Differences in memory performance and other clinical characteristics in patients with mesial temporal lobe epilepsy with and without hippocampal atrophy
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.
[Show abstract] [Hide abstract] ABSTRACT: Unilateral hippocampal atrophy (HA) is considered as a precursor of mesial temporal sclerosis (MTS) in some patients with temporal lobe epilepsy. However, in other cases, it has been suggested that HA without MTS may constitute a distinct epileptic entity. Hippocampal atrophy without MTS was defined as HA without T2-weighted hyperintensity, loss of internal architecture, or associated lesion seen on the MRI data. To date, no study has focused on the cognitive pattern of children with epilepsy with HA without MTS. The objectives of the present study were to characterize the cognitive profile of these children and to investigate the presence (or the absence) of material-specific memory deficits in these young patients, as found in patients with MTS. Toward this end, 16 young patients with epilepsy with either left or right HA without MTS completed a set of neuropsychological tests, assessing overall intelligence, verbal memory and nonverbal memory, and some aspects of attention and executive functions. Results showed normal intellectual functioning without specific memory deficits in these patients. Furthermore, comparison between patients with left HA and patients with right HA failed to reveal a material-specific lateralized memory pattern. Instead, attention and executive functions were found to be impaired in most patients. These results suggest that HA may constitute a distinct epileptic entity, and this information may help health-care providers initiate appropriate and timely interventions.0Comments 0Citations
- "However, compared with studies in adults, pediatric data could only partially confirm the notion of material-specific deficits in children with epilepsy with MTS [6,7,19, 20]. An association between left MTS and verbal memory problems has frequently been observed [18,212223, but there are no consistent findings for right MTS and nonverbal memory deficits [9,14,24] . For instance , Gargaro and colleagues  found the typical memory profile (e.g., left MTS and verbal memory problems and right MTS and nonverbal memory problems) in only 25% of their pediatric cohort. "
- "Comparing memory performance in patients with drug-resistant familial mTLE, with patients with " benign " familial mTLE and asymptomatic first-degree relatives, who had hippocampal atrophy, Alessio et al. (2004a) demonstrated that the interactions between hippocampal atrophy and drug-resistant epilepsy were associated with the poorest anterograde memory scores. Likewise, we recently reported in patients suffering from drug-resistant unilateral mTLE (Voltzenlogel et al., 2014), that the low seizure-frequency group performed significantly better than the high seizure-frequency group on anterograde memory tests (see also Alessio et al., 2004b; Hendriks et al., 2004; Wang et al., 2001). On a retrospective analysis of data from patients who had undergone a cognitive assessment on two occasions at an interval of more than 10 years, Thompson and Duncan (2005) demonstrated that complex focal seizures were associated with memory decline. "
[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.0Comments 5Citations
- "However, the extent of neuronal loss and the severity of cognitive deficits in this group were far less striking than those observed in the rats that had experienced motor SE. Thus, our findings add further weight to the evidence from former studies in animal models [9,53] and humans [4,6,63] showing that behavioral deficits in TLE correlate with the extent of hippocampal damage. "