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)

Twenty-four patients, including two with aplastic anemia and 22 with malignancy, underwent marrow transplantation after preparation with mechlorethamine, 0.3 to 2.0 mg/kg body weight. Fourteen of the 21 neurologically evaluable recipients developed immediate neurotoxicity a median of 4 days after treatment (range, 0 to 34 days). Confusion and disorientation were observed in six patients, headache in six, hallucinations n four, lethargy in four, tremors in three, paraplegia in one, seizure in one, and vertigo in one. Whereas acute symptoms cleared in 11 patients, three remained symptomatic until death. Twelve evaluable patients survived more than 60 days; all six with previous acute toxicity subsequently developed delayed onset of new neurologic findings (personality change, confusion, seizure, diplopia, or dementia) a median of 169 days (range, 70 to 248 days) after treatment. Cerebrospinal fluid analysis was usually normal but cerebral computed tomographic scans showed ventricular enlargement and electroencephalograms showed diffuse slowing. Postmortem histologic examination of brain showed neuronal degenerative changes with increased vascularity, gliosis, and perivascular fibrosis. Neurotoxicity appeared to increase with age and mechlorethamine dose and was commoner in patients given additional procarbazine or cyclophosphamide.
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PMID:Immediate and delayed neurotoxicity after mechlorethamine preparation for bone marrow transplantation. 704 28

This investigation examined the role of brain perfusion single-photon emission tomography (SPET) in traumatic head injury in 35 patients. The results were compared with those of X-ray computerized tomography (CT) and magnetic resonance imaging (MRI). CT and MRI detected brain contusions in seven patients, subarachnoid haemorrhage in one patient and both in nine patients. In 16 of the 17 subjects (94%), SPET with technetium-99m-hexamethylpropyleneamine oxime (Tc-HMPAO) revealed CT/MRI-negative abnormalities, such as hypoperfusion in the contre-coup region, frontal hypoperfusion related to personality change and cerebellar hypoperfusion associated with vertigo. In two patients presenting with diffuse axonal injury in the brainstem, hypoperfusion in the frontal cortex on the affected side was observed on SPET. SPET demonstrated hypoperfusion in the adjacent cortex, with no abnormality on either CT or MRI, in six of seven patients exhibiting acute epidural haematoma. SPET failed to provide additional information in two of five patients with acute subdural haematoma and in one of two patients displaying chronic subdural haematoma. In four of nine patients with post-traumatic amnesia, SPET detected hypoperfusion in the temporal lobe, with no abnormality on either CT or MRI. In five of eight patients with vertigo, SPET detected hypoperfusion in the morphologically normal cerebellum. In seven cases involving personality change, frontal hypoperfusion was observed in four; moreover, a markedly non-homogeneous pattern was evident in the remaining three. Overall, SPET afforded additional information in 26 patients (74%). CT possesses an advantage with respect to the detection of haemorrhagic lesions. MRI provides more precise information regarding contusions and axonal injury. Frequently, SPET may be the only examination to reveal perfusion abnormalities which are related to symptoms in the absence of other objective findings, such as post-traumatic amnesia, vertigo or personality change.
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PMID:Role of brain perfusion single-photon emission tomography in traumatic head injury. 1509 6

Mefloquine is a 4-methanolquinoline anti-malarial that in recent years has fallen out of favor for use as chemoprophylaxis against infection with chloroquine-resistant Plasmodium falciparum malaria owing in part to growing concerns of side effects and potential neurotoxicity. Despite over 20 years of licensed use, the pathophysiological mechanisms underlying mefloquine's neuropsychiatric and physical side effects and the clinical significance of the drug's neurotoxicity have remained poorly understood. In this report, an adverse reaction to mefloquine chemoprophylaxis is described characterized by prodromal symptoms of anxiety with subsequent development of psychosis, short-term memory impairment, confusion and personality change accompanied by complaints of disequilibrium and vertigo, with objective findings of central vestibulopathy. It is posited that these effects represent an idiosyncratic neurotoxic syndrome of progressive limbic encephalopathy and multifocal brainstem injury caused by the drug. This case provides insights into the clinical significance of mefloquine neuronal gap junction blockade and neurotoxicity demonstrated in animal models, points to recommendations for the management of affected patients including diagnostic considerations and appropriate referrals, and highlights critical implications for the continued safe use of the medication.
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PMID:Limbic encephalopathy and central vestibulopathy caused by mefloquine: a case report. 2249 97

Familial idiopathic basal ganglia calcification (Fahr`s disease) is a rare neurodegenerative disorder characterized by symmetrical and bilateral calcification of the basal ganglia. Calcifications may also occur in other brain regions such as dentate nucleus, thalamus, and cerebral cortex. Both familial and non-familial cases of Fahr`s disease have been reported, predominantly with autosomal-dominant fashion. The disease has a wide range of clinical presentations, predominantly with neuropsychiatric features and movement disorders. Psychiatric features reported in the literature include: cognitive impairment, depression, hallucinations, delusions, manic symptoms, anxiety, schizophrenia-like psychosis, and personality change. Other clinical features include: Parkinsonism, ataxia, headache, seizures, vertigo, stroke-like events, orthostatic hypotension, tremor, dysarthria, and paresis. Fahr`s disease should be considered in the differential diagnosis of psychiatric symptoms, particularly when associated with movement disorder. The disease should be differentiated from other conditions that can cause intracranial calcification. No specific treatment is currently available. Further research is needed to bridge the gap existing in our current knowledge of the prevalence, etiology, symptoms, and treatment of Fahr`s disease.
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PMID:Familial idiopathic basal ganglia calcification (Fahr`s disease). 2498 77