(Stroke. 1997;28:1648-1649.)
© 1997 American Heart Association, Inc.
Articles |
Division of Neurology, Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong
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We read with interest the case report, "Large Cerebral Infarction During Praziquantel Therapy in Neurocysticercosis," by Bang et al1 and would like to make the following comments.
From the first set of cerebrospinal fluid (CSF) findings, there was marked eosinophilia (41%), suggesting a heavy load of neurocysticercosis within the central nervous system. Together with the communicating hydrocephalus, there was strong evidence of significant inflammatory reactions at the skull base. Therefore, steroid therapy might have been advisable to prevent exacerbation of the inflammatory reactions due to the cysticidal effect of praziquantel.2 Cerebral angiitis and meningeal adhesion should have been anticipated. This is analogous to the treatment of tuberculous meningitis.3 In fact, steroid-dependent neurocysticercosis has been suggested as an inflammatory mechanism for neurological disturbances following praziquantel treatment.4
Second, praziquantel is known to cause seizures. Recently, we saw a 27-year-old Chinese woman who presented with subcutaneous nodules for several years. Skin biopsy confirmed cysticercosis. Although the skin nodules resolved after a course of praziquantel, she had two attacks of temporal lobe epilepsy with secondary generalization 1 month after treatment. She was rendered seizure free with sodium valporate. MRI of the brain revealed multiple small, ring-like lesions typical of neurocysticercosis.
A 30-year-old Nepalese woman presented with generalized
tonic-clonic seizure. CT of the head revealed a small, solitary,
ring-like enhancing lesion at the gray-white matter junction of the
right high parietal lobe, with marked perifocal edema. She was seizure
free while on sodium valporate. Praziquantel was started empirically by
a neurosurgeon. One
Department of Neurology, Yonsei University College of Medicine, Seoul, Korea
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