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Inflammation and Corticospinal Functioning in Multiple Sclerosis: A TMS Perspective.

Mario Stampanoni Bassi1, Fabio Buttari1, Luana Gilio1

  • 1Unit of Neurology & Neurorehabilitation, IRCCS Neuromed, Pozzilli, Italy.

Frontiers in Neurology
|August 1, 2020
PubMed
Summary
This summary is machine-generated.

Transcranial magnetic stimulation (TMS) reveals altered brain excitability in multiple sclerosis (MS). Inflammation-induced synaptopathy may underlie MS pathophysiology and symptoms, offering new insights into disease mechanisms.

Keywords:
Transcranial magnetic stimulation (TMS)cytokinesinflammationmultiple sclerosis (MS)synaptic transmission

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Area of Science:

  • Neuroscience
  • Clinical Neurology
  • Neurophysiology

Background:

  • Multiple sclerosis (MS) involves demyelination and neuronal loss, affecting corticospinal tract integrity.
  • Transcranial magnetic stimulation (TMS) assesses motor cortex function and corticospinal tract integrity in MS.
  • TMS has explored neurophysiological underpinnings of MS symptoms like fatigue, but study variability suggests other mechanisms.

Purpose of the Study:

  • To discuss if TMS-assessed corticospinal excitability alterations in MS patients can explain pathophysiological correlates.
  • To explore the relationship between these alterations and specific MS clinical characteristics and symptoms.
  • To review evidence on inflammatory synaptopathy in MS, its early presence, association with relapses, and disease progression.

Main Methods:

  • Review of existing literature on TMS studies in multiple sclerosis.
  • Integration of findings from experimental autoimmune encephalomyelitis (EAE) animal models.
  • Analysis of cerebrospinal fluid (CSF) biomarkers in relation to TMS measures.

Main Results:

  • TMS measures are associated with demyelination and neuronal loss in MS.
  • An imbalance between cortical excitation and inhibition is observed in MS patients via TMS.
  • Pro-inflammatory and anti-inflammatory molecules in CSF correlate with corticospinal hyperexcitability, suggesting inflammatory synaptopathy.

Conclusions:

  • Inflammatory synaptopathy is a key pathophysiological mechanism in MS.
  • Corticospinal excitability alterations measured by TMS may correlate with MS pathophysiology and clinical features.
  • Inflammatory synaptopathy may be an early feature, characterize relapses, and progress throughout the MS disease course.