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Heidi E Kirsch

Publications and source records attributed to Heidi E Kirsch.

7 recordsLinked to original sources
PubMed2006

Mechanisms of seizure propagation in a cortical model.

We consider a mathematical model of mesoscopic human cortical ictal electrical activity. We compare the model results with ictal electrocortical data recorded from three human subjects and show how the two agree. We determine that, in the model system, seizures result from increased connectivity between excitatory and inhibitory cell populations, or from decreased connectivity within either excitatory or inhibitory cell populations. We compare the model results with the disinhibition and 4-AP models of epilepsy and suggest how the model may guide the development of new anticonvulsant therapies.

4-Aminopyridine↗
PubMed2006

Bifurcation control of a seizing human cortex.

We consider as a mathematical model of human cortical electrical activity a system of fourteen ordinary differential equations. With appropriate parameters, the model produces activity characteristic of a seizure. To prevent such seizures, we incorporate feedback controllers into the model dynamics. We show that three controllers--a linear feedback controller, a differential controller, and a filter controller--can be used to eliminate seizing activity in the model system. We show how bifurcations induced by the linear controller alter those present in the original dynamics.

Action Potentials↗
PubMed2006

Complex visual hallucinations as post-ictal cortical release phenomena.

Visual hallucinations can be elementary or complex and appear in a wide variety of neurological disorders. Hallucinations associated with seizures can either be ictal or part of a post-ictal cortical release phenomenon, and their features may help distinguish their etiology. We describe two patients with suspected ictal occipital lobe lesions with elementary hallucinations that were followed by post-ictal complex hallucinations.The pathophysiologies of elementary and complex hallucinations are reviewed. The sequential occurrence of these two distinct types of hallucinations in these patients emphasizes the observation that hallucinations associated with seizures can result from both irritative and cortical release mechanisms.

Adolescent↗
PubMed2005

Social cognition and epilepsy surgery.

Human social behavior depends on a set of perceptive, mnemonic, and interpretive abilities that together may be termed social cognition. Lesion and functional imaging studies of social cognitive functions implicate the temporal lobes (in particular, the nondominant temporal lobe) and mesial temporal structures as critical at the front end of social cognitive processes. The frontal lobes, in turn, function to interpret and to modulate these processes via top-down control. Damage to frontal regions is associated with specific derangements in social behavior. Chronic focal-onset epilepsy and its surgical treatment commonly affect these neuroanatomic regions and might therefore impact social function. Postoperative social function helps determine quality of life for both patients and families. There is some evidence that resective seizure surgery affects social cognition, but there are significant weaknesses in our current knowledge that can be overcome with comprehensive longitudinal research.

Cognition↗
PubMed2005

Pathological pattern formation and cortical propagation of epileptic seizures.

The stochastic partial differential equations (SPDEs) stated by Steyn-Ross and co-workers constitute a model of mesoscopic electrical activity of the human cortex. A simplification in which spatial variation and stochastic input are neglected yields ordinary differential equations (ODEs), which are amenable to analysis by techniques of dynamical systems theory. Bifurcation diagrams are developed for the ODEs with increased subcortical excitation, showing that the model predicts oscillatory electrical activity in a large range of parameters. The full SPDEs with increased subcortical excitation produce travelling waves of electrical activity. These model results are compared with electrocortical data recorded at two subdural electrodes from a human subject undergoing a seizure. The model and observational results agree in two important respects during seizure: (i) the average frequency of maximum power, and (ii) the speed of spatial propagation of voltage peaks. This suggests that seizing activity on the human cortex may be understood as an example of pathological pattern formation. Included is a discussion of the applications and limitations of these results.

Cerebral Cortex↗
PubMed2004

Multimodal functional mapping of sensorimotor cortex prior to resection of an epileptogenic perirolandic lesion.

The effects of chronic epileptogenic lesions on functional anatomy are under debate. Our recent experience during mapping and resection of a lesion in sensorimotor cortex supports the idea that epileptogenic lesions may prompt development of alternate cortical motor representations. Multimodal mapping may uncover alternate areas of functionality that make surgery feasible even when conventional neuroanatomy suggests otherwise. Newer methods such as electrocorticographic spectral analysis may complement traditional electrical cortical stimulation mapping.

Adolescent↗