International Meeting for Autism Research: Empathy Deficits Associated with Alexithymia but Not Autism: Evidence From Brain Imaging

Empathy Deficits Associated with Alexithymia but Not Autism: Evidence From Brain Imaging

Friday, May 21, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
9:00 AM
G. Bird , Psychology Department, Birkbeck College, University of London, London, United Kingdom
G. Silani , Laboratory for Social and Neural Systems Research, University of Zurich, Zurich, Switzerland
R. Brindley , Institute of Psychiatry, Kings College London, London, United Kingdom
S. White , Institute of Cognitive Neuroscience, University College London, London, United Kingdom
U. Frith , Institute of Cognitive Neuroscience, University College London, London, United Kingdom
T. Singer , Laboratory for Social and Neural Systems Research, University of Zurich, Zurich, Switzerland
Background:

A lack of empathy is often described as a feature of Autism Spectrum Conditions (ASC). However, empirical studies of empathy in ASC have produced mixed results, with some evidence for an empathy deficit in ASC being provided by tasks that rely on skills that may be impaired in ASC (e.g. facial expression recognition). More problematic for claims of an empathy deficit in ASC is the high rate of alexithymia in ASC. Alexithymia is described as a subclinical phenomenon marked by difficulties in identifying and describing feelings and difficulties in distinguishing feelings from the bodily sensations of emotional arousal. Our previous work suggests that alexithymia results in empathic deficits, thus making it possible that ASC per se does not result in reduced empathy, but that previous findings of an empathy deficit may be due to the increased numbers of alexithymic individuals in this population.

Objectives:

To directly test empathy in individuals with ASC and to determine whether any deficits are due to their autism spectrum condition and/or a result of the increased level of alexithymia in this group.

Methods:

Using functional magnetic resonance imaging (fMRI), we tested empathy in a group of individuals with ASC selected to ensure a wide distribution of alexithymia scores and a matched control group (of individuals without an ASC) with the same wide distribution of alexithymia scores. Empathic brain responses were measured using an ‘empathy for pain’ paradigm which involves a real-life social setting and does not rely on attention to, or recognition of, facial affect cues. In this task participants lie in the scanner while a partner sits next to the scanner and rests their hand next to the participant’s hand. Both the participants and their partner receive brief electric shocks to the back of their hand. Coloured cues indicate whether the participant, or their partner, will receive the shock. This paradigm allows pain-responsive areas of the participant’s brain to be identified. Activity can be measured in these areas when the partner receives pain as an index of the participant’s level of empathy.

Results:

Importantly, after controlling for alexithymia, there were no differences in the level of empathic brain activity between the ASC and Control groups. In contrast, the degree of alexithymia was significantly associated with empathic brain activity in both groups. The relationship between alexithymia and empathic brain activity did not vary as a function of group.

Conclusions:

These findings suggest that the empathy deficits observed in ASC may be due to the large co-morbidity between alexithymic traits and ASC, rather than representing a necessary feature of the social impairments in autism.

See more of: Brain Imaging
See more of: Brain Imaging
See more of: Brain Structure & Function