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Mesial temporal lobe epilepsy: pathogenesis, induced rodent models and lesions
Alok K Sharma1, Rachel Y Reams, William H Jordan
1Department of Comparative Pathobiology, Purdue University, West Lafayette, IN, USA. Alok.Sharma@covance.com
Abstract:
Mesial temporal lobe epilepsy (MTLE), the most common epilepsy in adults, is generally intractable and is suspected to be the result of recurrent excitation or inhibition circuitry. Recurrent excitation and the development of seizures have been associated with aberrant mossy fiber sprouting in the hippocampus. Of the animal models developed to investigate the pathogenesis of MTLE, post-status epilepticus models have received the greatest acceptance because they are characterized by a latency period, the development of spontaneous motor seizures, and a spectrum of lesions like those of MTLE. Among post-status epilepticus models, induction of systemic kainic acid or pilocarpine-induced epilepsy is less labor-intensive than electrical-stimulation models and these models mirror the clinicopathologic features of MTLE more closely than do kindling, tetanus toxin, hyperthermia, post-traumatic, and perinatal hypoxia/ischemia models. Unfortunately, spontaneous motor seizures do not develop in kindling or adult hyperthermia models and are not a consistent finding in tetanus toxin-induced or perinatal hypoxia/ischemia models. This review presents the mechanistic hypotheses for seizure induction, means of model induction, and associated pathology, especially as compared to MTLE patients. Animal models are valuable tools not only to study the pathogenesis of MTLE, but also to evaluate potential antiepileptogenic drugs.
Insights
Mesial temporal lobe epilepsy (MTLE) is a common, intractable epilepsy. This review examines animal models, particularly post-status epilepticus models like kainic acid or pilocarpine induction, for studying MTLE pathogenesis and evaluating drugs.
Area of Science:
- Neuroscience
- Epileptology
- Pathology
Background:
- Mesial temporal lobe epilepsy (MTLE) is the most prevalent epilepsy in adults, often proving intractable.
- Pathogenesis is linked to recurrent excitation/inhibition imbalances and hippocampal mossy fiber sprouting.
- Animal models are crucial for understanding MTLE and testing therapies.
Purpose of the Study:
- To review mechanistic hypotheses for seizure induction in MTLE.
- To compare various animal models for their relevance to human MTLE.
- To highlight the utility of animal models in evaluating antiepileptogenic drugs.
Main Methods:
- Review of existing literature on MTLE pathogenesis and animal models.
- Comparison of post-status epilepticus models (kainic acid, pilocarpine) with other models (kindling, tetanus toxin, hyperthermia, etc.).
- Analysis of seizure induction mechanisms, model induction methods, and associated pathology.
Main Results:
- Post-status epilepticus models, especially kainic acid and pilocarpine-induced epilepsy, closely mimic MTLE's clinicopathologic features.
- These models exhibit a latency period, spontaneous seizures, and characteristic lesions.
- Other models like kindling and hyperthermia lack consistent spontaneous seizure development.
Conclusions:
- Post-status epilepticus models are superior for studying MTLE pathogenesis due to their clinical and pathological relevance.
- These models provide a platform for investigating seizure mechanisms and developing novel antiepileptogenic treatments.
- Further research using these validated models can advance understanding and treatment of intractable MTLE.
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