We describe 10 cases of lumbosacral plexus neuropathy in which no underlying condition was discovered on initial evaluation or on follow-up examination after an average of 6 years. The patients presented with pain and weakness. Recovery was delayed and often incomplete. When the lower plexus is involved, it may be confused with disk disease manifesting as "sciatica." This syndrome may be a counterpart to the well-described idiopathic brachial plexus neuropathy.

Among 10 patients with amyotrophic lateral sclerosis who had combined biopsy of muscle and cutaneous nerves, two had a history of paresthesia that suggested involvement of peripheral afferent neurons. Of four patients without paresthesia, two had unequivocal abnormalities of touch-pressure sensation of the toe. On morphometric evaluations of lateral fascicles of deep peroneal nerve, one nerve had an abnormally low myelinated fiber density and seven of 10 had abnormally high frequencies of teased-fiber abnormalities. Teased fibers in which myelin was degenerating into linear rows of myelin ovoids and balls occurred in 10.5 percent of fibers in amyotrophic lateral sclerosis nerves as compared with 1.7 percent in control nerves (0.01 less than p less than 0.025). Estimates of density of myelinated fibers were less sensitive than estimates of the frequency of various changes in teased fibers for detecting abnormality.

A new standardized surface technique for conduction studies of the superficial peroneal nerve was developed and applied to 35 normal subjects and 63 patients with peroneal mononeuropathies, lumbar radiculopathies, sciatic neuropathies, lumbosacral plexopathies, or peripheral neuropathies. The response amplitude was greater than 5 microV and the response peak latency was less than 4.1 msec in all normal subjects; however, 8.6% of normal subjects had at least one unelicitable superficial peroneal nerve response (6% of all limbs tested). These data were compared with those of previous studies. Although this technique did not improve the diagnosis of peroneal neuropathy, it did distinguish lumbosacral plexopathy and sciatic neuropathy from L5 radiculopathy and served as a second, easily approachable, sensory conduction study of the leg.

We reviewed the clinical and laboratory features of 81 patients who had trigeminal sensory neuropathy (TSN) and a connective tissue disease (CTD). The neuropathy developed before the symptoms of CTD in 6/81 patients (7%), and in 38/81 patients (47%) TSN and CTD were diagnosed concurrently. The most frequently associated CTDs were undifferentiated connective tissue disease (38/81, 47%), mixed connective tissue disease (21/81, 26%), and scleroderma (15/81, 19%). Of 66 patients followed for more than 1 year (median, 5 years; range, 1 to 26 years), 8/66 patients (12%) had mild improvement and 2/66 (3%) had marked improvement of numbness; no patient had complete return of sensation. The facial numbness was frequently associated with moderate to severe facial pain that was usually resistant to pharmacologic therapy. None of the patients developed clinical or laboratory evidence of systemic vasculitis. The etiology of this cranial sensory neuropathy remains obscure.

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