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Biomedical subjects

Mary L Phillips

Publications and source records attributed to Mary L Phillips.

At least 37 records · Page 2Linked to original sources

Perception of facial and vocal affect by people with schizophrenia in early and late stages of illness.

BACKGROUND: Emotion recognition impairments have been demonstrated in schizophrenia, but few studies have examined whether these reflect generalised or specific perceptual deficits or are associated with illness course. AIMS: To examine the nature of emotion recognition abnormalities in patients with schizophrenia at different stages of illness. METHOD: We examined the performance of 50 in-patients with early-stage schizophrenia, 50 with chronic schizophrenia and 50 healthy controls on the Benton Facial Recognition Test, Facial Emotion Recognition Test and Voice Emotion Recognition Test. RESULTS: Patients with chronic schizophrenia were significantly more impaired than other groups on the emotional tasks, even after controlling for impairments in non-emotional stimuli. Individual emotion recognition accuracy for the two sensory modalities was not significantly positively correlated for either group with schizophrenia. CONCLUSIONS: Emotion recognition deficits in schizophrenia are trait features of the disorder and increase with illness duration.

Adolescent↗

Subcortical and ventral prefrontal cortical neural responses to facial expressions distinguish patients with bipolar disorder and major depression.

BACKGROUND: Bipolar disorder (BD) is characterised by abnormalities in mood and emotional processing, but the neural correlates of these, their relationship to depressive symptoms, and the similarities with deficits in major depressive disorder (MDD) remain unclear. We compared responses within subcortical and prefrontal cortical regions to emotionally salient material in patients with BP and MDD using functional magnetic resonance imaging. METHODS: We measured neural responses to mild and intense expressions of fear, happiness, and sadness in euthymic and depressed BD patients, healthy control subjects, and depressed MDD patients. RESULTS: Bipolar disorder patients demonstrated increased subcortical (ventral striatal, thalamic, hippocampal) and ventral prefrontal cortical responses particularly to mild and intense fear, mild happy, and mild sad expressions. Healthy control subjects demonstrated increased subcortical responses to intense happy and mild fear, and increased dorsal prefrontal cortical responses to intense sad expressions. Overall, MDD patients showed diminished neural responses to all emotional expressions except mild sadness. Depression severity correlated positively with hippocampal response to mild sadness in both patient groups. CONCLUSIONS: Compared with healthy controls and MDD patients, BD patients demonstrated increased subcortical and ventral prefrontal cortical responses to both positive and negative emotional expressions.

Adult↗

Distinct neural correlates of washing, checking, and hoarding symptom dimensions in obsessive-compulsive disorder.

CONTEXT: Obsessive-compulsive disorder (OCD) is clinically heterogeneous, yet most previous functional neuroimaging studies grouped together patients with mixed symptoms, thus potentially reducing the power and obscuring the findings of such studies. OBJECTIVE: To investigate the neural correlates of washing, checking, and hoarding symptom dimensions in OCD. DESIGN: Symptom provocation paradigm, functional magnetic resonance imaging, block design, and nonparametric brain mapping analyses. SETTING: University hospital. PARTICIPANTS: Sixteen patients with OCD (11 inpatients, 5 outpatients) with mixed symptoms and 17 healthy volunteers of both sexes. Intervention All subjects participated in 4 functional magnetic resonance imaging experiments. They were scanned while viewing alternating blocks of emotional (washing-related, checking-related, hoarding-related, or aversive, symptom-unrelated) and neutral pictures, and imagining scenarios related to the content of each picture type.Main Outcome Measure Blood oxygenation level-dependent response. RESULTS: Both patients and control subjects experienced increased subjective anxiety during symptom provocation (patients significantly more so) and activated neural regions previously linked to OCD. Analyses of covariance, controlling for depression, showed a distinct pattern of activation associated with each symptom dimension. Patients demonstrated significantly greater activation than controls in bilateral ventromedial prefrontal regions and right caudate nucleus (washing); putamen/globus pallidus, thalamus, and dorsal cortical areas (checking); left precentral gyrus and right orbitofrontal cortex (hoarding); and left occipitotemporal regions (aversive, symptom-unrelated). These results were further supported by correlation analyses within patients, which showed highly specific positive associations between subjective anxiety, questionnaire scores, and neural response in each experiment. There were no consistently significant differences between patients with (n = 9) and without (n = 7) comorbid diagnoses. CONCLUSIONS: The findings suggest that different obsessive-compulsive symptom dimensions are mediated by relatively distinct components of frontostriatothalamic circuits implicated in cognitive and emotion processing. Obsessive-compulsive disorder may be best conceptualized as a spectrum of multiple, potentially overlapping syndromes rather than a unitary nosologic entity.

Adult↗

Social threat perception and the evolution of paranoia.

Rapid and efficient judgments about the significance of social threat are important for species survival and may recruit specialized neurocognitive systems, consistent with biological models of threat processing. We review cognitive, psychophysiological, neuropsychological, and neuroimaging evidence in support of specialized neural networks subserving the processing of facial displays of threat. Cognitive research suggests that faces depicting anger are detected quickly when presented amongst other facial expressions, on the basis of distinguishing facial features. Psychophysiological investigations using visual scanpath techniques provide evidence for increased foveal attention to facial features of threat-related expressions (anger, fear), which may facilitate rapid detection and subsequent appraisal of the significance of threat (such as the direction of impending threat). Neuropsychological and neuroimaging studies implicate a primary role for the amygdale and pre-frontal cortices in interpreting signs of danger from facial expressions and other social stimuli. Subtle disturbances in these neurocognitive systems underlying efficient threat detection (manifesting in attentional biases and aberrant neural activity) may result in abnormally heightened perception of social threat, as seen in clinical levels of social anxiety and/or persecutory delusions in schizophrenia. Clinical states of paranoia may therefore reflect normal variation (i.e. biases) in the adaptive mechanisms which have evolved, in the Darwinian sense, to facilitate efficient threat detection in humans. As such, clinical levels of paranoia may represent the inevitable cost of efficient threat perception--or 'justified' suspicion--that is necessary for survival of the human species.

Affect↗

Differential neural responses to overt and covert presentations of facial expressions of fear and disgust.

There is debate in cognitive neuroscience whether conscious versus unconscious processing represents a categorical or a quantitative distinction. The purpose of the study was to explore this matter using functional magnetic resonance imaging (fMRI). We first established objective thresholds of the critical temporal parameters for overt and covert presentations of fear and disgust. Next we applied these stimulus parameters in an fMRI experiment to determine whether non-consciously perceived (covert) facial expressions of fear and disgust show the same double dissociation (amygdala response to fear, insula to disgust) observed with consciously perceived (overt) stimuli. A backward masking paradigm was used. In the psychophysics experiment, the following parameters were established: 30-ms target duration for the covert condition, and 170-ms target duration for the overt condition. Results of the block-design fMRI study indicated substantial differences underlying the perception of fearful and disgusted facial expressions, with significant effects of both emotion and target duration. Findings for the overt condition (170 ms) confirm previous evidence of amygdala activation to fearful faces, and insula activation to disgusted faces, and a double dissociation between these two emotions. In the covert condition (30 ms), the amygdala was not activated to fear, nor was the insula activated to disgust. Overall, findings demonstrate significant differences between the neural responses to fear and to disgust, and between the covert presentations of these two emotions. These results therefore suggest distinct neural correlates of conscious and unconscious emotion perception.

Adult↗

Patterns of neural response to emotive stimuli distinguish the different symptom dimensions of obsessive-compulsive disorder.

Despite its heterogeneous symptomatology, obsessive-compulsive disorder (OCD) is currently conceptualized as a unitary diagnostic entity. Recent factor-analytic studies have identified several OCD symptom dimensions that are associated with different demographic variables, comorbidity, patterns of genetic transmission, and treatment response. Functional abnormalities in neural systems important for emotion perception, including the orbitofrontal cortex, lateral prefrontal cortex, anterior cingulate gyrus, and limbic regions, have been reported in OCD. In this review, we discuss the extent to which neurobiological markers may distinguish these different symptom dimensions and whether specific symptom dimensions, such as contamination/washing, are associated with abnormalities in emotion and, in particular, disgust, perception in OCD. Also discussed are findings that indicate that anxiety can be induced in healthy volunteers in response to OCD symptom-related material, and that associated increases in activity within neural systems important for emotion perception occur to washing- and hoarding-related material in particular in these subjects. Further examination of neural responses during provocation of different symptom dimensions in OCD patients will help determine the extent to which specific abnormalities in neural systems underlying emotion perception are associated with different symptom dimensions and predict treatment response in OCD.

Adult↗

Recognition accuracy and response bias to happy and sad facial expressions in patients with major depression.

Impaired facial expression recognition has been associated with features of major depression, which could underlie some of the difficulties in social interactions in these patients. Patients with major depressive disorder and age- and gender-matched healthy volunteers judged the emotion of 100 facial stimuli displaying different intensities of sadness and happiness and neutral expressions presented for short (100 ms) and long (2,000 ms) durations. Compared with healthy volunteers, depressed patients demonstrated subtle impairments in discrimination accuracy and a predominant bias away from the identification as happy of mildly happy expressions. The authors suggest that, in depressed patients, the inability to accurately identify subtle changes in facial expression displayed by others in social situations may underlie the impaired interpersonal functioning.

Adult↗

Dysregulation of arousal and amygdala-prefrontal systems in paranoid schizophrenia.

OBJECTIVE: The authors investigated impaired differentiation of limbic-prefrontal systems by autonomic arousal in schizophrenia. It was predicted that paranoid patients would be distinguished by a disjunction of hyperarousal but reduced amygdala and medial prefrontal activity relative to both healthy comparison subjects and patients with nonparanoid schizophrenia. METHOD: Pictures depicting facial expressions of fear were presented to 27 schizophrenia patients (13 paranoid, 14 nonparanoid) and 22 matched healthy comparison subjects in an implicit perception task to evoke limbic activity. Simultaneous functional magnetic resonance imaging and skin conductance arousal recordings were acquired during presentation of faces expressing fear or neutral emotion. Responses to fear stimuli were further examined by contrasting those that were associated with a skin conductance response ("with arousal") and those that were not ("without arousal"). RESULTS: In the comparison subjects, arousal dissociated amygdala/medial prefrontal ("visceral") networks and hippocampus/lateral prefrontal ("context") networks for fear perception. Excessive arousal responses were elicited in the schizophrenia subjects, but there was an associated reduction in amygdala/medial prefrontal activity. This disjunction was pronounced in paranoid patients relative to both healthy subjects and nonparanoid patients. Paranoid patients also showed a relatively greater prefrontal deficit for "without-arousal" responses. CONCLUSIONS: This is the first study to reveal a functional disconnection in autonomic and central systems for processing threat-related signals in patients with paranoid schizophrenia. Paranoid cognition may reflect an internally generated cycle of misattribution regarding incoming fear signals due to a breakdown in the regulation of these systems.

Adult↗

Medial prefrontal cortex activity associated with symptom provocation in eating disorders.

OBJECTIVE: The authors sought to identify neural correlates of eating disorders in order to contribute to the debate on the genesis and classification of eating disorders and provide endophenotypes for genetic research. METHOD: Twenty-six female patients with eating disorders (10 with bulimia nervosa, 16 with anorexia nervosa) and 19 healthy female comparison subjects matched for age and education were presented with food and aversive emotional images while brain activity was recorded with functional magnetic resonance imaging. RESULTS: Women with eating disorders identified the food stimuli as threatening and disgusting. In response to these stimuli, the women with eating disorders had greater activation in the left medial orbitofrontal and anterior cingulate cortices and less activation in the lateral prefrontal cortex, inferior parietal lobule, and cerebellum, relative to the comparison group. In addition, women with bulimia nervosa had less activation in the lateral and apical prefrontal cortex, relative to the comparison group. Between-group differences in response to nonspecific emotional stimuli were found in the occipital cortex, parietal cortex, and cerebellum. CONCLUSIONS: A medial prefrontal response to symptom-provoking stimuli was identified as a common feature of anorexia and bulimia nervosa. This finding supports a conceptualization of eating disorders as being transdiagnostic at the neural level. The abnormal prefrontal reaction is associated with symptom-related material, whereas the occipital and cerebellar differences are nonspecific. An abnormal propensity to activate medial prefrontal circuits in response to inappropriate stimuli is common to eating, obsessive-compulsive, and addictive disorders and may account for the compulsive features of behavior in these conditions.

Adult↗

Neurobiology of emotion perception I: The neural basis of normal emotion perception.

There is at present limited understanding of the neurobiological basis of the different processes underlying emotion perception. We have aimed to identify potential neural correlates of three processes suggested by appraisalist theories as important for emotion perception: 1) the identification of the emotional significance of a stimulus; 2) the production of an affective state in response to 1; and 3) the regulation of the affective state. In a critical review, we have examined findings from recent animal, human lesion, and functional neuroimaging studies. Findings from these studies indicate that these processes may be dependent upon the functioning of two neural systems: a ventral system, including the amygdala, insula, ventral striatum, and ventral regions of the anterior cingulate gyrus and prefrontal cortex, predominantly important for processes 1 and 2 and automatic regulation of emotional responses; and a dorsal system, including the hippocampus and dorsal regions of anterior cingulate gyrus and prefrontal cortex, predominantly important for process 3. We suggest that the extent to which a stimulus is identified as emotive and is associated with the production of an affective state may be dependent upon levels of activity within these two neural systems.

Animals↗

Neurobiology of emotion perception II: Implications for major psychiatric disorders.

To date, there has been little investigation of the neurobiological basis of emotion processing abnormalities in psychiatric populations. We have previously discussed two neural systems: 1) a ventral system, including the amygdala, insula, ventral striatum, ventral anterior cingulate gyrus, and prefrontal cortex, for identification of the emotional significance of a stimulus, production of affective states, and automatic regulation of emotional responses; and 2) a dorsal system, including the hippocampus, dorsal anterior cingulate gyrus, and prefrontal cortex, for the effortful regulation of affective states and subsequent behavior. In this critical review, we have examined evidence from studies employing a variety of techniques for distinct patterns of structural and functional abnormalities in these neural systems in schizophrenia, bipolar disorder, and major depressive disorder. In each psychiatric disorder, the pattern of abnormalities may be associated with specific symptoms, including emotional flattening, anhedonia, and persecutory delusions in schizophrenia, prominent mood swings, emotional lability, and distractibility in bipolar disorder during depression and mania, and with depressed mood and anhedonia in major depressive disorder. We suggest that distinct patterns of structural and functional abnormalities in neural systems important for emotion processing are associated with specific symptoms of schizophrenia and bipolar and major depressive disorder.

Brain↗

Neural correlates of anxiety associated with obsessive-compulsive symptom dimensions in normal volunteers.

BACKGROUND: The neural correlates of anxiety associated with obsessive-compulsive symptomlike provocation in normal volunteers are unknown. METHODS: Ten healthy volunteers participated in four functional magnetic resonance experiments. Subjects were scanned while viewing alternating blocks of emotional (normally aversive, washing-relevant, checking-relevant, or hoarding-relevant pictures) and neutral pictures, and imagining scenarios related to the content of each picture type. Nonparametric brain mapping analyses were used. RESULTS: In response to the provocative pictures in all experiments, increases in subjective anxiety and activation in bilateral ventral prefrontal, limbic, dorsal prefrontal, and visual regions were demonstrated. Anxiety related to different symptom dimensions was associated with different patterns of activation: provocation of washing-relevant anxiety predominantly activated dorsal and ventral prefrontal regions; checking-relevant anxiety predominantly activated dorsal prefrontal regions; and hoarding-relevant anxiety predominantly activated ventral prefrontal regions and the left amygdala. CONCLUSIONS: Our findings support a dimensional model of obsessive-compulsive disorder (OCD) whereby 1) the brain systems implicated in the mediation of anxiety in response to symptom-related material in normal subjects are similar to those identified in OCD patients during symptom provocation, and 2) anxiety associated with different symptom dimensions is associated with differential patterns of activation of these neural systems. Further investigation of the neural basis of OCD symptom dimensions is required.

Adult↗

Ketamine alters neural processing of facial emotion recognition in healthy men: an fMRI study.

Disruption of facial emotion perception occurs in neuropsychiatric disorders where the expression of emotion is dulled or blunted, for example depersonalization disorder and schizophrenia. It has been suggested that, in the clinical context of emotional blunting, there is a shift in the relative contribution of brain regions subserving cognitive and emotional processing. The non-competitive glutamate receptor antagonist ketamine produces such emotional blunting in healthy subjects. Therefore, we hypothesised that in healthy subjects ketamine would elicit neural responses to emotional stimuli which mimicked those reported in depersonalization disorder and schizophrenia. Thus, we predicted that ketamine would produce reduced activity in limbic and visual brain regions involved in emotion processing, and increased activity in dorsal regions of the prefrontal cortex and cingulate gyrus, both associated with cognitive processing and, putatively, with emotion regulation. Measuring BOLD signal change in fMRI, we examined the neural correlates of ketamine-induced emotional blunting in eight young right-handed healthy men receiving an infusion of ketamine or saline placebo while viewing alternating 30 s blocks of faces displaying fear versus neutral expressions. The normal pattern of neural response occurred in limbic and visual cortex to fearful faces during the placebo infusion. Ketamine abolished this: significant BOLD signal change was demonstrated only in left visual cortex. However, with ketamine, neural responses were demonstrated to neutral expressions in visual cortex, cerebellum and left posterior cingulate gyrus. Emotional blunting may be associated with reduced limbic responses to emotional stimuli and a relative increase in the visual cortical response to neutral stimuli.

Adult↗

Task instructions modulate neural responses to fearful facial expressions.

BACKGROUND: The amygdala, hippocampus, ventral, and dorsal prefrontal cortices have been demonstrated to be involved in the response to fearful facial expressions. Little is known, however, about the effect of task instructions upon the intensity of responses within these regions to fear-inducing stimuli. METHODS: Using functional magnetic resonance imaging, we examined neural responses to alternating, 30-sec blocks of fearful and neutral expressions in nine right-handed male volunteers during three different 5-min conditions: 1) passive viewing; 2) performance of a gender-decision task, with no explicit judgment of facial emotion; 3) performance of an emotionality judgment task - an explicitly emotional task. RESULTS: There was a significant effect of task upon activation within the left hippocampus and the left inferior occipital gyrus, and upon the magnitude of response within the left hippocampus, with maximal activation in these regions occurring during passive viewing, and minimal during performance of the explicit task. Performance of the gender-decision and explicit tasks, but not passive viewing, was also associated with activation within ventral frontal cortex. CONCLUSIONS: Neural responses to fearful facial expressions are modulated by task instructions.

Amygdala↗

Ketamine and fMRI BOLD signal: distinguishing between effects mediated by change in blood flow versus change in cognitive state.

No human fMRI studies have examined ketamine effects on the BOLD signal change associated with cognitive task performance. We wished to distinguish between effects on 1) cerebral blood flow, with resultant change in BOLD signal; and 2) cognition and neural mechanisms underlying BOLD signal change associated with task performance. Eight right-handed men (mean age 28.75 years) received ketamine or saline i.v. in a randomized, double-blind manner (bolus 0.23 mg/kg; 0.5 mg/kg over 45 min to a maximum 1 hr). Subjects viewed 10 alternating 30-sec blocks of faces with neutral expressions and a fixation cross and discriminated gender of faces. Gradient echo echoplanar images were acquired on a GE Signa 1.5 T Neurovascular system. One hundred T2-weighted images depicting BOLD contrast were acquired over 5 min (for each task) at each of 14 near-axial noncontiguous 7-mm thick planes. Ketamine significantly increased dissociative phenomena and negative symptoms, but did not affect performance of the gender discrimination task. Significant BOLD signal change was demonstrated predominantly in occipitotemporal cortex with both ketamine and placebo. Only two clusters in middle occipital gyrus (BA 18) and precentral gyrus (BA 4) showed significantly decreased BOLD signal change during ketamine compared to placebo. BOLD signal change was not significantly greater in any region during ketamine. Our findings demonstrate subtle rather than major differences between the effects of ketamine and placebo upon the BOLD signal change during perception of face-non face contrast. We suggest that they represent task-dependent effects of the drug/placebo, rather than task-independent effects of the drug per se, and indicate that the effects of ketamine on cerebral blood flow are predominantly focal and task-dependent, rather than global and task-independent.

Adult↗

Perception of emotions from faces and voices following unilateral brain damage.

The importance of the right hemisphere in emotion perception in general has been well documented but its precise role is disputed. We compared the performance of 30 right hemisphere damaged (RHD) patients, 30 left hemisphere damaged (LHD) patients, and 50 healthy controls on both facial and vocal affect perception tasks of specific emotions. Brain damaged subjects had a single episode cerebrovascular accident localised to one hemisphere. The results showed that right hemisphere patients were markedly impaired relative to left hemisphere and healthy controls on test performance: labelling and recognition of facial expressions and recognition of emotions conveyed by prosody. This pertained at the level of individual basic emotions, positive versus negative, and emotional expressions in general. The impairment remained highly significant despite covarying for the group's poorer accuracy on a neutral facial perception test and identification of neutral vocal expressions. The LHD group were only impaired relative to controls on facial emotion tasks when their performance was summed over all the emotion categories and before age and other cognitive factors were taken into account. However, on the prosody test the LHD patients showed significant impairment, performing mid-way between the right hemisphere patients and healthy comparison group. Recognition of positive emotional expressions was better than negative in all subjects, and was not relatively poorer in the LHD patients. Recognition of individual emotions in one modality correlated weakly with recognition in another, in all three groups. These data confirm the primacy of the right hemisphere in processing all emotional expressions across modalities--both positive and negative--but suggest that left hemisphere emotion processing is modality specific. It is possible that the left hemisphere has a particular role in the perception of emotion conveyed through meaningful speech.

Adult↗

A preferential increase in the extrastriate response to signals of danger.

This study examined neural responses in nine right-handed healthy individuals while they viewed mild and intense expressions of four emotions (fear, disgust, happiness, and sadness) contrasted with neutral faces in four event-related functional magnetic resonance imaging experiments. Orthogonal polynomial trend analysis revealed a significant linear increase in the fusiform extrastriate cortical response to increasing intensities of all four emotional expressions, which was significantly greater to increasing intensities of fear and disgust than happiness and sadness, and a significant linear decrease in response to sadness in another extrastriate region. The amygdala was activated by high-intensity fearful expressions, consistent with findings from previous studies, and by low- but not high-intensity sad expressions. Significant linear increases in response to increasing intensities of fear, disgust, and happiness occurred within the hippocampus, anterior insula, and putamen, respectively. Conversely, significant linear decreases in hippocampal and putamen responses occurred to increasing intensities of sadness. We provide the first demonstration of differential increases in extrastriate and limbic responses to signals of increasing danger than to those of other emotions, and significant decreases in these responses to signals of increasing sadness in others. We suggest that this differential pattern of response to different categories of emotional signals allows the preferential direction of visual attention to signals of imminent danger than to other, less-salient emotional stimuli.

Amygdala↗