The functional neuroanatomy in social behaviour in autistic disorder

Background and Aim : The neuropathological basis of autism has not been determined, and much of the work has focused on classic Kanner-type autism. However, a number of anatomical substrates have been suggested. Damasio and Maurer proposed that autism is due to dysfunction of mesolimbic (dopaminergic) brain areas (ventromedial prefrontal cortex, medial temporal lobe, striatum and limbic thalamus) because damage to these brain regions can cause features of autism (impaired social and emotional functioning, stereotyped behaviours, mannerisms and obsessionality) (Damasio and Maurer, 1978). This hypothesis is supported by studies which have reported that (i) in animals, social deficits and stereotypical behaviour are associated with damage to the medial temporal lobe in infancy (Bachevalier, 1994); (ii) in humans, autistic-type patterns of behaviour are associated with abnormalities in the temporal lobe caused by other neurodevelopmental disorders (e.g. tuberous sclerosis) (Bolton and Griffiths, 1997); and (iii) individuals with autism are impaired on frontal executive tasks (Ozonoff et al., 1991; Hughes et al., 1994). Non-limbic areas such as the parietal lobe have also been suggested as important in aetiology because the inattention of children with autism to salient social cues resembles inattention and neglect following parietal lobe damage (Bryson et al., 1990Methods : We studied nine high-functioning adult male volunteers [mean age ± standard deviation, 37 ± 7 years; FSIQ (full-scale IQ) 102 ± 15] clinically diagnosed, using ICD-10, as having Asperger syndrome (seven subjects) or autism (two subjects) (Table 1). Diagnosis was confirmed where possible with the Autism Diagnostic Interview (Lord et al., 1994), a structured interview of parental informants to aid the diagnosis of autism. We also studied nine right-handed adult male controls (27 ± 7 years; FSIQ 116 ± 10). Intelligence was measured using the Wechsler Adult Intelligence Scale—Revised (WAIS-R) (Wechsler, 1981), and subjects with autistic disorder were tested outside the scanner on their ability to recognize faces, using the Warrington recognition memory task for faces (Warrington, 1984)Results : Subjects with autistic disorder and controls were debriefed after scanning, and both groups reported no difficulties in viewing or judging the face stimuli. However, although the subjects with autistic disorder performed well above chance, performance data showed that they made more errors than controls during the explicit processing of facial expressionsConclusion : Although high-functioning individuals with autistic disorder (i.e. autism and Asperger syndrome) are of normal intelligence, they have life-long abnormalities in social communication and emotional behaviour. However, the biological basis of social difficulties in autism is poorly understood. Facial expressions help shape behaviour, and we investigated if high-functioning people with autistic disorder show neurobiological differences from controls when processing emotional facial expressions.

کلیدواژه ها:

neurobiological ، behaviour ، autistic