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Bilateral decrease in interictal hippocampal blood flow in unilateral mesiotemporal epilepsy

A Rougier1, D Lurton, B El Bahh

  • 1Department of Neurosurgery, Hôpital Pellegrin, Université Victor Segalen, Bordeaux, France. arougier@ar-luni.u-bordeaux2.fr

Journal of Neurosurgery
|February 9, 1999
PubMed
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In unilateral mesiotemporal epilepsy, asymmetrical hippocampal perfusion indicates restricted discharges, while bilateral hypoperfusion suggests spread. Regional cerebral blood flow (rCBF) changes reflect both functional and lesional origins.

Area of Science:

  • Neurology
  • Neuroimaging
  • Epilepsy Research

Background:

  • Unilateral mesiotemporal epilepsy is characterized by focal seizures originating in the temporal lobe.
  • Regional cerebral blood flow (rCBF) alterations have been observed in epilepsy, but their association with seizure spread is not fully understood.

Purpose of the Study:

  • To investigate the relationship between contralateral rCBF changes and the spatiotemporal organization of epileptic abnormalities in unilateral mesiotemporal epilepsy.

Main Methods:

  • Assessed hippocampal blood flow (HBF) using stable xenon-enhanced computed tomography in 19 patients.
  • Categorized patients into two groups based on seizure discharge spread (unilateral vs. contralateral).
  • Analyzed HBF data in relation to interictal spiking and ictal discharge organization via stereoelectroencephalography.

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Main Results:

  • Asymmetrical HBF was observed in patients with unilateral ictal discharges (Group 1).
  • Bilateral hippocampal hypoperfusion was found in patients with contralateral seizure spread (Group 2).
  • Statistical analysis revealed a significant interaction between HBF and seizure spread patterns.

Conclusions:

  • Asymmetrical interictal hippocampal perfusion correlates with unilateral ictal discharges.
  • Bilateral hippocampal hypoperfusion is associated with ictal discharges spreading to contralateral mesiotemporal structures.
  • Decreased rCBF in epilepsy has both functional and lesional components, independent of neuron loss.