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Different structural correlates for verbal memory impairment in temporal lobe epilepsy with and without mesial temporal lobe sclerosis.

ABSTRACT: Memory impairment is one of the most prominent cognitive deficits in temporal lobe epilepsy (TLE). The overall goal of this study was to explore the contribution of cortical and hippocampal (subfield) damage to impairment of auditory immediate recall (AIMrecall), auditory delayed recall (ADMrecall), and auditory delayed recognition (ADMrecog) of the Wechsler Memory Scale III (WMS-III) in TLE with (TLE-MTS) and without hippocampal sclerosis (TLE-no). It was hypothesized that volume loss in different subfields determines memory impairment in TLE-MTS and temporal neocortical thinning in TLE-no.T1 whole brain and T2-weighted hippocampal magnetic resonance imaging and WMS-III were acquired in 22 controls, 18 TLE-MTS, and 25 TLE-no. Hippocampal subfields were determined on the T2 image. Free surfer was used to obtain cortical thickness averages of temporal, frontal, and parietal cortical regions of interest (ROI). MANOVA and stepwise regression analysis were used to identify hippocampal subfields and cortical ROI significantly contributing to AIMrecall, ADMrecall, and ADMrecog.In TLE-MTS, AIMrecall was associated with cornu ammonis 3 (CA3) and dentate (CA3&DG) and pars opercularis, ADMrecall with CA1 and pars triangularis, and ADMrecog with CA1. In TLE-no, AIMrecall was associated with CA3&DG and fusiform gyrus (FUSI), and ADMrecall and ADMrecog were associated with FUSI.The study provided the evidence for different structural correlates of the verbal memory impairment in TLE-MTS and TLE-no. In TLE-MTS, the memory impairment was mainly associated by subfield-specific hippocampal and inferior frontal cortical damage. In TLE-no, the impairment was associated by mesial-temporal cortical and to a lesser degree hippocampal damage.

SUBMITTER: Mueller SG

PROVIDER: S-EPMC3259857 | biostudies-literature | 2012 Feb

REPOSITORIES: biostudies-literature

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Different structural correlates for verbal memory impairment in temporal lobe epilepsy with and without mesial temporal lobe sclerosis.

Mueller Susanne G SG Laxer Kenneth D KD Scanlon Cathy C Garcia Paul P McMullen William J WJ Loring David W DW Meador Kimford J KJ Weiner Michael W MW

Human brain mapping 20110324 2

<h4>Objectives</h4>Memory impairment is one of the most prominent cognitive deficits in temporal lobe epilepsy (TLE). The overall goal of this study was to explore the contribution of cortical and hippocampal (subfield) damage to impairment of auditory immediate recall (AIMrecall), auditory delayed recall (ADMrecall), and auditory delayed recognition (ADMrecog) of the Wechsler Memory Scale III (WMS-III) in TLE with (TLE-MTS) and without hippocampal sclerosis (TLE-no). It was hypothesized that vo ...[more]

PMID: 21438080

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Project description:RationaleHigh frequency oscillations (HFO; ripples = 80-200, fast ripples 200-500 Hz) are promising epileptic biomarkers in patients with epilepsy. However, especially in temporal epilepsies differentiation of epileptic and physiological HFO activity still remains a challenge. Physiological sleep-spindle-ripple formations are known to play a role in slow-wave-sleep memory consolidation. This study aimed to find out if higher rates of mesial-temporal spindle-ripples correlate with good memory performance in epilepsy patients and if surgical removal of spindle-ripple-generating brain tissue correlates with a decline in memory performance. In contrast, we hypothesized that higher rates of overall ripples or ripples associated with interictal epileptic spikes correlate with poor memory performance.MethodsPatients with epilepsy implanted with electrodes in mesial-temporal structures, neuropsychological memory testing and subsequent epilepsy surgery were included. Ripples and epileptic spikes were automatically detected in intracranial EEG and sleep-spindles in scalp EEG. The coupling of ripples to spindles was automatically analyzed. Mesial-temporal spindle-ripple rates in the speech-dominant-hemisphere (left in all patients) were correlated with verbal memory test results, whereas ripple rates in the non-speech-dominant hemisphere were correlated with non-verbal memory test performance, using Spearman correlation).ResultsIntracranial EEG and memory test results from 25 patients could be included. All ripple rates were significantly higher in seizure onset zone channels (p < 0.001). Patients with pre-surgical verbal memory impairment had significantly higher overall ripple rates in left mesial-temporal channels than patients with intact verbal memory (Mann-Whitney-U-Test: p = 0.039). Spearman correlations showed highly significant negative correlations of the pre-surgical verbal memory performance with left mesial-temporal spike associated ripples (rs = -0.458; p = 0.007) and overall ripples (rs = -0.475; p = 0.006). All three ripple types in right-sided mesial-temporal channels did not correlate with pre-surgical nonverbal memory. No correlation for the difference between post- and pre-surgical memory and pre-surgical spindle-ripple rates was seen in patients with left-sided temporal or mesial-temporal surgery.DiscussionThis study fails to establish a clear link between memory performance and spindle ripples. This highly suggests that spindle-ripples are only a small portion of physiological ripples contributing to memory performance. More importantly, this study indicates that spindle-ripples do not necessarily compromise the predictive value of ripples in patients with temporal epilepsy. The majority of ripples were clearly linked to areas with poor memory function.

Project description:ObjectiveHippocampal sclerosis is the most common neuropathologic finding in cases of medically intractable mesial temporal lobe epilepsy. In this study, we analyzed the gene expression profiles of dentate granule cells of patients with mesial temporal lobe epilepsy with and without hippocampal sclerosis to show that next-generation sequencing methods can produce interpretable genomic data from RNA collected from small homogenous cell populations, and to shed light on the transcriptional changes associated with hippocampal sclerosis.MethodsRNA was extracted, and complementary DNA (cDNA) was prepared and amplified from dentate granule cells that had been harvested by laser capture microdissection from surgically resected hippocampi from patients with mesial temporal lobe epilepsy with and without hippocampal sclerosis. Sequencing libraries were sequenced, and the resulting sequencing reads were aligned to the reference genome. Differential expression analysis was used to ascertain expression differences between patients with and without hippocampal sclerosis.ResultsGreater than 90% of the RNA-Seq reads aligned to the reference. There was high concordance between transcriptional profiles obtained for duplicate samples. Principal component analysis revealed that the presence or absence of hippocampal sclerosis was the main determinant of the variance within the data. Among the genes up-regulated in the hippocampal sclerosis samples, there was significant enrichment for genes involved in oxidative phosphorylation.SignificanceBy analyzing the gene expression profiles of dentate granule cells from surgically resected hippocampal specimens from patients with mesial temporal lobe epilepsy with and without hippocampal sclerosis, we have demonstrated the utility of next-generation sequencing methods for producing biologically relevant results from small populations of homogeneous cells, and have provided insight on the transcriptional changes associated with this pathology.

Project description:The Wada test is widely used in the presurgical evaluation of potential temporal lobectomy patients to predict postoperative memory function. Expected asymmetry (EA), defined as Wada memory lateralized to the nonsurgical hemisphere, or a higher score after injection of the surgical hemisphere would be considered favorable in terms of postoperative memory outcome. However, in some cases, nonlateralized memory (NM) results, with no appreciable asymmetry, may occur because of impaired scores after both injections, often leading to denial of surgery. The reason for such nonlateralized Wada memory in patients with intractable temporal lobe epilepsy (TLE) remains unclear. Given that quantitative morphometric magnetic resonance imaging studies in TLE patients have shown bilateral regional atrophy in temporal and extratemporal structures, we hypothesized that the volume loss in contralateral temporal structures could contribute to nonlateralized Wada memory performance. To investigate this, we examined the relationship between the volume changes of temporal structures and Wada memory scores in patients with intractable TLE with mesial temporal sclerosis (MTS) using an age- and gender-matched control group. Memory was considered nonlateralized if the absolute difference in the total correct recall scores between ipsilateral and contralateral injections was <11%. Among 21 patients, Wada memory was lateralized in 15 and nonlateralized in 6 patients, with all the nonlateralized scores being observed in left TLE. The recall scores after ipsilateral injection were significantly lower in patients with an NM profile than an EA profile (23 ± 14% vs. 59 ± 18% correct recall, p ? 0.001). However, the recall scores after contralateral injection were low but similar between the two groups (25 ± 17% vs. 25 ± 15% correct recall, p=0.97). Compared to controls, all the patients showed greater volume loss in the temporal regions. However, patients with a NM profile showed significantly more volume loss than those with a lateralized memory profile in both contralateral and ipsilateral temporal regions (p<0.05). Left hemispheric Wada memory performance correlated positively with the size of the left mesial and neocortical temporal structures (r=0.49-0.63, p=0.005-0.04). Our study suggests that volume loss in the nonsurgical temporal structures is associated with nonlateralized Wada memory results in patients with intractable TLE.

Dataset Information

Different structural correlates for verbal memory impairment in temporal lobe epilepsy with and without mesial temporal lobe sclerosis.

Publications

Different structural correlates for verbal memory impairment in temporal lobe epilepsy with and without mesial temporal lobe sclerosis.

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