Postictal Generalized Electroencephalography Suppression Research Articles

Asymmetrical cortical surface area decrease in epilepsy patients with postictal generalized electroencephalography suppression.

Postictal generalized electroencephalographic suppression is a possible electroencephalographic marker for sudden unexpected death in epilepsy. We aimed to investigate the cortical surface area abnormalities in epilepsy patients with postictal generalized electroencephalographic suppression. We retrospectively included 30 epilepsy patients with postictal generalized electroencephalographic suppression (PGES+), 21 epilepsy patients without postictal generalized electroencephalographic suppression (PGES-), and 30 healthy controls. Surface-based analysis on high-resolution T1-weighted images was conducted and cortical surface areas were compared among the three groups, alongside correlation analyses with seizure-related clinical variables. Compared with PGES- group, we identified reduced surface area in the bilateral insula with more extensive distribution in the right hemisphere in PGES+ group. The reduced right insular surface area was associated with younger seizure-onset age. When compared with healthy controls, PGES- group presented reduced surface area in the left caudal middle frontal gyrus; PGES+ group presented more widespread surface area reductions in the right posterior cingulate gyrus, left postcentral gyrus, middle frontal gyrus, and middle temporal gyrus. Our results suggested cortical microstructural impairment in patients with postictal generalized electroencephalographic suppression. The significant surface area reductions in the insular cortex supported the autonomic network involvement in the pathology of postictal generalized electroencephalographic suppression, and its right-sided predominance suggested the potential shared abnormal brain network for postictal generalized electroencephalographic suppression and sudden unexpected death in epilepsy.

Risks and predictive biomarkers of sudden unexpected death in epilepsy patient.

The current review updates our knowledge regarding sudden unexpected death in epilepsy patient (SUDEP) risks, risk factors, and investigations of putative biomarkers based on suspected mechanisms of SUDEP. The overall incidence of SUDEP in adults with epilepsy is 1.2/1000 patient-years, with surprisingly comparable figures in children in recently published population-based studies. This risk was found to decrease over time in several cohorts at a rate of -7% per year, for unknown reasons. Well established risk factors include frequency of generalized tonic-clonic seizures, while adding antiepileptic treatment, nocturnal supervision and use of nocturnal listening device appear to be protective. In contrast, recent data failed to demonstrate the predictive value of heart rate variability, periictal cardiorespiratory dysfunction, and postictal generalized electroencephalography suppression. Preliminary findings suggest that brainstem and thalamic atrophy may be associated with a higher risk of SUDEP. Novel experimental and human data support the primary role of generalized tonic-clonic seizure-triggered respiratory dysfunction and the likely contribution of altered brainstem serotoninergic neurotransmission, in SUDEP pathophysiology. Although significant progress has been made during the past year in the understanding of SUDEP mechanisms and investigation of numerous potential biomarkers, we are still missing reliable predictors of SUDEP beyond the well established clinical risk factors.

Postictal electroencephalographic (EEG) suppression: A stereo-EEG study of 100 focal to bilateral tonic-clonic seizures.

We aimed to describe intracerebral aspects of postictal generalized electroencephalography suppression (PGES) following focal to bilateral tonic-clonic ("secondarily generalized tonic-clonic") seizures (GTCS) recorded using stereoelectroencephalographic (SEEG), and to correlate these with electroclinical features. Three independent observers scored semiologic and SEEG features. Patient and epilepsy characteristics were collected. Descriptive statistics and multivariate analysis were performed. The operational definition of PGES on SEEG used strict criteria (absence of visible signal at 20μV/mm amplitude, in all readable channels). Postictal regional suppression (RS) was identified if only a subset of implanted electrodes showed absence of signal. We evaluated 100 seizures in 52 patients. Interobserver agreement was good (κ 0.72 for clinical features and 0.73 for EEG features). PGES was present in 27 of 100 and RS without PGES present in 42 of 100 seizures. Region of RS included epileptogenic zone in 43 of 51 (86%). No effect of sampling (multilobar or bilateral exploration) was seen. Oral tonicity (mouth opening and/or tonic vocalization during the tonic phase of GTCS) was associated with the presence of PGES (P=0.029; negative predictive value [NPV] 0.91). Bilateral upper limb extension during the tonic phase correlated with PGES (P=0.041; NPV 0.85). Association of both oral tonicity and bilateral upper limb extension had a high NPV of 0.96. SEEG recordings confirm true absence of signal during postictal EEG suppression. PGES is unlikely when both upper limb extension and oral tonicity are absent. We hypothesize that bilateral tonic seizure discharge at bulbar level brainstem regions is associated with the production of oral signs and may relate to mechanisms of PGES.

Cortical thinning in epilepsy patients with postictal generalized electroencephalography suppression.

The aim was to investigate the brain microstructural abnormalities in epilepsy patients with postictal generalized electroencephalographic suppression (PGES) using a cortical surface-based analysis. According to the video-electroencephalography records of epilepsy patients with generalized convulsive seizures, 30 patients with PGES (PGES+) and 21 patients without PGES (PGES-) were recruited. High-resolution T1-weighted images were acquired from each patient and 30 matched healthy control subjects. Cortical thickness was compared amongst the three groups using FreeSurfer software. Patients with PGES showed reduced cortical thickness in the right paracentral lobule, inferior parietal lobule, supramarginal gyrus and middle temporal lobe compared with patients without PGES. In relation to healthy control subjects, the PGES+ group presented reduced cortical thickness in the right superior parietal lobule and supramarginal gyrus, whilst the PGES- group presented reduced cortical thickness in the left precuneus, precentral gyrus, lateral occipital gyrus, parahippocampal gyrus, superior parietal lobule and right caudal middle frontal gyrus. Patients with PGES exhibited characteristic brain microstructural abnormalities, corroborating the PGES mechanisms at the brain level. The right-sided predominance of the detected PGES-related cortical thinning was the same as that of sudden unexpected death in epilepsy (SUDEP) cases and patients at high risk for SUDEP, implying that PGES and SUDEP may share a common abnormal brain substrate that is involved in the pathophysiology of these conditions.

Characteristics of postictal generalized EEG suppression in children

Although the pathophysiologic mechanism of sudden unexpected death in epilepsy (SUDEP) is unknown, autonomic dysfunction is thought to be the most likely. It has been hypothesized that respiratory depression resulting in SUDEP may be secondary to postictal generalized electroencephalography suppression (PGES). We sought to determine the characteristics of PGES in children. This included whether PGES was associated with ictally mediated autonomic changes and potential increased risk of SUDEP. Children admitted to our Pediatric Epilepsy Monitoring Unit between 3/2009 and 10/2011 were prospectively recruited. Clinical and electrophysiological data from children with PGES were compared to those without PGES. Data included the occurrence of peri-ictal tachycardia, bradycardia, and hypoxemia. Potential SUDEP risk was assessed using SUDEP-7 Inventory scores. Thirty seven children with 168 seizures were analyzed. PGES was observed following 27/168 (16.1%) seizures in 12/37 (32.4%) children. Only primary and secondarily generalized tonic clonic seizures were marked by PGES. PGES was significantly associated with peri-ictal tachycardia (p=0.019) and hypoxemia (p=0.005). Children with PGES had significantly higher SUDEP-7 Inventory scores than those without PGES (4.2 ± 1.3 versus 2.8 ± 1.4, p=0.007). SUDEP-7 scores were not significantly different between children with and without peri-ictal tachycardia (3.4 ± 1.3 versus 2.5±1.6, p=0.12), bradycardia (4 ± 2 versus 2.9 ± 1.4, p=0.45), or hypoxemia (3.4 ± 1.5 versus 2.4 ± 1.3, p=0.051). Based on our data, PGES is not rare in children. Children with PGES may be at greater risk for SUDEP as measured by the SUDEP-7 Inventory.