Niklaus Egloff

Nondermatomal somatosensory deficits in patients with chronic pain disorder: clinical findings and hypometabolic pattern in FDG-PET.

ABSTRACT Patients with chronic pain disorders often show somatosensory disturbances that are considered to be functional. This paper aims at a more precise clinical description and at a documentation of functional neuroimaging correlates of this phenomenon. We examined 30 consecutive patients with unilaterally accentuated chronic pain not explained by persistent peripheral tissue damage and ipsilateral somatosensory disturbances including upper and lower extremities and trunk. The patients were assessed clinically and with conventional brain CT or MRI scan. In the last 11 patients functional neuroimaging was carried out (18‐fluordeoxyglucose positron emission tomography = FDG‐PET). Depressive symptoms were assessed with the Hamilton depression scale (HAMD‐17) and pain intensity was rated with a visual analogue scale for pain (VAS). All patients suffered from mild to moderate depressive symptoms. All patients had experienced a prolonged antecedent phase of severe emotional distress; most of them remembered a “trigger episode of somatic pain” on the affected side. Somatosensory deficits were a replicable hyposensitivity to touch and heat perception of nondermatomal distribution. Conventional imaging procedures (brain CT or MRI scans) showed no structural changes. However, in 11 patients functional imaging with FDG‐PET showed a significant hypometabolic pattern of changes in cortical and subcortical areas, mainly in the post‐central gyrus, posterior insula, putamen, and anterior cingulate cortex. In summary, pain‐related nondermatomal somatosensory deficits (NDSDs) are a phenomenon involving biological as well as psychosocial factors with replicable neuroperceptive clinical findings and a complex neurodysfunctional pattern in the FDG‐PET. Abbreviations: ACC: anterior cingulate cortex; CRPS: complex regional pain syndrome; DLPFC: dorsolateral prefrontal cortex; DSM‐IV: diagnostic and statistical manual of mental disorders, fourth revision; FDG‐PET: 18‐fluordeoxyglucose positron emission tomography; fMRI: Functional magnetic resonance imaging; HAMD: Hamilton depression scale; ICD‐10: International classification of diseases, version 10; NDSD: nondermatomal somatosensory deficits; PFC: prefrontal cortex; PTSD: posttraumatic stress disorder; SPECT: single photon emission computerized tomography; SPM: Statistical parametric mapping; VAS: visual pain analogue scale.Patients with chronic pain disorders often show somatosensory disturbances that are considered to be functional. This paper aims at a more precise clinical description and at a documentation of functional neuroimaging correlates of this phenomenon. We examined 30 consecutive patients with unilaterally accentuated chronic pain not explained by persistent peripheral tissue damage and ipsilateral somatosensory disturbances including upper and lower extremities and trunk. The patients were assessed clinically and with conventional brain CT or MRI scan. In the last 11 patients functional neuroimaging was carried out (18-fluordeoxyglucose positron emission tomography = FDG-PET). Depressive symptoms were assessed with the Hamilton depression scale (HAMD-17) and pain intensity was rated with a visual analogue scale for pain (VAS). All patients suffered from mild to moderate depressive symptoms. All patients had experienced a prolonged antecedent phase of severe emotional distress; most of them remembered a ‘‘trigger episode of somatic pain” on the affected side. Somatosensory deficits were a replicable hyposensitivity to touch and heat perception of nondermatomal distribution. Conventional imaging procedures (brain CT or MRI scans) showed no structural changes. However, in 11 patients functional imaging with FDG-PET showed a significant hypometabolic pattern of changes in cortical and subcortical areas, mainly in the post-central gyrus, posterior insula, putamen, and anterior cingulate cortex. In summary, pain-related nondermatomal somatosensory deficits (NDSDs) are a phenomenon involving biological as well as psychosocial factors with replicable neuroperceptive clinical findings and a complex neurodysfunctional pattern in the FDG-PET. 2009 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. No support and no potential conflict of interest. term refers to a slightly different historical understanding of dis-

Vitamin D and Central Hypersensitivity in Patients with Chronic Pain

BACKGROUND Low vitamin D is implicated in various chronic pain conditions with, however, inconclusive findings. Vitamin D might play an important role in mechanisms being involved in central processing of evoked pain stimuli but less so for spontaneous clinical pain. OBJECTIVE This study aims to examine the relation between low serum levels of 25-hydroxyvitamin D3 (25-OH D) and mechanical pain sensitivity. DESIGN We studied 174 patients (mean age 48 years, 53% women) with chronic pain. A standardized pain provocation test was applied, and pain intensity was rated on a numerical analogue scale (0-10). The widespread pain index and symptom severity score (including fatigue, waking unrefreshed, and cognitive symptoms) following the 2010 American College of Rheumatology preliminary diagnostic criteria for fibromyalgia were also assessed. Serum 25-OH D levels were measured with a chemiluminescent immunoassay. RESULTS Vitamin deficiency (25-OH D < 50 nmol/L) was present in 71% of chronic pain patients; another 21% had insufficient vitamin D (25-OH D < 75 nmol/L). After adjustment for demographic and clinical variables, there was a mean ± standard error of the mean increase in pain intensity of 0.61 ± 0.25 for each 25 nmol/L decrease in 25-OH D (P = 0.011). Lower 25-OH D levels were also related to greater symptom severity (r = -0.21, P = 0.008) but not to the widespread pain index (P = 0.83) and fibromyalgia (P = 0.51). CONCLUSIONS The findings suggest a role of low vitamin D levels for heightened central sensitivity, particularly augmented pain processing upon mechanical stimulation in chronic pain patients. Vitamin D seems comparably less important for self-reports of spontaneous chronic pain.

Nondermatomal somatosensory deficits in chronic pain patients: are they really hysterical?

TOC summary Patients with chronic pain frequently show nondermatomal somatosensory deficits (NDSDs) that are considered to be functional. We hypothesize a multifactorial etiology of NDSDs, including stress. Abstract Patients with chronic pain disorders frequently show nondermatomal somatosensory deficits (NDSDs) that are considered to be functional. Typically, NDSDs show quadratomal or hemibody distribution ipsilateral to the areas of chronic pain. According to the Diagnostic and Statistical Manual of Mental Disorders, 4th edition and the International Classification of Diseases, 10th revision, such functional somatosensory deficits are classified in the chapter “conversion disorder.” Many publications also used the term “hysterical sensory loss.” However, doubts are increasing about this one‐sided psychiatric view. We aimed to better characterize the biopsychosocial factors associated with NDSDs. Therefore, we compared 2 groups of inpatients with chronic pain disorder, of whom 90 suffered from NDSDs and 90 did not. The patients with NDSDs all showed widespread somatosensory deficits with hemibody distribution. On logistic regression analysis, history of a prior physical trauma was positively predictive for patients with NDSDs. Personality disorder and adverse childhood experiences were positively predictive for the control group with chronic pain disorders without NDSDs. The frequencies of comorbid depression and anxiety disorder did not differ statistically between groups. In conclusion, pain patients with NDSDs are, psychopathologically, by no means more noticeable personalities than patients with chronic pain disorder without NDSDs. Similar to complex regional pain syndromes, we assume a multifactorial etiology of NDSDs, including stress. Based on our observations, terms like “hysteric” should not be applied any longer to patients with NDSDs who suffer from chronic pain.

Hypersensitivity and hyperalgesia in somatoform pain disorders

OBJECTIVE In psychiatry, pain disorders not explained by structural lesions have been classified for decades as somatoform pain disorders, the underlying concept being somatization. In a parallel move, somatic medicine has defined an expanding group of similar pain disorders, known as functional pain syndromes. Functional pain syndromes are characterized by enhanced pain sensitivity. The aim of our study was to investigate the proportion of patients with somatoform pain disorders who also meet the criteria of functional pain syndromes and the extent to which patients with somatoform pain disorders also show enhanced pain sensitivity. METHODS Data on pain sensitivity in 120 hospitalized patients were obtained by means of two algometric methods. The group of patients with somatoform pain disorders was further divided into two subsets: patients with and those without a co-diagnosis of a functional pain syndrome. Patients with nociceptive pain served as control group. RESULTS Of the 120 in-patients selected, 67 fulfilled the criteria of a somatoform pain disorder of which 41 (61%) also met the co-diagnosis of a functional pain syndrome. Patients with somatoform pain disorder differed from controls in that they showed enhanced pain sensitivity, irrespective of whether a functional pain syndrome was concomitantly present (P<.001). CONCLUSIONS Somatoform pain disorders show considerable overlap with functional pain syndromes, including enhanced pain sensitivity. This suggests the relevance of integrating somatosensory aspects of pain into a modified understanding of somatoform pain disorders.

Implications of proposed fibromyalgia criteria across other functional pain syndromes

Objectives: In 2010, the American College of Rheumatology (ACR) proposed new criteria for the diagnosis of fibromyalgia (FM) in the context of objections to components of the criteria of 1990. The new criteria consider the Widespread Pain Index (WPI) and the Symptom Severity Score (SSS). This study evaluated the implications of the new diagnostic criteria for FM across other functional pain syndromes. Method: A cohort of 300 consecutive in-patients with functional pain syndromes underwent a diagnostic screen according to the ACR 2010 criteria. Additionally, systematic pain assessment including algometric and psychometric data was carried out. Results: Twenty-five patients (8.3%) had been diagnosed with FM according to the ACR 1990 criteria. Twenty-one of them (84%) also met the new ACR 2010 criteria. In total, 130 patients (43%) fulfilled the new ACR 2010 criteria. A comparison of new vs. old cases showed a high degree of conformity in most of the pain characteristics. The new FM cases, however, revealed a pronounced heterogeneity in the anatomical pain locations, including several types of localized pain syndromes. Furthermore, patients fulfilling the ACR 2010 FM criteria differed from those with other functional pain syndromes; they had increased pain sensitivity scores and increased psychometric values for depression, anxiety, and psychological distress (p < 0.01). Conclusions: FM according to the ACR 2010 criteria describes the ‘severe half’ of the spectrum of functional pain syndromes. By dropping the requirement of ‘generalized pain’, these criteria result in a blurring of the distinction between FM and more localized functional pain syndromes.

Stressinduzierte Hyperalgesie (SIH) als Folge von emotionaler Deprivation und psychischer Traumatisierung in der Kindheit

ZusammenfassungDie Schmerzforschung der letzten Jahre hat gezeigt, dass bei vielen chronischen Schmerzstörungen Ausmaß und Stärke des individuell erlebten Schmerzes nicht mit dem Ausmaß der peripheren Gewebeschädigung oder der Aktivität der primär-afferenten und der spinal-nozizeptiven neuronalen Bahnen korrelieren. Insbesondere Stress und Angst üben einen modulierenden Einfluss auf das Schmerzerleben aus, wobei Art, Dauer und Schwere des Stressors sowie biographisch frühe Prägungen bei der Ausreifung des Stress- wie des Schmerzverarbeitungssystems bedeutsam sind. Bei einigen chronischen Schmerzstörungen, z. B. Fibromyalgiesyndrom, craniomandibuläre Dysfunktion (CMD) oder somatoforme Schmerzstörung, ist kein relevanter peripherer Input nachweisbar. Die Arbeit gibt einen Überblick über Studien, welche tierexperimentell ebenso wie beim Menschen die neurobiologischen Mechanismen und neuronalen Botenstoffe bei der stressinduzierten Hyperalgesie untersuchen. Daraus werden Konsequenzen für die aktuelle wie künftige Schmerztherapie abgeleitet.AbstractIt is now widely recognized that in many chronic pain syndromes the intensity and severity of individually perceived pain does not correlate consistently with the degree of peripheral nervous system tissue damage or with the intensity of primary afferent or spinal nociceptive neurone activity. In particular, stress and anxiety exert modulatory influences on pain depending on the nature, duration and intensity of the stressor and developmental influences on the maturation of the stress as well as the pain system. In some chronic pain syndromes, e. g. fibromyalgia, TMD or somatoform disorders, no nociceptive or neuropathic input is detectable. We summarise the studies investigating the neural substrates and neurobiological mechanisms of stress-induced hyperalgesia (SIH) in animals and humans. The review provides new perspectives and challenges for the current and future treatment of chronic pain.

Therapie zentralisierter Schmerzstörungen

Previous somatic pain experience (priming), psychobiographic imprinting (pain proneness), and stress (action proneness) are key to an enhanced centralised pain response. This centralised pain response clinically manifests itself in pain sensitization and chronification. The therapeutic approach to chronic centralised pain disorders is multimodal. The overarching aim of the various interventions of a multimodal treatment program is to activate anti-nociceptive areas of the cerebral matrix involved in pain processing. The lists of medications targeting neuropathic and somatoform pain disorder show considerable overlap. Psychotherapy helps patients with central pain sensitization to improve pain control, emotional regulation and pain behaviour.Previous somatic pain experience (priming), psychobiographic imprinting (pain proneness), and stress (action proneness) are key to an enhanced centralised pain response. This centralised pain response clinically manifests itself in pain sensitization and chronification. The therapeutic approach to chronic centralised pain disorders is multimodal. The overarching aim of the various interventions of a multimodal treatment program is to activate anti-nociceptive areas of the cerebral matrix involved in pain processing. The lists of medications targeting neuropathic and somatoform pain disorder show considerable overlap. Psychotherapy helps patients with central pain sensitization to improve pain control, emotional regulation and pain behaviour.

Widespread Pain and Low Widespread Pain Index Scores among Fibromyalgia-positive Cases Assessed with the 2010/2011 Fibromyalgia Criteria

Objective. Widespread pain is no longer required for fibromyalgia (FM) diagnosis according to the American College of Rheumatology (ACR) 2010 preliminary diagnostic criteria and its 2011 modification, but its absence may be of concern. We investigated whether the widespread pain definition was satisfactory and the consequences of having a small number of painful regions or of not satisfying the widespread pain criterion. Methods. We studied 5011 patients who satisfied the 2011 criteria. FM was identified using the Widespread Pain Index (WPI) and the Symptom Severity Scale (SSS): WPI ≥ 7 and SSS ≥ 5 or WPI 3–6 and SSS ≥ 9. Widespread pain was 4 quadrants plus axial pain, according to the 1990 ACR FM criteria. Results. There were 4700 patients (93.8%) who satisfied the ACR 1990 widespread pain criterion. Using a new strict definition for 5 pain regions based on the WPI sites, a modified widespread pain criterion requiring 4 of 5 regions identified 98.8% of criteria-positive patients. Patients without widespread pain or those in the low WPI/high SSS group had milder FM and no evidence of increased psychological or physical distress. Conclusion. In usual clinical and epidemiological studies, the 2011 and 2010 criteria work well, but are not as effective in patients with asymmetrical or regional pain who do not satisfy a widespread pain criterion. A ≥ 4-pain region widespread pain definition will eliminate regional pain false-positives and will identify 98.8% of current 2011 cases. Future revisions of the 2010/2011 criteria should consider incorporating the ≥ 4-region requirement to avoid misclassification.

traumatization and chronic pain: a further model of interaction

Up to 80% of patients with severe posttraumatic stress disorder are suffering from “unexplained” chronic pain. Theories about the links between traumatization and chronic pain have become the subject of increased interest over the last several years. We will give a short summary about the existing interaction models that emphasize particularly psychological and behavioral aspects of this interaction. After a synopsis of the most important psychoneurobiological mechanisms of pain in the context of traumatization, we introduce the hypermnesia–hyperarousal model, which focuses on two psychoneurobiological aspects of the physiology of learning. This hypothesis provides an answer to the hitherto open question about the origin of pain persistence and pain sensitization following a traumatic event and also provides a straightforward explanatory model for educational purposes.

Schmerzstörungen bei Traumatisierten - neurophysiologische Aspekte und klinische Phänomenologie

This overview portrays the salient physiological mechanisms being involved in the clinical manifestation of chronic pain in traumatized patients. A «hypermnesia-hyperarousal-model» is purported to support the neurophysiologic plausibility of the trauma-pain-relationship. We discuss seven characteristic clinical pain entities which alone or in combination can be found in patients with a previous psychological trauma.