Acute lesions that impair affective empathy.
Richard Leigh,Kenichi Oishi,John Hsu,Martin A. Lindquist,Rebecca F. Gottesman,Rebecca F. Gottesman,Samson Jarso,Ciprian M. Crainiceanu,Susumu Mori,Argye E. Hillis,Argye E. Hillis +10 more
TL;DR: Three studies converge in support of the proposal that affective empathy--making inferences about how another person feels--engages at least the following areas: prefrontal cortex, orbitofrontal gyrus, anterior insula, anterior cingulate cortex, temporal pole, amygdala and temporoparietal junction.
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Abstract: Functional imaging studies of healthy participants and previous lesion studies have provided evidence that empathy involves dissociable cognitive functions that rely on at least partially distinct neural networks that can be individually impaired by brain damage. These studies converge in support of the proposal that affective empathy—making inferences about how another person feels—engages at least the following areas: prefrontal cortex, orbitofrontal gyrus, anterior insula, anterior cingulate cortex, temporal pole, amygdala and temporoparietal junction. We hypothesized that right-sided lesions to any one of these structures, except temporoparietal junction, would cause impaired affective empathy (whereas bilateral damage to temporoparietal junction would be required to disrupt empathy). We studied 27 patients with acute right hemisphere ischaemic stroke and 24 neurologically intact inpatients on a test of affective empathy. Acute impairment of affective empathy was associated with infarcts in the hypothesized network, particularly temporal pole and anterior insula. All patients with impaired affective empathy were also impaired in comprehension of affective prosody, but many patients with impairments in prosodic comprehension had spared affective empathy. Patients with impaired affective empathy were older, but showed no difference in performance on tests of hemispatial neglect, volume of infarct or sex distribution compared with patients with intact affective empathy.
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Citations
Leukoaraiosis is independently associated with naming outcome in poststroke aphasia.
Amy E. Wright,Donna C. Tippett,Sadhvi Saxena,Rajani Sebastian,Bonnie L. Breining,Andreia V. Faria,Argye E. Hillis +6 more
TL;DR: Naming outcome after poststroke aphasia is influenced by the initial severity of right hemisphere leukoaraiosis independently of other variables, suggesting degree of recovery from aphasIA may depend on the integrity of the noninfarcted brain tissue.
Influence of age, lesion volume, and damage to dorsal versus ventral streams to viewer- and stimulus-centered hemispatial neglect in acute right hemisphere stroke
Adrian Suarez,Sadhvi Saxena,Kenichi Oishi,Kumiko Oishi,Alexandra Walker,Chris Rorden,Argye E. Hillis,Argye E. Hillis +7 more
TL;DR: The relative contributions of age, total lesion volume, and damage to subcortical and cortical grey matter regions as well as white matter tracts to both the severity and presence of significant viewer-centered and stimulus-centered neglect are identified, using multivariable regression tests.
Aphasia or Neglect after Thalamic Stroke: The Various Ways They may be Related to Cortical Hypoperfusion
Rajani Sebastian,Mara G. Schein,Cameron Davis,Yessenia Gomez,Melissa Newhart,Kenichi Oishi,Argye E. Hillis +6 more
TL;DR: Findings indicate that aphasia was observed in some cases of isolated left thalamic infarcts without cortical hypoerfusion due to arterial stenosis or occlusion, but neglect occurred after isolated right thalic infarCTs only when there was cortical hypoperfusiondue to arterIAL stenosisor occlusions.
A meta-analytic review of social cognitive function following stroke.
TL;DR: The results indicated that three of the four core domains of social cognitive function were significantly disrupted in people with stroke, and moderate to large deficits were identified for theory of mind, social perception, social behaviour, and social behaviour.
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