Epilepsia
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Twiddler's syndrome is the conscious or unconscious manipulation of implantable pulse generators (IPGs) or associated wire systems by the patient. Most commonly, this complication has been documented in patients with cardiac pacemakers, but there are reported cases in patients with deep brain stimulators. Twisting of stimulator systems results in dislodgement or damage to leads and loss of stimulation to the desired target. ⋯ Surgical revision achieved the desired stimulation and effects. On 4-month follow-up the deep brain stimulator remained stable and untwisted; however, it was subsequently removed in the fourth month because of infection at the extension site. In conclusion, twiddler's syndrome is a rare complication occurring in patients with deep brain stimulator implants and warrants awareness among neurologic and neurosurgical epilepsy specialists.
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Disrupted sleep patterns in children with epilepsy and their parents are commonly described clinically. A number of studies have shown increased frequency of sleep disorders among pediatric epilepsy patients; however, few have characterized the association between epilepsy and parental sleep quality and household sleeping arrangements. The purpose of this study was to explore the effect of pediatric epilepsy on child sleep, parental sleep and fatigue, and parent-child sleeping arrangements, including room sharing and cosleeping. ⋯ Pediatric epilepsy can significantly affect sleep patterns for both the affected child and his or her parents. Parents frequently room share or cosleep with their child, adaptations which may have detrimental effects for many households. Clinicians must not only be attentive to the sleep issues occurring in pediatric patients with epilepsy, but also for the household as a whole. These data provide evidence of a profound clinical need for improved epilepsy therapeutics and the development of nocturnal seizure monitoring technologies.
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In children with symptomatic or idiopathic focal epilepsies, their disease may evolve into an epileptic encephalopathy related to continuous spike and wave during slow sleep (CSWS) or electrical status epilepticus during slow sleep (ESES). ESES syndrome implies serious risks of neuropsychologic impairment, and its treatment has frequently been disappointing. The aim of this study is to present our experience using sulthiame as add-on treatment in 53 patients with ESES syndrome that was refractory to other antiepileptic drugs (AEDs). ⋯ We understand that sulthiame may be effective as add-on treatment in children with ESES syndrome.
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People with epilepsy are more likely than healthy people to experience comorbidities and complications in various medical situations. However, the prevalence of postoperative complications, mortality, and use of medical resources in surgical patients with epilepsy has not been studied. The purpose of this study is to examine whether epilepsy is an independent risk factor for postoperative adverse outcomes of patients receiving major surgery. ⋯ Stroke was identified as the most significant postoperative complication for surgical patients with epilepsy. Patients, especially those with previous hospitalization or emergency visits due to the disease, confronted significantly higher postoperative complication rates, and consumed more in-hospital medical resources without differences in overall mortality rates. Further revision of health care standards to provide early recognition of postoperative complications and better management for surgical patients with epilepsy is needed.
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To date, magnetic resonance imaging (MRI)-based studies of the cerebral cortex in mesial temporal lobe epilepsy (MTLE) have focused primarily on investigating cortical volume and thickness. However, volume is a composite of surface area and thickness, each reflecting distinct neurobiologic and genetic processes. The goal of this study was to investigate cerebral cortex (1) surface area, (2) surface geometric distortion, and (3) thickness in MTLE with hippocampal sclerosis (HS). ⋯ Our findings indicate that contraction in surface area, rather than cortical thinning, explains ipsilateral mesial and anterior temporal lobe atrophy in patients with MTLE with HS. Furthermore, the alterations in surface geometry indicate folding abnormality involving the same regions. Cortical surface changes may represent sequelae of the disease or deviant cortical development.