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Related Experiment Video

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Utilizing Repetitive Transcranial Magnetic Stimulation to Improve Language Function in Stroke Patients with Chronic Non-fluent Aphasia

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Secondary thalamic dysfunction underlies abnormal large-scale neural dynamics in chronic stroke.

Phillip R Johnston^1,2, John D Griffiths^3,4,5,6, Leanne Rokos^2,4

¹Department of Psychology, University of Toronto, Toronto, ON M5S 3G3, Canada.

Proceedings of the National Academy of Sciences of the United States of America

|November 6, 2024

Summary

Stroke causes widespread neural slowing due to secondary thalamic degeneration, not direct damage. This thalamic dysfunction disrupts corticothalamic circuits, impacting cognitive and language function after stroke.

Keywords:

aperiodic neural dynamics computational modeling magnetoencephalography stroke thalamus

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Electroencephalography Network Indices as Biomarkers of Upper Limb Impairment in Chronic Stroke

Electroencephalography Network Indices as Biomarkers of Upper Limb Impairment in Chronic Stroke

Published on: July 14, 2023

Area of Science:

Neuroscience
Neurology
Medical Imaging

Background:

Stroke frequently leads to widespread neural slowing and functional impairments.
The precise causes of these abnormal neural dynamics post-stroke remain largely unknown.
Secondary degeneration of the thalamus is increasingly recognized as a consequence of stroke.

Purpose of the Study:

To investigate the causes of post-stroke neural slowing.
To explore the role of the thalamus and corticothalamic circuits in post-stroke neural dynamics.
To determine the relationship between secondary thalamic degeneration and functional outcomes.

Main Methods:

Applied a neurophysiological corticothalamic circuit model to magnetoencephalography (MEG) power spectra from chronic stroke patients.
Compared model-estimated physiological parameters between patients and controls.
Analyzed correlations between spectral slowing, secondary thalamic degeneration (volume, microstructure, blood flow), and cognitive/language outcomes.

Main Results:

Stroke patients exhibited significantly lower intrathalamic inhibition in the lesioned hemisphere.
Spectral slowing strongly correlated with overall secondary degeneration of the ipsilesional thalamus.
Thalamic degeneration, mediated by thalamic disinhibition, was linked to abnormal brain dynamics and poorer cognitive/language outcomes, independent of lesion volume.

Conclusions:

Post-stroke neural slowing reflects disrupted corticothalamic circuit dynamics caused by secondary thalamic dysfunction.
Thalamic disinhibition plays a crucial role in linking secondary thalamic degeneration to abnormal neural activity.
The thalamus is a key target for understanding and potentially treating post-stroke brain dysfunction and associated disability.