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Infratentorial MRI Findings in Rasmussen Encephalitis Suggest Primary Cerebellar Involvement

Johannes T Reiter1, Bastian David1, Selma Enders1

  • 1From the Department of Epileptology (J.T.R., B.D., S.E., C.C.P., T.B., C.E.E., R.S., T.R.), University Hospital Bonn; Charité-Universitätsmedizin Berlin (D.A., A.M.K.), Department of Pediatric Neurology; Charité-Universitätsmedizin Berlin (D.A., A.M.K.), Center for Chronically Sick Children; Charité-Universitätsmedizin Berlin (A.T.), Institute of Neuroradiology; Charité-Universitätsmedizin Berlin (A.M.K.), Institute for Cell Biology and Neurobiology; Department of Neuroradiology (V.K., A.R.), University Hospital Bonn; Department of Radiology and Nuclear Medicine (V.K.), Vrije Universiteit Amsterdam Medisch Centrum, The Netherlands; Institute of Experimental Epileptology and Cognition Research (B.W.), University Hospital Bonn; and Section for Translational Epilepsy Research (A.J.B.), Department of Neuropathology, University Hospital Bonn, Germany.

Neurology(R) Neuroimmunology & Neuroinflammation
|August 14, 2021
PubMed
Abstract

Insights

Rasmussen encephalitis (RE) causes unilateral brain inflammation. This study reveals RE also involves cerebellar atrophy, suggesting a primary cerebellar role beyond secondary effects.

Area of Science:

  • Neurology
  • Neuroimaging
  • Neuroinflammation

Background:

  • Rasmussen encephalitis (RE) is a rare neurological disorder typically affecting one side of the brain.
  • Anecdotal reports suggest cerebellar atrophy in RE, but the extent and nature of infratentorial involvement remain unclear.
  • This study investigates cerebellar abnormalities in RE using advanced MRI techniques.

Purpose of the Study:

  • To morphometrically investigate cerebellar and brainstem involvement in Rasmussen encephalitis.
  • To differentiate between primary cerebellar involvement and secondary atrophy in RE.
  • To explore the relationship between cerebellar atrophy and white matter integrity.

Main Methods:

  • Voxel-based morphometry (VBM) and asymmetry indices (AIs) of the cerebellum and brainstem in 57 RE patients and 57 controls.
  • Fluid-attenuated inversion recovery (FLAIR) imaging to assess inflammation.
  • Diffusion tensor imaging (DTI) to evaluate the cortico-ponto-cerebellar (CPC) tract integrity.
  • Spatial independent component analysis (ICA) to analyze atrophy patterns.

Main Results:

  • Patients with RE exhibited bilateral cerebellar and ipsilesional mesencephalic atrophy.
  • Morphometric AIs correlated with FLAIR intensity AIs in cases of predominant ipsilesional atrophy.
  • Reduced fractional anisotropy in ipsilesional CPC tracts was observed, indicating white matter damage.
  • ICA identified distinct ipsilesional and contralesional atrophy components in RE patients.

Conclusions:

  • The study demonstrates cerebellar atrophy in RE, with ipsilesional atrophy likely due to primary inflammation.
  • Contralesional cerebellar atrophy is interpreted as secondary, resulting from damage to the crossed cerebellar pathway.
  • These findings suggest a more extensive involvement of the cerebellum in Rasmussen encephalitis than previously understood.

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