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Indian Journal of Medical Sciences, Vol. 60, No. 7, July, 2006, pp. 296-297 Letter To Editor HEMIPARESIS AND CEREBELLAR DYSFUNCTION COMPLICATING MIXED MALARIAL INFECTION WITH FALCIPARUM AND VIVAX MALARIA George IgeA, Varghese L, Mathews PK Dept. of Medicine -3, CMC Hospital Vellore, Tamil Nadu Code Number: ms06042 Sir, Cerebral malaria is a diffuse encephalopathy, in which focal neurological signs are relatively unusual. Focal neurological deficits in malaria like cerebellar ataxias, extrapyramidal rigidity, cranial nerve palsies and cortical blindness presenting with intact sensorium are rare, but reported.[1],[2] We report a case of mixed infection with Plasmodium falciparum and Vivax malaria, who presented with hemiparesis and cerebellar dysfunction with intact sensorium, due to its uncommon occurrence. A 21 yr. old man from a malaria endemic area presented with fever for 1 week and headache with vomiting for 5 days. The relatives noticed paucity of movements on the right side, from the 3rd day of illness. He had no history of seizures, loss of consciousness or bladder or bowel incontinence. At admission, he was disoriented but obeying commands (Glasgow coma score 14/15). His vital signs were stable and he had no icterus or neck stiffness. Cranial nerve examination showed bilateral nystagmus and right sided Upper Motor Neuron facial weakness. On motor examination, he had hemiparesis on the right side, with grade 3 power. He also had bilateral cerebellar signs (truncal ataxia bilateral past pointing and dysdiadochokinesia). Power on the left half of body was normal. He had an extensor plantar response on the right side, while on the left side, it was flexor. Sensory system examination was unremarkable. Fundus was normal. Routine biochemical and hematological examination was normal. Peripheral blood showed the evidence of a mixed malarial infection, with ring stages and gametocytes of P. falciparum and Vivax . Magnetic resonance imaging (MRI) of the brain and cerebrospinal fluid (CSF) examination was normal. He was treated with intravenous Quinine and Dextrose with oral Doxycycline. His fever responded and his hemiparesis and cerebellar signs improved by the 5th day of treatment. At 2 weeks follow- up, his power had improved to normal and there were no cerebellar signs. The striking feature of neurological deficits in malaria is that, most of them are either transient or resolve completely over a period of time.[3] The possible mechanisms of hemiparesis and cerebellar dysfunction in malaria include vascular infarction and immune-mediated demyelination. In falciparum infections, the parasitized red blood cells develop membrane protuberances on the surface, which extrude an adhesive protein, Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1) that mediates cytoadherence.[4] Plugging of cerebral capillaries and venules by clumped, parasitized red blood cells, is one hypothesis to explain its pathogenesis. Focal lesions suggesting infarction and hemorrhages have been demonstrated by few workers earlier.[5] The other is a humoral hypothesis, which proposes a immune-mediated, inflammatory response, with release of vasoactive substances capable of producing endothelial damage and alterations of permeability.[4] In this case, it is unlikely to have been due to a demyelinating process, as the MRI Brain and the CSF examination was normal. This case had focal neurological deficits of hemiparesis and cerebellar dysfunction, which resolved with adequate treatment of malaria. This case is being reported for its rarity and to highlight the role of early recognition and timely treatment, which leads to complete recovery. References
Copyright 2006 - Indian Journal of Medical Sciences |
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