Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions

Abstract

The intensity of acute and chronic pain depends on interactions between peripheral impulse input and CNS pain mechanisms, including facilitation and inhibition. Whereas tonic pain inhibition is a characteristic of most pain-free individuals, pain facilitation can be detected in many chronic pain patients. The capability to inhibit pain is normally distributed along a wide continuum in the general population and can be used to predict chronic pain. Accumulating evidence suggests that endogenous pain inhibition depends on activation of the prefrontal cortex, periaqueductal gray and rostral ventral medulla. Quantitative sensory test paradigms have been designed to acquire detailed information regarding each individual’s endogenous pain inhibition and facilitation. Such tests include: temporal summation of pain, which is mostly used to assess facilitatory pain modulation by measuring the change in pain perception during a series of identical nociceptive stimuli; and conditioned pain modulation, which tests pain inhibition by utilizing two simultaneously applied painful stimuli (the ‘pain inhibits pain’ paradigm). Considerable indirect evidence seems to indicate that not only increased pain facilitation but also ineffective pain inhibition represents a predisposition for chronic pain. This view is supported by the fact that many chronic pain syndromes (e.g., fibromyalgia, temporomandibular joint disorder, irritable bowel syndrome, headache and chronic fatigue syndrome) are associated with hypersensitivity to painful stimuli and reduced endogenous pain inhibition. However, future prospective studies will be necessary to provide definitive evidence for this relationship. Such research would not only provide important information about mechanisms relevant to chronic pain but would also permit identification of individuals at high risk for future chronic pain.

Endometriosis Is Associated With a Shift in MU Opioid and NMDA Receptor Expression in the Brain Periaqueductal Gray

“…59 Communication between the prefrontal cortex, the PAG, and the rostral ventrolateral medulla seems to be crucial in these chronic conditions. Studies have shown that PAG activity is increased in animal models of irritable bowel syndrome (IBS), which might be indirectly linked to visceral hypersensitivity in this chronic painful condition.…”

Altered Brain Complexity in Women with Primary Dysmenorrhea: A Resting-State Magneto-Encephalography Study Using Multiscale Entropy Analysis

“…First, significant group differences only emerged at larger scale factors (SFs) beginning from SF 52 (Figure 2a,b). Second, counts of significant group differences within each scale factor-interval were SFs 1~50 (0), 51~60 (4), 61-70 (8), 71~80 (6), 81~90 (10), and 91~100 (14). SF 92 was the most frequent feature (count = 4) that differentiated the brain complexity of PDMs from CONs, followed by SF 81 and SF 99 (3 counts each) (Figure 2a).…”

The Cerebrospinal Fluid in Severe Pain Conditions : Clinical, Pharmacological and Proteomic Aspects

“…For instance, it is widely recognized that affective factors like fear [264] and depression [140] are important to assess in pain patients, although the causal relationships are complex and difficult to disentangle [140,263]. The biopsychosocial model is consistent with the view of the brain as an active system that filters, selects and, through descending neural pathways, modulates nociceptive input from the periphery [153,154,179,231]. The biopsychosocial model is also consistent with the fact that pain is not just about an "inner" experience; pain is associated with behavioural changes, e.g.…”

“…Hence, strictly speaking, the concept of central sensitization should be restricted to the preclinical neurophysiological setting. Nonetheless, some authors use concepts like "central sensitivity syndromes" or "centralized pain" to characterize some of the clinical pain conditions listed above in this paragraph [48,231].…”

“…The PAG, which for obvious neuroanatomical reasons is one of the first areas exposed to BE released into the third ventricle (see above), is part of an intricate top-down system that modulates nociceptive inputs at the spinal level [179,231]. The best studied top-down descending pathway is the PAG-RVM system, which links the PAG to the spinal cord via the rostral ventromedial medulla (RVM) [108].…”