Differences in memory performance and other clinical characteristics in patients with mesial temporal lobe epilepsy with and without hippocampal atrophy

Alessio, Andréa; Damasceno, Benito Pereira; Camargo, Cândida Helena Pires de; Kobayashi, Eliane; Guerreiro, Carlos A. M.; Cendes, Fernando

doi:10.1016/j.yebeh.2003.10.010

Cited by 96 publications

(66 citation statements)

References 29 publications

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“…Other studies also found that left hippocampal atrophy is more evidently related to poorer memory function than right hippocampal atrophy [Bigler et al, 1996;Burgess et al, 2002;Kilpatrick et al, 1997;McConley et al, 2008]. This finding is in line with hippocampal lesion data [Alessio et al, 2004;Szabo et al, 2009]. These previous results and our present findings suggest that volumetric changes in the left hippocampus may be more important to memory performance than volumetric changes in the right hippocampus.…”

Section: Discussionsupporting

confidence: 92%

Ipsilateral hippocampal atrophy is associated with long‐term memory dysfunction after ischemic stroke in young adults

Schaapsmeerders

Uden

Tuladhar

et al. 2015

Human Brain Mapping

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Memory impairment after stroke in young adults is poorly understood. In elderly stroke survivors memory impairments and the concomitant loss of hippocampal volume are usually explained by coexisting neurodegenerative disease (e.g., amyloid pathology) in interaction with stroke. However, neurodegenerative disease, such as amyloid pathology, is generally absent at young age. Accumulating evidence suggests that infarction itself may cause secondary neurodegeneration in remote areas. Therefore, we investigated the relation between long-term memory performance and hippocampal volume in young patients with first-ever ischemic stroke. We studied all consecutive first-ever ischemic stroke patients, aged 18-50 years, admitted to our academic hospital center between 1980 and 2010. Episodic memory of 173 patients was assessed using the Rey Auditory Verbal Learning Test and the Rey Complex Figure and compared with 87 stroke-free controls. Hippocampal volume was determined using FSL-FIRST, with manual correction. On average 10 years after stroke, patients had smaller ipsilateral hippocampal volumes compared with controls after left-hemispheric stroke (5.4%) and right-hemispheric stroke (7.7%), with most apparent memory dysfunctioning after left-hemispheric stroke. A larger hemispheric stroke was associated with a smaller ipsilateral hippocampal volume (b=-0.003, P<0.0001). Longer follow-up duration was associated with smaller ipsilateral hippocampal volume after left-hemispheric stroke (b=-0.028 ml, P=0.002) and right-hemispheric stroke (b=-0.015 ml, P=0.03). Our results suggest that infarction is associated with remote injury to the hippocampus, which may lower or expedite the threshold for cognitive impairment or even dementia later in life.

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Section: Discussionsupporting

confidence: 92%

Ipsilateral hippocampal atrophy is associated with long‐term memory dysfunction after ischemic stroke in young adults

Schaapsmeerders

Uden

Tuladhar

et al. 2015

Human Brain Mapping

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“…As fraction of newly-born neurons develop into GABA-ergic interneurons (Liu et al, 2003) and TLE is associated with decreased numbers of GABA-ergic interneurons, declined neurogenesis during chronic epilepsy may contribute to increased seizure-susceptibility of the DG. Likewise, hippocampal-dependent learning and memory deficits and depression observed in chronic TLE (Brown-Croyts et al, 2000;Oddo et al, 2003;Alessio et al, 2004) could be linked at least partially to the declined neurogenesis. Thus, neuroprotective approaches that block both aberrant neurogenesis occurring during the early period after the SE and dramatically decreased neurogenesis occurring at extended time-points after the SE may be useful for preventing chronic epilepsy as well as learning and memory deficits observed after SE.…”

Section: Dentate Neurogenesis and Temporal Lobe Epilepsymentioning

confidence: 99%

“…In most patients presenting TLE, the development of seizures is preceded with an IPI such as the head trauma, stroke, SE, and infections like meningitis (Harvey et al, 1997;Fisher et al, 1998;Cendes, 2004). Nevertheless, it is difficult to predict the consequences of initial seizures in humans because of multiple contributing factors.…”

Section: Definition Causes and Consequences Of Seizuresmentioning

confidence: 99%

“…In a population of new patients presented with epilepsy, almost 30% of them have seizures originating from the temporal lobe of the brain (Manford et al, 1992). Individuals affected with TLE typically have comparable clinical description, including an initial precipitating injury (IPI) such as the status epilepticus (SE), head trauma, encephalitis or childhood febrile seizures (Harvey et al, 1997;Fisher et al, 1998;Cendes, 2004). There is usually a latent period of several years between this injury and the emergence of the chronic TLE characterized by spontaneous recurrent motor seizures (SRMS) originating from temporal lobe foci, and learning and memory impairments (Devinsky, 2004;Detour et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Progress in neuroprotective strategies for preventing epilepsy

Acharya

Hattiangady

Shetty

2008

Progress in Neurobiology

156

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Neuroprotection is increasingly considered as a promising therapy for preventing and treating temporal lobe epilepsy (TLE). The development of chronic TLE, also termed as epileptogenesis, is a dynamic process. An initial precipitating injury (IPI) such as the status epilepticus (SE) leads to neurodegeneration, abnormal reorganization of the brain circuitry and a significant loss of functional inhibition. All of these changes likely contribute to the development of chronic epilepsy, characterized by spontaneous recurrent motor seizures (SRMS) and learning and memory deficits. The purpose of this review is to discuss the current state of knowledge pertaining to neuroprotection in epileptic conditions, and to highlight the efficacy of distinct neuroprotective strategies for preventing or treating chronic TLE. Although the administration of certain conventional and new generation antiepileptic drugs is effective for primary neuroprotection such as reduced neurodegeneration after acute seizures or the SE, their competence for preventing the development of chronic epilepsy after an IPI is either unknown or not promising. On the other hand, alternative strategies such as the ketogenic diet therapy, administration of distinct neurotrophic factors, hormones or antioxidants seem useful for preventing and treating chronic TLE. However, long term studies on the efficacy of these approaches introduced at different time-points after the SE or an IPI are lacking. Additionally, grafting of fetal hippocampal cells at early time-points after an IPI holds considerable promise for preventing TLE, though issues regarding availability of donor cells, ethical concerns, timing of grafting after SE, and durability of graft-mediated seizure suppression need to be resolved for further advances with this approach. Overall, from the studies performed so far, there is consensus that neuroprotective strategies need to be employed as quickly as possible after the onset of the SE or an IPI for considerable beneficial effects. Nevertheless, ideal strategies that are capable of facilitating repair and functional recovery of the brain after an IPI and preventing the evolution of IPI into chronic epilepsy are still hard to pin down.

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“…In adults, there is a clear-cut relationship between hippocampal injury and memory impairment in patients with left TLE. In patients with right TLE, this relationship is not as clear (2,(6)(7)(8) . Memory deficit occurs mainly when epilepsy involves both temporal lobes and the dominant hemisphere (9) .…”

mentioning

confidence: 99%

Memory impairment in children with temporal lobe epilepsy: a review

Guimarães

Rzezak

et al. 2006

J. epilepsy clin. neurophysiol.

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Introduction:The authors present a review article on memory aspects of temporal lobe epilepsy in childhood. Methods: We performed a search in the literature. Results: Temporal lobe epilepsy (TLE) in childhood present with great clinical, electroencephalographic and etiological diversity. The neuropsychological features in children with TLE are not well-defined yet. The relationship between the lateralization of the lesion and performance on memory tests is not established. Conclusion: The studies performed in children with TLE show controversy data. This finding may be due to the etiological, clinical and electroencephalographic diversity seen in such group of children. Besides, most studies use different assessments. Therefore, it is clear that more studies are necessary to elucidate which neuropsychological deficits occur in children with TLE.

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Differences in memory performance and other clinical characteristics in patients with mesial temporal lobe epilepsy with and without hippocampal atrophy

Cited by 96 publications

References 29 publications

Ipsilateral hippocampal atrophy is associated with long‐term memory dysfunction after ischemic stroke in young adults

Ipsilateral hippocampal atrophy is associated with long‐term memory dysfunction after ischemic stroke in young adults

Progress in neuroprotective strategies for preventing epilepsy

Memory impairment in children with temporal lobe epilepsy: a review

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