Trial Information

Analysis of the Occurrence of Perilesional Edema and Seizures in Patients With Inactive Cysticercosis

Seizures are the most common clinical manifestation of cerebral cysticercosis and occur in
the presence of viable, dying, and calcified or non-calcified dead cysts. How calcified
cysts provoke seizures is not known but recent observations demonstrated edema around some
calcified lesions at the time of seizure activity and disappearance during periods when
seizures were not occurring. Edema associated with foci in idiopathic epilepsy is highly
unusual so that this observation suggests that the mechanism(s) associated with calcified
cysts is unique. Documenting and understanding this phenomenon is important for a number of
reasons. First, although by definition these lesions are inactive, e.g., not living larvae
and do not require anti-parasitic treatment, they are frequently mistaken for active lesions
and patients undergo unnecessary treatment. Second, a likely reason for perilesional edema
is intermittent antigen release and subsequent host immune response resulting in
inflammation and edema. If proved, then the treatment for this would not only involve
suppression of seizure activity with anti-seizure medication but also the use of
anti-inflammatory medications such as corticosteroids. The present protocol will
systematically assess the presence of edema associated with calcified lesions at the time of
seizure activity and attempt to determine why some calcified lesions in the same patient are
foci of seizures while others are clinically silent. There are three related but separate
questions. 1) What is the most sensitive MRI technique that can detect edema around
calcified or inactive lesions? It is essential to determine the most sensitive methods
initially because the use of insensitive techniques will lead to inaccurate assessments of
which lesions are prone to lead to seizure activity and how many patients are affected. 2)
How common is perilesional edema around calcified or inactive lesions associated with
seizure activity? 3) What factors determine which lesions are prone to cause seizure
activity? 4) Can perilesional edema be effectively treated or prevented? 5) Can
perilesional edema be treated? We have reported from long term longitudinal studies in a
handful of patients that only some of many lesions seem to be associated with seizure
activity and edema.