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Although somatosensory amplification is theorized to serve a critical role in somatization, it remains poorly understood neurobiologically. In this perspective article, convergent visceral-somatic processing is highlighted, and neuroimaging studies in somatoform disorders are reviewed. Neural correlates of cognitive-affective amplifiers are integrated into a neurocircuit framework for somatosensory amplification. The anterior cingulate cortex, insula, amygdala, hippocampal formation, and striatum are some of the identified regions. Clinical symptomatology in a given patient or group may represent dysfunction in one or more of these neurobehavioral nodes. Somatosensory amplification may, in part, develop through stress-mediated aberrant neuroplastic changes and the neuromodulatory effects of inflammation.
BACKGROUND - Historically, in both adult and pediatric populations, a lack of knowledge regarding complex regional pain syndrome (CRPS) and absence of clear diagnostic criteria have contributed to the view that this is a primarily psychiatric condition.
OBJECTIVE - To test the hypothesis that children with CRPS are more functionally disabled, have more pain and are more psychologically distressed than children with other pain conditions.
METHODS - A total of 101 children evaluated in a tertiary care pediatric pain clinic who met the International Association for the Study of Pain consensus diagnostic criteria for CRPS participated in the present retrospective study. Comparison groups included 103 children with abdominal pain, 291 with headache and 119 with back pain. Children and parents completed self-report questionnaires assessing disability, somatization, pain coping, depression, anxiety and school attendance.
RESULTS - Children with CRPS reported higher pain intensity and more recent onset of pain at the initial tertiary pain clinic evaluation compared with children with other chronic pain conditions. They reported greater functional disability and more somatic symptoms than children with headaches or back pain. Scores on measures of depression and anxiety were within normal limits and similar to those of children in other pain diagnostic groups.
CONCLUSIONS - As a group, clinic-referred children with CRPS may be more functionally impaired and experience more somatic symptoms compared with children with other pain conditions. However, overall psychological functioning as assessed by self-report appears to be similar to that of children with other chronic pain diagnoses. Comprehensive assessment using a biopsychosocial framework is essential to understanding and appropriately treating children with symptoms of CRPS.
BACKGROUND - This study examined how an interactive seminar focusing on two medically unexplained illnesses, chronic fatigue syndrome (CFS) and fibromyalgia, influenced medical student attitudes toward CFS, a more strongly stigmatized illness.
METHODS - Forty-five fourth year medical students attended a 90 minute interactive seminar on the management of medically unexplained illnesses that was exemplified with CFS and fibromyalgia. A modified version of the CFS attitudes test was administered immediately before and after the seminar.
RESULTS - Pre-seminar assessment revealed neutral to slightly favorable toward CFS. At the end of the seminar, significantly more favorable attitudes were found toward CFS in general (t (42) = 2.77; P < 0.01) and for specific items that focused on (1) supporting more CFS research funding (t (42) = 4.32; P < 0.001; (2) employers providing flexible hours for people with CFS (t (42) = 3.52, P < 0.01); and (3) viewing CFS as not primarily a psychological disorder (t (42) = 2.87, P < 0.01). Thus, a relatively brief exposure to factual information on specific medically unexplained illnesses was associated with more favorable attitudes toward CFS in fourth year medical students.
CONCLUSION - This type of instruction may lead to potentially more receptive professional attitudes toward providing care to these underserved patients.
Anger and how anger is regulated appear to affect acute and chronic pain intensity. The inhibition of anger (anger-in), in particular, has received much attention, and it is widely believed that suppressing or inhibiting the verbal or physical expression of anger is related to increased pain severity. We examine theoretical accounts for expecting that anger inhibition should affect pain, and review evidence for this claim. We suggest that the evidence for a link between trait anger-in (the self-reported tendency to inhibit anger expression when angry) and acute and chronic pain severity is quite limited owing to a number of factors including a inadequate definition of trait anger-in embodied in the popular anger-in subscale of Spielberger's Anger Expression Inventory, and a strong overlap between trait anger-in scores and measures of general negative affect (NA). We argue that in order to determine whether something unique to the process of anger inhibition exerts direct effects on subsequent pain intensity, new conceptualizations and approaches are needed that go beyond self-report assessments of trait anger-in. We present one model of anger inhibition and pain that adopts elements of Wegner's ironic process theory of thought suppression. Findings from this emerging research paradigm indicate that state anger suppression (suppression manipulated in the laboratory) may indeed affect sensitivity to subsequent painful stimuli, and we outline potentially productive avenues of future inquiry that build on this model. We conclude that although studies employing correlational designs and self-reports of trait anger-in have not upheld the claim that anger inhibition affects pain severity, evidence from studies using new models suggests that actually inhibiting anger expression during a provocative event may increase perceived pain at a later time.
Syndromes characterized by pain, fatigue, mood disorder, cognitive dysfunction, and sleep disturbance have been referred to as stress-related somatic disorders by virtue of the observation that onset and exacerbation of symptoms occur with stress. These syndromes include but are not limited to fibromyalgia, chronic fatigue syndrome, temporomandibular disorder, and irritable bowel syndrome. As with most chronic illnesses, genetic susceptibility and lifetime environmental exposures play a role in creating vulnerability to disease. Cumulative lifetime stress has been associated with a number of physiologic changes in the brain and body that reflect dysregulated hormonal and autonomic activity. Exposure to the stressor of violence is likely to create a state of vulnerability for the stress-related somatic syndromes and also to contribute to symptom expression and severity. Understanding the relationship between violence, stress, and somatic syndromes will help in clarifying the consequences of violence exposure to long-term health and health-related quality of life.
The role of the serotonin transporter protein (STP) in the development of somatoform [corrected] disorders was addressed in a correlational study of the levels of immunoreactive STP (IR-STP) using site-specific antibodies against the least conserved (among a group of other cotransporters) epitope at the C-terminal of STP and the level of anxiety symptoms in patients with somatoform [corrected] disorders. A total of 22 patients were studied, with DSM-IV diagnoses of somatoform [corrected] disorders, along with 32 mentally healthy subjects of comparable age and sex. Immunoblotting of IR-STP from patients from healthy donors produced a diffuse band between 68 and 105 kDal and a clear narrow band at 43 kDal. The 43-kDal IR-STP protein was almost completely absent from most patients, as compared with the levels of this protein in healthy donors. This result suggests an abnormality of STP processing or, perhaps, alternative splicing of the gene encoding STP in patients with somatoform [corrected] disorders, and this appears to reflect the dysfunction in serotoninergic transmission in the CNS in these patients.
The role of serotonin transporter (SERT) protein in the development of somatoform disorders (SD) was investigated. An association study was performed in terms of the evaluation of the level of SERT immunoreactive (IR-SERT) protein using site-specific antibodies directed at SERT C-terminus fragment, poorly conserved among the other cotransporters. The level of the anxious symptomatology was also estimated in the patients with SD. 22 patients, who met DSM-IV criteria for somatoform disorders, and 32 normals were examined. In platelets from normals, IR-SERT protein migrated as a difuse band between 68 and 105 kDa, and a major sharper band at 43 kDa. Almost complete disappearance of platelet 43 kDa IR-SERT protein band was observed in most of the patients with SD. These findings permitted to suggest a possibility of either biosynthetic or processing abnormality of SERTs in the affected population, that might reflect a dysfunction of serotonin neurotransmission in CNS of the patients with SD.
To elucidate the role of serotonin transporter (SERT) protein as a candidate target for somatoform disorders (SD), we have performed an association study of the SERT immunoreactive (IR-SERT) protein level by using site-specific antibodies directed at C-terminus epitope poorly conserved among other cotransporters. 22 patients who met DSM-IY criteria for SD and 32 healthy volunteers matched in sex and age participated in the study. In platelets from all healthy donors, IR-SERT proteins migrates as a diffuse band between 75 and 102 kDa and a major sharper band at 43 kDa. We revealed almost complete disappearance of platelet 43 kDa IR-SERT protein in all patients with SD. All patients were rated with Hamilton Depressive Rating Scale (HDRS). There were found a significant negative correlation between residual IR-SERT 43 kDa protein level and HDRS Scores [r = -0.83; P < 0.000001]. These findings suggest that a biosynthetic or processing abnormality may exist in SERTs in the affected population and may reflect the dysfunction of serotonin neurotransmission in CNS.
The utility of measuring both positive and negative affective states for assessing rheumatoid arthritis (RA) patients was examined in 3 independent samples of male and female RA patients (Sample A: 179 women, 48 men; Sample B: 177 women, 24 men; Sample C: 134 women, 38 men). Confirmatory factor analyses of each sample indicated that positive and negative affect constituted separate, negatively correlated factors. The relations among disease variables, coping, and affects were consistent with a model in which coping mediates the relationship between disease variables and positive and negative affect. Patients with higher pain and limitation from RA had higher levels of maladaptive coping, and maladaptive coping was associated with lower positive affect and higher negative affect. Those RAs with higher activity limitation also reported less adaptive coping, which was associated with less positive affect.