moderate anxiety, and below average social resilience. All of which were improved with the drumming sessions and all of which further improved after 6 weeks and further so after 10 weeks. They used a djembe drum (the one I have) and performed in a drum circle where the leader did not know about nor care to address any particular psychological pathologies.

    It would be interesting to know if there is a dose response relationship where increased weeks, sessions per week, or minutes per session led to further improvement, and then what is the optimal dose. Looking at the 10 week over 6 week improvements, it does not appear they were hitting a ceiling of benefits and improvements were largely maintained 3 months post. Personally I’d like to see the control group having some kind of intervention rather than continuing social activities as usual, even if they went out of their way to find a social control group.

    The above paper is also interesting to me in that it looked at inflammatory markers in relation to mental health and how they improved somewhat with the drumming. I read a number of papers looking at BDNF and mental health and blogged about it. I think this is worth further reading to find out whether and how much other favorite interventions of mine like exercise, caloric restriction and intermittent fasting might overlap with regards to systemic inflammatory mediators, and I’ll bet money they do. However, unlike exercise, diets, and fasting, drumming is actually fun.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Coracoid Pain Test does NOT diagnose Adhesive Capsulitis

    Coracoid pain test: a new clinical sign of shoulder adhesive capsulitis.Carbone S, Gumina S, Vestri AR, Postacchini R. Int Orthop. 2010 Mar;34(3):385-8.

    “Patients with adhesive capsulitis were clinically evaluated to establish whether pain elicited by pressure on the coracoid area may be considered a pathognomonic sign of this condition. The study group included 85 patients with primary adhesive capsulitis, 465 with rotator cuff tear, 48 with calcifying tendonitis, 16 with glenohumeral arthritis, 66 with acromioclavicular arthropathy and 150 asymptomatic subjects. The test was considered positive when pain on the coracoid region was more severe than 3 points (VAS scale) with respect to the acromioclavicular joint and the anterolateral subacromial area. The test was positive in 96.4% of patients with adhesive capsulitis and in 11.1%, 14.5%, 6.2% and 10.6% of patients with the other four conditions, respectively.”

    “The coracoid pain test could be considered as a pathognomonic sign in physical examination of patients with stiff and painful shoulder.”

    “In conclusion, digital pressure over the coracoid area elicits pain in the vast majority of patients with adhesive capsulitis and, thus, it can be considered an easy and reliable clinical test for identifying patients with or without this condition. Based on its sensitivity and predictive values, it may represent a “cardinal test” for this condition.”

    My comments:

    These authors are claiming that the “coracoid pain test” is useful for the diagnosis of frozen shoulder. I think they are mistaken, and here’s why:

    Adhesive capsulitis (aka frozen shoulder) is a common but poorly understood shoulder condition for which sufferers generally note diffuse yet severe shoulder pain, combined with a loss of active range of motion (AROM), or how far you can move you shoulder on your own and passive range of motion (PROM), or how far someone else can move your shoulder. The above authors are suggesting that a tender coracoid process is a cardinal/pathognomonic sign of adhesive capsulitis.

    I had to google the meaning of pathognomonic sign, which is “a particular sign whose presence means that a particular disease is present beyond any doubt.”

    Well, here’s doubt; which I describe at length in my blog Coracoidopathy the Missing Link in Shoulder Pain. The gist is that there are three tendons attaching to the coracoid process for which Karim 2005 thinks the coracobrachialis (CB) and the short head of the biceps (SHB) are the source of pain. Bhatia 2007 thinks the pectoralis minor (PM) tendon is the source of pain (I disagree but think they’re close), which I discuss specifically in my blog Bench Press Shoulder Pain. Gigante 2016 further confirmed Karim’s results where they diagnosed “coracoid syndrome” (what I call coracoidopathy) also treated with a corticosteroid injection to the coracoid process.

    One reason I think Karim and Gigante are correct (more so than Bhatia) is that, besides tenderness with palpation to the coracoid process, I also use an isometric Speed’s test as a strength test to stress the SHB and CB. I find the Speed’s test is often relatively weak and painful. Anatomically the Speed’s test should not stress the PM muscle because the PM does not act to flex the shoulder. Another reason I don’t primarily suspect the PM is that I find warming up with supinated front raises (SFRs) to strengthen the SHB and CB prior to bench pressing usually and immediately lessens bench press (if performed right after) associated shoulder pain. If the PM were the primary source of pain, the SFRs shouldn’t work (lessening pain by warming up the affected tendons) again because the PM does not flex the shoulder.

    Where I think Carbone 2010 (above), go wrong is they weren’t able to find either Karim’s or Bhatia’s paper in their lit review. As such, enthesitis, tendinitis, tendinosis or tendinopathy of the tendons attaching to the coracoid process appear not to have been a consideration for differential diagnosis. In my shoulder population only 18% of my coracoidopathy patients also had frozen shoulder, which I treat as two separate conditions. With coracoidopathy combined with frozen shoulder I just combined the treatments (coracoidopathy plus frozen shoulder) thus I strengthen the SHB and CB (often with rotator cuff (RTC) and scapular stabilization exercises as needed), plus shoulder stretching exercises given to treat the lost range of motion secondary to the adhesive capsulitis. A full 82% of my shoulder pain patients who had tenderness over coracoid process did not have the lost range of motion indicative of frozen shoulder. Researchers Karim, Bhatia, and Gigante didn’t report a loss of range of motion in their patients with coracoid process tenderness either.

    Consequences of misdiagnosing patients with adhesive capsulitis because of a tender coracoid process would include largely ineffective treatment with perhaps unnecessary stretches and misplaced intracapsular cortisone shots. When such treatment didn’t work it might result in an unnecessary and ineffective surgical treatment, perhaps an acromioplasty.

    The other thing that bothers me about using a tender coracoid process as the pathognomonic or cardinal sign of adhesive capsulitis is that it just doesn’t make any obvious sense. Adhesive capsulitis is thought to occur as the joint capsule of the shoulder becomes inflamed, adherent and shrinks resulting in pain and loss of range of motion. However the coracoid process is an extra-capsular structure, which means it lies outside the inflamed joint capsule, such that there is perhaps an association but no clear and causal link between one and the other.

    Plus adhesive capsulitis already has what I think is a cardinal sign, which lost shoulder PROM. Such that if I am doing my standard shoulder evaluation, looking at AROM, PROM, resistive tests, followed by palpation. I’m already going to find out if there is adhesive capsulitis. A patient with RTC tendinopathy or tearing might have difficulty, pain, and loss of AROM, combined with painful resistive tests of the RTC musculature, plus likely tenderness over one or more of the RTC tendons. However, PROM should be intract. A person with adhesive capsulitis will have limitations in both AROM and PROM while resistive tests are generally not that irritating. A patient with coracoidopathy will likely have pain and weakness with supinated shoulder flexion (isometric Speed’s test) and will, in my experience certainly be tender with palpation over the coracoid process.  I think combinations of the above are common, which can be very confusing if you are not aware that coracoidopathy is a potential diagnosis/confounder.

    So I think the “coracoid pain test” is certainly an important test that should be performed with every shoulder evaluation (it only takes 5 seconds) but I don’t think it’s indicative of a diagnosis of adhesive capsulitis. Rather I think it it is frequently comorbid with adhesive capsulitis.

    As noted the bulk of what I have to say about the diagnosis and treatment of coracoidopathy is here. In fact here’s a video of one patient (of many) with an obvious positive coracoid pain test and no loss of AROM or PROM, thus obviously not a pathognomonic sign of adhesive capsulitis.

    I’m gradually writing more about the coracoidopathy, comparing and contrasting with other diagnoses and treatments here.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Exercise and Neuropathy (Chad’s Review)

    I’m intending to make this blog a review of pertinent research on exercise and neuropathy and making comments with regards to my thoughts and how it affects my current treatment programs for neuropathy. I’ll be updating and adding studies to it as they come out (thus far there aren’t many) or as I locate them, with the most recent research being on top.


    Exercise increases cutaneous nerve density in diabetic patients without neuropathy. Singleton JR, Marcus RL, Jackson JE, K Lessard M1, Graham TE, Smith AG. Ann Clin Transl Neurol. 2014 Oct;1(10):844-9

    “Exercisers increased IENFD at both ankle and proximal thigh, while controls showed a small decline in IENFD at both sites.”

    “While other neuropathy measures were not significantly different between groups at 12 months there was a trend toward slower progression of UENS and other neuropathy measures in the exercise group.”

    “Together, these results support the concept that distal nerve fiber injury may occur in patients with diabetes prior to neuropathy symptom onset, and that cutaneous axons can regenerate in response to metabolic improvement.”

    “IENFD specifically evaluates distal unmyelinated axons and thus does not directly assess large myelinated fibers. However, IENFD is correlated to large fiber surrogates, including NCS, among patients with diabetic neuropathy.”

    My comments

    IENDF means “intraepidermal nerve fiber density” which is the number of nerve fibers in the skin, which is lessened in those with neuropathy and those about to get neuropathy.

    The exercise program was a year long. Aerobic exercise ramped up from a supervised 30 min per week at 65% of max heart rate (MHR) and progressed to 50 minutes at 85% MHR by week 7. They also lifted weights, doing 2-3 sets of 12 reps. They were given a non-described home exercise program consisting of both aerobic and strength training in addition to the supervised exercise. The subjects also received nutritional counseling.

    Unlike to the below (Kluding 2012) study this one was able to show distal (at the ankle) nerve regrowth. However it’s impossible to tell if that’s because the treatment program was longer (a year vs 10 weeks) or if it was because of non-described dietary interventions, or because the subjects had nerve fiber damage that hadn’t yet progressed to the point of neuropathy. Still it’s great news that diet and exercise can reverse peripheral nerve damage.


    The effect of exercise on neuropathic symptoms, nerve function, and cutaneous innervation in people with diabetic peripheral neuropathy. Kluding PM, Pasnoor M, Singh R, Jernigan S, Farmer K, Rucker J, Sharma NK, Wright DE. J Diabetes Complications. 2012 Sep-Oct;26(5):424-9.

    “Significant reductions in pain (-18.1±35.5 mm on a 100 mm scale, P=.05), neuropathic symptoms (-1.24±1.8 on MNSI, P=.01), and increased intraepidermal nerve fiber branching (+0.11±0.15 branch nodes/fiber, P=.008) from a proximal skin biopsy were noted following the intervention.”

    “This is the first study to describe improvements in neuropathic and cutaneous nerve fiber branching following supervised exercise in people with diabetic peripheral neuropathy. These findings are particularly promising given the short duration of the intervention, but need to be validated by comparison with a control group in future studies.”

    “Significant improvements were observed following exercise in the number of branches per fiber in the proximal biopsy site, although no significant improvements were noted in the distal IENF measures or proximal IENF density. This may reflect less extensive damage in proximal nerve fibers, or earlier response of these fibers to exercise-induced plasticity in a 10-week intervention. Although the change in IENF density was not statistically significant, the observed increase in this measure is consistent with modest 30% increase in IENF density following 1 year of lifestyle intervention (Smith et al. 2006).”

    My comments:

    The exercise program was 10 weeks long starting with 2 days per week of cardio (on various machines) 30 minutes per day at 50% VO2R (reserve aerobic capacity) and progressed to 50 minutes two days per week at 70% V02R. Strength training started with 1 set of 10 reps 1 day per week and progressed to 1 set of 20 reps a set 2 days per week. The strength training exercises were crunches, bicep curls, chest press, lat pulls, leg extensions, seated leg curls, seated rows, shoulder presses, squats, and tricep presses.

    None of the patients had increased neuropathic pain with the average reduction of pain being 18.1 points on a 100 mm scale. Converting that to common language, if you had neuropathy pain of 6/10 to start, after 10 weeks the pain was reduced about 2 points to a 4/10. Nerve fiber density was increased in the thigh but not at the ankle. So the good news is that the exercise seemed to help, but the bad news is that regarding neuron innervation it doesn’t sound like it helped as much lower down on the foot where it’s most needed.

    The subjects had a an average BMI of 35 (obese) that wasn’t changed at all with the exercise. So probably diet in addition to the exercise would help with weight loss, and would also lessen foot pressure when standing and walking, and likely have positive effects on nerve health as well.


    Lifestyle intervention for pre-diabetic neuropathy. Smith AG, Russell J, Feldman EL, Goldstein J, Peltier A, Smith S, Hamwi J, Pollari D, Bixby B, Howard J, Singleton JR. Diabetes Care. 2006 Jun;29(6):1294-9

    Baseline distal IENFD was 0.9 +/- 1.2 fibers/mm and proximal IENFD was 4.8 +/- 2.3 fibers/mm. Baseline distal IENFD correlated with fasting glucose (P < 0.001) and OGTT (P < 0.01). After 1 year of treatment, there was a 0.3 +/- 1.1-fiber/mm improvement in distal IENFD and a 1.4 +/- 2.3-fiber/mm improvement in proximal IENFD (P < 0.004). The change in proximal IENFD correlated with decreased neuropathic pain (P < 0.05) and a change in sural sensory amplitude (P < 0.03).

    These findings indicate that diet and exercise counseling for IGT results in cutaneous reinnervation and improved pain. Skin biopsy was the most sensitive measure of neuropathy change over 1 year. IENFD should be included as an end point in future neuropathy trials.

    All subjects received individualized counseling with goals of reducing weight by 7% and increasing weekly exercise to 150 min. Dietary counseling occurred quarterly.

    “However, subjects who had absent epidermal fibers and loss of the dermal nerve plexus were unlikely to experience significant reinnervation. However, some with absent epidermal but preserved dermal fibers did experience reinnervation. Only 31% of subjects noted improvement in distal IENFD. In contrast, 70% experienced reinnervation at the proximal biopsy site.”

    My comments:

    Details about the diet and exercise counseling or adherence were not given, but the combination was apparently effective enough that there was mild weight loss (decreasing BMI from 32.1 to 31) over the year they were studied. Also they were able to show distal (ankle) nerve reinnervation, though noted it seemed difficult to achieve than proximal (thigh) nerve regeneration, and they noted that there is maybe a threshold where peripheral nerves are too long gone to come back. That would indicate that early onset of diet and exercise interventions would be in the best interest of those with prediabetes.


    My overall take home message

    I expect that 20-30 minutes of exercise every day would do more than 50 minutes two days per week. The strength training programs if described didn’t sound too bad, but if I were trying to increase lower leg circulation I’d make sure to include calf raises. However, as much as I’m a fan of strength training, I don’t expect the weights are as important as the aerobic exercise for nerve reinnervation. I do expect the strength training to help with neuropathy related disabilities such as strength balance loss. Also it seems like optimal reinnervation takes a long time to achieve and it’s best started before it’s too late.

    Also no biopsies were taken from the sole of the foot, and I don’t think there are any good conventional exercises that target the foot intrinsic muscles on the plantar surface of the foot. On the contrary electric muscle stimulation (EMS) contracts exactly the muscle that’s underneath the electrode. Plus EMS specifically lessens neuropathic pain, and with the parameters I use it does so nigh immediately. EMS might also be an ideal adjunct because those with type 2 diabetes aren’t known to be big exercisers and EMS can be done while watching TV. Still if I had type 2 diabetes my first priority would be REVERSING said diabetes, which research is indicating is possible. You just have to suffer HARD for eight weeks.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Coracoidopathy Diagnosis Confirmed in New Study

    This paper just came out in June this year confirming what I call coracoidopathy (tendinopathy of the short head of the biceps and coracobrachialis muscles where they attach at the coracoid process). They called it “coracoid syndrome,” which I might as well, if they had named it before I did, however I do feel like “coracoid syndrome” sounds a lot like “coracoid impingement syndrome” which isn’t at all the same thing.

    For what might be easier reading my write up on how I diagnose and treat coracoidopathy, how it relates to the bench press exercise, and how it differs from coracoid impingement syndrome is available. Since I think the condition is very common, more common than even these researchers describe, I am glad to see it get more attention. Like Karim 2005, I think these guys nail the condition and they reference a number of the same studies I found. Also, like Karim, they treated it with a cortisone injection which was for the most part successful. However, since I think cortisone is generally fools gold for tendinopathy, I’m against it’s use, and I think the one failure they had was illustrative as to why. So I thought it would be good to quote some comments from the paper and comment how similar or different my experiences have been with the condition.

    Coracoid syndrome: a neglected cause of anterior shoulder pain. Gigante A, Bottegoni C, Barbadoro P. Joints. 2016 Jun 13;4(1):31-8. [FREE FULL TEXT]

    “Conclusions: the present study documents the existence, and characteristics, of a “coracoid syndrome” characterized by anterior shoulder pain and tenderness to palpation over the apex of the coracoid process and showed that the pain is usually amenable to steroid treatment. This syndrome should be clearly distinguished from anterior shoulder pain due to other causes, in order to avoid inappropriate conservative or surgical treatment.”

    I think this is exactly right and appreciating the diagnosis I think would go a long way towards presenting plenty of unnecessary acromioplasties.

    “Bench-presser’s shoulder is an overuse insertional tendinopathy of the pectoralis minor muscle usually affecting weightlifters and bodybuilders. On examination, medial juxta-coracoid tenderness is present and the active-contraction test and bench-press maneuver are positive (7).”

    Here I would differ with their conclusion. They are citing Bhatia 2007 and taking him at face value. However, as I explained in my Bench Press Shoulder Pain blog I expect that what Bhatia is calling “bench-presser’s shoulder” is really slightly misdiagnosed coracoidopathy. I don’t think the active contraction test or the bench-press maneuver are able to isolate the pectoralis minor from that of the short head of the biceps or coracobrachialis and that if an isometric Speed’s test were performed on his patients, I speculate it would have been positive as well.

    “In the course of the senior Author’s long experience with shoulder problems, a large number of patients have presented with anterior shoulder pain but no clinical signs of subacromial or subcoracoid impingement, rotator cuff or pectoralis minor tendinopathy, subscapularis or LHBt disorders, or symptoms and signs of instability.”

    I wholeheartedly agree with that.

    “The exclusion criteria were: pain symptoms elicited by digital pressure applied on an area of tenderness medial to the coracoid along the inferior-medial orientation of the muscle fibers, the anterolateral subacromial area and the apex of the contralateral coracoid process; symptoms, clinical signs (e.g. painful active contraction test and bench-press maneuver), X-ray, or MRi findings suggesting other shoulder girdle disorders, including tendon tears, adhesive capsulitis or coracoid impingement; previous or multiple shoulder problems; neck pain symptoms or clinical features indicating neck pathology; ipsilateral upper limb problems; suspected nerve compression; clinical signs or laboratory test findings of rheumatic disease, including fibromyalgia (19); and obesity, as this condition hampers digital palpation of the coracoid process.”

    I’m of the opinion that the authors exclusion criteria are too restrictive, such that a fair amount of patients with coracoidopathy/coracoid impingement were excluded. When I did the demographics on my patients with shoulder pain, I found that 88% of my patients with coracoidopathy also had something else, most frequently rotator cuff tendinopathy or adhesive capsulitis. I think for the purpose of Gigante’s study, the bulk of these exclusions were useful in that if they are going to treat the condition with a focused cortisone injection and see if it works, you want to do it on someone with an isolated condition. However, I think the exclusions based on obesity, previous shoulder problems, and particularly the “bench-press maneuver” lessen the true incidence of even isolated coracoidopathy which they describe as 5.28% compared to my 10.2%.

    I’m particularly concerned about their use of the “bench-press maneuver” (which is a simulated bench press motion against manual resistance) as an exclusion test because I think it will be positive in a fair number of patients with coracoidopathy who don’t bench press. Also, because all the patients I have had as of recent with anterior shoulder pain, and a tender coracoid process had coracoidopathy. While I am unaware of anyone doing an EMG test to confirm, it is widely thought that both the short head of the biceps and coracobrachialis both work in shoulder flexion and horizontal adduction (the combination thereof is what the upper arm does when bench pressing) and thus should be positive (painful with resistance in the bench press motion). In fact the authors report:

    “Eleven patients (73.33%) remembered performing abrupt, repetitive flexion and adduction movements of the shoulder against resistance with the elbow in extension (as when lifting a person from a bed) prior to symptom onset; the other 4 reported that their job involved movements of this kind.”

    The above is a pretty big clue that the “bench-press maneuver” should not be used to exclude someone from the diagnosis of coracoidopathy.

    Treatment, which as with Karim and Bhatia, was with a corticosteroid injection to the coracoid process, which seems to have been largely successful. In my main coracoidopathy paper, I go into detail with citations as to why I’m against the use of cortisone injections to damaged tendons, with the reason being that while smaller short term studies find cortisone injections beneficial, larger longer term studies find a high incidence of recurrence and increased risk of tendon rupture such that those who have corticosteroid injections are, on average, worse off than those who have had no treatment whatsoever. The patients in this paper were followed for two years and this does not seem to have been much of an issue, however they were largely sedentary patients and the ones who failed treatment I think is illustrative.

    “The last patient (6.66%) had residual pain (EQ-VAs: 22) and unsatisfactory shoulder function (sst: 66.67), and received a third infiltration. At 60 days this patient still complained of anterior shoulder pain and his scores were the same as at the previous visit, but he admitted that he had never stopped lifting heavy weights.”

    “A possible explanation for this case is that his coracoid syndrome, combined with an initially undiagnosed supraspinatus tendinitis, worsened with shoulder overuse and finally led to tendon inflammation, which does not respond to steroid treatment.”

    Here’s another possible explanation. In the active patient who continued to workout, the corticosteroid injection being catabolic (meaning it weakens the tissue where it’s injected) had reduced capacity to heal, which was worsened with each subsequent injection, only being offset by the anabolic (strengthening) action of their weight training. This would explain corticosteroid injections increase the risk of rupture (with more injections being worse) in collagenous type tissues and why in other types of tendinopathy corticosteroid injections have been shown to slow long term rates of healing in comparison to measured and progressive resistance training and also in comparison to no treatment whatsoever. As such I think the treatment that’s in the long term best interest in all patients to include both the active ones and sedentary ones. Given that resting tendons with tendinopathy isn’t particularly evidence based, and that tendinopathy generally isn’t inflammatory, I don’t find the authors’ explanation particularly compelling. Rather I think if they had added supinated front raises (as described with video in both my Coracoidopathy the Missing Link in Shoulder Pain and my Bench Press Shoulder Pain blogs) to an otherwise balanced exercise program, perhaps with some some internal and external rotation rotator cuff exercises, they might have had a complete resolution of symptoms.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Type 2 Diabetes Curable! But Mosley’s New Book has HUGE Typo

    I was over at a buddy’s house when he opened some mail, and in it was Michael Mosley’s new book The 8-Week Blood Sugar Diet. I was like, “Oh that’s the 5:2 guy, he’s cool he’s into intermittent fasting.” At the time I was familiar with Dr. Moseley from having watched his video on intermittent fasting “Eat, Fast, and Live Longer”. I still think it’s a great video and I wondered what he had new to say since he said he cured his own Type 2 diabetes by the The FastDiet or 5:2 diet, eating anything you want 5 days per week and doing a ‘modified’ fast (eating 500 calories if female and 600 if male) 2 days per week. So I was wondering what the new big deal was.

    The new book was to popularize Dr. Roy Taylor’s 2011 research, which Mosley wrote:

    “The volunteers stuck to the 800-calorie regime, and in just eight weeks–a remarkably short time–lost an average of 33 pounds. They also lost nearly 5 inches from their waist. By the end their blood sugar levels were all back in nondiabetic range.” pg 48

    “In Dr. Taylor’s studies, largely for reasons of convenience, the subjects were asked to lose weight by drinking commercial meal-replacement diet shakes for the whole eight weeks, supplemented with some nonstarchy vegetables.” pg 115

    “If you decide to start with meal-replacement diet shakes, you should aim to consume around 600 calories per day in shakes, plus 200 calories’ worth of nonstarchy vegetables.” pg 116

    “I think one of the main advantages of doing this diet with real food is that it will retrain your taste buds.”

    “What does 800 calories look like? More than you might think…”

    The above mentioned results were all seem legit, type 2 diabetes per the research was reversed. HOWEVER, it was all based 600 calories per day, not 800. I guess you could look at it one way and be like, it’s just 200 calories difference no biggie, but I have to think in real life, when you are mentally preparing to eat 800 calories day in and day out, being told it really should have been 200 less would be a little disheartening.

    I can’t imagine there was anything sinister going on here, he cited his source and probably some mental thing caused 8 weeks to be remembered as 800 calories. “8 weeks 800 calories” is catchy in a way that 8 weeks 600 calories isn’t. But man, I’m really surprised that nobody caught the discrepancy! Not a single proofreader? Nobody reads actual the actual research anymore? Do they even read the abstracts? Because it says in the front page, and in the text, the study participants only ate  600 calories per day.

    Anyway the book put me onto the research, well worth a read, with FREE FULL TEXT! Gotta love free full text.
    Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Lim EL1, Hollingsworth KG, Aribisala BS, Chen MJ, Mathers JC, Taylor R. Diabetologia. 2011 Oct; 54(10): 2506–2514.

    Some quotes:

    “Three individuals failed to comply with the diet (two during the first week and one during weeks 4–8), and one left the study for an unrelated medical reason. Hence 11 individuals (nine male and two female, age 49.5 ± 2.5 years) completed the study.”

    “After the baseline measurements, individuals with type 2 diabetes started the diet, which consisted of a liquid diet formula (46.4% carbohydrate, 32.5% protein and 20.1% fat; vitamins, minerals and trace elements; 2.1 MJ/day [510 kcal/day]; Optifast; Nestlé Nutrition, Croydon, UK). This was supplemented with three portions of non-starchy vegetables such that total energy intake was about 2.5 MJ (600 kcal)/day.”

    “Ongoing support and encouragement was provided by means of regular telephone contact.”

    “Average weight loss during the 8 weeks of dietary intervention was 15.3 ± 1.2 kg, equivalent to 15 ± 1% of initial body weight…”

    “This study demonstrates that the twin defects of beta cell failure and insulin resistance that underlie type 2 diabetes can be reversed by acute negative energy balance alone. A hierarchy of response was observed, with a very early change in hepatic insulin sensitivity and a slower change in beta cell function. In the first 7 days of the reduced energy intake, fasting blood glucose and hepatic insulin sensitivity fell to normal, and intrahepatic lipid decreased by 30%. Over the 8 weeks of dietary energy restriction, beta cell function increased towards normal and pancreatic fat decreased. Following the intervention, participants gained 3.1 ± 1.0 kg body weight over 12 weeks, but their HbA1c remained steady while the fat content of both pancreas and liver did not increase. The data are consistent with the hypothesis that the abnormalities of insulin secretion and insulin resistance that underlie type 2 diabetes have a single, common aetiology, i.e. excess lipid accumulation in the liver and pancreas.”

    Overall I think it’s exciting research. Since becoming interested in intermittent fasting myself, how it compares to other diets, and what conditions it’s good for (nigh everything), diabetes has been something I have been most frequently asked about by my patient population. Making diabetes something I have reading much about. In fact, I’m almost finished with the continuing education requirement necessary to become a Certified Diabetes Educator (CDE). Curiously, the above paper is 5 years old, and curing type 2 diabetes wasn’t mentioned in my CDE course material, rather just “management” was.

    Speaking of 600 calories a day, I suppose I could do that for 8 weeks if I had to, and with all the problems associated with diabetes, it would be worth it. I definitely don’t think I’d want to divide it into 3 meals of 200 calories each and I certainly wouldn’t take the time to prepare a 200 calorie meal. Rather, I’d just work all day on zero calories, and have a 600 calorie dinner exactly at the 8 pm hour.

    Final Thoughts

    Despite the 600-to-800 calorie typo I thought the book was great. It put me onto new research and emphasized how much better one’s life will be if they reverse your diabetes rather than just manage it. Plus it had some good warnings about telling your doctor you are going to do it, as they might have to adjust your medications to avoid too low a drop in blood sugar or blood pressure.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Coracoid Impingement Syndrome and Coracoidopathy

    This blog is probably only of interest to professionals since coracoid impingement syndrome (CIS) is thought to be a very rare, though important, shoulder pathology. CIS describes when the coracoid process is thought to physically impinge upon the lesser tuberosity of the humerus, pinching the subscapularis tendon and perhaps the long head of the biceps tendon in the process, thus causing pain and/or degeneration of said structures. Though even proponents of CIS report that it occurs infrequently, it has accumulated a fair amount of attention in the medical literature and is thought to be a potential cause of anterior shoulder pain either before or after surgery for it or other shoulder pathologies. While I wouldn’t say CIS is well known, it is at least known, which is more than I can say for what I think is the most underappreciated, easy to diagnose, and relatively easy to treat (for me at least) shoulder conditions; coracoidopathy.

    This blog is a long footnote to my main work Coracoidopathy, the Missing Link in Shoulder Pain, so if you haven’t read that one, I’d recommend you do so now to better understand where I’m coming from with regards to CIS. Another footnote, but not essential to his blog is coracoidopathy and bench press shoulder pain.

    What I intend to do here is go through the papers that I find most interesting regarding CIS, quote the relevant text, and compare and contrast with my thoughts regarding both CIS and coracoidopathy. I’ll also describe to what degree one diagnosis might be mistaken for the other. If I am correct in my observation that 84.7% of physical therapy shoulder referrals have some degree of coracoidopathy (and almost nobody knows about it) it stands to reason that it is more likely misdiagnosed as CIS (though I have never witnessed that happening in real life either) than vice versa.

    It’s difficult for me to say anything definitive about CIS because I have never made the diagnosis, nor in the 17 years I have been a physical therapist have I ever been referred a patient with CIS either pre- or post-op. Also, as you will see, a couple of the ways CIS is diagnosed is by analgesic injection or direct observation in surgery, and as a physical therapist I can’t do either. However, since tendinopathy in general and tendinopathy of the coracoid process (which I call coracoidopathy) is one of my things, I thought it would be worth writing about if, for no other reason than to make it clear that I covered all foreseeable bases.

    I’ll open up by quoting what Karim et. al. had to say about CIS in their paper describing “enthesitis of the biceps brachii short head and coracobrachialis at the coracoid process” (see why I had to give it my own name?) which shows they knew about CIS as well, but didn’t think it described at least some of the patients they saw. Without further adu:

    Enthesitis of biceps brachii short head and coracobrachialis at the coracoid process: a generator of shoulder and neck pain. Karim MR1, Fann AV, Gray RP, Neale DF, Escarda JD. Am J Phys Med Rehabil. 2005 May;84(5):376-80.

    “…[CIS] is hypothesized to be due to encroachment of the lesser tuberosity on the coracoid process because of overuse in flexion-internal rotation, which can lead to displacement of normal centering of the humeral head. Symptoms of coracoid impingement syndrome include anterior shoulder pain, occasionally radiating down the upper arm/forearm. Shoulder impingement signs are negative. Pain is made worse with passive flexion. On palpation there is tenderness over the coracoid process. The literature does not describe conservative treatment but rather describes confirmation of the diagnosis with local anesthetic injection between the coracoid process and the humeral head. This site of injection was different from ours, which was centered over the coracoid process. No conservative treatment was recommended or described in these studies. According to the studies, definitive treatment is coracohumeral decompression surgery, such as resection of the coracoid tip. This syndrome [CIS] seems to be similar to what we found in our patients in whom conservative treatment with steroid injection over the coracoid process improved or resolved our patients’ symptoms.

    I don’t have anything to add to the above except to say it sounds right, and per the references and quotes cited below, it’s clear that Karim had a pretty good handle on the CIS data up to 2005. Afterwards there was some more guidance/suggestions as to how to conservatively treat CIS, which is fairly in line with how I would treat basic rotator cuff (RTC) tendinopathy, that being global strengthening of the scapular stabilizing muscles, focused strengthening of the RTC, and perhaps some stretching and postural adjustments (if needed).

    The role of the coracoid process in the chronic impingement syndrome. Gerber C, Terrier F, Ganz R. J Bone Joint Surg Br. 1985 Nov;67(5):703-8.

    “Physical examination revealed an exquisitely tender coracoid tip.”

    “Forward flexion combined with medial rotation was chosen as the position in which to identify subcoracoid impingement by CT scan…”

    “We documented idiopathic subcoracoid impingement (Figs 3-7) clinically, computer-tomographically and operatively in four painful shoulders, and we had sufficient clinical evidence of its occurrence in 21 others.”

    “As in most cases of chronic idiopathic impingement, the symptoms could usually be treated conservatively.”

    “We carried out isolated resection of the anterolateral coracoid tip only once; this was when, at operation, we had unequivocal proof of coraco-humeral impingement whereas there was no impingement against the acromion or the coraco-acromial ligament. This patient had a completely painfree, physically normal shoulder 18 months after operation.”

    Most of the above sounds reasonable to me. While, not describing what conservative treatment is, they said it was usually effective. However, I would think that if the coracoid process was impinging on the lesser tuberosity/subscapularis/long head of the biceps, I would think those areas would be exquisitely tender, more so or at least equal to the coracoid tip. If the tenderness was isolated over the coracoid process (especially if confirmed with a weak or painful Speed’s test) then I would immediately suspect coracoidopathy. This makes me wonder if the 21 painful shoulders they diagnosed based on clinical evidence, that was not confirmed operatively or with a CT scan, were in fact coracoidopathy misdiagnosed as CIS.

    The coracoid impingement syndrome. Dines DM, Warren RF, Inglis AE, Pavlov H. J Bone Joint Surg Br. 1990 Mar;72(2):314-6.

    “The seven patients were seen over a period of six years.”

    All patients had tenderness in the anteromedial shoulder over the coracoid process.”

    “All patients had anterior shoulder pain made worse by forward flexion and medial rotation combined with horizontal adduction. This manoeuvre produced a painful click in seven of the 8 shoulders.”

    “Previous operations. Five patients had one or more surgical procedures, including diagnostic arthroscopy, glenoplasty, tenodesis of the long head of the biceps (four patients), and acromioplasty (two patients).”

    “Four patients had arthrograms pre-operatively. None of these helped with the diagnosis.”
    “After this, either the anterolateral aspect of the tip of the coracoid process or the whole tip is removed to open the coracohumeral space (Fig. 2a), about 1 to 1 .5 cm being removed. The conjoined tendon is then re-attached to the remaining base of the coracoid process (Fig. 2b). We now recommend the more radical excision.”

    “Six shoulders had complete resolution of preoperative symptoms and two had mild residual discomfort during stressful activity in the overhead position, but no pain at rest.”

    “Coracoid impingement is a rare cause of anterior shoulder pain, which should be considered especially after the failure of previous surgery for impingement, biceps tendon lesions, instability, or an operation on the coracoid…”

    Interesting, in this paper was the rareness of the CIS, 7 patients in 6 years. I have the same reservation as in the Gerber study in that they noted tenderness over the coracoid process, but they didn’t report further to see if they were tender over the lesser tuberosity of the humerus, where the coracoid process should be impinging. Two had a prior acromioplasty and five had prior prior tenodesis (the tendon was cut off), which makes me wonder if either or both might have encouraged anterior translation of the humeral head resulting in the coracoid impingement. Also, rotator cuff weakness/tendinopathy generally precedes long head of the biceps tendinopathy, for which it is often cut, and also precedes acromioplasty. As such, I think strengthening the rotator cuff and scapular stabilizing musculature would go a long way towards treating CIS and preventing the need for coracoid process excision. It does seem the excision helped, however if any of the patients did in fact have coracoidopathy, cutting the short head of the biceps, coracobrachialis, and pec minor loose, to reattach them on a shortened coracoid process might (in a roundabout way) eliminate the muscle/tendon pain as well as the impingement. Previous conservative treatment in this study was not described but if it were me I’d definitely want to give scapular stabilizing, rotator cuff exercises a try first, most certainly combined with my targeted exercise for coracoidopathy, the supinated front raise (SFR).

    Rotator interval lesions and their relation to coracoid impingement syndrome. Dumontier C1, Sautet A, Gagey O, Apoil A. J Shoulder Elbow Surg. 1999 Mar-Apr;8(2):130-5.

    “From 1984 to 1994 we operated on almost 500 patients with shoulder impingement syndrome. In reviewing the surgical records, with found that 12 patients (14 shoulders) had impingement of the rotator interval by the coracoid process or fibrous falx at the time of surgery.”

    “Preoperative imaging techniques were no help in diagnosis, even retrospectively…”

    Six patients had previously undergone shoulder operations. Three had been operated on for calcific tendinitis and 2 for subacromial impingement.”

    “Although we were aware of the possibility of coracoid impingement from the start, we discovered most of the impingement lesions during surgery.”

    “We believe that the tests devised by Yocum and Hawkins and Kennedy are most likely to yield positive results in cases of coracoid impingement. However, as Patete has already pointed out, none of these tests are specific…”

    “Contrary to authors who initially addressed the issue we believe that cases caused by an excessively lengthy coracoid process are rare and that no coracoid process can induce a cam effect.”

    “We chose to resect the coracoid process no further than the extent necessary to relieve impingement; we did not follow the recommendation of Dines et al that the tip of the coracoid process be removed.”

    “Three patients (4 shoulders) still had a fair amount of pain… Seven patients (9 shoulders) reported shoulder weakness…”

    “Whether coracoid impingement exists as a distinct syndrome and, if so, how variations of it should be classified, has yet to be fully established. We believe that lesions of the biceps and the subscapularis should not be attributed to coracoid impingement syndrome.”

    This paper all sounds very reasonable to me. 12 patients in 10 years, and 12/almost 500 impingement surgeries is “almost 2.4%” which does seem to back up the idea that CIS is uncommon, which is contrary to my findings coracoidopathy. I also like that they took a minimalist approach to excision of the coracoid process. Considering several of the patients still had shoulder pain and weakness after the procedure, it makes me wonder if they had coracoidopathy in addition to CIS, with the residual pain and weakness being secondary to the coracoidopathy still being there. As often as I find coracoidopathy with RTC tendinitis (74% of the time) I’d be surprised if they didn’t.

    Postoperative subcoracoid impingement syndrome in patients with rotator cuff tear. Suenaga N, Minami A, Kaneda K. J Shoulder Elbow Surg. 2000 Jul-Aug;9(4):275-8.

    “Previously reported cases of failed cuff surgery are as follows: (1) infection, (2) deltoid denervation, (3) deltoid detachment, (4) failure of the cuff repair, (5) rehabilitation failure, (6) re-tear, (7) remaining subacromial roughness, and (8) loss of superior stability. However, subcoracoid impingement syndrome has seldom been mentioned as a cause of failed anterior acromioplasty and rotator cuff surgery.”

    “Eleven cases of subcoracoid impingement syndrome were clinically diagnosed among 216 cases in which anterior acromioplasty and management of rotator cuff tear had been performed.”

    “The radiographic findings revealed slight upward migration of the humeral head in 8 cases and bony spurs of the coracoid and humerus in 5 cases. Bilateral CT scans were obtained in 7 cases. On CT scanning, the coracohumeral distance in the affected shoulder was seen to be, on average, 57.6% of that on the contralateral side…”

    “Subcoracoid impingement syndrome was diagnosed in terms of effective subcoracoid block. Effective subcoracoid block means that the symptom is alleviated after injection with 1.56 mL of 1% lidocaine and 0.5 mL of contrast medium fluoroscopically the site just posterior to the base of the coracoid.”

    “Coracoplasty was performed in 9 cases in which conservative treatment, consisting of physical therapy for more than 1 year and steroid injection at the base of the coracoid, had failed.”

    “Histopathologic findings of resected coracoid processes revealed hypertrophic changes to the fibrocartilage layer and the osseous trabecula at the posterior aspect. These findings suggest mechanical compression to the coracoid process of the tendinous rotator cuff or humeral head.”

    Results of this paper again sound reasonable. They didn’t report much in the way of hands on tests, and myself not having any experience with analgesic blocks, I do wonder if the subcoracoid block might also numb up the tip of the coracoid process similar to the analgesic injection given by Karim. They did noted the block was considered effective if pain with horizontal adduction was alleviated, which makes might or might not distinguish it from Karim’s injection.  Also, while they gave a picture of hypertrophic changes in the resected coracoid process, they did not say in what percentage of resected coracoid bone/cartilage this was found. Patients were given a year for physical therapy to work, which seems like more than enough time. However, what constituted physical therapy was not described, so it could have been progressive resistive exercise to the scapular muscles and RTC, which I think would help in the case of CIS, and be part of the treatment for coracoidopathy, but without a SFR I would expect coracoidopathy symptoms to remain. Physical therapy could have been, cold, heat, massage, stretching, ultrasound, acupuncture (the study was done in Japan), etc., all of which I expect would be relaxing but ultimately worthless (beyond placebo) for either condition.

    The coracoid impingement of the subscapularis tendon: a cadaver study. Radas CB, Pieper HG. J Shoulder Elbow Surg. 2004 Mar-Apr;13(2):154-9.

    “As opposed to sub-acromial impingement, an irritation of the subscapularis tendon seems to occur almost exclusively in shoulder joints that are pre-damaged or occurs post-operatively (subscapularis cyst or after arthroscopy, glenoplasty tenodesis of the long head of the biceps tendon, or acromioplasty)

    “…rupture of the subscapularis tendon seems to be much less frequent than the lesion of the upper/posterior cuff.”

    “We found ruptured subscapularis tendons to be the exception, only to be encountered when massive defects occurred in combination with lesions of the upper rotator tendons.”

    “The clinical symptoms of coracoid impingement primarily consist of pain in the anterior area of the shoulder above the lesser tuberosity with increased internal rotation and anteversion—the impingement position. Internal rotation is limited because of pain and can barely be performed actively if the subscapularis tendon is completely ruptured.”

    “A comparison of the subscapularis tunnel area between shoulders with and without degenerative changes or a ruptured subscapularis tendon revealed no significant differences (428 mm2 as compared with 427 mm2 on average).”

    “There seems to be a general disposition toward coracoid impingement, as the lesser tuberosity always makes contact with the coracoid process within the normal range of motion of the shoulder.”

    “…no significant difference was found between the tunnel areas of degenerated and healthy subscapularis tendons. Thus, a relationship between the coracoid impingement and the size of the subscapular tunnel area representing the size of the subcoracoid space can definitely be excluded.”

    “In conclusion, a coracoid impingement does not seem to be caused by anatomic variations as the main pathology. Instead, it seems to be the result of a functional problem, mainly anterior instability of the shoulder joint leading to a functional narrowing of the coracohumeral distance.

    Great paper, I don’t have any additional comments except to say it’s fascinating and sounds right.

    That’s all for the pre-Karim papers, below are a few that were published after Karim’s 2005 paper.

    Coracohumeral interval imaging in subcoracoid impingement syndrome on MRI. Giaroli EL, Major NM, Lemley DE, Lee J. AJR Am J Roentgenol. 2006 Jan;186(1):242-6.

    “…none of the subcoracoid impingement patients clinically suspected of having subcoracoid impingement had directly evident soft-tissue impingement or abnormal focal bone or soft-tissue signal.”

    “Subcoracoid impingement is clinically manifested as anterior shoulder pain after internal rotation, adduction, and forward flexion. These maneuvers are reproduced by the military parade rest position, perhaps explaining the predominance of soldiers among our patients with true-positive findings.”

    “Because subcoracoid impingement clinically is more apparent in internal rotation, perhaps repositioning the patient’s shoulder in internal rotation would yield more accurate measurements. However, given the prevalence of rotator cuff abnormalities and the relatively uncommon occurrence of subcoracoid impingement, positioning the patient’s shoulder in a standard neutral or external position is more practical and efficient.”

    “The average coracohumeral interval for females was 3 mm smaller than that for males. Using sex-adjusted data, we found a statistically significant difference between individuals with or without subcoracoid impingement in the axial coracohumeral interval (p = 0.01). This value, however, was poorly predictive…”

    “A sex-adjusted coracohumeral interval of 10.5–11.5 mm, although statistically significantly related to subcoracoid impingement, is poorly predictive of this diagnosis when acquired via routinely performed MRI.”

    “The morphology of the coracoid process and lesser tuberosity has no apparent predictive value.”

    This one is interesting because all 19 subjects were confirmed to have coracoid impingement per surgery and much like prior researchers reported with x-rays or CT scans, this one found an MRI didn’t help either. No data was given with regards to other clinical tests that might or might not have helped with pre-operative diagnosis, nor what other shoulder pathologies were present at the time of surgery. They seem to think that standing in the parade rest position was maybe causative of pain but that sounds unlikely to me as while the parade rest position has a lot of shoulder internal rotation, it lacks the the flexion and horizontal adduction reported to be needed to really hit the coracoid process, maybe.

    Coracoid impingement syndrome: a literature review. Okoro T1, Reddy VR, Pimpelnarkar A. Curr Rev Musculoskelet Med. 2009 Mar;2(1):51-5.

    “Patients with this syndrome typically present with a history of dull pain in the anterior aspect of the shoulder that is exacerbated by activities performed when the shoulder is in a forward flexed, adducted and internally rotated position.”

    “The coracoid impingement test is performed in a manner similar to that used to perform the Kennedy–Hawkins impingement sign, except that the patient’s shoulder is placed in a position of cross arm adduction, forward elevation, and internal rotation to bring the lesser tuberosity in contact with the coracoid .”

    The coracoid impingement test is passive on the part of the patient, and this is used to differentiate it from the superior labrum test which requires the patient to resist downward pressure on the arm.”

    “Another method that is used to evaluate whether a patient has coracoid impingement is to inject lidocaine into the subcoracoid region. Although it has been suggested that relief of pain with this injection can help to establish the diagnosis, this test has not been studied to determine either its validity or its accuracy. The proximity of multiple structures in the subcoracoid region, including the joint itself, makes the accuracy of these injections questionable.”

    “The first line of treatment for coracoid impingement should be a program of activity modification, with avoidance of the provocative positions of forward flexion and medial rotation, and physical therapy to strengthen rotator cuff muscles and scapular stabilizer musculature.”

    This is a review paper for which I am again largely in agreement. However, I’m skeptical that the O’Brien’s test (the active test they cited for superior labral pathology) is particularly diagnostic, in part because of this. I do like their use of the term “coracoid impingement test” because “passive shoulder flexion with internal rotation and horizontal adduction” is awkward to both say and write. I just don’t know if the “coracoid impingement test” works as well in practice as it sounds in theory.

    My other comment would be with regards to treatment. As I have commented above, I do think scapular stabilizing and RTC muscles should be strengthened, but I would definitely add in the SFR.

    The SFR being performed with active shoulder flexion and external rotation shouldn’t irritate CIS, and if ineffective would help rule out coracoidopathy and help rule in CIS. They mention activity modification to avoid provocative positions of flexion and internal rotation and I think that would help with distinguishing the two as well. With tendinopathy (in this case coracoidopathy), increased activity seems to warm up the tendon and make it feel better. This is also something I usually notice immediately with my treatments of SFRs. Physical impingement/impact however, I would expect to not warm up and feel better but rather worsen with increased stress of the offending activity.

    Subcoracoid impingement syndrome: a painful shoulder condition related to different pathologic factors. Garofalo R, Conti M, Massazza G, Cesari E, Vinci E, Castagna A. Musculoskelet Surg. 2011 Jul;95 Suppl 1:S25-9.

    “This study includes 13 consecutive patients suffering from subcoracoid impingement symptoms who underwent an arthroscopic treatment. Patients were identified from a database of 1678 consecutive patients treated with arthroscopy because of shoulder problems during a period of 3 years.”

    “All patients underwent an unsuccessful minimum 4-month course of conservative treatment consisting of activity modification, nonsteroidal anti-inflammatory medication, physical therapy and supervised exercise regimen before undergoing surgery.”

    “At one year of follow-up, VAS score decreased significantly passing from a mean preoperative value of 7.7 points (range 6-10) to a mean value of 1.2 points (range 0-3).”

    “The first line of treatment for coracoid impingement is a physical therapy program consisting in avoiding provocative positions, postural exercises to modify scapular anterior tilt, and exercise to strengthen rotator cuff muscles; however when this syndrome is refractory to non-operative treatment for at least 4-6 months, the patient may be a candidate for arthroscopic surgery.”

    I thought this was a good paper, again demonstrating rarity of the condition, 13 out of 1678 shoulder arthroscopies, is 0.77%. The post-operative rehab program was well described and reasonable, as were the pre-operative rehabilitation suggestions. HOWEVER, again I would suspect a fair number of patients with coracoidopathy to not have their pain satisfactorily resolved with an exercise program that didn’t directly target and strengthen the short head of the biceps and coracobrachialis muscles. Thus, with the above recommendations, not appreciating coracoidopathy as a diagnosis in and of itself, might result in an unnecessary arthroscopic surgery for which no signs of CIS were found, nor much of anything else was found. The result might be an acromioplasty while you are in there, because what else are you going to do? And this still wouldn’t fix the coracoidopathy! Also unnecessary acromioplasty may leave the shoulder less stable, perhaps predisposing one to legitimate RTC, CIS or other shoulder problems in the future. So I definitely wouldn’t let “anterior shoulder pain” be good enough as a complaint. Among other things the evaluation should including range of motion in planes and resistive tests to all relevant muscles. I’d definitely perform a Speed’s test (as a muscle test), as I think the short head of the biceps and coracobrachialis are particularly relevant. Plus directly palpating the coracoid process, adding SFRs to the exercise program if indicated.

    Coracoid impingement: diagnosis and treatment. Freehill MQ. J Am Acad Orthop Surg. 2011 Apr;19(4):191-7.

    “Goldthwait first described coracoid impingement in the anterior aspect of the shoulder in 1909.”

    “Gerber et al were the first to describe surgical management of coracoid impingement.”

    “In asymptomatic patients the coracoid itself may be tender to palpation. Such tenderness is not a reliable sign of coracoid impingement…”

    “A patient also may present with weakness of the subscapularis and pain on biceps testing (eg, Speed test…”

    “It is important to note, on clinical examination and imaging studies, associated pathology that may be causing the anterior shoulder pain, such as lesions of the subscapularis, rotator interval, biceps tendon.”

    Freehill writes a good history of CIS and points out what I would expect to find with CIS, which is tenderness in the interval between the coracoid process and lesser tuberosity. The downside, is that it’s pretty difficult to determine if that tenderness is due to impingement (pinching) between the two bones, or just tendinopathy of the subscapularis and maybe the long head of the biceps. He correctly notes that tenderness over the coracoid process is not a reliable indicator of CIS but does not appear to have read Karim’s paper to suspect tendinopathy at the coracoid process. He even notes, there may be pain with a Speed’s test. He’s so close! If he had only pluralized “biceps tendon.” Oh well, I guess we can’t all be visionaries.

    Overall from my research I saw further confirmation diagnosis coracoidopathy (tendinopathy of the muscles attaching to the coracoid process) was not a consideration in any of the papers prior to Karim 2005, or in any of the papers after Karim. So the word definitely did not get out.

    In general, CIS appears to be such a rare condition that it’s never hitherto been a consideration for me. I was well into developing my diagnosis and treatment for coracoidopathy before I gave it much thought. Preparing for this particular blog, I have given CIS more thought and just recently I was treating a patient for post-op lumbar fusion and she said “you know, my shoulder’s been hurting a lot too.” I asked where in the shoulder the pain was coming from and she had trouble saying where but finally pointed to her lateral deltoid (so much for all that talk about anterior shoulder pain). I did my basic shoulder tests, to include palpating the CP, which was very tender (while nothing else was) and my Speed’s test was both weak and painful (while nothing else was). I thought to add on a test of passive shoulder flexion/internal rotation/horizontal adduction, which was not provocative. I’m not sure if the coracoid impingement test is worthwhile or not, but I thought to throw it into my shoulder evaluations for a while and see if I could learn anything from it, and if it leads to any greater accuracy in shoulder diagnosis.

    So, if I had a patient with painful passive shoulder flexion/horizontal adduction/internal rotation, but with a strong and painless Speed’s test combined with tenderness over the coracoid process, the lesser tuberosity of the biceps and intervening soft tissue, and they didn’t respond favorably the SFR as part of a comprehensive scapular, UE, and RTC strengthening program then CIS might be a consideration. Nine times out of ten (or more) I’d expect that anterior shoulder pain and tenderness of the coracoid process is going to be coracoidopathy and my exercise program will work. I would expect if there is CIS there is likely coracoidopathy and RTC dysfunction as well, thus my SFR combined with my comprehensive RTC-type treatment program sounds right on the money for conservative treatment for CIS anyway. If that doesn’t work, it’s probably time for an MRI or a surgeon to go in there and fix what he finds.

    Next, in this hotly anticipated series will probably be coracoidopathy vs long head of the biceps tendinopathy and SLAP lesions. Anyway, review that peers.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Bench Press Shoulder Pain, Probably Coracoidopathy

    I’ve done my share of bench presses, mostly back in my bodybuilder years before I got involved in Olympic weightlifting. Back then (well before I was a physical therapist) if someone in the gym had shoulder pain with bench press, none of us knew what it was, and almost nobody thought to see a doctor or physical therapist about it. The general advice among lifters was to change the grip, lighten the weights, do higher reps, change the arc of motion, do dumbbells, do something, do anything different, all with greater or lesser amount of success and eventually something usually did “work.” That’s the thing with tendinopathy. It is usually self limiting, which means even if you do nothing it eventually gets better. The result is something is bound to be correlated and thus credited with the resolution of symptoms. “Post hoc ergo propter hoc” is the proper Latin term for the phenomenon of why people get all kinds of genuine well meaning and heart felt advice as to what ‘works’ to cure tendinopathy.

    Since I don’t want to type big words over and over here’s my abbreviations in one place:

    I go into it in nauseating detail in my most recent and what I think is my best blog ever: Coracoidopathy, the Missing Link in Shoulder Pain. However, I also think that blog might be an overkill of information and terminology for someone who just has some anterior shoulder pain when bench pressing. Plus, I had some things to say regarding bench press in particular that felt a bit out of place in the Missing Link paper. So I did another video (scroll near the bottom) in relation to coracoidopathy and bench press in more of a, “If it hurts here, do this” style. So if you have faith (thanks) just push play, if you need more convincing and some detail (you should) read below, and if you need a lot of convincing definitely click on my best blog ever above.

    Regarding the association between coracoidopathy and bench press, for me, it began when I was talking about coracoidopathy and SFRs and how with, SFRs the third/heavier set almost always feels better than the first/lighter set. One of my patients was listening, and mentioned his shoulder hurt with bench press and asked what if you did the SFRs right before you benched, would the benching feel better? I thought, “that’s a great question, let’s find out right now.” I tested his shoulder, and decided it was isolated coracoidopathy he had, and then proceeded by having him do SFRs for 3 sets of 15 with with 5, 8 and 10 pounds.  Immediately afterwards he did bench press, which was painless. In the months that followed several other friends (or friends of friends) with shoulder pain during bench presses reported similar (complete or much improved) acute relief of symptoms immediately after doing SFRs and with a full resolution of symptoms with continued use of the exercise.

    Then I got a patient who said he originally injured doing snatches in CrossFit, but his shoulder was bothering him a lot when he bench pressed. I diagnosed him with isolated coracoidopathy but when I tried the above protocol (with 5, 8, 10, 12, 15 lb, extra sets because 10 lb was too light) his typical bench press pain of 7/10 was reduced to 5/10. Now although this was good, it wasn’t good enough, so I made some changes to the program, in what I illustrate below as “Strategy-2”, which by his second visit decreased bench press pain to 1-2/10. By his 4th visit, he said he still had some soreness in CrossFit but was able to do everything (including snatches). By his 11th visit, 28 days later (doing SFRs daily between treatments), he worked up to doing 15-20-25 lb on SFRs for his 3 sets. At this point he reported he was 100% recovered, with no pain during any exercise or daily activities, including both bench pressing and CrossFit exercises.

    Only after all the above, as I was finalizing my write up on coracoidopathy did I come across the following study on “bench-presser’s shoulder”, which I think was in fact coracoidopathy, or if you prefer Karim 2005’s name for the condition “enthesitis of biceps brachii short head and coracobrachialis at the coracoid process” which I think is the true first with regards to the description of the diagnosis. Still I thought Bhatia’s paper, is important in that they confirmed the association between anterior shoulder pain and bench press coming from the coracoid process. Pain was eliminated with ‘almost’ exactly the same treatment, though slightly different explanation as Karim.

    From Bhatia’s Study

    The “bench-presser’s shoulder”: an overuse insertional tendinopathy of the pectoralis minor muscle. Bhatia DN, de Beer JF, van Rooyen KS, Lam F, du Toit DF. Br J Sports Med. 2007 Aug;41(8):e11. Epub 2006 Nov 30. [FREE FULL TEXT]

    Abstract
    BACKGROUND:
    Tendinopathies of the rotator cuff muscles, biceps tendon and pectoralis major muscle are common causes of shoulder pain in athletes. Overuse insertional tendinopathy of pectoralis minor is a previously undescribed cause of shoulder pain in weightlifters/sportsmen.

    OBJECTIVES:
    To describe the clinical features, diagnostic tests and results of an overuse insertional tendinopathy of the pectoralis minor muscle. To also present a new technique of ultrasonographic evaluation and injection of the pectoralis minor muscle/tendon based on use of standard anatomical landmarks (subscapularis, coracoid process and axillary artery) as stepwise reference points for ultrasonographic orientation.

    METHODS:
    Between 2005 and 2006, seven sportsmen presenting with this condition were diagnosed and treated at the Cape Shoulder Institute, Cape Town, South Africa.

    RESULTS:
    In five patients, the initiating and aggravating factor was performance of the bench-press exercise (hence the term “bench-presser’s shoulder”). Medial juxta-coracoid tenderness, a painful active-contraction test and bench-press manoeuvre, and decrease in pain after ultrasound-guided injection of a local anaesthetic agent into the enthesis, in the absence of any other clinically/radiologically apparent pathology, were diagnostic of pectoralis minor insertional tendinopathy. All seven patients were successfully treated with a single ultrasound-guided injection of a corticosteroid into the enthesis of pectoralis minor followed by a period of rest and stretching exercises.

    CONCLUSIONS:
    This study describes the clinical features and management of pectoralis minor insertional tendinopathy, secondary to the bench-press type of weightlifting. A new pain site-based classification of shoulder pathology in weightlifters is suggested.

    My thoughts on the study

    As for Bhatia, I think he’s more or less right that there is a definite association between coracoidopathy and the bench press exercise. Of the 60-70 ‘patients’ I have treated with some degree of coracoidopathy only one was referred from a doctor with pain related to bench press. However, of all the people I’ve known reporting pain with bench press (6 thus far since becoming aware of coracoidopathy as a diagnosis) have had isolated coracoidopathy, which responded favorably to my giving them SFRs as an exercise. So if you have anterior shoulder pain, particularly in the front of your shoulder with bench press, I think there’s a good chance that it is coracoidopathy.

    While I think Bhatia is correct about the association between bench press and coracoidopathy, I think it’s likely his group is incorrect when they implicate the PM as the primary irritated tendon. I’m also skeptical that their patients were tender with palpation over just the medial aspect of their coracoid process. This is because the coracoid process is quite small, such that everyone I have treated has been either tender there or not. Localization to a particular side maybe not impossible, but I think it is improbable to distinguish. I also don’t think the manual tests they used to implicate the PM were precise enough to effectively isolate and the implicate the PM tendon. Rather, I think that Karim 2005 nailed the diagnosis more precisely, even if they hid it behind an awkward name. My own experience combining tenderness with palpation of the coracoid process with pain and/or weakness with resistance through both the SHB and CB (with a Speed’s test) as well as a good treatment effect with SFRs (which is basically making the Speed’s test into an exercise) being the reasons why.

    Bhatia’s treatment, like Karim’s was an anesthetic and corticosteroid injection to the medial and coracoid process/PM tendon, which fully resolved symptoms. However, in my main coracobrachialis paper I go into detail (with citations) as to why I think cortisone for tendinopathy is a bad idea. The main reason is that cortisone makes tendons weaker, with several studies indicating pain may be reduced in the short term but on average patients are worse off in the long term. Besides, cortisone requires a doctor’s appointment and copay, while if you have dumbbells or a gym membership already, SFRs are free!

    My observations regarding coracoidopathy and the bench press exercise.

    Their coracoidopathy usually isn’t that bad. Not bad enough for most people to seek treatment. More than often, they just notice their shoulder hurts, but they usually just end up living with it because it’s not interfering with their daily lives much at all, it just interfered with their workouts, particularly bench press.

    To go along with their tendinopathy being more minor, while they are tender over their coracoid process their Speed’s test was still relatively strong and only a little painful in comparison to the average person with coracoidopathy. However, you can often tell a difference in relation to their other/good side.

    They tend to be more fit than average. Obviously they worked out doing bench press among other exercises so they don’t have to add a lot of exercise to their program to increase general upper body and/or shoulder stabilization strength. It is very likely that just adding the SFR to the routine is enough to cure the condition. If, on the contrary, there were muscle imbalances or other shoulder problems, additional exercises from my more comprehensive treatment program might be necessary.

    My two treatment strategies

    This leaves me with two strategies, for which I am not yet sure which is best.

    Strategy-1: Do SFRs 3 sets of 15 reps (easy-medium-hard) every day, and right before you do bench press. I’m aware of the fact that if people are going to bench press they are almost always going to do it first (I always did). That way your SHB and CB tendons/muscles will be warmed up before benching. It might also be a good idea to keep the reps higher (maybe 10-15s) on bench press itself for a while, until pain resolves. Doing SFRs only on bench days (rather than my preferred frequency of daily) will probably still work, but I find (and science agrees) that tendons heal better with daily treatment. Once cured, or nearly cured, I think it’s OK to drop the frequency back to just bench days. When fully cured I’d probably stop doing them, as I think of SFRs as a rehab exercise rather than for general fitness.

    Strategy-2: Strategy-2 is for worse case scenario, when a shoulder doesn’t react as well as I had hoped to with strategy-1. The plan would be to begin the workout with back exercises to further warm up the shoulder (as per my basic workout) then perform the SFRs mid workout, followed by bench press right after and towards the end of the workout. Although it’s conventional for lifters to train bench press first in a workout, some lifters have relatively overdeveloped chest, anterior deltoids, and shoulder internal rotation strength (compared to back, posterior delts, and shoulder external rotation strength). So, beginning with back might have several potential benefits such as letting you train the back harder, perhaps better correcting muscle imbalances that could have predisposed one to coracoidopathy in the first place.  It would also better warm up the shoulders making SFRs and bench press both feel better when you get there, thus less limited by pain. Lastly, training chest later in the workout, would have you a little more fatigued when you got there, so you would be less likely to use weights that might further injury.

    Other thoughts: Somewhere on chest day (before or after bench) it might be worthwhile to do dumbbell pullovers. I say this because I think it is a great exercise for both strength and stretch. I see a lot of shoulder patients, and older people in general who can’t get their arms all the way overhead, and pullovers are one of my favorite ways to stretch that. Also, if Bhatia is correct that the PM is a/or the source of coracoid process pain, then I think pullovers would be the best way to stretch, tension and strengthen the pec minor. The fact that all my people thus far respond so well to the SFR is the main reason think it isn’t the PM most of the time, however there is no reason it couldn’t be the pectoralis minor some of the time.

    As for where coracoidopathy hurts, and a SFR technique, it’s a lot easier to show than to tell, so here’s a demo by yours truly.

    Precautions 

    I should add that while I think coracoidopathy is often the cause of shoulder pain with bench press, it is obviously not the only cause, and my own data confirms that coracoidopathy very frequently co-occurs with RTC tendinopathy and other shoulder issues. As such, if one’s bench press shoulder pain isn’t coracoidopathy the SFRs aren’t going to work. If shoulder pain is more severe and more complicated than isolated coracoidopathy, and if the shoulder does not respond positively to the addition of the SFRs it might be worth seeing a doctor or physical therapist. If coracoidopathy (tendinopathy of the coracoid process) is part of the problem you’re probably going to have to educate your local health care provider about it because it’s generally not something they have heard about.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Coracoidopathy: The Missing Link in Shoulder Pain

    To cut to the chase, coracoidopathy (a term I made up) is an unbeknownst but common cause of shoulder pain. My preliminary data gathered from my shoulder pain referrals suggest it is present in up to 85% of people with shoulder pain. It is the primary diagnosis in over a third of them, and is the sole diagnosis in 10%. If my sample estimates hold up in other populations, it is more common than rotator cuff pathology for which it is often confused. It is easily diagnosed by sharp point tenderness with palpation over the coracoid process, further confirmed with weakness and/or pain with supinated shoulder flexion (aka an isometric Speed’s test). The good news is that in isolation coracoidopathy is easily treated by performing dumbbell supinated front raises. The problem is, apparently, NOBODY KNOWS ABOUT IT, which results in misdiagnosis, ineffective physical therapy, and likely unnecessary surgery after “conservative treatment” fails. Unfortunately surgery still doesn’t fix the problem because surgeons generally aren’t looking at the coracoid process either.

    Ad nauseum details below, and if you hate to read, a video is at the bottom.

    Abbreviations used below (FYI, I hate when all abbreviations are not given on page one of a paper)

    I became aware of the condition and came up with my treatment in 2012 when working with a patient who had persistent anterior shoulder pain months after having a RTC repair/subacromial decompression. I remember thinking, “it must be the long head of his biceps tendon,” but he wasn’t tender over his bicipital groove. When I closely read his op-report I found that the long head of his biceps had ruptured prior to his surgery and thus couldn’t be the source. After weeks of telling him the standard schtick, “the rotator cuff is known to refer pain to the front of the shoulder and down the arm,” I did more palpation and finally palpated his coracoid process, which was SHARPLY/ALARMINGLY tender. I then consulted my favorite physical therapy book, not one where someone tells you what to do but rather one that lets you see what you’ve got, Netter’s Atlas of Human Anatomy, which showed the coracoid process as the origin of the short head of the biceps and coracobrachialis muscles. The short head of the biceps and more so the coracobrachialis are the type of muscles you learn about for an anatomy test, but then forget because they’re inconsequential, or so I thought. I then did a pubmed.com search and came across only one paper that addressed those muscles as a site of pain at the coracoid process (Karim 2005). Karim injected the CP in six patients with anterior shoulder pain and tenderness over the CP with an anesthetic, which resulted in immediate and complete relief of pain. So I thought, “I bet that’s it.”

    With that knowledge in hand, and I already considering myself a tendinopathy specialist, I then thought my way through the mode of action of those muscles/tendons and decided a supinated front raise (SFR) would be the best way to target, tension, and strengthen the CB and SHB while minimizing deltoid contribution. The addition of the SFR to my patient’s treatment program lead to a near immediate reduction in symptoms and decreased tenderness over the CP.  From then on I started to look more closely at my shoulder patients and noticed they very often had CP tenderness and frequently had the weakness and pain with supinated shoulder flexion. It wasn’t a rare case, but almost the norm! At this point, having treated scores of patients with coracoidopathy and further refining my evaluation and treatment technique I figured it’s time to share.

    What is coracoidopathy?

    Coracoidopathy is tendin“opathy” of the tendons/muscles attaching to the “coracoid” process. See what I did there? Tendinopathy is a newer word for tendinitis, to reflect the fact that biopsies of painful tendons generally don’t find any inflammatory cells at the site of pain, for which the “itis” in tendinitis is in reference to. Tendinosis is another new word for tendinitis, for which more recent papers are distinguishing from tendinopathy, with tendinopathy used to describe the “painful condition” and tendinosis to describe the “tendon degeneration” that may or may not be associated with pain. To muddy things up a bit, some researchers are again arguing that there still is some inflammation present, at least early on, and as such, tendinitis isn’t always a misnomer. So tendinopathy, tendinosis, tendinitis, whatever you want to call it, it all depends on whose paper you read, but regardless, I know what you are talking about. What matters in this case is that the tendon pain/damage is coming from the coracoid process, a spot on the shoulder where three tendons attach. So if you want to call it coracoiditis, or coracoidosis I won’t argue, but yeah I thought of those too. Oh and to make things more complicated Crichton & Funk 2009 found the muscle fibers of the short head of the biceps and coracobrachialis insert directly into the coracoid process bypassing the existence of a “true tendon.” However, regardless of terminology, tendon type, or tendon existence, I find the same type of exercise program I used successfully for other tendinopathies to work as well or better with coracoidopathy.

    The three muscles/tendons potentially involved are the SHB, the CB, and the PM. I think that Karim’s group hit the nail on the head and deserves the credit for first describing the condition as involving the SHB and CB. They specifically noted:

    “No literature suggested tendons of the short head of the biceps brachii or coracobrachialis as a cause of pain.”

    I agree with Karim in that I have been unable to find any papers before, or giving them credit since, implicating either the SHB or CB as causes of shoulder pain. If my numbers are correct about the incidence this is a remarkable omission in the medical literature. It’s analogous to trying to treat elbow pain, without knowing tennis elbow exists. In fact several recent review papers specifically on the subject of biceps tendinopathy and anterior shoulder pain fail to mention the short head of the biceps or coracoid process whatsoever (Ryu 2010, Tuckman 2006, Singaraju 2008, Churgay 2009). Unfortunately, I think what prevented Karim and his group from achieving acclaim was that they couched their discovery behind a terrible name. “Enthesitis of the biceps brachii short head and coracobrachialis at the coracoid process” doesn’t exactly roll off one’s tongue. Coracoidopathy on the other hand…

    Certainly worthy of mention is Bhatia 2007 whose group, apparently unaware of Karim, came up with ‘almost’ the same treatment in what they described as “Bench Presser’s shoulder.” They also eliminated pain (this time in seven patients with tender CPs) with a localized injection of an anesthetic and corticosteroid at the CP. Bhatia targeted the medial aspect of the CP thinking that the PM was the primarily irritated tendon. However the CP being a small area, I expect relief of an irritated SHB and CB would also result.

    While I would not rule out PM involvement, the prevalence of pain reproduced with the Speed’s test, and relief of pain following treatment with the SFR, leads me to think that Karim is more correct in his assertion that the SHB and CB is of primary importance. I do, however, think that Bhatia is correct in his association of the condition with the bench press exercise. Most patients I have treated with shoulder pain were not working out with the bench press exercise, but all of the patients I have seen who complained of anterior shoulder pain with bench presses did have coracoidopathy, for which I intend to specifically address in another blog. [update 6-5-16 to add the bench press and coracoidopathy blog and video]

    If I had to limit it to one muscle/tendon as primary or most frequently irritated, I’d pick the CB. This is because resistive biceps testing at the elbow where the CB doesn’t act but which tensions the SHB plenty, is rarely provocative, while shoulder flexion, where the CB does act, most often is. Also it’s questionable how much the biceps, the long head at least, (Levy 2001) acts in shoulder flexion, and nobody has tested the short head. Also distinguishing between the SHB and CB is difficult as cadaver examination indicated they blend together at their origin at the CP, so differentiation is probably academic.

    How common is coracoidopathy?

    Retrospectively going through my patient charts after July of 2012 (thru the end of 2015) I had 59 shoulder referrals (after excluding post-op shoulder patients, recent fractures, or complaints related to systemic disease). I sought to determine how many had some degree of coracoidopathy. 10.2% (6/59) were diagnosed with isolated coracoidopathy, with no other apparent shoulder pathology. 35.6% (another 21/59) of shoulder patients were diagnosed with coracoidopathy as their primary diagnosis (CP the chief source of pain/Speed’s test most notable regarding pain and/or weakness) but had a secondary diagnosis. 40% (an additional 23/59) were given a diagnosis of coracoidopathy secondary to another shoulder pathology. Another way to look at it is 88% ((21+23)/50) of those with coracoidopathy also had another shoulder pathology. Of the included 59 shoulder referrals a total of 50 (84.7%) appeared to have some degree of coracoidopathy, of which 74% (37/50) had a codiagnosis of RTC pathology and 18% (9/50) also had adhesive capsulitis. Interestingly only 67.8% (40/59) of shoulder referrals were diagnosed with RTC pathology, indicating coracoidopathy may be more common. I have since started keeping track of my statistics prospectively, so it will be interesting to see if my numbers hold up, as well as what other clinicians find, as I’ll be embarrassed if my estimates turn out to be the result of confirmation bias.

    If coracoidopathy is so prevalent, how come nobody knows about it?

    That’s the big question for me. Now that I know about it, it’s obvious. However, (17 and counting now) I was a physical therapist for 13 years before I figured it out, and the standard “it’s referred pain” seemed to cover it. My data suggests there is usually more than just one problem, co-occurring with RTC issues 74% of the time, making the connection to the RTC an easy sell. Plus the RTC seems prone to tearing (perhaps because of all the cortisone injections the RTC gets whenever a person has coracoidopathy;) while the SHB/CB and PM do not, thus making the RTC the subject of more attention. Also there is the fact that the shoulder is a complicated joint, with lots of parts that can be injured, making it sometimes difficult to tell what’s what, while the CP sits just outside of what is often thought of as the shoulder joint (the glenohumeral joint). And of course, groupthink.

    I do think recognizing coracoidopathy goes a long way towards making the shoulder less complicated.

    How is coracoidopathy diagnosed?

    If it’s just coracoidopathy, it’s easy. I test the person in resistive supinated shoulder flexion (aka Speed’s test) performed with the elbow bent ~10 degrees, and then see if they are tender with palpation over the coracoid process and/or the muscles/tendons where they attach to it. A milder case of coracoidopathy may or may not have pain or noticeable weakness with the Speed’s test but it rarely goes the other way with a painful Speed’s test and no tenderness over the CP (that finding would make me suspect a LHB/SLAP lesion). As mentioned above the problem is that more often than not there is coracoidopathy and something else. As such it’s best to do a full orthopedic shoulder evaluation to include assessment of shoulder range of motion (active and passive), resistive tests of all relevant muscles, and perhaps some special tests for which I imagine physicians and physical therapists can debate indefinitely. The tests in my video were abbreviated a bit because, in Jaydah’s case, I already knew what her injury was. Sometimes I’ll clear for cervical symptoms by looking at cervical AROM, I’ll then do shoulder AROM in standing, and if there is a limitation I’ll test PROM in supine, followed by resistive tests in shoulder abduction, shoulder internal and external rotation, biceps, triceps, followed by supraspinatus. I now always add in the Speed’s test with the elbow slightly bent. I palpate the entire scapular and RTC region and I always palpate the coracoid process.

    So basically my shoulder evaluation is a fairly standard orthopedic shoulder evaluation, I just take an extra 1-2 minutes to add in the Speed’s test and palpate the coracoid process and it’s associated tendons.

    How is coracoidopathy treated?

    Both Karim and Bhatia reported they successfully treated the condition with a corticosteroid injection to the CP in their collective 13 patients. However, a number of studies have been published in recent years indicating that corticosteroid injections (on average) lead to short term improvement, at the expense of long term outcomes. Such that tendinopathy patients who get cortisone shots are (on average) WORSE OFF than if they had no treatment whatsoever. This is thought to be due to the catabolic nature of corticosteroids causing decreased tendon strength (Smidt 2009). Even a single injection in patients with plantar fasciitis (Lee 2014) results in an 19 fold increased risk of rupture, with another recent review concluding that corticosteroids resulted in significant long term harm to tendon tissue (Dean 2014). So I tell my patients the last thing I would do is get a cortisone shot. On the bright side, if you go to your doctor for anterior shoulder pain caused by coracoidopathy and ask for a cortisone shot, he’ll probably inject your RTC, so there’s that.

    Rather than cortisone I recommended exercise. Since this blog is the first description of an exercise based program for coracoidopathy, necessarily it’s based on my experience, anecdotes if you will. However, the use of progressive resistance exercise for tendinopathy is now well established in the research, with some of my favorite papers being Peterson 2014, Kongsgaard 2009, and Arampatzis 2007. I am largely just applying that type of research to the muscle/tendons attaching to the coracoid process, and if needed, basic strength and conditioning to other muscles stabilizing the shoulder joint. So for coracoidopathy, an initial sample exercise program might be as follows:

    • Standing Cable Rows (emphasizing scapular retraction)
    • Lat Pulldowns, moderately narrow grip (~18-20 inches) bar to front, emphasizing scapular retraction at the bottom and full stretch at the top)
    • Dumbbell Curls
    • Rope Tricep Pushdowns
    • Supinated Front Raise (SFR) (unilateral using the good shoulder first)

    The SFR is the primary operating exercise in my program directed at decreasing pain and increasing shoulder flexion strength targeting the SHB and CB. Resistive exercises themselves, particularly the SFR, usually make the tendon feel immediately better and starts the healing process, such that if one were to wait for pain to decrease first, they will be waiting for a really long time.

    I have my patients perform the SFR standing, one arm at a time (to better focus and prevent excessive body sway/back extension), and using the good shoulder first to obtain good technique before attempting it with the painful side. The elbow is slightly bent to lessen elbow stress and to increase SHB recruitment. The arm is fully supinated (palm up, trying to get the pinky higher than the thumb) to bring the SHB and CB muscles into what is likely their most advantageous position. The shoulder flexed to 90 degrees or where the upper arm is parallel to the floor. I think shoulder flexion to 90 degrees leads to the greatest tension and strengthening of the SHB and CB muscles, with minimal risk of shoulder impingement. Definitely check out the video, it’s way easier to just see it.

    Over time the entire program will be progressed in intensity and then some of the following exercises may be added as needed.

    • Standing Cable Internal Rotation
    • Standing Cable External Rotation
    • Dumbbell Pullovers (of my exercises I think pullovers best tension PM tendon, plus it’s a great shoulder stretch)
    • Bent Over Lateral Raises
    • Standing Cable Press (or Bench Press)
    • Dumbbell Military Press

    For rehab I start light and on each exercise, with the first set being a kind of warm-up. I have my patients do 3 sets (easy-medium-hard) of 15 reps. While I want most of the exercises to be painless, with the SFR I want the exercise intense enough to increase pain and if form is good I will continue to increase the weight, even if painful so long as it is not severe. If the person gets 15 reps with a full range of motion, pain or not, I increase the weight an increment for the second set. If they get 15 reps with full range of motion then, I again move the weight up for the third set. If the person gets full range of motion on the 3rd set, then the next day I have them start out with their ‘medium’ weight from before and move up from there. I want to quickly (over 2-3 days or so) get them to where they are unable to get all 15 reps on the third set. Only then do I stop increasing the weight until their strength progresses.

    Besides the SFR, I don’t usually want my patients working through pain. I’m particularly cautious with pressing motions. However, if both the patient and I are sure that their pain is coming from the CP I’ll sometimes let them work through it and see what happens. If the pain lessens over time, it’s a good sign, if it worsens, it’s bad and I’ll reduce weight or remove the exercise. It’s a bit subjective and those calls are why I get paid the big bucks, and also why I’ll usually introduce the pressing exercises, one at a time, later into the program after giving the SFR a chance to work.

    Once the patient is comfortable with the exercise, I recommend the SFR be performed daily (3 sets of 15 reps) with a home exercise program between therapy visits (preferably 3 times per week) where technique is observed and weights adjusted. My observation that SFRs performed daily speeds improvement, which was recently backed up by Lee 2014 who found resistance exercise performed 6 days per week superior to a frequency of 3 days per week in the treatment of lateral epicondylitis, which if you ask me is the same injury, just in a different location. The more comprehensive program (everything besides the SFR) if needed is performed at a lesser frequency (2-3 days per week) to build overall shoulder complex strength.

    To start off I’ll select a weight on the light side of what I expect to be appropriate for the patient based on their overall fitness level and strength/sensitivity assessed when I do my Speed’s test on them. So a weaker and/or more sensitive patient might start with just a 1 lb dumbbell, while a stronger/less painful weightlifter might use as much as 10-15 lbs to start. Too heavy and they might strain something, too light and I might not get the analgesic effect of the exercise, so I would rather select a weight that is too light on day one and maybe add an additional set or two to get them to a good resistance level. If I start too heavy I might lighten the weight or repeat a weight on subsequent sets.

    Reducing anxiety with painful exercise:

    Sometimes patients have anxiety about lifting weights with a painful tendon. As such I give them ‘my talk’ telling them what I expect will happen. As mentioned above I tell them that tendinopathies generally warm up with exercise, which is why if I’m giving them a comprehensive exercise program I’ll usually put the SFR towards the middle or end of their program. Naugle 2012 specifically talks about exercise induced hypoalgesia (pain lessening), which I expect that is part of the equation. However, I think there is more specific pain reduction secondary to directly and progressively tensioning the painful tendon with a progressively higher load. I tell them, “This is what happens in ~95/100 of my tendinopathy patients.” I say they may have increased pain during their first set of their focused exercise (in this case the SFR) which usually returns to baseline as soon as they are done. I tell them if their technique is good and they get all their reps I intend to increase the weight on the second set. Many patients are apprehensive about this because the first set with the lighter weight caused some pain. I tell them that’s what I ALWAYS do, and 95/100 of my patients report the second set, even though heavier, doesn’t hurt more than the first. I tell them if everything goes as I expect, the second set has good form, and they can get all 15 reps, I ALWAYS increase the weight an increment for the third set. I say people sometimes have anxiety about further increasing the weight for the last set, but 95/100 of my patients say, “You know the third set hurt less than the first,” and pain afterwards is usually less than at baseline. Telling my patients that always puts them at ease, and they almost always confirm that the third set felt better than the first.

    What to expect if it’s working:

    With tendinopathy in general there are two common responses. The first is that the pain goes away completely in a few weeks (maybe 3-6), the person is a lot stronger and able to do everything without pain. The second common response is that the pain gets 90% better in 3-6 weeks, the patient is a lot stronger, but there is still a little nagging pain (maybe a 1-2/10 with activity) that can last maybe 3-6 months.  While the second is the worst case, education from the start helps patients believe that it is still a good outcome. I used to rack my brain trying to figure out what to do with the residual 10% pain. Now I just accept it as what it is, STILL A GREAT OUTCOME, and if the person continues with their exercise program (if strength is fully restored and pain minimal I’ll reduce the SFR frequency to 2-3 times per week) eventually they’ll realize they don’t hurt anymore. However if they wimp out and get a cortisone shot, all bets are off.

    What about the cases where the person has coracoidopathy plus RTC tendinopathy, they are a post-op RTC repair and/or they have adhesive capsulitis?

    All of that goes beyond the scope of this blog, however in general, I’ll treat just as I would for those conditions (with some combination of stretching and strengthening as is appropriate) often very similar to my comprehensive exercise program above, plus stretches if ROM is limited. So basically I do my program for whatever else they have and add on the SFR. If it’s a post-op RTC repair, I wouldn’t add SFRs until 8 weeks post-op or so, when resistance exercises become appropriate, and my progression would be slower. If they are acute post-op I’m not going to even know if they have coracoidopathy, because palpation everywhere is going to be painful and I wouldn’t be doing any resistive tests.

    What else?

    I am a big fan of electric muscle stimulation (EMS) and I do use it for coracoidopathy and other tendinopathies but I think it’s benefits are definitely secondary to the exercises. I’ll usually place one electrode just inferior to the CP targeting the CB paired with the other electrode on the scapula targeting infraspinatus and teres minor, and I’ll usually put a second channel over the biceps and triceps. I figure on average EMS is good for maybe a 1 point drop in pain on a 10 point scale, which is less than I expect to get out of it for other conditions like back pain. So it’s certainly not essential.

    What if the treatment doesn’t work?

    The treatment responses I get with tendinopathy in general, and coracoidopathy in particular are consistent enough that if things don’t work out as I expect (the same and/or lessening pain as the person progresses from set to set, particularly by the third set, as well as relatively consistent pain relief day to day and week over week) then I begin to question my diagnosis. Also, if the patient notices catching pain that doesn’t warm up and feel better, or it makes them wince then I’ll start to suspect something worse, like a RTC tear or SLAP lesion in need of further diagnostic tests such as an MRI, and perhaps surgical correction. The Speed’s test has been shown to be a poor indicator of LHB or SLAP lesion pathology (as are all manual tests for LHB tendinopathy or SLAP lesions) however I think that’s because a positive Speed’s test is such a good indicator of coracoidopathy. However, if the patient has weak and/or painful Speed’s test, and they do not respond favorably to general strengthening as described, and focused strengthening with the SFR, it’s likely that something else is wrong in the shoulder with a LHB/SLAP lesion or RTC tear being at the top of the list.

    As promised, here’s a video:

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • My Continued Electric Stimulation Headache Data

    The following is headache patient results with electric muscle stimulation (EMS) and builds on a prior blog where I did the same thing but with somewhat different electrode placement, and slightly different parameters programmed into the EMS machines. Treatment results on 20 headaches had an average near immediate pain reduction of 90%, which is phenomenal, as presented in the table. Headache characteristics, pain intensity immediately before the treatment, immediately after, and 5 minutes after treatment, as well as how many milliamps the each patient worked up to. This is not what I think anyone should do, it’s not advice, it’s just what I did with my patients and what happened. Details and further discussion are below.

    Patient #Headache DescriptionPain BeforePain Immediately afterPain 5 min laterPoints Change% Changemax mA SONSmax mA ONSComments
    1occipital headache, worse on right4/100/100/104100%1437 
    23 frontal after MVA3/101/101/10266.67%1939 
    3bilateral frontal headache symmetrical5/100.5/100/105100.00%1431no pain over weekend
    4occipital headache & up to temples, frontal region, all day long7/103/100/107100.00%1433no pain over weekend
    5forehead, just came on, usually lasts all day, comes on for her when not stressed3/100/100/103100.00%1733no pain over weekend
    6temples, on right and right eye5/100/100/105100.00%1533 
    7posterior neck, and frontal5/101/100/105100.00%1749 
    8central top of head pain, 3-4 hour duration5.5/100/100/105.5100.00%1840 
    9occiptal5/101/100/105100.00%1740didn’t return for over a week
    10top center of head, since she woke up7/104/103/10457.14%1535repeated EMS but no additional change
    11temporal bilateral2.5/100/100/102.5100.00%1840says it felt like it “opened her up”
    12left eye and occiptal region, neck6/104/102.5/103.558.33%1844repeated EMS decreased HA to 1.5
    13occiptal2/101/101/10150.00%2042gone an hour later and did not return
    14mostly top of head, says it felt like her brain6.75/100/100/106.75100.00%2035 
    15left side occipital pain4/100/100/100100.00%1443gone 4 days before returning
    16cervical, subocciptal, temporal 2 day duration3.5/100.5/100/103.5100.00%918 
    17left temple, 5 hour duration, post MVA1/100/100/101100.00%1340says she could feel her muscles relaxing as she went, even in forehead, neck felt real good after, pain hadn’t returned by next day
    18supraorbital and temporal 30-40 min duration7/100/100/107100.00%1425normally gets HA weekly
    192 days constant due to eye strain, orbital/occipital6/101.5/101/10583.33%17340/10 20 min later, returned to 5/10 2 hours later and 6.5/10 3 hours later
    20frontal & occipital, on and off for a month10/102.0/102/10880.00%416 
    Averages 4.91.00.54.290%1535.35 

    Average pain reduction for these parameters has been 90% with combined occipital nerve stimulation (ONS) with channel 1 like before where I got 78% pain reduction. However with the second series I added a 2nd channel of supraorbital nerve stimulation (SONS) over the supraorbital nerves (on the forehead right above the eyes) thus attempting to mimic what was done in the percutaneous (surgically implanted) electrode studies where they noticed considerably better response than with occipital/suboccipital stimulation alone, and where it was determined safe in the Cefaly safety study. Here are the results, with comments and precautions below:

    Compared with my prior study, not only did I add the extra channel, but also changed my duty cycle with parameters as follows:

    • Pulse duration: 300 uS
    • Pulse amplitude: varied, generally considerably less for ONS (occipital nerve stimulation) than supraorbital nerve stimulation (SONS), see graph
    • Pulse frequency: 120 Hz
    • Ramp up: 1 second
    • Ramp down: 0 seconds
    • On time: 5 seconds
    • Off time: 15 seconds
    • Treatment time: 12 minutes

    Note that my pulse width and treatment frequency are higher than was established as safe in the Cefaly (basically a TENS headband) study so anyone looking to recreate my results is taking their health into their own hands. Again, I’m not advising anyone to copy me, I’m just sharing what I do and how well it has worked thus far. Know that every electrical stimulation device comes with a warning not to put the electrodes on your head.

    If you want to play it safe, and perhaps smart, the Cefaly parameters used in the treatment of 2313 headache sufferers were as follows:

    • Pulse duration: 250 uS
    • Pulse amplitude: 16 mA
    • Pulse frequency: 60 Hz
    • On time: ?
    • Off time: ?
    • Treatment time: 20 minutes

    The safe/smart approach might not work as well though. My larger pulse with delivers more current to the neck and head, but it’s been my observation that patients compensate for this by using less pulse amplitude (mA) thus keeping electrical charge (the best measure of dose) roughly equal. In my ongoing experiments I have switched from using the EV-906 machine to a Globus Genesy 300 with a pulse width of 450 uS and mA tolerated is proportionally less. I think my results may be better than the Cefaly results because of my use of the larger rubber carbon electrodes making more stimulation more comfortable, the use of two channels of stimulation instead of one, perhaps my higher pulse frequency or ‘rate’ maybe resulting in high-frequency fatigue of the painful nerves as I blogged about here. Also my programming 5 seconds on 15 seconds off, might be of benefit because when I later tried continuous stimulation, with otherwise identical parameters and it didn’t seem to work as well, though I only tried it on 7 headaches before I got a better idea to test.

    Also note that I put channel-1 electrodes on the back of the neck/occipital region, and channel-2 electrodes on the supraorbital. I do not mix and match them. Splitting the electrodes from one channel to the head and neck would result in ‘transcerebral brain stimulation’ with a machine that is a lot stronger than is known to be safe to do so, so I definitely would caution anyone against that, and I have not tried that on myself or anyone.  

    I switched to the Globus Genesy in part because it’s a true biphasic symmetric current, vs by biphasic asymmetric for the EV-906. In practical terms means both channels of the electrode feel of equal strength in the Globus, while on the EV-906 the ‘red’ wire feels maybe 30% weaker. For personal use on headaches I think this distinction is of minimal consequence, as even with the 30% weaker red wire of the EV-906 can be considerably stronger than anyone with a headache is going to want to use, and near immediate headache reduction of 90% speaks for itself. My switching to the Globus machines is because they became my go-to stimulator in my office where I’m mostly treating other body parts, because increased ease of use, durability, battery life, and power for stimulating other body parts. So for headaches I think the EV-906 is more than enough and about ⅓ the price of the Globus. A smaller ‘programmable’ two channel capable of hitting mine or Cefaly like parameters should be plenty, but I haven’t experimented with any two channel units to have a favorite as of yet.

    • The parameters in this study are still what I would call EMS (electric/electrical muscle stimulation) rather than TENS (transcutaneous electrical nerve stimulation) with EMS generally stronger and intermittent. EMS is type of TENS typically used to strengthen muscles but there is research that says it helps with pain better than TENS, and when I first applied it to the suboccipital region I had pretty good results acutely decreasing pain, at least seemingly better than that produced in the Cefaly research. Note however that I don’t use a control/placebo group, and at this point when I apply EMS/TENS to a patient for a headache I tell them I expect this is going to work. So there is certainly a positive expectation. Still the results presented above are remarkable so I do think there is a real effect going on.
    • A few observations is that it seems really good at knocking out periodic or frequent headaches, if not immediately, within 5 minutes afterwards of the cessation of stimulation.
    • The headaches appear to be gone for a long time, generally not returning for days to weeks.
    • It seems to help, but unfortunately does not always eliminate pain in people suffer chronic headaches, generally defined as 15 or more per month. I’ve only had two patients with chronic headaches and both said the the machines helped enough that they purchased an EV-906 for home use. However I’m still disappointed that they weren’t fully cured, hence I’m continuing read, research, and experiment with EMS/TENS parameters.
    • The other group that didn’t as well (just 4 patients, so I hesitate to draw conclusions) were those with headaches secondary or related to post-concussion syndrome.

    So that’s what I have thus far. I’m currently trying out a new series of tests using a program of frequency modulated TENS, which thus far (4 headaches) is 100%, but I’ll share that data and my program parameters if it turns out preferable.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Are Dietitians Wrong About Dinner Time?

    OK, are dietitians wrong about dinner time? I’m about to reinterpret some 20 year old research, which really got me thinking. Though I might be mistaken, I think the experts are wrong, and the research is on my side. Such that the oft made recommendation to have or finish dinner around 6 pm is not, how is it they say it? “Evidence Based” :

    Influences of fat and carbohydrate on postprandial sleepiness, mood, and hormones. Physiol Behav. 1997 May;61(5):679-86. Wells AS1, Read NW, Uvnas-Moberg K, Alster P.

    Abstract
    Paired studies were conducted in 18 healthy volunteers (9 men, 9 women) to investigate whether differences in mood and daytime sleepiness induced by high-fat-low-carbohydrate (CHO) and low-fat-high-CHO morning meals were associated with specific hormonal responses. Plasma insulin concentrations were significantly higher after low-fat-high-CHO meals, and cholecystokinin (CCK) concentrations were significantly higher after high-fat-low-CHO meals. Subjects tended to feel more sleepy and less awake 2-3 h after the high-fat-low-CHO meal, and ratings of fatigue were significantly greater 3 h after the high-fat-low-CHO meal than after the low-fat-high-CHO meal. The results of the present study are consistent with the hypothesis that there is an association between the lassitude experienced after a meal and the release of CCK.

    My comments:

    When I read the above research summary I get the impression that you really shouldn’t eat high fat meals if you need energy in the next couple hours. However, if you read the actual study and look at the graphs you see that both the high fat and high carb meals increased feelings of fatigue, and made the subjects feel more sleepy, with the high carb meal being just as bad or worse at various time periods of the 3 hours they looked. It’s not like they were hiding anything, it’s more that abstracts don’t always give the whole story. The paper had this fascinating quotes in the introduction:

    “…subjects report feeling more feeble, dreamy, and bored and less excited, clear headed, energetic, quick-witted, friendly, sociable, and elated after lunch than they do before eating.”

    stimulation of the mucosa of the small intestine, either by a small electrical current or by the inflation of a balloon, has been demonstrated to induce sleepiness and sleep in cats”

    “The pattern of afferent impulses evoked during stimulation are similar to those observed during the digestion of food, suggesting that digestive activity may contribute to the induction of drowsiness after eating.”

    So that, combined with a number of other papers I have been reading about meal timing, light/dark cycles and the disruption of circadian rhythms being associated with a number of problems including daytime fatigue, poor eating habits, and depression disorders, got me thinking.

    Maybe the best time to eat, and to subsequently feel tired is right before you want to go to sleep, duh. It definitely makes me think that after dinner is not the time for kids to do homework. Plus, there is the recent blog I did on a study that found people (in general) regardless of how you manipulate them are most hungry at 8 pm, and least hungry at 8 am. Yet all you hear from food experts is the importance of a good breakfast, and how you should finish your dinner early, generally 6 pm, particularly if you want to lose weight. So over the last year of my intermittent fasting I had mostly started eating at 5-6 pm, more recently 7 pm, but now I think I should start enjoying my dinner at 8 pm, live large, and sleep like a baby.

    Also it’s not that I haven’t been looking for research contrary to the late dinner idea. So far I have heard that late meals make sleeping difficult (OK maybe if you have acid reflux) but I have no difficulty sleeping after Thanksgiving dinner for sure. Thus far I have not been able to locate any research that found sleep compromised after eating in regular people. I’ve heard that early dinner’s help weight loss because they increase the fasting time after dinner and before breakfast. I’ll buy that, but it sure seems a Rube Goldberg way to go about it if a late meals do in fact make people tired (WHEN THEY NEED TO SLEEP) and people are naturally least hungry in the morning (WHEN THEY NEED TO BE AWAKE). It just seems to me a whole lot easier, more satisfying, productive, best for overall physical and mental health, to increase the post meal fasting period by skipping breakfast (and lunch while you’re at it). Why? I think because it’s more in accordance with nature. That would also mean that Megan Fox, General Stanley McChrystal and Herschel Walker aren’t wrong, even if they think they sometimes think they are.

    Diet experts, what are we missing?

    To me it makes no sense to eat dinner at 6 pm, feel fatigued afterwards such that all I have energy for the rest of the night to do is watch TV in a horizontal position, then go to sleep around 10 or 11, just in time for my  food coma (apparently well known to researchers as as postprandial somnolence) to be wearing off. So pending and likely regardless of any arguments to the contrary, I think for the next month I’m going to push my first meal of the day, dinner, to 8 pm and see what that feels like.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • EMS, High-Frequency Fatigue and Pain, Particularly Headaches & Back Pain

    I needed a break from fasting papers and, while I’m a big, BIG fan of EMS, and to a substantially lesser extent TENS, I am underwhelmed by high “kilohertz-frequency” alternating type currents as is commonly used in Russian stimulation for strength and interferential currents (IFC), sometimes used for both strength and pain. However, I thought this paper was a good review on both and concludes that neither Russian stimulation are ideal and that there are better forms of “kilohertz-frequency” electrical stimulation. I don’t doubt his conclusions but I think biphasic square wave currents are better still, such that this paper was almost academic for me.

    Electrical stimulation using kilohertz-frequency alternating current. Ward AR. Physical Therapy. 2009 Feb;89(2):181-90. [FREE FULL TEXT]

    Abstract
    Transcutaneous electrical stimulation using kilohertz-frequency alternating current (AC) became popular in the 1950s with the introduction of “interferential currents,” promoted as a means of producing depth-efficient stimulation of nerve and muscle. Later, “Russian current” was adopted as a means of muscle strengthening. This article reviews some clinically relevant, laboratory-based studies that offer an insight into the mechanism of action of kilohertz-frequency AC. It provides some answers to the question: “What are the optimal stimulus parameters for eliciting forceful, yet comfortable, electrically induced muscle contractions?” It is concluded that the stimulation parameters commonly used clinically (Russian and interferential currents) are suboptimal for achieving their stated goals and that greater benefit would be obtained using short-duration (2-4 millisecond), rectangular bursts of kilohertz-frequency AC with a frequency chosen to maximize the desired outcome.

    My comments:

    The above abstract and the paper were interesting to me because, the author does a good job of reviewing the research putting the slam on IFC, both in theory and in practice. However, the part I thought was fascinating and got me thinking about my use of electric stimulation for headaches was his section titled High-Frequency Fatigue:

    “When electrical stimulation is applied to elicit a motor response using PC frequencies higher than physiological or at the high end of the physiological range (ie, greater than about 50 Hz), it is possible to produce a blockage of muscle activity due to propagation failure or neurotransmitter depletion…This is responsible for the phenomenon of “high-frequency fatigue…”

    “…whether propagation failure or neurotransmitter depletion, a blockage of muscle contraction at stimulation frequencies around and above about 50 Hz is the result, and the effect is described as high-frequency fatigue.”

    So that got me thinking. In the above quotes, when talking about PC frequencies, the PC stands for ‘pulsed current’ for which the the biphasic square wave current I use is an alternating form of PC. I set all my machines at 120 hz, which is higher than most recommend for muscle strengthening, which I got from something the famous sprint coach Charlie Francis said he used with his sprinters (and unfortunately I can’t remember where I read it. Anyway, I have been programming my EMS machines with 120 hz ever since and it seems to work great. When I first tried EMS on my headache patients I used 120 hz (10 seconds on, 50 seconds off for 10-12 minutes) the same as I did for muscle strengthening and it worked great with my results being better than reported with the Cefaly studies. There are a few reasons why I think my results are better (use of much larger electrodes, use of rubber carbon electrodes) and I thought my higher frequency stimulation (120 hz vs 60 hz with the Cefaly) felt better. I tried 60 hz and thought it felt ‘prickly’ while the 120 hz felt like a comfortable buzz, and particularly when I started stimulating the supraorbital nerves, as the Cefaly device does. I wasn’t intending to strengthen any muscles, and utterly fatiguing out the sensory nerves sure is what it feels like was happening. So maybe that’s part of what’s going on, the higher frequency stim, which might be overkill (though still plenty effective) for muscle strengthening is fatiguing out the nerves eliminating headache pain. It also makes me wonder if the 120 hz frequency I use for core strengthening in low back pain patients explains why my patients get such a remarkable amount of immediate pain reduction. I always thought it was from the higher amount of current delivered which is implicit with EMS vs TENS, but maybe it’s higher than normal rate of delivery of said current. Reading this paper also makes me wonder if the faster muscle fatigue with the higher rate of stimulation leads to long term performance gains, and if the quicker muscle fatigue lets you tolerate higher amplitudes of stimulation, thus better exploiting gate control theory for pain reduction.

    So I don’t know, this paper gave me some ideas for which there aren’t yet definite answers. I like a higher frequency EMS than most think is ideal, and my reasons have been because I subjectively liked them better, and because that’s what Charlie Francis used. However, now I think I might be making better use of high-frequency fatigue, which might be at least part of the reason behind my (and my patients) subjective preferences.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Intermittent Fasting, BDNF, Depression, More

    Dietary restriction stimulates BDNF production in the brain and thereby protects neurons against excitotoxic injury. Duan W, Lee J, Guo Z, Mattson MP. J Mol Neurosci. 2001 Feb;16(1):1-12. [FREE FULL TEXT]

    Abstract
    Dietary restriction (DR) increases the lifespan of rodents and increases their resistance to several different age-related diseases including cancer and diabetes. Beneficial effects of DR on brain plasticity and neuronal vulnerability to injury have recently been reported, but the underlying mechanisms are unknown. We report that levels of brain-derived neurotrophic factor (BDNF) are significantly increased in the hippocampus, cerebral cortex, and striatum of rats maintained on a DR regimen compared to animals fed ad libitum (AL). Seizure-induced damage to hippocampal neurons was significantly reduced in rats maintained on DR, and this beneficial effect was attenuated by intraventricular administration of a BDNF-blocking antibody. These findings provide the first evidence that diet can effect expression of a neurotrophic factor, demonstrate that BDNF signaling plays a central role in the neuroprotective effect of DR, and proffer DR as an approach for reducing neuronal damage in neurodegenerative disorders.

    My comments:

    This paper dated in 2001 was written before “intermittent fasting” became a thing, so the results were a little hidden under the title “dietary restriction” but these rats were fasting nonetheless. One of the study authors here is Mark Mattson who did the TED talk on fasting and brain power. BDNF (brain derived neurotrophic factor) isn’t particularly catchy in the literature but appears immensely important to aging well, maintaining memory, preventing Alzheimer’s. So these findings relate to a lot of potential health benefits that are apparently easily achieve and underutilized.

    What I thought was most fascinating from the paper wasn’t just intermittent fasting increases BDNF, but rather how much it increases, which wasn’t just “statistically significant” but was EXTREMELY SUBSTANTIAL! Three months on an alternate day diet increased BDNF increased hippocampal BDNF ~519%. Brain researchers are apparently especially interested in hippocampus BDNF and nerve growth because atrophy and decline is especially associated with depression disorder, brain aging, memory loss and Alzheimer’s disease. There are even associations of low BDNF seen in anxiety disorders.

    There are a number of ways to increase BDNF and I first read about it in the book Spark, which was a great book about the effects of exercise on the brain. It had a chapter on depression and how aerobic exercise in particular increased BDNF and decreased depression symptoms. I had also read about BDNF due to my interest in electric stimulation for headaches, which then got me reading about electroconvulsive therapy (ECT), which is said to be the single most effective treatment for major depression disorder, for which a major pathway in which it is thought to work is by increasing BDNF and therefore new neuron growth in the hippocampus. A recent paper just looked at combining ECT with aerobic exercise and they found the effects to be additive, thus both ECT and exercise worked, but the combination worked better with regards to both increasing BDNF and decreasing symptoms. The downside of ECT doesn’t seem to be the ECT itself so much, but that it requires the patient to go under general anesthesia, each and every time over the course of the treatment, which regardless of effectiveness sounds like a bit of an ordeal.

    This paper also found the increases in BDNF were more widespread than just the hippocampus and rather increased in all parts of the brain in which they looked. Cerebral cortex BDNF was increased ~150%, and straitum BNDF increased ~282%. Nerve growth factor (NGF) was also increased with alternate day eating being increased ~64% in the hippocampus, 70% in the cortex and 89% in the straitum.

    As I read more and more papers about people using fasting, either intermittent or prolonged for weight loss, there are very frequent reports of improved well being and sometimes “frank euphoria” among the fasters. I had previously thought the ‘high’ you get from fasting was due to the increase in endorphins, and I’m sure part of it is, but it looks like BDNF and subsequent neurogenesis might also be part of it, particularly in the long term. So far I have not seen anyone put two and two together looking at intermittent fasting and mental health, but with major depression and associated disorders continuing to be such a problem, thinking inside the box is likely a sub-optimal strategy. It certainly looks worth a try, and combined with aerobic exercise might be a powerful long term fix that may lessen reliance on drugs which have serious side effects and are of debatable effectiveness. The side effects of intermittent fasting seem to be that you look better, age slower, and die older.

    So if you haven’t tried it, try it, you’ll probably feel better.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Exercise vs Intermittent Fasting for Longevity

    Differential effects of intermittent feeding and voluntary exercise on body weight and lifespan in adult rats. Goodrick CL, Ingram DK, Reynolds MA, Freeman JR, Cider NL. J Gerontol. 1983 Jan;38(1):36-45.

    Abstract
    Male wistar rats were housed in laboratory cages or activity-wheel cages at eight 10.5 or 18 months of age. Part of each cage group continued to be fed ad libitum, whereas the remaining animals were fed every other day. Compared with the ad libitum condition, intermittent feeding decreased body weight and increased lifespan at both ages in both caging conditions. Compared with the caged condition, voluntary exercise in activity wheels reduced body weight only in the 10.5-month-old group fed ad libitum but produced no effect on survival of either age group. The results suggest that intermittent feeding can enhance survival in mature rats even beyond ages at which body weight growth usually ceases, whereas voluntary exercise appears to have an early threshold beyond which increases in longevity are not observed.

    My comments:

    The “intermittent feeding” in this 1983 paper turns out to be what is now becoming somewhat popular as a version of intermittent fasting, and makes me wonder why nobody was talking about intermittent fasting back then. Instead everyone was talking about running, while intermittent fasting might have saved Jim Fixx.

    In this paper rats of two different ages were tested, starting with 10.5 month old rats (not quite mature, or not at peak body weight), and 18 month old rats (fully mature based on body weight). A number of things were interesting from this study, first being that the intermittent fasting diet improved lifespan a full 36% in the 10.5 younger rats, and 14% in the 18 mature rats. However the researchers said the difference and improvement was misleading because both fasting groups had a mean lifespan of 27 months, while the everyday eating rats in the younger experiment lives were shorter at 20 months compared to 23 months in the older ad lib eating rats, which they thought was likely due to survivorship bias in the older ad lib rats. Exercise surprisingly to me had no statistic or consistent effect on lifespan in either the ad lib or intermittent fasting animals, though roughly looking at their graphs the exercising groups generally did appear slightly ahead of the sedentary animals.

    In the discussion they mentioned limits with regards to the degree of dietary restriction generally being beneficial with survival. Restricting food intake >50% shortening lifespan and 10% restriction was beneficial, but increasing lifespan only 7%, less than usually seen with ~30% restriction or the every other day diet.

    Interestingly in this study the fasting rats given access to a running wheel did tend to spontaneously exercise more, 2-3 times as much compared to the ad lib rats with a running wheel. So it’s not like fasting animals get old and decrepit, doddering on in old age, but rather were apparently healthier and aging substantially slower.

    My favorite variety of intermittent fasting is still “time restricted feeding” variety which I think has a lot going for it, but in the research the every other day diet does have the preponderance of evidence behind it. I think we all hope (and some evidence suggests it’s true) that the every other day fasting findings are applicable to time restricted feeding. My apprehension regarding the every other day time plan has been that it’s supposed to be particularly arduous, while time restricted feeding soon becomes a pleasure. However I’m typing here on Tuesday afternoon, having not eaten anything since Sunday night. I’m calling mine “No Meals Mondays” and I have to say it’s not that bad. Last week around 42 hours of fasting I felt like I was entering an altered state of consciousness/feeling of calm or “meditative” state that made me wonder if this is what it feels like to not have ADHD. It was kind of like Adderall without the irritability. So we’ll see if I get that later today, but being almost 11 months into my intermittent fasting lifestyle, it’s kind of fun and definitely interesting to see what you can take and what it feels like.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Placebo Effect: You Probably Shouldn’t Know This, But…

    This is one of those papers where the abstract doesn’t quite cut it, and the whole paper was a fascinating read. I got thinking about it after reading my favorite paper on acupuncture, “Acupuncture is Theatrical Placebo” and I have since caught myself using the term “theatrical placebo” on the reg. That got me wondering and talking about the placebo effect and thinking the more theatrical the treatment the more effect you might get. Such that placebo shots would be more effective than placebo pills, and placebo surgery better still. It turns out, that’s pretty much the case but the details are fascinating. See my comments below the abstract for details.

    The “placebo” response in osteoarthritis and its implications for clinical practice. Doherty M, Dieppe P. Osteoarthritis Cartilage. 2009 Oct;17(10):1255-62. Apr 17. [FREE FULL TEXT AVAILABLE]

    Abstract
    Many observations support a major biological effect from the way in which people interpret the meaning of each component of their medical experience and the context in which this occurs. A recent systematic review of randomised controlled trials in osteoarthritis has demonstrated that the effect size of “placebo” is substantial and is usually greater than that obtained from the specific effect of an individual treatment. In the context of a randomised controlled trial, such a large placebo or “meaning” response is considered a nuisance, but in the context of clinical practice the optimisation of such meaning and contextual responses, through enhanced “care”, could greatly benefit people who suffer from osteoarthritis.

    My comments:

    As mentioned above the abstract doesn’t do this paper justice, and the full text is well worth a read, going well beyond the treatment arthritis. Reported findings include:

    1. With regards to osteoarthritis the effect size of the placebo (0.5-0.7) was much larger than that achieved with analgesic and anti-inflammatory drugs (0.2-0.3).
    2. Brand name placebo pills work better than generic placebo pills.
    3. Perceived price matters. Patients told their pills are expensive get a better effect than if they are told they got them discounted.
    4. Knowing, and seeing the intervention happening helps. Morphine administered directly into a PIC line led to faster pain relief than if it were concealed. Also open discontinuation of morphine administration resulted in a rapid return of pain, while concealed discontinuation did not.
    5. Yes, the more invasive the procedure, the better the placebo. Injections work better than placebo pills, and placebo surgery works better still.
    6. More placebo pills, injections, needles work better than fewer. Psychologically, acupuncture/dry needling which frequently uses a lot of needles would appear to have a has a lot going for it, though it’s unfortunate if you end up with a pneumothorax.
    7. Expectations matter a lot. If subjects are told what to expect, they’ll get more of that. They found ipecac (used to induce vomiting) can reduce nausea if subjects are told that’s what it does.
    8. A ‘new’ fake treatment works better than one where the treatment is established.
    9. Placebo response isn’t entirely psychological. There is evidence that placebo effects cause a real increase in endogenous opioids. (aka endorphins). This was one of the more interesting aspects of the paper to me and I’ll probably look up the references to see how much endorphin response there was from placebo treatments, how that relates to exercise, or other treatments (like TENS) reported increase endorphins to know if one increases them more than another. I’m also curious as to whether or not the more powerful placebo effects work all or in part by increased endorphin response.
    10. The nicer/more natural the environment/view (e.g. being able to look out the window and see trees) the better the outcomes of treatment.
    11. For irritable bowel syndrome (IBS) no treatment/waiting list was 28% effective, sham acupuncture (kind an oxymoron) with limited practitioner interaction was 44% effective, while sham acupuncture applied with positive practitioner intervention, with “warmth, attention and confidence” was 62% effective.
    12. An exorcism maybe works better than an aspirin if the patient really believes their possessed.
    13. If the provider is optimistic about the treatment, it improves outcomes. Provider pessimism does the opposite.
    14. A positive consultation for which the patient was given a confident diagnosis and told things would improve led to better (64% improvement) compared to a negative/indefinite consultation (39%) for which the doctor said “I cannot be certain what is the matter with you.” They said receiving a prescription made no difference. This overlaps with the optimism, but it seems a confident diagnosis matters. This is something I have noticed improves with experience and as important continued reading of the medical literature. Diagnosis do become more exact, and you sound better talking about it.

    The good news from all this is that most of the above benefits are not exclusive to sham interventions but generally come along free with real treatment. I could comment on this paper for hours, but for the most part it reminds of the review paper on optimism I blogged on. As such I think “real” treatment provided positively, with caring and confidence is the best of all worlds. I think using known or suspected placebo treatments is what practitioners do only if they ignorant of better ideas and/or  (more often the case) fooled themselves.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFITyoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Weight Loss, Set Point Theory, Metabolism and Thyroid Hormone

    Do adaptive changes in metabolic rate favor weight regain in weight-reduced individuals? An examination of the set-point theory. Weinsier RL, Nagy TR, Hunter GR, Darnell BE, Hensrud DD, Weiss HL. Am J Clin Nutr. 2000 Nov;72(5):1088-94. [FREE FULL TEXT]

    From the study:

    Abstract
    BACKGROUND:
    Obese persons generally regain lost weight, suggesting that adaptive metabolic changes favor return to a preset weight.

    OBJECTIVE:
    Our objective was to determine whether adaptive changes in resting metabolic rate (RMR) and thyroid hormones occur in weight-reduced persons, predisposing them to long-term weight gain.

    DESIGN:
    Twenty-four overweight, postmenopausal women were studied at a clinical research center in four 10-d study phases: the overweight state (phase 1, energy balance; phase 2, 3350 kJ/d) and after reduction to a normal-weight state (phase 3, 3350 kJ/d; phase 4, energy balance). Weight-reduced women were matched with 24 never-overweight control subjects. After each study phase, assessments included RMR (by indirect calorimetry), body composition (by hydrostatic weighing), serum triiodothyronine (T(3)), and reverse T(3) (rT(3)). Body weight was measured 4 y later, without intervention.

    RESULTS:
    Body composition-adjusted RMR and T(3):rT(3) fell during acute (phase 2) and chronic (phase 3) energy restriction (P: < 0.01), but returned to baseline in the normal-weight, energy-balanced state (phase 4; mean weight loss: 12.9 +/- 2.0 kg). RMR among weight-reduced women (4771 +/- 414 kJ/d) was not significantly different from that in control subjects (4955 +/- 414 kJ/d; P: = 0.14), and lower RMR did not predict greater 4-y weight regain (r = 0.27, NS).

    CONCLUSIONS:
    Energy restriction produces a transient hypothyroid-hypometabolic state that normalizes on return to energy-balanced conditions. Failure to establish energy balance after weight loss gives the misleading impression that weight-reduced persons are energy conservative and predisposed to weight regain. Our findings do not provide evidence in support of adaptive metabolic changes as an explanation for the tendency of weight-reduced persons to regain weight.

    My comments:

    This study is interesting for a number of reasons. First, the main finding was that putting overweight women on an 800 calorie per day diet did rapidly result in weight loss averaging 28 lb in an average of 15.4 weeks (12-20). That’s 1.82 pounds per week, so not bad at all. The diet did however decrease their thyroid hormone and did result in the resting metabolic rate of the dieters being decreased 6%. That sucks, however, once the weight was lost and the dieters were put on an isocaloric diet, both thyroid hormone and metabolism returned to a “weight adjusted” normal (by my math almost normal at least) and it took only 10 days for it to happen. It’s worth pointing out that “weight adjusted” means that as you lose weight, both the lean tissue and the fat lost results in a lesser metabolic rate. This means that skinny people burn fewer calories doing nothing than do fatter people. What they found however, was that after losing weight and establishing a maintenance diet, the formerly overweight subjects’ metabolisms were nearly the same as women their size should be, and based on metabolism they were not physically predisposed to gain their weight back. So that’s good news, and it means dieting works and you weren’t physically set up to fail afterwards.  At least that’s the statistical significant answer. Absolute numbers there was a 44 calorie daily difference in adjusted metabolic rate, which may not have been statistically significant and isn’t dooming, but certainly doesn’t help. If not normalized in time, doing the math 44 calories x 365 days / 3500 calories per pound of fat works out to gaining 4.6 pounds per year or 18.35 pounds over the 4 year follow up. That might not be enough to explain all the actual (24.4 lb) gain in the following 4 years, but it sure explains a lot of it. They said the “weight-gain tendency of obesity-prone persons appears to be caused by factors other than variations in metabolic rate” but I don’t know, a larger sample with the same findings probably would have been statistically significant. So to me the findings and the conclusions are a bit questionable.

    Which brings me to thinking about intermittent fasting (IF). The results of this study got me wondering about the results of short term but full-on fasting for four days.  With 4 days of fasting, metabolic rate increased over 10%. Such that I’d like to know and how this would relate to IF where short term fasts are continued regularly. I would also like to know what happens to thyroid levels and metabolic rate when intermittent fasting is and isn’t combined with caloric restriction. Caloric restriction generally (but not always) happens without trying when doing intermittent fasting. I would expect, or at least hope, the metabolic rate increase from fasting might help offset the short term metabolic slowdown from caloric restriction. Other research found less lean tissue loss with IF as compared to typical caloric restriction diets, which if true would have preserve a higher metabolic rate.

    Finally, I don’t think of IF as a weight loss diet. I don’t use it as such. Rather it’s a very simple healthy eating plan, that saves time and money and  lets you eat large meals of most anything you want. It just has the frequent side effects of fat loss, improved willpower, and breaking the connection/addiction to sugary/fatty foods which gradually makes you “want” to eat healthier. Such that it’s not something you go into with the idea of going off later on. Hence, I would expect the weight lost with IF to be lasting, so it will be interesting to see how this all plays out in the research going forward.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.

  • Intermittent Fasting and Circadian Rhythms

    I had a blog idea comparing various cleansing/detoxification schemes with intermittent fasting, with the gist being that there are some similarities. Both probably make you feel better for largely the same reasons, but that fasting is better and free. With detoxing and cleansing, it seems that someone is always trying to separate you from your money in some way.

    So anyway, I’m still planning that blog and in doing so I thought I would look up what “ScienceBasedMedicine.org” had to say about both. Generally they hate everything alternative, and predictably they put the smack down on cleansing/detoxifications for reasons I largely agree with. I was somewhat surprised to see they seemed overwhelmingly positive yet cautious about intermittent fasting, again for reasons I overwhelmingly agree with. Intermittent fasting really is getting a lot of science behind it, and my own experience has been (and continues to be) pretty great.

    So anyway, that’s not what this blog is about, but in reading the sciencebasedmedicine.org article on fasting, it cited a study about circadian rhythms that I have been looking for data on for some time. It’s funny, you go to pubmed.com enter in your search terms and things don’t always just pop up as you want. So anyway, here’s the paper I wanted to talk about with comments to follow:

    The internal circadian clock increases hunger and appetite in the evening independent of food intake and other behaviors. Obesity (Silver Spring). 2013 Mar;21(3):421-3. Scheer FA, Morris CJ, Shea SA.

    From the Abstract

    RESULTS:
    There was a large endogenous circadian rhythm in hunger, with the trough in the biological morning (8 AM) and peak in the biological evening (8 PM; peak-to-trough amplitude = 17%; P = 0.004). Similarly-phased significant endogenous circadian rhythms were present in appetites for sweet, salty and starchy foods, fruits, meats/poultry, food overall, and for estimates of how much food participants could eat (amplitudes 14-25%; all P < 0.05).

    CONCLUSIONS:
    In people who sleep at night, the intrinsic circadian evening peak in appetite may promote larger meals before the fasting period necessitated by sleep, whereas the circadian morning trough would theoretically facilitate the extended overnight fast. Furthermore, the circadian decline in hunger across the night would theoretically counteract the fasting-induced hunger increase that could otherwise disrupt sleep.

    My comments:

    This was interesting to me because I first learned about intermittent fasting by reading on wiki “The Warrior Diet”. It turns out that wasn’t true fasting because Ori Hofrichter ate (but ate in smaller amounts) during the day. I later became a fan of the Fast-5 diet because it was simpler. Bert Herring was a real faster, because he ate nothing during the day.  It also helps that Burt gives his book away, and even better, he didn’t try and sell you on hundreds of dollars worth of supplements every month.

    The thing that appealed to me was not having to prepare any meals, healthy or not, during the day, and just being able to eat as I wanted at night. Still I think both Ori and Bert were on to something about consuming the bulk of, or all of your calories at night. Night time seemed when most people want to eat. As such, I think when people try to lose weight with a lot of small meals as is typically recommended, you’ll be taking in some of those calories when you aren’t really hungry, or are otherwise busy. Then at night when you really are more hungry, and the refrigerator is right there, you have to chose between cheating or suffering.

    I also think the circadian rhythms would go a long way towards explaining eating disorders such as binge eating and bulimia, where the binge and subsequent purge is generally at night. While it hasn’t been researched yet, I have this suspicion that time restricted feeding with a night time eating window, is God’s gift to both disorders. Though probably not anorexia, where eating more calories is necessary.

    With the time restricted feeding variety of intermittent fasting, your eating won’t interrupt your day, that way at night when you are most hungry you can have big, satisfying meals. I had always thought this was the most efficient way to go, and the most psychologically satisfying. At the end of the day, you still had your big meal/reward to look forward too. If I recall correctly, Ori in The Warrior Diet talked about eating at night being the most natural, arguing that, lions have to be cunning and alert when hungry (in sympathetic mode), and then can relax after eating (in parasympathetic mode). This is something I never saw any research on, but I find his logic compelling.

    Finally I came across a paper that kind of backs up his theory that night eating is the most natural time to do it, and that there is more to it than psychology and convenience. 8 am is when we are least hungry, and our hunger peaks at 8 pm every night. The Warrior Diet’s 4 hour window of eating most of your food from 6-10 pm seems to hit that just right. The same is true of the Fast-5’s typical window of 5-10 pm. For what it’s worth, I now hybrid the two, eating all my calories in a 4 hour window like Ori, with no small meals like Burt, and it’s just as easy.  

    So to sum it all up, what’s that you hear about breakfast being the most important meal of the day? That’s called propaganda.

    Thanks for reading my blog. If you have any questions or comments (even hostile ones) please don’t hesitate to ask/share. If you’re reading one of my older blogs, perhaps unrelated to neck or back pain, and it helps you, please remember SpineFit Yoga for you or someone you know in the future.


    Chad Reilly is a Physical Therapist, obtaining his Master’s in Physical Therapy from Northern Arizona University. He graduated Summa Cum Laude with a B.S. Exercise Science also from NAU. He is a Certified Strength and Conditioning Specialist, and holds a USA Weightlifting Club Coach Certification as well as a NASM Personal Training Certificate. Chad completed Yoga Teacher Training at Sampoorna Yoga in Goa, India.