Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several neurological complications are associated with severe falciparum malaria. Cerebral malaria is one of the most life-threatening complications. A few patients may experience a neurological syndrome after complete recovery from Plasmodium falciparum infection. In the literature especially the postmalaria neurological syndrome (PMNS), acute disseminated encephalomyelitis (ADEM) and delayed cerebellar ataxia have been reported. We describe a case of a 53-year-old woman who was readmitted after an adequately treated P. falciparum infection with word-finding difficulties, confusion and tremor. Peripheral blood smears were repeatedly negative for malarial parasites. The clinical features best fitted a PMNS. Because of the severity of the syndrome she was treated with high-dose prednisone. She recovered completely. The possibility of ADEM is also discussed. Aetiology of these syndromes is still unknown, but it could be mediated by an immunological mechanism. PMNS or ADEM must be considered when neurological signs and symptoms occur after recovery from a P. falciparum infection.
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PMID:Neurological complications following Plasmodium falciparum infection. 1595 88

Neurologic signs and symptoms are common in acute malarial infection. However, after the parasites have been cleared from the blood and patients recover full consciousness, neurologic or psychiatric symptoms may occur or recur within 2 months after the acute illness. This phenomenon is called "postmalaria neurologic syndrome" (PMNS). We present a 50-year-old man who returned from the Republic of Malawi and soon developed Plasmodium falciparum malaria. Cerebral malaria, renal failure, hepatic failure, diffuse intravascular coagulation with thrombocytopenia, and upper gastrointestinal bleeding were noted during the acute stage. He was admitted to the infectious diseases ward and treated for 3 weeks. He was free from clinical general symptoms and parasites in blood smear when discharged. However, 2 weeks after discharge, he began to experience severe headache, dizziness, diplopia, mild hand tremor, unsteady gait, and easy falling. When readmitted to the neurologic ward, he presented with irritability, delirium, visual hallucination, and strange behavior. Neurologic examination was normal except for mild general weakness and evident truncal ataxia when walking. Brain magnetic resonance imaging revealed no structural lesions, and electroencephalography showed diffuse cortical dysfunction. Cerebral spinal fluid profile exhibited cytoalbuminologic dissociation. Brain single photon emission computed tomography showed diffuse cerebral parenchymal disorder. Nerve conduction studies revealed early sensory predominant polyneuropathy. The unsteadiness persisted for the initial 2 weeks of hospitalization until corticosteroid was administered. Intravenous methylprednisolone (80 mg/day) was continued for 3 days, followed by oral prednisolone (45 mg/day). His unsteadiness improved gradually after medication, and he absconded from the hospital on the 9th day of corticosteroid treatment with clear consciousness and free ambulation. The manifestation of PMNS is diverse and may present as an acute confusional state or psychosis, generalized seizure, fine tremors, cerebellar syndromes, postural hypotension, or malarial polyneuritis. Although the neurologic syndrome is primarily self-limited in most cases, corticosteroid may be beneficial in reversing PMNS.
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PMID:Postmalaria neurologic syndrome: a case report. 1711 25