BY SARAH OWENS
Recurrent seizures did not leave markers of cortical damage in patients with lifelong seizures caused by focal cortical dysplasia or cryptogenic epilepsy, according to a study of post-surgical brain tissue published online in the Annals of Neurology on August 30.
It has been a commonly held belief that recurrent seizures cause brain damage in regions involved in epileptogenesis that are remote from the primary site of injury. However, those assumptions are not supported by definitive clinical or experimental evidence, the study authors wrote.
"Despite the recurrence of thousands of focal seizures during a patient's lifetime, cortical areas that are involved in seizure generation show a normal structural appearance," the study authors, led by Laura Rossini, MSc, of the Carlo Besta Neurological Institute Foundation in Milan, Italy, wrote. "These findings suggest that seizure activity per se does not promote the expression of brain injury biomarkers, at least in the considered neocortical epilepsies."
For the study, researchers obtained postsurgical brain tissue from 20 patients with a lifelong history of seizures who underwent surgery for drug-resistant epilepsy at the Carlo Besta Neurological Institute Foundation and at the Claudio Munari Epilepsy Surgery Center at Niguarda Hospital in Milan, Italy. Of these patients, 16 had been diagnosed with focal cortical dsyplasia type II, showing disrupted cortical lamination, dysmorphic neurons, and balloon cells; and four had cryptogenic epilepsy, with no detectable structural lesions on imaging and neuropathological investigation.
The researchers used immunohistochemistry to evaluate the patients' brain tissue samples, looking for markers of brain tissue damage, including neuronal paucity, extended gliosis, presence of inflammatory molecules/cells, and protein extravasation. For patients with focal cortical dysplasia type-II, they analyzed three areas: the core of the lesion, which had the most cytoarchitectural alterations; an adjacent transition area called the perilesion, which had only minimal alterations; and the normal-appearing cortex. For cryptogenic patients, they analyzed the whole normal-appearing cortex.
They found that while markers of tissue damage were detectable in the core of the lesion in patients with focal cortical dysplasia-II, particularly patients with the type IIb subtype, there were no markers of tissue damage detectable in the adjacent perilesional and nonlesional areas. Similarly, there were no markers of tissue damage in the whole normal-appearing cortices of patients with cryptogenic epilepsy.
Additionally, nine of the 20 patients also underwent stereo-electroencephalography, which measures electrical activity in the epileptogenic zone. The researchers attempted to correlate the neuropathological findings with patterns of electrical activity; however, they found that the epileptogenic zone included regions that did and did not have neuropathological alterations. This, the researchers concluded, suggests that structural alterations in the epileptogenic zone are not directly related to seizures.
Still, the study author concluded, the findings "should not reduce the need to treat seizures and their intrinsic comorbidity risks that interfere with normal physiological brain functions, causing serious social and psychological disability."
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