Alexithymia, or "no words for feelings", is a personality trait which is associated with difficulties in emotion recognition and regulation. It is unknown whether this deficit is due primarily to ...regulation, perception, or mentalizing of emotions. In order to shed light on the core deficit, we tested our subjects on a wide range of emotional tasks. We expected the high alexithymics to underperform on all tasks.
Two groups of healthy individuals, high and low scoring on the cognitive component of the Bermond-Vorst Alexithymia Questionnaire, completed questionnaires of emotion regulation and performed several emotion processing tasks including a micro expression recognition task, recognition of emotional prosody and semantics in spoken sentences, an emotional and identity learning task and a conflicting beliefs and emotions task (emotional mentalizing).
The two groups differed on the Emotion Regulation Questionnaire, Berkeley Expressivity Questionnaire and Empathy Quotient. Specifically, the Emotion Regulation Quotient showed that alexithymic individuals used more suppressive and less reappraisal strategies. On the behavioral tasks, as expected, alexithymics performed worse on recognition of micro expressions and emotional mentalizing. Surprisingly, groups did not differ on tasks of emotional semantics and prosody and associative emotional-learning.
Individuals scoring high on the cognitive component of alexithymia are more prone to suppressive emotion regulation strategies rather than reappraisal strategies. Regarding emotional information processing, alexithymia is associated with reduced performance on measures of early processing as well as higher order mentalizing. However, difficulties in the processing of emotional language were not a core deficit in our alexithymic group.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Recognition of others' emotions is an important aspect of interpersonal communication. In major depression, a significant emotion recognition impairment has been reported. It remains unclear whether ...the ability to recognize emotion from facial expressions is also impaired in anxiety disorders. There is a need to review and integrate the published literature on emotional expression recognition in anxiety disorders and major depression.
A detailed literature search was used to identify studies on explicit emotion recognition in patients with anxiety disorders and major depression compared to healthy participants. Eighteen studies provided sufficient information to be included. The differences on emotion recognition impairment between patients and controls (Cohen's d) with corresponding confidence intervals were computed for each study. Over all studies, adults with anxiety disorders had a significant impairment in emotion recognition (d = -0.35). In children with anxiety disorders no significant impairment of emotion recognition was found (d = -0.03). Major depression was associated with an even larger impairment in recognition of facial expressions of emotion (d = -0.58).
Results from the current analysis support the hypothesis that adults with anxiety disorders or major depression both have a deficit in recognizing facial expression of emotions, and that this deficit is more pronounced in major depression than in anxiety.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Parkinson's disease (PD) is associated with a loss of neurons from the midbrain. The cause of PD is unknown, but it is established that certain neurotoxins can cause similar syndromes. The brain is ...normally protected from these noxious blood‐borne chemicals by the blood–brain barrier which includes specialized proteins on the inside of blood vessels in the brain. These act as molecular efflux pumps and P‐glycoprotein (P‐gp) is an abundant representative. Vulnerability to PD appears codetermined by the genotype for the P‐gp gene. We hypothesized that PD patients have reduced P‐gp function in the blood–brain barrier. We used positron emission tomography to measure brain uptake of 11C‐verapamil, which is normally extruded from the brain by P‐gp. Here, we show significantly elevated uptake of 11C‐verapamil (18%) in the midbrain of PD patients relative to controls. This is the first evidence supporting a dysfunctional blood–brain barrier as a causative mechanism in PD. Ann Neurol 2005;57:176–179
In patients who experience unilateral chronic pain, abnormal sensory perception at the non-painful side has been reported. Contralateral sensory changes in these patients have been given little ...attention, possibly because they are regarded as clinically irrelevant. Still, bilateral sensory changes in these patients could become clinically relevant if they challenge the correct identification of their sensory dysfunction in terms of hyperalgesia and allodynia. Therefore, we have used the standardized quantitative sensory testing (QST) protocol of the German Research Network on Neuropathic Pain (DFNS) to investigate somatosensory function at the painful side and the corresponding non-painful side in unilateral neuropathic pain patients using gender- and age-matched healthy volunteers as a reference cohort. Sensory abnormalities were observed across all QST parameters at the painful side, but also, to a lesser extent, at the contralateral, non-painful side. Similar relative distributions regarding sensory loss/gain for non-nociceptive and nociceptive stimuli were found for both sides. Once a sensory abnormality for a QST parameter at the affected side was observed, the prevalence of an abnormality for the same parameter at the non-affected side was as high as 57% (for Pressure Pain Threshold). Our results show that bilateral sensory dysfunction in patients with unilateral neuropathic pain is more rule than exception. Therefore, this phenomenon should be taken into account for appropriate diagnostic evaluation in clinical practice. This is particularly true for mechanical stimuli where the 95% Confidence Interval for the prevalence of sensory abnormalities at the non-painful side ranges between 33% and 50%.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Abstract Decreased prefrontal activation (hypofrontality) in schizophrenia is thought to underlie negative symptoms and cognitive impairments, and may contribute to poor social outcome. ...Hypofrontality does not always improve during treatment with antipsychotics. We hypothesized that antipsychotics, which share antagonism at dopamine receptors, with a relatively low dopamine receptor affinity and high serotonin receptor affinity may have a sparing effect on prefrontal function compared to strong dopamine receptor antagonists. We systematically investigated the relation between serotonin and dopamine antagonism of antipsychotics and prefrontal functioning by reviewing neuroimaging studies. The weight of the evidence was consistent with our hypothesis that antipsychotics with low dopaminergic receptor affinity and moderate to high serotonergic affinity were associated with higher activation of the prefrontal cortex. However, clozapine, a weak dopamine and strong serotonin antagonist, was associated with decrease in prefrontal activation. Future studies should further elucidate the link between prefrontal activation and negative symptoms using prospective designs and advanced neuroimaging techniques, which may ultimately benefit the development of treatments for disabling negative symptoms.
Major depressive disorder (MDD) has been associated with abnormal prefrontal-limbic interactions and altered catecholaminergic neurotransmission. The val158met polymorphism on the ...catechol-O-methyltransferase (COMT) gene has been shown to influence prefrontal cortex (PFC) activation during both emotional processing and working memory (WM). Although COMT-genotype is not directly associated with MDD, it may affect MDD pathology by altering PFC activation, an endophenotype associated with both COMT and MDD. 125 participants, including healthy controls (HC, n=28) and MDD patients were genotyped for the COMT val158met polymorphism and underwent functional magnetic resonance imaging (fMRI-neuroimaging) during emotion processing (viewing of emotional facial expressions) and a WM task (visuospatial planning). Within HC, we observed a positive correlation between the number of met-alleles and right inferior frontal gyrus activation during emotional processing, whereas within patients the number of met-alleles was not correlated with PFC activation. During WM a negative correlation between the number of met-alleles and middle frontal gyrus activation was present in the total sample. In addition, during emotional processing there was an effect of genotype in a cluster including the amygdala and hippocampus. These results demonstrate that COMT genotype is associated with relevant endophenotypes for MDD. In addition, presence of MDD only interacts with genotype during emotional processing and not working memory.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Alexithymia is a trait characterized by a diminished capacity to describe and distinguish emotions and to fantasize; it is associated with reduced introspection and problems in emotion processing. ...The default mode network (DMN) is a network of brain areas that is normally active during rest and involved in emotion processing and self-referential mental activity, including introspection. We hypothesized that connectivity of the DMN might be altered in alexithymia. Twenty alexithymic and 18 non-alexithymic healthy volunteers underwent a resting state fMRI scan. Independent component analysis was used to identify the DMN. Differences in connectivity strength were compared between groups. Within the DMN, alexithymic participants showed lower connectivity within areas of the DMN (medial frontal and temporal areas) as compared to non-alexithymic participants. In contrast, connectivity in the high-alexithymic participants was higher for the sensorimotor cortex, occipital areas and right lateral frontal cortex than in the low-alexithymic participants. These results suggest a diminished connectivity within the DMN of alexithymic participants, in brain areas that may also be involved in emotional awareness and self-referential processing. On the other hand, alexithymia was associated with stronger functional connections of the DMN with brain areas involved in sensory input and control of emotion.
Due to the lack of a specific diagnostic tool for neuropathic pain, a grading system to categorize pain as 'definite', 'probable', 'possible' and 'unlikely' neuropathic was proposed. Somatosensory ...abnormalities are common in neuropathic pain and it has been suggested that a greater number of abnormalities would be present in patients with 'probable' and 'definite' grades. To test this hypothesis, we investigated the presence of somatosensory abnormalities by means of Quantitative Sensory Testing (QST) in patients with a clinical diagnosis of neuropathic pain and correlated the number of sensory abnormalities and sensory profiles to the different grades. Of patients who were clinically diagnosed with neuropathic pain, only 60% were graded as 'definite' or 'probable', while 40% were graded as 'possible' or 'unlikely' neuropathic pain. Apparently, there is a mismatch between a clinical neuropathic pain diagnosis and neuropathic pain grading. Contrary to the expectation, patients with 'probable' and 'definite' grades did not have a greater number of abnormalities. Instead, similar numbers of somatosensory abnormalities were identified for each grade. The profiles of sensory signs in 'definite' and 'probable' neuropathic pain were not significantly different, but different from the 'unlikely' grade. This latter difference could be attributed to differences in the prevalence of patients with a mixture of sensory gain and loss and with sensory loss only. The grading system allows a separation of neuropathic and non-neuropathic pain based on profiles but not on the total number of sensory abnormalities. Our findings indicate that patient selection based on grading of neuropathic pain may provide advantages in selecting homogenous groups for clinical research.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The 'complex neural pulse'(TM) (CNP) is a neuromodulation protocol employing weak pulsed electromagnetic fields (PEMF). A pioneering paper reported an analgesic effect in healthy humans after 30 ...minutes of CNP-stimulation using three nested whole head coils. We aimed to devise and validate a stimulator with a novel design entailing a multitude of small coils at known anatomical positions on a head cap, to improve applicability. The main hypothesis was that CNP delivery with this novel device would also increase heat pain thresholds. Twenty healthy volunteers were enrolled in this double-blind, sham-controlled, crossover study. Thirty minutes of PEMF (CNP) or sham was applied to the head. After one week the other treatment was given. Before and after each treatment, primary and secondary outcomes were measured. Primary outcome was heat pain threshold (HPT) measured with thermal quantitative sensory testing. Other outcomes were warmth detection threshold, and aspects of cognition, emotion and motor performance. As hypothesized heat pain threshold was significantly increased after the PEMF stimulation. All other outcomes were unaltered by the PEMF but there was a trend level reduction of cognitive performance after PEMF stimulation as measured by the digit-symbol substitution task. Results from this pilot study suggest that our device is able to stimulate the brain and to modulate its function. This is in agreement with previous studies that used similar magnetic field strengths to stimulate the brain. Specifically, pain control may be achieved with PEMF and for this analgesic effect, coil design does not appear to play a dominant role. In addition, the flexible configuration with small coils on a head cap improves clinical applicability.
Dutch Cochrane Centre NTR1093.
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DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Structural neuronal plasticity is present in the nucleus para-retroambiguus (NPRA) and the commissural nucleus of the solitary tract/A2 group (NTScom/A2) in female hamsters. Both brainstem nuclei ...play a role in estrous cycle related autonomic adaptations. We investigated how aging affects the capillary condition in these adaptive brainstem regions. Senescent female hamsters (±95 weeks) were tested weekly for their 4-day estrous cycle. Subsequently morphological changes of NPRA and NTScom/A2 were compared with those of young (±20 weeks) females in an ultrastructural study. The medial tegmental field served as control area. In 841 capillaries (
n
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319 capillaries, young females (
N
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3);
n
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522 capillaries, aged females (
N
=
4)) vascular aberrations were classified into 3 categories: endothelial and tight junction, basement membrane and pericyte aberrations. In old animals, capillaries showed marked endothelial changes, disrupted tight junctions, and thickening and splitting of basement membranes. Aberrations were found in 40–60% of all capillaries. About 70% of the pericytes contained degenerative inclusions. Despite this generalized vascular degeneration, the reproductive cycle of female hamsters was unaffected by vascular senescence. Perivascular fibrosis as reported in aging rats was never observed, which suggests the existence of species differences.
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