to the editor: I would like to commend Dr. McKnight for an excellent review on paresthesias.1 I am particularly pleased that he categorized pathoetiologies based on central and peripheral phenomena. However, a number of inaccuracies and omissions of valuable information warrant discussion.
Entrapment of the lateral femoral cutaneous nerve is not “usually” without motor deficit. This nerve is pure sensory, and weakness suggests polyneuropathy, plexopathy, radiculopathy or another type of mononeuropathy. Recognition of the absence of weakness is important, as lateral thigh numbness with motor impairment secondary to plexopathy may indicate occult malignancy compressing the lumbar plexus.2 Tumor compressing the nerve at the root level with isolated paresthesias has been reported,3 indicating the merit of differentiation with electrodiagnostic testing.
Cubital tunnel syndrome is described in the article as being associated with leaning on the elbow and the presence of a shallow ulnar groove. In fact, cubital tunnel syndrome occurs when there is ulnar entrapment under the flexor carpi ulnaris in the proximal volar portion of the forearm. Entrapment at the ulnar groove results in compression at a more proximal, distinct site.4 Discrimination is important, as neurosurgical decompression must be precise to limit the extent of excision and accompanying morbidity.
The authors define the C6 dermatome as involving the lateral portion of the forearm, the thumb, and the index and middle fingers. It is commonly accepted that the C7 dermatome transmits afferent sensation from the entirety of the middle digit.5 As the authors point out, “Knowledge of sensory spinal root distribution and cutaneous nerve distribution is requisite to diagnosing paresthesias.” In fact, the American Spinal Injury Association defines the C7 dermatome spinal cord injury sensory level as being the middle digit. The importance of knowing right and left sensory and motor levels cannot be overemphasized. These levels are invaluable in monitoring response to emergent methylprednisolone in traumatic myelopathies. Similarly, rostral ascension of a level in an acute or chronic situation may suggest syrinx progression to the medullary respiratory centers with potential imminent ventilatory failure.
I was disappointed that historical clues to suggest paresthesias in multiple sclerosis were not accompanied by solicitation of visual symptoms, spasms, bowel/bladder deficits, or onset of similar episodes disseminated in space and time, commonly occurring in young female patients.
One final major concern is that of underappreciation of the value inherent to optimal evaluation with electromyography and nerve conduction studies. Electrodiagnosis can define severity and rate of progression, and can strongly suggest and differentiate axonal or demyelinating histopathology in peripheral polyneuropathies. Electrodiagnostic data can be invaluable in defining prognosis and can suggest the immediacy of further work-up or treatment. For example, data may suggest multifocal motor neuropathy with conduction block that is amenable to treatment and reversal of quadriparesis. Identical information can be collected in peripheral mononeuropathies to guide the neurosurgeon as to decompression of peripheral nerve, plexus, or root entrapment sites.
in reply: Our article, an overview of a complex neurologic disorder that is frequently seen by family physicians, was designed to provide a framework for these physicians to use when making a diagnosis.
Dr. Geller indicates that the lateral femoral cutaneous nerve is a pure sensory nerve, which is correct. The word “usually” should not have been in the article. Dr. Geller's points about weakness, etc., are also accurate. However, it was beyond the depth of this article to cover the entire neurologic spectrum of the persisting disorder. The purpose of the review article was to serve as an introduction for family physicians. A complete review of treatment could not have been placed on nine pages.
We researched the dermatomes mentioned by Dr. Geller in several sources that were validated by practicing neurologists. However—as one might expect—these sources did not completely agree, but they were the ones with which we felt most comfortable.
We appreciate Dr. Geller's point regarding our lack of emphasis on use of the erythrocyte sedimentation rate in diagnosis. However, we did not feel it was necessary to mention all of the specific diseases diagnosed through a given laboratory test or the potential significance of abnormal readings. Dr. Geller also mentioned our underappreciation of nerve conduction velocity studies and electromyography. We feel that these tests were mentioned correctly. It is our opinion that these tests serve best as useful adjuncts to the initial tests mentioned. Although the results can be very important, it is our experience that these tests rarely suggest a diagnosis that is not clinically apparent.