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Updated: May 8, 2026

Assessment of Memory Function in Pilocarpine-induced Epileptic Mice
Published on: June 4, 2020
Hippocampal atrophy and memory dysfunction in patients with juvenile myoclonic epilepsy
Katia Lin1, Gerardo Maria de Araujo Filho, Tatiana Frascareli Pascalicchio
1Unidade de Pesquisa e Tratamento das Epilepsias (UNIPETE), Universidade Federal de São Paulo (UNIFESP-EPM), São Paulo, SP, Brazil; Centro de Cirurgia de Epilepsia de Santa Catarina (CEPESC), Hospital Governador Celso Ramos (HGCR), Florianópolis, SC, Brazil.
Abstract:
Juvenile myoclonic epilepsy (JME) is a well-defined idiopathic generalized epilepsy (IGE) syndrome, being the most common IGE in adults and accounting for 5-11% of patients with epilepsy. While neuropsychological and neuroimaging studies have discussed the thalamofrontal dysfunction as the major pathophysiologic mechanism of JME, investigation on memory is scarce in patients with JME, with lack of objective assessments addressing common complaints and daily difficulties such as recalling telephone numbers, messages to pass on, and taking antiepileptic drugs regularly. The aim of this study was to objectively assess memory deficits in a group of patients with JME using neuropsychological examination combined with structural MRI of the hippocampi. After informed consent, a cohort of 56 consecutive patients with JME (29 males; mean age ± SD = 26.5 ± 9.01 years; range = 14.0-55.0 years) was included. The control group consisted of 42 healthy volunteers (18 males; mean age ± SD = 31.0 ± 8.54 years; range=20.0-56.0 years) without a family history of neuropsychiatric disorders. Patients and controls were submitted to a MRI and to a neuropsychological assessment, and comparisons between groups were performed, as well as a correlation study between hippocampal atrophy and neuropsychological performance in a group of patients with JME. The level of statistical significance was set at p<0.05. Significant hippocampal atrophy among patients with JME was observed, which was correlated with memory dysfunctions. The present findings reinforce the existence of functional-anatomic ictogenic networks that are not limited to frontal lobes, providing further support towards the concept of 'system epilepsies' in JME.
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