Clinical measures of pain sensitization in moderate to severe knee osteoarthritis
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Quantitative sensory testing
Gold standard (test)
Joint pain
Central Sensitization
Knee pain
Peripheral and central sensitization are neurophysiological processes that can prolong painful conditions. Painful shoulder conditions are often persistent, perhaps due to the presence of sensitization.This manuscript summarizes six studies that have evaluated those with musculoskeletal shoulder pain for the presence of sensitization.All six manuscripts report evidence of peripheral sensitization, while central sensitization was described in five of the studies. The chronicity of symptoms in subjects who were included in the studies is probably influencing this finding. The primary somatosensory test used to assess sensitization in these studies was Pressure Pain Threshold, a test for lowered nociceptive thresholds.It appears that peripheral sensitization manifests consistently in those with musculoskeletal shoulder pathology, probably due to the inflammatory processes related to tissue injury. Central sensitization, while not universally present, was reported in a majority of the manuscripts. Because central sensitization is thought to be a key step on the pathway to chronic pain, evidence for its presence in those with shoulder pain is significant. Clinicians should expect the presence of sensitization with shoulder pathology and make appropriate choices about interventions so as not to exacerbate pain.
Central Sensitization
Quantitative sensory testing
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Central Sensitization
Central pain
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In the Netherlands, 18% of the adults suffer from chronic pain.
Detection of central sensitization would
provide information about the patients nociceptive system that could enable mechanism-based therapy. The aim of this thesis was to set-up a process for the outpatient pain clinic in St. Antonius Hospital
for the detection of central sensitization in chronic pain patients with electrical Quantitative Sensory
Testing (eQST).
The preliminary results did not show significant differences in pain threshold for chronic low back
patients compared to healthy controls (t(95)=-0.131, p=0.896). The CSI score did show a significant
difference between the two populations (t(95)=5.395, p<0.001). Regarding of the baseline characteristics,
only gender seemed to be an influence related to the pain threshold.
This thesis offers a clinical process aligned with current clinical practice at the outpatient pain clinic
to eventually detect and monitor central sensitization. The monitoring process has successfully been
implemented at St. Antonius Hospital. So far, no differences between CLBP and healthy controls
in pain threshold were found, however still too few pain patients have been
included. Subsequently, it is too early to draw conclusions from these preliminary results. Thereby is
recommended to include more patients to evaluate the monitoring process of central sensitization.
Central Sensitization
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Stress and sensitization are central concepts in chronic pain. Both can be a consequence and a contributor to the pain experience. This chapter describes the psychobiology of stress and sensitization within a multilevel perspective, indicating the impact of various forms of stress and sensitization on multiple psychoneurobiological processes (i.e., autonomic, endocrine, immune, and central processes) related to chronic pain. As a result of disordered stress regulation, sensitization may occur as a mechanism that explains how acute pain problems can become chronic and how acute pain problems can extend or generalize to other body parts or modalities. The evidence for stress and sensitization as consequences of or as contributors to chronic pain is reviewed, and possible underlying mechanisms are discussed. Next, strategies to reduce stress and sensitization and foster desensitization processes are described. The chapter concludes by introducing a motivational account of chronic pain informed by the stress and sensitization literature.
Chronic Stress
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Nociplastic pain, the most recently proposed mechanistic descriptor of chronic pain, is the pain resulting from an altered nociceptive system and network without clear evidence of nociceptor activation, injury or disease in the somatosensory system. As the pain-associated symptoms in many patients suffering from undiagnosed pain would result from the nociplastic mechanisms, it is an urgent issue to develop pharmaceutical therapies that would mitigate the aberrant nociception in nociplastic pain. We have recently reported that a single injection of formalin to the upper lip shows sustained sensitization lasting for more than 12 days at the bilateral hindpaws, where there is no injury or neuropathy in rats. Using the equivalent model in mice, we show that pregabalin (PGB), a drug used for treating neuropathic pain, significantly attenuates this formalin-induced widespread sensitization at the bilateral hindpaws, even on the 6 day after the initial single orofacial injection of formalin. On the 10th day after formalin injection, the hindlimb sensitization before PGB injection was no more significant in mice receiving daily PGB injections, unlike those receiving daily vehicle injections. This result suggests that PGB would act on the central pain mechanisms that undergo nociplastic changes triggered by initial inflammation and mitigate widespread sensitization resulting from the established changes.
Pregabalin
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Pain, the primary symptom of osteoarthritis (OA), reduces both the quality and quantity of life for patients. The pathophysiology of OA pain is complex and often difficult to explain solely by radiological structural changes. One reason for this discrepancy is pain sensitization (peripheral sensitization [PS] and central sensitization [CS]) in OA. Thus, an understanding of pain sensitization is important when considering treatment strategies and development for OA pain. In recent years, pro-inflammatory cytokines, nerve growth factors (NGFs), and serotonin have been identified as causative agents that induce peripheral and central sensitization and are becoming therapeutic targets for OA pain. However, the characteristics of the clinical manifestations of pain sensitization elicited by these molecules remain unclear, and it is not well understood who among OA patients should receive the therapeutic intervention. Thus, this review summarizes evidence on the pathophysiology of peripheral and central sensitization in OA pain and the clinical features and treatment options for this condition. While the majority of the literature supports the existence of pain sensitization in chronic OA pain, clinical identification and treatment of pain sensitization in OA are still in their infancy, and future studies with good methodological quality are needed.
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Capsaicin
Central Sensitization
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Hyperalgesia has long time been attributed to sensitization of peripleral nociceptors. Sensitization and hyperexcitability of central neurons have now been demonstrated to play a critical role in initiation and maintenance of hyperalgesia; and a series of intracellular molecular events relating mainly to NMDA receptor-PKC-NO system is thought to involve in the development of hyperalgesia. Novel strategy for prevention and treatment of hyperalgesia is thus greatly expected based on the discovery of central sensitization and its molecular basis.
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Central Sensitization
Central pain
Open peer review
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The pathophysiology of the two most common primary headaches, migraine and tension-type headache, is complex and not yet fully understood. Recent animal and human studies examining these headaches indicate that the nociceptive input to the central nervous system (CNS) may be increased due to activation or sensitization of peripheral sensory afferents. The barrage of nociceptive impulses may result in sensitization of second- and third-order neurons in the CNS. In this way, sensitization may play a role in initiation and maintenance of migraine and tension-type headache. It is likely that the effects of established medication for both disorders may be partly due to a reduction in sensitization. Several interesting drugs that counteract sensitization are under development, and targeting this mode of action seems to be a promising way of improving the treatment for these prevalent disorders.
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