Neuroimaging - Cognitive and Clinical Neurosci.

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2-Minute Neuroscience: Neuroimaging

By contrasting the condition of empathy with that of ToM, greater activation was found in the PFC, medial frontal gyrus, and superior temporal gyrus when subjects engaged in ToM, and in the ACC and amygdala when subjects engaged in empathy contrast. Classical symptoms, such as delusion and hallucination, have been regarded as critical indicators of functional impairments in schizophrenia.


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  • INTRODUCTION.

More recently, researchers in clinical psychiatry have started to focus on neurocognitive factors including memory, attention, language, and executive functions as potential markers for predicting functional impairments in schizophrenia. Patients with schizophrenia often experience difficulty in social contexts, and tend to avoid social situations requiring communication with others. Rehabilitation programs focusing on interpersonal communication, such as social skill training SST , are widely applied clinically.

As the newly established research field of social neuroscience expands, psychiatrists have begun to examine whether impairment of social cognition in schizophrenia is distinct from impairments of neurocognition. Studies in social neuroscience have shown that deficits in the recognition of basic emotions, especially negative emotions, such as fear, were reported in patients with bilateral amygdala injury. Inspired by these studies, we investigated the relation between amygdala size and how well patients with schizophrenia recognize facial emotions 20 patients and 20 healthy controls.

Facial emotion recognition was assessed using 39 images stimuli selected from the Pictures of Facial Affect series, 28 including three neutral faces and 36 faces expressing happiness, sadness, fear, anger, disgust, or surprise six each. Compared with healthy controls, amygdala volume was smaller in patients with schizophrenia. Additionally, patients with schizophrenia performed poorly on the facial emotion—recognition test, particularly for the emotions of anger, disgust, surprise, and sadness. Further, the volume of the left amygdala was positively correlated with the score for recognizing sadness Fig.

Thus, this study demonstrated that amygdala neuropathology contributes to impaired facial emotion recognition in schizophrenia, and that social cognitive impairment in this disorder can be directly linked to physical abnormalities in the social brain. Volume of the amygdala was significantly smaller in patients with schizophrenia than in healthy controls.

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The scores on the facial emotion—recognition test were lower in the patient group for emotions of surprise, anger, disgust, and sadness. In the patients, the volume of the left amygdala was positively correlated with the score for sadness.


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  2. Neuroscience.
  3. Behavioural neuroscience;
  4. Healthy controls; Schizophrenia. Behaviorally, individuals with schizophrenia performed poorly on the PAT. Thus, in another study, gray matter volume, white matter integrity, and sulcal morphological patterns were measured in the anterior cingulate gyrus ACG , and their associations with performance on the PAT were examined 26 patients and 20 healthy controls. These results suggest that different types of pathology within a single gyrus can distinctly influence aspects of social cognitive function in schizophrenia, illustrating the importance of multimodal neuroimaging Fig.

    ToM ability is established early in life by age 3—5 years with deficits typically observed in autistic spectrum disorders ASD , but also in schizophrenia.

    Biological Psychiatry: Cognitive Neuroscience and Neuroimaging - Journal - Elsevier

    Together with neuroimaging studies from other groups, 33 , 34 our study indicates that abnormal STS structure is a common neural underpinning of both ASD and schizophrenia, which manifests as a common deficit in ToM. Alexithymia is characterized by a deficit in recognizing one's own emotional state — an ability thought to be critical for understanding the emotional states of others 37 — and is therefore considered to be related to social cognitive impairment. They also showed a significant bilateral FA reduction in the deep white matter of the frontal, temporal, parietal, and occipital lobes, a large portion of the CC, and the corona radiata.

    This suggests that different aspects of empathic ability have distinct neurological bases, and that the neuropathology underlying schizophrenia in different individuals can be specific for particular empathic deficits. Looking at the evidence described above, impairment of each specific aspect of social cognition in schizophrenia seems to be associated with the pathology of a specific set of brain region, although different social cognitive abilities also seem to have common neural underpinnings to some extent.

    Thus, a tentative conclusion here is that social cognitive impairment in schizophrenia is not a homogenous process based on a specific set of pathological brain regions, but a mixture of multiple cognitive impairments in which substantial individual variability is present. Lower scores on the Psychosocial subscale were associated with smaller dorsolateral PFC volumes.

    These results show that brain regions associated with poor QOL partially overlap with those associated with social cognitive impairment in schizophrenia. An unresolved question is whether standard pharmacotherapy can repair social cognition and the dysfunctional social brain. One study that explored the effect of antipsychotic medication on social cognition in schizophrenia during an acute episode showed that social cognition was improved after recovery, and was attributed to restored left mPFC activation. Some neuroimaging studies suggest that neuroimaging results have the potential to be biological predictors of responses to behavioral therapeutic interventions.

    An fMRI study has shown that after neurocognitive treatments and social cognitive training, brain activity in several cortical regions active during facial emotion recognition increased when patients engaged in this task. A growing body of literature details the neuronal underpinnings of social cognitive impairments in schizophrenia.

    The emerging picture is complex, and must take into account the multiple characteristics of social cognitive impairment, the multiple brain regions involved in each aspect of social cognitive impairment, and the substantial heterogeneity among schizophrenia patients.

    Second, we must note that most of the neuroimaging studies in this research field provide neural correlates of behavioral and psychological measures, but do not test their causality. The authors declare no conflict of interest. Volume 69 , Issue 5. The full text of this article hosted at iucr. If you do not receive an email within 10 minutes, your email address may not be registered, and you may need to create a new Wiley Online Library account. If the address matches an existing account you will receive an email with instructions to retrieve your username.

    Psychiatry and Clinical Neurosciences Volume 69, Issue 5. Carlo Altamura. By Massimo Silvetti and Tom Verguts. By Arlette Streri and Edouard Gentaz. Golaszewski, M. Seidl, M. Christova, E. Gallasch, A. Kunz, R.

    Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

    Nardone, E. Trinka and F. By Junning Li, Z. JaneWang and Martin J. By Chao Suo and Michael J. Alexander Diaz, Lizeth H.

    Sloot, Huibert D. Mansvelder and Klaus Linkenkaer-Hansen. Cheng, D. Veldhuijzen, J. Greenspan and F. This is made possible by the EU reverse charge method. Edited by Peter Bright. Edited by Theophanides Theophile. Edited by Chia-Hung Hsieh. Edited by Oleg Minin. Edited by Dr. Hande Turker. Edited by Bernhard Schaller. Edited by Philip Ainslie. Edited by Luca Saba.

    Edited by Nirmal Singh. Published: May 16th DOI: Triarhou Open access peer-reviewed 2.