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Anatomy and Pathophysiology of Chronic Pain and the Impact of Hypnotherapy

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Abstract

Chronic pain is thought to develop from intense repetitive nociceptive (acute) pain. This condition has various forms and can persist for longer than 3 months, such that finding efficacious treatment is challenging in the clinical setting. The essence of this review is to present a selection of studies highlighting anatomical changes in brain activity in acute and chronic pain. An overview of the interaction between pain and psychological conditions will also be examined followed by the physiological effect of hypnosis. The review concludes with recommendations for further work in developing robust pain management in clinical hypnotherapy practice.

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... This system is largely responsible for the resistance response to stress. Given that stress is a major factor contributing to depression and chronic pain, this may explain the physiological link that has been found between depression and chronic pain (Gill, 2018). ...
... To control the pain the technique of hypnosis can be an alternative, it is necessary to be given as a pre-surgery hypnosis, to change consciousness, the dissociation of peripheral consciousness, and increased responsiveness for cues provided, which is effective in controlling somatic pain in the long term (Gill, 2018). ...
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... 55 Studies of hypnotherapy in the chronic pain literature have shown that hypnotic suggestions for pain modulation also impact the prefrontal, insular, and somatosensory regions, and there is evidence for differing brain activations depending on whether the hypnotic suggestion is related to pain affect or pain intensity. 56 Moreover, a recent, well-designed, controlled study has shown that responders to hypnotherapy with moderate to severe IBS had attenuation of brain activity in the posterior insula and that improvement in symptoms was associated with normalization of evoked brain responses to painful visceral stimuli (Figure 3). 57 These data suggest that the use of gut-focused metaphors, hypnotic suggestions for physiological improvement, and imagery used during hypnotherapy, may select specific related peripheral and central gut-brain neuronal pathways, leading to favorable neuroplastic changes induced by practice and further re-enforcement during, and in between hypnotherapy sessions. ...
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Background Despite their high prevalence and advances in the field of neurogastroenterology, there remain few effective treatment options for functional gastrointestinal disorders (FGIDs). It is recognized that approximately 25% of sufferers will have symptoms refractory to existing therapies, causing significant adverse effects on quality of life and increased healthcare utilization and morbidity. Gut‐focused hypnotherapy, when delivered by trained therapists, has been shown to be highly effective in severe refractory FGIDs. However, hypnotherapy continues to be surrounded by much misunderstanding and skepticism. Purpose The purpose of this review is to provide a contemporary overview of the principles of gut‐focused hypnotherapy, its effects on gut‐brain interactions, and the evidence‐base for its efficacy in severe FGIDs. As supplementary material, we have included a hypnotherapy protocol, providing the reader with an insight into the practical aspects of delivery, and as a guide, an example of a script of a gut‐focused hypnotherapy session.
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Fibromyalgia (FM) is a disorder of unknown aetiology, characterized by chronic widespread pain, stiffness and sleep disturbances. In addition, patients frequently complain of memory and attention deficits. Accumulating evidence suggests that FM is associated with CNS dysfunction and with an altered brain morphology. However, few studies have specifically investigated neuropsychological issues in patients suffering from FM. We therefore sought to determine whether neuropsychological deficits found in FM patients may be correlated with changes in local brain morphology specifically in the frontal, temporal or cingulate cortices. Twenty FM patients underwent extensive testing for potential neuropsychological deficits, which demonstrated significantly reduced working memory and impaired non-verbal long-term memory (limited to free recall condition) in comparison with normative data from age- and education-matched control groups. Voxel-based morphometry (VBM) was used to evaluate for potential correlations between test results and local brain morphology. Performance on non-verbal working memory was positively correlated with grey matter values in the left dorsolateral prefrontal cortex, whereas performance on verbal working memory (digit backward) was positively correlated with grey matter values in the supplementary motor cortex. On the other hand, pain scores were negatively correlated with grey matter values in the medial frontal gyrus. White matter analyses revealed comparable correlations for verbal working memory and pain scores in the medial frontal and prefrontal cortex and in the anterior cingulate cortex. Our data suggest that, in addition to chronic pain, FM patients suffer from neurocognitive deficits that correlate with local brain morphology in the frontal lobe and anterior cingulate gyrus, which may be interpreted to indicate structural correlates of pain-cognition interaction.
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The role of the brain in chronic pain conditions remains speculative. We compared brain morphology of 26 chronic back pain (CBP) patients to matched control subjects, using magnetic resonance imaging brain scan data and automated analysis techniques. CBP patients were divided into neuropathic, exhibiting pain because of sciatic nerve damage, and non-neuropathic groups. Pain-related characteristics were correlated to morphometric measures. Neocortical gray matter volume was compared after skull normalization. Patients with CBP showed 5-11% less neocortical gray matter volume than control subjects. The magnitude of this decrease is equivalent to the gray matter volume lost in 10-20 years of normal aging. The decreased volume was related to pain duration, indicating a 1.3 cm3 loss of gray matter for every year of chronic pain. Regional gray matter density in 17 CBP patients was compared with matched controls using voxel-based morphometry and nonparametric statistics. Gray matter density was reduced in bilateral dorsolateral prefrontal cortex and right thalamus and was strongly related to pain characteristics in a pattern distinct for neuropathic and non-neuropathic CBP. Our results imply that CBP is accompanied by brain atrophy and suggest that the pathophysiology of chronic pain includes thalamocortical processes.
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In the past decade of pain research, a network of pain transmitting areas within the CNS has been established, based on both animal studies and findings from functional imaging studies in humans. Consequently, the neurobiology of pain is increasingly understood as an integration of activity in distinct neuronal structures. Evidence of altered local brain chemistry and functional reorganization in chronic back pain patients supports the idea that chronic pain could be understood not only as an altered functional state, but also as a consequence of central plasticity. Recently, local morphologic alterations of the brain in areas ascribable to the transmission of pain were detected in patients suffering from phantom pain, chronic back pain, irritable bowl syndrome, fibromyalgia and two types of frequent headaches. These alterations were different for each pain syndrome, but overlapped in the cingulate cortex, the orbito-frontal cortex, the insula and dorsal pons. These regions function as multi-integrative structures during the experience and the anticipation of pain. Although some authors discussed these findings as damage or loss of brain gray matter, one of the key questions is whether these structural alterations in the cerebral pain transmitting network precede or succeed the chronicity of pain. A very recent paper investigated patients with chronic pain due to primary hip osteoarthritis and found a characteristic gray matter decrease in patients compared to controls in the anterior cingulate cortex (ACC), right insular cortex and operculum, DLPFC, amygdala and brainstem. Following total hip replacement a subgroup of these patients were completely pain free and showed 6 weeks and 4 months after surgery, monitoring a gray matter increase in the DLPFC, ACC, amygdala and brainstem. As gray matter decrease is at least partly reversible when pain is successfully treated, the author suggests that the gray matter abnormalities found in chronic pain do not reflect brain damage, but are rather a reversible consequence of chronic nociceptive transmission, which normalizes when the pain is adequately treated.
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Much evidence from pain patients and animal models shows that chronic pain does not exist in a vacuum but has varied comorbidities and far-reaching consequences. Patients with long-term pain often develop anxiety and depression and can manifest changes in cognitive functioning, particularly with working memory. Longitudinal studies in rodent models also show the development of anxiety-like behavior and cognitive changes weeks to months after an injury causing long-term pain. Brain imaging studies in pain patients and rodent models find that chronic pain is associated with anatomical and functional alterations in the brain. Nevertheless, studies in humans reveal that lifestyle choices, such as the practice of meditation or yoga, can reduce pain perception and have the opposite effect on the brain as does chronic pain. In rodent models, studies show that physical activity and a socially enriched environment reduce pain behavior and normalize brain function. Together, these studies suggest that the burden of chronic pain can be reduced by nonpharmacological interventions.
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Objectives Chronic pain (CP; >3months) is a common condition that is associated with significant psychological problems. Many people with CP do not fit into discrete diagnostic categories, limiting the applicability of research that is specific to a particular pain diagnosis. This meta-analysis synthesized the large extant literature from a general CP, rather than diagnosis-specific, perspective to systematically identify and compare the psychological problems most commonly associated with CP. Methods Four databases were searched from inception to December 2013 (PsychINFO, The Cochrane Library, Scopus, and PubMed) for studies comparing the psychological functioning of adults with CP to healthy controls. Data from 110 studies were meta-analysed and Cohen's d effect sizes calculated. ResultsThe CP group reported experiencing significant problems in a range of psychological domains (depression, anxiety, somatization, anger/hostility, self-efficacy, self-esteem and general emotional functioning), with the largest effects observed for pain anxiety/concern and somatization; followed by anxiety and self-efficacy; and then depression, anger/hostility, self-esteem and general emotional functioning. Conclusions This study demonstrates, for the first time, that individuals with CP are more likely to experience physically focussed psychological problems than other psychological problems and that, unlike self-efficacy, fear of pain is intrinsically tied to the CP experience. This challenges the prevailing view that, for individuals with CP, problems with depression are either equal to, or greater than, problems with anxiety, thereby providing important information to guide therapeutic targets. Practitioner pointsPositive clinical implications This is the first time that the CP literature has been synthesized from a general perspective to examine psychological functioning in the presence of CP and provide practical recommendations for assessment and therapy. Individuals with CP were most likely to experience psychological problems in physically focussed areas - namely pain anxiety/concern and somatization. Although fear of pain was intrinsically tied to the CP experience, self-efficacy was not. CP was more strongly associated with anxiety than with depression. Limitations The study focuses on the general CP literature, adults and research-utilizing self-report measures. Meta-analyses are limited by the empirical literature on which they are based.
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Pain is an unpleasant experience which results from both physical and psychological responses to injury. A complex set of pathways transmits pain messages from the periphery to the central nervous system, where control occurs from higher centres. Primary afferent pain fibres synapse with second-order neurons in the dorsal horn of the spinal cord. Ascending spinothalamic and spinoreticular tracts convey pain up to the brain, where pain signals are processed by the thalamus and sent to the cortex. Descending tracts, via the midbrain periaquaductal grey and nucleus raphe magnus, have a role in pain modulation. When nerves are damaged, neuropathic pain results and various mechanisms have been proposed for how this takes place. These mechanisms involve both peripheral and central sensitization.
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Current evidence supports the efficacy of hypnosis for reducing the pain associated with experimental stimulation and various acute and chronic conditions; however, the mechanisms explaining how hypnosis exerts its effects remain less clear. The hypothalamic-pituitary-adrenal (HPA) axis and pro-inflammatory cytokines represent potential targets for investigation given their purported roles in the perpetuation of painful conditions; yet, no clinical trials have thus far examined the influence of hypnosis on these mechanisms. Healthy participants, highly susceptible to the effects of hypnosis, were randomized to either a hypnosis intervention or a no-intervention control. Using a cold pressor task, assessments of pain intensity and pain unpleasantness were collected prior to the intervention (Pre) and following the intervention (Post) along with pain-provoked changes in salivary cortisol and the soluble tumor necrosis factor-α receptor II (sTNFαRII). Compared with the no-intervention control, data analyses revealed that hypnosis significantly reduced pain intensity and pain unpleasantness. Hypnosis was not significantly associated with suppression of cortisol or sTNFαRII reactivity to acute pain from Pre to Post; however, the effect sizes for these associations were medium-sized. Overall, the findings from this randomized controlled pilot study support the importance of a future large-scale study on the effects of hypnosis for modulating pain-related changes of the HPA axis and pro-inflammatory cytokines.
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Chronic pain can develop from numerous conditions and is one of the most widespread and disabling health problems today. Unfortunately, the pathophysiology of chronic pain in most of these conditions, along with consistently effective treatments, remain elusive. However, recent advances in neuroimaging and neurophysiology are rapidly expanding our understanding of these pain syndromes. It is now clear that substantial functional and structural changes, or plasticity, in the central nervous system (CNS) are associated with many chronic pain syndromes. A group of cortical and subcortical brain regions, often referred to as the "pain matrix," often show abnormalities on functional imaging studies in persons with chronic pain, even with different pain locations and etiologies. Changes in the motor and sensory homunculus also are seen. Some of these CNS changes return to a normal state with resolution of the pain. It is hoped that this knowledge will lead to more effective treatments or even new preventative measures. The purpose of this article is to review recent advances in the understanding of the CNS changes associated with chronic pain in a number of clinical entities encountered in the field of physical medicine and rehabilitation. These clinical entities include nonspecific low back pain, fibromyalgia, complex regional pain syndrome, postamputation phantom pain, and chronic pain after spinal cord injury.
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The neuropsychological status of pain conditions such as fibromyalgia, commonly categorized as 'psychosomatic' or 'functional' disorders, remains controversial. Activation of brain structures dependent upon subjective alterations of fibromyalgia pain experience could provide an insight into the underlying neuropsychological processes. Suggestion following a hypnotic induction can readily modulate the subjective experience of pain. It is unclear whether suggestion without hypnosis is equally effective. To explore these and related questions, suggestions following a hypnotic induction and the same suggestions without a hypnotic induction were used during functional magnetic resonance imaging to increase and decrease the subjective experience of fibromyalgia pain. Suggestion in both conditions resulted in significant changes in reported pain experience, although patients claimed significantly more control over their pain and reported greater pain reduction when hypnotised. Activation of the midbrain, cerebellum, thalamus, and midcingulate, primary and secondary sensory, inferior parietal, insula and prefrontal cortices correlated with reported changes in pain with hypnotic and non-hypnotic suggestion. These activations were of greater magnitude, however, when suggestions followed a hypnotic induction in the cerebellum, anterior midcingulate cortex, anterior and posterior insula and the inferior parietal cortex. Our results thus provide evidence for the greater efficacy of suggestion following a hypnotic induction. They also indicate direct involvement of a network of areas widely associated with the pain 'neuromatrix' in fibromyalgia pain experience. These findings extend beyond the general proposal of a neural network for pain by providing direct evidence that regions involved in pain experience are actively involved in the generation of fibromyalgia pain.
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The transition from acute to chronic pain appears to occur in discrete pathophysiological and histopathological steps. Stimuli initiating a nociceptive response vary, but receptors and endogenous defence mechanisms in the periphery interact in a similar manner regardless of the insult. Chemical, mechanical, and thermal receptors, along with leucocytes and macrophages, determine the intensity, location, and duration of noxious events. Noxious stimuli are transduced to the dorsal horn of the spinal cord, where amino acid and peptide transmitters activate second-order neurones. Spinal neurones then transmit signals to the brain. The resultant actions by the individual involve sensory-discriminative, motivational-affective, and modulatory processes in an attempt to limit or stop the painful process. Under normal conditions, noxious stimuli diminish as healing progresses and pain sensation lessens until minimal or no pain is detected. Persistent, intense pain, however, activates secondary mechanisms both at the periphery and within the central nervous system that cause allodynia, hyperalgesia, and hyperpathia that can diminish normal functioning. These changes begin in the periphery with upregulation of cyclo-oxygenase-2 and interleukin-1β-sensitizing first-order neurones, which eventually sensitize second-order spinal neurones by activating N-methyl-d-aspartic acid channels and signalling microglia to alter neuronal cytoarchitecture. Throughout these processes, prostaglandins, endocannabinoids, ion-specific channels, and scavenger cells all play a key role in the transformation of acute to chronic pain. A better understanding of the interplay among these substances will assist in the development of agents designed to ameliorate or reverse chronic pain.
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It has been widely recognized that an appreciable proportion of chronic pain patients have depressive disorders. Although numerous studies and several literature reviews have examined the relationship between chronic pain and depression, disorders of mood come in many forms, and little attention has been paid to the different types of depressive disorders found among patients with chronic pain. In this article, the different ways in which a chronic pain patient may manifest depression are discussed. Diagnostic criteria for major depression, dysthymia, and atypical depression are described, and the relevance of these disorders and of masked depression to chronic pain is discussed. The medical illnesses and medications that can cause symptoms of depressive disorders are also briefly described. Depressive disorders and their concomitants are an integral part of the experience of chronic pain and are important in developing an optimal treatment plan. For these reasons, they should be carefully evaluated in all patients with chronic pain.
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Pain patients may be requested to complete pain charts as part of their evaluation at pain clinics. Inferences are made about the 'psychological content' of the patient's pain on the basis of the extent and distribution of the pain as illustrated in these drawings. In this study, the records of 328 patients from 4 distinct types of chronic pain service, were scored for how many body parts were included in the pain drawings and the percentage of body surface area involved. Four psychological instruments were used to quantify the psychological status of the patients. These included 2 measures of current psychological status (the General Health Questionnaire-28, and the Irritability/Depression and Anxiety Questionnaire), 1 measure of childhood quality (the Parental Bonding Index), and 1 measure of premorbid personality (the Hysteroid/Obsessoid Questionnaire). No significant correlation was found between the percentage of body surface area affected by pain, and the measures of childhood quality. Only very limited correlations were found between the percentage of the body surface area with pain and the measures of current psychological state and premorbid personality. Hence, strong emphasis should not be placed on the involvement of multiple areas as a sign of psychological illness.
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Defines and delimits the area of inquiry in hypnosis, i.e., the topics to be investigated regardless of explanatory theories. 4 such alternative explanations are presented and compared, showing how they variously deal with the interpretation of experimental and clinical evidence. (66 ref)
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The hippocampus is an important structure for declarative, spatial, and contextual memory and is implicated in the perception of chronic pain. The hippocampal formation is vulnerable to damage from seizures, ischemia, and head trauma and is particularly sensitive to the effects of adrenal glucocorticoids secreted during the diurnal rhythm and chronic stress. Adrenal steroids typically have adaptive effects in the short run, but promote pathophysiology when there is either repeated stress or dysregulation of the HPA axis. The damaging actions of glucocorticoids under such conditions have been termed "allostatic load", referring to the cost to the body of adaptation to adverse conditions. Adrenal steroids display both protective and damaging effects in the hippocampus. They biphasically modulate excitability of hippocampal neurons, and high glucocorticoid levels and severe acute stress impair declarative memory in a reversible manner. The hippocampus also displays structural plasticity, involving ongoing neurogenesis of the dentate gyrus, synaptogenesis under control of estrogens in the CA1 region, and dendritic remodeling caused by repeated stress or elevated levels of exogenous glucocorticoids in the CA3 region. In all three forms of structural plasticity, excitatory amino acids participate along with circulating steroid hormones. Glucocorticoids and stressors suppress neurogenesis in the dentate gyrus. They also potentiate the damage produced by ischemia and seizures. Moreover, the aging rat hippocampus displays elevated and prolonged levels of excitatory amino acids released during acute stress. Our working hypothesis is that structural plasticity in response to repeated stress starts out as an adaptive and protective response, but ends up as damage if the imbalance in the regulation of the key mediators is not resolved. It is likely that morphological rearrangements in the hippocampus brought on by various types of allostatic load alter the manner in which the hippocampus participates in memory functions and it is conceivable that these may also have a role in chronic pain perception.
Article
Investigation of the basic mechanisms of chronic pain not only provides insights into how the brain processes and modulates sensory information but also provides the basis for designing novel treatments for currently intractable clinical conditions. Human brain imaging studies have revealed new roles of cortical neuronal networks in chronic pain, including its unpleasant quality, and mouse studies have provided molecular and synaptic mechanisms underlying relevant cortical plasticity. This review paper will critically examine the current literature and propose a cortical network model for chronic pain.
Depression and Pain Comorbidity
  • M Bair
  • R Robinson
  • W Katon
  • K Kroenke
Bair, M., Robinson, R., Katon, W. & Kroenke, K. (2003). Depression and Pain Comorbidity. Archives of Internal Medicine, 163(20), 2433-2445.
Pain Perception and Hypnosis: F i n d i n g s F r o m R e c e n t F u n c t i o n a l N e u r o i m a g i n g Studies
  • Del Casale
  • A Ferracuti
  • S Rapinesi
  • C Serata
  • D Caltagirone
  • S Savoja
  • V Piacentino
  • D Callovini
  • G Manfredi
  • G Sani
  • G Kotzalidis
  • G Girardi
Del Casale, A., Ferracuti, S., Rapinesi, C., Serata, D., Caltagirone, S., Savoja, V., Piacentino, D., Callovini, G., Manfredi, G., Sani, G., Kotzalidis, G. & Girardi, P. (2015). Pain Perception and Hypnosis: F i n d i n g s F r o m R e c e n t F u n c t i o n a l N e u r o i m a g i n g Studies. International Journal of Clinical and Experimental Hypnosis, 63(2), 144-170.
Pain Perception and Hypnosis: n g Studies
  • A Del Casale
  • S Ferracuti
  • C Rapinesi
  • D Serata
  • S Caltagirone
  • V Savoja
  • D Piacentino
  • G Callovini
  • G Manfredi
  • G Sani
  • G Kotzalidis
  • P Girardi
Del Casale, A., Ferracuti, S., Rapinesi, C., Serata, D., Caltagirone, S., Savoja, V., Piacentino, D., Callovini, G., Manfredi, G., Sani, G., Kotzalidis, G. & Girardi, P. (2015). Pain Perception and Hypnosis: n g Studies. International Journal of Clinical and Experimental Hypnosis, 63(2), 144-170.