The findings on nerve conduction studies are varied, but they usually include findings that are consistent with a generalized but heterogeneous sensorimotor polyneuropathy that includes features of demyelination such as slowed nerve conduction velocities, temporal dispersion and occasionally, conduction block.
Treatment All forms of leprosy require long-term treatment with sulfones (dapsone being the most commonly used), rifampin, and clofazimine. The skin lesions of lepromatous leprosy are responsive to thalidomide, which itself may cause a sensory neuropathy (Barnhill and McDougall). Reactivation of disease, or a conversion from the tuberculoid to the lepromatous pattern, may occur during times of reduced immunity.
The status of this disorder is uncertain and the authors have not encountered a definite case. Although characteristic disturbances of skeletal muscle are known to complicate hypothyroidism, the demonstration of a definite polyneuropathy has been infrequent. However, a number of elderly myxedematous patients complain of weakness and numbness of the feet, legs, and, to a lesser extent, hands, for which no other explanation can be found. Loss of reflexes, diminution in vibratory, joint-position, and touch-pressure sensations, and weakness in the distal parts of the limbs are the usual findings (see Dyck and Lambert). The neuropathic manifestations are seldom severe. Nerve conduction velocities are slowed and the protein content of the CSF is usually increased to more than 100 mg/dL. Possibly the latter finding is a reflection of the increased protein content of the serum in the hypothyroid state. The subjective improvement and complete or near-complete reversibility of neuropathic signs following treatment with thyroid hormones provides evidence of a hypothyroid etiology. In biopsies of nerve, an edematous protein infiltration of the endoneurium and perineurium, a kind of metachromatic mucoid material, has been seen. Dyck and Lambert (who should be credited for drawing attention to this neuropathy) noted segmental demyelination in teased fiber preparations. In electron-microscopic sections, a slight increase in glycogen, acid mucopolysaccharides, and aggregates of glycogen and cytoplasmic laminar bodies in Schwann cells have been observed by others.
Polyneuropathy of sensorimotor type has also been observed in association with a syndrome of chronic lymphocytic thyroiditis and alopecia (Hart et al).
Idiopathic Small-Fiber Sensory Polyneuropathy (Numb, Burning Feet Syndrome)
This, of course, does not have the status of a single entity, but all neurologists encounter numerous cases of a relatively nonprogressive idiopathic sensory polyneuropathy, mainly in older patients. Paresthesias of feet and lower legs, sensory loss, and absent ankle reflexes are the usual findings. The hands may be mildly affected, but leg weakness and imbalance are absent or minor. A painful variety is also known (see later).
The most common situation in our experience has been one that affects elderly women with slowly progressive (over years) burning and numbness of the feet, ascending to the ankles or midcalves. There are few findings on examination. Often, there is only mild loss of pinprick and thermal sensation; ankle reflexes may or may not be reduced. There is little progression over the years. Most of these cases are idiopathic, but there is a broad differential diagnosis, including the diseases mentioned earlier, as outlined by Mendell and Sahenk (Table 43-5 is adapted from their discussion).