Association of Impaired Facial Affect Recognition with Basic Facial and Visual Processing Deficits in Schizophrenia

McLean Hospital, Belmont, Massachusetts, USA.
Biological psychiatry (Impact Factor: 10.26). 04/2009; 65(12):1094-8. DOI: 10.1016/j.biopsych.2009.01.026
Source: PubMed


Impaired emotion recognition has been reported in schizophrenia, yet the nature of this impairment is not completely understood. Recognition of facial emotion depends on processing affective and nonaffective facial signals, as well as basic visual attributes. We examined whether and how poor facial emotion recognition in schizophrenia is related to basic visual processing and nonaffective face recognition.
Schizophrenia patients (n = 32) and healthy control subjects (n = 29) performed emotion discrimination, identity discrimination, and visual contrast detection tasks, where the emotionality, distinctiveness of identity, or visual contrast was systematically manipulated. Subjects determined which of two presentations in a trial contained the target: the emotional face for emotion discrimination, a specific individual for identity discrimination, and a sinusoidal grating for contrast detection.
Patients had significantly higher thresholds (worse performance) than control subjects for discriminating both fearful and happy faces. Furthermore, patients' poor performance in fear discrimination was predicted by performance in visual detection and face identity discrimination.
Schizophrenia patients require greater emotional signal strength to discriminate fearful or happy face images from neutral ones. Deficient emotion recognition in schizophrenia does not appear to be determined solely by affective processing but is also linked to the processing of basic visual and facial information.

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    • "Our findings therefore suggest that impaired facial emotion perception in schizophrenia is due at least in part to under-recruitment of regions involved in processing perceptual features of faces and the detection of changes in facial expressions, in contrast or in addition to other processes that contribute to facial emotion perception (e.g., dysfunction at the level of associating a perception with emotional knowledge). Our findings are consistent with previous research reporting sensory contributions to facial emotion processing deficits in schizophrenia (e.g., Butler et al., 2009; Norton et al., 2009; Turetsky et al., 2007). Furthermore, the similar findings in core regions involved in face perception in relatives suggest that this under-recruitment is associated with the genetic/familial liability to schizophrenia. "
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    ABSTRACT: Deficits in facial emotion perception in schizophrenia may be a marker of disorder liability. Previous functional magnetic resonance imaging (fMRI) studies investigating these deficits have been limited by task demands that may recruit other impaired cognitive processes in schizophrenia. We used a family study design along with a passive viewing task during fMRI to investigate brain activation abnormalities underlying facial emotion perception in schizophrenia and examine whether such abnormalities are associated with the genetic liability to the disorder. Twenty-eight schizophrenia patients, 27 nonpsychotic relatives, and 27 community controls passively viewed images of facial emotions during an fMRI scan. Analyses revealed hypoactivation in face processing areas for both patients and relatives compared to controls, and hyperactivation in relatives compared to both patients and controls for frontal regions implicated in emotion processing. Results suggest that activation abnormalities during facial emotion perception are manifestations of the genetic liability to schizophrenia, and may be accompanied by compensatory mechanisms in relatives. Studying mechanisms in nonpsychotic relatives is a valuable way to examine effects of the unexpressed genetic liability to schizophrenia on the brain and behaviour. Copyright © 2015 Elsevier B.V. All rights reserved.
    Full-text · Article · Jul 2015 · Schizophrenia Research
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    • "The first explanation refers to the sensory deficit in schizophrenia. Several studies have reported a basic sensory disturbance in the processing of emotion in the facial (Turetsky et al., 2007; Wynn et al., 2008; Norton et al., 2009; Laprevote et al., 2010; McBain et al., 2010; Bedwell et al., 2013; Jahshan et al., 2013) and vocal (Leitman et al., 2005, 2007, 2010, 2011a; Gold et al., 2012; Kantrowitz et al., 2013) modalities. This is unlikely to be the case in our study since patients with basic sensory disturbances, as assessed with the Benton test and the PEGA, were excluded from our sample. "
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    ABSTRACT: There has been extensive research on impaired emotion recognition in schizophrenia in the facial and vocal modalities. The literature points to biases toward non-relevant emotions for emotional faces but few studies have examined biases in emotional recognition across different modalities (facial and vocal). In order to test emotion recognition biases, we exposed 23 patients with stabilized chronic schizophrenia and 23 healthy controls (HCs) to emotional facial and vocal tasks asking them to rate emotional intensity on visual analog scales. We showed that patients with schizophrenia provided higher intensity ratings on the non-target scales (e.g., surprise scale for fear stimuli) than HCs for the both tasks. Furthermore, with the exception of neutral vocal stimuli, they provided the same intensity ratings on the target scales as the HCs. These findings suggest that patients with chronic schizophrenia have emotional biases when judging emotional stimuli in the visual and vocal modalities. These biases may stem from a basic sensorial deficit, a high-order cognitive dysfunction, or both. The respective roles of prefrontal-subcortical circuitry and the basal ganglia are discussed.
    Full-text · Article · Aug 2014 · Frontiers in Psychology
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    • "Overwhelmingly, significant impairments in emotion perception are reported (7), and these appear present and stable from pre-onset to chronic multi-episode patients (2). A more recent line of inquiry has suggested that deficient facial emotion processing in schizophrenia may be underpinned by basic visuoperceptual deficits (8, 9), although electrophysiological evidence of this is not always demonstrated. Studies using neutral face stimuli have verified a primary deficit in the processing of configural information (described below), with a relative overreliance on facial feature processing by patients with schizophrenia (10, 11), and in ultra-high risk individuals (12). "
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    ABSTRACT: Background: Face processing impairment in schizophrenia appears to be underpinned by poor configural (as opposed to feature-based) processing; however, few studies have sought to characterize this impairment electrophysiologically. Given the sensitivity of event-related potentials to antipsychotic medications, and the potential for neurophysiological abnormalities to serve as vulnerability markers for schizophrenia, a handful of studies have investigated early visual P100 and face-selective N170 in “at risk” populations. However, this is the first known neurophysiological investigation of configural face processing in a non-clinical schizotypal sample. Methods: Using stimuli designed to engage configural processing in face perception (upright and inverted Mooney and photographic faces), P100 and N170 components were recorded in healthy individuals characterized by high (N = 14) and low (N = 14) schizotypal traits according to the Oxford–Liverpool Inventory of Feelings and Experiences. Results: High schizotypes showed significantly reduced N170 amplitudes to inverted photographic faces. Typical N170 latency and amplitude inversion effects (delayed and enhanced N170 to inverted relative to upright photographic faces, and enhanced amplitude to upright versus inverted Mooney faces), were demonstrated by low, but not high, schizotypes. No group differences were shown for P100 analyses. Conclusions: The findings suggest that neurophysiological deficits in processing facial configurations (N170) are apparent in schizotypy, while the early sensory processing (P100) of faces appears intact. This work adds to the mounting evidence for analogous neural processing anomalies at the healthy end of the psychosis continuum.
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