Cerebellar ataxia in patients with malaria treated with chloroquine.

Sir, Three male patients aged 35, 40 and 42 years, were admitted to our unit with a history of severe ataxia. All three patients had three attacks of malaria within a period of four months. All three were treated with chloroquine and they lived in a malarial area in the northern part of Sri Lanka. They developed ataxia approximately two weeks after treatment for the third attack of malaria. There was no history of numbness in the peripheries. No vertigo was reported at any time during the illness. They had not been given any other medication in the recent past. They were not alcoholics and had no history of contacts with any chemicals. On examination they were not anaemic, were afebrile and there was severe ataxia. Finger-nose test, heel-knee test were positive and showed severe uncoordination. There was no nystagmus. The patients were seen by an ear, nose and throat consultant who excluded any vestibulo-labyrinthine disorder. They were later seen by the neurophysician who confirmed the diagnosis of cerebellar ataxia. No specific treatment was given and all three patients started showing improvement two weeks after the onset of illness and were completely normal 6-8 weeks later. Neuromyotoxicity consisting of peripheral neuropathy, cardiomyopathy and proximal myopathy has been reported in patients who were given chloroquine for longer periods, as in systemic lupus erythematosus and rheumatoid arthritis.1' 2 The basic pathology in all the tissues was vacuolation, with accumulation of myeloid and curvilinear bodies. No ataxia was mentioned in any of these reports. Is the ataxia seen in these three patients due to a late manifestation recurrent malaria, to chloroquine toxicity or is it a post-infectious allergic manifestation of malaria similar to the Guillain-Barr6 syndrome? R.F. James Medical Units 16B'18B, General Hospital (Teaching), Jaffna, Sri Lanka