John Libbey Eurotext

Epileptic Disorders

The Educational Journal of the International League Against Epilepsy

Propagation of seizures in a case of lesional mid-cingulate gyrus epilepsy studied by stereo-EEG Volume 18, numéro 4, December 2016

Illustrations

  • Figure 1
  • Figure 2
  • Figure 3
Auteurs
1 The Department of Neurology, School of Medicine, Yale University New Haven, CT
2 The Epilepsy Center at Cleveland Clinic Foundation. Cleveland, Ohio, USA
3 Hôpital Erasme, ULB Cliniques universitaires de Bruxelles, Bruxelles, Belgium
* Correspondence: Rafeed Alkawadri 15 York Street, LCI 7-14B, New Haven, CT 06520, USA
  • Mots-clés : cingulate epilepsy, SEEG, hypermotor seizures, connectivity, propagation
  • DOI : 10.1684/epd.2016.0874
  • Page(s) : 418-25
  • Année de parution : 2016

Little is known about the propagation of seizures arising from the cingulate gyrus, as cingulate coverage with interhemispheric subdural electrodes is usually challenging and incomplete due to inherent anatomical and vascular limitations. We present a case of lesional mid-cingulate epilepsy confirmed by stereotactically implanted intracranial depth electrodes and subsequent surgical resection. Hypermotor symptomatology was seen during the first seven seconds of seizure onset while the seizure was still confined to the mid-cingulate gyrus contacts. The patient had brief contralateral clonic movements as seizure propagated to the primary motor cortex. There was a high concordance between the primary propagation contacts, as delineated by intracranial EEG, and the contacts, with higher coherence values in the connectivity matrix. Interestingly, cingulate-extra-cingulate connectivity and spread to the primary motor, premotor, and prefrontal cortex was seen preceding spread to other cingulate contacts, of which one was less than 15 mm from the onset contact. This report is one of a few published, documenting propagation of seizures arising from the mid-cingulate cortex. As illustrated by these data, hypermotor semiology correlated with direct activation of the cingulate cortex. Subsequent seizure propagation activated an extensive extra-cingulate rather than an intra-cingulate epileptogenic network. Interestingly, had the region of onset not sampled, the seizure onset would have appeared as non-localizing widespread rhythms over the fronto-parietal convexities. Further studies to explore the propagation of seizures arising from the cingulate gyrus and the physiological and pathological connectivity patterns within the cingulate gyrus in humans are needed, preferably using stereotactic implantation. Specific targets to be investigated are also discussed.