Asperger Syndrome: A Proton Magnetic Resonance Spectroscopy Study of BrainDeclan G.M. Murphy et al., Archives of General Psychiatry, Volume 59, October 2002.
Asperger Syndrome (AS; an autistic disorder) is associated with impaired social skills and obsessional/repetitive behaviour. Patients with autism have significant abnormalities in the frontal lobe and frontoparietal connectivity. Nobody has examined the relationship between abnormalities in the frontal and parietal lobes and clinical symptoms in people with AS. Subjects with AS have abnormalities in neuronal integrity of the prefrontal lobe, which is related to severity of clinical symptoms.
Changes in Cerebral Blood Flow in Asperger Syndrome during Theory of Mind Tasks
Presented by the Auditory Route T. Nieminen-Von Wendt, L. Metsahonkala, S. Aalto, T. Autti, R. Vanhala and L. Von-Wendt, European Child and Adolescent Psychiatry, 2003, 12: 178 - 189.
Lack of theory of mind (ToM) has been considered to be a key feature in Asperger Syndrome (AS). The main aim of the present study was to determine whether an exclusively auditory input of ToM stories activated the same brain areas as demonstrated previously using individual stimuli. Eight right-handed otherwise healthy men with AS and eight healthy right-handed male controls participated in the PET activation study using auditory given ToM stories and stories about physical events for induction. Both subjects with AS and controls showed increased activation in the occipitotemporal area bilaterally and in thalamus during ToM tasks. Both groups also showed activation in the medial frontal area during ToM tests. However, this activation was more intensive and extensive in the control group, especially when a more sensitive analysis method was used. As a group, unrelated unrelated to the tasks, the AS subjects showed increased activation of the cerebellum. It was concluded that the activation pattern was mainly in agreement with earlier studies using comparable stimuli administered differently. There was no support for a right hemisphere specific dysfunction.
Defining the Broader Phenotype of Autism: Genetic, Brain, and Behavioural PerspectivesGeraldine Dawson, Sara Webb, Gerard D. Schellenberg, Stephen Dager, Seth Friedman, Elizabeth Aylward, and Todd Richards, Development and Psychopathology, 14 (2002), 581 - 611.
In this article, the current state knowledge of the cognitive neuroscience of social and language impairments in autism is reviewed. Following from this, six candidate broader phenotype autism traits are proposed: (a) face processing, including structural encoding of facial features and face movements, such as eye gaze; (b) social affiliation or sensitivity to social award, pertaining to the social motivational impairments found in autism; (c) motor imitation ability, particularly imitation of body actions; (d) memory, specifically those aspects of memory mediated by the medial temporal lobe - prefrontol circuits; (e) executive function, especially planning and flexibility; and (f) Language ability, particularly those aspects of language that overlap with specific language impairment, namely, phonological processing.
Asperger Syndrome: A Proton Magnetic Resonance Spectroscopy Study of the Brain
G. Declan and Murphy et al., Archives of General Psychiatry, October 2002, 59, 885 - 891.
We used in vivo proton magnetic resonance spectroscopy to examine neutronal integrity of the medial prefrontal and parietal lobes in 14 non-learning disabled adults with AS and 18 control subjects (of similar sex, age and IQ). We obtained measures of the prefrontal lobe in 11, the parietal lobe in 13, and both lobes in 10 subjects with AS. We measured concentrations and ratios of N - acetylaspartate (NAA), creatine and phosphocreatine (Cr + PCr), and choline (Cho). Levels of NAA, Cr+ PCr, and Cho are indicators of neuronal density and mitochondrial metabolism, phosphate metabolism, and membrane turnover. Frontal metabolite levels were correlated with scores on the Yale-Brown Obsessive Compulsive Scale and the Autism Diagnostic Interview. Subjects with AS had significantly higher prefrontal lobe concentration of NAA (x = -3.1; P= .002), Cr + PCr (z= -2.2; P= .03) and Cho (z= -2.9; P= .003). Increased prefrontal NAA concentration was significantly correlated with obsessional behaviour (t = 0.72; P=.02). We found no significant differences in parietal lobe metabolite concentrations. Subjects with AS have abnormalities in neuronal integrity of the prefrontal lobe, which is related to severity of clinical symptoms.
Autism, A.S. and Brain Mechanisms for the Attribution of Mental States to Animated Shapes
F. Castelli, C. Frith, F. Happe and U. Frith, Brain (2002), 125, 1839 - 1849.
Ten able adults with autism or Asperger's Syndrome and 10 normal volunteers were PET scanned while watching animated sequences. The animations depicted two triangles moving about on a screen in three different conditions: moving randomly, moving in a goal-directed fashion, (clashing, fighting), and moving interactively with implied intentions (coaxing, tricking). The last condition frequently elicited descriptions in terms of mental states that viewers attributed to the triangles (mentalizing). The autism group gave fewer and less accurate descriptions of these latter animations, but equally accurate descriptions of the other animations compared with controls. While viewing animations that elicited mentalizing, in contrast to randomly moving shapes, the normal group showed increased activation in a previously identified mentalizing network (medial prefrontal cortex, superior temporal sulcus at the temporoparietal junction and temporal poles). The autism group showed less activation than the normal group in all these regions. However, one additional region, extrastriate cortex, which was highly active when watching animations that elicited mentalizing, showed the same amount of increased activation in both groups. In the autism group this extrastriate region showed reduced functional connectivity with the superior temporal sulcus at the temporo-parietal junction, an area associated with the processing of biological motion as well as with mentalizing. This finding suggests a physiological cause for the mentalizing dysfunction in autism: a bottleneck in the interaction between higher order and lower order perceptual processes.
The claim that individuals with autism spectrum disorders, regardless of general intelligence, have an impairment in the attribution of mental states, has been confirmed once again. Able individuals with high-functioning autism or Asperger's Syndrome gave fewer and less accurate interpretations of animations that elicited mentalizing.
- Brain Anatomy and Sensorimotor Gating in Asperger's Syndrome
- Evidence of Brain Overgrowth in the First Year of Life in Autism
- The Severity and Nature of Motor Impairment in Asperger’s Syndrome: A comparison with Specific Developmental Disorder of Motor Function
- Asperger’s Syndrome: Tests of Right Hemisphere Functioning and Interhemispheric Communication