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Persistent abnormality detected in the non-ictal electroencephalogram in primary generalised epilepsy
  1. J O Willoughby1,
  2. S P Fitzgibbon1,
  3. K J Pope2,
  4. L Mackenzie1,
  5. A V Medvedev1,*,
  6. C R Clark3,
  7. M P Davey1,†,
  8. R A Wilcox1
  1. 1Centre for Neuroscience and Department of Medicine (Neurology), Flinders University, Adelaide, South Australia, Australia
  2. 2School of Informatics and Engineering, Flinders University
  3. 3Cognitive Neuroscience Laboratory School of Psychology, Flinders University *A V Medvedev is now at Dept of Neuroscience, Georgetown University Medical Center, USA†M P Davey is now at Centre for Visual Sciences, Australian National University, Australia
  1. Correspondence to:
 Professor J O Willoughby, Department of Medicine (Neurology), Flinders University and Medical Centre, PO Box 2100 Adelaide SA, Australia 5001;John.Willoughby{at}flinders.edu.au

Abstract

Objectives: Gamma oscillations (30–100 Hz gamma electroencephalographic (EEG) activity) correlate with high frequency synchronous rhythmic bursting in assemblies of cerebral neurons participating in aspects of consciousness. Previous studies in a kainic acid animal model of epilepsy revealed increased intensity of gamma rhythms in background EEG preceding epileptiform discharges, leading the authors to test for intensified gamma EEG in humans with epilepsy.

Methods: 64 channel cortical EEG were recorded from 10 people with primary generalised epilepsy, 11 with partial epilepsy, and 20 controls during a quiescent mental state. Using standard methods of EEG analysis the strength of EEG rhythms (fast Fourier transformation) was quantified and the strengths of rhythms in the patient groups compared with with controls by unpaired t test at 1 Hz intervals from 1 Hz to 100 Hz.

Results: In patients with generalised epilepsy, there was a threefold to sevenfold increase in power of gamma EEG between 30 Hz and 100 Hz (p<0.01). Analysis of three unmedicated patients with primary generalised epilepsies revealed an additional 10-fold narrow band increase of power around 35 Hz–40 Hz (p<0.0001). There were no corresponding changes in patients with partial epilepsy.

Conclusions: Increased gamma EEG is probably a marker of the underlying ion channel or neurotransmitter receptor dysfunction in primary generalised epilepsies and may also be a pathophysiological prerequisite for the development of seizures. The finding provides a new diagnostic approach and also links the pathophysiology of generalised epilepsies to emerging concepts of neuronal correlates of consciousness.

  • primary generalised epilepsy
  • gamma oscillations
  • partial epilepsy
  • EEG, electroencephalography
  • PGE, primary generalised epilepsies

https://doi.org/10.1136/jnnp.74.1.51

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    Footnotes

    • Competing interests: none declared.

    • ↵* A V Medvedev is now at Dept of Neuroscience, Georgetown University Medical Center, USA

    • ↵† M P Davey is now at Centre for Visual Sciences, Australian National University, Australia