Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2009 Jan;14 Suppl 1(Suppl 1):32-7.
doi: 10.1016/j.yebeh.2008.09.017. Epub 2008 Oct 31.

Temporal lobe epilepsy: where do the seizures really begin?

Affiliations
Review

Temporal lobe epilepsy: where do the seizures really begin?

Edward H Bertram. Epilepsy Behav. 2009 Jan.

Abstract

Defining precisely the site of seizure onset has important implications for our understanding of the pathophysiology of temporal lobe epilepsy, as well as for the surgical treatment of the disorder. Removal of the limbic areas of the medial temporal lobe has led to a high rate of seizure control, but the relatively large number of patients for whom seizure control is incomplete, as well as the low rate of surgical cure, suggests that the focus extends beyond the usual limits of surgical resection. Reevaluation of the extent of the pathology, as well as new data from animal models, suggests that the seizure focus extends, at least in some cases, beyond the hippocampus and amygdala, which are usually removed at the time of surgery. In this review, we examine current information about the pathology and physiology of mesial temporal lobe epilepsy syndrome, with special emphasis on the distribution of the changes and patterns of seizure onset. We then propose a hypothesis for the nature of the seizure focus in this disorder and discuss its clinical implications, with the ultimate goal of improving surgical outcomes and developing nonsurgical therapies that may improve seizure control.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Basic circuitry of a neocortical seizure focus with a cortical excitatory driver, a subcortical seizure synchronizer and a number of neuromodulatory inputs (NM) that regulate excitability of synchronizer, driver or both.
Figure 2
Figure 2
Summary of Gloor’s absence circuitry experiments. A. Regular spike wave activity occurs in intact thalamocortical circuit. B. Separating cortex from the thalamus prevents regular spike and wave activity. C. Removal of cortex prevents abnormal activity from developing in the thalamus.
Figure 3
Figure 3
Connections between limbic structures and medial dorsal and midline thalamic nuclei. Simplified outline of significant known pathways between limbic sites that are strongly associated with seizure activity and the medial dorsal (MD) and midline thalamic nuclei. Direction of arrows indicates efferent and afferent pathways.
Figure 4
Figure 4
Modulation of limbic seizure activity through manipulation of the midline region of the thalamus. Seizure induced in anesthetized rat by stimulation of contralateral CA 3 in the hippocampus, with simultaneous seizure activity in CA 1 of the hippocampus and the medial dorsal thalamic nucleus (MD) before and after infusion of the GABA-A antagonist bicuculline. Seizure duration is significantly lengthened by bicuculline (arrows). First 10 seconds of each recording is stimulation artifact.
Figure 5
Figure 5
Variable pattern of limbic seizure onset according to the multiple independent generator hypothesis of limbic epilepsy. A. shows the situation in which all three sites contribute equally to seizure onset. B. displays a theoretical amygdala dominant seizure onset, whereas C. depicts a seizure in which the amygdala would play a minor role in relation to the other sites.

References

    1. Margerison JH, Corsellis JAN. Epilepsy and the temporal lobes. A clinical, electroencephalographic and neuropathological study of the brain in epilepsy, with particular reference to the temporal lobes. Brain. 1966;89:499–530. - PubMed
    1. Avoli M, Gloor P. Interaction of cortex and thalamus in spike and wave discharges of feline generalized penicillin epilepsy. Exp Neurol. 1982;76:196–217. - PubMed
    1. Steriade M. Sleep, epilepsy and thalamic reticular inhibitory neurons. Trends Neurosci. 2005;28:317–324. - PubMed
    1. Meeren HK, Pijn JP, Van Luijtelaar EL, Coenen AM, Lopes da Silva FH. Cortical focus drives widespread corticothalamic networks during spontaneous absence seizures in rats. J Neurosci. 2002;22:1480–1495. - PMC - PubMed
    1. Bertram EH, Zhang DX, Mangan P, Fountain N, Rempe D. Functional anatomy of limbic epilepsy: a proposal for central synchronization of a diffusely hyperexcitable network. Epilepsy Res. 1998;32:194–205. - PubMed

Publication types