Mesial temporal lobe epilepsy (MTLE) is usually accompanied by memory deficits due to damage to the hippocampal system. In most studies, however, the influence of hippocampal atrophy (HA) is confounded with other variables, such as: type of initial precipitating injury and pathological substrate, effect of lesion (HA) lateralization, history of febrile seizures, status epilepticus, age of seizure onset, duration of epilepsy, seizure frequency, and antiepileptic drugs (AEDs). To investigate the relationship between memory deficits and these variables, we studied 20 patients with MTLE and signs of HA on MRI and 15 MTLE patients with normal high-resolution MRI. The findings indicated that (1) HA, earlier onset of seizures, longer duration of epilepsy, higher seizure frequency, and AEDs (polytherapy) are associated with memory deficits; and (2) there is a close relationship between deficits of verbal memory and left HA, but not between visual memory and right HA.
"Temporal lobe epilepsy (TLE) can be associated with hippocampal cell loss (hippocampal sclerosis) and other structural changes in the medial temporal lobe region, such as fiber sprouting and synaptic reorganization , , . It has also been repeatedly reported that TLE patients with hippocampal sclerosis may show learning and memory deficits, increased anxiety, depression and mood disorders , , . Thus, it seems reasonable to assume that these behavioral changes are secondary to the TLE-related hippocampal neurodegeneration. "
[Show abstract][Hide abstract] ABSTRACT: Treating rats with kainic acid induces status epilepticus (SE) and leads to the development of behavioral deficits and spontaneous recurrent seizures later in life. However, in a subset of rats, kainic acid treatment does not induce overt behaviorally obvious acute SE. The goal of this study was to compare the neuroanatomical and behavioral changes induced by kainate in rats that developed convulsive SE to those who did not. Adult male Wistar rats were treated with kainic acid and tested behaviorally 5 months later. Rats that had experienced convulsive SE showed impaired performance on the spatial water maze and passive avoidance tasks, and on the context and tone retention tests following fear conditioning. In addition, they exhibited less anxiety-like behaviors than controls on the open-field and elevated plus-maze tests. Histologically, convulsive SE was associated with marked neuron loss in the hippocampal CA3 and CA1 fields, and in the dentate hilus. Rats that had not experienced convulsive SE after kainate treatment showed less severe, but significant impairments on the spatial water maze and passive avoidance tasks. These rats had fewer neurons than control rats in the dentate hilus, but not in the hippocampal CA3 and CA1 fields. Correlational analyses revealed significant relationships between spatial memory indices of rats and neuronal numbers in the dentate hilus and CA3 pyramidal field. These results show that a part of the animals that do not display intense behavioral seizures (convulsive SE) immediately after an epileptogenic treatment, later in life, they may still have noticeable structural and functional changes in the brain.
PLoS ONE 01/2014; 9(1):e84722. DOI:10.1371/journal.pone.0084722 · 3.23 Impact Factor
"In such instances, the left hemisphere may come to assume a dominant role for nonverbal episodic memory tasks as a mean of ensuring the preservation of function. This interpretation could also explain why several studies failed to find a direct relation between right hippocampal atrophy and deficits on any kind of episodic memory task [Alessio et al., 2004]. "
"Left HS correlated with impairments in verbal episodic memory while visuo-spatial working memory was affected in right HS  . In addition, deficiency of verbal memory in left HS and deficiency of visual memory in right HS were observed in patients with early-onset, long-term duration and highfrequency of seizures . Proton magnetic resonance spectroscopy ( 1 H MRS), which is assumed to be suitable for providing information about neuronal loss and gliosis, revealed correlation between 1 H MRS values and verbal memory scores . "
[Show abstract][Hide abstract] ABSTRACT: Calbindin expression of granule cells of the dentate gyrus is decreased in temporal lobe epilepsy (TLE) regardless of its etiology. In this study, we examined the relation between reduction of calbindin immunoreactivity and the verbal and visuo-spatial memory function of patients with TLE of different etiologies. Significant linear correlation was shown between calbindin expression and short-term and long-term percent retention and retroactive interference in auditory verbal learning test (AVLT) of patients including those with hippocampal sclerosis. In addition, we found significant linear regression between calbindin expression and short-term and long-term percent retention of AVLT in patients whose epilepsy was caused by malformation of cortical development or tumor and when no hippocampal sclerosis and substantial neuronal loss were detected. Together with the role of calbindin in memory established in previous studies on calbindin knock-out mice, our results suggest that reduction of calbindin expression may contribute to memory impairments of patients with TLE, particularly, when neuronal loss is not significant.
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