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Please read “What Everyone on Your Health Care Team Should Know About FMSand CMP”.
Fibromyalgia (FMS) and chronic myofascial pain (CMP) can have an impact onmany aspects of your patient care. FMS is a state of central sensitization causingallodynia and hyperalgesia (Russell 1998). In CMP, there are nodules inside tautbands in muscles that decrease range of motion and cause pain at the end ofrange of motion (Simons, Travell, Simons 1999). TrP pain may be referredelsewhere, with autonomic concomitants and proprioceptive dysfunction.
Myofascia can entrap nerves, blood and lymph vessels. Patients with FMS oftenexperience a decrease in libido. CMP may cause pediatric and adolescent pelvicpain (Schroeder, Sanfilippo, Hertweck 2000). Studies show that 50 % of thechildren of people with FMS may have an inherited tendency to develop FMS(Pellegrino, Waylonis and Sommer 1989), so female children of an FMS parentshould be monitored carefully during first menses.
FMS patients often have multiple hormonal and autonomic imbalances leading toprofound physiological and clinical consequences (Adler, Manfredsdottir, Creskoff2002). FMS can interact with and be affected by sex hormones (Carett,Dessureault, Belanger 1992) and reproduction (Ostensen, Rugelsjoen, Wigers1997). FMS is associated with hypothalamus-pituitary-adrenal (HPA) axisdysfunction. This imbalance can affect the hypothalamic-pituitary-gonadal (HPG)axis and other hormonal axes. Pituitary release of growth hormone and prolactinmay be abnormal in FMS (Griep, Boersma de Kloet.1994). Patients withendometriosis may have high rates of FMS (Sinaii, Cleary, Ballweg 2002). FMSand CMP can add to the severity of endometriosis symptoms. There seems to bean increased incidence of female urethral syndrome in FMS (Wallace 1990).
Female urethral syndrome is a description, not a diagnosis. Look for the cause.
TrPs which may cause or contribute to this syndrome include TrPs of the lowabdominal wall, low rectus abdominus TrPs, pelvic floor muscles, piriformis, andhigh adductor magnus muscles.
Severe menstrual cramping, delayed periods, irregular periods, long periods withexcess bleeding, late periods, missed periods, membranous flow, and/or bloodclots may be a part of the FMS and CMP picture. Menstrual cramping can becaused by coccygeus, iliocostalis, rectus abdominis, pyramidalis, and other pelvicand vaginal TrPs, as well as TrPs high on the adductor magnus muscle (Simons,Travell, Simons 1999). The high adductor magnus TrP, a common and frequentlymissed contributor, refers severe pain deep within the pelvis, and can compress What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 femoral blood vessels. These TrPs are found about 3/4 of the way back from thefront of the inner thigh and respond well to groin stretches. The referral zone caninclude the pubic bone, vagina, rectum, and bladder. In some patients, this painonly occurs during intercourse.
Fibrocystic breasts are often linked with FMS, but I believe that they may be dueto TrPs. The smooth muscles around the ducts have motor endplates, so it islogical the TrPs may form here. Large pendulous breasts can aggravate andperpetuate TrPs and promote the common TrP perpetuating factor of head-forward,round shouldered posture. Mammography can be painful for women with bothFMS and CMP. Myofascial TrPs generate the pain, and FMS amplifies it. Extramedication and massage before a mammogram, and an extra soft touch during it,may prevent pain that could further sensitize an already sensitized CNS.
Dyspareunia may be caused by vaginal and pelvic floor TrPs. Abdominal and low-back TrPs may cause aching and cramps during intercourse. Sharp pain may bepart of piriformis TrPs causing pudendal nerve entrapment. TrPs in any shortlateral rotator muscle can cause piriformis syndrome, including nerve entrapment.
These TrPs are often part of a conglomerate of hip and pelvis TrPs that aggravateeach other. These TrPs refer to the sacroiliac region, spreading sideways acrossthe buttock, over the hip, and to the upper 2/3 of the back of the thigh, in acomposite pain referral pattern. Pain from these TrPs is usually increased bysitting, standing and walking. The sciatic radiation of pain from nerve entrapmentcan extend down the back of the leg to the sole of the foot. Even spreading thethighs apart can be painful. Compression can also cause buttock, inguinal,perineal, and posterior thigh pain and parathesias. Piriformis TrPs also may resultin tightening or immobility of the sacroiliac, which causes further dysfunction.
Pelvic floor TrPs refer pain to an oval area between the buttocks from the base ofthe sacroiliac triangle to the base of the tailbone. The obturator internus TrP painpattern is more rounded, and there may be spillover pain in a V-shape down theback of the thigh. These TrPs may cause generalized symptoms such asdyspareunia, particularly during entry, as well as aching perineal pain. Specificmuscles cause specific symptoms as well. For example, TrPs in the levator animuscle refer pain to the perineum, vagina, coccygeal area, rectum, posterior pelvicfloor, and low back. They can cause stress incontinence, loss of ability to emptythe bladder thoroughly and low back pain, particularly in pregnancy. Post-coitalrectal pain may be prevented by oral clonidine or inhaled salbutamol, but the TrPsshould be treated as well.
TrPs in the ischiocavernosus muscle refer pain to the perineum and nearbyurogenital structures. These TrPs can contribute to dyspareunia, particularlyduring entry, as well as an aching pain in the perineum. Often pain and pressurein the vaginal and perineal area responds well to internal work on thebulbospongiosus. A pelvic exam may activate these TrPs, but this can often be What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 avoided by use of topical anesthetic. These TrPs may respond to finger pressure,but the topical anesthetic is mandatory. Allow time for it to work. These TrPs mayrespond to groin stretches and craniosacral release, and to diazepam or similarmedication taken before intercourse. For detailed information on specific pelvicfloor and related TrPs including diagnoses and treatment, see volume II of theTrigger Point Manuals (Travell and Simons, 1992).
TrPs can cause vulvodynia so severe that intercourse is impossible, and the abilityto sit (and work) may be severely curtailed. Vaginal TrP taut bands can often befelt during pelvic exam. Vaginismus may co-exist with TrPs in the pelvic area.
Some women experience post-coital increase in leg and back pain due to activationof myofascial TrPs. Adequate treatment should avoid this. A daily home stretchingprogram is very important. Some FMS patience experience post-coital weaknessso severe they may be unable to rise from the bed to use the bathroom. Theymay also experience intense heat sensations.
TrPs in scar tissue produced by surgical incision are common, especially in thevaginal cuff following hysterectomy. Lessen the chance of surgical scar TrPs byinjecting the incision area of the cuff as well as the outer layers of the initialincision with procaine immediately before surgery. Pelvic scar tissue TrPs cancause pain easily mistaken for menstrual cramps or bladder spasms.
Intercourse-induced headaches generally involve TrPs. This type of headache isusually localized at the occipital area, but it may be generalized. Coitus activatesthe TrPs. Latent TrPs are like time bombs waiting to go off, and they may do soright before or after orgasm. The TrPs need to be treated until they are gone, notjust latent. A beta blocker may be helpful to prevent this headache. Adequatetiming of medication is essential. Coitus may also cause sensory overload in FMSpatients. This does not always involve pain but can include a heightened sensi-tivity to noise or light, or hyperarousal insomnia from racing adrenalin.
Chronic pelvic congestion can cause chronic pelvic pain. This may be hormonal butmay have a circulatory component. S ome of the circulatory congestion may bedue to myofascial entrapment. Hormone therapy acts upon venous receptors(Charles, 1995). TrP entrapment can be treated with myofascial release, myo-therapy, or craniosacral release therapies. Anything that adds to the congestion ofthe pelvic area, such as an infection, can exacerbate the symptoms.
It is important to find out exactly what the patient’s hormone levels are. Othercells besides the ovaries are involved in estrogen generation. HRT is a mechanismfor replacement of hormones to normal levels. It is critical to identify the correctlevels of HRT replacement needed for each patient. Menopausal women experi-enced enhanced memory and learning capacity with estrogen replacement(Sherwin1997). This may be of importance for women with FMS cognitive deficits What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 (Starlanyl, Copeland 2001). Insulin resistance is a common perpetuating factor ofFMS and CMP. Estrogens raise glucose levels and can add to the risk of developinginsulin resistance. They boost sodium levels and may increase fluid retention.
Estrogen lack has a significant effect on carbohydrate and lipid metabolism(Grumbach, Auchus 1999).
Malabsorption is common in FMS. Some women may be unable to absorb oralestrogen. A transdermal formula of 1.0 mg estriol, 0.25 mg estrione and 0.25 mgestradiol per 0.1 cc can be formulated by a compounding pharmacist. Proges-terone transdermal cream can be applied separately to approximate normalhormone balance if needed, but progesterone may increase insulin resistance. Becautious when changing medications. For example, a change to Estrace vaginalcream in one patient activated abdominal and other TrPs, causing crippling painmimicking menstrual cramps, although the uterus and ovaries were gone. It tookweeks to inactivate the TrPs.
Perimenopause, as well as menopause itself, can begin early for FMS patients, withamplified symptoms. Insomnia can be intensified by hot flashes. HRT may pro-vide relief. Another therapeutical option is gabapentin (Guttuso, 2000), sometimesprescribed for the central sensitization of FMS. Patients experienced an average87 percent reduction in the frequency of hot flashes. Some postmenopausalsymptoms may be secondary to androgen deficiency. It is important to test freetestosterone. When there is low circulating bioavailable testosterone, adequatereplacement may relieve the symptoms (Davis,1999). In a study of women whohad symptoms that responded to estrogen but then returned, the patientsresponded to testosterone (Sarrel, 2000).
Some women find that the FMS symptoms worsen dramatically during menses.
There may be changes in the pattern of pain and other FMS symptoms(Anderberg, Marteinsdottir, Hallman et al. 1998). There may be irregular bloodflow, cramping, membraneous discharge (often with blood clots), and/or extremeblood flow. Vaginal discharge, sometimes with itch, is common. So is mittel-schmerz. One study showed a greater number of FMS tender points aftermenstruation than during menstruation, but not in users of oral contraceptives(Hapidou, Rollman 1998).
Painful menstrual periods should never be considered something to be endured.
There may be perpetuating factors such as endocrine imbalance or contributingmyofascial TrPs that can be remedied. Patients have had hysterectomies becausemenstrual pain was unbearable and dramatically interfered with function. Oftenthe ovaries were left, but in many cases were removed later to balance hormonalswings and prevent mittelschmirtz and/or hormone-activated migraines.
What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 Any chronic pain condition can result in failure to ovulate (Berga 1998). Excesshyaluronic acid has been found in patients with FMS (Yaron, Buskila, Shirazi et al.
1997). This may affect fertility. One study suggests a hyaluronidase inhibitor forcontraception (Reddy, Joyce, Zaneveld 1980). Check for hypometabolism andthyroid resistance, which will not show up on standard thyroid panels (Lowe,2000). Topical or oral T3 may be of use if hypothyroid symptoms are present(Starlanyl, Jeffrey, Roentsch, et al. 2001-2002).
Obesity may decrease fertility and increase insulin resistance (Crosignani, Vegetti,Columbo et al. 2002). Infertility may be enhanced by an anteriorly rotated pelvis,often due to myofascial TrPs. Exposure to bright light may be a useful treatmentfor infertility if there is abnormal melatonin metabolism (Partonen,1999). Guai-fenesin therapy, which some of us have found useful for FMS, has been used totreat infertility. It thins cervical secretions, making it easier for the sperm topenetrate the egg (Check, Adelson and Wu, 1982). Guaifenesin therapy mustproceed carefully, because each person with FMS has a personal best dosage. Anincorrect dosage can increase FMS symptoms, as can treatment without properdiet in cases of co-existing insulin resistance, reactive hypoglycemia or metabolicsyndrome (Starlanyl, Copeland 2001).
Most medications for FMS and CMP are not safe for pregnant or lactating women.
Perpetuating factors for FMS and TrPs must be identified and controlled as much aspossible to reduce symptoms. Some patients have reported that propranololhelped control pain. Explore non-medicinal pain and stress control options, suchas bodywork, mindwork, and life style changes such as attention to diet, sleephabits, exercise and stretching routine. Smoking is a huge perpetuating factor,and should be avoided. Some women have reported partial remission of FMSsymptoms during pregnancy, but symptom flare after birth. TrPs can worsenduring pregnancy. Pregnancy-induced hypertension may be caused by insulinresistance (Innes,Wimsatt 1999).
More than twenty FMS patients have reported 10-month gestations. All deliveredhealthy infants. This may be related to FMS biochemical irregularities, or even toTrP-induced contracture of muscles. Relaxin may be involved. Women with hipslocked in flexion due to TrPs are more likely to have trouble delivering. Ripening ofthe cervix requires loosening of collagen through changes in ground substance(Calder 1994), and FMS and CMP can alter ground substance (Starlanyl, Copeland2001). FMS patients may require pain medication earlier than healthy women, andmay also require induced labor. Myofascial pain may exceed analgesia provided byan epidural. TrP injections may be required for complete analgesia during labor(Tsen, Camann 1997) and may prevent or minimize postpartum TrPs.
What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 Adler GK, Manfredsdottir VF, Creskoff FW. 2002. Neuroendocrine abnormalities infibromyalgia. Curr Headache Rep 6(4):289-98.
Anderberg UM, Marteinsdottir I, Hallman J et al. 1998. Variablility in cyclicityaffects pain and other symptoms in female fibromyalgia syndrome patients. JMusculoskel Pain 6(4):5-22.
Berga SL. 1998. Hypothalamus pituitary gonadal axis: stress induced gonadalcompromise. J Musculoskel Pain 6(3):61-70.
Borg-Stein J. 2002. Management of peripheral pain generators in fibromyalgia.
2002. Rheum Dis Clin North Am 28(2):305-17.
Butkevich IP, Vershinina EA. 2003. Maternal stress differently alters nociceptivebehaviors in the formalin test in adult female and male rats. Brain Res961(1):159-65.
Calder AA. 1994. Prostaglandins and biological control of cervical function. Aust NZ Obstet Gynaecol 34(3):347-51.
Carrett S, Dessureault M, Belanger A. 1992. Fibromyalgia and sex hormones. JRheumatol 19(5):831.
Charles, G. 1995. [Congestive pelvic syndromes]. Rev Fr Gynecol Obstet90(2):84-90. [French] Check JH, Adelson HG, Wu CH. 1982. Improvement of cervical factor withguaifenesin. Fertil Steril 37(5):707–708.
Crosignani PG, Vegetti W, Columbo M. et al. 2002. Resumption of fertility with dietin overweight women. Reprod Biomed Online 5(1):60-4.
Davis SR. 1999. Androgen treatment in women. Med J Aust 170(11):545-9.
Griep EN, Boersma JW, de Kloet ER.1994. Pituitary release of growth hormoneand prolactin in the primary fibromyalgia syndrome. J Rheumatol 21(11):2125–2130.
Grumbach MM, RJ Auchus. 1999. Estrogen: consequences and implications ofhuman mutations in synthesis and action. Clin Endocrinol Metab 84(12):4677-94.
Guttuso Jr. TJ. 2000. Gabapentin’s effects on hot flashes and hypothermia.
Neurology 54(11):2161-2163.
What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 Hapidou EG, GB. 1998. Menstrual cycle modulation of tender points. Pain77(2):151-61.
Innes KE, Wimsatt JH. 1999. Pregnancy-induced hypertension and insulinresistance: evidence for a connection. Acta Obstet Gynecol Scand 78(4):263-84.
Lowe J. 2000. The Metabolic Treatment of Fibromyalgia. Boulder, CO: McDowellPublishing Company.
Ostensen M, Rugelsjoen A, Wigers SH. 1997. The effect of reproductive eventsand alterations of sex hormone levels on the symptoms of fibromyalgia. Scand JRheumatol 26(5):355–360.
Partonen T. 1999. Melatonin-dependent infertility. Med Hypotheses 52(3):269-70.
Pellegrino M, Waylonis GW, Sommer A. 1989. Familial occurrence of primaryfibromyalgia. Arch Phys Med Rehab 70(1):61–63.
Reddy JM, Joyce C, Zaneveld LJ. 1980. Role of hyaluronidase in fertilization: theantifertility activity of mycrisin, a nontoxic hyaluronidase inhibitor. J Androl1(1):28-32.
Russell IJ. 1998. Advances in fibromyalgia: possible role for central neuro-chemicals. Am J Med Sci 315(6):377-384.
Sarrel PM. 2000. Effects of hormone replacement therapy on sexual psycho-physiology and behavior in postmenopause. J Womens Health Gend Based Med9(Suppl 1):S25-32.
Schroeder B, Sanfilippo JS, Hertweck SP. 2000. Musculoskeletal pelvic pain in apediatric and adolescent gynocology practice. J Pediatr Adolesc Gynecol 13(2):90.
Sherwin BB. 1997. Estrogen’s effects on cognition in menopausal women.
Neurology 48(5 Suppl 7):A21-6.
Sinaii N, Cleary SD, Ballweg ML. 2002. High rates of autoimmune and endocrinedisorders, fibromyalgia, chronic fatigue syndrome and atopic diseases amongwomen with endometriosis: a survey analysis. Hum Reprod 17(10):2715-24.
Simons DG, Travell JG, and Simons LS. 1999. Travell and Simons’ Myofascial Painand Dysfunction: the Trigger Point Manual: Vol I, ed 2. Baltimore: Williams andWilkins.
Starlanyl DJ, Jeffrey JL, Roentsch G et al. 2001-2002. The effect of transdermalT3 (3,3’,5-triiodothyronine) on geloid masses found in patients with both What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003 fibromyalgia and myofascial pain: double-blinded, N of 1 clinical study. Myalgies2(2):8-18.
Starlanyl DJ, Copeland ME. 2001. Fibromyalgia and Myofascial Pain: A SurvivalManual. Ed. 2. Oakland: New Harbinger Publications.
Staud R, Smitherman ML. 2002. Peripheral and central sensitization in fibro-myalgia: pathogenic role. Curr Pain Headache Rep 6:259-266.
Tsen LC, Camann WR. 1997. Trigger point injections for myofascial pain duringepidural analgesia for labor. Reg Anesth 22(5):466-468.
Travell JG, Simons DG. 1992. Myofascial Pain and Dysfunction: The Trigger PointManual, Vol. II. Baltimore: Williams and Wilkins.
Wallace DJ. 1990. Genitourinary manifestations of fibrositis, and increasedassociation with female urethral syndrome. J Rheumatol 17(2):238–239.
Yaron I, Buskila D, Shirazi I et al. 1997. Elevated levels of hyaluronic acid in thesera of women with fibromyalgia. J Rheumatol 24(11):2221-4.
What Your OB/GYN Should Know About FMS and CMPby Devin J. Starlanyl 2003

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