OMM Case Studies

The purpose of this thread is to give DO students and premeds an idea of what is possible with Osteopathy. There is a fair bit of cynicism on SDN about osteopathy and OMM. I know some of you have had bad experiences in school or have been asked to believe things without evidence. Dont throw the baby out with the bathwater. AT Still was onto something huge, something that modern evidence based medicine will only clarify and enhance. Research on osteopathic methods/OMM is still thin. We need cases to spark ideas for good pilot studies- which are in turn required for large controlled well funded studies later. Cases are no substitute for good research- but they are the first step towards that goal.

I plan on posting cases here from my own practice. I have hundreds if not thousands of cases like this, so if you have any requests for particular conditions I can talk about what I have done or give a particular case (if I can remember it in detail or find my note).

If you have your own cases to post- that is fine, but there are rules-
1) it has to be a real case. No making up stories, and please dont fudge the details if you don't recall. Look up the chart if you need to, or be clear about where your memory fails you. The goal of this is understanding and teaching, and for that we need the truth.

2) try to provide as much relevant history and physical exam as possible. Don't waste our time with lots of extra information if it is not pertinent to the case. Do your best to be concise (a few paragraphs- history, physical, assessment, treatment, Plan/outcome/followup/rationale for success and relevant links to review sites or primary lit). Provide enough so that someone could replicate your approach and potentially get the same results.

3) pick impressive cases if possible- ideally office visits that have changed your patients life in a major way, prevented surgery, made a rare diagnosis, etc. If you know what you did to get this result- be specific as to your theory, but provide enough detail for alternative theories. If you just got lucky- provide as much detail as you can as to your approach and perhaps we can figure it out.

If you see stuff you like here, bump and request a sticky!

Case:
A woman in her late 20's presented to the clinic with chief complaint of hypertension.

History
This patient presents with a 3 month history of blood pressures averaging 150's systolic and 90's diastolic. She has had daily headaches for the past 6 years since a head injury (i don't recall the cause- i think it was a motor vehicle accident). At least 1 and usually 2-3 headaches per week were light sensitive and produced nausea. She takes mobic 3-4 days per week for her headaches. Over the counter remedies, Vicodin and muscle relaxers do not seem to help, and she has not tried other medications. She has one of her mild daily headaches today without light sensitivity. She also reports terrible sleep- waking many times per night. She denies N/V, dizziness or other symptoms at time of visit. No other relevant PMHx.

Objective
BP 150's systolic 90's diastolic
pulse normal range
physical exam- unimpressive except for severe cranial compression. Patient had transient reproduceable severe splitting headache, light sensitivity and nausea with compression through a horizontal vector encompassing the right greater wing of the sphenoid (reminiscent of her migraines).

Assessment:
1) hypertension probably due to medication side effect (Mobic)
2) post concussive migraines
3) post concussive sleep disturbance
4) probable medication overuse headaches
5) somatic dysfunction findings (don't recall all regions treated, head was of prime relevance)

Plan:
Treatment of the head using Ligamentous Articular Strain style technique- probably about 20 lbs of force. Compression resolved with treatment, and her migraine was no longer reproduceable despite significant force through the region. There was resolution of the patients mild headache that she came in with as well. I told her to stop taking her mobic, and to use only tylenol- and only if she gets a severe headache (do not medicate the mild ones). On 2 week follow up she was quite excited. Her sleep was normal for the first time in years. Her BP was 128/72 and she had only 1 mild headache during the follow up period, and did not use any pain medicine. I used a similar OMT approach, resolving whatever residual findings there were, and told her to follow up as needed if she had any more headaches or BP issues. She has not thus far followed up after 6 more weeks. In retrospect she had no rebound headache after quitting the mobic- so most of her headaches and migraines were probably due to the concussive syndrome/compression rather than medication overuse.

In my experience- cranial compressions from serious head trauma will cause migraines and sleep disturbance in many cases. All migraine patients I have worked on lately appear to have reproduceable migraine strain patterns as the above case- and in many such cases migraines resolve and do not return after a single successful treatment. I do not have evidence to support this claim- detailed studies using objective measures will be needed to validate these findings.

relevant articles:
http://www.uptodate.com/contents/postconcussion-syndrome
http://www.uptodate.com/contents/me...ache-etiology-clinical-features-and-diagnosis
http://www.uptodate.com/contents/nsaids-and-acetaminophen-effects-on-blood-pressure-and-hypertension

danzman said:

So I guess I don't understand what you are looking for? Anecdotal case studies, research, EBM? It seems that nearly every piece of work I read that praises OMT is poorly designed, and every decent study finds no solid evidence.

In all seriousness though, I would love some good EBM on the subject.

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I agree with your assessment. OMM research sucks. As much as possible I use primary lit and modern understanding of anatomy, physiology and pathophysiology to try to come to a correct diagnosis, and then reason- if possible using EBM as to its cause- once there, I try to determine how the diagnosis might be cured using minimally invasive techinques (in many cases OMM).

You are not expected to provide any cases if you don't have any- feel free to ask questions about the ones I present or ask questions about specific illnesses and I'll try to give examples of how I approach them.

CASE:

A woman in her 70's with severe left knee pain and a history of bone on bone osteoarthritis of the left knee, told she needed knee replacement by her rheumatologist and seeking a second opinion.

History:
Patient presents with a 13 year history of severe left knee pain, keeping her from walking without a severe limp. She has a visible moderate severity valgus deformity of the limb, which she states has been present since birth. She reports that the knee never bothered her until she fell on the ice 13 years ago resulting in sudden severe pain which has been present 100% of the time since this initial injury- but far worse with weight bearing and with extension. She has difficulty completely extending her knee without it "catching". She hurts worse going down stairs vs up stairs- but both are difficult for her. She has undergone several synvisc injections and steroid injections of the knee without relief. X ray of the knee revealed severe osteoparthritis with bone-on-bone.

Objective:
Vitals stable
exam of the knee revealed valgus deformity. There was a large stiff bulge in the lateral aspect of the popliteal fossa, and anterior pressure through this structure towards the lateral meniscus exactly reproduced her pain. Pain was also reproduced through extension, and she wasn't able to extend the knee fully (was restricted by about 10 degrees).

Assessment
1) lateral meniscal strain/malposition
2) somatic dysfunction of the lower extremity.

Plan
Based on the exam, I proceeded to use myofascial release to treat the popliteal fossa. While balancing the popliteal fossa in an indirect fascial position, she tolerated about 5-10 lbs of anterior force through the region. I maintained this until the soft tissue normalized. I then used mild traction through the knee, gently oscillated the region until several loud articulations occurred. She was then able to fully extend the knee. The patient proceeded to stand on her knee with no pain, and walked up and down the hallway with no pain. On 2 week follow up she only had mild pain when she was working and no pain during normal day to day activities, walking, going up or down stairs, or fully extending her knee.

I have seen this presentation/diagnosis about a dozen times in my practice this year (had 2 such cases actually last friday- one a 88 year old woman and one a ~50-some year old male physician- both convinced by other physicians they would need knee replacements, both pain free after one visit of OMM- though i obviously havent had follow up with them yet), several months ago I actually had one patient cancel her knee replacement surgery (a $20k procedure) that was due the following week because her knee pain was resolved, she had no pain at all at a 2 month follow up. I believe that many cases of extreme functional knee pain originate at the meniscus, and like the shocks of a car- they need to be positioned correctly relative to their surrounding structures to prevent wear and pain. The wear in most cases does not appear to be the cause of pain- it seems to be the poor biomechanics that cause both the wear and the pain- and fixing the mechanics should prevent the pain and resolve worsening of the abnormal wear (though im sure the arthritis is still there on x-ray). I have no objective evidence to make any claims about what is possible, just my experience. Obviously more studies need to be done.

Relevant articles:
http://emedicine.medscape.com/article/308054-overview
http://www.uptodate.com/contents/meniscal-injury-of-the-knee

CASE

A 2 ½ year old girl with developmental delay.

History
This patient initially presented 3 weeks ago with a history of developmental delay since birth. The mother reports no known birth trauma or childhood injuries and was born at term. The girl walked at 18 months (normal is 12), has a very limited vocabulary of only a few words that are repeated by memorization to get certain things (as if she doesn't understand them). She is “floppy” per the parents and has a partially spastic gate. She has always been a “good” kid, never making much noise or being very active. In fact, her 14 month old brother was outrunning her at time of first exam. The mother reports that the patient has frequent leg cramps at night and rarely sleeps more than a couple hours at a time- often screaming and crying between the hours of 2am and 4am.

Objective:
Vitals Stable
Gait is wide, unstable, halting. Child does not make eye contact, appears to be staring into space. I introduce myself and hold out my hand and she stands there staring. The mom tearfully reaches out and helps her take my hand. When asked to lie down the child does not comply but does not resist our attempts to position her.
Her OA is severely sidebent to the left, she has a severe posterior cranial compression involving the occiput and temporal bones. The rest of her neck appears to compensate for the upper cervical lesion by bending to the right.

Assessment
1) Developmental Delay.
2) Restless leg syndrome(?)
3) Somatic Dysfunction of the Head and cervical spine

Plan
Based on today exam, I used balanced indirect pressure (~15 lbs) on the child's skull to treat her compression resulting in normalization of tissue tone and symmetry of this region. I used fascial direct HVLA on her OA region, with normalization of her upper cervical spine, and the lower cervical spine straightened easily without intervention once the OA was normalized.

To me the leg cramping sounded like the way restless leg syndrome presents in adults. While a review of literature reveals many causes of RLS, I have seen consistently wonderful outcomes treating restless leg syndrome with Mangesium Sulfate (IM, IV or transdermal using epsom salts, though oral Mg does not seem to alter clinical outcomes). I thus empirically recommended that the parents bathe their daughter using epsom salt daily (not very scientific I know- but I didnt want to stick her to draw an RBC Mg level, nor did I want to give her an IM Mg shot if the transdermal may be as effective, and the risk was low).

On two week follow up I entered the room and didn't recognize the patient, and had to validate that she was the same girl I treated before. She was running around the room, smiling, laughing, talking in complete sentences. No coordination issues at all were visible, she made instant eye contact- greeted appropriately- showed no signs of shyness, followed orders perfectly. Essentially age-normal in every visible way. The mom reported that she didn't even recognize her daughter anymore either. After bringing her home the child slept through the night that night and every night thereafter without disturbance. She had no more leg cramps (presumably due to the epsom salt baths). She said “i cant really complain, but last week she's told me “no” for the first time. At least she's exerting her independence... even if I dont like it”

This result was more than I expected, and the best I've seen for this kind of case among my patients. A couple of old time osteopaths are quoted as saying that cranial compressions will shut down a child's development- and that if you fix the compression you can fix the child. This appears to be one such case- though an n of 1. I would love to do a large study if we can find many such cases in a concentrated area. One theory holds that up to 50% of autism-like disorders reflect seizure-like activity in the brain, and Mg has known anti seizure properties- so it is possible that some of the girls cognitive improvements could be attributable to this- and sleep quality may decrease muscle irritability in the neck as well. I do think the cranial treatment was the major factor in her recovery but I cannot prove it, and this is an alternative theory that may warrant further investigation.

Take home message:
In kids with developmental delay- fix any compressions you find.
Further research needed to see if these results can be repeated in larger groups with a control group. We also need to establish what- if anything is the mechanism of this change (perfusion of certain brain areas, release of physical stress on certain groups of neurons or axons, etc.). Perhaps we could use fMRI's with sedated children much like in the Autism article listed below- with before/after studies and the radiologist reading the studies and techs and parents blind to grouping.
Further research is needed to determine what percentage of children with this presentation actually are undergoing seizure-like activity in their brain, and whether Mg may help this in a subset of patients.
Research needed on RLS in adults and children, whether Mg can be consistently used to demonstrate positive outcomes in all cases or just a subset of cases. If found effective for some or all of these patients, different formulations of Mg should be tested for efficacy.

This is what I've found so far in terms of relevant research:

Developmental delay/PDD/Autism
http://www.cdc.gov/ncbddd/autism/hcp-dsm.html
http://www.webmd.com/brain/autism/n...rains-alike-very-different-from-normal-brains
http://www.ted.com/talks/aditi_shankardass_a_second_opinion_on_learning_disorders.html

Restless leg:
http://www.mgwater.com/transdermal.shtml
http://www.drugs.com/ppa/magnesium-sulfate.html
http://emedicine.medscape.com/article/1188327-overview
http://www.ncbi.nlm.nih.gov/pubmed/17557494
http://www.ncbi.nlm.nih.gov/pubmed/9703590
http://www.ncbi.nlm.nih.gov/pubmed/8363978

Tired said:

Did you have any imaging to verify that no cervical/cranial anatomic abnormalities were present prior to performing HVLA? Would the presence of a Chiari malformation or other skull-base deformity be affected by your manipulation?

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excellent question. I had no imaging- and while the patient does not fit the exact pattern for any of the types of Chiari it probably should be higher on my differential (RLS, balance problems, developmental delay could all be attributable to this, and she could have been having headaches- though the parents did not seem to think pain or nausea/vomiting were significant issues for her)- I'm not sure what your experience is with this condition- I would not expect type 1 to be symptomatic at this age (usually adult onset symptoms), and type 3+4 are very rare and often don't live this long. Type II is possible, though they are usually diagnosed at birth or prenatally on ultrasound.

The cranial treatment I would do regardless as I do not believe it would put a chiari malformation patient at risk and may potentially help their symptoms. As for the way I do fascial HVLA- using a precise localization on a direct fascial barrier- the total force is more of a gentle nudge to treat soft tissue than a forceful pop targeting bones like you might be imagining- I do this on newborns and 90 year olds with osteoporosis. Its very- very gentle or i wouldnt be doing it on a child like this. While I doubt it would damage a Chiari patient- if this had been higher on my differential i probably would have chosen a different technique like BLT to achieve the same results.

very good call. Now you got me wondering if I should go back and check her with an MRI out of curiosity- though now that she is asymptomatic justifying it might be difficult. This "tethering" of the C1-C2 area seen in Chiari might be much like what was functionally occurring in this patient due to her upper cervical spine lesions- so even if she had no chiari at all it may explain why some of her symptoms were similar to what are seen in chiari. I wonder how much of her improvement in RLS was due to the upper cervical lesion improvement vs the magnesium. Thanks for the input!

Tired said:

My experience with the Chiaris is limited to my time with the Neurosurgeons as an intern. Like you, I doubt a type I would be particularly troublesome or symptomatic (without provoking an argument, I was trained that the Chiari I's are asymptomatic period, regardless of how convinced the patient is that it's causing their headaches...). I ask because I'm not a DO and I'm not schooled up on OMM beyond a very rudimentary level, so wasn't really sure if that was even a consideration. Appreciate the detailed description of what you're doing; it makes sense to me now why you don't have to get an obligatory MRI first.

This case was interesting, because it really sounds like the motor symptoms are the most prominent aspect, even if that's not what mom is most concerned about. Walking at 18mo is a little late, and the spastic gait is interesting. I'm not overly impressed with a limited vocabulary at 2.5y; I think you could make an argument that that's normal variant, depending on the home environment and parents' educational level. I'm not really sure what to make of the eye-contact issue and general affect in a toddler. This seems to fall into that "FLK" category that the Pediatricians are fond of talking about, and so neuroimaging would be interesting though probably not all that illuminating...

Thanks for the case study, it was interesting to read, even for someone like me who's pretty separated from what you're doing. One other question since I just thought of it. Did you consider doing a "pre-supplementation" Mag level? I don't know if that really would have changed anything, but just curious. I've never given oral Mag to outpatients, so not really familiar with whether that's necessary.

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I appreciate your insight. The gait was a more objective finding its true, With a 2 1/2 year old daughter myself I guess I assume she's normal and this girl had a tiny fraction of my daughters words as the mom reported and that was corroborated by my brief observation of her. There was a huge difference before/after. Her mom was well educated and was actually a special ed teacher, so she might be more reliable about stuff like this than some.

The thought crossed my mind to get a pre-treatment mag level- but I decided I didn't want to stick the poor kid. Serum Mg isn't very helpful as it represents about 1-2% of the total body stores and its highly regulated- it doesn't well represent intracellular stores which is what we would be more interested in (it is less regulated in critically ill patients so it is more useful in the ER and ICU). In theory RBC Mg levels are better representative, but they are only about 50% sensitive for intracellular deficiency (and the test costs $180). there is a company that does send outs for buccal cell Mg levels which are supposed to be 100% sensitive but that test costs something like $600 which I cant justify.

With the low likelihood of side effects and the possible upside (like I said, seen great results in RLS patients) I figured it was worth the shot in the dark.

facetguy said:

Interesting case.

What do you feel is the mechanism for the fascial HVLA? Is it a mechanoreceptor/reflex thing, or more of an adhesion-rupturing effect? I don't even know if there's a solid answer; just curious as to your thoughts.

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As you probably know, the research as to the actual mechanism of all we do for treatment is um.. limited. What we do works (or at least it can in the right hands) and we have many theories as to how and why, but I doubt the theories are all that close to fact- and in all are fairly vague even if they are on the right track. We need to sit down with some geeks with fancy toys and work out the details

In the absence of facts, I can give you my theory. I don't think it is adhesions that are being treated, as you can obtain the same effect in fascia with indirect treatments like counterstrain which do not disrupt tissues.

It seems as if fascias and soft tissues have a "memory". When they are injured by a sudden jolt (such as a whiplash injury)- its like they all lock down in that position- perhaps a neurologically mediated reflex (spinal cord?, local effect? both? i don't know). typically the person tries to return to their normal life and drags the local joints back to their normal position and the local soft tissue is dragged along- leaving a strain pattern... bruises heal in days, bones heal in weeks, but this fascial pattern may persist for decades if its not addressed- and this seems to be the cause of much of the chronic pain we see.

Many of the "indirect treatments" like counterstrain, BLT, and LAS move the fascias or myofascial structures to their position of ease- i.e. position of injury, hold it there until the reflex releases and then return the joint to normal with the pull or strain no longer there. This would seem to depend on a spinal cord mediated reflex that is maintained by constant facilitation that is ultimately exhausted by lack of peripheral input for an extended time.

Neurofascial release appears to disrupt this same pathway at the spinal cord itself by sending conflicting signals that stop the facilitation from occurring.

In direct fascial HVLA you take the resistance in the fascia and exaggerate it to the point where its maximally stuff- localize perfectly on this stiiff barrier, then give it a nudge to disrupt the whole thing locally. This would seem to depend on a local component of the reflex for it to work... perhaps cancelling the long standing input to the CNS that is maintaining the feedback loop.

Any muscles or bones held in mal-alignment by the fascia seem to be returned to normal as the fascia releases (sometimes with a quiet 'click' in the case of bones, but it is different than the loud pop you hear with typical cervical high velocity techniques). It takes a substantial degree of localization, but the force needed once you're there is minimal. I prefer it over the traditional thrusting pops of the neck b/c putting all that force in such a sensitive region just makes me nervous- and I'd hate to one day make a disc herniation worse or dislodge some hardware, damage an unstable alar ligament or cause a vertebral artery dissection. Treating patients all day you're bound to miss something at some point and this way you're always safe.

Direct fascial HVLA also saves time, it can treat a region of fascia rather than a single joint at a time- and it takes a second or two to localize, then a nudge and you're done. Since it localizes through muscular structures you don't have to worry about your patient relaxing, you don't have to do soft tissue first, you don't have to do soft tissue after. Thus- a patient with 10 years of chronic neck and shoulder pain with several asymmetric vertebrae and local muscle spasms could in theory all be treated with a single well localized cervical fascial HVLA technique- with no soft tissue and no recurrence of symptoms after months of follow up... so long as the original injury was to this area and this wasn't simply a compensatory strain pattern from another region of the body.

Of course, if you're not good at localizing you'll need practice first.

MSmentor018 said:

great cases and discussion! do you have any experience or cases with acute OM in children? I met a DO at WVSOM that performed a study using OMT and decreasing the incidence? or duration of AOM. just wanted to hear your thoughts. thanks for the effort, keep it up.

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I have several kids that had serious recurrent OM infections- almost constant abx and I had some success (as in, it seemed like a marked reduction in incidence). Small n of maybe 4 or 5 over the past few years... and im not batting 100%- but 3 probably had 100% resolution over 1-3 treatments. One had ear tubes placed after my first treatment so I dont know how he would have done. Also, without a control group its hard to know how many would have had their last ear infection anyway even if I didnt work on them. I cant recall if I've seen the study you refer to- I saw one like it- and if its the one im thinking it was pretty small. We gotta do some bigger multicenter studies.


It is difficult to recall the details of any of the cases I saw off the top of my head. I can tell you most have bad temporal bone issues on the side of infections and you do your best to make the head symmetric and soft and you're good to go. I have heard that they claim poor temporal mobility reduces local lymph drainage and this results in a buildup of fluid for longer duration with normal viral infections- leading to eventual bacterial overgrowth.

I dont think we've been able to demonstrate this lymph theory yet- in fact i dont think we have a good way of evaluating a cranial bones "mobility" yet. There is an obvious difference by feel between the healthy side and the other, but this is hard to quantify objectively. I would be interested if anyone has ideas how we might do this.

Styria said:

At a Cranial Academy conference, Stefan Hagopian worked on my head using a considerable amount of force, more than I'd ever seen done with cranial. But it resolved dysfunction that had been ongoing for a year.

Where do you recommend learning the Ligamentous Articular Strain style? There's no mention of it in Speece's book and I don't recall it in Liem. Was it developed in Dallas or somewhere else? Should I attend an LAS course before learning it as a cranial style?

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The technique I described there for treating migraines I came up with myself, but it is a modification of some of the things I learned from Dr Speece in his LAS course in texas. In reality- he credits it all back to Rollin Becker, Sutherland and AT Still- "its all just osteopathy." You might go right to the LAS course- Dr Speece does address treating the head with balanced pressure, or you might check some of the more advanced cranial academy and SCTF courses, or you might seek out a mentor.

LAS and cranial osteopathy are a confusing bit of history. If you could study under Sutherland I think you'd see a practical guy who didn't talk about CRI, used a ton of force when treating heads and got good objective results with what he did. The same would be true of many of the old timers who did cranial, including Arbuckle, Fulford, Rollin Becker, Charlotte Weaver and probably AT Still himself. Time has a way of changing things with each generation though, and not always for the better when the emphasis is on tradition rather than innovation and validation. I recommend you pay most attention to those who get the best results... at least that is what I've done and I'm happy with where that has taken me. "the biscuit speaks for the cook" as AT Still was famously quoted.

Basically, old cranial is the same exact thing as LAS. LAS refers to lesions in joint structures, so probably BMT (referring to dural membranes) or simply cranial would be a more accurate description- but the principle is identical- compression or traction with balance of underlying structures until the region normalizes.

painmd87 said:

How do you think we could adequately control and standardize large, multicenter clinical trials with OMM?

So much of it involves very finely tuned senses and minute adjustments in force, velocity, etc. What you do could be functionally very different from what another practitioner does. You even identified a treatment that you developed yourself, and I've witnessed other attendings describing techniques they've created, and I've witnessed their successes and failures as well.

I think the standardization of treatment is the biggest impediment to quality, repeatable research.

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It does present a unique challenge- because I would argue as soon as you standardize an approach to a symptom, it is no longer osteopathy you are testing. I say this because any time you resign yourself to treating symptoms in chronic disease, your work will result in temporary success at best, or more likely failure. An example is GERD- which can be caused by sleep disturbance (sleep apnea, PTSD, etc), hiatal hernia, overstimulation of sympathetics (with associated tension around the celiac ganglion), irritation of the parasympathetics due to muscle tension around the OA, diaphragmatic spasm, abdominal pressure on the stomach due to pregnancy or obesity or malignancy, hormonal factors, over-production of stomach acid due to gastrinoma, etc. etc. If you pour through the primary lit published over the past 10 years you can validate each of these causes.

If a patient presents with GERD, the symptoms are probably caused by only one or two of the above factors. I have seen omm protocols for GERD that have every practitioner treat the epigastric area- you can imagine there are a lot of treatment failures in terms of objective outcomes for obvious reasons, and perhaps few if any objective successes (success would depend on the right causal diagnosis-just guessed at in such a protocol, and it would also depend on the skill of the practitioner which can be quite variable). Some of the studies involved "black box" protocols where practitioners can diagnose and treat everything in the patient to get symptoms better... in this case you don't know what they diagnosed or treated, how they did it, why, and any success is unlikely to be reproduced- and any failure is unexplained and you cannot improve on it for the next study... basically the study tells you nothing of consequence for the advancement of the science.

To make matters more complicated, the studies I've read for OMM and GERD involve mostly subjective outcomes- for which there are seemingly good results... the patients claim to feel "somewhat" better- but you assume a reporting bias (many times patients are giving results to the person who did the treatment, and thus they might not want to disappoint, and there are poor control conditions where patients probably know their grouping -or there just simply is no control group.

Any protocol for GERD would be hard pressed to address all of the above causal factors- most of your effort would be wasted for any given patient, and some causes are not directly addressed with OMM but rather lifestyle change (obesity, for example). All of these lifestyle factors would present a "failure" of OMM in such a study, when the failure is really in the study design for not excluding patients where such factors are the primary cause of their symptoms.

My suggestion would be:
1) to use a single objective causal diagnosis as part of inclusion criterion- for example GERD with objectively diagnosed hiatal hernia.

2) you need practitioners with knowledge and training to treat hiatal hernias- ideally ones that think they have achieves significant and consistent results in their outpatient patient base.

3) have grouping-blind technician or radiologist read objective measures of symptoms before treatment (pH monitoring, manometry or whatever).

4) have patients undergo treatment to the best of the practitioners ability, and for controls try to do a sham treatment that seems believable but does not target the exact hypothesized area). Practitioner should report their perceived success or failure for each patient, and detail regarding the technique or approach used (this can probably be standardized, given a known causal diagnosis). They should recheck for hiatal hernia post treatment in both control and treatment groups and give their perceived findings (it would be nice to know that the controls are not affected by the sham tx, and it would be nice to see whether subjective diagnosis is accurate if good outcomes are indeed seen).

5) have a grouping-blind technician or radiologist read repeated objective measures for each patient.

This is in essence a double blind study which evaluates conservative manipulative treatment for the condition of hiatal hernia. Most of the art of osteopathy is in the history and physical to get the the causal based diagnosis in the first place- and that is a given at the start of this study- but it would at least let us know whether the outcomes are possible given a correct diagnosis. It is a start. You would need a separate study to determine whether a certain palpatory approach is sensitive or specific to diagnosis of hiatal hernia. Too often studies lump everything together and ultimately tell you nothing.

If you find that the practitioner is unsuccessful- it is not a failure of osteopathy. This might just mean you need to ask a different practitioner with more skill or a different approach to put their stuff to the test until you find something that works (or you dont- and then resign that OMM as we currently understand it will not help that condition- at least then you know what to refer on to symptomatic oriented care or surgery).

This approach to research would result in a change in the way this material is taught in schools- which is a good thing. Students would actually be learning things of practical value rather than material that feels like its based on wishful thinking and optimistic theories... which is unfortunately a good bit of the OMM class at most schools now.

primadonna22274 said:

I really appreciate these case studies. I am OMS1 and a PA with 11 yr of practice experience...having a harder than expected time with OMM/OPP. I think I have been allopathically indoctrinated and I find it tough to wrap my mind around the mechanical concepts of osteopathy--although I am interested. I'm also not a very mechanically-minded person--more intuitive and conceptual. Any helpful advice? I want to get this and be good at it! Thanks.

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Your clinical experience will be invaluable to your studies- as it will give relevance to everything you cover in class and deepen your studies. As for OMM, my advice would be to focus on the concepts. Study the philosophy of osteopathy by reading AT Still's work and shadowing the most skilled OMM docs you can find who are willing to share their time. Check for OMM specialists in your area doing a successful cash-only practice, or those who everyone in your town keeps talking about. You might also want to look for student groups on campus that cover more advanced topics than what you get in class, and you can learn a lot at national conferences (AAO Convocation each march can be interesting, though it is expensive and there are some odd folks there...).

You will fiind anatomy and mechanics are important, but memorization and detail work doesn't have to be the centerpiece of your osteopathic education. You can study these topics in more of a general big picture way and be very successful at OMM.

You will find as your skill as a physician improves once you are out in practice, your brain will process lots of information very quickly and your instincts and intuition will become more and more correct. If you use this well it will saves a ton of time in patient encounters. Use your intuition to guide your history taking and physical exam so that you get to the correct diagnosis faster, and don't forget to rule out important things that might slip off your intuition radar.

bones said:

My suggestion would be:
1) to use a single objective causal diagnosis as part of inclusion criterion- for example GERD with objectively diagnosed hiatal hernia.

2) you need practitioners with knowledge and training to treat hiatal hernias- ideally ones that think they have achieves significant and consistent results in their outpatient patient base.

3) have grouping-blind technician or radiologist read objective measures of symptoms before treatment (pH monitoring, manometry or whatever).

4) have patients undergo treatment to the best of the practitioners ability, and for controls try to do a sham treatment that seems believable but does not target the exact hypothesized area). Practitioner should report their perceived success or failure for each patient, and detail regarding the technique or approach used (this can probably be standardized, given a known causal diagnosis). They should recheck for hiatal hernia post treatment in both control and treatment groups and give their perceived findings (it would be nice to know that the controls are not affected by the sham tx, and it would be nice to see whether subjective diagnosis is accurate if good outcomes are indeed seen).

5) have a grouping-blind technician or radiologist read repeated objective measures for each patient.

Click to expand...

For GERD, another issue is that many of the patients with sleep disturbance and GERD symptoms have central sensitization- and this sensitization may be more the reason for thier symptoms than objective findings at the lower esophageal sphicter. Perhaps the exclusion criterion could also exclude those with normal pH and manometry findings pre-treatment.

You can see any such study with so many exclusions could be expensive and require a big city and connections to a major GI center. Most DO schools are in rural areas and/or have few connections to major research sites. These are challenges but they are not insurmountable.

painmd87 said:

Thanks for the detailed reply. There are two big problems I see with constructing large scale trials.

1) You suggest selecting practitioners who feel they've had success in the past. This could be difficult to recruit, and will create results that are only applicable to that subset of DOs.

2) To a patient reviewing this data and choosing treatment (OMM vs. various pharmaceutical/surgical treatments for hiatal hernia, for example), it would be difficult to decide of ABC, D.O. is going to successfully treat him vs. DEF D.O. If the treatment fails because of selecting the wrong physician, then the likelihood of seeking further osteopathic treatment may be reduced.

I'm not trying to be antagonistic, but rather am seeking answers for some problems I have identified as I go through osteopathic medical school. What one person palpates may be different from what another feels. Your adjustment may differ from mine. And as such, the diagnoses and outcomes will vary. To the generally uneducated patient and public, this would come off as unreliable outcomes, and thus not worth the financial and physical risks.

With that said, I can't identify any way to increase the consistency of results. We're starting with inconsistent symptoms (or a very small sample size of specific symptoms), treating with varying treatments (or with a very small sample size of physicians), and reassessing those same inconsistent symptoms. Your suggestions would go a long way to closing those gaps, but further questions are created as well. The cases you've presented thus far are excellent examples of what results a skilled clinician can produce in complicated situations, especially where previous treatments haven't created optimal results.

Click to expand...

All good points.

Yes, not all DO's are made the same. Results may vary. I think placing more of AT Still's philosophy into the curriculum, and working hard to figure out what works best and focusing all educational efforts in the direction of what works would do wonders for consistently improving results universally.

My point is that if you really want to know what works- go to those that think they are succeeding in a major way and validate. If results are established, then it opens the door for others to follow in their footsteps. As you say, they might be difficult to recruit... they make a ton of money in private/cash practice, their income is not based on EBM, and many have poor research experience (it would be like recruiting a neurosurgeon to a study demonstrate whether some procedure in neurosurgery works- it takes them out of their cashflow and it doesnt directly help their practice since they get paid just as well regardless of the results). That said, some will be altruistic and want to help the future of DO's, and some will want to show off how great their results are- so I bet you'll be able to find some willing to cooperate.


I should add- the more serious the pathology the more obvious the biomechanical diagnosis- this should improve inter-rater reliability in serious cases (though- finding the "key" lesion and the true underlying cause of pathology is not always easier- and it is all the more important so you aren't there working all day).

As for #2 this is one of my biggest frustrations in my kind of practice. In the town i'm in now I have a personal reputation which supersedes any issues like this as far as patient care... but sometimes when I meet a DO and they ask what my specialty is and I say OMM they give me a look like I have a puss filled boil on the side of my face... lol. Little do they know I might not fit their preconceptions of an OMM guy. The MD's I meet dont have this reaction- and many are quite excited to work with me (just as many patients) probably because for those who haven't really had much of an experience with OMM or osteopathy- I and my description of it is their first impression of it.

History
A 28 year old woman presents to the hospital with a 10 year history of uncontrolled asthma, admitted for acute exacerbation. This is her 5th such admission for asthma over the past several years. She also has rib pain and low back pain (which is why the IM guys consulted OMM... typical). She reports that she has tried many different medications in the outpatient setting including high dose inhaled corticosteroids without relief. Nothing seems to relieve symptoms. Her symptoms bother her all day, and she has been unable to walk her dogs since she moved to the region due to her breathing problems.

Objective:
Vitals
Respirator rate 30-35
appears dyspnic/unconfortable/pale

Exam- very poor air movement through lungs bilaterally.

Patient displayed dermatographism globally (sustained severe erythema after light palpation lasting several minutes- thought to be due to hyperemia of the local capillaries)

All upper ribs especially ribs 2-4) were very stiff, with intercostal spasms. She had bilateral tender nodular irritation of the anterior C2-3 interspace (according to what we're taught- this would be consistent with Chapman's points for the airways- I suspend judgement- I haven't seen a lot of data supporting their diagnostic value yet).

C4 severe stiffness (remember C3-5 innervates the diaphragm through the phrenic nerve).

Severe suboccipital spasms (remember vagus passes through jugular foramen).

The nature of the above mechanical findings was very severe- unmistakably abnormal to even completely untrained hands.

Most of the rest of her physical exam was more or less normal. A few spasms in her trapezius accounted for her low back pain, but they seemed rather unimportant at the time.

Assessment:
1) Acute exacerbation of Asthma
2) Low back pain
3) Somatic dysfunction of head, cervical spine, ribs, upper extremity

Plan
OMM to above areas with resolution of abnormal findings in the ribs, neck and base of the skull. The anterior tender regions between the ribs were very painful and difficult to resolve until I adopted neurofascial release- and apparently altering the CNS through this mechanism resolved their stimulation.

A few minutes into the treatment the patient began breathing more slowly- re-evaluation of the lungs revealed good air movement but loud expiratory wheeze (to me an improvement over minimal air movement). To my great surprise, when I completed treating the above mechanical findings altogether and they were completely resolved, her lungs were completely clear. On repeat testing her dermatographism was gone as well (I still cannot explain that- though I am open to ideas). After completion of treatment, she walked up and down the hallway with no respiratory distress whatsoever, and her respiratory rate was about 12-16 range. Oh, and no low back pain... She went home the next day and followed up in my clinic in 2 weeks.

At clinic follow up, her lungs were clear. She stated that the day she went home she walked her dogs for the first time in 10 years, and she did so with no respiratory distress. She states that in her past 4 hospitalizations she was in bed for a week each time after going home. I had her follow up in my clinic PRN (as needed) and I have not heard back about her condition since this.



Here is some general discussion to consider (sorry if its long- I've just been thinking about it this weekend so its fresh in my head):

According to
(2011 Chest) http://www.ncbi.nlm.nih.gov/pubmed/21835905
there are probably 3 or more major subtypes of asthma, caused by:
1) GERD
2) bacterial pneumonia
3) eosinophilia in the lungs
4) a combination of the above
5) other factors (perhaps CNS neurologically mediated reflex as seen in irritant induced asthma).

#1- GERD
GERD is present in 50-80% of asthma cases, it may be caused by beta agonists, but it is likely also a contributing factor or even the prime causal factor in some asthma cases.
http://www.uptodate.com/contents/ga...result&search=GERD+ASTHMA&selectedTitle=1~150

To find the cause of GERD and cure it we must think broadly- much as we are doing for asthma itself (I would argue that GERD is even a more complicated disease). Prime things to consider

Sleep deprivation appears to cause increased GERD symptoms, so consider the diagnosis of sleep apnea, PTSD, post concussive sleep disturbance, anxiety disorder, etc. Fixing a cranial compression will typically fix post-head trauma sleep disturbance. Fixing celiac ganglion/epigastric tension and normalizing all of the rib heads will typically improve symptoms of anxiety or PTSD to where sleep normalizes. For sleep apnea you might encourage weight loss, you might treat the parahyoid muscles, or you might give CPAP.

Campbell CM, Bounds SC, Simango MB, Witmer KR, Campbell JN, Edwards RR, Haythornthwaite JA, Smith MT. Self-reported sleep duration associated with distraction analgesia, hyperemia, and secondary hyperalgesia in the heat-capsaicin nociceptive model. Eur J Pain. 2010 Dec 29.

Lautenbacher S, Kundermann B, Krieg JC.Sleep deprivation and pain perception.Sleep Med Rev. 2006 Oct;10(5):357-69.

Araujo P, Mazaro-Costa R, Tufik S, Andersen ML.Impact of sex on hyperalgesia induced by sleep loss. Horm Behav. 2011 Jan;59(1):174-9.

Orr W, PhDa, Chien Lin Chen, MD. Sleep and the Gastrointestinal Tract. Neurol Clin 23 (2005) 1007–1024.

Schey R, Dickman R, Parthasarathy S, Quan SF, Wendel C, Merchant J, Powers J, Han B, van Handel D, Fass R. Sleep deprivation is hyperalgesic in patients with gastroesophageal reflux disease. Gastroenterology. 2007 Dec;133(6):1787-95.

Dickman R, Colleen Green, M.S.1; Shira S. Fass, Ph.D.1; Stuart F. Quan, M.D.2; Roy Dekel, M.D.1; Sara Risner-Adler, B.S.1; Ronnie Fass, M.D. Relationships Between Sleep Quality and pH Monitoring Findings in Persons with Gastroesophageal Reflux Disease. Journal of Clinical Sleep Medicine, Vol. 3, No. 5, 2007.

One must also consider hiatal hernia (diaphragm spasm, phrenic nerve irritation), vagal irritation due to OA issues, splanchnic irritation and its direct affects on the LES, etc.

#2 Bacterial pneumonia
Atypical pneumonia may be a causal factor in chronic reactive airway disease- principle organisms may be mycoplasma pneumonia and chlamydia pneumonia.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC394343/
http://www.ncbi.nlm.nih.gov/pubmed/16750980
http://www.ncbi.nlm.nih.gov/pubmed/20013705
http://www.ncbi.nlm.nih.gov/pubmed/18079229
http://www.uptodate.com/contents/my...atypical+pneumonia+asthma&selectedTitle=1~150
http://www.uptodate.com/contents/cl...atypical+pneumonia+asthma&selectedTitle=4~150

Osteopathically I would approach this much like regular pneumonia patients.

Improve lymph drainage by:
normalizing rib mobility, normalize diaphragm function
make sure C3-5 are normal (normal phrenic nerve function)

Normalize immune function
-by normalizing sleep as above
-by normalizing sympathetic chain to avoid immune suppression (i.e. fix the ribs, treat epigastric region)
-addressing other causes of immune suppression if present and addressable (diet, comorbid infections).

Normalize blood sugars
proper administration if insulin, etc.

If you validate + PCR of mycoplasma sp or chlamydia sp in the blood, you might do antibiotics- probably doxycycline or macrolides.

#3 eosinophilia in the lungs
http://www.uptodate.com/contents/approach-to-the-patient-with-eosinophilia?source=see_link
http://www.uptodate.com/contents/ca...rch=eosinophilic+pneumonia&selectedTitle=3~77
http://www.uptodate.com/contents/cl...nic+eosinophilic+pneumonia&selectedTitle=6~17

Consider eosinophilic pneumonia, churg strauss (eosinophilic vasculitis), chronic fungal exposure, etc.
I think of eosinophilia as a starting point for fungal or parasytic workups, though there may be other factors. If patients test positive for sensitization to fungi, I would have them test their house for mold. For biomechanics, I treat much the same way as for bacterial pneumonia, but perhaps place more emphasis in the GI system in suspected parasitic organisms.
Antifungals and antiparasitic drugs may be considered, but if symptoms improve but then recur after treatment think about environmental exposures and biomechanical factors that might be contributing toward that patients sensitivity.


Irritant induced asthma
http://www.uptodate.com/contents/re...rch=irritant+induced+asthma&selectedTitle=1~8
I believe this is a central nervous system maintained smooth muscle spasm.
The mechanism may be similar to the mechanism for whiplash which is centrally maintained spasm due to sudden insult to the peripheral muscles... the sudden insult to smooth muscle fibers may result in chronic smooth muscle spasm due to a similar process.

This version of asthma may be nearly 100% curable with just OMM much in the way whiplash is so easy to fix with counterstrain or neurofascial release, and I imagine this is the only way to explain the rapid improvement before my eyes in the above case. Neurofascial release targets the central nervous system component of the feedback loop which maintains peripheral... thus I dont have to put my fingers in their bronchial tree to treat their hyperresponsivness (weird visual). Treat abnormalities in the sympathetic chain, issues with vagus OA region, and


I would imagine slow improvement for infectious causes or GERD once the body restored normal function, but a neurologically mediated bronchoconstriction could be reversed in seconds or minutes. I also imagine there is more risk for exacerbation in these cases during treatment- so care should be used with HVLA to the ribs... (you have been warned)

Anyway I have no proof of what I'm doing- only theories and cases. But the patient did get better, as have many others with less dramatic but equally compelling symptoms and results. I am willing to put this approach to the test if we can find anyone to test it.

The common mechanical considerations are: rib abnormalities are very important in asthma- and almost universally present. Carefully evaluate each of the top 8 ribs on both sides... there is a good chance you'll find lots of spasms in asthmatics. Fix with care- especially in acute exacerbations... #4 may result in a full blown asthma attack if you aggravate the nerves without fixing them (you have been warned).

Important considerations for long term outcomes are anything that influences efficiency of lymph drainage from the lungs or anything that modifies function of the diaphragm, and anything resulting in vagal abnormalities. In cases where causes #1-#3 are the prime issue, i would not expect instant results- but I would expect remission within a week's time if 100% of the anatomy is normal and it is indeed the anatomy that is preventing normal function (environmental factors are a consideration too). I think the majority of cases are curable in such a fashion, though I have no evidence other than a small series of promising cases to support this. Even if I'm wrong or you cannot reproduce these results, a thorough workup and appropriate antibiotics or anti-fungals or PPI should put a lot of these cases into remission without chronic steroid use- so you can use this approach to help your patients even if your hands are not developed.


I feel like House DO lol...
Imagine thinking of all this for your average every-day asthma patient instead of just tossing steroids at them for the rest of their life... but patients go into remission with the right treatment targeting the actual cause of their symptoms. As you get better thinking this way it does get faster. As the information becomes more second nature and you start recognizing patterns- soon it might take a few minutes instead of hours to figure these cases out. To me this is what osteopathy is supposed to be. It takes a lot of hard thinking but the challenge is fun and the rewards are spectacular.

History:
This patient was a 16 year old male with a multi year history of wheezing and difficulty keeping up with his classmates in athletics- especially those involving running. He had no symptoms at rest, nor symptoms during ordinary activity. He would regularly use his bronchodilator at sporting events, sometimes using it pre-running to try to perform better, but he would often wheeze anyway and find himself taking it again with prolonged activity. He would go all off season without feeling like he needed it. No other relevant past medical history. No history of smoking. I did not ask whether he coughed more laying down at night, or any other symptoms that might indicated GERD.

Objective:
Vitals Stable
Lungs: bilateral wheezing on exhalation.
Musculoskeletal: severe restricted motion for upper 4 ribs bilaterally.
Other findings unremarkable

Assessment:
1) Mild Intermittent Asthma
2) Somatic dysfunction of the ribs

Plan:
Based on today's exam, I treated the upper rib region first using myofascial release, then low amplitude articulatory technique. All of the ribs were normal after treatment. Wheezing persisted post treatment.

I saw the patient again about a month later. He reported to me that the day or two after the treatment he started coughing up “ropey gunk” from his lungs. Shortly thereafter he no longer wheezed when running and stopped using his bronchodilators. He reports having no difficulty keeping up with his classmates and hadn't used his bronchodilators since the treatment.


Discussion: See previous asthma case for a lot of detail. This patient was seen before I was thinking about a lot of that stuff, so I don't exactly know the etiology of his symptoms. Given that his symptoms improved over hours to days rather than immediately- and the material expelled from his lungs- I imagine his disease had a significant amount of tissue involvement which to me would suggest to me either a walking pneumonia or one of the eosinophilic diseases- though I cant say for sure given the limited history and the lack of lab work that I got. That said- ribs are a very high yield region to normalize in all asthma cases regardless of etiology. I have observed serious upper rib disturbance in every case of asthma I have seen thus far- and each time I have been successful in normalizing these ribs completely I have seen a corresponding normalization of lung function. There are certainly a couple of cases I haven't helped- and I knew it immediately because I couldn't figure out how to fix their ribs. I know a lot more now than I did then, and I suspect I might be able to help those same patients today if I saw them back. I do suspect other biomechanical factors are involved in some cases- as per my discussion in the last case, and I would bear these in mind as well.

Cuthbert said:

Your comments remind me of so many Chiropractors who have a high opinion of themselves. I have to convince parents daily that their child or infant's spine is not out of alignment and that there is not enough evidence based research to support the use of HVLA and other techniques on children. Furthermore, I spend time explaining how a good percentage of ear infections are viral and will go away even without treatment (be it an antibiotic or so called "movement of the skull bones").

If you want to do some good for OMT, start research. As you have previously stated, it is poor to say the least. Personally, I find this type of anecdotal evidence nauseating. It reminds me of the baseless information that was force fed during OMM classes and the multitudes of my classmates who took it at face value.

Click to expand...

Your lack of professionalism might hurt you down the road. Lets keep this civil and professional. If you find fault with one of my points and have evidence that persuades me I am all for changing my position.

You obviously didn't actually read my point about ear infections. I know that most ear infections clear themselves. The cases I am referring to are children with serious recurrent ear infections that would clearly need ear tubes following standard of care. The "successes" were cases where the infections stopped in 1-3 visits concurrent with OMM (over a period of 1-2 months). Keep in mind all of the kids in this category had infections for 6 months -3 years before seeing me- some almost continuously. I clearly stated this wasn't a study, and I didn't have a control group- so no way to know how many would have gotten better over that 1-2 month window anyway even if they weren't getting OMM. That said- my intervention did spare most of these kids from getting ear tubes, as that was the next logical step.

I said symmetry of the temporal bones is important- that implies normalizing soft tissue and muscle pull on these structures- not "moving the bone". Obviously since all living bone is flexible there may be some relative change in resting position, but it wont be a lot. More important-i think- is symmetry of tension through the bone and local soft tissue. The "mobility" theory pushed by cranial enthusiasts hasn't been validated yet, if that is what you are referring to- and I stated that as well. Though maybe that is just another way of saying what I'm saying about the relative stiffness.


I am sorry you had a bad experience at school. That doesn't mean that all of OMM is garbage.

Yes, I have a high opinion of osteopathy and what it can do based on my daily observations in my professional practice- and I am excited to be part of it. However, I would be nothing without my teachers along the way and I owe all of my success to them.

My intent with this thread is 2 fold.
1) to put some cases up so that pre-meds, students residents, and perhaps other attendings can use my experience to help them think about their own patients- and perhaps replicate my success in their practice.

2) provide ideas for future research in OMM. No one person can do the thousands of studies that are needed to validate or disprove the theories that we teach as fact in the OMM curriculum at most schools. My cases tell me, and hopefully they will tell others- that such research might be worthwhile (but i argue to start at what seems to work clinically rather than at the open ended theories of class). Hopefully there are enough ideas here and enough clarity of description that residents and attendings who have the resources and time and inclination to do research can turn some of these concepts into working projects. They must be able to replicate the results before they can test them however.

I have said repeatedly not to take what I'm saying at face value. Validate for yourself clinically before you accept what i say as possible, and research needs to be done and repeated several times before you can accept any theory as truth. This thread is nothing but a point to start research and begin the long process of validation.

I never promise any outcomes to my patients. Patients come to me because they have nowhere else to turn, or they want a second opinion before a major procedure, or because they just want to try something more permanent than medications. When patients come to me I do my best to get my patients well and out of my office after one or a few visits and never back to see me. I don't sell them any supplements or other crap to make money off their ignorance. I simply do my best to make them well as fast as possible, and do my best to educate them about their disease process. If I cant help them, I refer them on to someone who can at least help symptomatically. Yes I end up having a high turnover in patients this way, but for every patient that gets a great outcome- I end up getting lots of referrals from their referring doc or from the patients friends and family. My approach to patient care is very different than the "wellness" model i see sometimes with alternative health practitioners where you go back 3 times a week for years on end and end up spending lots of money for no obvious benefit.

Just trying to clarify

For those who this isn't obvious:
When it comes to learning new ideas, there seem to be 3 types of people.

Scientists- are those primarily interested in understanding the truth of something, despite convention, obstacles, or common sense which may tell them the answer is obvious. They look at available data, make hypotheses, and try to find ways to validate or disprove these hypotheses. Most of the work is trial and error- and there will be lots of error... but the reward is success and progress. AT Still fought hard for this principle- placing the discovery of new truth above all else in his life.

"You find that all men are successes or failures. Success is the stamp of truth. I will say all men who fail to place their feet on the dome of facts do so by not sieving all truth and throwing the faulty to one side."
Andrew Taylor Still

Believers- are those who believe anything that comes along that sounds plausible, even on thin evidence. They are open minded but lacking in discernment. They tend to get fooled easily, and are at risk for being swindled or falling victim to the latest fads and ideas. Often once you believe a few things that are not true- you build theories on these concepts- and before you know it there are many misconceptions which you hold as obvious truth. Though they may convince themselves of their success and may try to convince others (and perhaps succeed in the case of other "believers") they often fail to achieve any objective measure of success. Most will shy away from research because there is some underlying fear of finding out they might be wrong about what they hold so dear.

Skeptics- This encompasses those who disbelieve anything that doesn't perfectly fit with their understanding of the universe unless it comes from a very trusted source (or they learned it in school). This includes many in the scientific community- not the innovators, but many of the followers. They have great discernment but lack open mindedness. They are slow to adapt, slow to change, and slow to understand, and tend to miss the big opportunities of life. If something seems too good to be true, these individuals will tend to ridicule it and will rarely if ever take the time to check to see if its true (from the "you've won $1million in the mail to the latest cure all for cancer). This might save them a good bit of time, but what happens when a new crazy sounding idea is actually correct? Without investigating they will never know. Sometimes a whole generation needs to die off before new ideas can take hold.

Most of the OMM arguments in school and on SDN involve the believers against the skeptics. Whoever speaks louder will win that argument, but you are still no closer to the truth. Neither group is really even interested in the truth- they are more interested in being right.

I encourage everyone reading this to do their best to be scientists. Open minded with discernment. If you find yourself to have tendencies toward one of the latter 2 groups you can fight these and learn something new.


To the believers- I say put your ego aside. Realize that the truth- whatever it is, will allow you the best success that is possible with OMM- even if what results looks nothing like what you were taught, even if it means dedicating more time to learning. If there is truly no objective success to be had- wouldn't you want to know that as well? Then you could could toss OMM to the side and offer something else to your patients of true value. I wouldn't be here if I didn't think there was something of incredible value in OMM, but I think a lot of this value has been lost to several generations of DO's... and that means if we start looking for whats real there is going to be some pain when we find out whats not real. You might discover a lot of what we continue to teach in class is false. Everything must be validated before it is taught as truth in school to new students. You will always lose most of the smartest people in class once you ask people to believe something on thin evidence. Seriously. Cranial, spinal mechanics theories, chapmans points, viscerosomatic reflexes. None of these things are fact.

We must continue to teach our best theories so that the art of osteopathy isn't lost and so that the next generation can test these theories, but research methodology, reading primary literature, and open minded discussions where all possibilities are on the table must be a major emphasis in school.


To the skeptics- Before you start a rant about OMM and cranial and all the crap they tried to make you believe in school... just wait. If you wear the DO degree- every time you make fun of OMM and osteopathic philosophy you are degrading the very things that make you different from MD's... the very things that justify your degree. Don't you owe it to yourself and your colleagues to at least TEST to see if AT Still was onto something?
a few ways to do this:
1) find someone really good at OMM to permanently fix a life long problem you or your family member has had. If you cant find someone able to do this- one of 3 things has happened: either OMM is bunk, your problem is not fixable by OMM, or you haven't found the right doc yet. Find the best doc you can and put them to the test. Hopefully if you have one of the conditions I talk about in one of these cases you can find someone willing to put it to the test using that methodology even if nothing else has worked. You can see for yourself- what do you really have to lose other than some self respect and some time and a little money... seriously? The upside is you can say you tried it and it didn't work (and let me try to respond...) or you can be cured of your issue.

2) Shadow an OMM doc who everyone thinks is getting good results (shoot high or you will get exactly what you expect). See for yourself what is happening exactly. Are they fooling patients? are they fooling themselves? Could objective changes actually be happening? Maybe just shadow them for an afternoon rather than a whole rotation- that way your risk is minimal. See what you think.

3) Do research. Do lots of it. Find the best OMM docs you can find and make them do it in front of you under controlled conditions (even if you have to tie them down to accomplish this). You can ridicule them as their results come back negative for any effects if that is indeed what you find- but save your ridicule for then- don't jump the gun by ridiculing something you haven't tested in an objective manner. Test whoever you can find with the best reputation for real results with OMM. If they somehow succeed, you win and you can learn what they are doing and help your patients. If not, you can ridicule them to your hearts content. Either way you get paid for your time. Not bad.

ensuii said:

I'm not a skeptic, I'm someone that refuses to have smoke blown up their ass. Tenderpoints on patient's with an MI? Cranial for Asthma? Sorry buddy, but if your patient is an average joe who looks at you weird when you tell them you're going to treat their trouble breathing with manipulation of the bones in their skull, its not because they're a skeptic...it's because the entire idea of OMT seems more like science fiction than medicine. I mean, seriously, the modalities you access to prove your point are the same ones wielded by homeopaths.

Click to expand...

skeptic.

its okay, you're not alone. I don't know if its worth the effort to spar with someone who has already made up his mind when he obviously hasn't tested a drop of what I'm saying... even going so far as to make up things that he imagines I said and then railing against them and invoking homeopaths to prove his point.

counterstrain for an MI?
When I work the ER and a MI comes in I treat them like the next ER doc (actually I ship 'em to a place that does caths, but stabilization is the same). As I clearly said- and even AT Still said- you treat symptoms aggressively when life or limb are on the line. The difference is how you handle the other 90+% of cases you see.

Cranial and asthma... what?
Ribs first for asthma remember? I treat heads for sleep problems in post concussive patients... who in theory occasionally have GERD because of this, which might occasionally be the primary cause of asthma in a small subset of patients- a scenario i haven't seen yet... is that what you're referring to?

where are you getting this stuff?
the "modalities" I access are drugs, surgery, needles, my words and my hands. Not that different than other physicians really- but a lot different than homeopaths. I happen to be better with my hands than some other docs, and I tend to use them first line for certain conditions, but in a rational way that works. What makes me really different is the philosophy.

As for treating "average joes"... I live in the midwest- that is what I see all day... hard working farmers and factory workers, maintenance men and store clerks- and they are the ones sending me all their friends and family when I get them better

Cuthbert said:

Good clinicians practice evidence based medicine and do not subject their patients to unproven techniques. Techniques which could even lead to harm - it is unknown due to the fact that they lack evidence.

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um... thanks? but I think you called me a bad doctor. and you make it sound like i'm subjecting my patients to something dangerous or sinister.

Look at the guidelines for ACLS...

EVIDENCE BASED GUIDELINES

Because of the nature of resuscitation research, few randomized controlled trials have been completed in humans. Many of the recommendations in the American Heart Association's 2010 Guidelines for advanced cardiac life support (hereafter referred to as the 2010 ACLS Guidelines) are made based upon retrospective studies, animal studies, and expert consensus [5]
http://www.uptodate.com/contents/advanced-cardiac-life-support-acls-in-adults

sooo.... do we just say- lets not resuscitate the 45 year old with a Vfib rolling into our ER- there aren't good EBM guidelines for resuscitation, and I would be a bad doctor if I didn't have proof by double blind placebo controlled trials for what I'm doing... see ya sucker!

... or do we provide the best care we can given a limited evidence base and using our best judgement? I'd do CPR on the guy, and you might not- but that doesn't make me a bad doctor and you a good one.


Actually, if evidence based medicine were taken to its logical conclusion, you would be replaced by a nurse practitioner... after all, if you cannot prove you provide superior care in an evidence based manner, why should the insurance company pay for you? Can't prove it? then do something useful and set up a double blind quality control study between nurses and pediatricians for the next 6 months during your spare time... I hope you're up on your epidemiology research standards and grant writing...

read this:
http://www.arna.org/Main-Menu-Categ...N/APN/APNs-Making-a-Good-Strategy-Better.aspx

Ouch.

see my point though?

Do these sound like stupid analogies?
Telling me to look at a patient with persistent hand numbness and positive tinnels over the carpal tunnel and to NOT treat them due to a lack of evidence is almost identical to that resuscitation example to me. If I don't- they suffer for months in a stupid brace, get a nerve conduction study for $400, get injections several times for hundreds each, or get a $5k surgery that runs the risks of anesthesia and cutting the nerve (I've seen two botched carpal tunnel surgeries- essentially ruins a patients life... not pretty). If the doc has a bad physical exam or the NCS is inconclusive, you can add a $2k EMG and a $2k MRI of the neck to the bill.


The alternative is for me to spend 30 seconds- move whatever bone is pinching the carpal tunnel and bingo- no more numbness, negative tinnels, and in many cases it never comes back... so easy that it makes me crazy all the suffering patients go through over stuff like this- but when am I going to run these studies to prove to people like you that I can do this? ...When are you going to prove you dont need to be replaced by a nurse? I get paid good money whether there is EBM proof of what I do or not. If they arent going to take away your practice would you still take the time out of your day to run the study of pediatricians vs nurses? Maybe if you are altruistic or worried about the future and you have nothing better to do... but probably no you wouldn't. All pediatricians might suffer for it, but its impractical for the average doc in practice to drop everything for a study that doesn't change their pay or their way of life... unless of course they are a research nerd and that is what they love to do.

A lot of what I deal with in clinic is a lot like the carpal tunnel case or the resuscitation case above- its so obvious (with the proper training) that waiting for evidence to help your patients seems absolutely absurd... yet getting the evidence is still important- especially to help you refine your approach and improve outcomes/success rate. If outcomes and success are already excellent though- there is somewhat less motivation from a practical perspective... The success itself is one form of evidence, but its not the quality or breadth of evidence necessary to change the curriculum at schools or help the medical and scientific community as a whole understand what we do.

My simplistic solution is to post some cases on here when i find some time and hope that I can share the burden of research with others who might be interested. I'm hoping i will have motivation in the near future to run some studies of my own... but there is a TON of things that need to be looked at. it is a little overwhelming.

bones said:

CASE
A 2 ½ year old girl with developmental delay.

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I just got a heartfelt letter from the patient's mom this AM thanking me for giving them their daughter back after 2 years of deadends and heartache.

"she went from a rote, shell of a 2 year old to a full-of life, active, self-thinking, happy little girl"

The credit to AT Still and osteopathy.

After cases like this- I wonder how many kids like this are out there... how many families are affected, how many healthcare and special ed dollars are spent, and how much potential is lost with these children over the course of their lives. This is why I keep struggling to teach and to bother posting this stuff... every doc we get to practice this way and do it well will change many lives. More importantly, some may then turn this into successful large scale research so we can actually figure out specifically how this is possible and help many physicians to reliably reproduce these results- we may alleviate much human suffering.

fiznat said:

I too am a little wary of this case study/story telling version of EBM. Everyone has their n=1 but it's not science, it's anecdote.

I'm interested in OMM and I think it could be a really fantastic approach for our patients, but storytelling like this kinda makes me nervous-- especially when it is conducted in the relative absence of (or substitution for?) research.

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It is conducted only on the back of 120 years of experience and theory. One measure of a truth is success. Not a great measure, no- especially without controls, but cases come before pilot studies, and pilot studies come before large controlled trials... if nobody posts the cases where does it begin?

My options are as follows:
1) Shut up and keep my cases to myself- let the skeptics rant and the believers believe. This is what I did between '05 and now. Its easy to do, and its very safe. ...But nothing changes... in fact the rants against cranial and the mindless quoting of OMM class material continues almost word for word the same. DO schools keep popping up, quality weakens as quantity grows, and fewer and fewer people even know what osteopathy is or what it can do.

2) Post cases on here. Make a lot of people uncomfortable- get attacked by 90% of the SDN community that actually posts, and risk the AOA and colleagues of mine getting pissed at me for opposing their policies (its not that hard to figure out who I am). Am I crazy? Maybe... but I care more about the future of osteopathy than I do about my own comfort- or the comfort of anyone reading this. If even a few pre-meds or med students or residents latch on to these cases, learn from them- and reproduce the success in their practice... it was all well worth it (even more so if pilot studies or large controlled trials are inspired from this page). It is so hard to find someone willing to stick their neck out like this that the real material doesn't get taught.

Tired said:

EBM is a red-herring in this argument. The med students aren't getting worked up over the fact that the treatments described don't have evidence behind them, that's just their way of expressing discomfort with what sounds like snake oil to them. What I think they really want to say is, "This sounds crazy, and I can't believe a physician is actually doing these things!" It makes them feel like their chosen field is akin to faith healing, crystal therapy, and chiropractics. It makes them upset, which is why they're responding the way that they are.

I think your central point is important: there is a different between routine and emergent issues, and there is a difference between adjunctive therapy and substituting therapy. I would also add that the financial aspect of "alternative" therapies makes me extremely uncomfortable, but I have discussed that elsewhere and won't belabor the point.

There is really nothing that has been presented in these cases that makes me particularly uncomfortable, and I'm saying that as an MD somewhere in between my Orthopaedic Surgery training. Do I believe that you can manipulate the carpal bones and cure CTS? Absolutely not, because while the carpus is somewhat mobile, the position of the bones relative to each other is ligamentously fixed and cannot be altered without damage to these ligaments.

Still, if a patient is receiving medically/surgically-appropriate therapy, and you all are going to take a crack at OMM because they aren't improving or want to try it or whatever, I doubt many people would object. The key, at least in my mind, is knowing what constitutes generally accepted standard of care for a given condition, and ensuring that any non-traditional therapies are not being used when something else is more appropriate. That's what makes Osteopaths different from the fringe CAM people.

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You are one smart dude... and I appreciate your opinion and insight. Funny how most of the argumentative rants come from other DO's.

As for Carpal tunnel and other entrapment neuropathies- maybe you can help me then. I will describe my process, my observations and results and maybe you can give your opinion as to whats actually happening.

When I am presented with a patient with numbness or burning pain of the upper extremity I follow a logical course.

First from history I try to figure out the cause.

Sudden onset or slow onset?
Tied to an incident or unknown trigger?
Conditions producing swelling? Lymphadema? Pregnancy?
Jobs around time of symptom onset?
Sports around time of symptom onset?
Reproducible? What reproduces it?
Does it occur instantly like a shock or is it always slow onset, slow resolution
Associated only with winter and discoloration of the fingers

What is the distribution?
Follows a dermatome?
Follows a peripheral nerve pathway?
Follows part of a peripheral nerve pathway?
Follows no pathway at all- but specific patch of numbness?
Global symptoms in the extremity?
Glove like distribution?

Physical exam
I hope at this point I've figured out whether its vascular or neurologic in origin. For sake of brevity, lets assume its neurologic, and a perfect median nerve distribution, and it began after local trauma (a fall on an outstretched hand that occurred 2 years ago).

I will check the logical places for entrapment- I will do Tinels at the carpal tunnel, I will press at the distal interosseus membrane, and I will do Tinels or press at the proximal pronators. For completeness I will often apply pressure to the brachial plexus region on the ipsilateral side and do a Spurlings and palpate the lower cervical vertebrae.

All of these should be unremarkable in a normal case. If any of them exactly reproduce the pain or numbness that the patient is reporting (lets say- the carpal tunnel does this), I will palpate locally for any abnormal functional anatomy. With a positive Tinnels – there is invariably increased tissue resistance locally (perhaps it comes with practice- but I can clearly tell when a Tinels will be positive in many cases just by how much resistance there is in the local tissues as I tap).

Then I proceed to try to figure out the source of the local tissue resistance. Usually it feels like the proximal carpal bones that are at fault, but I havent been using any means to validate this. Invariably it seems like one or more of the carpal bones will be indented or protruding more than is normal- and very stiff and tender to the touch. I might gently apply traction and articulate the joint by taking it through a range of motion. Sometimes there is significant soft tissue resistance, and fascial techniques are required to normalize the local tissue. In any case, once the anatomy feels completely normal, you can recheck Tinels, if it is negative and they are asymptomatic at rest- you might be done. To be sure I typically tap 2-3x as hard on my recheck, and tap all around the region as well as right over the carpal tunnel. All should be 100% normal. If symptoms persist, recheck the local anatomy for any abnormalities you might have missed or treat areas that share innervation upstream or downstream that came up abnormal on exam.

With normalization of local anatomy after treatment- I have nearly 100% resolution of Tinels sign and nearly 100% resolution of symptoms at rest (except in cases of double crush- which i will explain below). If i think mechanics are better and symptoms persist- I recheck the joint and almost always find something abnormal that I missed... after fixing remaining mechanical problems, remaining symptoms are typically resolved. There are a few cases here and there where I cannot improve the local anatomy for whatever reason (an arthrogryposis case comes to mind- excess bone growth was pinching the carpal tunnel), and they do not improve symptomatically after the attempted treatment- this is a small minority of cases. The whole treatment process in many cases takes less than 30 seconds. The diagnostic process may take considerably longer, but with practice it has gotten pretty fast as well.


Some caveats:
1) in my experience, double crush phenomena is very common (more than one contributing location). This is often the case when nerve testing elicits a response that is not precisely in the distribution of the tested nerve, and leads to a lot of diagnostic confusion.

For example- a tap at the carpal tunnel triggers single finger distribution symptoms- I would say you probably have partial impingement at the carpal tunnel plus irritation at one of the digital nerves due to local mechanical problems. The finger or deep hand muscles are probably the primary issue (the rest of the median nerve doesn't seem to be symptomatic) but I would try to normalize both regions.

Another example may be a tap at the carpal tunnel triggering C6 distribution symptoms- which could be from partial carpal tunnel entrapment in conjunction with nerve root impingement at the C5-C6 interspace- again both regions should be addressed. (cervical radiculopathy needs to be treated with extreme care- Xray or CT first for -any- risk of fracture after recent trauma- and you can use indirect or "Still" technique for improvement with minimal risk in all other cases... most resolve easily with normalization of cervical spine motion).

You can see how middle finger distribution could be confusing when you're testing the median nerve- you'd want to check both the finger, the hand muscles and C7 nerve roots.

There are sometimes cases of triple or quadruple crush. If you have studied any neurology you know that once an axon is irritated it takes far less stimulation to trigger repeat potentials. Just fix irritation at each location (probably just one will be far worse and the most important).


2) if symptoms don't resolve entirely on the first treatment (a minority of cases)- at the end of the visit I consider a wider differential diagnosis which may include disc herniations, brain tumors, MS, B12 deficiency, etc. I may consider imaging or objective diagnostic testing at this point to help clarify what I'm missing.

3) Thoracic outlet syndrome is a common entity despite what the literature says. It is heavily underdiagnosed- I believe this is because most physicians dont know how to test for it with their physical exam. It can be purely neurologic, purely vascular or both. When light pressure at the supraclavicular space reproduces the patients neuropathy it is pretty clearly a neurologic TOS. Treatment of the offending muscle (and it is usually only one- either subscapularis, scalenes, subclavius, pec minor, or occasionally others)- and gentle separation of the first rib from the clavicle will often result in marked softening of the region and resolution of symptoms. LEARN HOW TO DO THIS- the few times it is properly diagnosed, most allopathic physicians want to cut out the first rib well, they don't want to- but they don't know what else to do. Fix it this way- its very easy.

4) Rarely I see cases where numbness does not conform to dermatomes and doesn't make sense. If distribution is vague and changes with each retest, the patient might be faking for whatever reason (think about reasons for secondary gain- workmans comp, drug seeking, attention, etc.), if distribution is discreet but doesn't make sense, it could be a "trigger point"- or put more simply a referred pain pattern. I still do not really understand the science behind these, but if you find something like this you can try to find a muscle- often trapezius, teres minor, subscapularis or some other local arm muscle that reproduces symptoms. This is far less than 10% of upper extremity neuropathies, and may be nothing more than the muscle spasm tugging on a structure that impinges a branch of the nerve in question. These lead to considerable diagnostic confusion, but must be accounted for in this kind of workup. If symptoms are discreet, consistent with repeat exams, don't conform to nerve pathways, and cannot be reproduced or fixed with mechanical testing and treatment - think about spinal cord lesions or brain lesions... MS or tumors. Don't miss those.


Other common entrapments:
Ulnar nerve- check Guyon's canal and the cubital tunnel (I do Tinels on Guyon's canal, and Tinel's on the soft tissue next to the cubital tunnel- as direct stimulation will always be positive even in normal individuals). Rule out lower brachial plexus irritation with local palpation.

Radial nerve- much more rare, and much harder to treat. For sensory loss only I look carefully at the posterior distal interosseus membrane (or at least the region around it)- try Tinel's there. In the few cases of radial nerve symptoms I've seen this is usually were the problem is. In theory it could be pinched as it travels along the humorus, but I havent seen this yet. I did have one with motor weakness and no sensory involvement- consistent with posterior interosseus syndrome. This was particularly challenging without immediate sensory feedback and I had to look up the anatomy- but his strength did recover to 4/5 (from 2/5) on my second attempt (that was pre-post treatment thumb extensor muscle strength testing). To treat this you must target the Arcade of Frohse (part of the supinator).




If you have a better anatomic theory as to how fixing these things is possible, I am very curious.
I have had many dozens of such cases that have resulted in remission of their day to day sensory symptoms, and 2 where muscle strength improved dramatically over the course of the treatment (one involved the radial nerve above, one was a median nerve entrapment case after a fall). When I see weakness I have a very low threshold for imaging and referral, but if sensory symptoms resolve and strength improves I might wait a week and see how they do before I push hard for surgery.

I dont typically get NCS or EMG on these patients because I dont want to charge them for something that physical exam gives me a clear answer for, especially when 30 seconds later they are often symptom free (and permanently so- even if they have had symptoms for years). For any study to be meaningful however objective testing will be necessary. I am sorry I do not have NCS findings before and after treatment as that would be far more interesting... honestly, I am not even sure if they would change- though I suspect they would. With resolved symptoms I am not sure it matters – they still wouldn't be getting more aggressive intervention if they are symptom free.

I don't expect you to believe me without better evidence- but if you try this method and it works for you... go for it. If it at least makes sense anatomically that's a start. Even without the ability to treat, this is a good approach to know whats going on diagnostically (the NCS is objective, but not nearly as helpful clinically). If you cut the wrong thing or the patient has double crush your outcomes wont be as good.

Tired said:

Do I believe that you can manipulate the carpal bones and cure CTS? Absolutely not, because while the carpus is somewhat mobile, the position of the bones relative to each other is ligamentously fixed and cannot be altered without damage to these ligaments.

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I'd challenge you to compare wrist flexibility good hand vs bad in the next 10 carpal tunnel cases you see. check range of motion in extreme flexion and extension. I think you'll find motion is limited in the affected side. Dont take my word for it- try it. It doesn't feel like the bones are very far out of normal position- just that they are particularly stiff and tender and often one or two are abnormally prominent. I don't know exactly what makes them prominent... the studies haven't been done. They are easy enough to normalize though and thats the end of story for carpal tunnel symptoms in most cases.

The hard part isn't the treatment- the hard part is finding out where the problem is... it takes a good working knowledge of dermatomes and peripheral nerve pathways and likely locations of impingement.

Lower extremity is just as challenging, but just as important clinically. Most cases of numbness down the leg are NOT disc herniations... but most docs get lumbar MRIs, and most patients have bulging disks somewhere- so it seems like everyone ends up getting all this aggressive stuff done, and with poor success rates. Do a good exam with a good working knowledge of nerve pathways and patients like this are easy to figure out. If you have good hands, they are easy to help too (very high success rate- and permanent improvement if you do it right).

Cuthbert said:

I don't think that a life threatening situation is comparable to using rib raising to treat asthma or any other example which you have given.

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Oh, so evidence based medicine is not important for life threatening medical situations? We are only to use it in non-critical cases?

and I never said anything about rib raising...

DrHogFan said:

I really enjoy reading about the case studies. I wish those with a bone to pick with OMT would make their case in a new thread so Bones could use his time on this one to post more studies. Whether you believe them or not I find them to be interesting.

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Thanks. I'd expect nothing less posting this stuff on SDN. It still surprises me just how unprofessional some physicians and med students can be though- this could be a major issue in their practice.

Still.. I think its worth it.

homeboy said:

it's always going to be viewed as snake oil...
...because the manner in which it is taught is--per Tired--akin to faith healing and chiropractic.

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That isn't what he said. read more carefully.

These outcomes seem too good to be true to someone without this training and way of thinking and this makes some people very uncomfortable... especially DO students that are already defensive about their title and think they will be labeled as snake oil salesmen by association. Most things that seem too good to be true definitely are. MOST. The best opportunities also seem too good to be true at first glance. The only way to distinguish snake oil from truth is to test it... right?