(1/88) A systematic history for the patient with chronic pelvic pain.
Chronic pelvic pain is a source of frustration to both the physician and the patient. Physicians have been ill equipped by their training to confront the multifaceted nature of the complaints of patients with chronic pelvic pain. Patients have experienced a repetitive dismissal of their complaints by physicians too busy in their practices to address their problems comprehensively. The approach to the patient with chronic pelvic pain must take into account six major sources of the origin of this pain: 1) gynecological, 2) psychological, 3) myofascial, 4) musculoskeletal, 5) urological, and 6) gastrointestinal. Only by addressing and evaluating each of these components by a very careful history and physical examination and by approaching the patient in a comprehensive manner can the source of the pain be determined and appropriate therapy be administered. This article was developed to provide the clinician with a set of tools and a methodology by which the patient with this complaint can be approached. (+info)
(2/88) Effectiveness of a home program of ischemic pressure followed by sustained stretch for treatment of myofascial trigger points.
BACKGROUND AND PURPOSE: Myofascial trigger points (TPs) are found among patients who have neck and upper back pain. The purpose of this study was to determine the effectiveness of a home program of ischemic pressure followed by sustained stretching for the treatment of myofascial TPs. SUBJECTS: Forty adults (17 male, 23 female), aged 23 to 58 years (mean=30.6, SD=9.3), with one or more TPs in the neck or upper back participated in this study. METHODS: Subjects were randomly divided into 2 groups receiving a 5-day home program of either ischemic pressure followed by general sustained stretching of the neck and upper back musculature or a control treatment of active range of motion. Measurements were obtained before the subjects received the home program instruction and on the third day after they discontinued treatment. Trigger point sensitivity was measured with a pressure algometer as pressure pain threshold (PPT). Average pain intensity for a 24-hour period was scored on a visual analog scale (VAS). Subjects also reported the percentage of time in pain over a 24-hour period. A multivariate analysis of covariance, with the pretests as the covariates, was performed and followed by 3 analyses of covariance, 1 for each variable. RESULTS Differences were found between the treatment and control groups for VAS scores and PPT. No difference was found between the groups for percentage of time in pain. CONCLUSION AND DISCUSSION: A home program, consisting of ischemic pressure and sustained stretching, was shown to be effective in reducing TP sensitivity and pain intensity in individuals with neck and upper back pain. The results of this study indicate that clinicians can treat myofascial TPs through monitoring of a home program of ischemic pressure and stretching. (+info)
(3/88) Lipid profile in patients with fibromyalgia and myofascial pain syndromes.
In this study serum lipid profile of patients with fibromyalgia syndrome (FMS) and myofascial pain syndrome (MPS) were investigated and compared with healthy controls. Thirty women who had FMS and 32 women who had MPS with the characteristic trigger points (TrP), especially on the periscapular region were included in this study. Thirty one age matched healthy women were assigned as a control group. All of the subjects were sedentary healthy housewives. Total cholesterol, triglyceride and high-density lipoprotein cholesterol (HDL-c) levels were not significantly different between the FMS and control groups. On the other hand the MPS group had total cholesterol (198.7 vs 172.9 mg/dL, p=0.003), triglyceride (124.7 vs 87.6 mg/dL, p=0.01), low-density lipoprotein cholesterol (LDL-c) (127.5 vs 108.4 mg/dL, p=0.02) and very low-density lipoprotein cholesterol (VLDL-c) (24.9 vs 17.3 mg/dL, p=0.008) levels, which were significantly higher than the controls. There was no significant difference between the lipid profiles in the FMS and MPS groups. Tissue compliance, which was measured from trigger points in the MPS group, correlated significantly with total cholesterol and LDL-c levels. In conclusion, a significant difference was found between the lipid levels of patients with MPS and the controls. More extensive investigation of lipid and lipoprotein levels is required to determine whether high lipid levels are the cause or result of MPS. (+info)
(4/88) Trigger points: diagnosis and management.
Trigger points are discrete, focal, hyperirritable spots located in a taut band of skeletal muscle. They produce pain locally and in a referred pattern and often accompany chronic musculoskeletal disorders. Acute trauma or repetitive microtrauma may lead to the development of stress on muscle fibers and the formation of trigger points. Patients may have regional, persistent pain resulting in a decreased range of motion in the affected muscles. These include muscles used to maintain body posture, such as those in the neck, shoulders, and pelvic girdle. Trigger points may also manifest as tension headache, tinnitus, temporomandibular joint pain, decreased range of motion in the legs, and low back pain. Palpation of a hypersensitive bundle or nodule of muscle fiber of harder than normal consistency is the physical finding typically associated with a trigger point. Palpation of the trigger point will elicit pain directly over the affected area and/or cause radiation of pain toward a zone of reference and a local twitch response. Various modalities, such as the Spray and Stretch technique, ultrasonography, manipulative therapy and injection, are used to inactivate trigger points. Trigger-point injection has been shown to be one of the most effective treatment modalities to inactivate trigger points and provide prompt relief of symptoms. (+info)
(5/88) Management of myofascial trigger point pain.
Successful management of myofascial trigger point (MTrP) pain depends on the practitioner finding all of the MTrPs from which the pain is emanating, and then deactivating them by one of several currently used methods. These include deeply applied procedures, such as an injection of a local anaesthetic into MTrPs and deep dry needling (DDN), and superficially applied ones, including an injection of saline into the skin and superficial dry needling (SDN) at MTrP sites. Reasons are given for believing that DDN should be employed in cases where there is severe muscle spasm due to an underlying radiculopathy. For all other patients SDN is the treatment of choice. Following MTrP deactivation, correction of any postural disorder likely to cause MTrP reactivation is essential, as is the need to teach the patient how to carry out appropriate muscle stretching exercises. It is also important that the practitioner excludes certain biochemical disorders. (+info)
(6/88) Superficial versus deep dry needling.
Ninety percent of my patients with myofascial trigger point (MTrP) pain have this alone and are treated with superficial dry needling. Approximately 10% have concomitant MTrP pain and nerve root compression pain. These are treated with deep dry needling. SUPERFICIAL DRY NEEDLING (SDN): The activated and sensitised nociceptors of a MTrP cause it to be so exquisitely tender that firm pressure applied to it gives rise to a flexion withdrawal reflex (jump sign) and in some cases the utterance of an expletive (shout sign). The optimum strength of SDN at a MTrP site is the minimum necessary to abolish these two reactions. With respect to this patients are divided into strong, average and weak responders. The responsiveness of each individual is determined by trial and error. It is my practice to insert a needle (0.3mm x 30mm) into the tissues immediately overlying the MTrP to a depth of 5-10 mm and to leave it in situ long enough for the two reactions to be abolished. For an average reactor this is about 30secs. For a weak reactor it is several minutes. And for a strong reactor the insertion of the needle and its immediate withdrawal is all that is required. Following treatment muscle stretching exercises should be carried out, and any steps taken to eliminate factors that might lead to the reactivation of the MTrPs. DEEP DRY NEEDLING (DDN): This in my practice is only used either when primary MTrP activity causes shortening of muscle sufficient enough to bring about compression of nerve roots. Or when there is nerve compression pain usually from spondylosis or disc prolapse and the secondary development of MTrP activity. Unlike SDN, DDN is a painful procedure and one which gives rise to much post-treatment soreness. (+info)
(7/88) Lesions of rat skeletal muscle after local block of acetylcholinesterase and neuromuscular stimulation.
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. To test this hypothesis in rats, small amounts of an acetylcholinesterase inhibitor [diisopropylfluorophosphate (DFP)] were injected into the proximal half of the gastrocnemius muscle, and the muscle nerve was electrically stimulated for 30-60 min for induction of muscle twitches. The distal half of the muscle, which performed the same contractions, served as a control to assess the effects of the twitches without DFP. Sections of the muscle were evaluated for morphological changes in relation to the location of blocked end plates. Compared with the distal half of the muscle, the DFP-injected proximal half exhibited significantly higher numbers of abnormally contracted fibers (local contractures), torn fibers, and longitudinal stripes. DFP-injected animals in which the muscle nerve was not stimulated and that were allowed to survive for 24 h exhibited the same lesions but in smaller numbers. The data indicate that an increased concentration of ACh in a few end plates causes damage to muscle fibers. 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. (+info)
(8/88) A practical approach to fibromyalgia.
Fibromyalgia is the name given to a collection of symptoms with no clear physiologic cause, The constellation of symptoms are clearly recognizable as a distinct pathologic entity. The diagnosis is made through clinical observations made by the examiner. Differential diagnosis must include other somatic syndromes as well as disease entities like hepatitis, hypothyroidism, diabetes mellitus, electrolyte imbalance, multiple sclerosis, and cancer. Diagnostic criteria are given as guidelines for the diagnosis, not as absolute requirements. Treatment of this condition remains individualized and relies heavily on having a therapeutic relationship with a provider. Treatment of this syndrome needs to be looked at as an ongoing process. Goal oriented treatment aimed at maintaining specific functions can be directed at helping a patient get restorative sleep, alleviating the somatic pains that ail the patient, keeping a person productive, regulating schedules or through goal oriented agreements made with the patient. Since this syndrome is chronic and may effect all areas of a persons functioning the family and social support system of the person being treated need to be evaluated. Patients often seek alternative medical treatments for this problem including diet therapy, acupuncture, and herbal therapy. Treatment must involve more than just the symptoms presented and the patient can only be treated successfully if they are willing to work at changing their own perceptions, and ways of relating to stressors in their world. (+info)