title: Autism spectrum disorders and schizophrenia: meta-analysis of the neural correlates of social cognition.
abstract: BACKGROUND
  Impaired social cognition is a cardinal feature of Autism Spectrum Disorders (ASD) and Schizophrenia (SZ). However, the functional neuroanatomy of social cognition in either disorder remains unclear due to variability in primary literature. Additionally, it is not known whether deficits in ASD and SZ arise from similar or disease-specific disruption of the social cognition network.
  
  
  OBJECTIVE
  To identify regions most robustly implicated in social cognition processing in SZ and ASD.
  
  
  METHODS
  Systematic review of English language articles using MEDLINE (1995-2010) and reference lists.
  
  
  METHODS
  Studies were required to use fMRI to compare ASD or SZ subjects to a matched healthy control group, provide coordinates in standard stereotactic space, and employ standardized facial emotion recognition (FER) or theory of mind (TOM) paradigms.
  
  
  METHODS
  Activation foci from studies meeting inclusion criteria (n = 33) were subjected to a quantitative voxel-based meta-analysis using activation likelihood estimation, and encompassed 146 subjects with ASD, 336 SZ patients and 492 healthy controls.
  
  
  RESULTS
  Both SZ and ASD showed medial prefrontal hypoactivation, which was more pronounced in ASD, while ventrolateral prefrontal dysfunction was associated mostly with SZ. Amygdala hypoactivation was observed in SZ patients during FER and in ASD during more complex ToM tasks. Both disorders were associated with hypoactivation within the Superior Temporal Sulcus (STS) during ToM tasks, but activation in these regions was increased in ASD during affect processing. Disease-specific differences were noted in somatosensory engagement, which was increased in SZ and decreased in ASD. Reduced thalamic activation was uniquely seen in SZ.
  
  
  CONCLUSIONS
  Reduced frontolimbic and STS engagement emerged as a shared feature of social cognition deficits in SZ and ASD. However, there were disease- and stimulus-specific differences. These findings may aid future studies on SZ and ASD and facilitate the formulation of new hypotheses regarding their pathophysiology.
authors: Department of Child and Adolescent Psychiatry, Institute of Psychiatry, King's College London, London, United Kingdom.
authors: Gisela
authors: G
authors: Sugranyes
authors: Marinos
authors: M
authors: Kyriakopoulos
authors: Richard
authors: R
authors: Corrigall
authors: Eric
authors: E
authors: Taylor
authors: Sophia
authors: S
authors: Frangou
mesh_terms: D002648:Child; D002659:Child Development Disorders, Pervasive / Q000503:physiopathology*; D003071:Cognition / Q000502:physiology*; D006801:Humans; D007398:Interpersonal Relations; D008279:Magnetic Resonance Imaging; D009420:Nervous System / Q000503:physiopathology*; D012559:Schizophrenia / Q000503:physiopathology*