(Stroke. 1997;28:1648-1649.)
© 1997 American Heart Association, Inc.
Articles |
Caution With Praziquantel in Neurocysticercosis
Division of Neurology, Department of Medicine, Queen Mary Hospital, Pokfulam Road, Hong Kong
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To the Editor:
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 week later, however, she had repeated seizures, requiring a combination of two anticonvulsants.
Praziquantel, an effective anthelmintic, kills both the adult and cysts of Taenia solium.5 Nevertheless, this effective medical treatment of neurocysticercosis can be complicated by seizures and cerebral infarction.1 2 6 The underlying mechanisms are unknown, but dying cysts may initiate intense inflammatory reactions leading to neuronal irritation or angiitis. Although coadministration of corticosteroid has been advocated,7 major cerebral infarction might not be preventable.2 We wonder whether CSF findings can be an indicator for prophylactic steroid therapy before praziquantel.
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1. Bang OY, Heo JH, Choi SA, Kim DI. Large cerebral infarction during praziquantel therapy in neurocysticercosis. Stroke.. 1997;28:211-213.
2. Woo E, Yu YL, Huang CY. Cerebral infarction precipitated by praziquantel in neurocysticercosis: a cautionary note. Trop Geogr Med.. 1988;40:143-146.[Medline] [Order article via Infotrieve]
3. Bharucha NE, Barucha EP, Bhabha SK. Bacterial infections. In: Bradley WG, Daroff RB, Fenichel GM, Marsden CD, eds. Neurology in Clinical Practice. Boston, Mass: Butterworth-Heinemann; 1996:1181-1243.
4. Lui SL, Fong KY, Chen WH, Yu YL. Steroid-dependent neurocysticercosis. Trop Geogr Med.. 1995;47:221-222.[Medline] [Order article via Infotrieve]
5.
Del Brutto OH. Medical treatment of
cysticercosis—effective. Arch Neurol.. 1995;52:102-104.
6. Levy AS, Lillehei KO, Rubinstein D, Stears JC. Subarachnoid neurocysticercosis with occlusion of the major intracranial arteries: case report. Neurosurgery.. 1995;36:183-188.[Medline] [Order article via Infotrieve]
7. Del Brutto OH, Sotelo J, Roman GC. Therapy for neurocysticercosis: a reappraisal. Clin Infect Dis.. 1993;17:730-735.[Medline] [Order article via Infotrieve]
Response
Department of Neurology, Yonsei University College of Medicine, Seoul, Korea
Key Words: neurocysticercosis • praziquantel \
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I would like to express my gratitude to Drs Fong and Cheung for their interest in our recently published article in Stroke.1 On behalf of my colleagues, I would like to address their comments.
First, I agree with the comment that steroids might have been given to our patient in the first course of praziquantel therapy. I usually reserve the use of steroids for toxic symptoms developed by acute inflammatory reaction when treating parenchymal cysticerci with praziquantel because its plasma levels are lowered by steroids.2 However, findings in our patient suggest that the early start of steroids may be mandatory in some patients, such as those with subarachnoid cysticerci, scheduled for the use of praziquantel. Albendazole, although not uniformly available in all countries, may have an advantage over praziquantel because albendazole has been reported to be highly effective for the treatment of subarachnoid cysticerci3 and plasma levels are increased in the presence of steroids.4
Second, Fong and Cheung mentioned that the treatment with praziquantel can be complicated by seizures as well as cerebral infarction, with brief reports of two patients who had developed seizures after 1 week and 1 month, respectively, of praziquantel therapy. It is uncertain whether their seizures were developed by the acute inflammatory reaction subsequent to the destruction of the cysts by praziquantel therapy or were a sign of neurocysticercosis itself. Descriptions regarding other toxic symptoms attributed to the acute inflammatory reaction are lacking, and epileptic seizures are the most common neurological sign of neurocysticercosis.5
Finally, they raised the question of whether CSF findings (eosinophils) can be an indicator for prophylactic treatment of steroids before the use of praziquantel in patients with neurocysticercosis.2 Eosinophils have capabilities of chemotaxis, phagocytosis, and microbicidal activity similar to those of neutrophils and are known to be associated with the degeneration and destruction of the cysticerci.6 Increased inflammatory cells, including eosinophils, in CSF may represent the severity of the inflammation. However, it appears that the site of an inflammation carries more risk in complicating stroke than the mere severity of an inflammation. Our and previous reports have continued to describe the importance of the subarachnoid form of cysticerci.1 7 Recently, it has been reported that subarachnoid cysticerci were found in 54 of the 65 patients with neurocysticercosis who developed stroke or TIA, while CSF eosinophils were evident in only 33.8
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References |
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TopIntroductionReferencesIntroduction References |
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1. Bang OY, Heo JH, Choi SA, Kim DI. Large cerebral infarction during praziquantel therapy in neurocysticercosis. Stroke.. 1997;28:211-213.
2.
Vasquez ML, Jung H, Sotelo J. Plasma levels of
praziquantel decrease when dexamethasone is given
simultaneously. Neurology.. 1987;37:1561-1562.
3.
Del Brutto OH, Sotelo J, Aguirre R, Diaz-Calderon E,
Alarcon A. Albendazole therapy for giant subarachnoid
cysticerci. Arch Neurol.. 1992;49:535-538.
4. Jung H, Hurtado M, Medina MT, Sanchez M, Sotelo J. Dexamethasone increases plasma levels of albendazole. J Neurol.. 1990;237:279-280.[Medline] [Order article via Infotrieve]
5.
Sotelo J, Guerrero V, Rubio F.
Neurocysticercosis: a new classification based on active and
inactive forms: a study of 753 cases. Arch Intern
Med.. 1985;145:442-445.
6. Molinari JL, Meza R, Tato P. Taenia solium: cell reactions to the larva (Cysticercus cellulosae) in naturally parasitized, immunized hogs. Exp Parasitol.. 1983;56:327-328.[Medline] [Order article via Infotrieve]
7.
Del Brutto OH. Cysticercosis and cerebrovascular
disease: a review. J Neurol Neurosurg
Psychiatry.. 1992;55:252-254.
8.
Cantu C, Barinagarrementeria F. Cerebrovascular
complications of neurocysticercosis: clinical and neuroimaging
spectrum. Arch Neurol.. 1996;53:233-239.
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