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Results for “Vestibular Neuronitis”

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At least 253 records · Page 14Linked to original sources
PubMed1995

Ultrastructural changes in superior vestibular commissural neurons following vestibular neurectomy in the cat.

The ultrastructural changes of the feline superior vestibular commissural neurons (CNs) were quantitatively assessed 8 weeks following ipsilateral vestibular neurectomy. Results indicated a slight degeneration of synaptic profiles (SPs; 25%) representing the primary vestibular afferent input onto CN soma. The synaptic vesicles of the remaining SPs, which likely originate from the cerebellum and the contralateral CNs, were smaller and rounder, suggesting a transition from an inhibitory to an excitatory mode of response. The SP loss had little impact on the CNs' capacity for protein synthesis and structural maintenance, since there was no change in the volume fraction of intracellular organelles. These data suggest that CNs do not degenerate and are likely functional after vestibular compensation. These findings support the role of the commissural pathway in vestibular compensation as proposed by Galiana et al, which is based on the assumption that the intervestibular commissural connections remain intact following vestibular neurectomy.

Animals↗
PubMed1989

Muscarinic regulation of spontaneously active medial vestibular neurons in vitro.

We examined the effects of cholinergic agonists and antagonists on spontaneously occurring action potentials extracellularly recorded from medial vestibular nucleus (MVN) neurons in rat brainstem slice preparation to elucidate the cholinergic mechanism involved in excitation. Addition of carbachol (10(-6)-10(-5) M) and muscarine (10(-6)-10(-5) M) into the bath dose-dependently increased the spontaneous firing rate, while nicotine (10(-5)-10(-4) M) had no effects. Acetylcholine (10(-6)-10(-5) M) in the presence of physostigmine (10(-7) M) also increased the firing rate in a dose-dependent manner. Conversely, atropine (10(-8)-3 x 10(-7) M) slightly decreased the firing and dose-dependently inhibited the carbachol-induced increase in the firing rate. These results suggest that the firing rate of spontaneously active MVN neurons are regulated by acetylcholine via muscarinic receptors.

Acetylcholine↗
PubMed2004

A prospective study on the course of anxiety after vestibular neuronitis.

OBJECTIVE: Critical life events trigger intense emotions. Anxiety is one of the most frequent of these emotions. It is unclear which factors determine the intensity and course of anxiety after a critical life event. METHOD: Anxiety levels of 92 patients in the 6 weeks after experiencing an acute vestibular disorder were examined. The influence of cognitive, personality and illness variables on the course of their anxiety was analyzed. RESULTS: Acute vestibular disorder is accompanied by intensive anxiety. In most patients, anxiety decreased as vertigo regressed. Catastrophizing and dysfunctional cognitions and different personality styles predicted 17.6% of the anxiety 6 weeks after the functional loss of vestibular equilibrium. CONCLUSIONS: Acute vestibular disorder is a critical life event. Most individuals cope successfully with acute vestibular disorder. However, dysfunctional cognitions are risk factors for the persistence of anxiety.

Acute Disease↗
PubMed1988

Morphology of physiologically identified second-order vestibular neurons in cat, with intracellularly injected HRP.

The morphology of horizontal canal second-order type I neurons was investigated by intracellular staining with horseradish peroxidase (HRP) and three-dimensional reconstruction of the cell bodies and axons. Axons penetrated in and around the abducens nucleus were identified as originating from type I neurons by their characteristic firing pattern to horizontal rotation and by their monosynaptic response to stimulation of the ipsilateral vestibular nerve. A total of 47 type I neurons were stained. The cell bodies were located in the rostral portion of the medial vestibular nucleus (MVN) and were large or medium sized and had rather elongated shapes and rich dendritic arborizations. The neurons were divided into two groups: those which projected to the contralateral side of the brain stem (type Ic neurons) and those which projected to the ipsilateral side of the brainstem (type Ii neurons). All stem axons of type Ic neurons crossed the midline and bifurcated into rostral and caudal branches in the contralateral medial longitudinal fasciculus (MLF). Two or three collaterals arising close to this bifurcation distributed terminals in a relatively wide area in the contralateral abducens nucleus. Some of these collaterals projected further to the contralateral MVN and thus are vestibular commissural axons. Some of the rostral and caudal stem axons had collaterals which projected to the contralateral nucleus prepositus hypoglossi (PH), nucleus raphe pontis, or medullary reticular formation. There were at least six classes of type Ii neurons, most of which distributed to a relatively limited region in the ipsilateral abducens nucleus and they were categorized according to their future projections into the following categories: A) no further collaterals beyond the abducens nucleus; B) collaterals in the abducens nucleus and a branch descending and terminating in ipsilateral PH; C) projected to the abducens nucleus, PH, and an area rostral to the abducens nucleus; D) projected to the abducens nucleus and to ipsilateral reticular formation rostral and caudal to the abducens nucleus; E) collaterals in the abducens nucleus and a thick caudal stem axon entering and descending in ipsilateral MLF; F) a thick caudal stem axon entering and descending in ipsilateral MLF and no collaterals to the abducens nucleus. Some type Ii neurons also had recurrent collaterals which projected back to the ipsilateral MVN; these may inhibit type II neurons during ipsilateral rotation.

Action Potentials↗