Affect Processing In Patients Research Articles

Hedonic Tone: A Bridge between the Psychobiology of Depression and its Comorbidities

Treatment of Major Depressive Disorder (MDD), in many cases, offers less than optimal results, resulting in loss of function and remaining impairment. This is partially explained by the high prevalence of comorbid psychiatric illnesses that share common features, likely resulting in less than adequate treatment outcomes among patients receiving traditional psychiatric treatment. The term anhedonia does not sufficiently capture the complex and multifaceted reward-associated deficits seen in neuropsychiatric disorders. Deficits in reward-related processes can lead to behaviors that may appear to be the loss of interest or pleasure, and may preclude an individual from engaging in goal-oriented action. Investigators have identified a lifelong poor hedonic responsiveness, manifested as altered sensitivity to reinforcement, in patients with Attention Deficit Hyperactivity Disorder (ADHD), and suggest it as a common endophenotype for depression and the inattentive symptoms of ADHD. Research into the neurobiology of anhedonia has focused on the centers in the brain related to reward and motivation, and has identified the dopaminergic and associated circuits as playing a key role. Studies have shown that lesions in reward and motivation circuits result in anhedonia, and that decreased activation in the medial frontal cortex is believed to underlie abnormal positive affect processing in patients. In this paper, we propose that a specific phenotype of depression, which is more likely to be described as “treatment resistant” is associated with high risk of comorbidity with dysthymia, ADHD, and substance abuse, specifically cocaine abuse. We believe these patients experience a chronically lower hedonic tone that results in chronic anhedonia (as opposed to acute state anhedonia noted in a major depressive episode) related to unique pathophysiology and requiring treatment of the dopaminergic deficiency that characterizes its unique collection of comorbidities.

Fearful face recognition in schizophrenia: An electrophysiological study

BackgroundEmotional expressions are important acts of communication, and impairment in facial emotion recognition has been shown to be related to impairments in social cognition in schizophrenia. We used an event-related potential (ERP) paradigm to identify and delineate the temporal characteristics in the electrophysiological cascade related to fearful facial affect processing in patients with schizophrenia as compared to healthy controls. MethodsTwenty-four subjects with schizophrenia and 24 individually matched healthy controls participated in an emotion recognition task. Ekman faces displaying neutral and fearful facial expressions were used as stimuli. ERPs were recorded using a 128-channel EEG system. ResultsBased on the analysis of Global Field Power (GFP) in the 150–190ms time window both groups differentiated between fearful and neutral faces. Schizophrenia patients showed an additional differential processing of fearful vs. neutral faces in the 330–450ms time window, and this ERP effect correlated with psychopathology. ConclusionsBoth patients and healthy controls differentiate fearful and neutral faces in early phases of emotion processing. Our results also indicate that schizophrenia patients show increased responsivity to fearful faces at a later processing stage. This could be related to the overrating of negative emotions, and the symptomatology associated with fear processing in patients with schizophrenia.

Evidence of diagnostic specificity in the neural correlates of facial affect processing in bipolar disorder and schizophrenia: a meta-analysis of functional imaging studies

Schizophrenia (SZ) and bipolar disorder (BD) may overlap in etiology and phenomenology but differ with regard to emotional processing. We used facial affect as a probe for emotional processing to determine whether there are diagnosis-related differences between SZ and BD in the function of the underlying neural circuitry. Functional magnetic resonance imaging (fMRI) studies published up to 30 April 2012 investigating facial affect processing in patients with SZ or BD were identified through computerized and manual literature searches. Activation foci from 29 studies encompassing 483 healthy individuals, 268 patients with SZ and 267 patients with BD were subjected to voxel-based quantitative meta-analysis using activation likelihood estimation (ALE). Compared to healthy individuals, when emotional facial stimuli were contrasted to neutral stimuli, patients with BD showed overactivation within the parahippocampus/amygdala and thalamus and reduced engagement within the ventrolateral prefrontal cortex (PFC) whereas patients with SZ showed underactivation throughout the entire facial affect processing network and increased activation in visual processing regions within the cuneus. Patients with BD showed greater thalamic engagement compared to patients with SZ; in the reverse comparison, patients with SZ showed greater engagement in posterior associative visual cortices. During facial affect processing, patients with BD show overactivation in subcortical regions and underactivation in prefrontal regions of the facial affect processing network, consistent with the notion of reduced emotional regulation. By contrast, overactivation within visual processing regions coupled with reduced engagement of facial affect processing regions points to abnormal visual integration as the core underlying deficit in SZ.

The impact of the Val158Met catechol-O-methyltransferase genotype on neural correlates of sad facial affect processing in patients with bipolar disorder and their relatives

The Met allele of the catechol-O-methyltransferase (COMT) valine-to-methionine (Val158Met) polymorphism is known to affect dopamine-dependent affective regulation within amygdala-prefrontal cortical (PFC) networks. It is also thought to increase the risk of a number of disorders characterized by affective morbidity including bipolar disorder (BD), major depressive disorder (MDD) and anxiety disorders. The disease risk conferred is small, suggesting that this polymorphism represents a modifier locus. Therefore our aim was to investigate how the COMT Val158Met may contribute to phenotypic variation in clinical diagnosis using sad facial affect processing as a probe for its neural action. We employed functional magnetic resonance imaging to measure activation in the amygdala, ventromedial PFC (vmPFC) and ventrolateral PFC (vlPFC) during sad facial affect processing in family members with BD (n=40), MDD and anxiety disorders (n=22) or no psychiatric diagnosis (n=25) and 50 healthy controls. Irrespective of clinical phenotype, the Val158 allele was associated with greater amygdala activation and the Met158 allele with greater signal change in the vmPFC and vlPFC. Signal changes in the amygdala and vmPFC were not associated with disease expression. However, in the right vlPFC the Met158 allele was associated with greater activation in all family members with affective morbidity compared with relatives without a psychiatric diagnosis and healthy controls. Our results suggest that the COMT Val158Met polymorphism has a pleiotropic effect within the neural networks subserving emotional processing. Furthermore the Met158 allele further reduces cortical efficiency in the vlPFC in individuals with affective morbidity.

Event-related potential patterns and gender effects underlying facial affect processing in schizophrenia patients

This study was designed to clarify the consecutive temporal mechanisms and gender effects underlying facial affect processing in patients with schizophrenia and normal controls through electrophysiological measurements. The following four event-related potential (ERP) components were chosen as indexes of four distinct stages: P100, N170, N250, and P300. A total of 38 schizophrenia patients (22 females) and 38 normal controls (20 females) were recruited. ERPs were recorded while participants identified emotions in images of faces showing three different states: happy, fearful and neutral. The mean peak amplitude of N170 was significantly lower in schizophrenia patients than in normal controls. The mean peak amplitudes of N170 and N250 for fearful emotion were significantly higher than that for happy emotion. The latencies of N170, and P300 were longer in schizophrenia patients than in normal controls. Gender effects were found for P100 peak amplitude and N170 latency, and significant interactions with gender were found for P300 amplitudes and P100 latency. Our results provide evidences of the dysfunctional ERP patterns underlying facial affect processing in schizophrenia patients. Furthermore, the results suggest that gender could be an important controlling factor for facial affect processing in schizophrenia patients.

Effects of emotion and identity on facial affect processing in schizophrenia

We used facial affect labeling and matching tasks to study effects of (1) emotion and (2) identity on facial affect processing in patients with remitted schizophrenia ( n=30) compared with healthy controls ( n=30). The patients (1) had a specific deficit for labeling facial affects of sadness and anger but not happiness, disgust and fear; they (2) performed as well as controls in matching facial affects in one face but were impaired in matching facial affects in two different faces. The patients' impairment in facial affect processing may be emotion-specific. The effects of identity on facial affect processing are discussed in the light of several hypotheses (a deficit of context processing, a global–local processing impairment or a selective attention deficit), and may be related to frontal, prefrontal or amygdala dysfunctions.

Attenuation of the neural response to sad faces in major depression by antidepressant treatment: a prospective, event-related functional magnetic resonance imaging study.

Depression is associated with interpersonal difficulties related to abnormalities in affective facial processing. To map brain systems activated by sad facial affect processing in patients with depression and to identify brain functional correlates of antidepressant treatment and symptomatic response. Two groups underwent scanning twice using functional magnetic resonance imaging (fMRI) during an 8-week period. The event-related fMRI paradigm entailed incidental affect recognition of facial stimuli morphed to express discriminable intensities of sadness. Participants were recruited by advertisement from the local population; depressed subjects were treated as outpatients. We matched 19 medication-free, acutely symptomatic patients satisfying DSM-IV criteria for unipolar major depressive disorder by age, sex, and IQ with 19 healthy volunteers. Intervention After the baseline assessment, patients received fluoxetine hydrochloride, 20 mg/d, for 8 weeks. Average activation (capacity) and differential response to variable affective intensity (dynamic range) were estimated in each fMRI time series. We used analysis of variance to identify brain regions that demonstrated a main effect of group (depressed vs healthy subjects) and a group x time interaction (attributable to antidepressant treatment). Change in brain activation associated with reduction of depressive symptoms in the patient group was identified by means of regression analysis. Permutation tests were used for inference. Over time, depressed subjects showed reduced capacity for activation in the left amygdala, ventral striatum, and frontoparietal cortex and a negatively correlated increase of dynamic range in the prefrontal cortex. Symptomatic improvement was associated with reduction of dynamic range in the pregenual cingulate cortex, ventral striatum, and cerebellum. Antidepressant treatment reduces left limbic, subcortical, and neocortical capacity for activation in depressed subjects and increases the dynamic range of the left prefrontal cortex. Changes in anterior cingulate function associated with symptomatic improvement indicate that fMRI may be a useful surrogate marker of antidepressant treatment response.