Adhesive Capsulitis

[HeadStrongPT]

Ok Diane...so it shall be done. Here's the new thread extending from our previous discussion on the relationship between pain and manual therapy.

I think I am trying to better understand the 10 steps by applying it to a specific clinical scenario. In this case: adhesive capsulitis. I was trying to reconcile rule #9 in the context of this pathology. To me there must be a relationship between the tissue's architecture and the pain levels present.

As an example (please for give not having the specific reference right now - I will post it). Numerous RCT have examined the positive relationship between an increase in glenohumeral ROM and self-reported pain and function resulting from manual mobilizations. How can this be reconciled with rule #9?

[Luke Rickards]

Roderick,

I take it that the mobilisations referred to here involve some kind of stretching. Here are some references on the mechanisms behind increase ROM with stretching.

Both static stretching and ballistic stretching increase range of motion, most likely as a result of enhanced stretch tolerance rather than changes in muscle elasticity. (LaRoche,2006)

The constancy of the muscle resting tension suggests that merely the subjects' tolerance to higher stretching strain brings about the enlargement of ROM after short-term stretching exercises. (Weimann,1997)

Long term stretching increases joint range of motion as a result of elevated stretch tolerance rather than a viscoelastic accomodation.] [ The effectiveness of different stretching techniques is attributed to a change in stretch tolerance rather than passive properties." (Magnusson, 1998)

I haven't read the RCTs so can you tell us, did they show that the increase in ROM was not actually a result of decreased pain following the application of manual therapy? Did they show that the manual therapy was directly responsible for a change in the tissue length (rather than tolerance from neurological change), leading to increased ROM? And, were non-specific factors ruled out?

I understand that eventually the associated tissue changes will improve, but is this a result of the manual therapy, or due simply to a resolution of the disease mechanisms and return of function?

[HeadStrongPT]

Roderick,

I take it that the mobilizations referred to here involve some kind of stretching. Here are some references on the mechanisms behind increase ROM with stretching.



I haven't read the RCTs so can you tell us, did they show that the increase in ROM was not actually a result of decreased pain following the application of manual therapy? Did they show that the manual therapy was directly responsible for a change in the tissue length, leading to increased ROM? And, were non-specific factors ruled out?

Actually I was incorrect. Only one of the studies I mentioned was an RCT. I'll need to do some more homework on the clinical trials. Here are a few of the articles I typically reference. I included the abstract of one of the articles as it is the only one conducted with the patient under a brachial plexus block.

You bring up a good point. A limitation of these studies is that they do not state the manual therapy was directly responsible for change in tissue length. However, the Hinricus study reports significant changes in capsular volume measured via arthrogram following the mobilization protocols. The changes in volume do seem to correlate well with the increases in ROM. This does lend support that there is a connection between the mobilization and tissue architecture.

I think there is evidence to acknowledge that manual therapy can directly influence connective tissue in the case of adhesive capsulitis. There may be other mechanisms (plausible or otherwise) at work as well that were not addressed within the study.

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Jing-lan Yang, Chein-wei Chang, Shiau-yee Chen, Shwu-Fen Wang, and Jiu-jenq Lin. Mobilization Techniques in Subjects With Frozen Shoulder Syndrome: Randomized Multiple-Treatment Trial Physical Therapy 2007 87: 1307-1315.

Henricus M Vermeulen, Piet M Rozing, Wim R Obermann, Saskia le Cessie, and Thea PM Vliet Vlieland. Comparison of High-Grade and Low-Grade Mobilization Techniques in the Management of Adhesive Capsulitis of the Shoulder: A Randomized Controlled Trial. Physical Therapy 2006 86: 355-368.

Placzek JD, Roubal PJ, Freeman DC, Kulig K, Nasser S, Pagett BT. Long-term effectiveness of translational manipulation for adhesive capsulitis. Clin Orthop. 1998;356:181-91.

Long term effects of glenohumeral joint translational (gliding) manipulation on range of motion, pain, and function in patients with adhesive capsulitis were studied. Thirty-one patients underwent brachial plexus block followed by translational manipulation of the glenohumeral joint. Changes in range of motion and pain were assessed before manipulation with the patient under anesthesia, immediately after manipulation with the patient still under anesthesia, at early follow up (5.3±3.2 weeks), and at long-term follow up (14.4±7.3 months). Passive range of motion increased significantly for flexion, abduction, external rotation, and internal rotation. Significant decreases in visual analog pain scores between initial evaluation and the follow up assessments also occurred. Furthermore, Wolfgang's criteria score increased significantly between initial evaluation and follow up assessments. Translational manipulation provides a safe, effective treatment option for adhesive capsulitis.

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[Luke Rickards]

Here's a tidbit from eMedicine that looks useful here.

To date, no robust pathophysiologic model explains the relationship between the principal characteristics of this disease (ie, pain, contracture). Neurologic factors seem to be the principle mediators of the pain, whereas a process resembling fibromatosis causes the contracture, as described in the above text. Why the pain precedes the contracture and why it resolves before the contracture does in most subjects remain unclear. The fact that the pain of FS often precedes stiffening of the joint tends to support the notion that the initial pain probably does not stem from altered mechanics of the glenohumeral joint.

I think Jason posted a research paper ages ago that concluded doing nothing was not statistically different to manipulation. We should look at that one too. Perhaps Jason will remember it.

[HeadStrongPT]

I couldn't agree more from an empirical standpoint. AC really has many features of CRPS at times, suggesting a systemic or autoimmune component. However, the emedicine article does indicate there are both central and connective tissue mediators of the pathology.

In context with clinical trials demonstrating that specific mobilizaton techiques result in changes in capsular volume and ROM, I believe this leaves room for further discussion of rule #9.

Please understand I am not saying it is entirely mechanical - far from it. Nor would it be reasonable to say it is entirely neurological, autoimmune etc...

So Luke. I've got one for you: If AC is profoundly mediated by the nervous system. Wouldn't it's presentation change considerably with the patient under anesthesia? How does this account for the effectiveness of manipulation under anesthesia?

[Jon Newman]

So Luke. I've got one for you: If AC is profoundly mediated by the nervous system. Wouldn't it's presentation change considerably with the patient under anesthesia? How does this account for the effectiveness of manipulation under anesthesia?--Roderick

I know this was asked of Luke but as Luke mentioned elsewhere, I had concerns about number 9 myself and these were essentially my thoughts at the time

Manipulation under anesthesia seems to have a direct effect on the connective tissue. Doctors realize the lack of specificity and bluntness of the procedure as they are cautious about breaking a bone during the procedure. This must mean that bones are as likely to break as adhesions are after a certain amount of force. Since the patient is unconscious during the procedure, reflexive changes aren't likely to account for any ROM gains. More likely there was a change in form of some sort. Of course those range of motion gains are unlikely to be lasting without helpful behavior following the procedure but for some people, it seems to be an important part of their recovery.

Regardless, the qualifier "almost never" and the boolean "and" in "clinically relevant AND lasting" in point #9 gives some wiggle room for this sort of thing.--Jon

I would add that mobilization of a painful joint has to be significantly easier with an unconscious patient--at least if the intended consequence was a direct effect on the tissue architecture itself.

The list we created was to address issue of pain and in no way does it mean that there are not other aspects to be concerned about regarding our care of a patient.

Roderick, (I've been using Rod, but I see you signature is Roderick so sorry if I was too informal earlier), what do you mean by presentation when you asked "Wouldn't it's presentation change considerably with the patient under anesthesia?"

[Luke Rickards]

I believe this leaves room for further discussion of rule #9.

These aren't rules, so there's always room for further discussion.

If AC is profoundly mediated by the nervous system. Wouldn't it's presentation change considerably with the patient under anesthesia?

I don't think that AC is profoundly mediated by the nervous system. I think pain is. I have no doubt that the pain of AC changes profoundly under anesthesia.

I guess the question here is do we know that the fibroblastic changes and reduction in ROM are the cause of the pain. You noted yourself that pain shows up before significant tissue changes, and it often resolves before the tissue returns to normal.

More from the article-

Sympathetic dysfunction in patients with FS is believed to mediate hyperresponsiveness of peripheral alpha adrenoreceptors in the nerve endings of somatosensory neurons, including various joint nociceptive and proprioceptive fibers of the shoulder. This hyperresponsiveness probably contributes to the pain (allodynia) produced with gentle, passive mobilization of the shoulders observed in patients with FS.
Ischemia of the soft tissues may link the apparently distinct and separate pathophysiologic entities observed in FS, namely, neurologically mediated pain and fibromatosis-like contracture.........hypersensitization of peripheral vasomotor alpha-adrenergic receptors and a pain-induced increase in local vasomotor tone also can contribute to ischemia of the local connective tissues of the shoulder.

If this is true then the pain mechanism is likely to be hypersensitivity of somatosensory neurons and concurrent local ischemia, ie predominantly chemical in nature and not a direct result of tissue hyperplasia.

Regarding the correlations between manual therapy and increased ROM, we should therefore also look at other mechanisms operating beyond direct lengthening of CT. Mobilisation can result in reflexive autonomic changes and increased blood flow, reflexive change in tissue stretch tolerance and local muscle tone, descending pain inhibition, etc. Mobilisation might also directly stretch the CN. Where this is the case, are we sure that it is responsible for the changes in ROM and reduction in pain?

[Diane]

Lest we forget,

Ischemia of the soft tissues

... some of those "soft tissues" are likely to be nociceptively/interoceptively screaming neural structures, i.e., nerves around the shoulder, deep and superficial, underneath and on top, innervating mesoderm in the area or just minding its own business, passing by on its way to the elbow, or past the elbow to the hand.

I'd be interested in expanding the search for the "cause" to include these other areas of neural destination. What are the neurodynamics like at the wrist? Elbow?

At another concentric circle of influence altogether, what about the nerves that are segmental, around the neck/trunk (i.e., superficial cervical plexus with its extensive drape of supraclavicular nerves out to shoulder, lateral cutaneous under the arm, intercostobrachialis, dorsal cutaneous between the scap)?

[HeadStrongPT]

I think I wasn't as clear as I could have been earlier, so I will restate: I agree with the statements regarding pain and manual therapy in principle. I agree that pain is a fundamental and often under appreciated component of orthopedic conditions. Ignorance of this fact results in inefficient treatment.

I also agree that manual therapy, at least the way it is often delivered, is insufficient to elicit plastic changes within soft tissue to result in long-standing improvements in function. This certainly leaves plenty of room for a neurological / systemic explanation as has been proposed on this forum.

I find many patients in early stages of AC to be highly sensitized. My approach to these individuals likely falls in line with the opinions of those on this forum: desensitization, gentle periarticular mobilization, even gentler articular mobilization (we cavemen call them grade 1-2 ). I find patients AROM often improves without the slightest mechanical assault on the capsule itself.

HOWEVER. There are instances where a mechanical approach directly influences the mechanical properties of the tissue such to permit an increase in ROM. I believe the most direct evidence of this was the increase in capsular volume following capsular mobilization. Of course one could theorize that the increase in volume is due to some complex neurological cascade, but this would be far less plausible than the explanation that a mechanical treatment elicited a mechanical response. Occam would likely agree with me on this.

I concede that the mechanical changes manual therapists claim to elicit are drastically overstated, AND that is very annoying for me as well. Coming from a background in exercise, where there is a much stronger appreciation for neurophysiology than physical therapy, I was appalled at what highly educated individuals were willing to believe. You certainly have an ally in this regard.

I think the debate could be resolved by agreeing that there is a strong likelihood that both neural and local factors are at play here. The degree to which each contributes is up for debate not only on this forum, but among professionals in the medical community who research it directly. Until the answer is found with a larger degree of certainty, this debate is likely to continue with little chance of a resolution.

Of course I do enjoy the mental exercise a debate like this provides. Thanks! If I didn't answer some specific questions addressed to me, I will review and respond.

[HeadStrongPT]

Roderick, (I've been using Rod, but I see you signature is Roderick so sorry if I was too informal earlier), what do you mean by presentation when you asked "Wouldn't it's presentation change considerably with the patient under anesthesia?"

I knew I missed a question. Feel free to call me Rod or Roderick. No worries either way. I think the question was meant to illustrate that if AC were predominantly a neurological phenomenon, then ROM would likely improve considerably with the patient under sedation.

Since this does not occur (I'm lucky to be present during some MUA) and since ROM certainly does improve following an MUA, a logical conclusion is that there must be a biomechanical component to AC. Again, I'm not implying that 100% of the therapeutic effort should be directed at assaulting the capsule. I am also saying that there must be some balance between acknowledging the roles of the nervous and MSK systems.

This brings us back to #9 and my obsession of "relatively little" and "almost never". Again, the debate is likely an exercise in futility, but it has certainly given my cortex a workout.

[Jon Newman]

Hi Rod,

Perhaps it would help if you offered an amended version of number 9 that better captures what you have in mind. That's how we did it.

Actually anyone can chime in. That's sort of the point.

I'm currently content with how it reads until someone offers something better.

[HeadStrongPT]

Hi Rod,

Perhaps it would help if you offered an amended version of number 9 that better captures what you have in mind. That's how we did it.

Actually anyone can chime in. That's sort of the point.

I'm currently content with how it reads until someone offers something better.

#9 There is insufficient evidence to suggest a direct connection between tissue length, form or symmetry and the prevalence of pain. Manually applied forces as they are often applied in the clinic are unlikely to directly result in clinically relevant and lasting change in tissue length, form or symmetry. While evidence exists supporting the notion that mechanical therapies elicit some form of mechanical response in connective tissue, the effects of manual therapy must also be regarded as the result of reflexive neurophysiological responses.

I was going to put something in there about me being awesome but it got a little wordy. Kidding of course. I'll natually welcome any criticism or comment. #9 could be broken up into their own statements.

[Diane]

Rod, I'd lay odds on any favorable change happening in a wide-awake, conscious, pain-perceiving patient receiving manual treatment being completely a function of the two nervous systems interacting, not a function of a mechanical change to connective tissue caused by the manual application of force to it - this latter point is mostly perceptual fantasy/conceptual hallucination IMO.

[HeadStrongPT]

Rod, I'd lay odds on any favorable change happening in a wide-awake, conscious, pain-perceiving patient receiving manual treatment being completely a function of the two nervous systems interacting, not a function of a mechanical change to connective tissue caused by the manual application of force to it - this latter point is mostly perceptual fantasy/conceptual hallucination IMO.

I think there is only a small amount of disagreement here. I simply would replace the words "any" and "completely" with "some" and "partially". How do you reconcile a significant change in capsular volume following a mechanical treatment as perceptual or fantastic?

In this instance, I have provided measurable support to at least implicate a mechanical treatment in iliciting a mechanical change in the glenohumeral joint capsule.

Do you have any direct or measurable support for the two nervous systems interacting in adhesive capsulitis? What neurological event could cause an expansion of capsular volume? I can't think it should be too much of a strech to say some mechanical event is at play. I am prepared to eat crow here.

[Luke Rickards]

Here's something else that might be helpful here.

Schleip, 2003-

"Immediate fascial plasticity cannot be understood by mechanical properties alone. Fascia is densely innervated by mechanoreceptors. Manual stimulation of these sensory endings probably leads to tonus changes in motor units which are mechanically linked to the tissue under the practitioner’s hand."

"fascial mechanoreceptors can trigger immediate viscosity changes of the ground substance."