HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Haller, L. Articles by Dago, A. Search for Related Content PubMed PubMed Citation Articles by Haller, L. Articles by Dago, A.

Clinical and Pathological Aspects of Human African Trypanosomiasis (T. B. Gambiense) with Particular Reference to Reactive Arsenical Encephalopathy

L. Haller^*, H. Adams, F. Merouze AND A. Dago

^* WHO/TDR Programme, Tryprespro, Daloa, Ivory Coast, Africa ,
Department of Neuropathology, Southern General Hospital, Glasgow G51 4TF, Scotland ,
Rural Health Sector, Daloa, Ivory Coast, Africa,
and Department of Pathology, CHU Treichville, Abidjan, Ivory Coast, Africa

Fourteen of 330 patients treated with melarsoprol (Mel B) for human African trypanosomiasis (HAT) developed a severe reactive arsenical encephalopathy (RAE). Six of these cases were fatal and postmortem examination was performed on 5 patients. Symptoms of "sleeping sickness" were compared with symptoms after treatment with arsenicals and the subsequent onset of RAE. There are 3 characteristic syndromes of RAE: convulsive status associated with acute cerebral edema, rapidly progresive coma without convulsions, and acute nonlethal mental disturbances without neurological signs. Three subjects revealed hypoxic brain damage with acute cerebral edema, and multiple hemorrhages of brain stem in those comatose. The pathology of the underlying HAT (chronic perivascular inflammation and plasma cytic infiltration of the brain) and the pathology of the RAE (characterized by acute vasculitis) are distinct. RAE occurs in the first as well as in the second stage (CNS involvement) of trypanosomiasis but the reason for this is unclear; an exclusive toxicity of the drug, or a Herxheimer reaction are possible but seem unlikely. Both clinical and laboratory findings point rather to a drug-related, delayed immune response.

Accepted for publication August 27, 1985.

This article has been cited by other articles:

				H. M.H. Braakman, F. J.J.M. van de Molengraft, W. W.A. Hubert, and D. H. Boerman Lethal African trypanosomiasis in a traveler: MRI and neuropathology Neurology, April 11, 2006; 66(7): 1094 - 1096. [Abstract] [Full Text] [PDF]

				N. Kumar, R. Orenstein, D. Z. Uslan, E. F. Berbari, C. J. Klein, and A. J. Windebank Melarsoprol-associated multifocal inflammatory CNS illness in African trypanosomiasis Neurology, April 11, 2006; 66(7): 1120 - 1121. [Full Text] [PDF]