A 17‐year‐old male with chronic epilepsy status post remote functional hemispherectomy

Differential Regulation of Wnt/β-catenin Signaling in Acute and Chronic Epilepsy in Repeated Low Dose Lithium-Pilocarpine Rat Model of Status Epilepticus

Predictors of Drug-Resistant Epilepsy After Perinatal Stroke.

The surgical treatment of chronic pharmacoresistant epilepsies is increasing rapidly. Although several studies have reported on histopathological findings in temporal lobe epilepsy, little is known about the surgical pathology of other seizure disorders. Here we report the histopathological findings in 63 consecutive surgical specimens of patients who were operated for chronic pharmacoresistant epileptic seizures other than temporal lobe epilepsy (37 corticectomies, 19 functional hemispherectomies, 5 lobectomies, 1 multilobectomy, and 1 frontal lobe deafferentiation combined with a temporal lobectomy). There were structural lesions in 85.7% of the specimens. In 16 cases (25.4%) the predominant lesions were malformative (focal glioneuronal hamartias and hamartomas, vascular malformations, abundant ectopic neurons in the white matter, microgyria, and arachnoid cyst). Lesions indicating pre- or perinatal necrosis such as porencephaly, ulegyria, and congenital hemiatrophy were present in 7 cases (11.1%). Twelve specimens (19.0%) contained low-grade neoplasms (7 gangliogliomas, 3 astrocytomas, 1 oligodendroglioma and 1 oligoastrocytoma). There were 3 cases of Rasmussen encephalitis, 1 specimen with atrophy and gliosis due to previous herpetic encephalitis and 1 case with an old abscess wall. Posttraumatic or postoperative changes were the predominant finding in 7 specimens (11.1%). In 7 patients there were only nonspecific changes such as cortical atrophy and gliosis or old hemorrhage. No structural alterations were identified in 9 specimens (14.3%). The findings suggest that the structural lesions observed in the great majority of the specimens were closely related to the pathogenesis of intractable seizures.

Purpose of ReviewSudden Unexpected Death in Epilepsy (SUDEP) is the commonest cause of epilepsy-related premature mortality in people with chronic epilepsy. It is the most devastating epilepsy outcome. We describe and discuss risk factors and possible pathophysiological mechanisms to elucidate possible preventative strategies to avert SUDEP.Recent FindingsSudden death accounts for a significant proportion of premature mortality in people with epilepsy compared to the general population. Unmodifiable risk factors include a history of neurologic insult, younger age of seizure-onset, longer epilepsy duration, a history of convulsions, symptomatic epilepsy, intellectual disability, and non-ambulatory status. Modifiable risk factors include the presence of convulsive seizures, increased seizure frequency, timely and appropriate use of antiseizure medications, polytherapy, alcoholism, and supervision while sleeping. Pathophysiology is unclear, but several possible mechanisms such as direct alteration of cardiorespiratory function, pulmonary impairment, electrocerebral shutdown, adenosine dysfunction, and genetic susceptibility suggested.SummaryMethods to prevent SUDEP include increasing awareness of SUDEP, augmenting knowledge of unmodifiable risk factors, obtaining full seizure remission, addressing lifestyle factors such as supervision and prone positioning, and enacting protocols to increase the detection of and intervention for SUDEP. Further studies are required to characterize precisely and comprehensively SUDEP risk factors and pathophysiological drivers and develop evidence-based algorithms to minimize SUDEP in people with epilepsy.

OBJECTIVESDepression is a common psychiatric complication of temporal lobe epilepsy. This study examined the effect of depressed mood on neuropsychological performance among patients with chronic temporal lobe epilepsy.METHODSSeventy consecutive surgery...

The aim of the research was to study the wide range of anticonvulsant effects of new 3- and 4-benzoylpyridines oxime derivatives in comparison with the reference drug valproic acid, it included assessment of motor and EEG convulsive state manifestations and epileptic status. To identify the most effective compound we studied the anticonvulsant effects in the models of generalized convulsions caused by maximal electroshock seizure test and subcutaneous administration of pentylenetetrazole. Later, the most active compound was studied in the models of chronic cobalt-induced epilepsy and epileptic status caused by neurotoxin d, l-homocysteine thiolactone. The original compounds prevent convulsions and protect 100% of animals against death in a dose-dependent manner in the maximal electroshock seizure test with superiority over valproic acid. In the pentylenetetrazole epilepsy model the compounds decrease the latent period of the first clonic seizure onset. The leader compound GIZH-298 (60 mg/kg) has a pronounced anticonvulsant effect on primary and, especially, on secondary epileptic foci in the cobalt-induced epilepsy model that generates seizure activity in various brain structures with a predominant effect in the cortex and hypothalamus. GIZH-298 (60 mg/kg, 50 min after administration) completely eliminates the secondary-generalized tonic-clonic seizures (SGTCS) and protects 100% of animals against death in the stable stage of the epileptic status caused by the administration of d, l-homocysteine thiolactone. Valproic acid (100 mg/kg) does not fully eliminate the SGTCS and protects against death only 71% of animals. 3- and 4-benzoylpyridine oxime derivatives have pronounced anticonvulsant activity with superiority over valproic acid.

The role for ketogenic diets in epilepsy and status epilepticus in adults

Rasmussen’s encephalitis (RE) is a rare, devastating neurological condition characterized by chronic unihemispheric brain inflammation, refractory epilepsy, and progressive neurological decline and hemiplegia with an etiology that remains elusive and a pediatric-skewed epidemiology. The deleterious nature of RE on the patient’s neurocognitive development necessitates early medical intervention. RE is diagnosed on the basis of clinical features, MRI, EEG and biopsy obtained after surgery. While medical management often proves ineffective, surgical intervention has shown durable seizure freedom and control. This review comprehensively explores the surgical techniques in the management of RE including the steps involved in modified functional hemispherectomy, peri-insular, vertical-parasagittal and endoscopic hemispherotomies. We have summarized how each procedure aims to disconnect the affected hemisphere from the healthy hemisphere through different corridors of approach. Hemidecortication procedures offer good functional and cognitive outcomes overall despite the expected hemianopia, hemiplegia and loss of fine motor skills. We also review the importance of selecting appropriate candidates for surgery, as well as comprehensive pre- and postoperative management, along with the most likely outcomes of surgery.