Social cognition in individuals with agenesis of the corpus callosum

Fuller Graduate School of Psychology, Pasadena, CA, USA.
Social neuroscience (Impact Factor: 2.66). 02/2010; 5(3):296-308. DOI: 10.1080/17470910903462419
Source: PubMed


Past research has revealed that individuals with agenesis of the corpus callosum (ACC) have deficits in interhemispheric transfer, complex novel problem-solving, and the comprehension of paralinguistic aspects of language. Case studies and family reports also suggest problems in social cognition. The performance of 11 individuals with complete ACC and with normal intelligence was compared to that of 13 IQ- and age-matched controls on three measures of social cognition. Individuals with ACC were indistinguishable from controls on the Happe Theory of Mind Stories and the Adult Faux Pas Test, but performed significantly worse on various portions of the Thames Awareness of Social Inference Test (TASIT) involving interpretations of videotaped social vignettes. Further analysis of the TASIT indicated that individuals with ACC showed deficiency in the recognition of emotion, weakness in understanding paradoxical sarcasm, and particular difficulty interpreting textual versus visual social cues. These results suggest that the tendency for deficient social cognition in individuals with ACC stems from a combination of difficulty integrating information from multiple sources, using paralinguistic cues for emotion, and understanding nonliteral speech. Together, these deficits would contribute to a less robust theory of mind.

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    • "Verbal-Performance deficits (Chiarello, 1980; Sauerwien et al. 1994). Socially, they exhibit impaired comprehension of higher-order aspects of communication, affecting language pragmatics and humor (Brown, Paul, Symington, & Dietrich, 2005; Brown, Symington, Van Lancker-Sidtis, Dietrich, & Paul, 2005; Paul, Van Lancker, Schieffer, Dietrich, & Brown, 2003), theory of mind (Symington, Paul, Symington, Ono, & Brown, 2010), and interpersonal relations (Brown & Paul, 2000; Turk, Brown, Symington, & Paul, 2010). It has been suggested that AgCC involves a core cognitive deficit in complex novel problem-solving (Brown & Paul, 2000; Gott & Saul, 1978; Sauerwein & Lassonde, 1994; Smith & Rourke, 1995; Solursh, Margulies, Ashem, & Stasiak, 1965). "
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    ABSTRACT: The role of interhemispheric interactions in the encoding, retention, and retrieval of verbal memory can be clarified by assessing individuals with complete or partial agenesis of the corpus callosum (AgCC), but who have normal intelligence. This study assessed verbal learning and memory in AgCC using the California Verbal Learning Test-Second Edition (CVLT-II). Twenty-six individuals with AgCC were compared to 24 matched controls on CVLT-II measures, as well as Donders' four CVLT-II factors (i.e., Attention Span, Learning Efficiency, Delayed Memory, and Inaccurate Memory). Individuals with AgCC performed significantly below healthy controls on the Delayed Memory factor, confirmed by significant deficits in short and long delayed free recall and cued recall. They also performed less well in original learning. Deficient performance by individuals with AgCC during learning trials, as well as deficits in all forms of delayed memory, suggest that the corpus callosum facilitates interhemispheric elaboration and encoding of verbal information.
    Full-text · Article · Jun 2014 · Neuropsychologia
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    • "Additional deficits in AgCC include impairments in social problem solving (Symington et al., 2010), abstract reasoning (Brown and Paul, 2000), generalization (Solursh et al., 1965) and processing speed (Marco et al., 2012). Overall, AgCC often involves pronounced real-world social impairments similar to those seen in high-functioning people with autism, encompassing diminished social self-awareness (Brown and Paul, 2000), difficulty imagining the social perspective of others (Symington et al., 2010; Turk et al., 2010), poor conversation skills (O'Brien, 1994) and restricted verbal expression of emotional experience (similar to alexithymia; Buchanan et al., 1980; O'Brien, 1994). Autism spectrum disorder (ASD) is a complex neuropsychiatric disorder whose diagnosis is based on deficits in communication and social interaction, as well as patterns of stereotyped, restricted and repetitive behaviours. "
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    ABSTRACT: The corpus callosum, with its ∼200 million axons, remains enigmatic in its contribution to cognition and behaviour. Agenesis of the corpus callosum is a congenital condition in which the corpus callosum fails to develop; such individuals exhibit localized deficits in non-literal language comprehension, humour, theory of mind and social reasoning. These findings together with parent reports suggest that behavioural and cognitive impairments in subjects with callosal agenesis may overlap with the profile of autism spectrum disorders, particularly with respect to impairments in social interaction and communication. To provide a comprehensive test of this hypothesis, we directly compared a group of 26 adults with callosal agenesis to a group of 28 adults with a diagnosis of autism spectrum disorder but no neurological abnormality. All participants had full-scale intelligence quotient scores >78 and groups were matched on age, handedness, and gender ratio. Using the Autism Diagnostic Observation Schedule together with current clinical presentation to assess autistic symptomatology, we found that 8/26 (about a third) of agenesis subjects presented with autism. However, more formal diagnosis additionally involving recollective parent-report measures regarding childhood behaviour showed that only 3/22 met complete formal criteria for an autism spectrum disorder (parent reports were unavailable for four subjects). We found no relationship between intelligence quotient and autism symptomatology in callosal agenesis, nor evidence that the presence of any residual corpus callosum differentiated those who exhibited current autism spectrum symptoms from those who did not. Relative to the autism spectrum comparison group, parent ratings of childhood behaviour indicated children with agenesis were less likely to meet diagnostic criteria for autism, even for those who met autism spectrum criteria as adults, and even though there was no group difference in parent report of current behaviours. The findings suggest two broad conclusions. First, they support the hypothesis that congenital disruption of the corpus callosum constitutes a major risk factor for developing autism. Second, they quantify specific features that distinguish autistic behaviour associated with callosal agenesis from autism more generally. Taken together, these two findings also leverage specific questions for future investigation: what are the distal causes (genetic and environmental) determining both callosal agenesis and its autistic features, and what are the proximal mechanisms by which absence of the callosum might generate autistic symptomatology?
    Full-text · Article · Apr 2014 · Brain
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    • "In mice 40 days post-injury, we found elevated levels of activated microglia in the corpus callosum as assessed by Iba1 immunoreactivity. The corpus callosum carries interhemispheric connections that are important for the processing of social and emotional information in humans [38,39], and loss of the corpus callosum in mice impacts emotional memory more than object memory [40]. Iba1 positive cells were elevated in the corpus callosum of rcTBI injured animals compared to shams, regardless of their shock stress status. "
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    ABSTRACT: The debilitating effects of repetitive concussive traumatic brain injury (rcTBI) have been increasingly recognized in both military and civilian populations. rcTBI may result in significant neurological, cognitive, and affective sequelae, and is often followed by physical and/or psychological post-injury stressors that may exacerbate the effects of the injury and prolong the recovery period for injured patients. However, the consequences of post-injury stressors and their subsequent effects on social and emotional behavior in the context of rcTBI have been relatively little studied in animal models. Here, we use a mouse model of rcTBI with two closed-skull blunt impacts 24 hours apart and social and emotional behavior testing to examine the consequences of a stressor (foot shock fear conditioning) following brain injury (rcTBI). rcTBI alone did not affect cued or contextual fear conditioning or extinction compared to uninjured sham animals. In the sucrose preference test, rcTBI animals had decreased preference for sucrose, an anhedonia-like behavior, regardless of whether they experienced foot shock stress or were non-shocked controls. However, rcTBI and post-injury foot shock stress had synergistic effects in tests of social recognition and depression-like behavior. In the social recognition test, animals with both injury and shock were more impaired than either non-shocked injured mice or shocked but uninjured mice. In the tail suspension test, injured mice had increased depression-like behavior compared with uninjured mice, and shock stress worsened the depression-like behavior only in the injured mice with no effect in the uninjured mice. These results provide a model of subtle emotional behavioral deficits after combined concussive brain injury and stress, and may provide a platform for testing treatment and prevention strategies for social behavior deficits and mood disorders that are tailored to patients with traumatic brain injury.
    Preview · Article · Sep 2013 · PLoS ONE
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