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In this experiment, the effects of ischemia on neural conduction in the monkey spinal cord were studied. In six monkeys generalized ischemia of the spinal cord was created by bleeding the animals to a hypotensive level below the lower limits of autoregulation in the spinal cord. The progressive development of spinal cord ischemia was documented by blood-flow measurement using the hydrogen clearance method. Physiological integrity of the spinal cord was monitored and recorded by the spinal evoked response. The spinal evoked response did not disappear until at least 10 minutes of profound ischemia. At levels of ischemia 20% to 25% of normal blood flow, the spinal evoked response was unchanged. It is concluded that long-tract neural conduction in the spinal cord is relatively resistant to the effects of ischemia.
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Fourteen patients with chronic glomerulonephritis and with Alport's syndrome were treated. Haemodialysis was performed 2--3 times weekly. The duration of treatment was from 10 months to 9 years. Serum levels of electrolytes, urea and creatinine were determined, the neurological condition was examined and nerve conduction velocity was measured in the lower and upper extremities. The determinations were done before and after haemodialysis. Subclinical manifestations of polyneuropathy were demonstrated with reduced motor-nerve conduction velocity in the lower extremities. A direct effect of single haemodialysis was far from uniform: usually the conduction velocity increased after haemodialysis and in some cases it decreased. There was no correlation between the serum levels of electrolytes, urea and creatinine and motor-nerve conduction velocity.
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Local anesthetics administered intrathecally seen more effective when in hypobaric solution than when in hyperbaric solution. To test whether an unrecognized osmotic effect might be playing a part in this, sheathed vagus nerves of rabbit were incubated in electrolyte-deficient or electrolyte-free media of various degrees of hypo-osmolarity. The nerves gained weight over a period of 15 min. They lost nearly half their sodium, but very little potassium, within 5 min. Electrolyte depletion by incubation in sucrose solutions depressed the amplitude of the C-fiber component of the compound action potential more rapidly in hypo-osmotic than in iso-osmotic solutions. In iso-osmotic sucrose, 50 per cent depression developed in 61 +/- 12 min (mean +/- SD, n = 5), but in 0.6 iso-osmotic sucrose, 50 per cent depression was reached in 17 +/- 3 min (n = 5). Lidocaine, 100 microM (approximately 0.003 g/100 ml) in iso-osmotic sucrose was without observed effect; lidocaine, 100 microM in 0.6 iso-osmotic sucrose produced 50 per cent depression in 7 +/- 2 min (n = 4). Thus, osmotic swelling plus electrolyte depletion, but not electrolyte depletion alone, markedly intensified inhibition of conduction by lidocaine. All effects were reversible by returning the nerves to isotonic physiologic incubation medium. The results suggest that intrathecal osmotic swelling of neural tissue may contribute to the conduction block in hypobaric spinal anesthesia.
H reflex on the soleus muscle and motor tibial nerve conduction velocity are used to study peripheral nervous system maturation in 68 healthy children, from birth to 4 years of age. Proximal an distal conduction velocities develop in a parallel and approximately exponential way but proximal conduction velocities remain always faster. The latencies slightly decrease during the first 18 months of life and then increase very slowly.
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A case of scleroedema is reported in a 28-year-old man with severe neuromuscular involvement. Failure in neural conduction as well as muscular degeneration and necrosis were seen. Histopathological study showed resorption and formation of scar tissue probably secondary to ischaemia. In addition there was increase in neutral, sulphated and non-sulphated mucosubstances in the dermal and endomysial connective tissue.
The segmental and supraspinal innervation of the detrusor muscle and periurethral striated musculature was studied in 27 patients with diabetes mellitus by gas cystometry, integrated sphincter electromyography, and spinal evoked-response latency measurements. Slowing of neural conduction velocities was a consistent finding in all the patients, even when cystometry did not show abnormalities. Thus, neuropathy in the segmental innervation of the bladder and urethra was documented.
A rapid visual resolution test conducted on available equipment reveals the presence of rapid falloff in acuity in a case of probable multiple sclerosis. Intense large field illumination was used, and grating acuity was tested using laser red light. The effect is so large that minor anomalies (not subjectively appreciated) or the residuum of earlier minor attacks of retrobulbar optic neuritis can be readily detected. A related "visual fatigue or saturation-like syndrome" was described earlier. In bright environments these patients' vision fades. Briefly closing the eyes restores visual sensitivity. Providing filters or lowering the light level tends to maintain vision. This test must be studied intensively. It offers a noninvasive simple means of showing underlying anomalies in neural conduction of the visual signal. Such anomalies can be prognostic and previously have been revealed only with sophisticated electrophysiological techniques.