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At least 163 records · Page 9Linked to original sources
PubMed2000

A new color vep procedure discloses asymptomatic visual impairments in optic neuritis and glaucoma suspects.

OBJECTIVE: To evaluate the reliability of visual evoked potentials obtained with a set of multiple chromatic and achromatic patterns (C-VEPs) in differentiating asymptomatic perifoveal retinal impairment from central conduction impairment. METHODS: We propose a set of colored pattern stimuli that allows relatively differential activation of the magnocellular and parvocellular pathways. The system runs on a standard Pentium PC with peripherals that present stimuli and collect, analyze and print data. P1 latencies of C-VEPs obtained with achromatic (black/white) and chromatic (blue/black and red/black isocontrast) checkerboards were evaluated in normal subjects and patients with subclinical retinal impairment (glaucoma suspects) or mild neural conduction impairment (optic neuritis), none of whom had subjective visual defects. RESULTS: The procedure evoked robust cortical signals and statistically distinguished the 3 groups of subjects. The achromatic and chromatic stimuli used distinguished controls from glaucoma suspects and patients with optic neuritis. Glaucoma suspects had greater impairment of C-VEPs to blue/black checkerboards whereas patients with optic neuritis had greater impairment of responses to red/black stimuli. CONCLUSIONS: Our data suggest that chromatic patterns (color/ black, red and blue), that may activate the parvocellular and magnocellular systems differentially but not selectively, can distinguish between mild perifoveal or foveal conduction impairment. They have the additional advantage of evoking large, stable responses across all the subjects.

Adult↗
PubMed2005

Are somatosensory saccades voluntary or reflexive?

The present study examines whether the distinction between voluntary (endogenous) and reflexive (stimulus-elicited) saccades made in the visual modality can be applied to the somatosensory modality. The behavioural characteristics of putative reflexive pro-saccades and voluntary anti-saccades made to visual and somatosensory stimuli were examined. Both visual and somatosensory pro-saccades had much shorter latency than voluntary anti-saccades made in the direction opposite to a peripheral stimulus. Furthermore, erroneous pro-saccades were made towards both visual and somatosensory stimuli on approximately 11-13% of anti-saccade trials. The observed difference in pro- and anti-saccade latency and the presence of pro-saccade errors in the anti-saccade task indicates that a somatosensory stimulus can elicit a form of reflexive saccade comparable to pro-saccades made in the visual modality. It is proposed that a peripheral somatosensory stimulus can elicit a form of reflexive saccade and that somatosensory saccades do not depend exclusively on higher level endogenous control processes for their generation. However, a comparison of the underlying latency distributions and of peak-velocity profiles of saccades made to visual and somatosensory stimuli showed that this distinction may be less clearly defined for the somatosensory modality and that modality-specific differences (such as differences in neural conduction rates) in the underlying oculomotor structures involved in saccade target selection also need to be considered. It is further suggested that a broader conceptualisation of saccades and saccade programming beyond the simple voluntary and reflexive dichotomy, that takes into account the control processes involved in saccade generation for both modalities, may be required.

Adult↗
PubMed1979

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↗
PubMed1988

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↗
PubMed2002

[The influence of haemodialysis on hearing organ of children with chronic renal failure].

Haemodialysis applied in terminal phase of chronic renal failure causes considerable metabolic and electrolyte disturbances within a few hours in human organism. The aim of the work was an evaluation of the influence of those disturbances on hearing organ as potential factors being responsible for perceptive hearing loss in considerable number of the patients with chronic renal failure (CRF). Examination was conducted on 20 children with CRF, aged 10-18 years. In each case, before and after dialysis, on the same day, ENT examination, pure tone audiometry, brain auditory evoked potentials (BAEP) and acoustic otoemissions (TEOAE, DPOAE) were performed. Audiometric tests revealed significantly worse hearing in children with CRF in comparison to healthy subjects with not statistically significant improvement after dialysis. Significantly elongated I, III, V peak latencies as well as I-III and I-V interpeak latencies in BAEP of children with CRF before dialysis were considerable shorter after dialysis except III-V but in 2 of them they appeared after dialysis. In 8 CRF cases DPOAE was present after dialysis in the range of frequencies absent before and in 9 CRF cases there was an increase of the response on the level of 10-15 dB for some frequencies. There were no any changes after dialysis in 3 cases with CRF. The results of our studies reflect subclinical disturbances in neural conduction of auditory pathway and its significant improvement after normalisation of blood parameters (uremic toxins, hyperkalaemia). This fact suggests central component of ureic axonopathy in the pathogenesis of hearing impairment in children with CRF. Dynamism of the changes in TEOAE and DPOAE reflects also the influence of those disturbances on auditory cells on the level of the labyrinth.

Adolescent↗
PubMed1985

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↗
PubMed1977

Auditory evoked brain stem potentials in a case of "locked-in" syndrome.

Auditory evoked brain stem potentials were measured in a patient with occlusion of the basilar artery about 7 mm above its origin, resulting in the "locked-in" syndrome due to infarction at the junction of the lower one third and upper two thirds of the pons. The first three waves of the evoked response originating from the acoustic nerve and auditory nuclei in the caudal pons were normal in wave form, peak latency, and voltage level. Waves IV and V, generated in the region of the lateral lemniscus and inferior colliculus in rostral pons and caudal midbrain, demonstrated prolonged peak latency and reduced voltage, indicative of slowed neural conduction in the pons above the level of the superior olivary complex. These findings suggest that auditory evoked potential recordings may have considerable value in the localization of brain stem disorders.

Acoustic Stimulation↗
PubMed1978

Internuclear ophthalmoplegia. II. Pursuit, optokinetic nystagmus, and vestibulo-ocular reflex.

Smooth pursuit, optokinetic nystagmus (OKN) and the vestibulo-ocular reflex (VOR) were studied in four patients with internuclear ophthalmoplegia (two with bilateral and two with unilateral lesions). Horizontal smooth pursuit by an adducting eye on the side of a medial longitudinal fasciculus (MLF) lesion was normal in three of four patients; vertical pursuit was abnormal in all four. The horizontal VOR gain of slow components made by an adducting eye on the side of an MLF lesion was normal in all four patients. The vertical VOR gain was decreased in the two patients tested. It is concluded that either there are pathways independent of the MLF for horizontal pursuit and vestibular signals that are not available to vertical signals, or vertical pursuit and vestibular eye movements require a higher rate of oculomotor neuron firing than equal-velocity horizontal eye movements.

Adult↗
PubMed1979

Dominant optic atrophy. The clinical profile.

We examined 24 individuals in four family pedigrees with dominantly inherited optic atrophy (DOA); 12 patients met the criteria for diagnosis of DOA and two were suspect. Our data indicate that (1) insidious onset usually occurred in childhood, but subjective visual symptoms may evolve in adulthood; (2) visual function was minimally (20/25) to moderately (20/400) abnormal, could be strikingly asymmetric in an individual (eg, 20/30 in the right eye and 20/200 in the left eye), and showed considerable intrafamilial and interfamilial variation; (3) visual field defects consisted of central and centrocecal scotomas, but no peripheral isopter abnormalities were found; (4) color-vision screening with Hardy-Rand-Rittler plates revealed dyschromotopsias, but only Farnsworth-Munsell 100-hue examination disclosed the typical tritan defects; (5) pattern-reversal visual-evoked responses were characterized by diminished amplitudes and prolonged latencies, consistent with neural conduction defects; (6) disc pallor was limited to the temporal segment in all cases, and 16 of 24 eyes showed focal temporal excavation, which is probably pathognomonic of DOA.

Adolescent↗
PubMed1976

Central vestibular compensation. Effect of the bilateral labyrinthectomy on neural activity in the medial vestibular nucleus.

An attempt was made to reconstruct the central events that occurred in the various stages of vestibular compensation after a bilateral labyrinthectomy in the cat. Bilateral labyrinthectomized cats showed no nystagmus, but had unsteady head movements and wide gaits. Neural activity in both sides of the medial vestibular nuclei (MVN) was depressed during the critical stage of compensation; however, the neural activity was full and normal during the acute and compensated stage. The experimental results suggest that removing crossed inhibitory influence and reducing the cerebellar inhibitory influence by bilateral labyrinthectomy enhances the process of recovering neural activity in the vestibular nuclei during central compensation, and that the contralateral vestibular end organ is not a source of the driving force responsible for regeneration of electrical activity in the deafferented MVN after a unilateral labyrinthectomy.

Animals↗
PubMed1997

Functional connectivity of the transected brachial plexus after intercostal neurotization in monkeys.

Microsurgical reconstructions of brachial plexuses were performed on twelve monkeys by using ipsilateral intercostal nerves (T3-9). Reinnervation in individual nerves was evaluated monthly by observations of neuromuscular and electromyographic improvements. The electromyographic studies revealed reappearance of motor unit potentials. According to a motor scale ranging from 0 to 4, the mean muscle power 6 months after operation improved to 2.75 in the deltoid muscles, 2 in the biceps muscles, 1.22 in the triceps muscles, 1.13 in the flexor carpi radialis muscles, and 1.6 in the intrinsic muscles of the hands. Retrograde transport of horseradish peroxidase (HRP) from the neuromuscular junctions of the reconstructed musculocutaneous nerves 6 months after complete brachial plexus lesion in four animals demonstrated HRP-labeled neurons in the anterior horns, spinal ganglia and sympathetic ganglia of the thoracic spinal cords. It suggested that the regenerated afferent and efferent circuits in the thoracic cords innervating the transected brachial plexuses were able to generate the movements in the paralyzed upper limbs. However, as evidenced by the behavior patterns and the fact that retrograde-labeled neurons were all found in the thoracic cords, the novel movements observed in the reconstructed brachial plexuses were in synchrony with respiration. These results suggested that the plasticity of central neural networks is limited between two widely separated areas, such as between the midcervical and midthoracic motor cortical areas in the present studies, and therefore, the efforts to reconstruct neural networks, both centrally and peripherally, should aim at rebuilding situations as nearly to the original status as possible.

Animals↗
PubMed1995

Subclinical neurotoxicity of mercury vapor revealed by a multimodality evoked potential study of chloralkali workers.

Pattern visual, brainstem auditory, and somatosensory evoked potential (EP) studies were performed on 26 chloralkali workers. The intensity of mercury vapor exposure in these workers was estimated from the individual working history. Mercury levels in blood, urine, and hair were determined with atomic absorption spectrometry. The EP findings were compared with those from individually matched normal subjects. In brainstem auditory and somatosensory EP studies, prolonged neural conduction times in the central nervous system (CNS) were found in workers exposed to mercury vapor. In the pattern visual EP study, mercury workers had higher interpeak amplitudes. Findings of this study suggested that chronic exposure to mercury vapor would affect the CNS functions. A multimodality EP study is a useful adjunct in evaluation of chronic mercury neurotoxicity, especially in an epidemiological study.

Adult↗
PubMed1986

Phenytoin: mechanisms of its anticonvulsant action.

Phenytoin is a major anticonvulsant drug that is very effective in controlling a wide variety of seizure disorders while impairing neurological function little, if at all. Early work suggested the hypothesis that the drug's effects were due to a selective block of high-frequency neuronal activity. This theory is reevaluated in the light of accumulated observations on the effects of phenytoin in many neuronal and synaptic preparations. Most of these observations can be explained by a use- and frequency-dependent suppression of the sodium action potential by phenytoin, with a consequent filtering out of sustained high-frequency neuronal discharges and synaptic activity. The molecular mechanism for this is a voltage-dependent blockade of membrane sodium channels responsible for the action potential. Through this action, phenytoin obstructs the positive feedback that underlies the development of maximal seizure activity, while normal brain activity, proceeding at lower neuronal firing rates, is spared its depressant action. Other mechanisms of action that may contribute to the drug's efficacy and selectivity are also discussed.

Action Potentials↗
PubMed1995

Blockade of sensory neuron action potentials by a static magnetic field in the 10 mT range.

To characterize the inhibitory effect of a static magnetic field, action potentials (AP) were elicited by intracellular application of 1 ms depolarizing current pulses of constant amplitude to the somata of adult mouse dorsal root ganglion neurons in monolayer dissociated cell culture. During the control period, < 5% of stimuli failed to elicit AP. During exposure to an approximately 11 mT static magnetic field at the cell position produced by an array of four permanent center-charged neodymium magnets of alternating polarity (MAG-4A), 66% of stimuli failed to elicit AP. The number of failures was maximal after about 200-250 s in the field and returned gradually to baseline over 400-600 s. A direct or indirect effect on the conformation of AP generating sodium channels could account for these results because 1) failure was preceded often by reduction of maximal rate of rise, an indirect measure of sodium current; 2) recovery was significantly prolonged in more than one-half of neurons that were not stimulated during exposure to the MAG-4A field; and 3) resting membrane potential, input resistance, and chronaxie were unaffected by the field. The effect was diminished or prevented by moving the MAG-4A array along the X or Z axis away from the neuron under study and by increasing the distance between magnets in the XY plane. Reduction of AP firing during exposure to the approximately 0.1 mT field produced by a MAG-4A array of micromagnets was about the same as that produced by a MAG-4A array of the large magnets above. The approximately 28 mT field produced at cell position by two magnets of alternating polarity and the approximately 88 mT field produced by a single magnet had no significant effect on AP firing. These findings suggest that field strength alone cannot account for AP blockade.

Action Potentials↗
PubMed2002

Neurons labeled from locomotor-related ventrolateral funiculus stimulus sites in the neonatal rat spinal cord.

Spinal cord/brainstem preparations from 5- to 8-day-old rats, maintained in vitro, were used to determine the cells of origin and regions of termination of fibers in the superficial ventrolateral funiculus (VLF) at a site from which rhythmic locomotor-like activity can be induced. Rhythmic locomotor-like activity was recorded from lumbar ventral roots after short trains of stimuli (50 Hz for 0.5-2 seconds) delivered to the VLF. Field potential mapping revealed that single VLF stimuli elicited responses in the ipsilateral ventrolateral medulla. Tract-tracing experiments by using biocytin, pressure-injected into the VLF, showed that only a small number of brainstem neurons were labeled and these were scattered bilaterally in the ventrolateral and lateral medulla. Dense concentrations of nerve terminals were found in the lateral reticular nucleus ipsilateral to the stimulation site. Labeled spinal cord neurons included a primary population of large cells distributed bilaterally in lamina VII from T13 to L4, with peak numbers in L2 ipsilaterally and in L3 contralaterally. Intracellular recordings revealed that some L2 and L3 neurons with rhythmic responses to VLF stimulation could be activated antidromically from the VLF, with latencies of less than 1.0 msec. These observations led us to speculate that the superficial VLF carries a locomotor-related tract originating bilaterally in lumbar lamina VII and terminating in the ipsilateral medulla, including the lateral reticular nucleus. This pathway may be part of the spinoreticular or spinoreticulotectal pathway that has been described in many species, the function of which has only loosely been ascribed.

Animals↗
PubMed2002

Modulation of responses of feline ventral spinocerebellar tract neurons by monoamines.

Ventral spinocerebellar tract neurons located in laminae V-VII of cat lumbar spinal cord were tested for the effects of ionophoretically applied monoamines and receptor selective agonists. Extracellularly recorded responses, monosynaptically evoked by group I afferents in a muscle nerve, were compared before, during, and after ionophoresis. They were analyzed with respect to changes in the number of evoked spikes and in the latency. Both serotonin (5-HT) and noradrenaline (NA) were found to facilitate responses of all neurons tested. Ionophoresis of three serotonin subtype receptor agonists (5-carboxamidotryptamine maleate, 5 methoxytryptamine HCl, and alpha-methyl 5-hydroxytryptamine) and of two NA receptor agonists (phenylephrine and isoproterenol) likewise had a facilitatory effect. However, three other 5-HT receptor agonists (8-hydroxy-dipropylaminotetraline hydrobromide), 2-methyl 5-hydroxytryptamine, and 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl and two NA receptor agonists (tizanidine and clonidine) had the opposite effect because they depressed responses of the tested neurons. These results show that information forwarded by means of the ventral spinocerebellar tract may be modulated by monoamines and that several receptor subtypes, located pre- or postsynaptically, may be involved. The results also demonstrate that transmission by means of group I muscle afferents may not only be facilitated by monoamines but also depressed by selective receptor subtype activation.

Action Potentials↗