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The cerebral mechanisms of traits associated with depersonalization-derealization disorder (DPRD) remain poorly understood.
Happy and sad emotion expressions were presented to DPRD and non-referred control (NC) subjects in an implicit event-related functional magnetic resonance imaging (fMRI) design, and correlated with self report scales reflecting typical co-morbidities of DPRD: depression, dissociation, anxiety, somatization.
Significant differences between the slopes of the two groups were observed for somatization in the right temporal operculum (happy) and ventral striatum, bilaterally (sad). Discriminative regions for symptoms of depression were the right pulvinar (happy) and left amygdala (sad). For dissociation, discriminative regions were the left mesial inferior temporal gyrus (happy) and left supramarginal gyrus (sad). For state anxiety, discriminative regions were the left inferior frontal gyrus (happy) and parahippocampal gyrus (sad). For trait anxiety, discriminative regions were the right caudate head (happy) and left superior temporal gyrus (sad).
The ascertained brain regions are in line with previous findings for the respective traits. The findings suggest separate brain systems for each trait.
Our results do not justify any bias for a certain nosological category in DPRD.
This chapter focuses on recent developments in functional neuroimaging that have highlighted functional abnormalities in key neural regions and neural systems underlying different executive control and emotional processes that are impaired in major depressive disorder (MDD). It then turns to findings from studies that employed functional neuroimaging techniques to examine functional neural abnormalities during rest, executive control and emotional challenge in individuals with MDD during depressed episode. The chapter describes new directions in functional neuroimaging of MDD, including functional neuroimaging studies. It also examines the newer neuroimaging analysis techniques that can be employed in the study of MDD, including functional and resting-state connectivity analyses. The chapter presents an integration of the major findings from these studies that have led to the development of neural models of MDD. Finally, it highlights the key neural system functional abnormalities that may represent potential biomarkers of MDD.
The amygdala has a key role in automatic non-conscious processing of emotions. Highly salient emotional stimuli elicit amygdala activity, and happy faces are among the most rapidly perceived facial expressions. In backward masking paradigms, an image is presented briefly and then masked by another stimulus. However, reports of amygdala responses to masked happy faces have been mixed. In the present study, we used functional magnetic resonance imaging (fMRI) to examine amygdala activation to masked happy, sad, and neutral facial expressions. Masked happy faces elicited greater amygdala activation bilaterally as compared to masked sad faces. Our findings indicate that the amygdala is highly responsive to non-consciously perceived happy facial expressions. (JINS, 2010, 16, 383–387.)
Depersonalisation disorder is characterised by emotion suppression, but the cerebral mechanisms of this symptom are not yet fully understood.
To compare brain activation and autonomic responses of individuals with the disorder and healthy controls.
Happy and sad emotion expressions in increasing intensities (neutral to intense) were presented in an implicit event-related functional magnetic resonance imaging (fMRI) design with simultaneous measurement of autonomic responses.
Participants with depersonalisation disorder showed fMRI signal decreases, whereas the control group showed signal increases in response to emotion intensity increases in both happy and sad expressions. The analysis of evoked haemodynamic responses from regions exhibiting functional connectivity between central and autonomic nervous systems indicated that in depersonalisation disorder initial modulations of haemodynamic response occurred significantly earlier (2s post-stimulus) than in the control group (4–6s post-stimulus).
The results suggest that fMRI signal decreases are possible correlates of emotion suppression in depersonalisation disorder.
The recognition of negative facial affect is impaired in people with schizophrenia. The neural underpinnings of this deficit and its relationship to the symptoms of psychosis are still unclear.
To examine the association between positive and negative psychotic symptoms and activation within the amygdala and extrastriate visual regions of patients with schizophrenia during fearful and neutral facial expression processing.
Functional magnetic resonance imaging was used to measure neural responses to neutral and fearful facial expressions in 11 patients with schizophrenia and 9 healthy volunteers during an implicit emotional task.
No association between amygdala activation and positive symptoms was found; the activation within the left superior temporal gyrus was negatively associated with the negative symptoms of the patients.
Our results indicate an association between impaired extrastriate visual processing of facial fear and negative symptoms, which may underlie the previously reported difficulties of patients with negative symptoms in the recognition of facial fear.
It has been suggested that people with psychopathic disorders lack
empathy because they have deficits in processing distress cues (e.g.
fearful facial expressions).
To investigate brain function when individuals with psychopathy and a
control group process facial emotion.
Using event-related functional magnetic resonance imaging we compared six
people scoring ⩾25 on the Hare Psychopathy Checklist–Revised and nine
non-psychopathic healthy volunteers during an implicit emotion processing
task using fearful, happy and neutral faces.
The psychopathy group showed significantly less activation than the
control group in fusiform and extrastriate cortices when processing both
facial emotions. However, emotion type affected response pattern. Both
groups increased fusiform and extrastriate cortex activation when
processing happy faces compared with neutral faces, but this increase was
significantly smaller in the psychopathy group. In contrast, when
processing fearful faces compared with neutral faces, the control group
showed increased activation but the psychopathy group decreased
activation in the fusiform gyrus.
People with psychopathy have biological differences from controls when
processing facial emotion, and the pattern of response differs according
to emotion type.
Three main approaches are used to explore the neural correlates of mood disorder: neuropsychological studies, neuroimaging studies and post-mortem investigations. Lesion studies implicate disturbances in the frontal lobe, basal ganglia, striatum and anterior temporal cortex. Early neurocognitive and neuropathological investigations led to a ‘hypofrontality’ hypothesis of unipolar and bipolar depression, but functional neuroimaging has revealed a more complex picture. Thus, increased metabolism may occur in the subgenual anterior cingulate gyrus in resting-state studies of depression and sad-mood induction. Antidepressants may reduce this activity. Amygdala hyperactivation also is associated with affective disorders. Task-related studies reveal abnormal biases in memory, the experience of pleasure and the perception of emotional facial expressions. There is still little clarity whether the abnormalities in brain activation represent state or trait characteristics of affective disorders.
Work on implicit memory in normal subjects has demonstrated
the influence of stimulus modality on the retrieval of semantic
information. The present study examined the effects of auditory
and visual semantic priming on the recognition of visual words
using a lexical decision task. Performance was studied in a
group of 20 patients with DSM–IV schizophrenia and 26
normal volunteers of similar age and sex. There were two versions
of the task: ipsimodal, in which the word or nonword visual
target followed 400 ms after the onset of a visual word prime
which may or may not be semantically related to the target;
and cross-modal, in which the visual target followed 400 ms
after the onset of an auditory word prime. Both groups showed
significant priming in both modality conditions, although the
schizophrenia patients exhibited significantly greater priming
in the cross-modal condition. Priming effects in the ipsimodal
condition did not differ substantially between patients and
controls. The priming effects in the two conditions correlated
with each other in the schizophrenia patients only. The results
suggest that priming may occur through amodal semantic
representations. In schizophrenia, there appears to be increased
cross-modal connectivity (reduced modality modularity and
informational encapsulation) between lexical representations
that could result in impaired language, particularly speech,
processing. (JINS, 2002, 8, 884–892.)
This article will concentrate on insight into serious mental disorder. Not psychoanalytic insight – nor indeed, the insight all of us have, to a greater or lesser extent, into our own attitudes, motives and behaviour – but the insight which patients with psychosis have into their mental pathology. This is no longer considered an all-or-none phenomenon, but rather a dimensional one, so that subjects can have different levels of awareness into their illness. The suggestion was first mooted by Aubrey Lewis (1934) in his seminal work on insight. Conceptual exploration of insight has been activated in the past decade and is proceeding in parallel with the construction of special scales to measure insight and research into its cognitive, biological, social and cultural basis.
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