Interictal epileptiform discharges show distinct spatiotemporal and morphological patterns across wake and sleep.

Presurgical evaluation of mesial temporal and neocortical focal pharmacoresistant epilepsy patients using intracranial EEG recordings has led to the generation of extensive data on interictal epileptiform discharges, located within or remotely from seizure onset zones. In this study, we used this data to investigate how interictal epileptiform discharges are modulated and how their spatial distribution changes during wake and sleep and analysed the relationship between these discharge events and seizure onset zones. Preoperative evaluation data from 11 adult patients with focal pharmacoresistant epilepsy were extracted from the Epilepsiae database. Interictal epileptiform discharges were automatically detected during wakefulness and over several hours of continuous seizure-free sleep (total duration of EEG recordings:106.7 h; mean per patient: 9.7 h), and analysed across four brain areas (mesial temporal, lateral neocortical, basal cortical and the temporal pole). Sleep stages were classified manually from scalp EEG. Discharge events were characterized according to their rate and morphology (amplitude, sharpness and duration). Eight patients had a seizure onset zone over mesial areas and three patients over lateral neocortical areas. Overall, discharge rates varied across brain areas during wakefulness and sleep [wake/sleep stages × brain areas interaction; Wald χ 2(df = 6) = 31.1, P < 0.0001]. N2-N3 non-rapid eye movement sleep increased interictal epileptiform discharges in mesial areas compared with wakefulness and rapid eye movement sleep (P < 0.0001), and to other areas (P < 0.0001 for all comparisons). This mesial pattern was observed both within and outside of seizure onset zones. During wakefulness, the rate of interictal epileptiform discharges was significantly higher than during N2-N3 non-rapid eye movement sleep (P = 0.04), and rapid eye movement sleep (P = 0.01) in lateral neocortical areas (referred to as lateral neocortical pattern), a finding that was more pronounced in seizures onset zones (P = 0.004). The morphological characteristics of the discharge events were modulated during wakefulness and sleep stages across brain areas. The effect of seizure onset zones on discharge morphology was conditioned by brain area and was particularly marked in temporal pole areas. Our analysis of discharge patterns in relation to cerebral localization, vigilance state and the anatomical affiliation of seizure onset zones revealed the global and local aspects of the complex relationship between interictal discharges, sleep and seizure onset zones. This novel approach may lead to a better understanding of cognitive decline and responses to therapy, as well as to adaptation of surgical interventions for epileptic patients.

Zero-crossing patterns reveal subtle epileptiform discharges in the scalp EEG.

Clinical diagnosis of epilepsy depends heavily on the detection of interictal epileptiform discharges (IEDs) from scalp electroencephalographic (EEG) signals, which by purely visual means is far from straightforward. Here, we introduce a simple signal analysis procedure based on scalp EEG zero-crossing patterns which can extract the spatiotemporal structure of scalp voltage fluctuations. We analyzed simultaneous scalp and intracranial EEG recordings from patients with pharmacoresistant temporal lobe epilepsy. Our data show that a large proportion of intracranial IEDs manifest only as subtle, low-amplitude waveforms below scalp EEG background and could, therefore, not be detected visually. We found that scalp zero-crossing patterns allow detection of these intracranial IEDs on a single-trial level with millisecond temporal precision and including some mesial temporal discharges that do not propagate to the neocortex. Applied to an independent dataset, our method discriminated accurately between patients with epilepsy and normal subjects, confirming its practical applicability.

Autosomal recessive cortical myoclonic tremor and epilepsy: association with a mutation in the potassium channel associated gene CNTN2.

We characterize a consanguineous Egyptian family with an autosomal recessively inherited familial cortical myoclonic tremor and epilepsy. We used multipoint linkage analysis to map the causative mutation to a 12.7 megabase interval within 1q31.3-q32.2 with a log of odds score of 3.6. For further investigation of the linked region in an efficient and unbiased manner, we performed exome sequencing. Within the suspected region we identified a homozygous single base pair deletion (c.503_503delG) leading to a frameshift in the coding region of the sixth exon of CNTN2 alias TAG-1 (p.Trp168fs), which segregated in the respective family. Many studies point towards an important role of the CNTN2 product contactin 2 in neuronal excitability. Contactin 2, a glycosylphosphatidylinositol-anchored neuronal membrane protein, and another transmembrane protein called contactin associated protein-like 2 (CNTNAP2 alias CASPR2) are together necessary to maintain voltage-gated potassium channels at the juxtaparanodal region. CNTN2 knockout mice were previously reported to suffer from spontaneous seizures and mutations in the CNTNAP2 gene have been described to cause epilepsy in humans. To further delineate the role of CNTN2 in patients with epilepsy, we sequenced the coding exons in 189 Caucasian patients with epilepsy. No recessive mutation was detected and heterozygote carriers of rare CNTN2 variants do not seem to be predisposed to epilepsy. Given the severity of the mutation and the proposed function of the gene, we consider this mutation as the most likely cause for cortical myoclonic tremor and epilepsy in this family.

Use of magnetic resonance imaging in assessment of constrictive pericarditis: a Moroccan center experience.

BACKGROUND: The diagnosis of constrictive pericarditis continues to be a clinical challenge. Magnetic resonance imaging provides excellent visualization of the pericardium. The aim of our study is to clarify the contribution of this non invasive exploration in the diagnosis of constrictive pericarditis in our center. METHODS: we conducted a prospective study over a period of two years, since 2008, covering a series of patients (n = 11), mean age 44 ± 15 years, in whom constrictive pericarditis was suspected clinically and on transthoracic echocardiography. We studied its characteristics on magnetic resonance imaging. RESULTS: Magnetic resonance imaging confirmed the diagnosis showing pericardial thickening in all cases, measuring 8.2 +/- 2.6 mm on average, circumferential in 64%, and localized in 36%. The imaging data, particularly pericardial thickening and its topography, were confirmed by surgical exploration, and results were concordant in all cases. CONCLUSION: Magnetic resonance imaging is a powerful tool to establish constrictive pericarditis diagnosis.

QT interval dispersion pattern in patients with acute ischemic stroke: Does the site of infarction matter?

BACKGROUND: QT interval dispersion (QTD) is an independent predictor of outcome following acute neurological events. OBJECTIVES: To explore QTD patterns and their relation to the affected cerebral region in patients with acute ischemic stroke. METHODS: Thirty patients with first acute ischemic stroke (the first stroke the patients had ever experienced) (study group) and 30 healthy controls (control group) were enrolled. Patients underwent magnetic resonance imaging to confirm and localize cerebral damage. Patients in the study group were further subdivided according to the site of infarction into four subgroups - namely, cortical, subcortical, brain stem and cerebellar infarctions, as well as according to insular involvement. All included subjects underwent 12-lead electrocardiography to measure QTD and corrected QT dispersion (QTcD). RESULTS: In the study group, both QTD and QTcD on the first hospitalization day were significantly higher than in the control group (P<0.05 for both). Similarly, in the study group, both QTD and QTcD values on the first hospitalization day were significantly higher than the respective values on the third day (P<0.001 for both). No significant differences were found among the four territorial subgroups, or between right- and left-sided subgroups, regarding QT interval measurements, whether on the first or third day (P>0.05 for all). However, 'first-day' QTD and QTcD of patients with insular involvement were significantly higher than in those without such involvement (P<0.001 for both). CONCLUSIONS: Both QTD and QTcD increased significantly in patients with acute ischemic stroke during the first hospitalization day. This increase of 'first-day' QTD and QTcD was significantly higher in patients with insular involvement than in those without such involvement.

Pilomotor seizures associated with sequential changes in magnetic resonance imaging.

Piloerection is rarely described in seizures. This symptom has been most frequently observed in patients with temporal lobe epilepsy and is rarely the principal clinical feature of seizures. No specific etiology of epilepsy associated with pilomotor seizures has been reported. We present the first case of a patient who experienced sudden and transitory epilepsy with pilomotor seizures occurring several times a day for months, and associated with sequential changes of the left hippocampus demonstrated by magnetic resonance imaging. [Published with video sequences].