WHY CARPAL TUNNEL SURGERY IN SOME PATIENTS IS DOOMED TO FAIL

Carpal tunnel syndrome is an entrapment neuropathy involving the median nerve at the wrist – and when the median nerve is entrapped physically  in the tunnel through which it passes; the patient may experience tingling, pain, or weakness, with or without muscle atrophy, in the first four fingers of the affected hand.

The “tunnel” is formed by the carpal bones in the wrist and the transverse carpal ligament. The median nerve passes through the tunnel along with the flexor tendons of the fingers. Tenosynovitis of these flexor tendons from repeat movement often occurs in middle aged women. Premenstrual edema, sewing, driving or operating computers can all cause pressure on the median nerve. It can also be caused by gout deposits or calcium. Rheumatoid arthritis or acromegaly  sometimes lead to these symptoms in the hand.

There can be numbness in the palm of the hand extending to the thumb, index, and middle fingers. Pain can occur. Weakness and loss of muscle mass can occur even without pain or sensory symptoms at the base of the thumb. This can make it hard to forcefully oppose the thumb to the tips of any fingers in the same hand, or squeeze objects. Pinpricking any of the first three fingers is sometimes accompanied by exaggerated painful response: a hallmark of conditions affecting single nerves. This is called “hyperpathia.” [ allodynia ]

The logical approach to curing this condition is relieving the pressure inside the carpal tunnel by cutting the tranverse carpal ligament during an operation. It would seem to make sense, since this is the only portion of the border around the  tunnel which is amenable to cutting to relieve   the pressure on the median nerve.  Over the years different surgical  techniques have been employed, including the use of an endoscopic cutting technique.

Prior to operating, it has been the custom of many centers to perform nerve conduction studies to confirm the diagnosis by  measuring conduction velocities across the median nerve.  More recent studies would seem to indicate that the problem of speed of conductivity may not be a good way to predict improved outcome from simply relieving pressure on the – ‘presumably’ – already damaged nerve. In fact, the prognosis may lie in the brain, and not in the amount of pressure on the median nerve, or how long the nerve has been under pressure.

Electroneurography  findings do not always correlate with symptoms or variations in central nervous system plasticity. Decreased median nerve sensory conduction velocity may not be suitable to confirm the degree of pain experienced by each individual patient. Pain is transmitted by A-delta and small c fibers.  Paresthesia signals are carried by A-beta fibers and are caused by ectopic firing of damaged nerves. It is not a new concept that electromyograpy studies have variable predictabilty in diagnosing peripheral nerve lesions.

The answer may be  how much gray matter a person has in the precentral gyrus, or across the entire thickness of the brain.  The amount of gray matter thickness may determine whether one feels pain, as a predominant feature, or paresthesia and numbness, as another alternative predominant feature; in the contralateral hand experiencing the pain or numbness and tingling. At least one study confirms the correlation between thicker gray matter cortices and complaints of pain. If such is the case…then perhaps MRI would be more sensitive and specific compared to electrodiagnostic studies.

We already know that chronic low back pain – despite what the recent CDC guidelines claim is a condition which should only be treated for several days with opioids – is associated with altered gray matter density in the prefrontal cortex of the brain. This finding supports two concepts. The first is that chronic pain exists; and  presumably should be treated with whatever works to alleviate pain. This means that when everything else has failed, it’s OK to use opioids as a last choice. But to limit dosage or amount of time they can be given, goes against all scientifically supported reasoning  regarding the cause of pain and that some patients [ as we know from genetic studies of opioid-receptors ] need much more medicine for pain than do others. Given this fact…it seems cruel to place arbitrary limits on opioids just because a good percentage of our American population takes pain pills for recreation. That is no reason to punish legitimate pain sufferers’.

The second reason or concept is quite evident in support of long-term opioid use, and flies in the face of conventional, and incorrect, thinking which has for years proclaimed that if you can’t identify the disease, then there is no pain complaint that has any legitimacy. Well,the fact that carpal tunnel syndrome [ and other irritation neuropathies ] may have the basis for its long-term prognosis hidden in the brain cortex thickness, would certainly be a “wake up call” to those who have been saying that if you can’t see or measure pain – then it does not exist. In carpal tunnel syndrome, the “pain is measured in the brain” and not in the wrist.  Therefore; our whole previous basis upon which we seemed to rely to determine if pain really exists in some patients is now called into question. Lots of patients continue to have wrist pain and numbness after they had undergone carpal tunnel surgery.  That’s because the brain was never “fixed,” only the wrist.  But the problem is that the pain “lives in the brain” and not in the wrist. One could say, without fear of contradiction, that the brain was “predisposed” toward chronicity of the pain – long before the patient in question took that factory job requiring repetitive movements of the hand while operating his machine or lathe. Thus, the pain is “centrally-mediated”  and  “predetermined.”

The reason I state my claim that “long-term opioid use” is indicated here is because the patient had already run out of treatment options of a more conservative nature: that’s why surgeons operate.  While traditional thought teaches that opioid-narcotics do not work well in neuropathic pain – nothing can be further from the truth. Recent genetic studies on opioid receptor physiology support the use of opioids by inference gleaned from substantial research outcomes using opioids in neuropathic pain: even though that was not the primary intent of the research, the methodology clearly was linked to positive outcome using opioids. [ This will be the subject of an upcoming blog ].

With regard to carpal tunnel syndrome; it has been shown that “paresthesia dominant” patients – using brain MRI to calculate gray matter cortical thickness across entire brains –  had “significantly reduced” cortical thickness in pre-central and post- central gyri contralateral to the more affected hand; and decreased median nerve sensory conduction velocity compared to “pain dominant” patients.

In the “pain dominant” patients,  cortical gray matter thickness correlated with pain severity,  but not paresthesia severity.

All of this suggests that a neuroanatomical substrate exists and may lead to improved therapeutic approaches based on these findings. [ See: PAIN 2016 May;157 (5): 1085-93 doi: 10, 1097 j.  Pain 0000000000000486   Maeda, et al. – Primary somatosensory/motor cortical thickness distinguishes paresthesia-dominant from pain-dominant carpal tunnel syndrome. ]

Thus, not all patients can be expected to improve from carpal tunnel surgery; and some patients will undergo procedures which are doomed to fail.

William Mangino II, M.D.