Typical versus atypical absence seizures: network mechanisms of the spread of paroxysms.
OBJECTIVE
Typical absence seizures differ from atypical absence seizures in terms of semiology, EEG morphology, network circuitry, and cognitive outcome, yet have the same pharmacological profile. We have compared typical to atypical absence seizures, in terms of the recruitment of different brain areas. Our initial question was whether brain areas that do not display apparent paroxysmal discharges during typical absence seizures, are affected during the ictal event in terms of synchronized activity, by other, distant areas where seizure activity is evident. Because the spike-and-wave paroxysms in atypical absence seizures invade limbic areas, we then asked whether an alteration in inhibitory processes in hippocampi may be related to the spread seizure activity beyond thalamocortical networks, in atypical seizures.


METHODS
We used two models of absence seizures in rats: one of typical and the other of atypical absence seizures. We estimated phase synchronization, and evaluated inhibitory transmission using a paired-pulse paradigm.


RESULTS
In typical absence seizures, we observed an increase in synchronization between hippocampal recordings when spike-and-wave discharges occurred in the cortex and thalamus. This indicates that seizure activity in the thalamocortical circuitry enhances the propensity of limbic areas to synchronize, but is not sufficient to drive hippocampal circuitry into a full paroxysmal discharge. Lower paired-pulse depression was then found in hippocampus of rats that displayed atypical absence seizures.


CONCLUSIONS
These observations suggest that circuitries in brain areas that do not display apparent seizure activity become synchronized as seizures occur within thalamocortical circuitry, and that a weakened hippocampal inhibition may predispose to develop synchronization into full paroxysms during atypical absence seizures.
Velazquez
Jose L Perez
JL
Programme for Neuroscience and Mental Health and Division of Neurology, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada. jose-luis.perez-velazquez@sickkids.ca
Huo
Jeanne Zhen
JZ
Dominguez
L Garcia
LG
Leshchenko
Yevgen
Y
Snead
O Carter
OC
D015107:4-Butyrolactone / Q000494:pharmacology; D000200:Action Potentials / Q000502:physiology*; D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology*; D013181:Cortical Spreading Depression / Q000502:physiology; D003344:Cortical Synchronization / Q000706:statistics & numerical data; D004195:Disease Models, Animal; D004567:Electrodes, Implanted; D004569:Electroencephalography / Q000706:statistics & numerical data; D004832:Epilepsy, Absence / Q000139:chemically induced / Q000145:classification / Q000503:physiopathology*; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology; D008959:Models, Neurological; D009433:Neural Inhibition / Q000502:physiology; D009434:Neural Pathways / Q000503:physiopathology; D051381:Rats; D020318:Rats, Long-Evans; D011999:Recruitment, Neurophysiological / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*; D013788:Thalamus / Q000503:physiopathology; D001371:trans-1,4-Bis(2-chlorobenzaminomethyl)cyclohexane Dihydrochloride / Q000494:pharmacology
D001371:trans-1,4-Bis(2-chlorobenzaminomethyl)cyclohexane Dihydrochloride; D015107:4-Butyrolactone