Amygdala damage in experimental and human temporal lobe epilepsy

Pitkänen, Asla; Tuunanen, Jarkko; Kälviäinen, Reetta; Partanen, Kaarina; Salmenperä, Tuuli

doi:10.1016/s0920-1211(98)00055-2

Cited by 208 publications

(154 citation statements)

References 60 publications

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“…In support of this idea, children and adults who have a history of temporal lobe epilepsy or status epilepticus, and have damage to the amygdala, also have a greater likelihood of ictal fear (Cendes et al 1994). This suggests that local alterations in inhibitory circuits may contribute to a lowered seizure threshold, and greater excitability within the amygdala, which may led to ictal fear (Pitkanen et al 1998). Additionally, results from a recent positron emission tomography (PET) study showed that during a modified Stroop task, bilateral amygdala activation was significantly greater during color naming of threat words than during color naming of neutral words in healthy subjects (Isenberg et al 1999).…”

Section: Discussionmentioning

confidence: 97%

A pilot study of amygdala volumes in pediatric generalized anxiety disorder

Bellis

Casey

Dahl

et al. 2000

Biological Psychiatry

304

196

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Section: Discussionmentioning

confidence: 97%

A pilot study of amygdala volumes in pediatric generalized anxiety disorder

Bellis

Casey

Dahl

et al. 2000

Biological Psychiatry

304

196

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“…The involvement of amygdala networks in TLE is highly documented by several studies from both humans and animal models (Gloor, 1992;Pitkanen et al, 1998;Aroniadou-Anderjaska et al, 2008), where this limbic area often represents the primary focus of epileptic seizures. In the absence of pathological conditions, the amygdala is under strong inhibitory GABAergic control provided by local circuits (Le Gal La Salle, 1976;Le Gal La Salle and Ben-Ari, 1981;Rainnie et al, 1991;Kemppainen and Pitkänen, 2000;Martina et al, 2001).…”

Section: Amygdala Network Drive Epileptiform Activity In Pilocarpinementioning

confidence: 99%

In vitro ictogenesis and parahippocampal networks in a rodent model of temporal lobe epilepsy

Panuccio

D’Antuono

Guzman

et al. 2010

Neurobiology of Disease

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Temporal lobe epilepsy (TLE) is a chronic epileptic disorder involving the hippocampal formation. Details on the interactions between the hippocampus proper and parahippocampal networks during ictogenesis remain, however, unclear. In addition, recent findings have shown that epileptic limbic networks maintained in vitro are paradoxically less responsive than non-epileptic control (NEC) tissue to application of the convulsant drug 4-aminopyridine (4AP). Field potential recordings allowed us to establish here the effects of 4AP in brain slices obtained from NEC and pilocarpinetreated epileptic rats; these slices included the hippocampus and parahippocampal areas such as entorhinal and perirhinal cortices and the amygdala. First, we found that both types of tissue generate epileptiform discharges with similar electrographic characteristics. Further investigation showed that generation of robust ictal-like discharges in the epileptic rat tissue is (i) favored by decreased hippocampal output (ii) reinforced by EC-subiculum interactions and (iii) predominantly driven by amygdala networks. We propose that a functional switch to alternative synaptic routes may promote network hyperexcitability in the epileptic limbic system.

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“…20 and 21). Subcortical brain regions are often studied for vulnerability to seizure-induced injury (21)(22)(23)(24)(25)(26)(27); however, a recent study by Karbowski et al (28) observed reduction of neurons in cortical layers 5 and 6 in the frontal lobes of rats with seizures. Seizure-induced neuronal damage in the cortex has also been previously demonstrated in baboons with convulsive status epilepticus (29).…”

mentioning

confidence: 99%

Epileptic baboons have lower numbers of neurons in specific areas of cortex

Young

Szabó

Phelix

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Significance We examined the variability of neuron packing densities across cortical regions and areas in two baboons with spontaneous, untreated epilepsy and two baboons without epilepsy. The two baboons without epilepsy had the distribution of neocortical neurons expected for Old World monkeys and baboons, whereas the baboons with untreated epilepsy had reduced numbers of cortical neurons overall, with the greatest reductions in motor and frontal areas of the cortex, and with little or no reduction in the primary visual cortex. The results suggest that neuron loss may follow untreated seizure activity, and this loss is greatest in areas of the cortex related to motor functions.

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Amygdala damage in experimental and human temporal lobe epilepsy

Cited by 208 publications

References 60 publications

A pilot study of amygdala volumes in pediatric generalized anxiety disorder

A pilot study of amygdala volumes in pediatric generalized anxiety disorder

In vitro ictogenesis and parahippocampal networks in a rodent model of temporal lobe epilepsy

Epileptic baboons have lower numbers of neurons in specific areas of cortex

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