Benign Childhood Epilepsy with Centrotemporal Spikes: An Ictal EEG

Abstract

Benign childhood epilepsy with centrotemporal spikes (BECTS) is common during childhood, but there are few reports in the literature recording the EEG during a seizure. We studied an 8-year-old boy with oropharyngeal seizures during wakefulness and sleep. Both his neuropsychomotor development and neurological examination were normal. While awake, the subjects's electroencephalogram (EEG) showed normal background activity and epileptiform activity characterized by spikes in the temporal regions (mid and anterior), central region of the right cerebral hemisphere and in the median central and parietal regions. During sleep, his EEG recorded an epileptic seizure that lasted 46 seconds. In the initial phase, the EEG showed an increase in the number of spikes with higher potential in the median central and parietal regions, followed by slow waves associated with the increase in slow waves in the right hemisphere. This was followed by a brief decrease in amplitude of the background activity, and then by rhythmic, diffuse discharges predominantly in the right centrotemporal region, of sharp waves at 12-13 Hz, with increasing potential. Slow waves of high amplitude then occurred for 5 seconds, and finally very high potential spikes reappeared in the central and temporal regions of the right cerebral hemisphere with normalization of the background activity. During these critical phases of the EEG, clonic lip movements and pouting could be observed with the mouth locked shut, associated with "throat noises," but there were no other motor manifestations. The child did not wake up during the seizure and there were no postictal signs or symptoms. Although there are some aspects in common in recordings of BECTS seizures, such as a reduction in amplitude followed by rhythmic discharges of increasing amplitude, differences exist that possibly correspond to the diverse characteristics of the electrical generators.

Localization of ictal pouting in frontal lobe epilepsy: A case report

“…Because of its anatomical complexity and interconnectivity, mesial FLE involving ACC presents with various clinical features, including complex stereotypic movements (in particular, thrashing, kicking, grasping, and running with or without vocalization), behavioral disturbances (motor or verbal aggression), paranoid delusions, and personality changes (autistic, obsessive–compulsive, and self-mutilating behavior). Fear with or without a matching facial expression and laughter without mirth may be early manifestations of mesial frontal lobe seizures [9], [12], consistent with reports that negative emotional stimuli activate the mesial prefrontal lobe and ACC [13]. The IP semiology is a behavioral manifestation rather than a motor manifestation and is presumed to be a response to stimuli with an affective or a cognitive component [3].…”

Benign Rolandic epilepsy: widespread increases in connectivity in a focal epilepsy syndrome

“…Volume conduction contributes to coherence (Thatcher et al, 2008; Thatcher, 2008, 2012a). The cross‐spectrum is the sum of the in‐phase potentials ( i.e .…”

“…During sleep, the seizures are often convulsive in type. From the published ictal recordings, it can be inferred that at least the majority of the generalized tonic-clonic seizures follow Rolandic activation and are therefore secondary generalized tonic-clonic seizures (Dalla Bernardina and Tassinari, 1975;Clemens, 2002;Panayiotopoulos et al, 2008;Tedrus et al, 2009). The EEG features of BRE consist of centrotemporal spikes (CTS), focal, high-amplitude (usually > than 150 V) central or mid-temporal surface negative spike or sharp waves of ∼ 70-80 milliseconds with a following slow wave (figure 1) (Kellaway, 2000).…”

“…During sleep, the seizures are often convulsive in type. From the published ictal recordings, it can be inferred that at least the majority of the generalized tonic‐clonic seizures follow Rolandic activation and are therefore secondary generalized tonic‐clonic seizures (Dalla Bernardina and Tassinari, 1975; Clemens, 2002; Panayiotopoulos et al, 2008; Tedrus et al, 2009).…”

Comorbidade Epilepsia e TDAH

“…(anteriores e médias), centrais e parietais, unilaterais, seguido do decréscimo da freqüência da atividade e reaparecimento da atividade interictal, não sendo observado um alentecimento focal pós crítico 30,44,45 .…”