[Studies on nerve conduction in neural muscular atrophy and Friedreich's hereditary ataxia].
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Results for “Neural Conduction”
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Conduction of neural impulses in human mechanoreceptive cutaneous afferents.
1. It was the aim of the present study to isolate and identify the components underlying the human sensory compound action potential and to study their axonal conduction velocities and refractory periods. For this purpose the technique of percutaneous microneurography was combined with intradermal electrical stimulation of nerve fibre terminals. Sixty-four median and ulnar nerve afferents innervating the glabrous skin of the digits were isolated and type identified. 2. The range of axonal conduction velocities was wide (20-60 m/s), but similar for each afferent category (20-60 m/s). Most afferents conducted slower than expected from the intrafascicularly recorded compound potential (50-60 m/s) and their conduction velocities generally decreased from the base to the tip of the digits. 3. The duration of the absolute axonal refractory periods of all types of afferents ranged from 0.7 to 3.5 ms. The duration of the total refractory periods ranged from 3 to 9 ms. Both absolute and total axonal refractory periods were inversely correlated (r = -0.70 and r = -0.67) with their axonal conduction velocities. 4. The size of individual action potentials was significantly correlated with axonal conduction velocities, although the correlation coefficient was relatively low (r = 0.43), even after correction for variability due to electrode resistance (partial correlation r = 0.44). 5. The results showed that different types of cutaneous afferents cannot be separated on the basis of their axonal conduction properties. The data demonstrate features of neural impulse conduction along the entire axonal tree and which are inaccessible to routine electrodiagnostic procedures. The present approach provides a sensitive means for assessing, in health and disease, nerve conduction in terminal axons.
Action Potentials↗
A "convertible pore" model of neural membrane conductance.
Instead of the single-channel pore proposed earlier [Wooldridge, D. E. (1984) Proc. Natl. Acad. Sci. USA 81, 5609-5612] for the transit of conductance ions through the neural membrane, a pore with a second channel for "influence ions" of calcium or magnesium is considered in this paper. By entering trapping centers at the closed inner ends of the new channels, the influence ions are postulated to alter the rates of chemical reactions that change the configurational state of the gates guarding the inner ends of the nearby conductance channels. This makes the permeability of the conductance channels strongly dependent on voltage. Using a four-state reaction scheme for both the sodium and potassium pore systems, a computer model of the membrane conductance is constructed. When suitable values are assigned to its parameters, the model closely reproduces the results of the Hodgkin-Huxley voltage-clamp and action potential experiments.
Action Potentials↗
Relation between RBE and LET to inhibit neural impulse conduction.
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Action Potentials↗
[Hypertonicity of the dialysis fluid on the neural motor conduction in patients in chronic hemodialysis. Short term study].
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Adolescent↗
Compression of rat spinal cord in vitro: effects of ethanol on recovery of axonal conduction.
The effect of ethanol on recovery of neural conduction after spinal cord compression was evaluated in an isolated rat spinal cord preparation. Controlled compression of 50 to 75 percent of the cord cross-section was delivered using a piezoelectric translator. Postcompression compound action potential (CAP) amplitude, latency, and refractory periods were measured relative to pre-compression values. Recovery of CAP's was compared for spinal cords exposed to ethanol in vitro (100 mg/dl bath concentration, started one hour prior to compression) versus those maintained in normal artificial CSF. The in vitro effects of ethanol were evaluated on spinal cords from rats maintained on a normal diet and from those repeatedly intoxicated with ethanol for 15 days prior to the acute experiment. Compression of the cord resulted in an immediate 68% decrease in CAP peak amplitude and an increase in latency (171%) and refractory period (256%). In normal bathing medium, CAP amplitude recovered to 83% of pre-compression values 180 minutes after compression. The addition of ethanol to the artificial CSF did not directly affect CAP parameters, but combined with compression, CAP amplitude recovered to only 42% of pre-compression values 180 minutes after impact (p less than .01). Recovery was less affected by acute ethanol exposure in cords from ethanol pretreated animals. CAP amplitude recovered to 83% of pre-compression levels and was not different from compression-only recovery (p less than 0.10). The data suggest that direct effects of ethanol on axonal membranes may affect the sensitivity of axons to mechanical trauma or their capacity to recover normal function. Since spinal cords from repeatedly exposed animals are less sensitive to the acute effects of ethanol, ethanol may be acting to "fluidize" the axonal membrane.
Alcoholic Intoxication↗
Brainstem auditory evoked responses in chronic renal failure and the effect of hemodialysis.
Brainstem auditory evoked responses (BAER) were recorded in patients with chronic renal failure before commencement of chronic dialysis treatment, and in patients with end-stage renal failure on chronic hemodialysis for several years. Both groups of patients had delayed latencies of the third and fifth waves. The patients on hemodialysis revealed delayed latency of interpeak I-V as well. There was no correlation between wave latency, serum urea, creatinine, PTH or duration of chronic hemodialysis treatment. A hemodialysis session led to a slight shortening of the third wave. This study suggests that neural conduction along the brainstem in patients with chronic renal failure is delayed even before hemodialysis is started. Although 1 dialysis session may have some beneficial effect, long-term hemodialysis treatment does not seem to shorten the delay in neural conduction observed in patients with chronic renal failure.
Adolescent↗
Nervous impulse propagation along peripheral and central fibres in patients with chronic renal failure.
In thirty-one patients with chronic renal failure we measured the conduction velocities in the proximal regions of median and peroneal nerves and concurrently evaluated the propagation properties of an afferent input along the related central (spinal and supraspinal) sensory pathways. In 26 of these patients the sensorimotor velocities of median, peroneal and sural nerves were also calculated. Lower limb peripheral conduction was more frequently abnormal than that of upper limb, the distal segment being involved to a greater degree. Since central propagation was more impaired during lower (11 out of 27 cases) than during upper limb (1 out of 27 patients) stimulation and the intracranial propagation time was rarely prolonged, a predominantly spinal defective impulse conduction was hypothesized. Neurophysiological data seem to confirm that early stages of defective neural conduction in CRF are in agreement with the model of central-peripheral distal axonopathy. However, an abnormal impulse propagation was also rarely found in proximal districts of peripheral fibres as well as along the intracranial sensory pathways. Correlations were found between some of the impulse propagation properties and the duration of CRF or dialysis. Serum parathyroid hormone, creatinine and BUN levels were correlated with some peripheral and central conduction indexes.
Adolescent↗
Compression induced damage on in-situ severed and intact nerves.
The effect of rapid as well as sustained compressive forces applied to the surface of intact and severed peroneal nerves of rabbits was studied. Considerable effort was taken to ensure a quantitative and consistent experimental paradigm. Stimuli were delivered to the sciatic nerve, and the compound action potential was recorded in the peroneal nerve, with compressive forces applied more proximally on the peroneal nerve. It was found that the conduction of action potentials on the larger nerve fibers was more sensitive to compressive force than that of the smaller nerve fibers, although all nerve fibers stopped conducting when sufficient compression was applied to the nerve. The effect on the conduction of action potentials on the nerve fibers appeared to be determined both by Laplace's law (as previously reported by others) and the viscoelastic properties of the entire nerve. Relatively low compressive forces (20 gm applied over approximately 7 sq mm) were found to decrease the neutral conduction of the larger nerve fibers for at least two hours, whereas stagnation of blood circulation was not found to affect measurably the neural conduction of all the nerve fibers for up to two hours.
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Scleroedema (Buschke). A case report.
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.
Adult↗
Electrophysiologic responses of human sural nerve to temperature.
The purpose of this study was to assess the conduction, specifically the latency and amplitude of the sensory nerve action potential (SNAP), of the sural nerve as a function of intraneural temperature of the leg. The electrophysiologic responses of the sural nerve were determined at different temperatures in 22 healthy adults. Distal sensory latency and amplitude of the sural SNAP was determined at 1 degree C intervals over a limb temperature range of 23 degrees to 40 degrees C. Limb temperature was monitored with a thermistor probe placed subcutaneously near the sural nerve. Ice bath soaks were used for cooling and infrared radiation for warming the limbs. An analysis of covariance was performed for the SNAP latencies and amplitudes to determine the effect of gender and leg (right or left) at each temperature level. No effect of gender or leg on neural conduction was detected in individual subjects. A regression analysis was then used on pooled data to determine the effect of temperature on sural SNAP latency and amplitude. An inverse linear change in the latency of sural SNAP was observed over the temperature ranges used. Mean latency increased 0.1 msec per 1 degree C increase in subcutaneous temperature. A direct relationship between amplitude of the SNAP and temperature was determined. Mean amplitude increased 0.3 muV per 1 degree C increase in subcutaneous temperature. The results of this study support previous reports, which state that SNAP latency is indirectly related to the intraneural temperature. Clinical electromyographers must monitor the temperature of the lower leg and foot whenever sensorineural conduction of the lower limbs is performed.
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Early detection of diabetic visceral neuropathy. An electrophysiologic study of bladder and urethral innervation.
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.
Adolescent↗
Electrophysiologic evaluation of the facial nerve in Bell's palsy. A review.
Facial nerve paralysis is the most common mononeuropathy and idiopathic facial paralysis (Bell's palsy) the most common seventh nerve disease electromyographers may be asked to evaluate. The electrophysiologic method of choice to assess the facial nerve is side-to-side evoked amplitude comparison with the affected side expressed as a percentage of the nonaffected side. This examination should be performed on days 3, 5, 7, 9, 11 and 13 after onset of paralysis. If the percentage of surviving axons falls below 10% within the first 14 days, an incomplete recovery is suggested. Electromyography may assist in prognosticating a functional return, determining neural conduction across the site of injury and following reinervation in the recovery period. The persistence or early return of an absent R1 component of the blink reflex may qualitatively suggest a satisfactory functional outcome in facial paralysis. Supramaximally exciting the facial nerve at the stylomastoid foramen and comparing the clinical response on the affected and nonaffected side, maximum stimulation test, can also predict eventual seventh nerve return. Observing a minimal twitch, utilizing the nerve excitability test or measuring the facial nerve latency have yielded poor correlations with functional return and are of limited usefulness in the prognostication of acute facial palsies. Trigeminal somatosensory evoked potentials can be employed to evaluate the status of the trigeminal nerve as approximately 50% of patients with Bell's palsy also have lesions involving the fifth nerve. Side-to-side amplitude comparison and electromyography are the two most valuable electrophysiologic methods of assessing facial nerve functioning.
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The effects of carbamazepine and sodium valproate on SEPs and BAEPs.
SEPs and BAEPs were studied in 36 previously untreated epileptics receiving either carbamazepine (CBZ) or sodium valproate (VPA) monotherapy. CBZ prolonged central conduction times in SEPs and BAEPs. SEP latency prolongation correlated with serum CBZ levels. VPA had minimal effects on evoked potentials. The present study gives evidence of similar effects of carbamazepine and phenytoin on central neural conduction.
Adult↗
Visual resolution in a patient exhibiting a visual fatigue or saturation-like effect: probable multiple sclerosis.
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.
Adult↗
Beta-adrenoceptors on duodenal mucosal cells mediate venous serotonin release.
We have previously documented predominant intraluminal release of serotonin (5-HT) following activation of muscarinic receptors on enterochromaffin cells. Gronstad et al. reported that portal venous release of 5-HT in response to vagal stimulation was mediated by beta-adrenergic receptors. The purpose of this study was to determine whether 5-HT release induced by the beta-adrenergic agonist, isoproterenol, is mediated by enteric nerves or is a direct action at the enterochromaffin cell level. We mounted rabbit duodenal mucosal sheets stripped of muscularis in modified Ussing chambers and measured release of 5-HT in response to 10(-5) M isoproterenol, in the presence and absence of the neural conduction blocker tetrotoxin, 10(-6) M. Serotonin was measured in the buffer bathing the mucosal and submucosal surfaces by HPLC. In the presence of isoproterenol, total (mucosal and submucosal) 5-HT release (21.0 +/- 4.9 ng/cm2/45 min) was significantly (P less than 0.05) greater than that in untreated controls (7.8 +/- 2.7 ng/cm2/45 min); release was predominantly toward the submucosal surface. In the presence of tetrodotoxin alone, net 5-HT release was significantly (P less than 0.05) increased to 12.8 +/- 2.8 ng/cm2/45 min. In tetrodotoxin-treated mucosa, isoproterenol increased 5-HT release to 28.6 +/- 5.3 ng/cm2/45 min which was significantly greater (P less than 0.05) than that with tetrodotoxin alone. Since 5-HT release was increased even in the presence of neural blockade, these results suggest that activation of beta-adrenergic receptors on or near enterochromaffin cells induces release of 5-HT predominantly toward the submucosal surface.
Animals↗
The role of phosphatidyl serine in neural excitation and conduction.
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Spinal mechanisms of the analgesic action of electroconvulsive shock.
The present study investigated the spinal systems involved in the analgesic action of electroconvulsive shock (ECS). To identify such systems complete spinal transections and discrete lesions within the dorsal half of the spinal cord were performed. Complete spinal transection eliminated ECS analgesia totally, demonstrating that the observed analgesic effect is attributable to neural conduction. Lesions within the region of the dorsolateral funiculus (DLF) caused a pronounced, but incomplete, attenuation of ECS analgesia. Larger lesions of the dorsal aspects of the spinal cord including both the DLF and the dorsal column area did not result in further attenuation of analgesia. Thus, it appears that within the dorsal cord the area of the DLF contains the fibers mediating the antinociceptive action of ECS. Additional experiments were conducted to determine the neuromediators involved in ECS analgesia. Of a wide range of antagonists injected intraperitoneally (methysergide, phentolamine, haloperidol, diphenhydramine, naloxone, picrotoxin, theophylline and scopolamine), only methysergide produced a significant attenuation of ECS analgesia. In contrast, following intrathecal injections of antagonists a dose-related decrease of analgesia could be seen after the injections of methysergide, phentolamine and naloxone implicating spinal serotonin, noradrenaline and the enkephalins in the analgesic action of ECS. To assess further the interaction between the action of these neurotransmitter systems, we evaluated the effect of drug pair combinations on ECS analgesia. Intrathecal phentolamine + naloxone, methysergide + naloxone and methysergide + phentolamine were injected at doses that caused maximal attenuation of analgesia.(ABSTRACT TRUNCATED AT 250 WORDS)
Analgesia↗