Enlargement of cerebral ventricles as an early indicator of encephalomyelitis

PLoS One. 2013 Aug 22;8(8):e72841. doi: 10.1371/journal.pone.0072841. eCollection 2013.

Abstract

Inflammatory disorders of the central nervous system such as multiple sclerosis and acute disseminated encephalomyelitis involve an invasion of immune cells that ultimately leads to white matter demyelination, neurodegeneration and development of neurological symptoms. A clinical diagnosis is often made when neurodegenerative processes are already ongoing. In an attempt to seek early indicators of disease, we studied the temporal and spatial distribution of brain modifications in experimental autoimmune encephalomyelitis (EAE). In a thorough magnetic resonance imaging study performed with EAE mice, we observed significant enlargement of the ventricles prior to disease clinical manifestation and an increase in free water content within the cerebrospinal fluid as demonstrated by changes in T2 relaxation times. The increase in ventricle size was seen in the lateral, third and fourth ventricles. In some EAE mice the ventricle size started returning to normal values during disease remission. In parallel to this macroscopic phenomenon, we studied the temporal evolution of microscopic lesions commonly observed in the cerebellum also starting prior to disease onset. Our data suggest that changes in ventricle size during the early stages of brain inflammation could be an early indicator of the events preceding neurological disease and warrant further exploration in preclinical and clinical studies.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cerebral Ventricles / abnormalities*
  • Encephalomyelitis, Autoimmune, Experimental / diagnosis
  • Encephalomyelitis, Autoimmune, Experimental / pathology*
  • Female
  • Magnetic Resonance Imaging
  • Mice

Grants and funding

This work was supported by a university grant from the Experimental and Clinical Research Center (ECRC2010-2013), a research grant from Novartis and research grants from the German Research Foundation (DFG Exc 257 to FP, WA 2804/1-1 to SW). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.