Difficulties in the cognitive processing of emotions--including difficulties identifying and describing feelings--are assumed to be an integral part of autism. We studied such difficulties via self-report in 27 high-functioning adults with autistic spectrum disorders, their biological relatives (n = 49), and normal adult controls (n = 35), using the 20-item Toronto Alexithymia Scale and the Beck Depression Inventory. The individuals with autism spectrum disorders were significantly more impaired in their emotion processing and were more depressed than those in the control and relative groups.

The aim of this investigation was to identify neural systems supporting the processing of intentional and unintentional transgressions of social norms. Using event-related fMRI, we addressed this question by comparing neural responses to stories describing normal behaviour, embarrassing situations or violations of social norms. Processing transgressions of social norms involved systems previously reported to play a role in representing the mental states of others, namely medial prefrontal and temporal regions. In addition, the processing of transgressions of social norms involved systems previously found to respond to aversive emotional expressions (in particular angry expressions); namely lateral orbitofrontal cortex (Brodmann area 47) and medial prefrontal cortex. The observed responses were similar for both intentional and unintentional social norm violations, albeit more pronounced for the intentional norm violations. These data suggest that social behavioural problems in patients with frontal lobe lesions or fronto-temporal dementia may be a consequence of dysfunction within the systems identified in light of their possible role in processing whether particular social behaviours are, or are not, appropriate.

Alexithymia is characterized by difficulties in identifying, differentiating and describing feelings. A high prevalence of alexithymia has often been observed in clinical disorders characterized by low social functioning. This review aims to assess the association between alexithymia and the ability to decode emotional facial expressions (EFEs) within clinical and healthy populations. More precisely, this review has four main objectives: (1) to assess if alexithymia is a better predictor of the ability to decode EFEs than the diagnosis of clinical disorder; (2) to assess the influence of comorbid factors (depression and anxiety disorder) on the ability to decode EFE; (3) to investigate if deficits in decoding EFEs are specific to some levels of processing or task types; (4) to investigate if the deficits are specific to particular EFEs. Twenty four studies (behavioural and neuroimaging) were identified through a computerized literature search of Psycinfo, PubMed, and Web of Science databases from 1990 to 2010. Data on methodology, clinical characteristics, and possible confounds were analyzed. The review revealed that: (1) alexithymia is associated with deficits in labelling EFEs among clinical disorders, (2) the level of depression and anxiety partially account for the decoding deficits, (3) alexithymia is associated with reduced perceptual abilities, and is likely to be associated with impaired semantic representations of emotional concepts, and (4) alexithymia is associated with neither specific EFEs nor a specific valence. These studies are discussed with respect to processes involved in the recognition of EFEs. Future directions for research on emotion perception are also discussed.