Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024530 (malaria)
 44,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of neuromyopathy due to chronic chloroquine intoxication is reported. The neuromyopathy developped 9 months after malaria suppression therapy with chloroquine was started. The clinical picture was that of a peripherical neuropathy in the lower limbs and of a generalized myasthenic syndrome. Muscular biopsy showed typical pictures of "vacuolar myopathy". The metabolism of the drug was normal. The patient improved soon after chloroquine was discontinued.
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PMID:[Chloroquine neuromyopathy. One case in prophylactic maleriatherapy (author's transl)]. 20 Aug 90

From January 1980 to December 1990, six cases of malaria were observed; three cases were caused by plasmodium (P.) vivax and three by P. falciparum. Following a malaria episode, two cases (33.3%), developed cerebral malaria. Both of them were infected by P. falciparum. Neurological and electrodiagnostic investigations were scheduled throughout their clinical course. The first case manifested as a grand mal seizure, followed by myoclonic jerk and a comatous state. A suppression burst EEG observed before anti-malarial therapy was initiated. In the second case, a manifestation of encephalo-myelo-neuropathy was confirmed clinically and electrophysiologically. Although both cases occurred suddenly and were extremely severe, early anti-malarial therapy resulted in good responses without sequelae. The complete reversibility of the pathological event depends on early recognition and comprehensive therapy. Further, electrophysiological assessment is recommended for the detection of regional involvement in cerebral malaria.
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PMID:Clinical and electrophysiological assessment of cerebral malaria. 205 62

Nerve biopsies were performed in four patients with suspected chloroquine induced neuromyopathy. Three of the patients were treated with high doses of chloroquine for connective tissue disease, while one patient was taking this drug as malaria prophylaxis. Morphological studies demonstrated the presence of segmental demyelination and remyelination in all cases. Cytoplasmic inclusions were observed in Schwann cells, in perineurial and endothelial cells, and in some interstitial cells. They were never observed within axons. Occasional curvilinear profiles were seen in perineurial and Schwann cells. Perineurial calcifications were observed in two cases. The results of this morphological study suggest that chloroquine neuropathy is essentially due primary involvement of Schwann cells.
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PMID:Morphological study of peripheral nerve changes induced by chloroquine treatment. 283 92

In a Nigerian town with a stable population of 20,000, a door-to-door survey was conducted, using a questionnaire involving a complete census and a simple neurological evaluation which had previously showed a 95% sensitivity and an 80% specificity for detecting neurological disease. Positive responders were evaluated and categorised, using agreed criteria for diagnoses. Nearly 100% cooperation was obtained. Life prevalence ratio for at least one episode of headache was 51/1000. Crude point prevalence ratio for migrainous headache was 5.3/100, and peak age-specific ratio was in the first decade. Prevalence ratio for epilepsy was 533/100,000 and peak age-specific prevalence ratio occurred in the 5-14 years age groups. The prevalence ratio for peripheral nerve disorders was 268/100,000, and age-specific prevalence ratio for tropical neuropathy increased with age. Prevalence ratio for stroke was rather low at 58/100,000, but was probably due to the people's attitude to the disabled elderly and high mortality of stroke which showed annual mortality rate of 70/100,000 which increased with age to 1519/100,000 per year in the eighth decade. Crude prevalence ratios (cases per 100,000) for others are 112 for neurological complications (including sciatica) of spondylosis, 15 each for poliomyelitis, motor neurone disease, development speech disorders, 10 each for syncope, hereditary neuropathies. Parkinson's disease, benign essential tremor, primary cerebellar degeneration, cerebral palsy, mental retardation, organic psychosis (probable intracranial tumor) and 5 each for muscular dystrophy, pyomyositis, spina bifida occulta, alcohol dependence and cerebral malaria. The implications of the findings are important for development of community neurological services in the developing countries.
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PMID:Neurological disorders in Nigerian Africans: a community-based study. 303 73

The spectrum of movement disorders in the tropics is different from that seen in the industrialized nations of the west. This is not surprising given the unique combination of environmental and population characteristics in the tropics. Infections seldom encountered in the west such as tuberculous meningitis, typhoid fever, Japanese encephalitis, malaria, trypanosomiasis or cysticercosis are often seen in the tropics and with global patterns of travel and immigration these conditions are becoming more common worldwide. Movement disorders associated with these infections, HIV, slow virus and prion disease are discussed. Taking into account the diverse etiologies of movement disorders in the tropics, movement disorders with a nutritional basis such as the infantile tremor syndrome, seasonal ataxia and tropical ataxic neuropathy, and manganese neurotoxicity are also reviewed. Finally, certain special characteristics of ubiquitous disorders such as Parkinson's disease, and disorders with a genetic basis such as Wilson's disease and spinocerebellar degeneration are described.
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PMID:Movement disorders in the tropics. 1247 95

A 3 year review of neurologic admissions into the adult medical wards at the UCH, Ibadan, Nigeria between January 1998 and December 2000 is presented. The study design involved the scrutiny of the records of all the neurological admissions, male and female to the medical ward. The identified cases were then classified and only cases confirmed as neurological were further analysed. Stroke, predominantly non-hemorrhagic accounted for 50.4% of cases for the period of study. Stroke is therefore the most common cause of adult neurologic admissions on medical wards of UCH. Central nervous system infections, comprising mainly of tetanus and meningitis accounted for 14.2% (111) and 12.4% (97) of case respectively. The myelopathies were the cause of neurologic admissions in 8.1% (63) of cases followed by seizure disorders. Headache was the reason for admission in 0.9% (7) of cases. Parkinsons disease, hypertensive encephalopathy, Guillian Barne syndrome, seasonal ataxic neuropathy, cavernous sinus thrombophlebitis, normal pressure hydrocephalus were rarely the cause of admission. Similarly, dystonia, and cerebral malaria recorded 0.13% (1) of cases each. A case is made for the establishment of regional stroke units in Nigeria.
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PMID:A 3-year review of neurologic admissions in University College Hospital Ibadan, Nigeria. 1452 26

We describe a case of a woman who developed a peripheral polyneuropathy shortly after completing 4 weekly doses of mefloquine hydrochloride (250 mg) malaria prophylaxis. Although mefloquine-related central nervous system neuropathy is well described in the literature, peripheral polyneuropathy similar to this case has been documented only once before, to our knowledge.
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PMID:Case report: Peripheral polyneuropathy and mefloquine prophylaxis. 2214 35