Recurrent seizures may cause hippocambal damage in temporal lobe epilepsy

Kälviäinen, Reetta; Salmenperä, Tuuli; Partanen, Kaarina; Vainio, Pauli; Riekkinen, Paavo; Pitkänen, Asla

doi:10.1212/wnl.50.5.1377

Cited by 205 publications

(129 citation statements)

References 14 publications

Supporting

Mentioning

113

Contrasting

Unclassified

Order By: Relevance

“…However, by adolescence or early adulthood, it frequently becomes refractory (21,22). Most of the patients with MTLE have histopathologic and MRI evidence of neuropathologic damage (23,24).…”

Section: Is Refractory Epilepsy Progressive?mentioning

confidence: 99%

“…In one study, patients with a unilateral seizure focus in the hippocampus and chronic drugresistant seizures had significantly smaller hippocampal volume on the side of the focus than did normal controls or patients with newly diagnosed or well-controlled temporal lobe seizures (24). The greater the number of seizures reported, the greater the loss of volume in the hippocampus, suggesting that the loss might be induced by seizure activity (24).…”

Section: Clinical Datamentioning

confidence: 99%

See 1 more Smart Citation

Is Refractory Epilepsy Preventable?

et al. 2002

View full text Add to dashboard Cite

Summary: About a third of the patients diagnosed with epilepsy will not be fully controlled with antiepileptic drugs (AEDs), and many of them will have frequent and disabling seizures. These patients will undergo multiple drug trials, most often without complete seizure remission. Moreover, refractory epilepsy is associated with increased morbidity (from seizures and medications), social isolation, unemployment, and overall reduced quality of life. There is evidence that refractory epilepsy can be a progressive disorder, which, if controlled early, might never develop into a full syndrome with all of its associated sequelae. The difficulty lies in identifying at an early stage patients who are likely to progress to intractability. No currently known markers enable clinicians to make this identification with confidence. Advances in pharmacogenomics and our understanding of pharmacologic responsiveness in epilepsy may change this situation. Even now, we are able to identify many patients with a poor prognosis earlier than before, particularly in the pediatric population, in which syndromic classification may provide an approach to predict intractability. The early initiation of aggressive therapy may improve outcome and overall quality of life.

show abstract

Section: Is Refractory Epilepsy Progressive?mentioning

confidence: 99%

Section: Clinical Datamentioning

confidence: 99%

Is Refractory Epilepsy Preventable?

et al. 2002

View full text Add to dashboard Cite

show abstract

“…The typical pattern is asymmetric hippocampal volume loss with greater abnormality in the ipsilateral hippocampus compared to the contralateral hippocampus. In addition, both disease course features (e.g., duration) and neurodevelopmental features (e.g., history of complex febrile seizures in childhood) have been implicated in hippocampal atrophy [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

MRI volume loss of subcortical structures in unilateral temporal lobe epilepsy

Pulsipher

Seidenberg

Morton

et al. 2007

Epilepsy & Behavior

View full text Add to dashboard Cite

Few studies have examined the relative degree of brain volume loss in both the hippocampi and subcortical structures in unilateral temporal lobe epilepsy (TLE), and their association with clinical seizure correlates. In this study, quantitative MRI volumes were measured in the hippocampus, thalamus, caudate, putamen, and corpus callosum in 48 unilateral TLE patients (26 rights, and 22 lefts) and compared to 29 healthy controls. The ipsilateral hippocampus, corpus callosum, and bilateral thalami showed the greatest volume loss, reflected by large to moderate effect size differences compared to controls. Bilaterally, the putamen showed the next highest volume reduction. The contralateral hippocampus and bilateral caudate nuclei showed the least volume reduction, characterized by small effect sizes. Furthermore, clinical seizure characteristics (e.g, duration of epilepsy) showed different patterns of association with the volume reductions observed across these structures. Findings suggest that distinct neurodevelopmental features may play a role in the volume abnormality observed in these regions.

show abstract

“…[1][2][3] Experimental and now human studies suggest that programmed cell death and/or apoptosis may contribute to the mechanism of neuronal death following seizures based on apoptotic morphology (blebbing, condensation of the nucleus), DNA fragmentation, upregulation of BCL-2 family proteins and activation of the caspase (cysteinyl aspartatespecific protease) family of cell death enzymes in affected cell populations. [4][5][6][7][8][9][10] Mitochondria are critical sites for the initiation and reinforcement of cell death pathways, being a source of apoptogenic factor (e.g.…”

Section: Introductionmentioning

confidence: 99%

Seizure-like activity leads to the release of BAD from 14-3-3 protein and cell death in hippocampal neurons in vitro

et al. 2003

View full text Add to dashboard Cite

Seizure-induced neuronal death may involve engagement of the BCL-2 family of apoptosis-regulating proteins. In the present study we examined the activation of proapoptotic BAD in cultured hippocampal neurons following seizures induced by removal of chronic glutamatergic transmission blockade. Kynurenic acid withdrawal elicited an increase in seizure-like electrical activity, which was inhibited by blockers of AMPA (CNQX) and NMDA (MK801 and AP5) receptor function. However, only NMDA receptor antagonists inhibited calcium entry as assessed by fura-2, and cell death of hippocampal neurons. Seizures increased proteolysis of caspase-3 and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) of cells. Seizure-like activity induced dephosphorylation of BAD and the disruption of its constitutive interaction with 14-3-3 proteins. In turn, BAD dimerized with antiapoptotic BCL-Xl after seizures. However, the absence of neuroprotective effects of pathway intervention suggests that BAD may perform a reinforcement rather than instigator role in cell death following seizures in vitro.

show abstract

Recurrent seizures may cause hippocambal damage in temporal lobe epilepsy

Abstract: In patients with cryptogenic epilepsy, recurrent seizures may cause damage to the hippocampus throughout the lifetime of the patient.

Cited by 205 publications

References 14 publications

Is Refractory Epilepsy Preventable?

Is Refractory Epilepsy Preventable?

MRI volume loss of subcortical structures in unilateral temporal lobe epilepsy

Seizure-like activity leads to the release of BAD from 14-3-3 protein and cell death in hippocampal neurons in vitro

Contact Info

Product

Resources

About