Neurologic Changes in Visceral Leishmaniasis

Faisal A. HashimLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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Ammar E. AhmedLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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M. El HassanLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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Murtada H. El MubarakLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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Hashim YagiLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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El Neim IbrahimLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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Mohammed S. AliLeishmaniasis Research Group, National Research Council, Department of Physiology and Department of Surgery, Faculty of Medicine, University of Khartoum, Khartoum, Sudan

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Neurologic changes in visceral leishmaniasis (VL) are rarely reported. From January 1992 to April 1993, 111 patients with VL were seen at Soba University Hospital in Khartoum, Sudan. Fifty-two (46%) patients had neurologic symptoms or signs; the most common symptom was a sensation of burning feet. Four patients had foot drop. Five patients had deafness and one patient had multiple cranial nerves palsies. None of our patients had vitamin deficiency or any of the other known causes of neuropathy. Nerve conduction studies in 15 patients showed evidence of axonal degeneration and demyelination, which were confirmed by histopathology and electron microscopy of nerve biopsies. There was no direct parasitic infection of the nerve and there was no neuritis. In most patients, the sensory symptoms disappeared within two weeks in most of our patients after specific anti-leishmanial treatment. Motor recovery was much slower. Audiographic studies in five patients with deafness showed it to be sensory-neural. Hearing returned to normal after treatment with sodium stibogluconate. Further studies are needed to define the etiology of the nerve pathology in patients with VL.

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