Calcific neurocysticercosis and epileptogenesis
Abstract
Neurocysticercosis is responsible for increased rates of seizures and epilepsy in endemic regions. The most common form of the disease, chronic calcific neurocysticercosis, is the end result of the host’s inflammatory response to the larval cysticercus of Taenia solium. There is increasing evidence indicating that calcific cysticercosis is not clinically inactive but a cause of seizures or focal symptoms in this population. Perilesional edema is at times also present around implicated calcified foci. A better understanding of the natural history, frequency, epidemiology, and pathophysiology of calcific cysticercosis and associated disease manifestations is needed to define its importance, treatment, and prevention.
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Received: June 20, 2003
Accepted: December 9, 2003
Published online: June 7, 2004
Published in issue: June 8, 2004
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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
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.