Objective: Anti-seizure medications (ASMs) are discontinued in the course of intracranial EEG (iEEG) monitoring for presurgical evaluation. The ASM withdrawal facilitates an emergence of seizures but may also precipitate seizure clusters (SC) and status epilepticus (SE). The aim of this study was to compare the rates of SC and SE during the ultra-rapid withdrawal (URW) and rapid withdrawal (RW) of ASMs during iEEG.
Methods: We performed a retrospective observational study of all consecutive patients with drug resistant epilepsy who completed iEEG at our comprehensive epilepsy center from 2012-2018. SC was defined as three or more seizures in 24 h with a return to baseline between the events. SE was defined as ≥ 5 min of clinical seizure or ≥ 10 min of ictal electrographic activity or series of seizures with no return to the neurological baseline between the events.
Results: Of 107 patients who completed iEEG with intracranial grid or strip electrodes, 46 (43%) were male. Median age at the time of iEEG was 35.4 years (interquartile range [IQR], 26.4 - 44.9). Ninety patients (84.1%) had all AEDs held on admission, while 16 patients (15%) underwent a rapid taper. The median time to first seizure was 15.1 (8.2 - 22.6) h. Sixty-two patients (57.9%) developed SC, while 10 (9.4%) developed SE. Twenty-six patients (36.1%) with these complications required intravenous lorazepam or other rescue ASMs, while the remaining patients had spontaneous resolution of seizures; intubations were not required. While there were differences in the proportions in patients who experienced SC, SE, or neither in the URW and RW groups, these differences were not significant at the 0.05 alpha level.
Significance: Ultra-rapid and rapid ASM withdrawal are accompanied by SC and SE the majority of which terminate spontaneously. These data support the use of either approach of the medication taper for seizure provocation in iEEG.
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http://dx.doi.org/10.1016/j.eplepsyres.2021.106756 | DOI Listing |
Pharmacol Rep
December 2024
Department of Experimental and Clinical Pharmacology, Centre for Preclinical Research and Technology (CEPT), Medical University of Warsaw, Banacha 1B, Warszawa, 02-097, Poland.
Sudden cessation of the drug can cause withdrawal syndrome, discontinuation syndrome, or rebound effect. The common feature of these phenomena is a quick onset, usually limited duration depending on the drug's half-life and remission after restarting the therapy. They are characterized by varying clusters of somatic, autonomic, and psychiatric symptoms.
View Article and Find Full Text PDFAm J Hum Genet
December 2024
Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, Guangdong, China. Electronic address:
Neurotherapeutics
December 2024
Department of Neurology and Neuroscience Brain Institute University of Virginia, School of Medicine, Health Sciences Center, Box 801330, Charlottesville, VA 22908-1330, USA. Electronic address:
Generalized Convulsive status epilepticus (SE) is a neurological emergency because prolonged convulsions can cause respiratory compromise and neuronal injury. Compromised GABA-mediated inhibition is a defining feature of SE, and many current therapies are benzodiazepines, which are allosteric modulators of GABA-A receptors. Many patients with medically refractory epilepsy are at risk for SE.
View Article and Find Full Text PDFRinsho Shinkeigaku
December 2024
Department of Neurology, Nakamura Memorial Hospital.
The patient was a 69-year-old right-handed woman. She had sensory aphasia, and the brain MRI revealed a subacute phase hemorrhage in the left subcortical temporal lobe. We speculated that the patient had post-ictal aphasia due to symptomatic epileptic seizures associated with cerebral hemorrhage.
View Article and Find Full Text PDFFront Netw Physiol
November 2024
Yale Comprehensive Epilepsy Center, Department of Neurology, Yale School of Medicine, New Haven, CT, United States.
To date, there is no neurophysiologic or neuroimaging biomarker that can accurately delineate the epileptogenic network. High-frequency oscillations (HFO) have been proposed as biomarkers for epileptogenesis and the epileptogenic network. The pathological HFO have been associated with areas of seizure onset and epileptogenic tissue.
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