Brain Basis of Empathy in
“Hypersocial” Williams Syndrome
Individuals
- A Meta-Analytical Approach –
-
1
Stanford University School of Medicine, Center for Interdisciplinary Brain Sciences Research (CIBSR), United States
-
2
Salk Institute for Biological Studies, Laboratory for Cognitive Neuroscience, United States
-
3
Harvard Medical School, Department of Neurology, United States
-
4
University of Zagreb, Department of Psychology, United States
-
5
Cedars-Sinai Medical Center at UCLA, Department of Pediatrics, United States
Statement of Purpose: Williams syndrome (WS) is a neurodevelopmental disorder caused by a hemizygous deletion of up to 28 genes on chromosome 7q11.23. One striking feature of the syndrome that distinguishes it from other disorders is excessive sociability and empathy for others (Meyer-Lindenberg et al. Nature Reviews Neuroscience 2006). The mirror neuron system (MNS) including the inferior frontal gyrus (IFG) to ventral precentral gyrus (vPrCG) and inferior parietal lobule (IPL), as well as the posterior superior temporal gyrus (pSTG) which provides visual input to the MNS, have been linked to empathy and socialization (Rizzolatti and Craighero, Annual Review of Neuroscience, 2004). Further, in separate lines of studies, empathy has been linked to brain regions such as the sensorimotor regions, limbic and paralimbic regions (anterior cingulate cortex,ACC; insula) (Vignemont and Singer, Trends Cogn Sci, 2006), and theory of mind (ToM) to the medial frontal cortex (mPFC), temporal poles (TP), and temporoparietal junction (TPJ) (Ciaramidaro et al. Neuropsychologia, 2007). In WS, it has been suggested that the cognitive component of theory of mind (ToM) is impaired whereas the perceptual component of ToM may be spared (Tager-Flusberg and Sullivan, Cognition, 2000). Therefore, it may be hypothesized that individuals with WS show differential impairment in brain regions implicated in cognitive and perceptual components of these systems.
Methods: In this preliminary study, we pooled previously collected functional magnetic resonance imaging (fMRI) data from 4 studies of affect and gaze processing. We compared brain activation in WS compared to typically developing (TD) control individuals. We also examined brain regions that are associated with empathy scores in WS and in TD individuals. Finally, diffusion tensor imaging (DTI) data was examined to test our hypothesis.
Results: Relative to TD individuals the WS group showed decreased activation in the “social brain”, namely the IFG, vPrCG, insula, TP, fusiform and amygdala regions. On the other hand, WS compared to the TD group showed increased activation in the right IPL/pSTG. Regressing out task type, age, gender, task performance, and voxel-based gray matter morphometry did not change the results. Further, whereas the anterior “social brain” (mPFC, IFG/PrCG/insula, STG) showed positive correlation with empathy scores in TD individuals, WS patients showed positive correlation with more posterior and “perceptual” regions (IPL, occipital regions, thalamus). Finally, DTI of the superior longitudinal / arcuate fascicule showed negative association with empathy scores, similar to the previously found negative associations found with cognitive abilities (Hoeft et al. J Neurosci, 2007).
Discussion: This study shows promising initial results suggesting putative neural systems associated with empathy in WS. The results support the hypothesis of the dissociation between the cognitive and perceptual components of empathy in WS. Future studies using tasks that more effectively target the neural systems involved in empathy are warranted.
Conference:
12th International Professional Conference on Williams Syndrome, Garden Grove,CA, United States, 13 Jul - 14 Jul, 2008.
Presentation Type:
Oral Presentation
Topic:
SESSION 3: Neuroimaging and Brain Functioning in Williams Syndrome
Citation:
Hoeft
F,
Karchemskiy
A,
Haas
BW,
Bellugi
U,
Galaburda
A,
Mills
DL,
Korenberg
JR and
Reiss
AL
(2009). Brain Basis of Empathy in
“Hypersocial” Williams Syndrome
Individuals
- A Meta-Analytical Approach –.
Conference Abstract:
12th International Professional Conference on Williams Syndrome.
doi: 10.3389/conf.neuro.09.2009.07.010
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Received:
29 Apr 2009;
Published Online:
29 Apr 2009.
*
Correspondence:
F. Hoeft, Stanford University School of Medicine, Center for Interdisciplinary Brain Sciences Research (CIBSR), Stanford, CA, United States, fumiko.hoeft@ucsf.edu