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Snead Lab

Research interests

The goal of Dr. Snead's clinical research is to devise therapeutic and diagnostic strategies that will improve the outcomes of children with infantile spasms undergoing treatment for that disorder.  Similarly, Dr. Snead has focused upon the development of improved diagnostic protocols for selection of children with extra temporal localization-related epilepsy for surgical treatment of their epilepsy.  Dr. Snead and his team have generated data that shows the value of magnetoencepahlography in this regard.

Snead lab is developing animal models of epilepsy syndromes that are unique to children and to investigate mechanisms of epileptogenesis in these models.  Dr. Snead and his team have defined and standardized the g-hydroxybutyrate (GHB) rat model of generalized  absence seizures which is now utilized worldwide to screen for anti-absence activity of putative anti-epileptic compounds and to investigate basic mechanisms of absence seizures.  The lab has shown that GABAB receptor (GABABR) agonists exacerbate, that both GHB and GABABR antagonists block, experimental absence seizures.  More recently, Snead lab has developed, characterized, and standardized an animal model of atypical absence epilepsy in rat and mouse.  This model is created by inhibiting cholesterol synthesis in the brain by AY 9944 (AY) during postnatal brain development.  Atypical absence seizures in children are a component of epilepsy syndromes in children which are hard to treat and which have a very poor neurodevelopmental outcome.  The AY model of atypical absence epilepsy in rat is clinically relevant because it reliably and accurately mirrors the EEG, behavioural, pharmacological and developmental characteristics of the human condition.  Depth electrode recordings indicate that hippocampal circuitry shows epileptiform activity during atypical absence seizure activity in the AY model.  This is in contradisctinction to typical absence epilepsy where the hippocampus is silent.  These data suggest that whether absence epilepsy is typical or atypical appears to be circuitry-dependent.  Snead lab staff are currently focusing upon putative GABABR-mediated mechanisms in this new model of atypical absence epilepsy, particularly in regard to putative perturbations ofo the molecular biology of the GABABR in this model.  To investigate this hypothesis further, Snead lab has developed GABABR transgenic mice that over-express the GABABR.  In addition, Snead lab is working with the Ts65Dn mouse model of Down syndrome as a substrate for other clinical models of epilepsy and is investigating mechanisms of epileptogenesis in the succinic semialdehyde knockout mouse.

Dr. Miguel Cortez is interested in experimental epileptogenesis, sleep modulation and chronophysiology of epilepsies, through the window of EEG and VEEG, for the characterization of animal models for refractory epileptic syndromes requiring active investigation such as West, Lennox-Gastaut, Rasmussen and Rett's. He provides assistance with monitoring of genetic animal models with seizure-like phenotype form other laboratories at SicKids and other research laboratories in Toronto. He is a member of the Eastern Association of Electroencephalographers and the American Epilepsy Society and has been actively involved in teaching of clinical and experimental neurophysiology.

Dr. Perez-Velazquez's scientific research is the understanding of the relation between brain function and behaviour.  One of his main research themes is the investigation of the patterns of coordinated activity in brain networks, associated with pathology and cognitive function.  Recent collaboration with clinicians at SickKids and other hospitals has resulted in projects involving magnetoencephalographic recordings to determine brain coordination dynamics and work is extending to brain dynamics resulting from traumatic injury and autism.  These studies are complimented with more theoretical investigations using dynamic system theory to elaborate frameworks that at least capture the essence of cellular interacations in the brain and their relation to behaviour.