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OBJECTIVE: For the clinical application of neuromagnetic recordings in neural conduction block, the patterns of magnetic fields in the region should be clarified. Using an experimental in vitro model, the spatiotemporal course of the neuromagnetic fields at the site of complete conduction block was examined. Additionally, the magnetic compound action fields (CAFs) and electric compound action potentials (CAPs) were compared and correlated. METHODS: In a chamber containing Ringer's solution, 10 isolated sciatic nerves of rabbits were electrically stimulated. Both evoked CAPs and CAFs were measured before and after the ligation of the nerve. The sequential positions of the current dipoles and the location of the conduction block were estimated by the least-squares search. RESULTS: The magnetic contour maps of the CAFs showed a characteristic quadrupolar pattern propagating along the nerve. The peak of the leading magnetic field ceased and disappeared at the position of the nerve ligation, while the trailing magnetic field became attenuated before reaching that position. The positions of the conduction blocks were localized by magnetic recordings within a difference of 2mm. CONCLUSIONS: The neuromagnetic recordings could visualize the change of the magnetic fields at the site of the complete conduction block and closely localize that position. SIGNIFICANCE: The neural conduction block was visualized and localized by neuromagnetic recordings.
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.
BACKGROUND: The aim of our work was to evaluate neural conduction in visual pathways in subjects with ocular hypertension and glaucoma. METHODS: We assessed simultaneous recordings of pattern electroretinograms (PERG) and visual evoked potentials (VEP) in 16 subjects with ocular hypertension (OHT), in 16 subjects with primary open-angle glaucoma (POAG) and in 15 age-matched controls. The visual stimuli were checkerboard patterns (the check edges subtend 15 min of visual arc; contrast 70%) reversed at the rate of 2 reversals/s. RESULTS: In OHT and POAG patients we found PERG and VEP latencies significantly longer than in controls. The P50-N95 PERG amplitudes were significantly reduced in OHT and POAG eyes. VEP amplitudes were significantly reduced in POAG eyes, while in OHT they were similar to controls. The retinocortical time (RCT; difference between VEP P100 latency and PERG P50 latency) was longer in POAG patients than in controls; no differences between patients with OHT and controls were observed. Moreover, we observed that in POAG the longer RCT was inversely related to the PERG amplitude. CONCLUSION: Our results suggest that involvement of the innermost retinal layers in POAG is accompanied by slowed neural conduction in the visual pathways.
BACKGROUND: A decreased content of n-3 fatty acids in erythrocyte membrane of type 1 diabetic patients, which is inversely related to plasma levels of HbA(1c), has been reported previously. Our aim in this study was to observe the changes after a low-dose n-3 fatty acid (330 mg/day docosahexaenoic acid and 630 mg/day eicosapentanoic acid) dietary intervention in the lipid composition of cell membrane and metabolic control (measured according to plasma HbA(1c) levels). Since changes in both parameters may alter transmembrane sodium transport or influence parameters measuring target organ damage, we also studied the neural conduction quality and activity of four sodium transporters. METHODS: Eighteen type 1 diabetic patients were randomly assigned to continue their usual diet (control group) or to supplement their diet with a daily low dose of n-3 fatty acids (supplemented group). The changes between baseline and end values of the following parameters were compared: HbA(1c), lipid and phospholipid composition of cell membrane, activity of four ion carriers and neural conduction quality. RESULTS: The dietary supplementation caused statistically significant changes in membrane lipid composition, particularly an increase of C22:6 (n-3) and the total n-3 fatty acid (respectively +0.90+/-1.14% vs. -0.44+/-1.23% and +1.36+/-1.62% vs. -0.5+/-1.80%, p<0.05). After the dietary supplementation, we also observed a significant decrease of HbA(1c) (-2.00+/-1.9% vs. -0.13+/-0.48%, p<0.05), without significant changes in the dose of insulin required, an increase in the motor conduction velocity by the median nerve (+2.12 +/-1.35 m/s vs. -0.8+/-2.34 m/s, p<0.05) and a decrease of the V(max) of the Na(+)-Li(+) countertransport (-96.6+/-111.2 vs. +58.1+/-81.3 micromol/l cell/h(-1), p<0.01). CONCLUSION: A low-dose omega-3 fatty acid dietary supplementation may change the fatty acid composition of the cell membrane and improve the metabolic control of diabetes. Using this dose, we also observed a decrease of the maximal rate of Na(+)-Li(+) countertransport and a slight improvement of neural conduction.
Pediatric lead (Pb) intoxication remains a major medical challenge in some developing countries where Pb is used in glazing industries. Pb exposure is reported to induce neurophysiological and neurocognitive impairment in children. However, the threshold and level of Pb intoxication necessary to induce neuropathology have not been established. Brainstem auditory evoked responses (BAERs) have been used widely as a sensitive biomarker for Pb-induced neurotoxicity. In this field study, BAER neural conduction time was used as a biomarker for central nervous system impairment in Andean children living in areas of high Pb contamination from Pb-glazing cottage industries. The mean Pb level in blood (PbB) for 112 Pb-exposed children was 49.25 microg/dL (SD, 270 microg/dL range, 4.4-119.1 microg/dL). Although BAERs in some children showed prolongations in neural conduction times, regression analyses revealed no significant correlation between PbB levels and BAER interpeak conduction times for 112 replicate recordings (I-III, r = 0.008, P = 0.93; II-V, r = 0.13, P = 0.16; I-V, r = 0.09, P = 0.35; and I-VI, r = 0.14, P = 0.27). A subgroup of 69 children in the study area with PbB levels in the United States Centers for Disease Control and Prevention (CDC) medical intervention-emergency classifications (CDC IV and V; mean, 67.0 microg/dL, SD, 15.8 microg/dL; range, 45.1-119.1 microg/dL) showed no significant correlation between PbB and BAER interpeak interval and no significant differences in BAER than a normal subgroup (t test, P > 0.05). The results demonstrate some evidence of abnormal possibly Pb-induced neural conduction delays in some individual children but a remarkable overall neurobiological functioning in severe, chronic pediatric Pb intoxication without measurable impairment of brainstem auditory nuclei and tracts, as evidenced by neurophysiological conduction times. The findings also demonstrate the variability in the threshold level and duration of Pb exposure necessary to induce brainstem neuropathology.
OBJECTIVES: Visual evoked potentials (VEPs) show abnormal responses in newly-diagnosed insulin-dependent diabetic (IDDM) patients. Electrophysiological methods allow one to dissect and explore different structures contributing to neural conduction in the visual pathways. The aim of our work was to assess whether the VEP abnormalities are due to impaired function of the retinal layers and/or a delayed conduction in the postretinal visual pathways. METHODS: Simultaneous recordings of VEP and pattern-electroretinogram (PERG) were performed at two intervals (at entry of the study and after 3 months) in 14 newly-diagnosed IDDM patients (age: 24.8+/-6.8 years; duration of disease: 3+/-1.5 months), and in 14 age-matched control subjects. RESULTS: In comparison with control subjects, IDDM patients showed: VEP P100 latencies significantly delayed (P < 0.01), a significant impairment of all PERG parameters (P < 0.01) and retinocortical time (RCT, difference between VEP P100 and PERG P50 latencies) and latency window (LW, difference between VEP N75 and PERG P50 latencies) also significantly increased (P < 0.01). All electrophysiological parameters were not significantly changed when retested after 3 months. No correlations were found between VEP P100 latency, RCT, LW and PERG parameters. CONCLUSIONS: Impaired PERG indicates an involvement of the innermost retinal layers; increased values of RCT and LW represent an index of delayed neural conduction in the postretinal visual pathways. Therefore two sources, one retinal (impaired PERG) and one postretinal (delayed RCT and LW), may independently contribute in to the abnormal responses of VEP observed in newly-diagnosed IDDM patients. Three months of relatively-stable metabolic control have not normalized the VEP and PERG impairment.
In this experiment, the vulnerability of long tract neural conduction in the spinal cord to progressive hypoxia was studied. The physiological integrity of nonsynaptic spinal cord conduction was monitored with the spinal evoked response (SER). Focal spinal cord blood flow was measured with the hydrogen clearance method. Progressive hypoxia was created by progressively increasing the amount of nitrogen in the inspired gas mixture. The SER was seen to fail only after extended periods of severe hypoxia. Multisynaptic cerebral condition monitored by the cerebral evoked response (CER) seemed more sensitive in the three animals in which both SER and CER were recorded. Spinal cord blood flow (SCBF) was not affected by progressive hypoxia until the PO2 was below 40 torr, and then the SCBF rose dramatically with further progression of the hypoxia.
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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The sites and magnitude of evoked potential response alterations induced by varying masses and concentrations of epidurally administered bupivacaine were assessed from electrodes positioned along the conducting pathways of the monkey. The mass of bupivacaine was the major factor in determining the level and degree of response alterations. At the lower levels of total drug mass, effects were limited to the dorsal root entry zone, whereas higher levels of mass not only increased the response attenuation at the gray matter level but resulted in additional changes in those responses recorded from the spinal cord white matter tracts. With all other factors stable, increasing concentration was associated with a greater degree of response attenuation, especially at the lower levels of total mass. These findings indicate that the mass of the drug is the major factor in determining the magnitude and level of bupivacaine-induced epidural analgesia. Increased concentration influences the local anesthetic's penetration at the dorsal root entry zone and, to a lesser degree, at the white tracts of the spinal cord.
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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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