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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.
On the ground of experiments on 6 baboons the authors tried to determined changes in the amplitude of the N10 somatosensory potential and the time of central neural conduction in relation to changes of the cerebral blood flow in subarachnoid haemorrhage. The following conclusions have been reached: the time of central neural conduction as well as the amplitude of the N10 cortical potential may serve as indicators of brain ischaemia after subarachnoid haemorrhage. The amplitude of the N10 potential seems to be an earlier indicator of ischaemia than the time of central neural conduction. The relationship of the changes in somatosensory evoked potentials and the brain blood flow is doubtless, but this relationship is not directly caused by changes in the cerebral blood flow.
Fifty patients occupationally exposed to organic solvents were examined using EEG, neural conduction velocity test, peripheral blood testing and psychological examination. A correlation between degree of CNS damage and time of exposure was observed. Also, subclinical changes detected using EEG and neural conduction velocity test were reported.
Nerve conduction velocities (NCVs) and multimodality evoked potentials were studies in 28 manic-depressive patients under lithium prophylaxis with serum lithium levels between 0.320 and 0.980 mEq/L. Slowing of motor and sensory NCVs and prolonged central neural conduction times obtained from somatosensory and brainstem auditory evoked potentials were found to correlate with serum lithium levels. Lithium-induced changes in cell membrane conductivity and in the synaptic transmission are considered responsible for the neurotoxic effects of lithium.
In 19 patients aged 19 to 45 years on long-term dialysis treatment during 12.6 +/- 18.2 months the concentrations of Rb and Cs were determined by atomic spectrometry in whole blood before and behind the dialyser at the beginning and end of dialysis. At the same time the concentrations of these elements were determined in the dialysing fluid. In all patients the velocity of conduction in the motor fibres in the upper and lower extremities was determined before and after dialysis. Damage to the peripheral neurons was demonstrated in the lower extremities mainly in 79% of cases. Increased velocity of motor conduction in at least one nerve related directly proportionally to the Cs concentration of the serum was demonstrated in 56-70% of the patients after one dialysis.
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Signal processing in neural networks will inevitably include delays due to the finite conduction velocity of the neurones and their interconnections. Diamond proposed a method for finding these delays in the case of (visual) steady-state responses. Alignment of response features, when represented in a time domain plot, would, allegedly, yield the delay. We show that filter action, by introducing frequency-dependent phase shifts, is bound to distort the time domain plot considerably, thereby aligning the response features in such a way that a wrong value for the delay is found. This makes that analysis method of doubtful significance.
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