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Electrophysiological and ultrastructural studies on reversible neural conduction disturbance after high voltage discharge.

High-voltage condenser discharges exerting a field strength of up to 1000 V/cm (discharge time constant 0.24-8 msec) applied to isolated sciatic frog nerve lead to disturbances of the propagation of action potentials including transient complete block of conduction. Such conduction disturbances are normally reversible within minutes. Inhibition of the activity of the membrane-bound Na+-K+ATPase prevents the recovery from conduction block. Withdrawal of external Ca2+ also prevents recovery, whereas blockade of protein synthesis by cycloheximide has no influence. The velocity of recovery depends on the temperature, with temperature coefficients (Q10) from 1.31 to 1.84 between 2 degrees and 30 degrees C. Transmission electron microscopy of nerves subjected to strong discharges shows alterations of the myelin sheath (splitting and cleft formation) which are, however, not specific for this mechanism of injury. No alterations are seen in the region of the free axoplasmic membrane of the node of Ranvier or in organelles. The results suggest a breakdown of the transmembrane ionic gradient causing the conduction disturbance.

Action Potentials↗

[Neural conduction velocity in patients on hemodialysis].

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.

Adolescent↗

Neural conduction velocity of the human auditory nerve: bipolar recordings from the exposed intracranial portion of the eighth nerve during vestibular nerve section.

We measured the conduction velocity of the intracranial portion of the auditory nerve in 3 patients undergoing vestibular nerve section to treat Ménière's disease. The conduction velocity varied from patient to patient, with an average value of 15.1 m/sec. The latency of peak III of the brain-stem auditory evoked potentials (BAEPs) increased by an average of 0.5 msec as a result of exposure of the eighth nerve, and if that increase is assumed to affect the entire length of the auditory nerve (2.6 cm) evenly, then the corrected estimate of conduction velocity would be 22.0 m/sec. Estimates of conduction velocity based on the interpeak latencies of peaks I and II of the BAEP, assuming that peak II is generated by the mid-portion of the intracranial segment of the auditory nerve, yielded similar values of conduction velocities (about 20 m/sec).

Electroencephalography↗