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)

Antihistaminergic drugs are currently used for the symptomatic treatment of vestibular-related syndromes such as vertigo and motion sickness. We therefore investigated whether histamine could modulate the firing of medial vestibular nuclei neurons (MVNn). Recently, we have demonstrated that different cell types are present among MVNn in guinea-pig brainstem slices. Bath-application of histamine at 10(-4) or 10(-5) M induced a small membrane depolarization accompanied by a slight decrease in membrane resistance and a reversible increase in spontaneous firing in all MVN cell types. These effects were presumably postsynaptic as they persisted in a low-calcium/high-magnesium solution. Using a variety of agonists and antagonists of histamine receptors (H1, H2 and H3), we conclude that these effects are mediated by H2 receptors. The companion paper is concerned with an in vivo study of the histaminergic modulation of the vestibular function (Yabe et al., in press).
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PMID:Medial vestibular nucleus in the guinea-pig: histaminergic receptors. I. An in vitro study. 838 29

Due to the age-associated increase in morbidity, many elderly subjects are in need of multiple drug treatment. Multimedications, however, carry a high risk for adverse drug reactions (ADR) and drug-drug interactions (DDI). This risk is especially increased in very old patients since age and morbidity lead to significant changes in body composition and organ functions. Nonetheless, representative and specific information on cumulative risks for adverse effects of multimedications in the aged is not yet available. We used data of the ongoing, population-based Berlin Aging Study (N = 516; age range 70-103 years) to evaluate the cumulative potential for ADR and DDI in a subgroup of participants taking five or more drugs (N = 221; 44.4% of the parent population [estimated]; mean age 85.2 +/- 8.3 years). Computerized algorithms were used to screen all medications for potential ADR and DDI based on standardized information which was derived from the German Physician's Desk Reference and a frequently used textbook on ADR and DDI. As expected, the analyses revealed a significant potential for adverse effects of multimedications. Cumulative totals of 12,221 different potential ADR (54.9 per subject) and 1016 different potential DDI (4.6 per subject) were identified. With regard to ADR, the most prevalent ADR-risks were for gastrointestinal upset (99%), headache (96%), postural hypotension (95%), and vertigo (94%). With respect to these risks, the minimum mean number of potentially offending drugs was 2.3, the maximum was 4.5 per subject. Additionally, 89% were at risk for drowsiness, 87% for blurred vision and 67% for confusion. Altogether, diuretics, digitalis and calcium antagonists accounted for 46% of ADR-risks. With regard to DDI, 85% had at least one drug-combination potentially leading to enhanced drug action, 52% had at least one combination potentially leading to reduced action. Most frequently involved in potential DDI were calcium antagonists (20%), digoxin (18%), and thiazides (17%). Most prevalent specific risks due to DDI were postural hypotension (48%), glycoside intoxication (26%), toxic CNS-effects (22%) and hypokalemia (19%). In conclusion, risks for ADR and DDI should be considered carefully and regularly monitored in elderly patients on multimedications. Stopping unnecessary medications, especially with regard to diuretics, digitalis and calcium antagonists, will lead to a marked reduction of the cumulative risks associated with multimedications in old age.
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PMID:[Potential side-effects and interactions in multiple medication in elderly patients: methodology and results of the Berlin Study of Aging]. 858 61

The approach to drug treatment of vertigo is almost exclusively symptomatic. There are 3 major goals for drug treatment of vertigo. The first one is to eliminate the hallucination of motion. Drugs with vestibular 'suppressant' properties are used for this purpose. The major vestibular suppressants are anticholinergic and antihistamine drugs. The second goal is to reduce the accompanying neurovegetative and psychoaffective signs (nausea, vomiting, anxiety). Antidopaminergics are used for this purpose. The third goal is to enhance the process of 'vestibular compensation' to allow the brain to find a new sensory equilibrium in spite of the vestibular lesion. Until now, the pharmacological manipulation of vestibular compensation has been assessed in animals but not in humans with vestibular lesions. Vestibular suppressant drugs delay rather than enhance compensation. A variety of other drugs is also used in the treatment of vertigo, including benzodiazepines, histaminergic agents, sympathomimetics and calcium antagonists. Their mechanism of action is poorly understood. The data base derived from clinical trials evaluating antivertigo medications is often questionable because of methodological limitations. This explains why habits of prescription are mainly empirical, and why striking differences can be noticed from one country to another. We can hope that new treatments may emerge from the present interest in receptor subclasses and neuromodulators of the vestibular system, and we must be ready to evaluate these potential new pharmacological agents with reliable clinical methods in humans.
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PMID:Antivertigo medications and drug-induced vertigo. A pharmacological review. 858 26

Levosimendan belongs to a new group of heart failure drugs, the calcium sensitizers. Because these compounds are not yet available for clinical use, the adverse drug events (ADEs) during levosimendan treatment cannot be predicted in detail. To evaluate the tolerability of levosimendan in human subjects, ADEs, safety laboratory values before and after treatment, and ambulatory ECG findings have been collected from several phase I and phase II clinical studies. By June 1994, approximately 200 subjects had received levosimendan. The most common ADE seen in healthy volunteers is headache, reported by some 40% of subjects in oral dosing but only 10% in i.v. dosing. The incidence of headache does not correlate well with the total daily dose of the drug. However, the controlled release formulations tested appear to cause vasodilatory symptoms more frequently than i.v. or rapid release oral formulations. The other typical vasodilatory ADEs seen in healthy volunteers are nausea, palpitation, and dizziness. Symptomatic hypotension is rarely encountered. It appears that heart failure patients tolerate the vasodilatory actions of the drug better than healthy volunteers. Only individual cases of headache, vertigo, and flushing have been reported, and injection site irritation has been the most commonly reported ADE (with an incidence <5%). However, because the longest administration of the i.v. infusion has been only 24 h, the duration of exposure to the drug is too short to allow any definitive conclusions to be drawn. All patients who have received levosimendan have been monitored with an ambulatory ECG. Even though some increase in heart rate is seen with high doses of the drug, there are thus far no signs of an increased incidence of ventricular tachyarrhythmias, nor have there been any noteworthy changes in the clinical laboratory safety tests. The experience with levosimendan is limited thus far and long-term data are lacking. It can be concluded, however, that at least in i.v. dosing the drug is devoid of ADEs with significant medical seriousness.
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PMID:Safety of levosimendan and other calcium sensitizers. 890 34

We describe a family with severe progressive cerebellar ataxia involving the trunk, the extremities, and speech. The proband, who has prominent atrophy of the cerebellum, shown by magnetic resonance imaging, was confined to a wheelchair at the age of 44 years. Two sons have episodes of vertigo and ataxia that are not responsive to acetazolamide. Quantitative eye-movement testing showed a consistent pattern of abnormalities localizing to the cerebellum. Genotyping suggested linkage to chromosome 19p, and SSCP showed an aberrant migrating fragment in exon 6 of the calcium-channel gene CACNA1A, which cosegregated with the disease. Sequencing of exon 6 identified a G-->A transposition in one allele, at nucleotide 1152, resulting in a predicted glycine-to-arginine substitution at codon 293. The CAG-repeat expansion associated with spinocerebellar ataxia 6 was not present in any family members. This family is unique in having a non-CAG-repeat mutation that leads to severe progressive ataxia. Since a great deal is known about the function of calcium channels, we speculate on how this missense mutation leads to the combination of clinical symptoms and signs.
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PMID:Progressive ataxia due to a missense mutation in a calcium-channel gene. 934 7

Neurotologic symptoms are common with migraine, yet relatively little is known about the pathophysiology of such symptoms. Motion sensitivity with bouts of motion sickness occurs in about two thirds of patients with migraine. Episodes of vertigo occur in about one fourth of patients and, in some, vertigo is the only symptom (so-called "migraine equivalent"). Phonophobia is the most common auditory symptom, but fluctuating hearing loss and acute permanent hearing loss occur in a small percentage. Migraine can mimic Meniere's disease and so-called "vestibular Meniere's disease" is usually associated with migraine. The recent discovery of a mutation in a brain calcium-channel gene in families with hemiplegic migraine and in families with episodic vertigo and ataxia suggests a possible mechanism for neurotologic symptoms in patients with more common varieties of migraine. A defective calcium channel, primarily expressed in the brain and inner ear, could lead to reversible hair cell depolarization and auditory and vestibular symptoms. This hypothesis is currently being investigated in other families with migraine headaches and neurotologic symptoms. Hopefully, such studies will lead to improved diagnosis and better treatments in the future.
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PMID:Neurotology of migraine. 943 80

It is well known that most episodes of benign paroxysmal positional vertigo (BPPV), even in untreated, recover spontaneously in 2 to 6 weeks. In the present study, we put forward the hypothesis that this is mainly due to the fact that endolymph, owing to its low calcium content (20 microM) is able to dissolve otoconia. To support this, the fate of frog saccular otoconia immersed in normal endolymph (Ca2+ content 20 microM) and in Ca2+-rich endolymphatic fluids (up to 500 microM) was studied by observing the crystals at regular intervals for 3 weeks. The results demonstrated that normal endolymph can dissolve otoconia very rapidly (in about 20 hours). When the endolymphatic Ca2+ content was increased (50 to 200 microM) otoconia dissolution time was slowed down (about 100 to 130 hours, respectively) and completely stopped when the endolymphatic Ca2+ content was of 500 microM. The present results therefore suggest that the major process involved in the spontaneous recovery of BPPV episodes is the capability of the endolymph to dissolve dislodged otoconia.
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PMID:Why do benign paroxysmal positional vertigo episodes recover spontaneously? 965 82

Benign paroxysmal positional vertigo (BPPV) is one of the most common and treatable causes of vertigo. We examined BPPV types and the effectiveness of physical therapy in each type. BPPV is caused by a utricular statoconium that blocks the semicircular canal. Statoconia can block any of the semicircular canals, but they generally affects the posterior canal. Diagnosis is based on a typical history and characteristic eye movements elicited by the Dix-Hallpike test. Treatment involves a physical maneuver designed to mobilize the free calcium particles from the semicircular canal to the utricle. Canalith repositioning is the mainstay of treatment. The maneuver is illustrated in detail and other forms of treatment and their indications are discussed.
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PMID:[Diagnosis and therapeutic options in benign paroxysmal positional vertigo]. 1021 83

Frequently, noise-induced hearing loss is associated with the symptom of tinnitus. Preliminary results in the animal model after noise exposure suggest that the calpain inhibitor leupeptin may protect against noise-induced hearing loss. A final common pathway for cell destruction and cell death (i.e., apoptosis) is the calpain hypothesis. Calpain is a normal, intracellular, cytosolic protease activated by excess intracellular calcium. Calpain inhibitors (AK275, AK295) have been shown to provide neuroprotection in the central nervous system. A collaboration of basic science and clinical research efforts focusing on calpain antagonists and inhibitors was established in New York in 1997; the initiators are attempting to develop neuroprotective drug therapy regimens for hearing and balance system complaints, particularly hearing loss, tinnitus, and vertigo. Both calpain inhibitors and antagonists are being developed and are being investigated wth perfusion techniques of the inner ear, in vitro and in vivo, for their effects on peripheral and central portions of the cochleovestibular system.
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PMID:Noise, Calpain, Calpain Inhibitors, and Neuroprotection: A Preliminary Report of Tinnitus Control. 1075 2

Benign paroxysmal positional vertigo (BPPV) is the most common and most treatable cause of vertigo. In most cases, a simple maneuver that takes less than a few minutes to do resolves the problem. BPPV is caused by misplaced calcium carbonate crystals (otoconia) in the semicircular canal of the inner ear that have broken free from the utricle. When these crystals break free, they either remain loose in one of three different semicircular canals or attach to the hair cells within a canal. Several different types of treatment maneuvers have been described. The maneuver to use varies according to the semicircular canal involved and whether the crystals are loose or attached to the hair cells.
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PMID:Benign paroxysmal positional vertigo. 1189 59


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