This "rare" form of TOS, is actually, not so rare, but possibly under-recognized, under-reported.

Once a person is dx'd with RSD, any muscle loss, even in dermatomal patterns (not usually a "sign" of RSD, unless a specific nerve is damaged, and the consequence is RSD/causalgia), then most doctors will [want to] believe that observed muscle loss is connected to either pain guarding, disuse, pain avoidance, hysteria, attention seeking; and not, a loss of nerve function. Also, even when they accept that there is "dermatomal" dennervation signs, they may still believe in the RSD dx, as having caused TOS (from muscle atrophy causing compression on the brachial plexus). Obviously, not all docs feel this way, but, in my own experience, anything is possible.

Unfortunately, once a person has signs of muscle wasting, atrophy, nerve dysfunction, motor loss, that IS NOT a consequence of RSD, most doctors will also [still want to] believe that this is so rare, that it couldn't be an actual nerve dysfunction (looping disbelief medicine), and try to attribute [it] to anything else, including pain guarding, disuse, pain avoidance, hysteria, attention seeking, than seek the actual cause of this nerve dysfunction.

Why? I assume that once a patient has observable wasting, atrophy, motor dysfunction, from a real nerve dysfunction/dennervation, the doctors have been taught that regaining what has been lost, even after nerve decompression, is quite low, statistically. Why should this matter? I assume that many docs, who don't see "success" in a patient's future, may not want to get involved, even though, correcting the nerve dennervation, and halting its progression, should be considered, heroic [my opinion], and preserving nerve function, whatever is left, should be a priority to everyone.

Anyways, what one would think would be a sure indicator of a true neurologic dysfunction, most doctors would rather believe, especially in the case of a possible TOS dx, that there is actually something else at play that could better explain this muscle wasting (nerve dysfunction).

What does that mean? Those whose atrophy, wasting, is a consquence of a BP compression, will more than likely have their "wasting" attributed to pain guarding, disuse, inactivity, (being a weenie) and, they will more than likely not get the timely diagnosis that would help them actually preserve nerve function.

What does that mean? That they will either have to deal with their condition on their own, in the hopes that it does not progress to very severe deficit, or try to get help, but have to convince every doctor that they come across that they indeed use their hand(s), finger(s), wrist(s), and are not "faking".

It is very difficult to develop wasting, especially wasting in a nerve dennervation pattern, without immobilizing the hand/arm/fingers in question. One would be surprised how much muscles "move" even when not doing much. It is quite difficult to remain still, even when something "hurts".

As a matter of fact, things that hurt, especially from a nerve dysfunction, actually cramp, burn, sting, go numb, curl, etc., and a patient is actually more likely to keep it moving in order to distract oneself from those symptoms.

So, the likelihood of having observable wasting, in a nerve dennervated fashion is highly unlikely the result of "disuse", "inactivity", "pain guarding". Most docs don't get this, as they probably haven't had this pleasure.

Apparently, though, there are people (notice, I did not use the word, patient) that go from doctor to doctor, feigning curled over limbs/fingers, for attention, or proof of disability, and/or demonstrative of hysteria, and that is what is the first thought in any physician who looks at a deformed, wasted, atrophied limb, and/or ulnar contracted fingers (regardless of gender).

If they do recognize that the atrophy/wasting is occuring in very obvious nerve dysfunction patterns, they will more than likely want to believe and diagnose that this patient is actually suffering from a more "fixable" nerve compression syndrome, like carpal tunnel, cubital tunnel, trigger finger, etc, than consider the more "rare" likelihood of a true neurogenic TOS.

Now, that is not to say that there have been no patients that had their TOS nerve dysfunction recognized and had timely intervention, but that may not be the norm.

True neurogenic TOS does occur, and in my opinion, isn't as "rare" as is advertised. Most people who present with very obvious dysfunction, in a very obvious nerve dysfunction pattern, often do get diagnosed and get some chance to halt the nerve dennervation.

Others, who get this "disuse", "inactive", "guarding" label, may not be as successful. Those whose obvious nerve dysfunction, even when supported by emg/ncs, may still be doubted, for any number of reasons. This is why it would really be nice if there was more "belief" in the possibility for this "rare" disorder, and less bias, less belief that patients are actually "doing this to themselves" for attention. Wouldn't that be nice.

Oh, and muscle wasting/atrophy can be viewed on MRI. Remember, nerves innervate different areas of the body. These nerve dysfunctions can start at the spinal nerve, down to direct compressions, resulting in wasting/muscle loss (despite use) in the muscle sets that they are meant to innervate. The loss of muscle mass on MRI, can be attributed to nerve dysfunction, but a certain assymetry may be expected if doctors think that certain people [read, women] even those who lift weights, favor the dominate side of their body, and are naturally "wasted", undeveloped on their non-dominate side.

It is the correlation of visual studies (MRI, MRA, MR Neurogram, etc), electrodiagnostics (emg/ncs), and clinical patient assessment that would hopefully allow as accurate a diagnosis as is medically possible. I would hope that social bias (towards patients on W/C, ligitation, disability) would not play a part in the workup of a patient.

Unfortunately, I don't think this is that case. Best to all.