Damage to white matter pathways in subacute and chronic spatial neglect: A group study and 2 single-case studies with complete virtual “in vivo” tractography dissection
Cerebral Cortex. 2012-11-15; 24(3): 691-706
DOI: 10.1093/cercor/bhs351
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1. Cereb Cortex. 2014 Mar;24(3):691-706. doi: 10.1093/cercor/bhs351. Epub 2012 Nov
15.
Damage to white matter pathways in subacute and chronic spatial neglect: a group
study and 2 single-case studies with complete virtual “in vivo” tractography
dissection.
Thiebaut de Schotten M(1), Tomaiuolo F, Aiello M, Merola S, Silvetti M, Lecce F,
Bartolomeo P, Doricchi F.
Author information:
(1)Natbrainlab, Department of Forensic and Neurodevelopmental Sciences, Institute
of Psychiatry, King’s College London, London, UK.
The exact anatomical localization of right hemisphere lesions that lead to left
spatial neglect is still debated. The effect of confounding factors such as acute
diaschisis and hypoperfusion, visual field defects, and lesion size may account
for conflicting results that have been reported in the literature. Here, we
present a comprehensive anatomical investigation of the gray- and white matter
lesion correlates of left spatial neglect, which was run in a sample 58 patients
with subacute or chronic vascular strokes in the territory of the right middle
cerebral artery. Standard voxel-based correlates confirmed the role played by
lesions in the posterior parietal cortex (supramarginal gyrus, angular gyrus, and
temporal-parietal junction), in the frontal cortex (frontal eye field, middle and
inferior frontal gyrus), and in the underlying parietal-frontal white matter.
Using a new diffusion tensor imaging-based atlas of the human brain, we were able
to run, for the first time, a detailed analysis of the lesion involvement of
subcortical white matter pathways. The results of this analysis revealed that,
among the different pathways linking parietal with frontal areas, damage to the
second branch of the superior longitudinal fasciculus (SLF II) was the best
predictor of left spatial neglect. The group study also revealed a subsample of
patients with neglect due to focal lesion in the lateral-dorsal portion of the
thalamus, which connects the premotor cortex with the inferior parietal lobule.
The relevance of fronto-parietal disconnection was further supported by complete
in vivo tractography dissection of white matter pathways in 2 patients, one with
and the other without signs of neglect. These 2 patients were studied both in the
acute phase and 1 year after stroke and were perfectly matched for age,
handedness, stroke onset, lesion size, and for cortical lesion involvement. Taken
together, the results of the present study support the hypothesis that anatomical
disconnections leading to a functional breakdown of parietal-frontal networks are
an important pathophysiological factor leading to chronic left spatial neglect.
Here, we propose that different loci of SLF disconnection on the rostro-caudal
axis can also be associated with disconnection of short-range white matter
pathways within the frontal or parietal areas. Such different local disconnection
patterns can play a role in the important clinical variability of the neglect
syndrome.
DOI: 10.1093/cercor/bhs351
PMID: 23162045 [Indexed for MEDLINE]