QJM. Cerebellar syndrome in Plasmodium falciparum malaria. Sir, logical checkup was done fortnightly, and these patients took 6 to 16 weeks for complete ...
Q J Med 1999; 92:233–234
Correspondence QJM Cerebellar syndrome in Plasmodium falciparum malaria Sir, There are reports in the literature of patients with P. falciparum malaria presenting without impairment of consciousness but with signs of cerebellar dysfunction.1 Most of these cases have been reported from the Indian subcontinent. Cerebellar ataxia is also commonly reported in cerebral malaria survivors after recovery from coma in both children and adults. More recently, a syndrome of delayed cerebellar ataxia (DCA) has also been described from Sri Lanka and India in which ataxia developed after an afebrile period of a few days to weeks after an attack of fever attributable to P. falciparum malaria.1–4 In this prospective hospital-based clinical study of 3188 adult patients with P. falciparum malaria admitted to the PBM hospital attached to S.P. Medical College Bikaner (Rajasthan) India between January 1992 and June 1998, cerebellar syndrome was observed in 49 patients at different stages of malarial infection. All patients were managed according to WHO guidelines after confirmation of diagnosis.5 All patients received oral or i.v. quinine and were managed by similar treatment protocols. Cerebellar ataxia during the acute stage of the illness with normal level of consciousness was observed in nine patients (part of this study has already been published6). There was selective involvement of cerebellum without any other neurological deficit except convulsions in three patients. These patients were treated on the line of cerebral malaria as according to WHO recommendation.5 Seven patients recovered completely at the end of the fourth week and another two by the end of the second month without any residual neurological deficit. Cerebellar ataxia as a neurological sequela in survivors of cerebral malaria was found in 22 of a total of 440 patients with strictly defined cerebral malaria. Involvement of lower limbs was more common than that of the upper limbs. Nystagmus was present in 14, cerebellar dysarthria in nine, and truncal ataxia in eight patients. A detailed neuro© Association of Physicians 1999
logical checkup was done fortnightly, and these patients took 6 to 16 weeks for complete recovery after regaining consciousness. The possible aetiological factors for causation of neurological sequelae in patients of cerebral malaria are anaemia, hypoglycaemia, deep coma and persistent seizures.7,8 DCA was observed in 18 patients (part of this study has already been published2). Mean delay between onset of fever and onset of cerebellar ataxia was 13 days (7–21 days). Apart from isolated case reports, DCA is mainly described from Sri Lanka and India.1–4 This unusual complication has an acute onset with signs suggesting predominantly midline cerebellar lesions without any evidence of cerebral involvement. There is bilateral involvement of the cerebellum or its connections or both. Lower limbs are involved more often than the upper limbs. Other causes of cerebellar ataxia in this setting, such as effects of drugs, neurotropic viruses, fever, etc., were ruled out by relevant investigations. DCA is presumed to be a variety of post-malaria neurological syndrome9 described mainly in the Indian subcontinent. The majority of these patients recovered by the end of the fourth week; three required the use of corticosteroids at the end of the eighth week and recovered completely by the end of the fourth month. The appearance of a mutant strain of Plasmodium falciparum, with a probable immunological mechanism, as few patients improved with corticosteroids, is likely to be the cause of this complication.3 Apart from the direct relation of Plasmodium falciparum and cerebellar dysfunction, such an ataxia has also been reported after the use of drugs such as chloroquine, artesunate and mefloquine, but we found no such patient in our study, despite keeping a close watch on drug toxicity in these patients. Cerebellar involvement in Plasmodium falciparum malaria can occur (i) during acute stage of fever, (ii) as a sequelae of cerebral malaria in survivors, (iii) in the form of delayed cerebellar ataxia and, (iv) as a side effect of drugs. Thus in a malaria
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endemic area, all patients with cerebellar ataxia and fever should be investigated for malaria infection. Most of these complications are self-limiting in nature, and once the diagnosis is established, the patients should not be subjected to costly investigations. D.K. Kochar Shubhakaran B.L. Kumawat I. Thanvi N Agrawal Department of Medicine, Neurology Section S.P. Medical College Bikaner India
References 1. Warrell DA. Cerebral malaria. In: Shakir RA, Newman PK, Poser CM, eds. Tropical neurology. London, W.B. Saunders, 1996; 213–45.
2. Kochar DK, Kumawat BL, Kochar SK, et al. Delayed cerebellar ataxia—a complication of plasmodium falciparum malaria. JAPI 1996; 44:686–8. 3. Senanayke N. Delayed cerebellar ataxia. A new complication of falciparum malaria. Br Med J 1987; 294:1253–4. 4. Senanayke N, Desilva HJ. Delayed cerebellar ataxia complicating falciparum malaria, a clinical study of 74 patients. J Neurol 1994; 241:456–9. 5. World Health Organization. Division of Control of Tropical Disease. Severe and complicated malaria. Trans Roy Soc Trop Med Hyg 1990; 84(Supplement 2):1–65. 6. Kochar DK, Shubhakaran, Joshi A, et al. Neurological manifestations of falciparum malaria. JAPI 1997; 45:898–9. 7. White NJ, Bremen JG. Harrison’s principles of internal medicine, 13th edn. Singapore, McGraw Hill, 1994:887. 8. Bajiya HN, Kochar DK. Incidence and outcome of neurological sequelae in survivors of cerebral malaria. JAPI 1996; 44:679–81. 9. Nguyen Thi HM, Nicholas PJ Day, LV Van Choung, et al. Post malaria neurological syndrome. Lancet 1996; 348:917–21.
