Myofascial Pain Syndrome Presenting as Chronic Pelvic Pain

 

by Nancy Molina,DC

 

A.S. is a 44-year-old woman with a two-year history of lower abdominal pain. Her menses were regular, of six to seven days' duration, but had become progressively heavier over the past two years, which was attributed to fibroids. She reported a recent six-month history of lower back pain that worsened one week before menses and continued throughout the menstrual cycle. She obtained modest relief from nonsteroidal anti-inflammatory drugs. (Tylenol, aspirin, etc.)

 

 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 hypo-thyroidism 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.

 

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