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PubMed2003

The effects of infrared laser and medical treatments on pain and serotonin degradation products in patients with myofascial pain syndrome. A controlled trial.

In this controlled study of 46 patients with myofascial pain syndrome, we investigated the effects of infrared (IR) laser application to trigger points and medical treatment on pain reduction and serotonin and its degradation products. Retaining double-blind trial principles, the patients were randomly assigned to two groups. The treatment group received IR laser treatment, whereas the control group received sham laser. However, both groups received medical treatment. In the treatment group, laser was applied once a day for 10 consecutive days at a dose of 1.44 J/cm2. The effect of the laser treatment on pain was evaluated by visual analog scale. Urinary excretion of 5-hydroxy indole acetic acid (5-HIAA) and serotonin + 5-hydroxy tryptophan (5-HT+5-HTP) was studied by column chromatography. At the end of the treatment, there was a statistically significant difference between the VAS values of the treatment and control groups. The 24-h urinary excretion of the 5-HIAA and 5-HT+5-HTP was significantly higher in the laser treatment group than in the placebo group. In conclusion, IR laser is an effective modality in the treatment of MPS which increases an important mediator of pain inhibition, serotonin.

5-Hydroxytryptophan↗
PubMed2003

Investigation of the effect of GaAs laser therapy on cervical myofascial pain syndrome.

Low-energy laser therapy has been applied in several rheumatoid and soft tissue disorders with varying rates of success. The objective of our study was to investigate the effect of laser therapy on cervical myofascial pain syndrome with a placebo-controlled double-blind prospective study model. It was performed with a total of 53 patients (35 females and 18 males) with cervical myofascial pain syndrome. In group 1 (n = 23), GaAs laser treatment was applied over three trigger points bilaterally and also one point in the taut bands in trapezius muscle bilaterally with a frequency of 1000 Hz for 2 min over each point once a day for 10 days during a period of 2 weeks. In group 2 (n = 25), the same treatment protocol was given, but the laser instrument was switched off during applications. All patients in both groups were instructed to perform daily isometric exercises and stretching just short of pain for 2 weeks at home. Evaluations were performed just before treatment (week 0), immediately after (week 2), and 12 weeks later (week 14). Evaluation parameters included pain, algometric measurements, and cervical lateral flexion. Statistical analysis was done on data collected from three evaluation stages. The results were evaluated in 48 patients (32 females, 16 males). Week 2 and week 14 results showed significant improvement in all parameters for both groups. However, comparison of the percentage changes both immediately and 12 weeks after treatment did not show a significant difference relative to pretreatment values. In conclusion, the results of our study have not shown the superiority of GaAs laser therapy over placebo in the treatment of cervical myofascial pain syndrome, but we suggest that further studies on this topic be done using different laser types and dosages in larger patient populations.

Arsenicals↗
PubMed2002

Interstitial cystitis, pelvic pain, and the relationship to myofascial pain and dysfunction: a report on four patients.

Treatment of chronic pelvic pain (CPP), interstitial cystitis (IC), prostatodynia, and irritative voiding symptoms can be frustrating for both patients and physicians. The usual approaches do not always produce the desired results. We found that when we treated myofascial trigger points (TrP) in pelvic floor muscles as well as the gluteus, piriform, infraspinatus, and supraspinatus muscles, symptoms improved or resolved. Various palpation techniques were used to isolate active myofascial TrPs in these muscles of four patients with severe CPP, IC, and irritative voiding symptoms. Injection and stretch techniques for these muscles were performed. Visual twitch responses at the skin surface and in the muscles were used to verify successful needle piercing of a TrP. The patients were asked to verbally describe exactly where the flash of distant pain was felt, a process that permitted an accurate recording of the precise pattern of pain referred by that TrP. The findings involved with the four patients substantiate the need for myofascial evaluation prior to considering more invasive treatments for IC, CPP, and irritative voiding symptoms. Referred pain and motor activity to the pelvic floor muscles (sphincters), as well as to the pelvic organs, can be the sole cause of IC, CPP, and irritative voiding dysfunction and certainly needs further investigation.

Adult↗
PubMed2006

[5-HT3 receptor antagonist als analgetics in rheumatic diseases].

Various rheumatic diseases like fibromyalgia, systemic inflammatory rheumatic disorders and localized diseases, such as arthritides and activated arthroses, tendinopathies and periarthropathies, as well as trigger points can be improved considerably by treatment with the 5-HT3 receptor antagonist tropisetron. Particularly in the latter group of diseases, local injections have done surprisingly rapid analgesic action. This effect matches that of local anesthetics, but lasts considerably longer and is comparable to local injections of local anesthetics combined with corticosteroids. The action of the 5-HT3 receptor antagonists can be attributed to an antinociceptive effect that occurs at the same time as an antiphlogistic and probably also an immunosuppressive effect. Whereas an inhibited release of substance P from the nociceptors, and possibly some other neurokins as well, seems to be the most likely explanation for the antinociceptive action, the antiphlogistic effect is primarily due to an inhibited formation of various different phlogistic substances; in some conditions, like systemic inflammatory rheumatic diseases, for example, the 5-HT3 receptor antagonists may exert an immunosuppressive effect in addition to this.

Analgesics↗
PubMed2004

Glomus tumor of the lateral aspect of the knee joint.

BACKGROUND: We report a rare case of glomus tumor that occurred in the lateral joint of the knee. A 54-year-old man was referred to us with a 3-year history of lateral pain in the left knee and the diagnosis of lateral meniscus injury. Physical examination revealed a small trigger point localized just on the lateral joint space. Magnetic resonance imaging (MRI) showed a very small round mass in the subcutaneous tissue at the level of the lateral joint space. TREATMENT: Excisional biopsy was performed, and the histology was characteristic of a glomus tumor. The patient was asymptomatic immediately after the operation. At the 3-year follow-up after the operation, no recurrence was seen.

Glomus Tumor↗
PubMed2004

Neurobiological basis for the use of botulinum toxin in pain therapy.

The various serotypes of botulinum toxin (BoNT) exert their action by inhibiting the exocytosis of acetylcholine (ACh) on cholinergic nerve endings. BoNT cleaves proteins (e.g. SNAP-25 or VAMP) that are necessary for the docking of the ACh vesicle to the presynaptic membrane. Without docking, no ACh can be released into the synaptic cleft and the innervated structure is paralyzed. This article focuses on the neuromuscular endplate. The main targets of BoNT therapy are states of muscle hyperactivity such as contractures (in the physiological sense), or spasm and focal dystonias. CONTRACTURES: The "integrated hypothesis" of the formation of myofascial trigger points suggests that a lesion of a muscle damages the endplate so that excessive ACh is released. This causes a local contracture (partial contraction of a muscle fiber) underneath the endplate. The contracture compresses small blood vessels, and the tissue becomes ischemic. Ischemia leads to the release of bradykinin (BKN) and sensitization or excitation of nociceptors. BoNT is a causal therapy in these cases, because it stops the excessive ACh release. SPASM: Reflex spasm in a given muscle can be induced by nociceptive input from neighboring joints or muscles. If the force generated by a spasm is relatively high, it will compress the large blood vessels supplying the muscle. The final effect again is ischemia. In this case a drop in pH may accompany the ischemia and BKN are known to be effective stimulants for muscle nociceptors. DYSTONIA: In cases of weak dystonias, a compression of blood vessels is unlikely. However, the tonic contraction will cause a lowering of pH and a release of ATP. Muscle cells contain ATP at concentrations sufficient to excite muscle nociceptors. In cases of spasm and dystonia, BoNT can abolish the pain by relaxing the muscle. Since many patients report alleviation of their pain before the muscle relaxing effect of BoNT has set in, a direct analgesic action of BoNT is being discussed. Most hypotheses rest on the assumption that BoNT inhibits not only the exocytosis of ACh but also of their neurotransmitters. Such an action could be analgesic if the release of neuropeptides from nociceptive nerve endings is prevented. This way, BoNT could alleviate the pain of neuropathies and various types of headache where neurogenic inflammation plays a role. Another site of an analgesic action could be the postganglionic sympathetic nerve ending that uses norepinephrine and ATP as transmitters. Norepinephrine is known to increase cases of chronic pain, and ATP is a stimulant of muscle nociceptors. If BoNT inhibits the release of these transmitters, it could be analgesic in cases of sympathetically maintained pain including the complex regional pain syndrome.

Analgesia↗
PubMed2004

Botulinum toxin in migraine prophylaxis.

Migraine is a chronic headache disorder manifesting in attacks lasting 4-72 hours. Characteristics of headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity, and association with nausea, photophobia and phonophobia. The migraine aura is a complex of neurological symptoms, which occurs just before or at the onset of migraine headache. Botulinum toxin A represents a completely new option for patients with chronic pain conditions. Numerous retrospective open-label chart reviews and 4 double-blind, placebo-controlled studies have demonstrated that botulinum toxin type A is significantly effective in migraine prophylaxis and reduces the frequency, severity, and disability associated with migraine headaches. Studies have generally reported a good and consistent efficacy. The differential therapeutic use of botulinum toxin appears to be worth attempting in migraine patients with the following characteristic features: (1) Muscular stress as migraine trigger, e. g., in craniocervical dystonia, pericranial painful muscular trigger points or tender points, oromandibular dysfunction, (2) concurrent chronic tension-type headache with the aggravating factors of muscular stress or oromandibular dysfunction, (3) chronic migraine with frequent migraine attacks on more than 15 days per month for longer than 3 months and if other therapeutic options have been either ineffective or have not been tolerated. The use of the agent does not cause CNS side effects. Migraine patients in particular, often suffer greatly, as a result of the adverse effects of the drugs used, from fatigue, dizziness, reduced concentration, loss of appetite, weight gain, hair loss and changes in libido. These side effects are not known in association with botulinum toxin A. To date, neither organic damage nor allergic complications have been reported. Thus, both the tolerability and the safety of this therapeutic measure are high. The mode of action by which botulinum toxin is effective in migraine prophylaxis is not fully understood and is under investigation. Currently, a number of other randomized, placebo-controlled, clinical trials are being conducted to evaluate the efficacy, optimal dosing, and side-effect profile of botulinum toxin type A in the prophylaxis of migraine and other headache entities.

Animals↗
PubMed2004

Botulinum toxin (BoNT) and back pain.

Myofascial pain syndrome is defined as subacute or chronic pain with sensory, motor and autonomic symptoms referred from active trigger points with associated painful dysfunctions. Authors present the usefulness of botulinum toxin A or B (BoNT/A or BoNT/B) injected into target muscles since the toxin is capable of controlling not only the muscular spasm but mostly the pain by alternative mechanisms of action, which are discussed. Posology of BoNT, technical aspects and results are presented. BoNT represents an interesting and useful tool for an adequate management of patients with myofascial pain.

Anti-Dyskinesia Agents↗
PubMed2005

Repetitive magnetic stimulation: a novel therapeutic approach for myofascial pain syndrome.

The aim of this study was to evaluate the short, medium and long-term effects of peripheral repetitive magnetic stimulation (rMS) on myofascial pain compared with transcutaneous electrical nerve stimulation (TENS).Fifty-three subjects with myofascial trigger points (TPs) at the level of the superior trapezius muscle were allocated randomly to three groups. The first group (n=17) was treated with rMS, the second (n=18) with TENS and the third (n=18) received a placebo treatment. Each treatment consisted of ten daily 20-minute sessions. Patients were evaluated before and immediately following treatment, and at one and three months after the end of treatment. Outcome measures were: the "neck pain and disability visual analogue scale" (NPDVAS), an algometric evaluation of pain, an evaluation of the TP characteristics, and the range of cervical bending and rotation contralateral to the affected trapezius muscle. At the end of treatment, the rMS group showed a significant improvement in the NPDVAS, algometry, TP characteristics, and cervical contralateral rotation. This improvement also persisted at one and three months post-therapy. After treatment, the TENS group showed significant improvement in the same outcome measures except for algometry. At the one month follow-up visit, this improvement had returned to non significant levels in all outcome measures with the exception of NPDVAS. No significant effect of TENS was seen at the three-month follow-up visit. The placebo group showed no significant improvement in any measure. Our results strongly suggest that at medium and longer term intervals peripheral rMS may be more effective than TENS for the treatment of myofascial pain.

Adult↗
PubMed2003

[Local treatment of rheumatic diseases with the 5-HT3 receptor antagonist tropisetron].

Local injection of the 5-HT3 receptor antagonist tropisetron manifests a distinct analgesic effect in various local diseases of the locomotor system such as tendinopathies, peri-arthropathies,myofascial pain syndrome, in trigger points, and in inflammatory joint processes.This effect corresponds to that exerted by local anesthetics in general use such as lidocaine and prilocaine among others, but the effect lasts considerably longer. The reason for this finding is found in a simultaneous antiphlogistic effect of the 5-HT3 receptor antagonist as evidenced by animal experiments and clinical data.

Humans↗
PubMed2001

[Pathophysiology of low back pain and the transition to the chronic state - experimental data and new concepts].

The present article concentrates on mechanisms that lead to the excitation of nociceptors in soft tissues and nociceptive neurones in the spinal dorsal horn. These mechanisms may contribute to the so-called unspecific low back pain. Properties of nociceptors in soft tissues: A nociceptive ending in soft tissue contains a multitude of receptor molecules in its membrane. The molecular receptors include binding sites for algesic substances that are released during painful stimulation or pathologic alterations of the tissue: bradykinin (BK), serotonin (5-HT), prostaglandin E2 (PG E2), adenosine triphosphate (ATP) and protons (H(+)). The excitation and sensitisation of nociceptors by these substances can be explained by the binding of the substances to the receptor molecules in the membrane of the receptive ending and ensuing opening of ion channels or activation of metabolic cascades. Purinergic receptor molecules in the membrane of nociceptors are activated by ATP. These receptors may be of particular importance for deep somatic pain, because ATP is present in large amounts in muscle tissue and is released during muscle damage. ATP-sensitive nociceptors appear to be distinct from nociceptors that can be excited by protons. The conduction of nociceptive information from muscle to the spinal cord is partly carried by unmyelinated fibres that possess tetrodotoxin-resistant (TTX-r) Na(+)-channels. Therefore, a drug that specifically blocks TTX-r Na(+)-channels would be a new attractive tool in the treatment of patients with deep somatic pain. Chronic muscle lesions such as a myositis have been shown to be associated with a higher innervation density of the tissue with free nerve endings that contain the neuropeptide substance P (SP). Many of these endings are likely to be nociceptors. Since a painful stimulus that acts on a muscle with increased nociceptor density will excite more nociceptors and elicit more pain, the increase in nociceptor density constitutes a peripheral mechanism for hyperalgesia. In muscle free nerve endings - many of which are nociceptive - the neuropeptides SP, calcitonin gene-related peptide (CGRP) and somatostatin have been shown to be present. These substances are released from the receptive endings in muscle when they are stimulated. SP and CGRP have a strong effect on blood vessels and induce local vasodilatation and oedema. The local oedema in the vicinity of the nociceptor is associated with the release of BK from plasma proteins, which increases the excitability of the nerve ending (see below). Thus, a local vicious cycle forms that may contribute to the formation of trigger points. Sensitisation of nociceptors and peripheral hyperalgesia: Nociceptors are easily sensitised, i.e. following a conditioning stimulus they are more sensitive to the unconditioned stimulus. In animals and humans, the responses to injections of BK can be increased by 5-HT or PG E2. The responses of muscle nociceptors to mechanical stimuli are likewise enhanced after administration of BK. During overuse, ischemia or inflammation of soft tissues, the tissue concentrations of BK, PG E2, and 5-HT are elevated and sensitise muscle nociceptors. A sensitised nociceptor is excited and elicits pain when innocuous mechanical stimuli act on the muscle, e.g. during contractions or stretch. Therefore, in chronically altered soft tissues, weak everyday stimuli are likely to cause pain. Mechanisms at the spinal level: In experiments on rats in which a myositis of the gastrocnemius-soleus (GS) muscle was induced experimentally, the effects of a peripheral painful lesion on the discharge behaviour of sensory dorsal horn neurones were studied. One of the main effects of the myositis was an expansion of the input (target) region of the muscle nerve, i.e. the population of dorsal horn neurones responding to an electrical standard stimulus applied to the GS muscle nerve grew larger. One reason for the myositis-induced expansion of the input region is hyperexcitability of the neurones caused by the release of SP and glutamate from the spinal terminals of muscle afferents with ensuing activation of NMDA channels in dorsal horn neurones (central sensitisation). The central sensitisation is of clinical importance because it can explain the hyperalgesia and spread of pain in patients. In contrast to excitability, the resting activity of dorsal horn neurones - which is likely to induce spontaneous pain in patients - does not appear to depend on the release of SP and glutamate but on the concentration of nitric oxide (NO) in the spinal cord. A pharmacological block of the NO synthesis led to a significant increase in background activity without affecting the excitability of the dorsal horn neurones. Such an increase in background activity was observed exclusively in nociceptive neurones, i.e. a local lack of NO in the spinal cord induces spontaneous pain. According to data from animal experiments, a decrease in the spinal NO concentration occurs as a sequel of a chronic muscle lesion; therefore, a lack of NO is a probable factor for the induction of chronic spontaneous pain. Normally, lesion-induced pain subsides and does not develop into chronic pain. The mechanisms governing the return to normal neuronal behaviour after a peripheral lesion are not well studied. Probably, the activation of inhibitory mechanisms, e.g. increased spinal synthesis of GABA or elevated activity of the descending antinociceptive system contribute to the restoration of normal function. The final step in the transition from acute to chronic pain are structural changes that perpetuate the functional changes. In the rat myositis model, an increase in the number of synapses on the surface of NO-snythesizing cells was present 8 h following induction of the myositis. These data show that structural changes appear quite early in the development of a painful disorder. A novel hypothesis for the development of chronic pain states that a strong nociceptive input to the spinal cord leads to cell death predominantly in inhibitory interneurones. Most of these interneurones are assumed to be tonically active; when their number decreases, the nociceptive neurones are chronically disinhibited and elicit continuous pain also in the absence of a noxious stimulus.

Animals↗
PubMed1998

[Differential diagnosis of polyarthritis pain syndrome of the locomotor apparatus].

Widespread pain syndromes of the musculoskeletal system present to general practitioners, internists, neurologists and orthopedic surgeons every day. The syndromes may result both from organic diseases (inflammatory joint diseases, rheumatic manifestations of organ diseases) as well as dysfunctional syndromes, the latter including mainly biomechanically induced syndromes and fibromyalgia. The approach is predominantly clinically oriented and requires laboratory means or technical procedures only in a limited extend. The duration of history, the recognition of synovitis and of myofascial trigger points or of integumental tender points allow in most patients to achieve appropriate diagnostic criteria.

English Abstract↗
PubMed2005

Outcome of invasive treatment modalities on back pain and sciatica: an evidence-based review.

Within the framework of evidence-based medicine high-quality randomised trials and systematic reviews are considered a necessary prerequisite for progress in orthopaedics. This paper summarises the currently available evidence on surgical and other invasive procedures for low back pain. Results of systematic reviews conducted within the framework of the Cochrane Back Review Group were used. Data were gathered from the latest Cochrane Database of Systematic Reviews 2005, Issue 2. The Cochrane reviews were updated using the evidence summary on surgery and other invasive procedures from the COST B13 European Guidelines for the Management of Acute and Chronic Non-Specific Low Back Pain. Facet joint, epidural, trigger point and sclerosant injections have not clearly been shown to be effective and can consequently not be recommended. There is no scientific evidence on the effectiveness of spinal stenosis surgery. Surgical discectomy may be considered for selected patients with sciatica due to lumbar disc prolapses that fail to resolve with the conservative management. Cognitive intervention Combined with exercises is recommended for chronic low back pain, and fusion surgery may be considered only in carefully selected patients after active rehabilitation programmes during 2 years time have failed. Demanding surgical fusion techniques are not better than the traditional posterolateral fusion without internal fixation.

Humans↗
PubMed2006

The effect of gallium arsenide aluminum laser therapy in the management of cervical myofascial pain syndrome: a double blind, placebo-controlled study.

The efficacy of low-level laser therapy (LLLT) in myofascial pain syndrome (MPS) seems controversial. A prospective, double-blind, randomized controlled trial was conducted in patients with chronic MPS in the neck to evaluate the effects of low-level 830-nm gallium arsenide aluminum (Ga-As-Al) laser therapy. The study group consisted of 64 MPS patients. The patients were randomly assigned into two groups. In group 1 (n = 32), Ga-As-Al laser treatment was applied over three trigger points bilaterally for 2 min over each point once a day for 15 days during a period of 3 weeks. In group 2 (n = 32), the same treatment protocol was given, but the laser instrument was switched off during applications. All patients in both groups performed daily isometric exercise and stretching exercises for cervical region. Parameters were measured at baseline and after 4 weeks. All patients were evaluated with respect to pain (at rest, movement, and night) and assessed by visual analog scale, measurement of active range of motion using an inclinometer and a goniometer, and the neck disability index. In both groups, statistically significant improvements were detected in all outcome measures compared with baseline (p < 0.05). However, no significant differences were obtained between the two groups (p > 0.05). In conclusion, although the laser therapy has no superiority over placebo groups in this study, we cannot exclude the possibility of effectivity with another treatment regimen including different laser wavelengths and dosages (different intensity and density and/or treatment interval).

Adult↗
PubMed2000

Difficult problems and their solutions in patients with cancer pain of the head and neck areas.

Pain management can be especially difficult in patients with head and neck cancer due to the erosive nature of the neoplasms that invade the region, the rich innervation of the head and neck, and other factors. Consequently, diagnosis is a complex process that cannot be dealt with in a cursory fashion. Furthermore, tumor pain can mimic noncancer conditions, nonmalignant orofacial disorders can be suggestive of tumor growth, and antineoplastic treatment-related conditions can be difficult to distinguish from tumor recurrence. A series of case reports illustrates key elements of diagnosis and pain management in patients with head and neck cancer. These elements include 1) detailed assessment of pain intensity and characteristics; 2) appropriate use of analgesic adjuvant medications; 3) use of diagnostic and therapeutic nerve blocks and myofascial trigger point injections; and 4) a high index of suspicion regarding tumor recurrence pain.

Adult↗
PubMed2001

Interventional approaches to the management of myofascial pain syndrome.

Interventional therapies are a valuable addition to our armamentarium when treating myofascial pain syndromes. When combined with other therapies, interventional techniques can be an effective adjunct in the multidisciplinary management of pain. This article describes current interventional therapies that are employed in treating myofascial pain syndromes. The mainstay of injection therapies, the myofascial trigger point injection, is emphasized. More recent advances, such as the use of botulinum toxin, are also discussed. In addition, other techniques such as acupuncture and the use of laser therapy are mentioned.

Acupuncture↗
PubMed2002

Myofascial pain syndrome and its suggested role in the pathogenesis and treatment of fibromyalgia syndrome.

Myofascial pain syndrome is a chronic muscle pain disorder in one or more muscles or groups of muscles accompanied by local and referred pain, decreased range of motion, weakness, and often autonomic phenomena. Patients are readily recognized by their history of muscle pain and the presence of myofascial trigger points, which are specific areas of hyperirritability in a muscle that cause local and referred pain on palpation. Failure to recognize MPS often leads to over-investigation, unnecessary medical intervention, and iatrogenic harm with serious cost implications. The purpose of this review is to present clinically relevant data regarding myofascial pain syndrome and to discuss its possible role in the pathophysiology and optimal treatment of fibromyalgia syndrome.

Autonomic Nervous System↗
PubMed2002

The relationship of neck injury and post-traumatic headache.

Although there may be several causes of post-traumatic headache, neck injury is perhaps the most common. This paper primarily reviews the relationship of neck injury, whiplash, and post-traumatic headache. Mechanisms may include structural damage from acceleration or extension of the neck, development of myofascial pain and trigger points, interaction of the trigeminal nociceptive system with the upper cervical (occipital) nerves, and psychologic and emotional factors. Although some healing will occur, the outcome may depend on a number of human factors (awareness of an impending collision) and the fact that repaired tissue is different from normal, uninjured tissue.

Headache Disorders↗