Predisposed Susceptibility and Partial Seizure Disorder

Many partial epilepsy patients appear to begin their illness with a completed form of electroclinical expression that will become habitual without further change, even when medication is discontinued. Another group of patients may begin their illness with a maximal electroclinical expression of generalized convulsive seizures. Their condition then may regress to a nonconvulsive form, with a subsequent intermittent breakthrough of convulsive seizures, particularly when medication is reduced or discontinued. By contrast, patients whose electroclinical expression evolves sequentially over an extended period from nonconvulsive to convulsive appear to represent a distinct minority. Our study of presurgical seizure patterns made comparisons between objectively and historically documented patterns in 60 patients who became seizure free after temporal lobectomy, and confirmed our clinical impression that partial epilepsy announces its onset with a completed form that subsequently becomes habitual. This observation raises the question of the validity of kindling as a model of partial seizures, because relentless electroclinical progression with eventual development of a contralateral positive transfer effect, reminiscent of secondary epileptogenesis, is the cardinal feature of kindling. Evidence of secondary epileptogenesis in humans is scarce and is the subject of debate. Furthermore, the kindling model suggests that a permanent change of brain function occurs as a consequence of repeated seizures, but this tenet is not consistent with the well-recognized remission that occurs in some partial onset epilepsy patients. Thus, kindling as a model for the human condition faces two conceptual difficulties: lack of overt “progression” in patients with partial epilepsy, and failure to accommodate the clinical reality of remission (i.e., the “erosion” of epileptogenesis). The kindling phenomenon interacts with both ontogeny and phylogeny. Ontogenetic studies of kindling have generated new understanding of the developmental aspects of partial epilepsy. By contrast, phylogenetic studies of kindling are limited, because of the obvious technical challenges of studies using higher mammals. Controversies about the clinical relevance of kindling may arise from extrapolation of data derived primarily from the rodent temporal limbic system. The clinical relevance of kindling will depend on phylogenesis and the brain structures that are involved in kindling in the model system and in patients. Brain anatomy differs significantly among species. Findings derived from animals phylogenetically closer to humans are more likely to be clinically relevant. Several partial epilepsies that currently are known to have a benign course originate in the neocortex. This presentation reviews selectively our observations on kindling in five different primate species. Analysis of the predisposition to kindling conferred by certain species and certain brain sites provides insight into the diverse courses and neuroplastic consequences of partial seizure disorders in humans.

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