Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004134 (ataxia)
 15,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The novel benzodiazepine derivative, meclonazepam (3-methylclonazepam) has been found to be orally effective at high doses against all stages of schistosomiasis. Animals studies have shown it to have a high therapeutic index and a profile of behavioural activity typical of the benzodiazepines. The effects of single oral doses of meclonazepam, 1, 2 and 4 mg on central arousal, psychomotor performance and subjective mood were studied in two double-blind placebo controlled studies in healthy volunteers. In doses exceeding 1 mg, meclonazepam caused marked dose-related impairment in cognitive and psychomotor functions as well as shifts in mood reflecting sedation and ataxia. These effects were most prominent in the first 3 h after administration, with moderate sedation still present 6 h after the 4 mg dose. The implications of these findings for the use of benzodiazepine agents in the treatment of schistosomiasis are discussed.
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PMID:Central effects in man of the novel schistosomicidal benzodiazepine meclonazepam. 405 98

Schistosomiasis is a parasitic disease caused by blood flukes of the genus Schistosoma. Currently more than 200 million people worldwide are affected. Neuroschistosomiasis constitutes a severe presentation of the disease. Neurological symptoms result from the inflammatory response of the host to egg deposition in the brain and spinal cord. Neurological complications of cerebral schistosomiasis include delirium, loss of consciousness, seizures, dysphasia, visual field impairment, focal motor deficits and ataxia. Cerebral and cerebellar tumour-like neuroschistosomiasis can present with increased intracranial pressure, headache, nausea and vomiting, and seizures. Myelopathy (acute transverse myelitis and subacute myeloradiculopathy) is the most common neurological complication of Schistosoma mansoni infection. Schistosomal myelopathy tends to occur early after infection and is more likely to be symptomatic than cerebral schistosomiasis. The conus medullaris and cauda equina are the most common sites of involvement. Severe schistosomal myelopathy can provoke a complete flaccid paraplegia with areflexia, sphincter dysfunction and sensory disturbances. Schistosomicidal drugs, steroids and surgery are the currently available treatments for neuroschistosomiasis. Rehabilitation and multidisciplinary team care are needed in severely disabled patients.
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PMID:Neurological complications of Schistosoma infection. 1790 71

Schistosomiasis (bilharzia) is a neglected tropical disease caused by digenetic trematode platyhelminths of the genus Schistosoma. Neuroschistosomiasis is one of the most severe clinical outcomes associated with schistosome infection. Neurological complications early during the course of infection are thought to occur through in situ egg deposition following aberrant migration of adult worms to the brain or spinal cord. The presence of eggs in the CNS induces a cell-mediated Th2-driven periovular granulomatous reaction. The mass effect of thousands of eggs and the large granulomas concentrated within the brain or spinal cord explain the signs and symptoms of increased intracranial pressure, myelopathy, radiculopathy and subsequent clinical sequelae. Myelopathy (acute transverse myelitis and subacute myeloradiculopathy) of the lumbosacral region is the most common neurological manifestation of S. mansoni or S. haematobium infection, whereas acute encephalitis of the cortex, subcortical white matter, basal ganglia or internal capsule is typical of S. japonicum infection. Cerebral complications include encephalopathy with headache, visual impairment, delirium, seizures, motor deficits and ataxia, whereas spinal symptoms include lumbar pain, lower limb radicular pain, muscle weakness, sensory loss and bladder dysfunction. The finding of eggs in the stool or a positive serology, provides supportive but not direct evidence of neuroschistosomiasis. A definitive diagnosis can only be made with histopathological study showing Schistosoma eggs and granulomas. Schistosomicidal drugs (notably praziquantel), steroids and surgery are currently used for the treatment of neuroschistosomiasis. During the 'acute phase' of the disease, neuroschistosomiasis is treated with corticosteroids which are augmented with a course of praziquantel once female worm ovipositioning commences. Surgery should be reserved for special cases such as in those with evidence of medullary compression and in those who deteriorate despite clinical management.
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PMID:Neuroschistosomiasis. 2167 95

Schistosomiasis is a parasitic disease caused by blood flukes of the genus Schistosoma. Currently 200 million people worldwide are infected. Neurological manifestations are a result of the inflammatory response of the host to egg deposition in the brain and spinal cord and is usually seen in patients with recent infection with no evidence of systemic illness. Cerebral and cerebellar disease can result in headache, seizure, and increased intracranial pressure. Cerebral schistosomiasis is more common in Schistosoma japonicum, but increasing cases due to Schistosoma mansoni are being reported in the literature. Other complications of cerebral schistosomiasis include delirium, loss of consciousness, visual field impairment, focal motor deficits, and ataxia. Myelopathy is the most common neurological manifestation of Schistosoma mansoni and the conus medullaris and cauda equine are the most common sites of involvement. Severe disease can result in flaccid paraplegia with areflexia, sphincter dysfunction, and sensory disturbance. Early recognition and prompt treatment are essential when physicians are faced with schistosomiasis involving the central nervous system. Schistosomicidal drugs, such as praziquantel, steroids and surgery, are the mainstay of therapy for this severe form of schistosomiasis.
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PMID:Schistosomiasis of the nervous system. 2382 18