Referred Muscle Pain Research Articles

REFERRED MUSCLE PAIN, SOME CONSIDERATIONS OF ITS SIGNIFICANCE IN PRACTICE

Muscle pain is a common symptom in many musculoskeletal disorders. When it is local as a result of a muscle injury, correct diagnosis does not appear difficult. Referred muscle pain is a symptom associated with diagnostic and therapeutic challenges. It can be a consequence of an injury that develops elsewhere in the body: a skeletal muscle in another area or joint, or it can often be associated with a visceral injury (in this case we have referred muscle pain or secondary muscle pain). The aim of this article is to make a review of the available literature studying the nature, diagnosis, and treatment of referred pain and its relevance to clinical practice. Materials and Methods: In this review, the available scientific articles concerning the field of reflected pain are reviewed: Google Scholar, Pubmed, Science Direct Web of Science, Scopus, and scientific articles in Cyrillic) databases were reviewed. The search results included keywords that define the current problem: muscle pain, referred muscle pain, nociceptive pain, neuropathic pain, radicular pain, somatic, viscera, visceral pain, hyperalgesia, central sensitization, spinal sensitization, visceral hyperalgesia; viscerosomatic convergence; descending modulation, muscle contraction, muscle hypotrophy. Results: When searching for topical scientific results, not many publications have been found. Some of them were older, in some possible mechanisms of pathogenetic manifestation of referred muscle pain were discussed. One article suggested the existence of another possible mechanism besides the generally described ones. Several hypotheses concerning the occurrence of this secondary pain were found to exist, without giving priority to any theory. Most articles described different localizations of symptoms of referred pain and their relationship to other body structures (muscle or joint in a distant region) or internal organ dysfunction or disease. Most of the authors emphasized on the need of better knowledge of this type of pain and the distinction between local, nociceptive, radicular, and neuropathic pain that has a precise clinical characteristic and evidence of a specific injury to an underlying body structure. Conclusion: Knowledge and diagnosing of referred muscle pain is important for clinical practice. Differentiation from primary skeletal muscle pain is still a challenge, but a good knowledge of the problem can provide solutions, although the pathogenetic mechanisms of its occurrence remain unclear. It is likely that the totality of central-nervous mechanisms, the convergence of information from different somatic areas in the dorsal horn and/or its facilitation in it as well as at the level of the thalamus, and the phenomenon of hyperexcitability are essential, although the notion that referred muscle pain has a peripheral origin should not be ignored. Knowledge and targeted search for referred secondary pain could prevent some diagnostic problems and at the same time treat it with appropriate treatments, including the means of physiotherapy.

Active Muscle Trigger Points Are Associated with Pain and Related Disability in Patients with Plantar Heel Pain: A Case-Control Study.

Pain experienced by patients with plantar heel pain has been associated with fascia thickness. It is possible that referred muscle pain may also be related to symptoms experienced by these patients. Our aim was to systematically investigate if the referred pain elicited by trigger points in the leg and foot musculature reproduces the symptoms in individuals with plantar heel pain and to determine the association of trigger points (TrPs) with pain and related disability. A case-control study was conducted. Thirty-five individuals with unilateral chronic plantar heel pain and 35 matched comparable healthy controls participated. An assessor blinded to the subject's condition explored TrPs in the flexor hallucis brevis, adductor hallucis, quadratus plantae, and internal gastrocnemius. Pain and related disability were assessed with a numerical pain rating scale (0-10), the Foot Function Index, and the Foot Health Status Questionnaire. The number of TrPs for each patient with plantar heel pain was 4 ± 3 (2.5 ± 2 active TrPs, 1.5 ± 1.8 latent TrPs). Healthy controls only had latent TrPs (mean = 1 ± 1). Active TrPs in the quadratus plantae (N = 20, 62.5%), and flexor hallucis brevis (N = 19, 59%) were the most prevalent in patients with plantar heel pain. A greater number of active, but not latent, TrPs was associated with higher foot pain variables (0.413 < rs < 0.561, P < 0.01), higher impact of foot pain (0.350 < rs < 0.473, P < 0.05) and worse related disability (-0.447 < rs < -0.35456, P < 0.05). The referred pain elicited by active TrPs in the foot muscles reproduced the symptoms in patients with plantar heel pain. A greater number of active TrPs was associated with higher pain and related disability in patients with plantar heel pain.

Characteristics of referred muscle pain to the head from active trigger points in women with myofascial temporomandibular pain and fibromyalgia syndrome

Our aim was to compare the differences in the prevalence and the anatomical localization of referred pain areas of active trigger points (TrPs) between women with myofascial temporomandibular disorder (TMD) or fibromyalgia (FMS). Twenty women (age 46 ± 8 years) with TMD and 20 (age 48 ± 6 years) with FMS were recruited from specialized clinic. Bilateral temporalis, masseter, sternocleidomastoid, upper trapezius, and suboccipital muscles were examined for TrPs. TrPs were identified by palpation and considered active when the pain reproduced familiar pain symptom experienced by the patient. The referred pain areas were drawn on anatomical maps, digitalized and also measured. A new analysis technique based on a center of gravity (COG) method was used to quantitative estimate of the localization of the TrP referred pain areas. Women with FMS exhibited larger areas of usual pain symptoms than women with myofascial TMD (P < 0.001). The COG coordinates of the usual pain on the frontal and posterior pain maps were located more superior in TMD than in FMS. The number of active TrPs was significantly higher in TMD (mean ± SD 6 ± 1) than in FMS (4 ± 1) (P = 0.002). Women with TMD exhibited more active TrPs in the temporalis and masseter muscles than FMS (P < 0.01). Women with FMS had larger referred pain areas than those with TMD for sternocleidomastoid and suboccipital muscles (P < 0.001). Significant differences within COG coordinates of TrP referred pain areas were found in TMD, the referred pain was more pronounced in the orofacial region, whereas the referred pain in FMS was more pronounced in the cervical spine. This study showed that the referred pain elicited from active TrPs shared similar patterns as usual pain symptoms in women with TMD or FMS, but that distinct differences in TrP prevalence and location of the referred pain areas could be observed. Differences in location of referred pain areas may help clinicians to determine the most relevant TrPs for each pain syndrome in spite of overlaps in pain areas.

Muscle symptoms and creatine phosphokinase elevations in patients receiving raltegravir in clinical practice: results from a multicenter study

7-11 November 2010, Tenth International Congress on Drug Therapy in HIV Infection, Glasgow, UK To further investigate CPK increases and muscle symptoms in a cohort of HIV-infected patients receiving raltegravir-based HAART compared with a control cohort with similar characteristics receiving darunavir-based HAART. The SCOLTA Project is a prospective, observational, multicenter study created to assess the incidence of adverse events in patients receiving new antiretroviral drugs in clinical practice. Muscle symptoms where classified according to the American Heart Association guidelines and CPK elevations were graded according to the DAIDS table. A total of 391 HIV-infected patients were included in the study, 258 (66.0%) males. CDC stage was C in 152 (38.9%) patients. Mean age at enrolment was 44.5 ± 9.0 years, mean CD4 cell count 348 ± 260 cell/µL and mean HIV-RNA 3.26 ± 1.54 log10 cp/ml; 135 (35.2%) patients were HCV Ab+ and 155 (39.6%) had a diagnosis of lipodystrophy. Sixteen (4.1%) were naive to antiretrovirals. No statistical difference was observed regarding baseline characteristics when comparing patients receiving raltegravir (n=293) and darunavir-based HAART (n=98). Thirteen patients (5.4%) receiving raltegravir referred muscle pain and 12 (5.0%) muscle weakness compared with 1 (1.1%) and 0 (0%) receiving darunavir (p=0.20 and p=0.04), respectively. Seventeen (5.8%) patients developed muscle pain and/or weakness in the raltegravir cohort in respect of 1 (1.0%) in the darunavir cohort (p=0.05). No statistical difference was observed when considering CPK increases (>200 U/L) that were reported in 26 (8.9%) patients treated with raltegravir and 11 (11.2%) receiving darunavir. No relation emerged between CPK increase and muscle pain/weakness. Of note, no patient discontinued raltegravir due to CPK elevations or worsening muscle symptoms and no cases of rhabdomyolysis were reported. CPK elevations occurred in >10% of patients receiving both raltegravir and darunavir suggesting a multifactorial aetiology in HIV-infected patients treated with HAART. Raltegravir-treated patients had a significantly higher proportion of muscle symptoms, especially muscle weakness. However, these symptoms did not cause therapy discontinuation, in our cases. Although the limited clinical significance to date, our data suggest the monitoring of muscle symptoms, including both pain and weakness, in patients receiving raltegravir and further diagnostic evaluations if they persist.

Assessment of mechanisms in localized and widespread musculoskeletal pain

The aim of this Review is to give a short presentation of the manifestations, assessment methods, and mechanisms underlying localized and widespread musculoskeletal pain, deep somatic tissue hyperalgesia and chronification. Hyperalgesia can be explained by increased pain sensitivity of nociceptors located in deep tissue (peripheral sensitization) or by increased responses from dorsal horn neurons (central sensitization). The spreading of pain and sensitization is related to increased synaptic activity in central neurons and to changes in descending control from supraspinal centers. Manifestations related to the different aspects of sensitization can be assessed quantitatively using sensory tests, such as pressure algometry (quantitative palpation) and cuff-algometry. Repeated pressure stimulation can evaluate the degree of temporal summation, which is a proxy for the level of central sensitization, as is expanded referred muscle pain area. The transition of acute localized musculoskeletal pain into chronic widespread pain is related to the progression of peripheral and central sensitization. This sensitization for the chronification of pain should be assessed by adequate pain biomarkers. Furthermore, pain prevention should target early intervention strategies and new anti-hyperalgesic compounds should be developed.

A New Muscle Pain Detection Device to Diagnose Muscles as a Source of Back and/or Neck Pain

Trigger point (TrPs) identification has become the mainstay of diagnosis for the treatment of Myofascial Pain Syndrome; however, manual pressure (MP) to identify TrPs by determining low-pressure pain threshold has low interrater reliability and may lack validity since it is done on inactive muscles. To elicit contractions and mimic an active muscle or movement that "causes" pain, a Muscle Pain Detection Device (MPDD) has been developed. A selected muscle is stimulated and painful muscles are precisely detected, allowing distinctions between primary and referred muscle pain as well as distinguishing other functional muscle pain thought to cause MPS. An IRB approved randomized controlled study is presented of MP (20 patients) control vs MPDD (20 patients) to identify which muscle(s) was the source of pain in subjects presenting to the NYU Pain Management Center with a minimum 3 months history of back pain. Patients were unaware of their diagnostic method. Subjects were injected in 1-3 sites identified via MP or MPDD by a separate, blinded physician. Prior to, and following treatment at one week and one month, the patients were administered Oswestry and visual analog scale pain questionnaires by a blinded evaluator, and their range of motion was measured by a blinded physical therapist. The MPDD group reported significantly larger improvements in pain, mood and Oswestry scores compared with the control (P < 0.05). Moreover, the MPDD group reported 82.5% pain relief at 1 month, compared with 53.2% in the control (P < 0.001). The range of motion measurements failed to reveal any significant difference between the groups. Using the MPDD appears to be more valid and potentially more reliable than palpation to identify muscles causing regional pain that could benefit from injections.

Effects of Intramuscular Anesthesia on the Expression of Primary and Referred Pain Induced by Intramuscular Injection of Hypertonic Saline

Intramuscular injection of hypertonic saline produces pain in the belly of the injected muscle (primary pain) and, often, pain that projects distally (referred pain). While it is known that referred pain can be induced during complete sensory block of the distal site, there is little evidence as to whether the perception of referred pain depends on ongoing input from the primary stimulus. We assessed whether blocking the noxious input following the induction of pain blocks the primary but not the referred pain. A cannula was inserted into the tibialis anterior muscle in 15 subjects (8 male, 7 female). In a quasi-random crossover design conducted over 2 experimental sessions, each subject received a bolus intramuscular injection of .5 mL of 5% hypertonic saline, followed 90 seconds later by either: A) A second bolus injection or; B) An injection of 2 mL lignocaine through the same cannula. Protocol A was followed 60 seconds later by either a sham injection or an injection of lignocaine, while protocol B was followed 60 seconds later by either a sham injection or an injection of hypertonic saline. Subjects mapped the areas of primary and referred pain, and rated the intensities at these sites every 30 seconds until the cessation of pain. In all subjects, the area and intensity of primary pain rapidly disappeared within 7.5 minutes of intramuscular lignocaine injection (P < .02 relative to the nonanesthesia condition). With the exception of 2 subjects, in whom the referred pain continued in the absence of primary pain, the referred pain declined in parallel with local pain: the mean total pain intensity declined by 74% in both regions. We conclude that the maintenance of referred muscle pain usually depends on ongoing noxious inputs from the site of primary muscle pain. Referred pain is a significant clinical problem, and commonly occurs with pain originating in muscle but not from skin. It is important to know the primary source of the pain so that treatment can be directed to this site rather to the site of referral.

Associations between psychological traits and experimental muscle pain are sex-dependent

Consistent with the biopsychosocial pain model, pain catastrophizing (PCS), assessed during or after pain, and fear of pain (FPQ) have both demonstrated significant correlations with a variety of pain models. Relatively less is known regarding the personality trait, neuroticism (N) somatosensory amplification (SSAS). These psychological constructs have not been compared with exogenous local or, in particular, referred muscle pain, a centrally-mediated phenomenon. Thus, this study aimed to determine the correlations between four psychological traits (N, PCS, FPQ, SSAS) and pain perception at local and referred sites using experimental muscle pain in both men and women.

Nociceptive and Non-nociceptive Hypersensitivity at Latent Myofascial Trigger Points

The aim of the study was to evaluate whether or not there exists nociceptive and non-nociceptive hypersensitivity at latent myofascial trigger points (MTrPs). Eleven healthy volunteers participated in this study, which consisted of 3 sessions of electromyography-guided intramuscular injection with a minimum of a week interval in between. In each session, a bolus of either hypertonic saline (6%, 0.1 mL, each), glutamate (0.1 mL, 0.5 M, each), or isotonic saline (0.9%, 0.1 mL, each) was randomly injected into a latent MTrP and a non-MTrP located in the right or left gastrocnemius medialis muscles. After each injection, participants were asked to rate the perceived pain intensity on an electronic visual analog scale (VAS) and to mark the pain areas on pain drawings. Maximal pain intensity (VAS(peak)), the area under the curve (VAS(auc)), and local and referred pain areas were extracted. Injections of either hypertonic saline, glutamate, or isotonic saline into the latent MTrPs induced a higher VAS(peak) and larger VAS(auc) than the non-MTrPs (all, P<0.05). Furthermore, the MTrPs with referred pain after painful injections were found to show higher VAS(peak) and larger VAS(auc) than those without referred pain (both, P<0.001). These results confirm the existence of nociceptive hypersensitivity at latent MTrPs and provide the first evidence that there exists non-nociceptive hypersensitivity (allodynia) at latent MTrPs. Finally, the occurrence of referred muscle pain is associated with higher pain sensitivity at latent MTrPs.

Validity of Cross-friction Algometry Procedure in Referred Muscle Pain Syndromes

Deep cross-friction pressure with a finger or an elbow in the proximal gluteal region causes a sciaticlike pain along the side of the thigh and the leg as a clinical presence of referred pain (RP) in patients with nonspecific low back pain (LBP). This study investigated the reliability and discriminative ability of experimentally provoked RP as a result of deep cross-friction with the aid of a Fischer algometer. The new clinical examination method measures the provoked RP threshold resulting in an outcome, expressed in kg/cm2. Forty two patients with subacute LBP (3 to 12 wk) participated in a prospective clinical trial. The outcome was assessed by means of the standard (perpendicular) pressure pain thresholds (PPT) measured with the aid of a Fischer algometer on both sides of the gluteus medius, the provoked RP pain thresholds (PPT-RP) at the location of the medial superior cluneal nerve, the Oswestry Disability Index , and the McGill Pain Questionnaire. The diagnostic criteria for the clinical presence of RP were determined by the patient on the pain chart drawings of the McGill Pain Questionnaire. The criteria for provoked RP were determined by means of PPT-RP with the aid of a Fischer algometer until the patient pointed out the RP zone in the thigh and/or the leg. The interobserver reliability was sufficient for both sides with and without RP (intraclass correlation coefficient>0.97). The test-retest performed independently of the observers ranking, showed a perfect reliability of the PPT-RP measurements (intraclass correlation coefficient>0.98). The PPT-RP at the level of the medial superior cluneal nerve in the subgroup with a clinical presence of RP (N=20) was significantly higher (3.5 kg/cm2) than in the subgroup patients without RP (N=22). The correlation between the factor RP and the PPT-RP was high (R=0.91, P<0.001). The clinically important difference between provoked and clinical presence of RP was found to be higher or lower than 5.6 kg/cm2. The standard PPT measurement of the gluteus medius revealed no significant differences between the subgroups with and without RP. This clinical study support the reliability and discriminative ability of a new method of experimentally provoked RP, using deep cross-friction pressure with the aid of a Fischer algometer in patients with LBP. The experimentally "provoked referred pain threshold" (PPT-RP) values lower than 6 kg/cm correspond clinically with the presence of a referred muscle pain area in the thigh and/or the leg. Further studies of a similar kind are nevertheless needed to confirm those conclusions and to assess the responsiveness of the provoked RP measurements in different treatment follow-up periods.

Muscle Pain: Sensory Implications and Interaction With Motor Control

Muscle hyperalgesia and referred pain plays an important role in chronic musculoskeletal pain. New knowledge on the involved basic mechanisms and better methods to assess muscle pain in the clinic are needed to revise and optimize the treatment regimes. Increased muscle sensitivity is manifested as (1) pain evoked by a normally non-nociceptive stimulus (allodynia), (2) increased pain intensity evoked by nociceptive stimuli (hyperalgesia), or (3) increased referred pain areas with associated somatosensory changes. Quantitative sensory testing provides the possibility to evaluate these manifestations in a standardized way in patients suffering from musculoskeletal pain or in healthy volunteers. Some manifestations of sensitisation, such as expanded referred muscle pain areas in chronic musculoskeletal pain patients, can be explained from animal experiments showing extrasegmental spread of sensitisation. An important part of the pain manifestations (eg, tenderness and referred pain) related to chronic musculoskeletal disorders may be due to peripheral and central sensitization, which play a role in the transition from acute to chronic pain. In recent years, it has become evident that muscle pain can interfere with motor control strategies and different patters of interaction are seen during rest, static contractions, and dynamic conditions.

Discrete Changes in Cortical Activation during Experimentally Induced Referred Muscle Pain: A Single-Trial fMRI Study

Noxious stimulation of skeletal muscle evokes pain that is often referred into distal areas. Despite referred pain being of significant clinical importance, the brain regions responsible for the perception of referred pain remain unexplored. The aim of this investigation is to define these regions using functional magnetic resonance imaging. We induced muscle pain by hypertonic saline injections (0.5 ml) into the tibialis anterior (TA) or flexor carpi radialis (FCR) muscle. TA injections evoked pain that was referred to the ankle/foot in 10/17 subjects, whereas FCR injections evoked pain that was projected into the wrist/hand in 6/12 subjects. Regional brain responses were statistically tested by convolving the temporal profile of the subjective pain intensity rating with the hemodynamic response function. For all subjects, signal increased in the region of primary somatosensory cortex (SI), which represents the leg or arm, that is, the area corresponding to the injection site. However, for those subjects who reported referred pain, signal intensity increases also occurred in the SI region representing the foot or hand. Interestingly, differential signal changes also occurred in anterior cingulate, cerebellar, and insular cortices. This is the first study to provide evidence of cortical differentiation in the processing of primary and referred pain.

Referred muscle pain is primarily peripheral in origin: The “barrier-dam” theory

The mechanisms leading to the frequent occurrence of referred muscle pain (RP) are largely unknown. It is possible that RP is caused by the increased sensitivity of local muscle nociceptors and/or by a central sensitisation. When deep pressure by palpation is used on a subject with smooth fibrotic lesions (myofibrosis) in a muscle, RP can originate as a hyperalgesic cutaneous area, adjacent to, or totally apart from the pressure pain locus. It is currently postulated that a chain reaction is activated implicating triggering of an ever-increasing number of afferent neurons and facilitation of the synaptic connection at the level of the spinal cord, causing more distally a distributed RP via convergent efferent pathways. The human interpretation of this phenomenon can be misleading when the tested person positions, after a few seconds, his RP distally from the site of pressure to the distally located RP area. As a result of what we have found in our experimentally induced RP probes, we hypothesize that deep pressure on a myofibrosis will, in the first place, within a few seconds, increase the nociceptive excitability of the afferent sensitive nerves from the RP area to the local spot of pressure on the muscle, which in return will, in the second place, excite the whole dependent RP area. The mechanism for referred muscle pain proposed in this article is linked to the "pre-local hyper-excitability theory" or "barrier-dam theory". The afferent sensitive peripheral nerves might be entrapped in local muscle hardenings (barrier-dam) with the consequence of the hyper-excitation of pre-local nerves between the distally referred pain area and the local muscular zone of tenderness. The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa. Clinical and fundamental studies with experimentally induced RP are nevertheless needed to examine the hypothesis.

Sympathetic facilitation of hyperalgesia evoked from myofascial tender and trigger points in patients with unilateral shoulder pain

ObjectiveTo provide evidence for the sympathetic–sensory interaction within a trigger point, which may contribute to local and referred pain and sympathetic symptoms in myofascial pain syndrome. MethodsPressure pain threshold (PPT) was measured from a trigger point in the painful side, from a tender point in the non-painful side in the infraspinatus muscles, and from a normal control point in the tibialis anterior muscle in 21 patients with unilateral shoulder pain. In addition, pressure threshold for eliciting referred pain (referred pain threshold, PTRP) was determined, then the intensity was measured of local and referred pain evoked by a pressure equal to 1.5 times PRPT, applied at the trigger point, in 11 patients. All measurements were taken during normal respiration and elevated intrathoracic pressure (EITP). ResultsPPT was significantly lower at the trigger than tender points during normal respiration (P=0.001). PPT decreased significantly at both the tender and trigger points during EITP compared with normal respiration (P<0.001). Significant decreases in referred pain threshold and increases in local and referred pain intensities were seen during EITP than normal respiration (all, P<0.01). ConclusionsThese results provide evidence of sympathetic facilitation of mechanical sensitization and the local and referred muscle pain. SignificanceSympathetic hyperactivity needs to be considered during the clinical evaluation and management of myofascial pain syndrome.

Clinical study of hip joint referred pain

Hip joint associated pain is known to distribute widely in affected thigh or lower leg and generally not restricted in hip joint area.However detail feature of hip joint associated referred pain is not sufficiently clarified. Therefore the aim of this study is to characterize the types of distribution of hip joint related pain and to give our opinion about underlying neurophysiological mechanisms of hip joint referred pain. Of 36 severe osteo-arthritis joints, 83% of the joints showed remote pain area and 18% of the joints showed pain restricted only in inguinal area. Fourteen percent of the joints had far remote pain in lower leg area. L5 root block study was conducted in 7 cases. In all cases remote referred pains were attenuated at least 2 or 3 days and long lasting pain improvement was achieved in one case. These results suggest that referred pain observed in severe hip osteoarthritis cases may initially triggered by hip joint itself but prolonged referred muscle pain may become a possible generator for triggering and maintaining of mal-pain circuit.

Assessment of muscle pain and hyperalgesia. Experimental and clinical findings

It is evident that muscle hyperalgesia and referred pain have an important role in chronic musculoskeletal pain. More knowledge of the basic mechanisms involved and better methods of assessing muscle pain in clinical practice are needed so that treatment regimens can be revised and improved. Methods of quantitative sensory testing of muscle pain and associated phenomena are described. These methods make it possible to evaluate manifestations of muscle pain in a standardised way both in patients suffering from musculoskeletal pain and in healthy volunteers. Elevated muscle sensitivity becomes manifest as (1) pain evoked by a normally non-noxious stimulus (allodynia), (2) abnormally intense pain evoked by noxious stimuli (hyperalgesia), or (3) unusually large areas of referred pain with associated somatosensory changes. These changes can occur as increased somatosensory sensitivity of deep somatic tissues or of the skin in areas of pain referral. Some manifestations of sensitisation in chronic musculoskeletal pain patients, such as expansion of the areas of referred muscle pain, can be explained by the extra segmental spread of central sensitisation seen in animal experiments. An important part of the manifestations of pain in chronic musculoskeletal disorders may be due to peripheral and central sensitisation processes, which are also involved in the transition from acute to chronic pain. Knowledge of these processes has expanded enormously in recent years; it should be utilised when new intervention strategies are designed.

Referred muscle pain/hyperalgesia and central sensitisation.

Referred muscle pain, resulting from algogenic conditions in viscera or other deep somatic structures (another muscle, a joint), is most often accompanied by secondary hyperalgesia and trophic changes (hypotrophy). Referred pain/ hyperalgesia from viscera is partly due to central sensitisation of viscero-somatic convergent neurons (triggered by the massive afferent visceral barrage) but also probably results from a reflex arc activation (the visceral input triggers reflex muscle contraction in turn responsible for sensitisation of muscle nociceptors). Referred pain/hyperalgesia from deep somatic structures is not explained by the mechanism of central sensitisation of convergent neurons in its original form, since there is little,convergence from deep tissues in the dorsal horn neurons. It has been proposed that these connections, not present from the beginning, are opened by nociceptive input from skeletal muscle, and that referral to myotomes outside the lesion results from the spread of central sensitisation to adjacent spinal segments.

Central sensitization in fibromyalgia and other musculoskeletal disorders.

Muscle hyperalgesia and referred pain play an important role in chronic musculoskeletal pain. New knowledge on the involved basic mechanisms and better methods to assess muscle pain in the clinic are needed to revise and optimize treatment regimens. Increased muscle sensitivity is manifested as pain evoked by a normally non-nociceptive stimulus (allodynia), increased pain intensity evoked by nociceptive stimuli (hyperalgesia), or increased referred pain areas with associated somatosensory changes. Some manifestations of sensitization, such as expanded referred muscle pain areas in patients with chronic musculoskeletal pain, can be explained from animal experiments showing extrasegmental spread of sensitization. An important part of the pain manifestations (eg, tenderness and referred pain) related to chronic musculoskeletal disorders may result from peripheral and central sensitization, which may play a role in the transition from acute to chronic pain.

Experimental muscle pain provokes long-lasting alterations of thermal sensitivity in the referred pain area

This study explores thermal sensitivity and thermal nociception for signs of central sensitization in the area of referred muscle pain. Two groups of 24 healthy subjects (ss) each, and with mean ages of, respectively, 27 and 55 years, were first trained in quantitative sensory testing and pain rating. Then, in a second session, referred pain was evoked by injection of 6% hypertonic saline into the infraspinatus muscle. Cold and warm thresholds, synthetic heat threshold (SHT – evoked by an alternating pattern of adjacent cold and warmth), and thermal pain thresholds were measured within the referred pain area at a rate of 1/20 min for 60–120 min. All ss of both groups experienced referred pain mostly in the upper arm and of medium intensity. Pain lasted for approximately 12 min with a shorter duration in the older group ( p<0.02). The cold threshold increased significantly ( p<0.001), and the warm threshold slightly, after the injection and remained high for the whole observation period (i.e. lower and higher temperatures were necessary to elicit cold and warmth, respectively). Threshold recovery was more delayed in the older age group. Of those 28 ss in whom cold pain threshold could be followed during the whole observation period, 18 ss showed an immediate threshold decrease of average 6 °C which outlasted the observation period. Four ss responded with a threshold increase. Heat pain thresholds were not affected in the referred pain area. Average synthetic heat threshold did not change; there were, however, distinct and lasting individual threshold shifts in either direction. Ss with lowered cold pain thresholds or evident threshold shifts for synthetic heat had also higher pain ratings. The results demonstrate that experimental muscle pain can induce long-lasting changes in thermal sensitivity and nociception. The unexpected cold threshold increase may tentatively be explained as an expression of long-term depression. The decrease of cold pain threshold or SHT in subgroups of ss may indicate central sensitization. However, the observed changes in this experiment do not provide an unambiguous indicator for central sensitization which seems to be rather individual and might depend on pain intensity and proneness to express central mechanisms of sensitization. Therefore in clinical pain states the individual pattern of sensory abnormalities has to be analysed and interpreted in addition to the pain parameters to assess central involvement.

Síndrome dolorosa miofascial

A síndrome dolorosa miofascial (SDM) é condição comum. Pode ser primária ou resultante de anormalidades orgânicasou funcionais músculo-esqueléticas, neurogênicas, viscerais e ou psicológicas. É caracterizada pela ocorrência de dor muscular localizada ou referida, pontos gatilhos, bandas de tensão, reprodução da dor por digito pressão e reação muscular contrátil localizada. O diagnóstico é clínico e deve excluir outras afecções concomitantes. O tratamento consiste na utilização de analgésicos antiinflamatórios não hormonais, miorrelaxantes, psicotrópicos e ou opióides, medidas fisiátricas que incluem cinesioterapia (alongamentoe condicionamento físico) agulhamento ou injeção anestésica de pontos gatilhos e psicoterapia. A remoção dos fatorescausais e perpetuantes é fundamental para o sucesso do tratamento. Procedimentos neurocirúrgicos funcionais eventualmente podem ser recomendados em alguns casos.