The cognitive consequences of epilepsy

Duncan, John S.; Thompson, Pam

doi:10.1002/ana.10710

Cited by 18 publications

(12 citation statements)

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“…The results showed that the step‐down latency was significantly decreased and transfer latency was significantly increased in pentylenetetrazole‐kindled rats as compared to the control group of animals which suggested significant memory impairment in the pentylenetetrazole‐kindled rats. This observation is in line with reported clinical studies that showed significant cognitive decline in epileptic patients [18]. When carbamazepine was administered to the pentylenetetrazole‐kindled and non‐kindled groups of rats, both groups showed significant decrease in step‐down latency and increase in transfer latency, thereby suggesting a cognitive impairment in both groups of animals.…”

Section: Discussionsupporting

confidence: 90%

“…It has been reported that epilepsy as well as the drugs which are used to treat this CNS disorder can produce several adverse outcome, among which the cognitive decline and increased oxidative stress are particularly important factors that significantly affect the patient’s quality of life [18]. Cognitive decline has long been recognized as a sequel of intractable epilepsy [18,19]. However, it is not clear whether it is the phenomenon of epileptogenesis or oxidative stress or both which might be contributing to the decline in cognitive function.…”

Section: Discussionmentioning

confidence: 99%

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Effect of Carbamazepine and Lamotrigine on Cognitive Function and Oxidative Stress in Brain during Chemical Epileptogenesis in Rats

Arora

Mehta

Sharma

et al. 2010

Basic Clin Pharma Tox

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The present study assessed the effect of carbamazepine and lamotrigine on cognitive function and oxidative stress in brain during chemically induced epileptogenesis in rats. Epileptogenesis was induced by administration of pentylenetetrazole (30 mg ⁄ kg, s.c.) on alternate days (three times ⁄ week) for 9-11 weeks or until stage 4 of seizure score was achieved. The neurobehavioural parameters used for cognitive assessment were step-down latency in continuous avoidance apparatus and transfer latency in elevated plus maze test paradigm. Carbamazepine and lamotrigine were administered intraperitoneally in doses of 60 mg ⁄ kg and 25 mg ⁄ kg, respectively, according to the groups, once a day for 11 weeks. Oxidative stress was assessed in isolated homogenized whole brain samples and estimated for the levels of malondialdehyde, reduced glutathione, catalase and superoxide dismutase. The results showed that lamotrigine did not produce any change in cognitive function, while carbamazepine produced cognitive dysfunction. Cognitive decline seen in the carbamazepine-treated pentylenetetrazole-kindled group was also associated with increased oxidative stress. Lamotrigine treatment had no effect on oxidative stress parameters alone, while it significantly decreased oxidative stress in the pentylenetetrazole-kindled group as compared to the pentylenetetrazole-kindled carbamazepine-treated group.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Effect of Carbamazepine and Lamotrigine on Cognitive Function and Oxidative Stress in Brain during Chemical Epileptogenesis in Rats

Arora

Mehta

Sharma

et al. 2010

Basic Clin Pharma Tox

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“…Mesial temporal lobe epilepsy is the most prevalent form of drug refractory epilepsy, and memory dysfunction is its most common neuropsychological effect (Duncan and Thompson, 2003). Over half of patients with epilepsy rate their memory problems as moderate to severe (Corcoran and Thompson, 1992), contributing significantly to their adverse quality of life (Fisher et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Fluoxetine restores spatial learning but not accelerated forgetting in mesial temporal lobe epilepsy

Barkas

Redhead

Taylor

et al. 2012

Brain

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Learning and memory dysfunction is the most common neuropsychological effect of mesial temporal lobe epilepsy, and because the underlying neurobiology is poorly understood, there are no pharmacological strategies to help restore memory function in these patients. We have demonstrated impairments in the acquisition of an allocentric spatial task, in patients with unilateral hippocampal sclerosis. We also show that patients have accelerated forgetting of the learned spatial task and that this is associated with damage to the non-dominant hippocampal formation. We go on to show a very similar pattern of chronic allocentric learning and accelerated forgetting in a status epilepticus model of mesial temporal lobe epilepsy in rats, which is associated with reduced and abnormal hippocampal neurogenesis. Finally, we show that reversal of the neurogenic deficit using fluoxetine is associated with reversal of the learning deficit but not the accelerated forgetting, pointing to a possible dissociation in the underlying mechanisms, as well as a potential therapeutic strategy for improving hippocampal-dependant learning in patients with mesial temporal lobe epilepsy.

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“…A number of factors have been identified as having a role, including underlying pathology, seizures, and medication (2,3). Of the main factors identified, the role of seizures has been less well studied, and the available evidence does not indicate as strong a relation as might be anticipated from clinical experience and animal studies.…”

mentioning

confidence: 99%

Cognitive Decline in Severe Intractable Epilepsy

2005

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Summary:Purpose: To explore the relation between seizurerelated variables and cognitive change in patients with severe intractable epilepsy.Methods: A retrospective analysis of data from 136 patients who had undergone a cognitive assessment on two occasions at an interval of ≥10 years. Cognitive measures included tests of memory and executive skills in addition to intelligence quotients (IQ). Details were available regarding seizure type and frequency in the intertest interval.Results: Cognitive decline was severe and occurred across a wide range of cognitive functions. The frequency of generalised tonic-clonic seizures was the strongest predictor of decline. Complex partial seizure frequency was associated with a decline in memory and executive skills but not in IQ. Seizurerelated head injuries and advancing age carried a poor cognitive prognosis, whereas periods of remission were associated with a better cognitive outcome. Early age at onset was not implicated, and duration of epilepsy was a much less potent predictor of cognitive decline than has been reported in cross-sectional studies. No evidence indicated that a higher level of cognitive function protected against cognitive decline.Conclusions: Our findings, together with those from animal studies and surgically treated patients, suggest that seizures can have a direct adverse effect on cognition and that good seizure control even after years of intractability can have a beneficial impact on cognitive prognosis. This study was based on individuals who merited two cognitive assessments ≥10 years apart and hence is biased in favor of those with the most severe forms of refractory epilepsy and those with decline. Key Words: Epilepsy-SeizuresIntelligence-Cognitive decline.Cognitive decline has long been recognized as a sequel of intractable epilepsy (1). A number of factors have been identified as having a role, including underlying pathology, seizures, and medication (2,3). Of the main factors identified, the role of seizures has been less well studied, and the available evidence does not indicate as strong a relation as might be anticipated from clinical experience and animal studies. Research involving animal models of epilepsy has demonstrated that status epilepticus and frequent recurrent chemically and electrically induced seizures can result in cognitive impairment (4-7).Cross-sectional studies of humans have provided some evidence of a relation between seizure frequency and cognitive impairment (8-10). Longer duration of epilepsy has been reported to be associated with greater cognitive impairments (11-13). The negative impact of duration may be in part due to the cumulative impact of seizures, but also to other factors including antiepileptic drug (AED) treatment and pathologic interictal brain activity. Two studies

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The cognitive consequences of epilepsy

Cited by 18 publications

References 17 publications

Effect of Carbamazepine and Lamotrigine on Cognitive Function and Oxidative Stress in Brain during Chemical Epileptogenesis in Rats

Effect of Carbamazepine and Lamotrigine on Cognitive Function and Oxidative Stress in Brain during Chemical Epileptogenesis in Rats

Fluoxetine restores spatial learning but not accelerated forgetting in mesial temporal lobe epilepsy

Cognitive Decline in Severe Intractable Epilepsy

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