Different EEG frequency band synchronization during nocturnal frontal lobe seizures

OBJECTIVE In this article we describe the course of synchronization between different EEG channels during nocturnal seizures in one patient with nocturnal frontal lobe epilepsy (NFLE). METHODS The functional interactions between the different EEG channels during the nocturnal seizures were analyzed by means of the so-called synchronization likelihood (SL). SL is a measure of the dynamical interdependencies between a time series (EEG channel) and one or more other time series. In contrast to coherence, SL measures linear as well as non-linear interdependencies and it can do so as a function of time, making it suitable for non-stationary time series. RESULTS The main result of our single-patient study is the demonstration of a significant hyper-synchronization during NFLE seizures in the 8-12 Hz band which seems to be stopped by an increase in synchronization in the 0.5-4 Hz band, towards the end of each ictal episode. CONCLUSIONS We suggest that a self-inhibiting complex mechanism might be responsible for the termination of ictal episodes which might take place at the level of the cortical layers and might involve mainly pyramidal neurons. SIGNIFICANCE This study shows that advanced EEG analysis methods can help the current understanding of ictal manifestations of NFLE.

[1]  G Plazzi,et al.  Nocturnal frontal lobe epilepsy. A clinical and polygraphic overview of 100 consecutive cases. , 1999, Brain : a journal of neurology.

[2]  F. L. D. Silva,et al.  The cortical source of the alpha rhythm , 1977, Neuroscience Letters.

[3]  D. Contreras,et al.  The slow (< 1 Hz) oscillation in reticular thalamic and thalamocortical neurons: scenario of sleep rhythm generation in interacting thalamic and neocortical networks , 1993, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[4]  C. Stam,et al.  Nonlinear synchronization in EEG and whole‐head MEG recordings of healthy subjects , 2003, Human brain mapping.

[5]  D. Tucker,et al.  EEG coherency. I: Statistics, reference electrode, volume conduction, Laplacians, cortical imaging, and interpretation at multiple scales. , 1997, Electroencephalography and clinical neurophysiology.

[6]  F. L. D. Silva,et al.  Basic mechanisms of cerebral rhythmic activities , 1990 .

[7]  C. Marsden,et al.  Autosomal dominant nocturnal frontal-lobe epilepsy: genetic heterogeneity and evidence for a second locus at 15q24. , 1998, American journal of human genetics.

[8]  M Steriade,et al.  Spike-wave complexes and fast components of cortically generated seizures. II. Extra- and intracellular patterns. , 1998, Journal of neurophysiology.

[9]  G. Plazzi,et al.  Epileptic nocturnal wanderings. , 1995, Sleep.

[10]  C. Marsden,et al.  Autosomal dominant nocturnal frontal lobe epilepsy. A distinctive clinical disorder. , 1995, Brain : a journal of neurology.

[11]  J. Schlag,et al.  Basic sleep mechanisms , 1974 .

[12]  C. Stam,et al.  Synchronization likelihood: an unbiased measure of generalized synchronization in multivariate data sets , 2002 .

[13]  Theiler,et al.  Spurious dimension from correlation algorithms applied to limited time-series data. , 1986, Physical review. A, General physics.

[14]  G. Plazzi,et al.  From nocturnal paroxysmal dystonia to nocturnal frontal lobe epilepsy , 2000, Clinical Neurophysiology.

[15]  F. H. Lopes da Silva,et al.  Nonlinear dynamics of epileptic seizures on basis of intracranial EEG recordings , 2005, Brain Topography.

[16]  Cornelis J Stam,et al.  Non-linear EEG analysis in children with epilepsy and electrical status epilepticus during slow-wave sleep (ESES) , 2001, Clinical Neurophysiology.

[17]  C. Guilleminault,et al.  Episodic nocturnal wanderings responsive to anticonvulsant drug therapy , 1977, Annals of neurology.

[18]  A. Ballabio,et al.  A new locus for autosomal dominant nocturnal frontal lobe epilepsy maps to chromosome 1 , 2000, Neurology.

[19]  W. Trzeciak,et al.  Evidence for S284L Mutation of the CHRNA4 in a White Family with Autosomal Dominant Nocturnal Frontal Lobe Epilepsy , 2003, Epilepsia.

[20]  F. Vogel,et al.  Refinement of the localization of the gene for neuronal nicotinic acetylcholine receptor alpha 4 subunit (CHRNA4) to human chromosome 20q13.2-q13.3. , 1994, Genomics.

[21]  D. Tucker,et al.  EEG coherency II: experimental comparisons of multiple measures , 1999, Clinical Neurophysiology.

[22]  R. Macdonald.  Carbamazepine: mechanisms of action , 1995 .

[23]  D. Contreras,et al.  Cellular basis of EEG slow rhythms: a study of dynamic corticothalamic relationships , 1995, The Journal of neuroscience : the official journal of the Society for Neuroscience.

[24]  F. H. Lopes da Silva,et al.  Relative contributions of intracortical and thalamo-cortical processes in the generation of alpha rhythms, revealed by partial coherence analysis. , 1980, Electroencephalography and clinical neurophysiology.

[25]  F. Takens.  Detecting strange attractors in turbulence , 1981 .

[26]  D. Spencer,et al.  Complex partial seizures of frontal lobe origin , 1985, Annals of neurology.

[27]  C. Marsden,et al.  Autosomal dominant frontal epilepsy misdiagnosed as sleep disorder , 1994, The Lancet.