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The EEG in E200K familial CJD: relation to MRI patterns.

Shmuel A Appel1, Joab Chapman, Isak Prohovnik

  • 1Department of Neurology, The Sagol Neuroscience Center, and Chaim Sheba Medical Center affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, 52621, Tel-Hashomer, Israel.

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In familial Creutzfeldt-Jakob Disease (fCJD) with the E200K mutation, electroencephalogram (EEG) abnormalities correlate with cortical MRI changes, not basal ganglia involvement. Periodic sharp wave complexes (PSWC) reflect cortical pathology in these prion disease patients.

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Area of Science:

  • Neuroscience
  • Neurology
  • Medical Imaging

Background:

  • Familial Creutzfeldt-Jakob Disease (fCJD) is a rare neurodegenerative disorder.
  • The E200K mutation is a common genetic cause of fCJD.
  • Understanding the relationship between EEG and MRI findings is crucial for diagnosis and understanding disease mechanisms.

Purpose of the Study:

  • To investigate the correlation between electroencephalogram (EEG) abnormalities and magnetic resonance imaging (MRI) findings in E200K mutation-positive fCJD patients.
  • To determine if EEG patterns, specifically periodic sharp wave complexes (PSWC), relate more closely to cortical or basal ganglia pathology.

Main Methods:

  • A prospective study involving 13 patients with E200K fCJD.
  • Comprehensive evaluations including EEG and diffusion-weighted imaging (DWI) MRI.
  • Analysis of the relationship between EEG abnormalities and DWI hyperintensities.

Main Results:

  • EEG showed classical CJD periodic sharp wave complexes (PSWC) in 38% of patients and slow activity in 62%.
  • Cortical MRI changes were observed in 6 patients, with 83% showing concordance between MRI and EEG findings.
  • EEG abnormalities correlated primarily with cortical pathology (DWI hyperintensities) rather than basal ganglia involvement.

Conclusions:

  • EEG findings in E200K fCJD patients resemble those in sporadic CJD (sCJD).
  • EEG abnormalities, particularly PSWC, are indicative of cortical pathology in E200K fCJD.
  • This suggests cortical involvement is a primary driver of EEG abnormalities in prion diseases.