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VIEWS & REVIEWS: T. E. Nash, O. H. Del Brutto, J. A. Butman, T. Corona, A. Delgado-Escueta, R. M. Duron, C. A.W. Evans, R. H. Gilman, A. E. Gonzalez, J. A. Loeb, M. T. Medina, S. Pietsch-Escueta, E. J. Pretell, O. M. Takayanagui, W. Theodore, V. C.W. Tsang, and H. H. Garcia Calcific neurocysticercosis and epileptogenesis Neurology 2004; 62: 1934-1938 [Abstract] [Full text] [PDF]

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Calcific neurocysticercosis and epileptogenesis

Walter Oleschko Arruda, MD   (7 July 2004)

Reply to Arruda

Theodore E. Nash, MD   (7 July 2004)

Calcific neurocysticercosis and epileptogenesis 7 July 2004
Walter Oleschko Arruda, MD, Universidade Federal do Parana Rua Goncalves Dias 713, 80240-340 Curitiba, Brazil Send Correspondence to journal: Re: Calcific neurocysticercosis and epileptogenesis warruda{at}hc.ufpr.br Walter Oleschko Arruda, MD	I read with great interest the article by Nash et al [1], where the authors cite only one retrospective study performed in Brazil. [2] A prior prospective study with 210 patients living in urban area was done and showed that neurocysticercosis accounted for 27.1% of cases [3]---a much higher number. Furthermore, another study where the cranial computed tomography (CT) scan findings of 2,000 cases of mild head trauma in Curitiba, Southern Brazil, showed that several calcifications (2.4%) (probably neurocysticercosis (NC) in most cases) was an incidental finding, because they were not found in patients with epilepsy. [4] We also reviewed reviewed 3093 CT scans out of 2554 randomized neurological patients from our Service evaluated during a one year period. NC was diagnosed in 236 patients based on tomographic criteria. Two-hundred and nineteen (92.8%) patients had the inactive form of NC, 195 (89%) had isolated intraparenchymal calcifications, and 24 had calcifications plus hydrocephalus. Active forms were observed in 14 patients: eight with degenerating cysts; four with viable cysts; one with intraventricular cyst; and one with racemose form. Three patients had both forms, active (cysts) and inactive (calcifications). I agree with the authors that brain calcifications due to cysticercosis may be related to an increased rate of epilepsy where cysticercosis is still endemic. In addition, most of our knowledge about the actual casual relationship between NC (in special the calcified forms, without edema) is based on anecdotal reports and serial observations. Prospective and controlled studies are necessary to determine the natural history and pathophysiology of this condition. More importantly, the complete eradication of the complex taeniasis/cysticercosis should be considered a priority in public health policy in all countries where this condition is still endemic. References 1. Nash TE, Del Brutto OH , Butman TA et al. Calcific neurocysticercosis and epileptogenesis. Neurology 2004; 62: 1934-1938 2. Trentin AP, Teive HA, Tsubouchi MH, de Paola L, Minguetti G. [Tomographic findings in 1000 consecutive patients with antecedents of epileptic seizures.] Arq Neuropsiquiatr. 2002; 60: 416–419. 3. Arruda WO. Etiology of epilepsy. A prospective study of 210 cases. Arq Neuropsiquiatr. 1991;49:251-4 4. Bordignon KC, Arruda WO. CT scan findings in mild head trauma: a series of 2,000 patients. Arq. Neuro-Psiquiatr. 2002; 60:204-210. 5. Narata AP, Arruda WO, Uemura E et al. Neurocysticercosis: a CT- scan study in a series of neurological patients. Arq. Neuro- Psiquiatr.1998; 56(2):245-249. The author Walter Oleschko Arruda, MD, has no conflict of interest
Reply to Arruda 7 July 2004
Theodore E. Nash, MD, Head, Gastrointestinal Parasites Section NIH, DHHS, 9000 Rockville Pike, Bldg. 4 Rm B1-06, Bethesda, MD, 20892 Send Correspondence to journal: Re: Reply to Arruda tnash{at}niaid.nih.gov Theodore E. Nash, MD	One of the types of data supporting the role of calcified cysticercal granulomas as a cause of seizures in exposed populations is their presence as the only abnormality in particular populations with seizures or epilepsy. As seen in the published Table [1], calcifications are frequently present in endemically exposed populations with seizures, epilepsy, or both and is often the most common finding. We thank Dr. Arruda for pointing out additional studies [2,3], including his own that were unintentionally not included in our review. These studies agree with our conclusion that indicate a high prevalence of typical calcified lesions in patients with epilepsy. Calcifications are common in other populations from endemic regions not known to suffer from seizures. [4,5] Degenerating cysts are a known cause of seizures in endemic population and was not the focus of our review. The body of the review provides additional more specific reasons that support calcified granulomas as foci of seizures. [1] Dr. Arruda agrees with our recommendations [1] that more definitive studies are required to determine the natural history, importance and pathophysiology of seizures associated with calcific neurocysticercosis. References 1. Nash TE, Del Brutto OH, Butman JA et al. Calcific neurocysticercosis and epileptogenesis. Neurology 2004;62:1934-1938. 2. Trentin AP, Teive HA, Tsubouchi MH, de Paola L, Minguetti G. Tomographic findings in 1000 consecutive patients with antecedents of epileptic seizures. Arq Neuropsiquiatr 2002;60:416-419. 3. Arruda WO. Etiology of epilepsy. A prospective study of 210 cases. Arq Neuropsiquiatr 1991;49:251-254.. 4. Bordignon KC, Arruda WO. CT scan findings in mild head trauma: a series of 2,000 patients. Arq Neuropsiquiatr 2002;60:204-210. 5. Narata AP, Arruda WO, Uemura E, et al. Neurocysticercosis. A tomographic diagnosis in neurological patients. Arq Neuropsiquiatr 1998;56:245-249.