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Wawrzyniak, M.

Publications and source records attributed to Wawrzyniak, M..

2 recordsLinked to original sources

Spatial neglect after subcortical stroke: sometimes a cortico-cortical disconnection syndrome

Background and ObjectivesSpatial neglect is commonly attributed to lesions of a predominantly right-hemispheric cortical network. Although spatial neglect was also repeatedly observed after lesions to the basal ganglia and the thalamus, many anatomical network models omit these structures. We investigated if disruption of functional or structural connectivity can explain spatial neglect in subcortical stroke. MethodsWe retrospectively investigated data of first-ever, acute stroke patients with right-sided lesions of the basal ganglia (n = 27) or the thalamus (n = 16). Based on lesion location, we estimated i) functional connectivity via lesion-network mapping with normative resting state fMRI data, ii) structural white matter disconnection and iii) tract-wise disconnection of association fibres based on normative tractography data to investigate the association of spatial neglect and disconnection measures. ResultsApart from very small clusters of functional disconnection observed in inferior/middle frontal regions in lesion-network symptom mapping for basal ganglia lesions, our analyses found no evidence of functional or structural subcortico-cortical disconnection. Instead, the multivariate consideration of lesion load to several association fibres predicted the occurrence of spatial neglect (p = 0.0048; AUC = 0.76), which were the superior longitudinal fasciculus, inferior occipitofrontal fasciculus, superior occipitofrontal fasciculus, and the uncinate fasciculus. ConclusionDisconnection of long (cortico-cortical) association fibres can explain spatial neglect in subcortical stroke. Like the competing theory of remote cortical hypoperfusion, this mechanism does not require the assumption of a genuine role for subcortical grey matter structures in spatial neglect.

neuroscience↗

Thalamocortical networks involved in Pusher Syndrome

Indirect quantification of functional and structural disconnection increases the knowledge derived from focal brain lesions by inferring subsequent brain network damage from the respective lesion. We applied both measures to a sample of 124 stroke patients to investigate brain disconnection in pusher syndrome - a disorder characterized by a disturbed perception of ones own upright body posture. Our results suggest a hub-like function of the posterior and lateral portions of the thalamus in the perception of ones own postural upright and identified dysfunction in a thalamo-cortical network as one likely cause of pusher syndrome. Lesion network-symptom-mapping investigating functional disconnection indicated cortical diaschisis in cerebellar, frontal, parietal, occipital, and temporal areas in patients with thalamic lesions suffering from pusher syndrome, but there was no evidence for functional diaschisis in cortical stroke and no evidence for the convergence of thalamic and cortical lesions onto a common functional network. Structural disconnectivity mapping identified several thalamo-cortical disconnections. Many of the thalamic and cortical regions disconnected by lesions that lead to pusher behavior correspond to previously reported lesion sites associated with pusher syndrome. Thus, while the presence of both, isolated thalamic and cortical lesions in context with pusher behavior has been reported previously and led to the conclusion that the correct estimation of ones own postural upright might depend on a thalamo-cortical network, our analyses offer the first evidence for a direct thalamo-cortical (or cortico-thalamic) interconnection and, more importantly, shed light on the location of the respective thalamo-cortical disconnections.

neuroscience↗