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Neurocysticercosis is the most common cause of acquired epilepsy in developing countries [55, 59].
Therefore, the current study was conducted in a rat pilocarpine model of acquired epilepsy.
Post-traumatic epilepsy is one of the most common and difficult to treat forms of acquired epilepsy worldwide.
Neurocysticercosis, which arises when larvae of the pork tapeworm Taenia solium penetrate the central nervous system, is the major cause of acquired epilepsy worldwide.
However, neurocysticercosis resulting from penetration of T. solium larvae into the central nervous system is the major cause of acquired epilepsy worldwide.
Interestingly, recent studies demonstrated that CB1 receptor expression undergoes a long-term redistribution in the hippocampus following epileptogenesis in the pilocarpine model of acquired epilepsy [6], [20].
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Post-traumatic epilepsy is the architype of acquired epilepsies, wherein a brain insult initiates an epileptogenic process culminating in an unprovoked seizure after weeks, months or years.
Hypertrophic neurones and astrocytes with BC-like morphology have been documented in the context of acquired epilepsy-associated pathologies, including hippocampal sclerosis (HS) [ 12– 16] and Rasmussen's encephalitis (RE) [ 17– 17].
The types and proportions of acquired epilepsies with known causes differ across populations.
Kindling, which is a model of epileptogenesis for acquired epilepsies, shares some of the similar mechanisms with long-term potentiation (LTP) [ 57].
Neurocysticercosis is major cause of adulthood acquired epilepsy [ 16], making T. solium a great public health risk in endemic communities [ 17].
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