Given the STG’s important roles in language processing (left hemisphere) and social perception (right hemisphere), the main goal of this study was to examine STG volumes in a sample of children and adolescents with autism. It was hypothesized that STG volumes would be greater in subjects with autism compared to healthy controls based on the replicable finding of brain overgrowth (which is associated with dysfunction) which is more prominent in the frontal/temporal lobes. The results of this study provide support to this hypothesis. Enlarged right STG in the autism group was the only statistically significant finding observed in the current study, but only after controlling for age and TBV. Notably, in the present study, there were no significant differences in the right-left asymmetry of the STG between the two groups, a finding which is also consistent with most, but not all studies investigating STG asymmetry in autism (De Fosse et al., 2004
; Gage et al., 2009
; Herbert et al., 2002
; Herbert et al., 2005
The STG volumetric findings reported in the current study differ from the only known study to date specifically examining whole STG volume in autism. Bigler and colleagues measured whole STG volumes in a sample of children and adolescent males with autism and compared them with matched typically developing subjects (Bigler et al., 2007
). Their study consisted of 30 subjects with autism (mean age = 12.6±3.5 years, FSIQ = 100.1±22.2, TBV = 1398.0±137.2 cc) and 26 typically developing subjects (mean age = 11.8±3.7 years, FSIQ = 105.7±17.8, TBV = 1436.8±145.9 cc). They did not find any significant between-group differences in STG volumes. The reason for this inconsistency is unclear, but likely owing to differences in study procedures including site differences in subject samples, scanning parameters, morphometric measurements, and image-processing methods. Notable differences with the current study include subject characteristics. The subjects with autism in the present investigation have slighter larger TBV than control subjects; however, the opposite is true in the Bigler study. While the TBV differences are not significant in both studies, controlling for TBV in the current study draws out additional significant enlargements of STG volumes in the autism group. Group-wise comparison of STG volumes in the Bigler study were not performed controlling for TBV. Other clear differences that might contribute to lack of agreement include imaging protocol (i.e. magnet strength, resolution, etc) and method used to measure STG volumes (i.e. software package, tracing procedures, etc).
In contrast, the findings reported here are concordant with mounting evidence suggesting STG abnormalities in autism as supported by postmortem, neuroimaging, and electrophysiology studies. In a postmortem study of the cytoarchitecture of the cerebral cortex, Casanova and colleagues reported abnormal cortical minicolumns in the posterior STG of autistic patients compared to controls; cell columns in the brains of autistic patients were significantly smaller and less compact in their configuration, with less neuropil space in their periphery (Casanova et al., 2002
). In a voxel-based investigation of brain structure in male adolescents with autism, Waiter and colleagues found the brains in the autism group to be associated with increased grey matter volume in the superior and middle temporal cortices when compared to controls (Waiter et al., 2004
). Several PET studies have also reported temporal lobe abnormalities (Boddaert et al., 2003
; Castelli et al., 2002
; Muller et al., 1999
; Zilbovicius et al., 1995
). In their PET study, Boddaert and colleagues reported abnormal STG activation in autistic patients while listening to speech-like sounds (Boddaert et al., 2003
). Castelli and colleagues showed diminished activation in Brodmann areas 21/22 (superior temporal sulcus) in a group with autism and Asperger’s syndrome while performing mentalizing tasks (Castelli et al., 2002
). Muller and colleagues demonstrated reduced bilateral temporal activations in adults with autism while performing an auditory task when compared to a group of control subjects (Muller et al., 1999
). Zilbovicius and colleagues reported significant hypoperfusion in the bilateral STG in a group of children with autism (Zilbovicius et al., 1995
). SPECT studies have also shown a reduction in regional cerebral blood flow in the superior temporal region of children and adults with autism (Mountz et al., 1995
; Ohnishi et al., 2000
). In an fMRI study using a theory of mind task, Baron-Cohen and colleagues demonstrated greater STG activation in a group of individuals with autism when compared to controls (Baron-Cohen et al., 1999
). In a more recent fMRI study, Gomot and colleagues reported reduced activation in the bilateral superior temporal region during a novelty detection task in children with autism (Gomot et al., 2006
). Finally, ERP (Bruneau et al., 2003
; Bruneau et al., 1999
) and MEG (Gage et al., 2003
; Roberts et al., 2010
; Rojas et al., 2008
) studies have also revealed STG abnormalities in autism. Although heterogeneous, these abnormal findings across multiple research modalities involving the STG strongly suggest a possible link between STG dysfunction/structure and autistic behavior.
At first glance, the finding of right-sided STG abnormalities appears counterintuitive given that language (one core impairment in autism) is usually left-lateralized. However, this finding is consistent with the right STG’s key role in social perception. Social perception refers to the processing of face expressions, eye gaze, body movements, and other type of biological motion with the overall goal of gauging the mental states of others (Allison et al., 2000
). Abnormality in social interaction is the sine qua non of autism spectrum disorders, and is essential for the diagnosis of autistic disorder, Aspeger’s disorder, and pervasive developmental disorder not otherwise specified (APA, 2000
). A large number of reports comparing groups with autism to healthy controls have reported abnormal activity in the superior temporal region (STG and the related superior temporal sulcus) using fMRI in conjunction with tasks tapping social perception skills (Redcay, 2008
). Abnormal volume of this structure supports the possible existence of structural defects which may help explain the array of aforementioned functional abnormalities. Perhaps more intriguing, however, is the finding of increased right posterior STG volume in the post-hoc analysis. This region includes the well-known posterior superior temporal sulcus, an area of intense research which has been implicated in explaining the social perceptual deficits in autism (Pelphrey and Carter, 2008b
To date, this is study is one of few specifically addressing whole STG volume in autism, reporting increased right-sided STG volume in children and adolescents with autism. However, the findings of this study must be interpreted in the context of several limitations. First, the sample size was relatively small; therefore, type I error cannot be excluded, especially in light of a previously reported negative study (Bigler et al., 2007
). Second, the sample consisted of only high-functioning males with autism ages eight to 18 years. This narrow demographic profile limits the generalizability of the results. Moreover, it may not be the case that the STG alterations found in HFA are also found in lower-functioning autism because their underlying etiology and neurobiology may differ. Third, clinical characterization of the HFA group is limited and detailed assessments of social and language deficits are unavailable for correlation with imaging data. Fourth, the volumetric measures obtained in this study are for the whole STG only and do not separate gray and white matter volumes; therefore, it is not possible to know what type of brain tissue is driving this effect. Finally, significant results were apparent only after exclusion of an extreme outlier in the control group. This strategy, while not ideal, was necessary to avoid the risks of artificially skewing the statistical analysis by a single outlier in a small study sample.
The STG is a critical node of the social brain as evidenced by its role in language processing (left hemisphere) and social perception (right hemisphere), and anatomical interconnection to association cortices and the limbic system. Therefore, abnormalities in this structure could possibly explain some of the core and secondary symptoms of autism. While preliminary, this study provides evidence for structural abnormalities of the right STG, and its posterior subdivision, in a sample of children and adolescent males with autism. This finding is consistent with the numerous reports of superior temporal abnormalities using a multitude of research modalities. Most notable are right posterior STG (right superior temporal sulcus) abnormalities detected using fMRI during tasks tapping social perceptual skills. However, in light of the aforementioned limitations, additional studies are needed before any conclusions can be made regarding abnormal STG structure in individuals with autism. Additional cross-sectional and longitudinal studies using larger sample sizes are warranted. Future studies ideally should include subjects carefully matched for age and sex and should incorporate periodic longitudinal clinical evaluations to assess relationships between imaging and clinical data. Finally, combining multiple neuroimaging modalities such as high-resolution structural MRI, MR spectroscopy, fMRI, and diffusion tensor imaging would also be helpful in understanding the role of the STG and help clarify its altered development in individuals with autism.