Good news!
"... shows how the thalamus – a sort of central networking hub that regulates functions such as language, memory, attention and movement – is affected months or years after a person has experienced a stroke, even though it was not directly damaged itself. ..."
From the significance and highlights:
"Significance
It is not currently understood why stroke causes a prominent slowing of neural activity, nor the associated functional impairment. Using a computational corticothalamic circuit model, we find that thalamic dysfunction is central to this abnormal activity as measured by magnetoencephalography (MEG), despite the absence of direct damage to the thalamus itself. The model indicated that slowing was caused by thalamic disinhibition, which was in turn associated with secondary thalamus degeneration. These findings highlight secondary thalamus disruption as an important determinant of corticothalamic circuit dysfunction and poststroke patient outcomes, and demonstrate how noninvasive measures of brain activity like MEG can be linked to underlying stroke pathophysiology via computational modeling.
Abstract
Stroke causes pronounced and widespread slowing of neural activity. Despite decades of work exploring these abnormal neural dynamics and their associated functional impairments, their causes remain largely unclear. To close this gap in understanding, we applied a neurophysiological corticothalamic circuit model to simulate magnetoencephalography (MEG) power spectra recorded from chronic stroke patients. Comparing model-estimated physiological parameters to those of controls, patients demonstrated significantly lower intrathalamic inhibition in the lesioned hemisphere, despite the absence of direct damage to the thalamus itself. We hypothesized that this disinhibition could instead be related to secondary degeneration of the thalamus, for which growing evidence exists in the literature. Further analyses confirmed that spectral slowing correlated significantly with overall secondary degeneration of the ipsilesional thalamus, encompassing decreased thalamic volume, altered tissue microstructure, and decreased blood flow. Crucially, this relationship was mediated by model-estimated thalamic disinhibition, suggesting a causal link between secondary thalamic degeneration and abnormal brain dynamics via thalamic disinhibition.
Finally, thalamic degeneration was correlated significantly with poorer cognitive and language outcomes, but not lesion volume, reinforcing that thalamus damage may account for additional individual variability in poststroke disability. Overall, our findings indicate that the frequently observed poststroke slowing reflects a disruption of corticothalamic circuit dynamics due to secondary thalamic dysfunction, and highlights the thalamus as an important target for understanding and potentially treating poststroke brain dysfunction."
SFU study sheds new light on what causes long-term disability after a stroke and offers new path toward possible treatment (original news release)
Secondary thalamic dysfunction underlies abnormal large-scale neural dynamics in chronic stroke (no public access)
No comments:
Post a Comment