Literature DB >> 12143363

Effects of chronic epilepsy on declarative memory systems.

C Helmstaedter1.   

Abstract

Memory is systematically affected by temporal lobe epilepsy. Since surgery is a promising alternative to pharmacological treatment the questions which memory system is affected and what the long-term prognosis of memory is are more relevant than ever. We address these issues by cross-sectional and longitudinal analysis of memory performance in large series of patients with temporal lobe epilepsy (TLE). The findings indicate that episodic memory rather than semantic memory is impaired in TLE, in particular in TLE with mesial temporal pathology. With the exception that mesial functions appear increasingly affected by chronic non-mesial TLE, memory decline in TLE is not different from that observed in healthy control subjects. However, since patients perform poorer than controls at any age, normal senescence brings patients to mnesic disability at a younger age. Semantic memory seems unaffected by this process but early cortical lesions appear to interfere with knowledge acquisition. Longitudinal data come to a different conclusion regarding the contribution of epilepsy/seizures to memory decline. Conservative treatment is associated with significant decline in figural memory and 37% of the patients experience some memory decline in the long run. Surgery partly anticipates the decline observed with conservative treatment, but losses are most marked after left temporal lobe surgery. After surgery, quite stable memory or even late recovery from surgery is indicated. Leaving aside the surgical intervention, the data provide evidence that the longitudinal memory outcome in TLE is determined by seizure control, seizure severity, mental reserve capacities, and the retest interval. Thus early and efficient seizure control and the prevention of any cerebral damage from the beginning of epilepsy are demanded.

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Mesh:

Year:  2002        PMID: 12143363     DOI: 10.1016/S0079-6123(02)35041-6

Source DB:  PubMed          Journal:  Prog Brain Res        ISSN: 0079-6123            Impact factor:   2.453


  44 in total

1.  Neuroanatomical correlates of cognitive phenotypes in temporal lobe epilepsy.

Authors:  Kevin Dabbs; Jana Jones; Michael Seidenberg; Bruce Hermann
Journal:  Epilepsy Behav       Date:  2009-06-26       Impact factor: 2.937

2.  Morphometry of hilar ectopic granule cells in the rat.

Authors:  Joseph P Pierce; Daniel P McCloskey; Helen E Scharfman
Journal:  J Comp Neurol       Date:  2011-04-15       Impact factor: 3.215

3.  Speed modulation of hippocampal theta frequency correlates with spatial memory performance.

Authors:  Gregory R Richard; Ali Titiz; Anna Tyler; Gregory L Holmes; Rod C Scott; Pierre-Pascal Lenck-Santini
Journal:  Hippocampus       Date:  2013-08-05       Impact factor: 3.899

4.  Theta Rhythmopathy as a Cause of Cognitive Disability in TLE.

Authors:  Tristan Shuman; Benjamin Amendolara; Peyman Golshani
Journal:  Epilepsy Curr       Date:  2017 Mar-Apr       Impact factor: 7.500

5.  Subventricular zone-derived neural stem cell grafts protect against hippocampal degeneration and restore cognitive function in the mouse following intrahippocampal kainic acid administration.

Authors:  Panagiota Miltiadous; Georgia Kouroupi; Antonios Stamatakis; Paraskevi N Koutsoudaki; Rebecca Matsas; Fotini Stylianopoulou
Journal:  Stem Cells Transl Med       Date:  2013-02-15       Impact factor: 6.940

6.  Unraveling the Role of the Hippocampus in Reversal Learning.

Authors:  Adrià Vilà-Balló; Ernest Mas-Herrero; Pablo Ripollés; Marta Simó; Júlia Miró; David Cucurell; Diana López-Barroso; Montserrat Juncadella; Josep Marco-Pallarés; Mercè Falip; Antoni Rodríguez-Fornells
Journal:  J Neurosci       Date:  2017-06-07       Impact factor: 6.167

7.  Recurrent seizures induce a reversible impairment in a spatial hidden goal task.

Authors:  Hai Lin; Gregory L Holmes; John L Kubie; Robert U Muller
Journal:  Hippocampus       Date:  2009-09       Impact factor: 3.899

8.  Hippocampal interictal epileptiform activity disrupts cognition in humans.

Authors:  Jonathan K Kleen; Rod C Scott; Gregory L Holmes; David W Roberts; Melissa M Rundle; Markus Testorf; Pierre-Pascal Lenck-Santini; Barbara C Jobst
Journal:  Neurology       Date:  2013-05-17       Impact factor: 9.910

Review 9.  Glutamate receptor antibodies in neurological diseases: anti-AMPA-GluR3 antibodies, anti-NMDA-NR1 antibodies, anti-NMDA-NR2A/B antibodies, anti-mGluR1 antibodies or anti-mGluR5 antibodies are present in subpopulations of patients with either: epilepsy, encephalitis, cerebellar ataxia, systemic lupus erythematosus (SLE) and neuropsychiatric SLE, Sjogren's syndrome, schizophrenia, mania or stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor's expression, impair glutamate-induced signaling and function, activate blood brain barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and ataxia in animal models, and can be removed or silenced in some patients by immunotherapy.

Authors:  Mia Levite
Journal:  J Neural Transm (Vienna)       Date:  2014-08-01       Impact factor: 3.575

10.  A selective interplay between aberrant EPSPKA and INaP reduces spike timing precision in dentate granule cells of epileptic rats.

Authors:  Jérôme Epsztein; Elisabetta Sola; Alfonso Represa; Yehezkel Ben-Ari; Valérie Crépel
Journal:  Cereb Cortex       Date:  2009-08-14       Impact factor: 5.357

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