On initial presentation, she reported marked fatigue and constant pain in the lower back and the right lower quadrant of the abdomen. The pain was worse with physical activity. She denied any urologic or neurologic symptoms, but did complain of a recent increase in intestinal gas and bloating. She had declined a colonoscopy from an internist. She later developed difficulty arising from bed because of back pain and right leg pain. There is no loss of bowel, bladder, or sexual function. She works in data entry and does a lot of sitting, which she reports "causes her pain after prolonged seated activity."
The patient's medical history includes uterine fibroids, lower back and abdominal sensations of pressure, and constant mild pain that had been attributed to the fibroids. An immediate total abdominal hysterectomy and bilateral salpingo-oophorectomy had been recommended, which she declined. She reported history of previous trauma to the region in a vehicular accident 15 years ago, but denied significant residual effects other than joint stiffness. She takes no medications.
Examination revealed an ill-appearing woman complaining of severe pain in the right lower abdominal quadrant and the lumbosacral region. Physical examination was negative, except for moderate lower abdominal tenderness to deep palpation. She was afebrile; her white blood cell count and differential were normal; and her red blood cell count was borderline low with a slight increase in MCV and MCH. Ferriten and percent saturation confirmatory serum studies were obtained and tested positive for chronic anemia. Laboratory diagnostics ruled out hypothyroidism and folic acid deficiency.
She could forward flex to 70 degrees without pain and exhibited a positive Minor's sign on arising, with complaints of localized low back pain. The patient was without paresthesias, muscle weakness or hyporeflexia to indicate any specific nerve root involvement. Magnetic resonance imaging of the spine was the diagnostic test of choice to rule out neurologic disease when the situation warranted.
Range of motion of her hips and joints in the lower extremities does not reproduce her pain. The distal vascular exam is normal. She presents with a functional right short leg. Palpable trigger point bands, purposeful withdraw, and referred pain were demonstrated on digital examination of the thoracolumbar iliocostalis, gluteus medius and quadratus lumborum. Chiropractic assessment yields joint fixation of T10-12, L1-L2 vertebrae and pelvis. Postural examination revealed a head-forward, round-shouldered posture that maintained the pectoral muscles in a shortened and digitally painful position.
Radiographic weightbearing imaging studies were performed to evaluate her lumbar spine. The curvature was somewhat hypolordotic. There was mild loss in disc height of the fifth lumbar and first sacral levels.
Incidental findings: Fergerson's gravational line falls anterior to the sacrum. There were proliferative osteophytes and mild traction spurring demonstrated at the first and second lumbar intraspinous levels. There was laterolisthesis of the spinous processes accompanied by pelvic declination. The acetabuli and hip joint spaces were well-maintained. The bone density and soft tissue structures were unremarkable. There was no evidence of any gross pathology, congenital findings or obvious fracture.
Impression: spondylosis and postural changes.
Discussion: Myofascial Pain Syndrome (a hyperirritable spot within a taut band of skeletal muscle or fascia) This case illustrates the typical clinical findings of myofascial pain syndrome (MPS) presenting as chronic pelvic pain. Although the patient does have mild mechanical low back pain, her major difficulties are related to the chronic pelvic pain disorder.
Clinical Features
There are seven clinical features of MPS due to trigger points (TPs) that warrant discussion. First, there is the exquisite local tenderness of the TP that is well explained by sensitization of the nerve endings of group III and group IV muscle nociceptors. Substances known to make tissues sensitize include bradykinins, prostaglandins, histamine and leukotrienes. Awad biopsied a tender nodular area in the muscles of 10 subjects. Electron microscopy showed discharging mast cells and blood platelets, each of which is a source of histamine and serotonin. Mense et al. discovered that group III and IV muscle nociceptors are most responsive to bradykinins. The afferent nerves of these muscle groups are also capable of generating nerve action potentials that can lead to the referral of pain, and autonomic phenomena to areas some distance from the TP.
Third, there is a palpable band that is characteristic of myofascial pain and helps localize the involved muscles. Of valuable objective clinical identification is the local twitch response of the taut band associated with the TP. The rope-like sensation produced on digital examination of the involved muscle fibers at the TP can be explained by contracture.
Clinically, the patient will experience pain whenever tension is placed on the taut band muscle fibers. There is a perceived weakness without atrophy, and increased fatigability, that may be explained by localized shortening of a group of muscle fibers, and can be expected to cut off local circulation of the capillaries in the TP zone strong enough to produce localized tissue hypoxemia. This leads to an energy crisis that also explains the more rapid onset of fatigue in muscles afflicted with active TPs compared to muscles free of TPs. This may also offer a reasonable explanation as to why leaving the afflicted muscle in a contracted (shortened) position (i.e., while sleeping at night or prolonged seated activity) initiates pain. Patients often report being aware of pain within a specific muscle group upon awakening in the morning.
Current clinical and research evidence indicates that the TP phenomenon begins primarily as a neuromuscular (histochemical) dysfunction resulting from muscle overload. Active TPs then can progress at an unpredictable rate to a dystrophic phase and demonstrate pathological changes.
MPS is a condition that is treatable by eliminating the specific trigger points that are the immediate cause of pain and correcting those factors that predispose to recurrence. Metabolic, endocrine, toxic, inflammatory and other systemic disorders can stress muscle and impair its ability to heal. The most common systemic factors associated with MPS are hypothyroidism, folic acid and iron insufficiency. Subclinical hypothyroidism is often overlooked because its symptoms are subtle, including widespread multiple TPs, cold intolerance, and fatigue. Iron is essential for the conversion of T4 to the active form of T3 thyroid hormone. Cholesterol is often elevated, and hyperactivity, while an unexpected sign, is often present and caused by constant body movement in an attempt to generate body heat. The most useful test is the highly sensitive thyroid stimulating hormone assay. A level in the upper range of normal should lead to further clinical correlation.
Patients with lowered folic acid levels feel cold and have lower cholesterol levels in contrast to hypothyroidism, which is accompanied by headaches, disturbed sleep and restless leg syndrome. Measurement of serum folate, serum vitamin B12 and red blood cell folate gives the most complete assessment of folate status. Iron deficiency is often seen in patients with MPS, usually women in premenopause that have inadequate iron stores. Consuming NSAIDs may lead to depletion of iron stores. Among systemic illness, fibromyalgia is sadly, too often confused with MPS.
Of special concern in these pelvic pain patients is the evolving disc herniation of the lumbar spinal segments. By exerting pressure over the dorsal afferent spinal nerve roots, the evolving disk herniation can produce a pain syndrome before any development of pain typically associated with radiculopathy, e.g., radiating pain and/or numbness of extremity occurs. Early close clinical monitoring of neurological status is warranted.
The chiropractic profession has long utilized manual treatment of MPS, most commonly in addressing the mechanical factors that include structural inadequacies, such as the short leg syndrome, postural stresses, and ultimately, correction of the vertebral subluxation complex. Additionally, many chiropractic practitioners, often at pre-adjustment, utilize digital ischemic compression of the TP for 15-30 seconds, rhythmic percussion of the TP at about two-second intervals to provide a counter-irritant to disrupt the TP and Ultrasound, or electrical stimulation heat application to stimulate endorphin production. Personally, I find that chiropractic adjustments prior to the administration of physiotherapy can significantly shorten the treatment plan duration.
A.S was treated 22 times over a 12-week period under my direction. Conservative chiropractic treatment included high-velocity thoracic, lumbar and pelvic adjustments. Percussor therapy, ultrasound with trigger-point head, and myofascial release with digital ischemic pressure was utilized. Finally, she was taught to recognize activities that would aggravate the pain and to distinguish the TP distribution. A stretch-conditioning muscle program was prescribed for use at a local gym.
Early in the course of care, she was given a referral for gynecological consultation and examination, and was consequently treated concurrently with a local OB/GYN. My medical colleague's report showed upon pelvic examination, a tender cervix and uterus, with tender adnexa as well. No palpable masses were detected. Pelvic ultrasonography was also negative for any mass. This patient's exam had yielded benign uterine fibroids, secretory endometrium, and ovaries with no pathologic change. She was instructed that the total abdominal hysterectomy and bilateral salpingo-oophorectomy that had been previously recommended was, in all likelihood, years away from any clinical consideration. She had a moderate number of white blood cells on a vaginal saline wet prep and was treated with a short-term trial of antibiotics. She received iron supplementation for three months, B12 injections twice weekly for one month, and six sessions of intravaginal electrical muscle stimulation of the levator ani muscle groups to disrupt active TPs.
In working closely with OB/GYN medical practitioners, I have discovered about 30 percent of their patients with pelvic pain belong in my practice; conversely, some of my patients in their practices. This recognition has afforded mutual respect, opportunity for co-referrals, and mutual cooperation when it comes to patient care.
References
- Gatterman MI. Disorders of the Pelvic Ring. Chiropractic Management of Spine-Related Disorders. Williams & Wilkins, 1990; 7: 112-127.
- Gerwin RD. The management of myofascial pain syndromes. Journal of Musculoskeletal Pain (The Haworth Press, Inc) Vol. I, No. 314, 1993, pp. 83-94.
- Travell JG, Simmons DG. Myofascial Pain and Dysfunction: The Trigger Point Manual. Williams & Wilkins, 1992.
- Simmons DG. Myofascial pain due to trigger points. International Rehabilitation Medicine Association, IRMA Monograph Series Number 1, Nov 1987.
- Travell JG, Simmons DG. Myofascial origins of low back pain. Postgraduate Medicine, Low Back Pain, Part I, Vol. 73, No 2, February 1983.
- Rubin, D. Myofascial trigger point syndromes: an approach to management. Arch Phys Rehabil Vol. 62, March 1981.
- Travell JG, Rinzler SH. The myofascial genesis of pain. Postgraduate Medicine Vol. II, No. 5, May 1952.
- Kraus H. Evaluation and treatment of muscle function in athletic injury. Amer Journal of Surg, Vol. 98, September 1959.
- Awad EA. Interstitial myofibrositis. Arch Phys Mid 54:449-453. 1973.
- Mense S. Nervous outflow from skeletal muscle following chemical noxious stimulation. J Physiol 267:75-88, 1977.
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