Disease relevance of Myofascial Pain Syndromes

• A comparative trial of botulinum toxin type A and methylprednisolone for the treatment of myofascial pain syndrome and pain from chronic muscle spasm [1].
• 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 [2].
• For 42 patients (91%) the principal cause of the pain was of muscular origin, with frequent features of myofascial pain syndromes (MPS, 50%) and fibromyalgia (FMS, 26%) [3].
• The patients with painful tendinopathies and myofascial pain syndromes were treated with local injections of 5-10 mg tropisetron, and patients with degenerative processes were treated for 5 days with an intravenous (i.v.) bolus injection of 5 mg tropisetron (Navoban) [4].
• Statistical analyses were performed on this remaining patient group with myofascial pain syndrome without a secondary diagnosis of neuropathic/deafferentation pain and partially responsive to clonazepam [5].

High impact information on Myofascial Pain Syndromes

• Botulinum toxin A versus bupivacaine trigger point injections for the treatment of myofascial pain syndrome: a randomised double blind crossover study [6].
• The superiority of water-diluted 0.25% to neat 1% lidocaine for trigger-point injections in myofascial pain syndrome: a prospective, randomized, double-blinded trial [7].
• Botulinum toxin type A injections often reduce the pain associated with conditions such as cervical dystonia, achalasia, rectal fissures, and myofascial pain syndrome [8].
• This paper introduces and relates the presentations made in a symposium entitled "Myofascial Pain Syndromes: Where are we? Where are we going?" at the 47th Annual Assembly of the American Academy of Physical Medicine and Rehabilitation in Kansas City October 2, 1985 [9].
• RESULTS: Local injections of tropisetron as a treatment for trigger points in myofascial pain syndrome also brought about rapid and prolonged relief in the majority of cases [10].

Chemical compound and disease context of Myofascial Pain Syndromes

• The results support the assumption that a dysfunctional end plate exhibiting increased release of ACh may be the starting point for regional abnormal contractions, which are thought to be essential for the formation of myofascial trigger points [11].
• There are, however, no data on the efficacy of clonazepam for chronic pain (CP) associated with myofascial pain syndrome (MFPS) [5].
• The effects of infrared laser and medical treatments on pain and serotonin degradation products in patients with myofascial pain syndrome. A controlled trial [12].

Biological context of Myofascial Pain Syndromes

• Clinical evaluation included parameters for measurement of pain levels using the neck pain and disability visual analogue scale (NPDVAS) and algometry, evaluation of myofascial trigger point characteristics and measurement of the range of cervical movement (range of motion, ROM) [13].

Anatomical context of Myofascial Pain Syndromes

• In skeletal muscle, a local increase of acetylcholine (ACh) in a few end plates has been hypothesized to cause the formation of contraction knots that can be found in myofascial trigger points [11].

Gene context of Myofascial Pain Syndromes

• RESULTS: The FREMS group showed a significant improvement in the NPDVAS, algometry, in myofascial trigger point characteristics, and in the ROM (homolateral rotation, controlateral rotation, bending and extension) after the end of treatment and at 1 and 3 months follow-up evaluation [13].
• OBJECTIVES: After it had been proven that systemic application of the 5-HT3 receptor antagonist tropisetron exerts an analgesic effect on musculoskeletal pain in fibromyalgia, we investigated the efficacy of the substance in tendinopathies and myofascial pain syndromes [10].

References