Fibromyalgia Syndrome: An Introduction (paper)

Note: This paper was writ­ten as an assign­ment for a med­ical com­mu­ni­ca­tions course. I’ve pub­lished it here after receiv­ing sev­er­al requests that I do so.

Fibromyal­gia Syn­drome (FMS) is a debil­i­tat­ing neu­ro­log­i­cal dis­or­der char­ac­ter­ized by chron­ic wide­spread pain and fatigue. It affects approx­i­mate­ly 2% of the pop­u­la­tion, and is more com­mon in women than in men. Cen­tral ner­vous sys­tem sen­si­ti­za­tion affects the entire body, lead­ing to many sec­ondary symp­toms. This paper will cov­er the his­to­ry, symp­toms, and caus­es of FMS as well as recent research and known treat­ments for the syn­drome.

Description

Fibromyal­gia has been described as a full-body migraine. Anoth­er com­mon expla­na­tion is to com­pare every­day life with FMS as being sim­i­lar to the aches and pains asso­ci­at­ed with a severe case of influen­za.

FMS patients expe­ri­ence inter­mit­tent flares, which are episodes of increased symp­to­mol­o­gy. Flares usu­al­ly occur in response to phys­i­cal or emo­tion­al stress—a sched­ule change, an ill­ness or injury, a new job, the birth of a child, etc. While fibromyal­gia is not con­sid­ered a degen­er­a­tive dis­or­der, its symp­toms usu­al­ly become more severe if the patient also has a degen­er­a­tive dis­or­der such as arthri­tis.

Diagnosis

First, a patient must have expe­ri­enced con­tin­u­ous pain in all four quad­rants of the body for at least three months (Wolfe et al., 1990). Doc­tors will usu­al­ly order many dif­fer­ent tests in order to rule out arthri­tis, Lyme dis­ease, and oth­er con­di­tions which might be con­fused with fibromyal­gia.

The key diag­nos­tic tool for FMS is the ten­der point exam. No more than 4kg/1.54km2 of pres­sure is applied to 18 spe­cif­ic points (see Table 1). If there is sig­nif­i­cant pain in at least 11 of the 18 points, the patient may be diag­nosed with fibromyal­gia.

Table 1: Ten­der Point Sites (Wolfe et al., 1990)
Occiput: bilat­er­al, at the sub­oc­cip­i­tal mus­cle inser­tions.
Low cer­vi­cal: bilat­er­al, at the ante­ri­or aspects of the inter­trans­verse spaces at C5C7.
Trapez­ius: bilat­er­al, at the mid­point of the upper bor­der.
Supraspina­tus: bilat­er­al, at ori­gins, above the scapu­la spine near the medi­al bor­der.
Sec­ond rib: bilat­er­al, at the sec­ond cos­to­chon­dral junc­tions, just lat­er­al to the junc­tions on the upper sur­faces.
Lat­er­al epi­condyle: bilat­er­al, 2 cm dis­tal to the epi­condyles.
Gluteal: bilat­er­al, in upper out­er quad­rants of but­tocks in ante­ri­or fold of mus­cle.
Greater trochanter: bilat­er­al, pos­te­ri­or to the trochanteric promi­nence.
Knee: bilat­er­al, at the medi­al fat pad prox­i­mal to the joint line.

There are so many com­mon sec­ondary symp­toms that it is not unusu­al for a patient to be treat­ed by mul­ti­ple spe­cial­ists for those symp­toms over a peri­od of years before she is diag­nosed with FMS. Sec­ondary symp­toms need not be present for diag­no­sis, and will vary from one patient to the next.

Table 2: Sec­ondary Symp­toms
Migraine or ten­sion-type headaches Tem­per­o­mandibu­lar joint dis­or­der
Irri­ta­ble bow­el dis­or­der Gas­troe­sophageal reflux
Impaired mem­o­ry and con­cen­tra­tion Periph­er­al neu­ropa­thy
Rest­less leg syn­drome and oth­er sleep dis­or­ders Sjogren’s syn­drome
Raynaud’s phe­nom­e­na Peri­od­ic mus­cle spasms and cramps
Myofas­cial pain syn­drome Impaired coor­di­na­tion
Inter­mit­tent hear­ing loss or ring­ing nois­es Skin sen­si­tiv­i­ty, itch­ing, burn­ing
Insom­nia Inter­sti­tial cys­ti­tis
Dizzi­ness Chem­i­cal sen­si­tiv­i­ty
Sen­si­tiv­i­ty to light, smells and sounds Fatigue
Cos­to­chon­dri­tis Dif­fuse pelvic pain
Nau­sea Dys­pare­u­nia
Rash­es Der­matographia
Chron­ic sinusi­tis/­post-nasal drip Eye irri­ta­tion, burn­ing or dry­ness

History

The night racks my bones, and the pain that gnaws me knows no rest,” laments Job (The Holy Bible: New Revised Stan­dard Ver­sion, Job 30:17). It’s easy to imag­ine that Job suf­fered from FMS.

Uni­ver­si­ty of Edin­burgh sur­geon William Bal­four described fibromyal­gia, which he called rheuma­tism, in 1815 (Bal­four, 1815, as cit­ed in Star­lanyl, 1999). Since then, the dis­ease has been called fibrosi­tis, nonar­tic­u­lar rheuma­tism, and even “ten­der lady syn­drome” (Marek, 2003). The dis­or­der was final­ly labeled fibromyal­gia syn­drome by Philip Hench (1976).

The Amer­i­can Col­lege of Rheuma­tol­ogy pub­lished its cri­te­ria for the diag­no­sis of fibromyal­gia in 1990 (Wolfe et al.). The Amer­i­can Med­ical Asso­ci­a­tion accept­ed the cri­te­ria in 1987, fol­lowed by the World Health Orga­ni­za­tion in 1992 (WHO, 2004).

Cause

After almost two cen­turies of study, the eti­ol­o­gy of fibromyal­gia is still a mat­ter of much debate. There are no lab tests for FMS. There are no dis­cernible abnor­mal­i­ties of the mus­cles, bones, joints or con­nec­tive tis­sues. It is known to involve cen­tral ner­vous sys­tem changes (Star­lanyl and Copeland, 2001), but those changes may be caused by or be the cause of the dis­or­der. Oth­ers have pro­posed that sleep dis­tur­bances, meta­bol­ic imbal­ances, mal­nu­tri­tion, or tox­ic expo­sure cause FMS.

For the last 25 years, most prac­ti­tion­ers have treat­ed FMS as an autoim­mune dis­or­der, sim­i­lar to arthri­tis. Lev­els of anti­nu­clear anti­bod­ies are used to diag­nose autoim­mune dis­or­ders, but the pres­ence of those anti­bod­ies is sim­i­lar in most FMS patients and healthy con­trols (Star­lanyl & Copeland, 2001).

Trav­ell and Simons believed that untreat­ed myofas­cial trig­ger points caused fibromyal­gia (1999, as cit­ed in Davies, 2001). Trig­ger points, though, refer pain to dif­fer­ent parts of the body. Ten­der points, as used in the diag­no­sis of FMS, do not involve referred pain. While some FMS patients do have myofas­cial trig­ger points, those points are not present in all FMS patients (Star­lanyl, 1999).

Some doc­tors per­sist in believ­ing that FMS is a psy­chi­atric dis­or­der, but researchers have been unable to dis­tin­guish between FMS, rheuma­toid arthri­tis and oth­er patients who expe­ri­ence chron­ic pain using psy­chi­atric tech­niques (Star­lanyl & Copeland, 2001). Some physi­cians have reclas­si­fied fibromyal­gia as a “func­tion­al somat­ic syn­drome,” claim­ing that it is char­ac­ter­ized more by dis­abil­i­ty than med­ical expla­na­tion, sug­gest­ing behav­ioral and psy­chi­atric treat­ment rather than any oth­er ther­a­pies (Barsky & Borus, 1999). While the inci­dence of psy­chi­atric dis­or­ders such as depres­sion is no high­er in patients with FMS than in those with oth­er chron­ic pain dis­or­ders, the num­ber of fibromyal­gia patients who have expe­ri­enced acute or long term trau­ma or abuse is far high­er than that of the gen­er­al pop­u­la­tion (Romans et al., 2002 and Van Houden­hove et al, 2004).

Research

In the last ten years, sev­er­al new tech­nolo­gies have been used to prove that FMS is a phys­i­cal dis­or­der. Func­tion­al mag­net­ic res­o­nance imag­ing (fMRI) and sin­gle positron emis­sion com­put­ed tomog­ra­phy (SPECT) scans of FMS patients’ brains show sig­nif­i­cant abnor­mal­i­ties in region­al cere­bral blood flow (Grace­ley et al., 2002 and Mountz et al., 1998). FMRIs also demon­strate sig­nif­i­cant­ly increased activ­i­ty in pain-rel­e­vant areas of the brain in response to stim­uli when com­pared to a con­trol group (Cook et al., 2004). Ital­ian researchers have found ele­vat­ed lev­els of the neu­ropep­tide sub­stance P, which is involved in the per­cep­tion of pain, in the spinal flu­id of FMS patients (De Ste­fano et al, 2000). Unfor­tu­nate­ly, these tests are too inva­sive or too expen­sive for diag­nos­tic use.

Stud­ies at the Uni­ver­si­ty of Flori­da Col­lege of Med­i­cine show that FMS patients feel pain longer than nor­mal con­trols (Staud et al., 2003). One of the researchers, Roland Staud, also found that once a sub­ject with fibromyal­gia is exposed to painful stim­uli, that patient stays more sen­si­tive to fur­ther stim­uli. Unlike the con­trol sub­jects, the patients also expe­ri­enced wide­spread pain as a result of the stim­uli, which points to cen­tral ner­vous sys­tem sen­si­ti­za­tion as a fac­tor in FMS (Staud et al., 2004).

Van Houden­hove et al. cite mul­ti­ple stud­ies regard­ing the effect of long-term stres­sors on the cen­tral ner­vous sys­tem on var­i­ous mam­mals, includ­ing humans.

Human stud­ies also sug­gest that the cumu­la­tive effects of phys­i­cal or psy­choso­cial bur­den may increase sus­cep­ti­bil­i­ty to stress in lat­er life, either through sen­si­ti­za­tion or failed inhi­bi­tion of the HPA-axis, pos­si­bly due to glu­co­cor­ti­coid-relat­ed hip­pocam­pal dam­age. For exam­ple, ret­ro­spec­tive stud­ies have shown that emo­tion­al, phys­i­cal or sex­u­al abuse dur­ing child­hood may not only increase future risks for anx­i­ety, depres­sion and soma­ti­sa­tion, but even organ­ic dis­eases such as coro­nary dis­or­ders, CVS, dia­betes, CPOD and viral infections—which may be relat­ed to life­long hyper­re­ac­tiv­i­ty of the LC-NE and HPA axes. (2004, p. 268).

Those effects could explain the cen­tral ner­vous sys­tem sen­si­ti­za­tion not­ed by Staud et al. Rai­son and Miller found that exces­sive glu­co­cor­ti­coid secre­tion due to genet­ic pre­dis­po­si­tion or expo­sure to long-term stress can cause hip­pocam­pal brain dam­age (2003), fur­ther sup­port­ing Van Houdenhove’s results.

Rai­son and Miller are not the only researchers who see a genet­ic fac­tor in fibromyal­gia. Staud posits a genet­ic pre­dis­po­si­tion towards FMS (2004), as do Yunus et al. (1999) and Pel­le­gri­no et al., 1989. Van Houden­hove, how­ev­er, points out that gen­er­a­tional behav­ioral cycles, such as those often seen in abu­sive fam­i­lies, could explain some of the appar­ent hered­i­ty (2004).

Treatment

Most treat­ment of FMS is lim­it­ed to man­age­ment of symp­toms. Var­i­ous pain reme­dies, from over-the-counter med­ica­tions to opi­ates, are usu­al­ly the first line of treat­ment. Mus­cle relax­ants, phys­i­cal ther­a­py, and mas­sage help some patients. Trig­ger point ther­a­py and injec­tions are anoth­er pos­si­bil­i­ty. Many FMS patients expe­ri­ence dif­fi­cul­ties in achiev­ing rest­ful sleep, so physi­cians com­mon­ly pre­scribe seda­tives and tran­quil­iz­ers. Low dos­es of anti-seizure med­ica­tions and atyp­i­cal antipsy­chotics, such as Requip and Sero­quel, have been found to be effec­tive in help­ing some fibromyal­gia patients to achieve restora­tive sleep.

Selec­tive sero­tonin reup­take inhibitors (SSRIs), tri­cyclic anti­de­pres­sants and oth­er med­ica­tions that affect neu­ro­trans­mit­ters help some fibromyal­gia patients (Marek, 2003). Cym­bal­ta, a new med­ica­tion which inhibits both sero­tonin and nor­ep­i­neph­rine reup­take, seems to improve pain and reduce the num­ber of ten­der points in FMS patients (Arnold et al., 2004).

Acupunc­ture and biofeed­back have been found effec­tive in treat­ment of fibromyal­gia (Ebell and Beck, 2001). Gen­tle, non-aer­o­bic exer­cise such as Tai Chi and some forms of yoga may help patients, as well.

Stress reduc­tion is one of the most impor­tant fac­tors in improv­ing the qual­i­ty of life for fibromyal­gia patients (Williamson, 1998). Regard­less of whether the dis­or­der is caused by stress or not, it is aggra­vat­ed by stress. While it is impos­si­ble for any per­son to com­plete­ly avoid stress, it is pos­si­ble to reduce expo­sure to known stres­sors and learn to bet­ter cope with those that must be endured.

Mind­ful­ness-based stress reduc­tion (MBSR) pro­grams are rel­a­tive­ly new in the treat­ment of fibromyal­gia in the US. In Full Cat­a­stro­phe Liv­ing, Jon Kabat-Zinn defines mind­ful­ness as, “the com­plete ‘own­ing’ of each moment of your expe­ri­ence, good, bad, or ugly” (1990, p. 11). The the­o­ry is that mind­ful­ness can allow patients to reduce their reac­tions to stress, improv­ing their abil­i­ty to cope with stres­sors. “In devel­op­ing the capac­i­ty to step back and observe the flow of con­scious­ness, mind­ful­ness can short­cir­cuit the fight or flight reac­tion char­ac­ter­is­tic of the sym­pa­thet­ic ner­vous sys­tem, allow­ing indi­vid­u­als to respond to the sit­u­a­tion at hand, instead of auto­mat­i­cal­ly react­ing to it on the basis of past expe­ri­ences.” (Proulx, 3002, p. 201) MBSR pro­grams typ­i­cal­ly last from 8 to 12 weeks and include instruc­tion in med­i­ta­tion, breath­ing tech­niques, phys­i­cal aware­ness, and yoga. They often uti­lize jour­nal­ing and group dis­cus­sions regard­ing atti­tudes and pos­i­tive think­ing. While MBSR par­tic­i­pa­tion does not nec­es­sar­i­ly lead to improve­ment of the phys­i­cal symp­toms of fibromyal­gia, it can lead to improved qual­i­ty of life for the fibromyal­gia patient.

Conclusion

It is unlike­ly that a cure will be found for fibromyal­gia as long as its eti­ol­o­gy is not ful­ly under­stood. Even as the con­tribut­ing fac­tors are iden­ti­fied, though, the com­plex­i­ty of the syn­drome leads one to believe that it is unlike­ly that any one treat­ment will pro­vide a panacea. The progress made in the last fif­teen years, though, has led to the reclas­si­fi­ca­tion of the dis­ease and improved treat­ments, hence an improved prog­no­sis for all fibromyal­gia patients.

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