Reduced sensory and motor nerve conduction velocities in moderate drinkers.

The mechanism responsible for peripheral nerve dysfunction in chronic alcoholism has not been fully elucidated either in terms of its relationship to the quantity of alcohol consumed or to nutritional status. As part of a series of studies to address these issues, the effects of moderate drinking (60-90 g ethanol per day) or heavy drinking (> 100 g ethanol per day) on peripheral nervous function and thiamine status was measured in 73 patients admitted to a detoxification unit. Electromyographic evaluation revealed significant reductions in median and ulnar sensory and motor nerve conduction velocities in both moderate drinkers (n = 30) and heavy drinkers (n = 43) compared to age-matched controls. Twelve moderate drinkers and 25 heavy drinkers manifested clinical neurological signs of peripheral neuropathy. Thiamine deficiency, as revealed by erythrocyte transketolase activation assay, was detected in two moderate drinkers and seven heavy drinkers but was not significantly correlated with electromyographic alterations with the exception of ulnar nerves. These findings provide evidence for significant early peripheral nerve dysfunction in moderate drinkers and a possible contributory role of thiamine deficiency to the ulnar nerve conduction deficits. Whether deficits in other water-soluble vitamins or a direct neurotoxic effect of ethanol are implicated in alcoholic peripheral neuropathy awaits further studies.

Abnormalities of peripheral nerve conduction in relation to thiamine status in alcoholic patients.

Thiamine status was evaluated using the erythrocyte transketolase activation assay in 20 alcoholic patients admitted on a voluntary basis to a Detoxification Unit. Electromyographic evaluation revealed significant reductions of motor and sensory conduction velocities in the alcoholic group. 38% of alcoholic patients showed significant erythrocyte transketolase activation deficits indicative of severe thiamine deficiency. In the case of peroneal nerve, reduced conduction velocities were negatively correlated with abnormal transketolase parameters. These findings are consistent with a contributory (but not exclusive) role of thiamine deficiency in the pathogenesis of alcoholic peripheral neuropathy. Deficiencies of other vitamins as well as direct neurotoxic effects of alcohol could also be involved in this phenomenon.

Peripheral neurological complications of aortoiliac vascular disease.

Six patients with an aortoiliac vascular disease and a peripheral neurological deficit are presented. Clinical and electromyographic findings revealed lumbosacral plexus, sciatic and femoral nerve lesions. A correlation is made between the level of the vascular lesion (aortic, aortoiliac or distally) and the type of peripheral nerve deficit observed. In a patient complaining of pain, weakness, or numbness in a leg, the differential diagnosis should include aortoiliac vascular disease. The peripheral neurological symptoms may be the initial manifestation of the vascular disease or may appear in the early post-operative period.

Sensory nerve conduction in chronic uremic patients during the first six months of hemodialysis.

In an attempt to find the best electrophysiological indicator of improvement for the neuropathy present in patients with chronic renal failure undergoing hemodialysis, several types of nerve conduction were studied at the beginning of dialysis and six months later. Sural nerve conduction and late response latencies were recorded in addition to conventional motor and sensory nerve conductions. After six months of hemodialysis, sensory nerve conduction velocities in the median, ulnar and sural nerves were improved. These values appear to be the most sensitive indices of the beneficial effect of hemodialysis on the neuropathy.

The importance of studying sural nerve conduction and late responses in the evaluation of alcoholic subjects.

Motor conduction velocities of median, ulnar, peroneal, and tibial nerves and sensory conduction velocities of median and ulnar nerves were studied in 30 alcoholic subjects and a similar group of control subjects. The results were compared to sural nerve conduction velocities and late response latencies (H reflex, F response). The latter two techniques improved the diagnostic yield by 20%: Whereas 73% of our patients showed an abnormality of conduction with conventional techniques, 93% had an abnormality of sural nerve conduction, late response latencies, or both. Abnormalities of motor and sensory conduction, which were more prominent in the lower limbs than the arms, could be documented in patients who did not have any clinical evidence of peripheral neuropathy. The electrophysiologic studies performed in the present study suggest that "axonal degeneration" is the underlying pathologic process in alcoholic peripheral nerve disease.