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摘要


急性瘧疾感染出現神經學症狀是常見的,然而在瘧原蟲已從患者血中消失而且患者完全恢復意識之後,在急性瘧疾感染後兩個月之內仍然可能會發生神經方面的症狀,這種現象稱爲瘧疾後神經症候群。我們報告一例從馬拉威共和國工作的五十歲男性台灣人,於回國後罹患熱帶瘧原蟲瘧疾。急性發作時並發有腦性瘧疾、肝腎衰竭、瀰漫性血管內血液凝固症及上胃腸道出血。他於感染科病房住院及治療三週;於出院時並沒有明顯臨床症狀,而血液抹片也沒有找到瘧原蟲。他於出院二週後出現頭痛、頭暈、複視、手抖、走路不穩以及容易跌倒等症狀。他於神經科住院期間有躁動,譫妄,視幻覺以及怪異行爲等表現。神經學檢查大致正常,除了輕微全身乏力,以及走路時有明顯的軀體運動失調。腦部核磁共振沒有明顯構造異常,腦波顯現瀰漫性皮質功能異常,脊髓液檢查呈現細胞白蛋分離現象,腦單光子電腦斷層攝影顯示瀰漫性腦實質疾病,而神經傳導檢查則是出現早期多發性神經病變現象。步態不稱於住院後兩週一直持續存在,直到使用皮質類固醇後才有改善的情形。我們使用甲基類固醇,每日80 mg點滴滴注連續三日,之後換成品服類固醇每日45 mg。步態不穩於使用類固醇後有逐漸改善情形,於使用類固醇九日後逃院。瘧疾後神經症候君的表現是多樣化,可能會有急性混亂或精神病、抽搐、震顫、小腦症狀、姿勢性低血壓或多發性神經炎等臨床表現。大部份的病例都能自行康復,而皮質類固醇可能有益於加速症狀改善。

並列摘要


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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