Biomedical subjects

B M Seemungal

Publications and source records attributed to B M Seemungal.

4 recordsLinked to original sources

PubMed2004

Perceptual and nystagmic thresholds of vestibular function in yaw.

A technique for simultaneous measurement of conscious (perceptual) and reflex (nystagmus) thresholds of vestibular function is described. We used an automated modified binary search algorithm with simultaneous infrared oculography in determining perceptual and VOR nystagmic thresholds respectively, during discrete whole body rotations in the dark. In a young group of 14 normal subjects (mean age 23 years) angular acceleration thresholds were significantly higher for perceptual detection (1.18 deg/s/s) than for nystagmus generation (0.51 deg/s/s). Only nystagmic thresholds were slightly raised (0.87 deg/s/s) in an older group of 9 normal subjects (mean age 63 years). The finding that nystagmic thresholds are lower than perceptual ones indicates a higher sensitivity of brainstem than cortical vestibular mechanisms. This technique would be of particular value in clinical situations where a dissociation between reflex and conscious vestibular mechanisms is expected, e.g. in patients with cortical lesions or in elderly patients with falls.

Adult↗

PubMed2001

The endocrine system, vertigo and balance.

Steroid, amine and peptide hormones affect the peripheral vestibular system. Vasopressin hypersensitivity of the endolymphatic sac may be implicated in the pathogenesis of Meniere's disease. Specific vasopressin antagonists will help define the role of vasopressin in Meniere's disease. The modulation of central vestibular pathways by neuroactive steroids may involve effects on gamma-aminobutyric acid-ergic and glutaminergic pathways. The vestibular nuclei also express enzymes that are important in the synthesis of steroids and the modulation of their activity. Steroids mediate both facilitatory and deleterious effects of stress on vestibular compensation. The quality and quantity of stressor that determines the pattern of hormonal output, may be important. Clinical observation suggests that episodic ataxia type 2, a P/Q calcium channelopathy, may be phenotypically modulated by endocrine fluctuations. Steroid hormones may affect the episodic ataxia type 2 phenotype by modulation of voltage-gated calcium channel activity via second messenger systems and ion channel subunit expression. Despite evidence to support the link, the role of the endocrine system in vestibular function and disease is as yet virtually unexplored.

Animals↗

PubMed1996

A hot ankle.

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Adult↗

PubMed1990

Antagonism of the effects of 5-hydroxytryptamine on the rabbit isolated vagus nerve by BRL 43694 and metoclopramide.

Depolarization and reduction in the C fibre compound action potential (C spike) in response to 5-HT were recorded simultaneously from rabbit isolated vagus nerve. 5-HT (0.1-100 mumol/l) was applied cumulatively and EC50 and IC50 values measured from individual concentration-response curves. Blockade of 5-HT responses by the 3-indazole carboxamide, BRL 43694, was investigated and compared with the blocking action of metoclopramide. BRL 43694 was a selective antagonist of 5-HT responses. A concentration of 10 nmol/l BRL 43694, which nearly abolished the depolarization and reduction of the C spike evoked by 5-HT (100 mumol/l), had no effect on similar responses evoked by DMPP (100 mumol/l) or GABA (100 mumol/l). Blockade of 5-HT responses by BRL 43694 (0.3 nmol/l) was slow in onset, a plateau blockade occurring after equilibrium of tissue with antagonist for 2 to 3 h. Metoclopramide induced a blockade of rapid onset. The maximal blockade was apparent within 30 min of application. Full recovery in the responsiveness of the tissue to 5-HT was observed within 30 min of washing out metoclopramide. BRL 43694 at concentrations of 0.3, 1, 3 and 10 nmol/l caused a progressive rightward shift of the concentration-response curves to 5-HT. At the highest concentration of antagonist, there was some depression of the maximal 5-HT response. The apparent pA2 estimated from the Schild equation was 10.03 +/- 0.09 (mean +/- SEM, n = 20) against 5-HT depolarization and 10.31 +/- 0.1 against C spike reduction. Schild plots had slopes not significantly different from 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗