Epilepsia
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Investigate whether patients on vigabatrin demonstrated new-onset and reversible T(2)-weighted magnetic resonance imaging (MRI) abnormalities. ⋯ MRI abnormalities attributable to vigabatrin, characterized by new-onset and reversible T(2)-weighted hyperintensities and restricted diffusion in thalami, globus pallidus, dentate nuclei, brainstem, or corpus callosum were identified in 8 of 23 patients. Young age and relatively high dose appear to be risk factors.
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Posttraumatic epilepsy is a common complication of traumatic brain injury (TBI), occurring in up to 15-20% of patients with severe brain trauma. Trauma accounts for approximately 5% of chronic epilepsy in the community. Because it is a common condition, and because of the relatively short latency period between injury and onset of chronic seizures, posttraumatic epilepsy represents a good model to test antiepileptogenic therapies. ⋯ Furthermore, closed head injury often produces diffuse concussive injury, with shearing of axons and selective damage to vulnerable brain regions, such as the hippocampus. The clinical, neurophysiologic, imaging, and neuropathologic features or epileptogenicity differ between these alternate mechanisms. It is likely that better understanding of the subtypes of epilepsy resulting from brain trauma will be required to successfully identify antiepileptogenic therapies.
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A large number of animal models of traumatic brain injury (TBI) are already available for studies on mechanisms and experimental treatments of TBI. Immediate and early seizures have been described in many of these models with focal or mixed type (both gray and white matter damage) injury. Recent long-term video-electroencephalography (EEG) monitoring studies have demonstrated that TBI produced by lateral fluid-percussion injury in rats results in the development of late seizures, that is, epilepsy. ⋯ Moreover, despite the multiple preclinical pharmacologic and cell therapy trials, there is no information available describing whether these therapeutic approaches aimed at improving posttraumatic recovery would also affect the development of lowered seizure threshold and epilepsy. To make progress, there is an obvious need for information exchange between the trauma and epilepsy fields. In addition, the inclusion of epilepsy as an outcome measure in preclinical trials aiming at improving somatomotor and cognitive recovery after TBI would provide valuable information about possible new avenues for antiepileptogenic interventions and disease modification after TBI.
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To determine the electroclinical significance and histopathological correlates of cortical gamma-aminobutyric acid(A)(GABA(A)) receptor abnormalities detected in and remote from human neocortical epileptic foci. ⋯ Focal decreases of cortical GABA(A) receptor binding on PET may include cortical regions remote from the primary focus, particularly in patients with high seizure frequency, and these regions are commonly involved in rapid seizure propagation. Although these regions may not always need to be resected to achieve seizure freedom, a careful evaluation of cortex with decreased GABA(A) receptor binding prior to resection using intracranial EEG may facilitate optimal surgical outcome in patients with intractable neocortical epilepsy.
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The purpose of the present investigation was to quantify alterations in GABA(A) receptor density in vivo in rats subjected to amygdala kindling. ⋯ Both the GABA(A) receptor density (B(max)), and possibly also the blood-brain barrier transport of FMZ (V(Br)) are altered after kindling. Furthermore, this study indicates the feasibility of conducting PET studies for quantifying moderate changes in GABA(A) receptor density in a rat model of epilepsy in vivo.