Central Sensitization

Fibromyalgia syndrome (FMS) is now a recognized clinical entity causing chronic and disabling pain. For several centuries, muscle pains have been known as rheumatism and then as muscular rheumatism. The term fibrositis was coined by Gowers in 1904 and was not changed to fibromyalgia until 1976. Smythe laid the foundation of modern FMS in 1972 by describing widespread pain and tender points. The first sleep electroencephalogram study was performed in 1975. The first controlled clinical study with validation of known symptoms and tender points was published in 1981. This same study also proposed the first data-based criteria. The important concept that FMS and other similar conditions are interconnected was proposed in 1984. The first American College of Rheumatology criteria were published in 1990 and neurohormonal mechanisms with central sensitization were developed in the 1990s. Serotonergic/norepinephric drugs were first shown to be effective in 1986.

Tl;dr: Referred muscle pain seems to be a neurological issue: https://www.youtube.com/watch?v=8QscW0wZ_5s.

Despite imagery’s regular use in massage therapy there are few studies examining its effectiveness. This experimental study examined the effect of imagery on manual trigger point release. Forty individuals (11 male and 29 female), aged 19-51 (M = 26.13, SD = 8.05) and divided into two groups; one focusing on deep, diaphragmatic breathing and the second on a rich imagery script, imagining their trigger point being a “ball of butter melting”. Manual trigger point release was applied four successively deeper times to the same point in the dominant upper trapezius muscle following the common “searching for 7” pain scale protocol. Significant differences were found in self-reported pain tolerance scores for participants using the breathing (M = 2/10, SD = 1.8/10) versus imagery scripts (M = 1/10, SD = 1.2/10), t(37) = 2.10, p = .043. A trend only approaching statistical significance was observed between treatments in both average press release (imagery: M = 25.6 s, SD = 15.5 s, breathing: M = 30.0 s, SD = 27.3 s, t(38) = 0.62, p = .540) and total treatment time (imagery: M = 2:15 m, SD = 1:08 m, breathing: M = 2:36 m, SD = 2:04 m, t(38) = 0.67, p = .507), with largest differences in the final two presses.

However, analyzing the above while taking local v. referred pain presence into account showed significant main effects of pain on the first press (local/breathing: M = 43.2 s, SD = 24.8 s; local/imagery: M = 31.5 s, SD = 16.1 s; referred/breathing: M = 23.2 s, SD = 12.5 s, referred/imagery: M = 28.1 s, SD = 12.2 s; F1,30 = 4.53, p = .042) and significant interaction effects of both pain and treatment type on total treatment time (local/breathing: M = 3:32 m, SD = 2:34 m; local/imagery: M = 2:07 m, SD = 1:12 m; referred/breathing: M = 1:50 m, SD = 1:11 m, referred/imagery: M = 2:22 m, SD = 1:08 m; F1,30 = 4.64, p = .039). Based on this study, therapists should include breathing techniques in manual trigger point release for patients experiencing referred pain and imagery scripts for patients experiencing only local pain.

Desde 1990 observamos que algunos pacientes con antecedentes de procesos periféricos (lesiones ortopédicas, post cirugía torácica o abdominal, hemiplejías, etc) presentaban un cuadro de amplificación del área dolorosa, intensificación de dolor expontáneo y manifestaciones clínicas al examen de los tegumentos

Recent advances have shed insight on the pathophysiologic mechanisms of fibromyalgia and migraine, especially in the chronic form. A growing body of evidence supports the involvement of peripheral and central sensitization disturbances of pain-related processes underlying both disorders. They involve increased glutamate transmission through interaction with its ionotropic and metabotropic receptors. Few studies supporting the implication of this excitatory amino acid in chronic migraine and primary fibromyalgia demonstrated increased levels of glutamate in the cerebrospinal fluid of affected patients. These findings have implications for future therapies directed against glutamate receptors (in particular, N-methyl-D-aspartate receptors). Limited clinical experience in this regard, although promising, does not exclude additional mechanisms contributing to the maintenance of pain, which can be the target of therapeutic approaches in both disorders.

Following injury and inflammation, pain to light stroking (dynamic mechanical allodynia) might develop at the damaged site (primary area) or in adjacent normal tissue (secondary area). Using fMRI we mapped changes in the spinal trigeminal nucleus (spV), and supraspinal brainstem nuclei following heat/capsaicin-induced primary and secondary dynamic mechanical allodynia in the human trigeminal system. The role of these structures in dynamic mechanical allodynia has not been clarified yet in humans. During the control session we applied the same mechanical stimuli to the same untreated trigeminal area. Primary and secondary mechanical allodynia showed equal levels of perceived pain intensity, and compared to control mechanical stimulation exhibited similar responses in the ipsilateral spV and contralateral ventrolateral periaqueductal gray (vlPAG). Activity in the spV was significantly higher during both conditions versus the control mechanical stimulation, indicating that central sens...

Tumor necrosis factor-alpha (TNF-α) is a principal mediator in pro-inflammatory processes that involve necrosis, apoptosis and proliferation. Experimental and clinical evidence demonstrate that peripheral nerve injury results in activation and morphological changes of microglial cells in the spinal cord. These adjustments occur in order to initiate an inflammatory cascade in response to the damage. Between the agents involved in this reaction, TNF-α is recognized as a key player in this process as it not only modulates lesion formation, but also because it is suggested to induce nociceptive signals. Nowadays, even though the function of TNF-α in inflammation and pain production seems to be generally accepted, diverse sources of literature point to different pathways and outcomes. In this review, we systematically searched and reviewed original articles from the past 10 years on animal models of peripheral nervous injury describing TNF-α expression in neural tissue and pain behavior.

Fibromyalgia (FM) pain is frequent in the general population but its pathogenesis is only poorly understood. Many recent studies have emphasized the role of central nervous system pain processing abnormalities in FM, including central sensitization and inadequate pain inhibition. However, increasing evidence points towards peripheral tissues as relevant contributors of painful impulse input that might either initiate or maintain central sensitization, or both. It is well known that persistent or intense nociception can lead to neuroplastic changes in the spinal cord and brain, resulting in central sensitization and pain. This mechanism represents a hallmark of FM and many other chronic pain syndromes, including irritable bowel syndrome, temporomandibular disorder, migraine, and low back pain. Importantly, after central sensitization has been established only minimal nociceptive input is required for the maintenance of the chronic pain state. Additional factors, including pain relate...

Hypersensitivity due to central pain mechanisms can influence recovery and lead to worse clinical outcomes, but the ability of quantitative sensory testing (QST), an index of sensitisation, to predict outcomes in chronic musculoskeletal disorders remains unclear. We systematically reviewed the evidence for ability of QST to predict pain, disability and negative affect using searches of CENTRAL, MEDLINE, EMBASE, AMED, CINAHL and PubMed databases up to April 2018. Title screening, data extraction, and methodological quality assessments were performed independently by 2 reviewers. Associations were reported between baseline QST and outcomes using adjusted (β) and unadjusted (r) correlations. Of the 37 eligible studies (n=3860 participants), 32 were prospective cohort studies and 5 randomised controlled trials. Pain was an outcome in 30 studies, disability in 11 and negative affect in 3. Meta-analysis revealed that baseline QST predicted musculoskeletal pain (mean r=0.31, 95%CI: 0.23 to 0.38, n=1057 participants) and disability (mean r=0.30, 95%CI: 0.19 to 0.40, n=290 participants). Baseline modalities quantifying central mechanisms such as temporal summation (TS) and conditioned pain modulation (CPM) were associated with follow-up pain (TS: mean r=0.37, 95%CI: 0.17 to 0.54; CPM: r=0.36, 95%CI: 0.20 to 0.50), whereas baseline mechanical threshold modalities were predictive of follow-up disability (mean r=0.25, 95%CI: 0.03 to 0.45). QST indices of pain hypersensitivity might help develop targeted interventions aiming to improve outcomes across a range of musculoskeletal conditions.

We examined the relation between ectopic afferent firing and tactile allodynia in the Chung model of neuropathic pain. Transection of the L5 spinal nerve in rats triggered a sharp, four- to six-fold increase in the spontaneous ectopic discharge recorded in vivo in sensory axons in the ipsilateral L5 dorsal root (DR). The increase, which was not yet apparent 16 h postoperatively, was complete by 24 h. This indicates rapid modification of the electrical properties of the neurons. Only A-neurons, primarily rapidly conducting A-neurons, contributed to the discharge. No spontaneously active C-neurons were encountered. Tactile allodynia in hindlimb skin emerged during precisely the same time window after spinal nerve section as the ectopia, suggesting that ectopic activity in injured myelinated afferents can trigger central sensitization, the mechanism believed to be responsible for tactile allodynia in the Chung model. Most of the spike activity originated in the somata of axotomized DRG...