scholarly journals CENTRAL SENSITIZATION OF PAIN IN PHYSIOTHERAPY

Author(s):  
Elżbieta Skorupska

Nowadays, there are three main pain descriptors: nociceptive pain, neuropathic pain, and nociplastic pain. The last one is the newest expression defining pain as ‘Pain that arises from altered nociception, despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain’ (International Association for the Study of Pain). The implementation of modern pain neuroscience in practice is said to be the most important for musculoskeletal physical therapists around the world. One of the examples of the nociplastic pain mechanism can be myofascial trigger points that are connected with central sensitization (one of the subtypes of nociplastic pain). Central sensitization (CS) is defined as an amplification of neural signaling within the central nervous system that elicits pain hypersensitivity and ongoing neuronal excitation which outlasts the initial nociceptor input. Features typical of that state are abnormally low peripheral thresholds for pain from pressure, temperature, electrical, and other stimuli and it has been proposed that trigger points may function as peripheral mediators of CS.

2021 ◽  
pp. 901-905
Author(s):  
James C. Watson

The International Association for the Study of Pain defines neuropathic pain as pain that is initiated or caused by a lesion or disease affecting the somatosensory system in either the peripheral nervous system or the central nervous system. Several well-recognized descriptors for neuropathic pain suggest a neuropathic rather than nociceptive pathophysiology (hot, burning, painful cold, freezing, prickling or tingling, pins and needles, electrical, shooting, stabbing, lancinating, and itching). However, whether the pain descriptors are used alone or incorporated into questionnaires to identify neuropathic pain, their sensitivity and specificity are limited (generally 70%-85%); therefore, verbal pain descriptors are insufficient for making the diagnosis of neuropathic pain.


2020 ◽  
Vol 78 (6) ◽  
pp. 321-330 ◽  
Author(s):  
Silvia Regina Dowgan Tesseroli de SIQUEIRA ◽  
Manoel Jacobsen TEIXEIRA ◽  
José Tadeu Tesseroli de SIQUEIRA

ABSTRACT Background: Diagnostic tools are necessary for the anamnesis and examination of orofacial pain, in order to fulfill diagnostic criteria and to screen potential causes of pain. Objective: To evaluate the Orofacial Pain Clinic Questionnaire (EDOF-HC) in the assessment and diagnosis of orofacial pain. Methods: Overall, 142 patients were evaluated and classified according to the criteria of the International Headache Society and International Association for the Study of Pain. All of them were evaluated with the EDOF-HC questionnaire, which consists of the orofacial and medical history, as well as the orofacial examination. Data were statistically analyzed with chi-square test and Bonferroni correction, one-way ANOVA with Tukey post hoc test, the two-step cluster and decision tree methods. Results: There were diferences in pain descriptors, pain in maximum mouth opening, number of trigger points, and history of previous surgery between the groups, which were classified into trigeminal neuralgia, burning mouth syndrome, temporomandibular disorders and trigeminal posttraumatic neuropathic pain with classification analysis. Conclusions: The EDOF-HC is a clinical supportive tool for the assessment of orofacial pain. The instrument may be used to support data collection from anamnesis and examination of patients according to the diagnostic criteria of most common orofacial conditions. It is also useful in the investigation of local and systemic abnormalities and contributes for the diagnosis of conditions that depend on exclusion criteria.


Cephalalgia ◽  
2007 ◽  
Vol 27 (5) ◽  
pp. 383-393 ◽  
Author(s):  
C Fernández-de-las-Peñas ◽  
ML Cuadrado ◽  
L Arendt-Nielsen ◽  
DG Simons ◽  
JA Pareja

Present pain models for tension-type headache suggest that nociceptive inputs from peripheral tender muscles can lead to central sensitization and chronic tension-type headache (CTTH) conditions. Such models support that possible peripheral mechanisms leading to pericranial tenderness include activation or sensitization of nociceptive nerve endings by liberation of chemical mediators (bradikinin, serotonin, substance P). However, a study has found that nonspecific tender points in CTTH subjects were not responsible for liberation of algogenic substances in the periphery. Assuming that liberation of algogenic substances is important, the question arising is: if tender muscle points are not the primary sites of on-going neurogenic inflammation, which structure can be responsible for liberation of chemical mediators in the periphery? A recent study has found higher levels of algogenic substances, and lower pH levels, in active myofascial trigger point (TrPs) compared with control tender points. Clinical studies have demonstrated that referred pain elicited by head and neck muscles contribute to head pain patterns in CTTH. Based on available data, an updated pain model for CTTH is proposed in which headache can at least partly be explained by referred pain from TrPs in the posterior cervical, head and shoulder muscles. In this updated pain model, TrPs would be the primary hyperalgesic zones responsible for the development of central sensitization in CTTH.


2021 ◽  
Vol 101 (3) ◽  
Author(s):  
Jorge Sánchez-Infante ◽  
Marcos J Navarro-Santana ◽  
Alfredo Bravo-Sánchez ◽  
Fernando Jiménez-Diaz ◽  
Javier Abián-Vicén

Abstract Objective The main objective of this systematic review and meta-analysis was to determine the short-, medium-, and long-term effectiveness of dry needling (DN) applied by physical therapists to myofascial trigger points for the treatment of pain. Methods PubMed, Scopus, SportDiscus, and Web of Science databases were searched from their inception to February 2020. Randomized controlled trials that compared DN with other treatments or placebo and measured pain with a visual analog Scale or another numerical pain rating scale were included. Two authors used a personalized form to collect the following data relevant to the objectives of the review from each article independently: study design, purpose, sample size, diagnosis, characteristics of DN intervention, characteristics of placebo intervention, outcome measures, period of assessment, body region, DN technique, and number of sessions. The initial search identified 1771 articles. After the selection, 102 articles were assessed for eligibility; 42 of these articles measuring pain were used for the meta-analysis. Four meta-analyses were performed according to the follow-up period from the last reported treatment. Results This meta-analysis found a large effect to decrease pain within 72 hours (standardized mean difference [SMD] = −0.81; 95% CI = −1.21 to −0.40), a moderate effect in 1 to 3 weeks (SMD = −0.69; 95% CI = −1.02 to −0.35), a large effect in 4 to 12 weeks (SMD = −0.85; 95% CI = −1.30 to −0.40), and a large effect in 13 to 24 weeks (SMD = −0.81; 95% CI = −1.64 to −0.03). The risk of bias was generally low; however, the heterogeneity of the results downgraded the level of evidence. Conclusions Low-quality evidence that the immediate to 72-hour (large) effect, 4- to 12-week (large) effect, 13- to 24-week (large) effect, and moderate-quality 1- to 3-week (moderate) effect suggested that DN performed by physical therapists was more effective than no treatment, sham DN, and other therapies for reducing pain. Impact DN is commonly used by physical therapists to treat musculoskeletal pain, and it is very important for physical therapists to know the clinical conditions and time periods for which DN is effective in reducing pain in their patients.


2018 ◽  
pp. 17-26
Author(s):  
Jianguo Cheng

Neuropathic pain arises as a direct consequence of a lesion or a disease affecting the somatosensory system. The mechanisms of neuropathic pain are often complex and difficult to study given the diversity of causes, pathology, and clinical presentation of various neuropathic pain conditions. Common mechanisms include peripheral and central sensitizations. Peripheral sensitization refers to increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields. Central sensitization refers to the augmented response of central signaling neurons. The mechanisms of peripheral and central sensitization are understood at the cellular and molecular levels. The processes of neuroplasticity involve activation of inflammatory cells, such as macrophages (and microglia in the central nervous system) and other immune cells, and release of inflammatory mediators, such as cytokines, chemokines, and a host of other mediators. Interactions of these mediators with specific receptors in the nociceptors or the spinal cord neurons may lead to phosphorylation or changes in expression of ion channels, receptors, transporters, and other effectors through specific signaling pathways. These events ultimately lead to changes in excitability, conductivity, and transmissibility of neurons in the pain processing pathways. Other factors may include disinhibition of interneurons, changes in descending inhibitory and excitatory pathways, and reorganization of the cortical areas and their interconnections.


2019 ◽  
Author(s):  
Valerie Evans ◽  
Michael Behr ◽  
Kei Masani ◽  
Dinesh Kumbhare

Abstract Background: Myofascial pain syndrome (MPS) is a prevalent chronic pain disorder primarily characterized by myofascial trigger points (MTrP). There is limited knowledge on the pathophysiology and mechanisms underlying MTrP and its development. Research has previously demonstrated the identification of MTrPs using ultrasound and vibration sonoelastography, although there is some contradictory evidence regarding if MTrPs present as hyper or hypoechoic regions. Electromyography (EMG) investigations of MTrP have demonstrated that MTrP are usually located proximal to innervation zones where the peak surface EMG signals are obtained from. Central sensitization has been proposed as the primary mechanism underlying MTrP development. Central sensitization is associated with hyperexcitability of neuronal responses to normal or noxious stimuli. There is a need for a study that measures ultrasound image textural changes and motor unit activity responses in the muscle following sensitization. The purpose of this study is to determine whether sensitizing healthy muscle using capsaicin induces a regional change in image texture variables within the specific and surrounding muscles, as well as the motor unit frequency and amplitude changes that accompany them.This is an exploratory trial that aims to provide preliminary evidence on whether central sensitization is a direct cause of taut band and MTrP development. Methods: The study conforms to the Consolidated Standards of Reporting Trials recommendations. Ethical approval will be sought from the University Health Network (UHN) Research Ethics Board. This proposed study is a single centered, factorial, randomized placebo-controlled trial with two independent variables, depth of capsaicin application and dose of capsaicin, for a total of four treatment arms and two control treatment groups. Discussion: This will be the first study that assesses the B-mode ultrasound image texture of induced sensitized muscles, and will provide more evidence on muscle motor unit activity and regional changes of central sensitization. Findings from this study may support one of few hypotheses proposed delineating the involvement of central sensitization in the development of trigger points.


Trials ◽  
2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Valerie Evans ◽  
Michael Behr ◽  
Kei Masani ◽  
Dinesh Kumbhare

Abstract Background Myofascial pain syndrome (MPS) is a prevalent chronic pain disorder primarily characterized by myofascial trigger points (MTrPs). There is limited knowledge on the pathophysiology and mechanisms underlying MTrP and its development. Research has previously demonstrated the identification of MTrPs using ultrasound and vibration sonoelastography, although there is some contradictory evidence regarding if MTrPs present as hyper or hypoechoic regions. Electromyography (EMG) investigations of MTrP have demonstrated that MTrPs are usually located proximal to innervation zones where the peak surface EMG signals are obtained from. Central sensitization has been proposed as the primary mechanism underlying MTrP development. Central sensitization is associated with hyperexcitability of neuronal responses to normal or noxious stimuli. There is a need for a study that measures ultrasound image textural changes and motor unit activity responses in the muscle following sensitization. The purpose of this study is to determine whether sensitizing healthy muscle using capsaicin induces a regional change in image texture variables within the specific and surrounding muscles, as well as the motor unit frequency and amplitude changes that accompany them. This is an exploratory trial that aims to provide preliminary evidence on whether central sensitization is a direct cause of taut band and MTrP development. Methods Ethical approval was obtained from the University Health Network (UHN) Research Ethics Board. This proposed study is a single centered, factorial, randomized placebo-controlled trial with two independent variables, depth of capsaicin application and dose of capsaicin, for a total of six treatment arms and three control treatment groups. Discussion This will be the first study that assesses the B-mode ultrasound image texture of induced sensitized muscles and will provide more evidence on muscle motor unit activity and regional changes of central sensitization. Findings from this study may support one of few hypotheses proposed delineating the involvement of central sensitization in the development of trigger points. Trial registration National Institutes of Health ClinicalTrials.gov NCT03944889. Registered on May 07, 2019


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