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Grey and white matter network disruption is associated with sensory deficits after stroke.

ABSTRACT: Somatosensory deficits after ischaemic stroke are common and can occur in patients with lesions in the anterior parietal cortex and subcortical nuclei. It is less clear to what extent damage to white matter tracts within the somatosensory system may contribute to somatosensory deficits after stroke. We compared the roles of cortical damage and disruption of subcortical white matter tracts as correlates of somatosensory deficit after ischaemic stroke. Clinical and imaging data were assessed in incident stroke patients. Somatosensory deficits were measured using a standardized somatosensory test. Remote effects were quantified by projecting the MRI-based segmented stroke lesions onto a predefined atlas of white matter connectivity. Direct ischaemic damage to grey matter was computed by lesion overlap with grey matter areas. The association between lesion impact scores and sensory deficit was assessed statistically. In 101 patients, median sensory score was 188/193 (97.4%). Lesion volume was associated with somatosensory deficit, explaining 23.3% of variance. Beyond this, the stroke-induced grey and white matter disruption within a subnetwork of the postcentral, supramarginal, and transverse temporal gyri explained an additional 14% of the somatosensory outcome variability. On mutual comparison, white matter network disruption was a stronger predictor than grey matter damage. Ischaemic damage to both grey and white matter are structural correlates of acute somatosensory disturbance after ischaemic stroke. Our data suggest that white matter integrity of a somatosensory network of primary and secondary cortex is a prerequisite for normal processing of somatosensory inputs and might be considered as an additional parameter for stroke outcome prediction in the future.

SUBMITTER: Kessner SS

PROVIDER: S-EPMC8163991 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Over 90% of children with Autism Spectrum Disorders (ASD) demonstrate atypical sensory behaviors. In fact, hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment is now included in the DSM-5 diagnostic criteria. However, there are children with sensory processing differences who do not meet an ASD diagnosis but do show atypical sensory behaviors to the same or greater degree as ASD children. We previously demonstrated that children with Sensory Processing Disorders (SPD) have impaired white matter microstructure, and that this white matter microstructural pathology correlates with atypical sensory behavior. In this study, we use diffusion tensor imaging (DTI) fiber tractography to evaluate the structural connectivity of specific white matter tracts in boys with ASD (n = 15) and boys with SPD (n = 16), relative to typically developing children (n = 23). We define white matter tracts using probabilistic streamline tractography and assess the strength of tract connectivity using mean fractional anisotropy. Both the SPD and ASD cohorts demonstrate decreased connectivity relative to controls in parieto-occipital tracts involved in sensory perception and multisensory integration. However, the ASD group alone shows impaired connectivity, relative to controls, in temporal tracts thought to subserve social-emotional processing. In addition to these group difference analyses, we take a dimensional approach to assessing the relationship between white matter connectivity and participant function. These correlational analyses reveal significant associations of white matter connectivity with auditory processing, working memory, social skills, and inattention across our three study groups. These findings help elucidate the roles of specific neural circuits in neurodevelopmental disorders, and begin to explore the dimensional relationship between critical cognitive functions and structural connectivity across affected and unaffected children.

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Grey and white matter network disruption is associated with sensory deficits after stroke.

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