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Over the past nine years, more than 12 million people exposed to Onchocerca volvulus infection have received at least one dose of ivermectin, almost all without serious adverse reactions. Since 1991, however, several cases with neurologic manifestations, including coma, have been reported after ivermectin treatment of persons infected with O. volvulus who also had concomitant Loa loa infection with very high microfilaremia (Ͼ 50,000 microfilariae/ml of blood). In 1995, four criteria were established to define probable cases of Loa encephalopathy temporally related to treatment with ivermectin (PLERI). The present paper describes three PLERI cases recorded in Cameroon and compares them with two others reported previously. Disorders of consciousness began 3-4 days after treatment. The objective neurologic signs were variable. The conditions improved favorably in three patients who benefited from early hospitalization and good nursing; their disorders of consciousness lasted only 2-3 days; the results of clinical examination became normal after one month and electroencephalographic abnormalities disappeared after 5-7 months. Conversely, late diagnosis and delay in proper management in two others probably led to worsening of the condition and to fatal outcome related to the usual complications of coma. In addition to these cases, patients w with high Loa microfilaremia also developed milder neurologic manifestations causing functional impairment lasting for at least one week after treatment. Before launching mass ivermectin distribution programs to control onchocerciasis in central Africa, communities in which the intensity of concomitant L. loa microfilaremia is high need to be identified, and specific educational measures and monitoring strategies should be developed and applied before they are treated.

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In August 2002, 65 cases of Loa-associated neurological Serious Adverse Events were reported after ivermectin treatment. The first signs, occurring within the 12–24 hours following treatment, included fatigue, generalized arthralgia, and sometimes agitation, mutism, and incontinence. Disorders of consciousness, including coma, generally appeared between 24 and 72 hours, and showed a rapid variation with time. The most frequent objective neurological signs were extrapyramidal. The patients presented with haemorrhages of the conjunctiva and of the retina. Biological examinations showed a massive Loa microfilaruria, the passage of Loa microfilariae into the cerebrospinal fluid, haematuria, and an increase in the C-reactive protein, all of which have been correlated with the high intensity of the initial Loa microfilaraemia. Eosinophil counts decreased dramatically within the first 24 hours, and then rose again rapidly. Electroencephalograms suggested the existence of a diffuse pathological process within the first weeks; the abnormalities disappearing after 3–6 months. Death may occur when patients are not properly managed, i.e. in the absence of good nursing. However, some patients who recovered showed sequelae such as aphasia, episodic amnesia, or extrapyramidal signs. The main risk factor for these encephalopathies is the intensity of the initial Loa microfilaraemia. The disorders of consciousness may occur when there are >50,000 Loa microfilariae per ml. The possible roles of co-factors, such as Loa strains, genetic predisposition of individuals, co-infestations with other parasites, or alcohol consumption, seem to be minor but they should be considered. The mechanisms of the post-ivermectin Loa-related encephalopathies should be investigated to improve the management of patients developing the condition.