Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042571 (vertigo)
 7,148 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although glucocorticoids are sometimes used for the treatment of vertigo in certain disorders such as Meniere's disease, the mechanism underlying anti-vertigo effect remains unknown. The present study was performed to examine the effects of a glucocorticoid, dexamethasone, on neuronal activity in the medial vestibular nucleus (MVN) to determine whether or not the drug acts directly on the MVN neuron using alpha-chloralose-anesthetized cats which were fixed in a stereotaxic instrument placed on a turn-table. Single neuronal activities in the MVN were extracellularly recorded with a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. Each pipette was filled with dexamethasone phosphate (0.1 M), monosodium glutamate (1 M), glutamic acid diethylester (GDEE) (0.05 M: a non-selective glutamate receptor antagonist), CoCl2, (0.1 M: a non-specific calcium channel blocker), RU38486 (0.01 M: glucocorticoid receptor antagonist) or potassium canrenoate (0.1 M: a mineralo-cortical receptor antagonist). These chemicals were microiontophoretically applied to the immediate vicinity of the target neuron being recorded. The effects of the drugs were examined on type I neurons which were identified according to responses to rotation: the neuron showed an increase and a decrease in firing with ipsilateral and contralateral rotation to the recording site, respectively. Microiontophoretically applied dexamethasone (50-200 nA) dose-dependently increased spontaneous firing of MVN neurons. However iontophoretic application of GDEE did not affect the dexamethasone-induced increase in firing of the MVN neurons but inhibited glutamate- and rotation-induced firing. Microiontophoretically applied Co2+ did not affect dexamethasone-, glutamate- and rotation-induced firing. However, dexamethasone-induced firing was dose-dependently suppressed by iontophoretic RU38486, but not by canrenoate. Then a microdialysis study using alpha-chloralose-anesthetized cats was performed to determine whether or not dexamethasone affects the release of glutamate from vestibular nerve terminals. The microdialysis probe (CMA/10, 2 mm) was inserted into the MVN and perfused with Ringer solution at 2 ml/min. Samples were collected at 10-min intervals. Endogenous glutamate was measured using the HPLC-ECD method. When repetitive stimuli (200 microseconds duration, 0.5 mA and 5 Hz) were given to the vestibular nerve for 10 min, an increase in the release of glutamate was observed. Dexamethasone did not produce spontaneous or stimulation-induced release of glutamate. These results suggest that dexamethasone acts directly on the MVN neuron to excite neuronal activity through glucocorticoid receptors on neuron membranes, but the excitation is not due to the release of glutamate.
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PMID:[Excitatory effects of glucocorticoids on neuronal activity in the medial vestibular nucleus--mediation by glucocorticoid receptor on the membrane]. 791 23

In any grade of distortion of the cervical spine as a result of acceleration forces in addition to cervical symptoms cerebral symptoms like headache, vertigo, auditory disturbances, tinnitus, disturbances in concentration and memory, difficulties in swallowing, impaired vision and temporo-mandibular dysfunctions may appear. These symptoms can persist and become invalidating. Cerebral single-photon emission tomography (SPECT) and positron emission tomography (PET) enable new diagnostic horizons for neurotraumatology. In this article we summarize the actual findings of these nuclear medical methods in neuropsychologically deficient patients with distortion of the cervical spine as a result of acceleration forces. Especially the latest results of the group of Basle (University Hospital Basle, Clinic of Rehabilitation Rheinfelden, Switzerland) are illustrated. This group found parieto-occipital hypoperfusion by relative quantitation using SPECT and bicisate (Neurolite, ECD). A first pilot study using PET and F-18-fluoro-deoxyglucose (FDG) could verify the above observation. The group's working hypothesis is that parieto-occipital hypoperfusion may be caused by activation of nociceptive afferences from the upper cervical spine. A critical approach to interpreting new functional methods and, on the other hand, openness in new scientific findings may contribute to answering the lasting controversial medico-legal discussion with more objectivity.
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PMID:[Cerebral findings following cervical spine distortion caused by acceleration mechanism (whiplash injury). Assessment of current diagnostic methods in nuclear medicine]. 892 81

Epileptic nystagmus (EN) describes repetitive eye movements that result from seizure activity. We describe a patient with EN and vertigo first noted at the age of 4 yr and 10 mo. Brain MRI did not show anomalies. Ictal EEG recordings revealed epileptic activity during three episodes of horizontal, left-beating nystagmus not crossing the midline. Ictal 99mTc-ECD SPECT demonstrated the presence of active foci in multiple cerebral regions including bilateral prefrontal, bilateral parieto-temporo-occipital and the left parieto-insular-vestibular areas. A wide area of hypoperfusion was also evident in the right hemisphere, prevailing in the parieto-occipital regions and the medial prefrontal gyrus. Topiramate was started at a dose of 2 mg/kg/d with complete seizure control after 14 d. EEG and SPECT were repeated after a seizure-free period of 1 mo; disappearance of epileptic activity and modification of cerebral perfusion were evident. This case reaffirms the cortical origin and involvement of temporo-occipital and frontal cortex in the genesis of saccadic epileptic nystagmus. Rapid complete control of clinical events coincided with the normalization of EEG and improvement of the SPECT pattern.
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PMID:Epileptic nystagmus: description of a pediatric case with EEG correlation and SPECT findings. 2083 24