Extensive cortical inflammation is associated with epilepsy in multiple sclerosis

Massimiliano Calabrese1, Nicola De Stefano, Matteo Atzori

  • 1The Multiple Sclerosis Centre of Veneto Region, First Neurology Clinic, Dept. of Neurosciences, University Hospital of Padova, Via Giustiniani 5, 35128 Padova, Italy. calabresem@hotmail.it

Journal of Neurology
|January 30, 2008
PubMed
Abstract

Insights

Epilepsy is more common in multiple sclerosis (MS). Intracortical lesions (ICLs) detected by double inversion recovery (DIR) MRI are more prevalent in relapsing remitting MS (RRMS) patients with epilepsy, suggesting ICLs cause seizures in MS.

Area of Science:

  • Neurology
  • Neuroimaging
  • Neuroinflammation

Background:

  • Epilepsy occurs 3-6 times more frequently in multiple sclerosis (MS) patients than the general population.
  • Conventional MRI may not detect pure intracortical lesions (ICLs) linked to seizures in MS.
  • The double inversion recovery (DIR) sequence offers improved detection of ICLs.

Purpose of the Study:

  • To investigate the relationship between intracortical lesions (ICLs) and epileptic seizures in relapsing remitting MS (RRMS).
  • To clarify the role of ICLs in epilepsy development in MS patients.

Main Methods:

  • Utilized the DIR MRI sequence to detect ICLs in 20 RRMS patients with epilepsy (RRMS/E).
  • Compared findings with 80 age-, gender-, and disease-matched RRMS patients without a history of seizures.
  • Matched patients based on disease duration, EDSS, and T2 lesion volume.

Main Results:

  • ICLs were detected in 90% of RRMS/E patients versus 48% of RRMS patients (p=0.001).
  • RRMS/E patients exhibited significantly more ICLs (7.2 vs 1.5) and a larger total ICL volume (1.2 cm³ vs 0.2 cm³).
  • No significant differences in juxtacortical lesions or T2-weighted lesion volume were found between groups.

Conclusions:

  • RRMS patients with epilepsy show more extensive cortical inflammation than those without seizures.
  • Inflammatory intracortical lesions are strongly implicated as a cause of epilepsy in MS.

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