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Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
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Pathophysiological associations of transcallosal dysfunction in ALS.

Mehdi A J van den Bos1, Mana Higashihara1,2, Nimeshan Geevasinga1

  • 1Westmead Clinical School, University of Sydney, Sydney, NSW, Australia.

European Journal of Neurology
|November 21, 2020
PubMed
Summary
This summary is machine-generated.

Amyotrophic lateral sclerosis (ALS) involves reduced transcallosal inhibition, impacting motor cortex excitability. This dysfunction correlates with faster disease progression and increased disability in ALS patients.

Keywords:
ALS pathophysiologyTMScortical neurophysiologytranscallosal inhibition

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Area of Science:

  • Neuroscience
  • Neurology
  • Motor Neuron Diseases

Background:

  • The corpus callosum's involvement in amyotrophic lateral sclerosis (ALS) is known from neuropathological studies.
  • Understanding transcallosal function alterations is crucial for ALS pathogenesis.

Purpose of the Study:

  • To investigate if altered transcallosal function contributes to ALS development and progression.
  • To correlate transcallosal function changes with functional disability in ALS patients.

Main Methods:

  • Assessed transcallosal function and motor cortex excitability in 17 ALS patients and healthy controls.
  • Measured transcallosal inhibition, short interval intracortical facilitation (SICF), and short interval intracortical inhibition (SICI).
  • Utilized clinical and neurophysiological assessments for patient staging.

Main Results:

  • ALS patients showed significantly reduced transcallosal inhibition compared to controls.
  • Cortical hyperexcitability, indicated by reduced SICI and increased SICF, was observed in ALS.
  • Reduced transcallosal inhibition correlated significantly with faster disease progression and muscle strength decline.

Conclusions:

  • Transcallosal circuit dysfunction is a key pathophysiological mechanism in ALS.
  • This dysfunction is linked to increased patient disability and accelerated disease progression.
  • Therapies targeting transcallosal circuit restoration may benefit ALS treatment.