Sunday, June 28, 2009

Tony Conigliaro: Right Fielder for the Red Sox. Reason for Wearing Helmets, when Playing Sports and other Activities!

Edited From Wikipedia

Tony Conigliaro: Red Sox Number 25

Tony? Yes, I liked him! Before a game that I went to with a group, some of the players were walking around the field. I saw a player with a number 25, and I knew it was him!

It is crucial for children to wear a protective helmet, when playing contact sports!

It is essential for Children and Adults to wear "Protective Helmets":

*Bike Riding:
Always supervise your children. Tell your young children never go outdoors without you. Tell your older children to tell you where they are always going. Suggest to them when they get to their destination to call you. Older children, like their privacy. Their safety is more important than their privacy, so do tell them to call by cell phone every fifteen to twenty minutes.

*Roller Blading
*Skate Boarding
*Dirt Bikes

*Equestrian Riding

Tony Conigliaro
Right fielder
Born: January 7, 1945(1945-01-07)
Revere, Massachusetts
Died: February 24, 1990 (aged 45)
Salem, Massachusetts
Batted: Right Threw: Right
MLB debut
April 16, 1964 for the Boston Red Sox
Last MLB appearance
June 12, 1975 for the Boston Red Sox
Career statistics
Batting average .264
Home runs 166
Runs batted in 516
Career highlights and awards

Anthony Richard Conigliaro (January 7, 1945 - February 24, 1990), nicknamed "Tony C" and "Conig",[1][2] was a Major League Baseball outfielder and right-handed batter who played for the Boston Red Sox (1964-67, 1969-1970, 1975) and California Angels (1971). He was born in Revere, Massachusetts, and was a 1962 graduate of St. Mary's High School (Lynn, Massachusetts).

Baseball Career

In his 1964 rookie season, Conigliaro batted .290 with 24 home runs and 52 RBI in 111 games, but broke his arm and his toes in August. Tony Oliva won American League Rookie of the Year honors.

In his sophomore season in 1965, Conigliaro led the league in home runs (32). He was selected for the All-Star Game in 1967. In that season, at age 22, he became the youngest player to reach a career total of 100 home runs.[3]

On August 18, 1967, the Red Sox were playing the California Angels at Fenway Park. Conigliaro, batting against Jack Hamilton, was hit by a pitch on his left cheekbone, and was carried off the field on a stretcher. He sustained a broken cheekbone and severe damage to his left retina. The batting helmet he was wearing did not have the protective ear-flap that has since become standard.

A year and a half later, Conigliaro made a remarkable return, hitting 20 homers with 82 RBI in 141 games, earning Comeback Player of the Year honors. In 1970, he reached career-high numbers in HRs (36) and RBI (116). That season he and his brother Billy formed two-thirds of the Red Sox outfield. After a stint with the Angels in 1971, he returned to the Red Sox briefly in 1975, but was forced to retire because his eyesight had been permanently damaged.

Conigliaro batted .267, with 162 home runs and 501 RBI during his 802-game Red Sox career. With the Angels, he hit .222, 4, 15, in 74 games. He holds the MLB record for most home runs (25) hit by a teenaged player. He is the 2nd youngest player to hit his 100h homer (after Mel Ott in 1931). Sports

Back in uniform after his injury, Tony Conigliaro leads the cheers from the dugout. Back in uniform after his injury, Tony Conigliaro leads the cheers from the dugout. (FRANK O'BRIEN/GLOBE STAFF/file 1967)

Mike Andrews, former teammate:

"He was destined for the Hall of Fame. There was no question in my mind. He just had everything going for him. He was as good a clutch hitter as I've ever seen."

Dick Williams, manager of 1967 Red Sox, on whether Boston could have won the World Series that year with a healthy Conigliaro:

"Oh, yes. We could have won more than '67."

Carl Yastrzemski, former teammate:

"He was just starting to come into his own as a big-league ballplayer all around."

Johnny Pesky, former Sox shortstop and longtime coach:

"He was a great player. The best 19-year-old I ever saw. That's one of the tragedies of baseball. When he got hurt, he was the best-looking young player I ever saw. I've said that many times. There's a lot of coulda, shoulda. We'll never know."

Mike Lowell, who wears Tony C's number 25 for the Red Sox and received the 1999 Tony Conigliaro Award for overcoming adversity after beating testicular cancer:

"It's a good name to be intertwined with, as opposed to something that might be negative. . . . I got some fan mail from people who say that they're proud that I'm wearing 25 because they're big Conigliaro fans. So that's got to be a pretty substantial compliment. I take it as good. . . . But I think it's just a shame that someone who was so highly touted like that. . . . It's sad to think that one moment really can change that so much."

Dick Bresciani, Red Sox historian, on Conigliaro's abbreviated 1975 comeback attempt:

"It was sad to see a guy who probably should have been still in his prime and all of a sudden he just couldn't perform well anymore."

Dick Johnson, curator of New England Sports Museum:

"I saw him when he'd been retired for about two years. He was a broadcaster out in the [San Francisco] area. They had a home-run-hitting contest and Tony C took part in it in street clothes, white shoes, checked polyester sport coat, a pair of bell-bottoms. And he gets in the batter's box, and my recollection is that he hit six of 10 pitches out of the park. It was remarkable. My brother and I were going crazy."

Jim Lonborg, former teammate:

"We were in spring training. We had a series with the Yankees down in St. Thomas and St. Croix. There were day games at very funky fields, pretty rough shape. I can remember being out at a wonderful restaurant up on top of a hill, Mike Ryan, and Rico [Petrocelli], Tony, and myself. Having dinner and then cocktails and then singing all kinds of great doo-wop songs. It was a wonderful night."

Rico Petrocelli, former teammate, on Conigliaro's comeback:

"Absolutely [amazing]. I thought he'd never come back. The hole in his eye. Geez, the damage. How can you hit if you can't see well? I thought it was one of the greatest comebacks of all time. I think we all did."

Billy Conigliaro, younger brother, on his memory of Aug. 18, 1967:

"The sound of the ball hitting him. It was just a big whack, a thud. The ball just went straight down. It didn't glance off. It didn't skip to the backstop. It just kind of fell right there."

Compiled by Maureen Mullen

Continued Edited From Wikipedia

Final years

On January 3, 1982 Conigliaro, in Boston to interview for a broadcasting position, suffered a heart attack while being driven to the airport by his brother Billy. Shortly thereafter, he suffered a stroke and lapsed into a coma. Conigliaro remained in basically a vegetative state until his death more than 8 years later. He lived these final years at his parents' home in Nahant, Massachusetts. In February, 1990 he died in Salem, Massachusetts at the age of 45. In commemoration, the Red Sox wore black armbands that season.

Currently, the Tony Conigliaro Award is given annually to the player who best overcomes an obstacle and continues to thrive through

Conigliaro's Corner

For the start of the 2007 season, Red Sox ownership added a new 200-seat bleacher section on the right field roof, providing an additional 16,000 available tickets for the season.[4] It was named "Conigliaro's Corner" in honor of Tony Conigliaro. The seats are being marketed specifically towards families.[4] As of May 2007, the section is reserved for Red Sox Nation members on Saturdays and Red Sox Kid Nation members on Sundays.[4]

Thursday, June 25, 2009

What is Spinal Cord Injury?

It was Chrisipher Reeves who brought Spinal Cord Injuries into the lime light. He was at his Equestian Meet, and fell off his horse. If he did not receive medical treatment as quickly as he did; he would have died on the spot. His neck was broken very high. In addition to his intial standard treatment, it was required that the doctors insert a "stainless steel arch" in his neck to support his head. He greatly advanced the treatment for persons with Spinal Cord Injuries. With his tireless advocacy, he advanced treatment for all persons with disabilities.

A spinal cord injury usually begins with a sudden, traumatic blow to the spine that fractures or dislocates vertebrae. The damage begins at the moment of injury when displaced bone fragments, disc material, or ligaments bruise or tear into spinal cord tissue. Most injuries to the spinal cord don't completely sever it. Instead, an injury is more likely to cause fractures and compression of the vertebrae, which then crush and destroy the axons, extensions of nerve cells that carry signals up and down the spinal cord between the brain and the rest of the body. An injury to the spinal cord can damage a few, many, or almost all of these axons. Some injuries will allow almost complete recovery. Others will result in complete paralysis.

Is there any treatment?

Improved emergency care for people with spinal cord injuries and aggressive treatment and rehabilitation can minimize damage to the nervous system and even restore limited abilities. Respiratory complications are often an indication of the severity of spinal cord injury About one-third of those with injury to the neck area will need help with breathing and require respiratory support. The steroid drug methylprednisolone appears to reduce the damage to nerve cells if it is given within the first 8 hours after injury. Rehabilitation programs combine physical therapies with skill-building activities and counseling to provide social and emotional support.

What is the prognosis?

Spinal cord injuries are classified as either complete or incomplete. An incomplete injury means that the ability of the spinal cord to convey messages to or from the brain is not completely lost. People with incomplete injuries retain some motor or sensory function below the injury. A complete injury is indicated by a total lack of sensory and motor function below the level of injury. People who survive a spinal cord injury will most likely have medical complications such as chronic pain and bladder and bowel dysfunction, along with an increased susceptibility to respiratory and heart problems. Successful recovery depends upon how well these chronic conditions are handled day to day.

What research is being done?

The National Institute of Neurological Disorders and Stroke (NINDS) conducts spinal cord research in its laboratories at the National Institutes of Health (NIH) and also supports additional research through grants to major medical institutions across the country. Advances in research are giving doctors and patients hope that repairing injured spinal cords is a reachable goal. Advances in basic research are also being matched by progress in clinical research, especially in understanding the kinds of physical rehabilitation that work best to restore function. Some of the more promising rehabilitation techniques are helping spinal cord injury patients become more mobile.

Wednesday, June 24, 2009

Trigeminal Neuralgia (TN) - Does a Virus Cause It?

Trigeminal neuralgia (TN), also called tic douloureux or the suicide disease, is a chronic (long-lasting) condition affecting the fifth cranial (trigeminal) nerve, one of the largest nerves in the head. Trigeminal neuralgia symptoms include sudden, sharp, stabbing, shock-like, or shooting pain in the face­—usually on the right side—often in the jaw or cheek. Medical professionals describe trigeminal neuralgia pain as the worst a person can experience. The attacks usually last a few seconds but may appear and disappear at any time and go on for days, months, or years. Talking, chewing, or swallowing can trigger agonizing pain and difficulty in coping, which is why it's called the suicide disease. Trigeminal Neuralgia is more common among women than men, usually occurs after the age of 50.

How NUCCA treatment can help TN

trigeminal neuralgia symptoms;trigeminal neuralgia TNThere is no clear-cut cause for trigeminal neuralgia (TN). Some say that TN is caused by trauma to the nerve as it passes from the skull to the muscles and tissue of the face. This trauma compresses the nerve, causing the nerve cell to shed its protective and conductive coating. Others believe the cause of TN is a biochemical change in the nerve tissue. Recently, it has been proposed that an abnormal blood vessel compresses the nerve as it exits from the brain. In all cases, an excessive amount of activity from a damaged nerve causes the painful attacks.

Over time, trigeminal neuralgia pain and its symptoms usually increases in severity and frequency. TN patients often require increased doses and more continuous usage of medications. As a result, many TN patients whose pain was initially well controlled with medication find that over time they must increase their medications to toxic levels in order to control their pain. At this point, unless they are willing to exist with the pain or in a toxic state, surgical intervention is suggested.

NUCCA can help trigeminal neuralgia symptoms by correcting the misalignments of the spine caused by trauma, and removing compression of the brain stem and surrounding nerves. After nerve irritation has been removed, proper communication is restored between the brain and spinal cord, and the surrounding nerves. The NUCCA procedure can be helpful by releasing the pressure of the artery or vein pressing on the trigeminal nerve at the base of the brain.

Specific imaging studies of the cervical (upper neck) region are conducted to locate a misalignment of the vertebrae. Insight Millenium technology is used to scan and measure the nervous system for possible irritation. If a misalignment has been found to affect the function of the nervous system, very specific gentle adjustments are made, by hand, to correct the misaligned vertebrae in the neck. After the adjustments have been performed, follow-up imaging studies and nervous system scans are taken to confirm a successful spinal correction

Hydrocephalus: Newborns -- Children -- Adults

September, 2005

What is Hydrocephalus?

Hydrocephalus and head enlargement in an infantThe term hydrocephalus is derived from two words: "hydro" meaning water, and "cephalus" referring to the head.

Hydrocephalus is a condition in which excess cerebrospinal fluid (CSF) builds up within the ventricles (fluid-containing cavities) of the brain and may increase pressure within the head. Although hydrocephalus is often described as "water on the brain," the "water" is actually CSF, a clear fluid surrounding the brain and spinal cord. CSF has three crucial functions: 1) it acts as a "shock absorber" for the brain and spinal cord; 2) it acts as a vehicle for delivering nutrients to the brain and removing waste; and 3) it flows between the cranium and spine to regulate changes in pressure within the brain. Hydrocephalus can occur at any age, but is most common in infants and adults age 60 and older. According to the National Institute of Neurological Disorders and Stroke, hydrocephalus is believed to affect approximately one in every 500 children. The majority of these cases are often diagnosed before birth, at the time of delivery, or in early childhood.

Common Causes of Hydrocephalus

Although rare, hydrocephalus can be inherited genetically or may be associated with developmental disorders, including spina bifida (congenital defect of the spine) and encephalocele (hernia of the brain). Other causes can include bleeding within the brain, brain tumors, head injuries, complications of premature birth such as hemorrhage, or diseases such as meningitis or other infections. In some cases, normal flow of CSF within the brain is blocked, resulting in fluid build-up.

Symptoms of hydrocephalus vary greatly from person to person. According to the Hydrocephalus Association, some of the most common symptoms are listed below as a reference.

Symptoms of Hydrocephalus in infants Abnormal enlargement of the head; soft spot (fontanel) is tense and bulging; scalp can appear thin; bones separated in baby's head; prominent scalp veins; vomiting; drowsiness; irritability; downward deviation of baby's eyes; seizures; or poor appetite.

Symptoms of Hydrocephalus in toddlers/children
Abnormal enlargement of baby's head; headache; nausea; vomiting; fever; blurred or double vision; unstable balance; irritability; sleepiness; delayed progress in walking or talking; poor coordination; change in personality; inability to concentrate; loss of sensory motor functions; seizures; or poor appetite. Older children may experience difficulty in remaining awake or waking up.

Symptoms of Hydrocephalus in young and middle-aged adults
Headache; difficulty in remaining awake or waking up; loss of coordination or balance; bladder control problems; impaired vision and cognitive skills that may affect job performance and personal skills.

Symptoms of Hydrocephalus in older adults
Loss of coordination or balance; shuffling gait, memory loss; headache; or bladder control problems. Hydrocephalus is often categorized for age groups as either congenital or normal pressure hydrocephalus. Congenital hydrocephalus refers to conditions that are caused by conditions existing at birth. Primary symptoms include headache, nausea, vomiting and drowsiness. Normal pressure hydrocephalus (NPH) is the accumulation of cerebrospinal fluid that causes the ventricles in the brain to become enlarged, with little or no increase in pressure. Adult-onset NPH mainly occurs in adults age 60 and older. Patients with NPH often get misdiagnosed with Alzheimer’s disease or dementia, as some of the symptoms mimic these two conditions.

Diagnosing Hydrocephalus

Before your doctor can recommend a course of treatment, he or she will:

  • Review your medical history, and perform a physical examination
  • Perform a complete neurological examination including diagnostic testing if needed
  • Ask specific questions to determine if symptoms are caused by hydrocephalus

The neurological examination will also help to determine the severity of your condition. Further tests such as an ultrasound (if the patient is an infant), computed tomography (CT or CAT scan), or magnetic resonance imaging (MRI) may be ordered. The tests may reveal useful information about the severity of the condition and its likely cause.

When Surgery is Necessary

Diverting FluidHydrocephalus can be treated in a variety of ways. The problem area may be treated directly (by removing the cause of CSF obstruction), or indirectly (by diverting the fluid to somewhere else; typically to another body cavity). Indirect treatment is performed by implanting a device known as a shunt to divert the excess CSF away from the brain. The body cavity in which the CSF is diverted is usually the peritoneal cavity (the area surrounding the abdominal organs).

In some cases, two procedures are performed, one to divert the CSF, and another at a later stage to remove the cause of obstruction (e.g., a brain tumor). Once inserted, the shunt system usually remains in place for the duration of a patient's life (although additional operations to revise the shunt system are sometimes needed). The shunt system continuously performs its function of diverting the CSF away from the brain, thereby keeping the intracranial pressure within normal limits.

An alternative operation called endoscopic third ventriculostomy utilizes a tiny camera to look inside the ventricles, allowing the surgeon to create a new pathway through which CSF can flow.


Your neurological function will be evaluated post surgery. If any neurological problems persist, rehabilitation may be required to further your improvement. However, recovery may be limited by the extent of the damage already caused by the hydrocephalus and by your brain's ability to heal.

Because hydrocephalus is an ongoing condition, long-term follow-up by a doctor is required. Follow-up diagnostic tests including CT scans, MRIs and x-rays, are helpful in determining if the shunt is working properly. Do not hesitate to contact your physician if you experience any of the following postoperative symptoms:

  • Redness, tenderness, pain or swelling of the skin along the length of the tube or incision
  • Irritability or drowsiness
  • Nausea, vomiting, headache or double vision
  • Fever
  • Abdominal pain
  • Return of preoperative neurological symptoms


The prognosis for hydrocephalus depends on the cause, the extent of symptoms, and the timeliness of diagnosis and treatment. Some patients show a dramatic improvement with treatment while others do not. In some instances of NPH, dementia can be reversed by shunt placement. Other symptoms such as headaches may disappear almost immediately if the symptoms are related to elevated pressure.

In general, the earlier hydrocephalus is diagnosed, the better the chance for successful treatment. The longer the symptoms have been present, the less likely it is that treatment will be successful. Unfortunately, there is no way to accurately predict how successful surgery will be for each individual. Some patients will improve dramatically while others will reach a plateau or decline after a few months.

Shunt malfunction or failure may occur. The valve can become clogged or the pressure in the shunt may not match the needs of the patient, requiring additional surgery. In the event of an infection, antibiotic therapy may be needed. A shunt malfunction may be indicated by headaches, vision problems, irritability, fatigue, personality change, loss of coordination, difficulty in waking up or staying awake, a return of walking difficulties, mild dementia or incontinence. Fortunately, most complications can be dealt with successfully.

Safe Haven Laws - No Questions Ask!

Edited From Wikipedia

Baby Safe Haven Sign

on Longwood Ave. in front of Children Hospital, Boston

Safe Haven Law

Safe Haven law, also known in some states as Baby Moses law, is the popular name for United States laws that decriminalize leaving unharmed infants with statutorily designated private persons so that the child becomes a ward of the state. "Safe Haven" laws typically let parents remain nameless to the court, often using a numbered bracelet system as the only means of linking the baby to the mother. [1] Some States treat safe haven surrenders as child dependency or abandonment, with a complaint being filed for such in juvenile court. The parent either defaults or answers the complaint. Other States treat safe haven surrenders as adoption surrenders, hence a waiver of parental rights (see parental responsibility).

Police stations, hospitals, rescue squads, and fire houses are all typical locations to which the safe haven law applies.[2]


Supporters of safe haven laws claim that the laws save lives by encouraging parents to surrender infants safely instead of aborting, killing, or discarding them. Detractors claim that, because safe haven laws do not require parents to be under stress, parents will use the law largely to avoid notice to the non-surrendering parent.

Detractors also claim that safe haven laws undercut temporary surrender laws, which were enacted specifically for parents who are unsure about whether to keep or relinquish their children. Supporters counter by arguing that anonymity is the only way to convince certain parents not to harm their infants, and that the benefit outweighs any claimed detriment.

Controversy has arisen out the safe haven law enacted in Nebraska in July 2008. The Nebraska law has been interpreted to define a child as anyone under 18,[3] and has resulted in the desertion of teenage children.[4] The law was changed in November 2008, allowing infants up to thirty-days old to be abandoned. Thirty-six children were dropped off in Nebraska hospitals in a four month span. None were infants.[5]


As of January 8, 2006, only one case had challenged the constitutionality of a safe haven law. Unable to allege personal harm, the plaintiff argued that all parents needed to know ahead of time that the State would not help parents hide children from each other. Further, because anonymity deprived a non-surrendering parent of a remedy from the outset, and could apply to any parent for any reason, the law threatened the public at large. The court dismissed the case, however, finding that the alleged harm did not rise to the level necessary to justify a public action. [6] Accordingly, the plaintiff's claim that the safe haven law violated the separation of powers doctrine by circumventing the Supreme Court's rule-making authority was not addressed.

But in late 2007, an Ohio Court of Common Pleas ruled that the entire Ohio Deserted Child Act was void for violating the Supreme Court's rule-making authority. In re Baby Boy Doe, 145 Ohio Misc.2d 1, 2007-Ohio-7244. There, the mother had left the child at the hospital, expressing an intent to leave the child there and to have the child adopted. The mother never contacted the hospital or the state agency later regarding the child. The alleged father's identity and location were not fully known. After being granted temporary custody, the state agency moved for permanent custody, as needed for adoption. The attorney and the guardian ad litem for the child challenged the constitutionality of the safe haven law, arguing that certain statutes of it violated the separation of powers doctrine under Art IV, Sec. 5(B) of the Ohio Constitution. The court agreed, finding that the safe haven laws' notice and anonymity statutes conflicted with the notice provisions of Juvenile Rule 15 and the due diligence requirements of other court rules. Juv.R. 15 required issuing summons to the parties ordering them to appear before the court. Under Juv.R. 2(Y) parents were mandated parties. Because the underlying purpose of the safe haven law was to keep parents anonymous and immune from prosecution, Juvenile Rule 15 undermined the safe haven laws' purpose. But the anonymity and notice statutes being procedural, the court rules governed. Then, because the notice and anonymity statutes could not be reconciled with the remaining safe haven statutes, the entire safe haven law was of no force and effect. The original safe haven complaint and permanent custody motion were dismissed. The case does not appear to have been appealed.[7]

Secret Safe Place for Newborns

Secret Safe Place for Newborns is a program that originated in Mobile, AL, in 1998 in response to concerns raised by reporter Jodi Brooks, then working for WPMI-TV, over a series of child abandonment stories.[8] The program was developed by John Tyson Jr., and allows new mothers to leave their newborns at emergency rooms anonymously without fear of prosecution. This program has since been adopted by over 40 states.[9]

Current status

In the spring of 2008 Nebraska and Alaska both passed their safe haven laws. Currently all 50 states have a form of Safe Haven law.[10]

John Walsh Leads Teens in Discussion of Sexting and Cyberbullying at Cox's National Summit on Internet and Wireless Safety

Monday, June 22, 2009

ATLANTA, June 22, 2009 /PRNewswire via COMTEX/ ----For the fourth consecutive year, teens from across the country will gather in Washington, D.C. for the Cox National Teen Summit on Internet and Wireless Safety held in partnership with the National Center for Missing & Exploited Children(R) (NCMEC).

As a part of Cox's Take Charge! program developed to keep kids safer online, America's Most Wanted host and children's advocate John Walsh will guide teen participants from Cox Communications' markets across the country in a discussion of Internet and wireless safety, with a focus on ways parents, guardians and teen mentors can help children be safer online, at home and on the go. Discussion topics include sexting, cyberbullying and parental controls.

Results of a new survey conducted by Cox in conjunction with NCMEC about the behavior of young people online and a recap of the summit will be presented during a virtual media conference on BlogTalkRadio. John Walsh, Harris Interactive and select teens will be available to answer questions. On June 25, the teens will deliver the news directly to Capitol Hill in meetings with members of Congress.

WHAT: Cox Communications' National Teen Summit on Internet &
Wireless Safety
WHEN: Wednesday, June 24, 2009
-- 7:00 a.m., Complete Survey Results available at
-- 9:00 a.m. Teen Summit
-- 11:00 a.m. Virtual Media Conference with John Walsh &
Harris Interactive
-- Call-In Phone Number: (646) 200- 4633
WHERE: National Cable & Telecommunications Association
25 Massachusetts Avenue, NW - Suite 100
Washington, DC 20001

Last year's key findings from the Summit include the following tips for parents/guardians:

-- Use parental controls like those available with Cox High Speed Internet
-- Proactively ask questions about what your teen is doing online and how
they are accessing the Internet.
-- Know the Internet, its popular sites and its capabilities, especially in
the social networking arena.

-- Set your conversation in a casual, non-threatening situation.

"Teens are connected online and through their cell phones. A dangerous new trend is sexting. One in five teens readily admits they participate in sexting, despite the fact that they believe it's dangerous," said John Walsh. "Knowledge is power. Parents need to arm themselves, and regularly talk with their teens in a non-confrontational manner about safe behavior with computers and wireless devices."

About Cox Communications:

Cox Communications is a multi-service broadband communications and entertainment company with 6.2 million total residential and commercial customers. The third-largest cable television company in the United States, Cox offers an array of advanced digital video, high-speed Internet and telephony services over its own nationwide IP network. Cox Business is a full-service, facilities-based provider of communications solutions for commercial customers, providing high-speed Internet, voice and long distance services, as well as data and video transport services for small to large-sized businesses. Cox Media offers national and local cable advertising in traditional spot and new media formats, along with promotional opportunities and production services. Cox Communications wholly owns and operates the Travel Channel. More information about the services of Cox Communications, a wholly owned subsidiary of Cox Enterprises, is available at,, and

About Cox's Take Charge Initiative:

Cox's Take Charge! program was launched in 2004 to educate parents and guardians about the importance of Internet safety and to help families get the most out of mass media in the home. It provides scores of resources to help parents and guardians manage what their children's' use of the TV, Internet and wireless devices -- from instructions on setting parental controls, to a guide to the lingo teens use online, to tips for more constructive conversations between parents and kids. Teaching young children and teens how to stay safer online is a major element of the Take Charge program, thanks in part to Cox's partnership with the NetSmartz(R) Workshop, NCMEC's Internet safety resource available at Cox has donated more than $30 million worth of advertising time to NetSmartz and NCMEC to encourage safer online behavior among children. More information on Take Charge! is available at and

About the National Center for Missing & Exploited Children:

The National Center for Missing & Exploited Children is a 501(c)(3) nonprofit organization. Since it was established by Congress in 1984, the organization has operated the toll-free 24-hour national missing children's hotline which has handled more than 2,377,000 calls. It has assisted law enforcement in the recovery of more than 138,500 children. The organization's CyberTipline has handled more than 699,500 reports of child sexual exploitation and its Child Victim Identification Program has reviewed and analyzed more than 23,796,800 child pornography images and videos. The organization works in cooperation with the U.S. Department of Justice's office of Juvenile Justice and Delinquency Prevention.

To learn more about NCMEC, call its toll-free, 24-hour hotline at 1-800-THE-LOST or visit its web site at

About the Survey

This survey was conducted online within the United States by Harris Interactive on behalf of Cox Communications between April 9 and 21, 2009 among 655 U.S. teens ages 13-18. No estimates of theoretical sampling error can be calculated; a full methodology is available.

SOURCE Cox Communications

Copyright (C) 2009 PR Newswire. All rights reserved

Tuesday, June 23, 2009

From Wikipedia, A Non-Disease? Fibromyalgia


Fibromyalgia (new lat., fibro-, fibrous tissue, Gk. myo-, muscle, Gk. algos-, pain), meaning muscle and connective tissue pain (also referred to as FM or FMS), is a disorder classified by the presence of chronic widespread pain and a heightened and painful response to gentle touch (tactile allodynia).[1] Other core features of the disorder include debilitating fatigue, sleep disturbance, and joint stiffness. In addition, persons affected by the disorder frequently experience a range of other symptoms that involve multiple body systems, including difficulty with swallowing,[2] functional bowel and bladder abnormalities,[3] difficulty breathing,[4] diffuse sensations of numbness and tingling (non-dermatomal paresthesia),[5] abnormal motor activity (i.e. nocturnal myoclonus, sleep bruxism),[6] and cognitive dysfunction.[7] An increased prevalence of affective and anxiety-related symptoms is also well known.[8] While the criteria for such an entity have not yet been thoroughly developed, the recognition that fibromyalgia involves more than just pain has led to the frequent use of the term "fibromyalgia syndrome".[9] Not all affected persons experience all the symptoms associated with the greater syndrome.

Fibromyalgia is considered a controversial diagnosis, with some authors contending that the disorder is a ‘non-disease’, due in part to a lack of abnormalities on physical examination, objective laboratory tests or medical imaging studies to confirm the diagnosis.[10] While historically considered either a musculoskeletal disease or neuropsychiatric condition, evidence from research conducted in the last three decades has revealed abnormalities within the central nervous system affecting brain regions that may be linked both to clinical symptoms and research phenomena.[11] Although there is as yet no generally accepted cure for fibromyalgia, there are treatments that have been demonstrated by controlled clinical trials to be effective in reducing symptoms, including medications, patient education, exercise, and behavioral interventions.[12]

* 1 Signs and symptoms
* 2 Causation hypotheses
o 2.1 Genetic predisposition
o 2.2 Stress-induced pathophysiology
o 2.3 Consequence of sleep disturbance
o 2.4 Central dopamine dysfunction (hypodopaminergia)
o 2.5 Abnormal serotonin metabolism
o 2.6 Deficient human growth hormone (HGH) secretion
o 2.7 Psychological factors
o 2.8 Other hypotheses
* 3 Pathophysiology
o 3.1 Sleep disturbances
o 3.2 Poly-modal sensitivity
o 3.3 Neuroendocrine disruption
o 3.4 Sympathetic hyperactivity
o 3.5 Cerebrospinal fluid abnormalities
o 3.6 Brain imaging studies
* 4 Diagnosis
* 5 Treatment
o 5.1 Pharmaceutical
+ 5.1.1 Analgesics
+ 5.1.2 Antidepressants
+ 5.1.3 Anti-seizure medication
+ 5.1.4 Dopamine agonists
+ 5.1.5 Insomnia
o 5.2 Investigational medications
o 5.3 Physical treatments
o 5.4 Psychological/behavioural therapies
* 6 Prognosis
* 7 Epidemiology
* 8 History
* 9 Controversies
* 10 See also
* 11 References
* 12 External links

Signs and symptoms
Common signs and symptoms of fibromyalgia.[13]

The defining symptoms of fibromyalgia are chronic, widespread pain and painful response to touch (allodynia). Other symptoms can include moderate to severe fatigue, needle-like tingling of the skin, muscle aches, prolonged muscle spasms, weakness in the limbs, nerve pain, functional bowel disturbances,[14] and chronic sleep disturbances.[15] Sleep disturbances may be related to a phenomenon called alpha-delta sleep, a condition in which deep sleep (associated with delta waves) is frequently interrupted by bursts of alpha waves, which normally occur during wakefulness. Slow-wave sleep is often dramatically reduced.[citation needed]

Many patients experience cognitive dysfunction[16] (known as "brain fog" or "fibrofog"), which may be characterized by impaired concentration,[17] problems with short[17][18] and long-term memory, short-term memory consolidation,[18] impaired speed of performance,[17][18] inability to multi-task, cognitive overload,[17][18] diminished attention span, anxiety, and depressive symptoms.[18] "Brain fog" may be directly related to the sleep disturbances experienced by sufferers of fibromyalgia.[citation needed]

Other symptoms often attributed to fibromyalgia that may possibly be due to a comorbid disorder include myofascial pain syndrome also referred to as Chronic Myofascial Pain, diffuse non-dermatomal paresthesias, functional bowel disturbances and irritable bowel syndrome (possibly linked to lower levels of ghrelin,[19] genitourinary symptoms and interstitial cystitis, dermatological disorders, headaches, myoclonic twitches, and symptomatic hypoglycemia. Although fibromyalgia is classified based on the presence of chronic widespread pain, pain may also be localized in areas such as the shoulders, neck, low back, hips, or other areas. Many sufferers also experience varying degrees of facial pain and have high rates of comorbid temporomandibular joint disorder.

Eye problems such as eye pain, sensitivity to light, blurred vision, and fluctuating visual clarity, can also be a symptom of the condition.[20] As a consequence of this, sufferers who wear glasses or contact lenses may have to change their lens prescription frequently.

Symptoms can have a slow onset, and many patients have mild symptoms beginning in childhood, that are often misdiagnosed as growing pains.[citation needed] Symptoms are often aggravated by unrelated illness or changes in the weather.[citation needed]They can become more or less tolerable throughout daily or yearly cycles; however, many people with fibromyalgia find that, at least some of the time, the condition prevents them from performing normal activities such as driving a car or walking up stairs. The disorder does not cause inflammation as is characteristic of rheumatoid arthritis, although some non-steroidal anti-inflammatory drugs may temporarily reduce pain symptoms in some patients. Their use, however, is limited, and often of little to no value in pain management.[21]

An epidemiology study consisting of an internet-based survey of 2,596 people with fibromyalgia[22] reported that the most frequently cited factors perceived to worsen fibromyalgia symptoms were emotional distress (83%), weather changes (80%), sleeping problems (79%), strenuous activity (70%), mental stress (68%), worrying (60%), car travel (57%), family conflicts (52%), physical injuries (50%) and physical inactivity (50%). Other factors included infections, allergies, lack of emotional support, perfectionism, side effects of medications, and chemical exposures.

Causation hypotheses

The cause of fibromyalgia is currently unknown. However, several hypotheses have been developed:

Genetic predisposition

There is evidence that genetic factors may play a role in the development of fibromyalgia. For example, there is a high aggregation of fibromyalgia in families.[23][24] The mode of inheritance is currently unknown, but it is most probably polygenic.[25] Research has demonstrated that fibromyalgia is associated with polymorphisms of genes in the serotoninergic,[26] dopaminergic[27] and catecholaminergic systems.[28] However, these polymorphisms are not specific for fibromyalgia and are associated with a variety of allied disorders (e.g. chronic fatigue syndrome,[29] irritable bowel syndrome[30]) and with depression.[31]

Stress-induced pathophysiology

Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia.[32] Accordingly, it has been proposed that fibromyalgia may result from stress-induced changes in the function and integrity of the hippocampus.[33] This proposition was based in part on the observation that preclinical studies in non-human primates have shown that exposure to psychosocial duress results in material changes to the very tissues of the brain, including atrophic and metabolic changes in the hippocampal complex.[34][35] Evidence in support of this hypothesis have been generated by two studies that employed single-voxel magnetic resonance spectroscopy (1H-MRS) to demonstrate metabolic abnormalities within the hippocampal complex in patients with fibromyalgia with significant correlations between hippocampal metabolic abnormalities and severity of clinical symptoms.[36][37]

Other authors have proposed that, because exposure to stressful conditions can alter the function of the hypothalamic-pituitary-adrenal (HPA) axis, the development of fibromyalgia may stem from stress-induced disruption of the HPA axis.[38] This proposition is supported in part by the observation from a prospective epidemiology study which found that variations in HPA function characterized by high levels of circulating cortisol following dexamethasone suppression testing, low levels of morning salivary cortisol and high levels of evening salivary cortisol are all associated with the development of chronic widespread pain.[39]

Consequence of sleep disturbance

Electroencephalography (EEG) studies have shown that people with fibromyalgia lack slow-wave sleep and that circumstances that interfere with stage four sleep (pain, depression, serotonin deficiency, certain medications or anxiety) may cause or worsen the condition.[40] According to the sleep disturbance hypothesis, an event such as trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder. The hypothesis supposes that stage four sleep is critical to the function of the nervous system, as it is during that stage that certain neurochemical processes in the body 'reset.' In particular, pain causes the release of the neuropeptide substance P in the spinal cord which has the effect of amplifying pain and causing nerves near the initiating ones to become more sensitive to pain. Under normal circumstances, areas around a wound become more sensitive to pain but if pain becomes chronic and body-wide this process can run out of control. The sleep disturbance hypothesis holds that deep sleep is critical to reset the substance P mechanism and prevent this out-of-control effect, and that an ongoing lack of sleep for any reason could become a source for the condition.

Central dopamine dysfunction (hypodopaminergia)

The 'dopamine hypothesis of fibromyalgia’ proposes that the central abnormality responsible for symptoms associated with fibromyalgia is a disruption of normal dopamine-related neurotransmission. Dopamine is a catecholamine neurotransmitter perhaps best known for its role in the pathology of schizophrenia, Parkinson's disease and addiction. There is also strong evidence for a role of dopamine in restless leg syndrome,[41] which is a condition found frequently in patients with fibromyalgia.[42] In addition, dopamine plays a critical role in pain perception and natural analgesia. Accordingly, musculoskeletal pain complaints are common among patients with Parkinson's disease,[43] which is characterized by drastic reductions in dopamine owing to neurodegeneration of dopamine-producing neurons, while patients with schizophrenia, which is thought to be due (in part) to hyperactivity of dopamine-producing neurons, have been shown to be relatively insensitive to pain.[44][45] Patients with restless leg syndrome have also been demonstrated to have an increased sensitivity to pain to static mechanical stimulation.[46]

As noted above, fibromyalgia has been commonly referred to as a "stress-related disorder" due to its frequent onset and worsening of symptoms in the context of stressful events.[47][48] Hence, it was proposed that fibromyalgia may represent a condition characterized by low levels of central dopamine that likely results from a combination of genetic factors and exposure to environmental stressors, including psychosocial distress, physical trauma, systemic viral infections or inflammatory disorders (e.g. rheumatoid arthritis, systemic lupus erythematosus).[49] This conclusion was based on three key observations; fibromyalgia is associated with stress, chronic exposure to stress results in a disruption of dopamine-related neurotransmission[50] and dopamine plays a critical role in modulating pain perception and central analgesia in such areas as the basal ganglia[51] including the nucleus accumbens,[52] insular cortex,[53] anterior cingulate cortex,[54] thalamus,[55] periaqueductal gray[56] and spinal cord.[57][58]

In support of the dopamine hypothesis of fibromyalgia, a reduction in dopamine synthesis has been reported by a study that used positron emission tomography (PET) and demonstrated a reduction in dopamine synthesis among fibromyalgia patients in several brain regions in which dopamine plays a role in inhibiting pain perception, including the mesencephalon, thalamus, insular cortex and anterior cingulate cortex.[59] A subsequent PET study demonstrated that, whereas healthy individuals release dopamine into the caudate nucleus and putamen during a tonic experimental pain stimulus (i.e. hypertonic saline infusion into a muscle bed),[60] fibromyalgia patients fail to release dopamine in response to pain and, in some cases, actually have a reduction in dopamine levels during painful stimulation.[61] Moreover, a substantial subset of fibromyalgia patients respond well in controlled trials to pramipexole, a dopamine agonist that selectively stimulates dopamine D2/D3 receptors and is used to treat both Parkinson's disease and restless leg syndrome.[62]

Abnormal serotonin metabolism

Serotonin is a neurotransmitter that is known to play a role in regulating sleep patterns, mood, feelings of well-being, concentration and descending inhibition of pain. Accordingly, it has been hypothesized that the pathophysiology underlying the symptoms of fibromyalgia may be a dysregulation of serotonin metabolism, which (it was proposed) may explain in part many of the symptoms associated with the disorder.[63] This hypothesis is supported by the observation of decreased serotonin metabolites in patient plasma[64] and cerebrospinal fluid.[65] However, selective serotonin reuptake inhibitors (SSRIs) have met with limited success in alleviating the symptoms of the disorder, while drugs with activity as mixed serotonin-norepinephrine reuptake inhibitors (SNRIs) have been more successful.[66] Accordingly, duloxetine (Cymbalta), a SNRI originally used to treat depression and painful diabetic neuropathy, has been demonstrated by controlled trials to relieve symptoms of some patients. It should be noted, however, that the relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate.[67] Complicating the analysis, one of the more effective types of medication for the treatment of the disorder (i.e. serotonin 5-HT3 antagonists) actually block some of the effects of serotonin.[68]

Deficient human growth hormone (HGH) secretion

An alternate hypothesis suggests that stress-induced problems in the hypothalamus may lead to reduced sleep and reduced production of human growth hormone (HGH) during slow-wave sleep. People with fibromyalgia tend to produce inadequate levels of HGH.[citation needed] Most patients with fibromyalgia with low IGF-I levels failed to secrete HGH after stimulation with clonidine and l-dopa.[citation needed] This view is supported by the fact that those hormones under the direct or indirect control of HGH, including IGF-1, cortisol, leptin and neuropeptide Y are abnormal in people with fibromyalgia,[69] In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep[70][71][72][73] though there is disagreement about the proposition.[74]

Psychological factors

There is strong evidence that major depression is associated with fibromyalgia, although the nature of the association is controversial. A comprehensive review into the relationship between fibromyalgia and major depressive disorder (MDD) found substantial similarities in neuroendocrine abnormalities, psychological characteristics, physical symptoms and treatments between fibromyalgia and MDD, but currently available findings do not support the assumption that MDD and fibromyalgia refer to the same underlying construct or can be seen as subsidiaries of one disease concept.[75] Indeed, the sensation of pain has at least two dimensions: a sensory dimension which processes the magnitude of the pain, and an affective-motivational dimension which processes the unpleasantness. Accordingly, a study that employed functional magnetic resonance imaging to evaluate brain responses to experimental pain among fibromyalgia patients found that depressive symptoms were associated with the magnitude of clinically-induced pain response specifically in areas of the brain that participate in affective pain processing, but not in areas involved in sensory processing which indicate that the amplification of the sensory dimension of pain in fibromyalgia occurs independently of mood or emotional processes.[76]

An alternative hypothesis regarding the development of fibromyalgia in relationship to psychological conflict proposes that the disorder may be a psychosomatic illness as described by John E. Sarno's writing related to "tension myositis syndrome," in which chronic pain is proposed to be a psychic diathesis of the mind's subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, and in some cases, psychotherapy are proposed as treatments.[77]

Other hypotheses

Other hypotheses have been proposed related to various toxins from the patient's environment,[78][79] viral causes such as the Epstein-Barr Virus,[80] an aberrant immune response to intestinal bacteria,[81] and erosion of the protective chemical coating around sensory nerves.[82] Still another hypothesis regarding the cause of fibromyalgia symptoms proposes that affected individuals suffer from vasomotor dysregulation resulting in sluggish or improper vascular flow.[83]


Sleep disturbances

The first objective findings associated with the disorder were reported in 1975 by Moldofsky and colleagues who reported the presence of anomalous alpha wave activity (typically associated with arousal states) on sleep electroencephalogram (EEG) during non-rapid-eye-movement sleep.[63] In fact, by disrupting stage IV sleep consistently in young, healthy subjects Moldofsky was able to reproduce a significant increase in muscle tenderness similar to that experienced by fibromyalgia but which resolved when the subjects were able to resume their normal sleep patterns.[84] Since that time a variety of other EEG sleep abnormalities have also been reported in subgroups of fibromyalgia patients.[85]

Poly-modal sensitivity

Results from studies examining responses to experimental stimulation have shown that fibromyalgia patients display sensitivity to pressure, heat, cold, electrical and chemical stimulation.[86] Experiments examining pain regulatory systems have shown that fibromyalgia patients also display a dysregulation of diffuse noxious inhibitory control,[87] an exaggerated wind-up in response to repetitive stimulation,[88] and an absence of exercise-induced analgesic response.[89] Together these results point to dysregulation of the nociceptive system at the central level.

Neuroendocrine disruption

Patients with fibromyalgia have been demonstrated to have a disruption of normal neuroendocrine function, characterized by mild hypocortisolemia,[90] hyperreactivity of pituitary adrenocorticotropin hormone release in response to challenge, and glucocorticoid feedback resistance.[91] A progressive reduction of serum growth hormone levels has also been documented—at baseline in a minority of patients, while most demonstrate reduced secretion in response to exercise or pharmacological challenge.[92] Other abnormalities include reduced responsivity of thyrotropin and thyroid hormones to thyroid-releasing hormone,[93] a mild elevation of prolactin levels with disinhibition of prolactin release in response to challenge[94] and hyposecretion of adrenal androgens.[95] These changes might be attributed to the effects of chronic stress, which, after being perceived and processed by the central nervous system, activates hypothalamic corticotrophin-releasing hormone neurons. Thus, the multiple neuroendocrine changes evident in fibromyalgia have been proposed to stem from chronic overactivity of corticotropin-releasing hormone releasing neurons, resulting in a disruption of normal function of the pituitary-adrenal axis and an increased stimulation of hypothalamic somatostatin secretion, which, in turn, inhibits the secretion of a multiplicity of other hormones.[96]

Sympathetic hyperactivity

Functional analysis of the autonomic system in patients with fibromyalgia has demonstrated disturbed activity characterized by hyperactivity of the sympathetic nervous system at baseline[97] with reduced sympathoadrenal reactivity in response to a variety of stressors including physical exertion and mental stress.[98][99] Fibromyalgia patients demonstrate lower heart rate variability, an index of sympathetic/parasympathetic balance, indicating sustained sympathetic hyperactivity, especially at night.[100] In addition, plasma levels of neuropeptide Y, which is co-localized with norepinephrine in the sympathetic nervous system, have been reported as low in patients with fibromyalgia,[101] while circulating levels of epinephrine and norepinephrine have been variously reported as low, normal and high.[102][103] Administration of interleukin-6, a cytokine capable of stimulating the release of hypothalamic corticotropin-releasing hormone which in turn stimulates activity within the sympathetic nervous system, results in a dramatic increase in circulating norepinephrine levels and a significantly greater increase in heart rate over baseline in fibromyalgia patients as compared to healthy controls.[104]

Cerebrospinal fluid abnormalities

The most reproduced laboratory finding in patients with fibromyalgia is an elevation in cerebrospinal fluid levels of substance P, a putative nociceptive neurotransmitter.[105][106][107] Metabolites for the monoamine neurotransmitters serotonin, norepinephrine, and dopamine—all of which play a role in natural analgesia—have been shown to be lower,[108] while concentrations of endogenous opioids (i.e., endorphins and enkephalins) appear to be higher.[109] The mean concentration of nerve growth factor, a substance known to participate in structural and functional plasticity of nociceptive pathways within the dorsal root ganglia and spinal cord, is elevated.[110] There is also evidence for increased excitatory amino acid release within cerebrospinal fluid, with a correlation demonstrated between levels for metabolites of glutamate and nitric oxide and clinical indices of pain.[111]

Brain imaging studies

Evidence of abnormal brain involvement in fibromyalgia has been provided via functional neuroimaging. The first findings reported were decreased blood flow within the thalamus and elements of the basal ganglia and mid-brain (i.e., pontine nucleus).[112][113] Differential activation in response to painful stimulation has also been demonstrated.[114][115] Brain centers showing hyperactivation in response to noxious stimulation include such pain-related brain centers as the primary and secondary somatosensory cortex, anterior cingulate cortex and insular cortex, while relative hypoactivation at subjectively equal pain levels appears to occur within the thalamus and basal ganglia. Patients also exhibit neural activation in brain regions associated with pain perception in response to nonpainful stimuli in such areas as the prefrontal, supplemental motor, insular, and cingulate cortices. Evidence of hippocampal disruption indicated by reduced brain metabolite ratios has been demonstrated by studies using single-voxel magnetic resonance spectroscopy (1H-MRS).[36][37] A significant negative correlation was demonstrated between abnormal metabolite ratios and a validated index of the clinical severity (i.e. the Fibromyalgia Impact Questionnaire).[116] Correlations between clinical pain severity and concentrations of the excitatory amino acid neurotransmitter glutamate within the insular cortex have also been demonstrated using 1H-MRS.[117] An acceleration of normal age-related brain atrophy has been demonstrated using voxel-based morphometry (VBM) with areas of reduced gray matter located in the cingulate cortex, insula and parahippocampal gyrus.[118] Studies utilizing positron emission tomography have demonstrated reduced dopamine synthesis in the brainstem and elements of the limbic cortex.[119] A significant negative correlation between pain severity and dopamine synthesis was demonstrated within the insular cortex. A subsequent study demonstrated gross disruption of dopaminergic reactivity in response to a tonic pain stimulus within the basal ganglia with a significant positive correlation between the defining feature of the disorder (i.e. tender point index) and dopamine D2 receptor binding potential specifically in the right putamen.[120] Finally, reduced availability of mu-opioid receptors in the ventral striatum/nucleus accumbens and cingulate cortex has been demonstrated, with a significant negative correlation between affective pain levels and receptor availability in the nucleus accumbens.[121]

The location of the nine paired tender points that comprise the 1990 American College of Rheumatology criteria for fibromyalgia.

There is still debate over what should be considered essential diagnostic criteria. The difficulty with diagnosing fibromyalgia is that, in most cases, laboratory testing appears normal and that many of the symptoms mimic those of other rheumatic conditions such as arthritis or osteoporosis. In general, most doctors diagnose patients with a process called differential diagnosis, which means that doctors consider all of the possible things that might be wrong with the patient based on the patient's symptoms, gender, age, geographic location, medical history and other factors. They then narrow down the diagnosis to the most likely one. The most widely accepted set of classification criteria for research purposes was elaborated in 1990 by the Multicenter Criteria Committee of the the American College of Rheumatology. These criteria, which are known informally as "the ACR 1990," define fibromyalgia according to the presence of the following criteria:

* A history of widespread pain lasting more than three months—affecting all four quadrants of the body, i.e., both sides, and above and below the waist.
* Tender points—there are 18 designated possible tender or trigger points (although a person with the disorder may feel pain in other areas as well). During diagnosis, four kilograms-force (39 newtons) of force is exerted at each of the 18 points; the patient must feel pain at 11 or more of these points for fibromyalgia to be considered.[122] Four kilograms of force is about the amount of pressure required to blanch the thumbnail when applying pressure.

This set of criteria was developed by the American College of Rheumatology as a means of classifying an individual as having fibromyalgia for both clinical and research purposes. While these criteria for classification of patients were originally established as inclusion criteria for research purposes and were not intended for clinical diagnosis, they have become the de facto diagnostic criteria in the clinical setting. It should be noted that the number of tender points that may be active at any one time may vary with time and circumstance.


As with many other syndromes, there is no universally accepted cure for fibromyalgia, and treatment is typically aimed at symptom management. Developments in the understanding of the pathophysiology of the disorder have led to improvements in treatment, which include prescription medication, behavioral intervention, exercise, and alternative and complementary medicine. Indeed, integrated treatment plans that incorporate medication, patient education, aerobic exercise and cognitive-behavioral therapy have been shown to be effective in alleviating pain and other fibromyalgia-related symptoms.[12] In 2005, the American Pain Society produced the first comprehensive guidelines for patient evaluation and management.[123] More recently, the European League Against Rheumatism (EULAR) issued updated treatment guidelines.[124]



A number of analgesics are used to treat the pain symptoms resulting from fibromyalgia, including nonsteroidal anti-inflammatory drugs (NSAID) and COX-2 inhibitors.[citation needed]


There is growing evidence that fibromyalgia symptoms are associated with the abnormal processing of pain in the central nervous system.[125] Dysfunction of serotonin and norepinephrine in the pain-inhibitory pathways is thought to contribute to chronic pain[citation needed], and antidepressants which increase the activity of these neurotransmitters may alleviate the pain symptoms.

A study published in JAMA on January 14 of 2009 underlined and supported the increasing body of research that antidepressants as a group are helpful in treating pain, depression, fatigue, sleep disturbances, and quality of life in individuals suffering from fibromyalgia.[126]

Tricyclic antidepressants continue to be widely prescribed for fibromyalgia, although their efficacy in treating fibromyalgic symptoms appears to be limited, with the largest improvement being in sleep quality. Tricyclics also have many side-effects due to interaction with adrenergic, cholinergic or histaminergic receptors, and sodium channels.

Recent meta-analyses show that selective serotonin reuptake inhibitors (SSRIs) and selective norepinephrine reuptake inhibitors (SNRIs) have the greatest benefit in reducing pain, with SNRIs having the most significant benefit.[citation needed] Additionally, SSRIs and SNRIs do not have the side-effects that are associated with tricyclics. A pooled meta-analysis of multiple medications showed that SSRIs had a significant symptomatic benefit that was moderate for sleep, overall well being, and pain severity[citation needed], and mild for fatigue and number of tender points[citation needed]. The results were mixed, showing that the SSRIs that had dual effects on norepinephrine and serotonin had the greatest benefit in pain reduction.

Recent research has focused on SNRIs, such as duloxetine. Although no meta-analyses are available, two placebo-controlled clinical trials have shown that duloxetine results in a significant reduction in pain compared to placebo. It was also found that the reduction in pain was independent of both comorbid depression and of any reduction in depression or anxiety. It should be noted, however, that in the first study the pain reduction was only found in women, not men, and the second study only looked at women. More research needs to be done to determine whether duloxetine has any pain reducing effect for men.[127]

Anti-seizure medication

Anti-seizure drugs are also sometimes used, such as gabapentin (Neurontin)[128] and pregabalin (Lyrica). Gabapentin is not approved or labeled for use in treatment of neuropathic pain or fibromyalgia. Pregabalin, originally labeled for the treatment of nerve pain suffered by diabetics, has been cleared by the US Food and Drug Administration for treatment of fibromyalgia.[129] A randomized controlled trial of pregabalin 450 mg/day found that 6 patients is the number needed to treat for one patient to have a 50% reduction in pain.[130]

Dopamine agonists

Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole(ReQuip) have been studied for use in the treatment of fibromyalgia with good results.[62] A trial of transdermal rotigotine is currently ongoing.[131]


As fibromyalgia sufferers often have insomnia, and insomnia is also believed to increase fibromyalgia pain, they should consider Zolpidem/Ambien CR or Zaleplon (insomnia medications seeming least disruptive to normal sleep architecture).[132] Some studies suggest these may be taken 7 to 10 days without the dependencies of other insomnia medications. If taken for longer periods then tapering of the medications are recommended to prevent the rebound of insomnia. [133]

Investigational medications

Milnacipran, a serotonin-norepinephrine reuptake inhibitor (SNRI), until recently, was only available in parts of Europe where it has been safely prescribed for other disorders. On May 22, 2007, a Phase III study demonstrated statistically significant therapeutic effects of Milnacipran as a treatment of fibromyalgia syndrome and in January 2009, the FDA approved the use of Milnacipran for chronic pain related to fibromyalgia, lupus and neuropathy.

Dextromethorphan is an over-the-counter cough medicine with activity as an NMDA receptor antagonist. It has been used in the research setting to investigate the nature of fibromyalgia pain;[134][135] however, there are no controlled trials of safety or efficacy in clinical use.

A study comprising a 3-month open trial of oral∆9-tetrahydrocannabinol(THC) in nine fibromyalgia patients reported a significant reduction in daily recorded pain and electronically induced pain in the 4 subjects who completed the study.[136] A subsequent controlled trial to evaluate the potential benefits of nabilone (a synthetic cannabinoid) in pain management and quality of life improvement in 40 patients with fibromyalgia reported significant decreases in comparison to baseline in the visual analog scale for pain (-29%), Fibromyalgia Impact Questionnaire score (-18%) and anxiety (-28%) following four weeks of therapy. No statistically significant differences were observed in any of the outcome measures in the placebo group. Patients receiving nabilone experienced more side effects, which included drowsiness (7/15), dry mouth (5/15), vertigo (4/15), and ataxia (3/15).[137] Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,[138] particularly in the treatment of cancer pain and neuropathic pain,[139][140] both of which are poorly treated by conventional opioids. As a result, some experts have suggested that cannabinoid agonists would be applicable for the treatment of chronic pain conditions unresponsive to opioid analgesics, and they propose that the disorder may be associated with an underlying clinical deficiency of the endocannabinoid system.[141]

Among the more controversial therapies involves the use of guaifenesin; called St. Amand's protocol or the guaifenesin protocol[142] the efficacy of guaifenesin in treating fibromyalgia has not been proven in properly designed research studies. Indeed, a controlled study conducted by researchers at Oregon Health Science University in Portland failed to demonstrate any benefits from this treatment,[143] and the lead researcher has suggested that the anecdotally reported benefits were due to placebo suggestion.[144] The results of the study have since been contested by Dr St. Amand, who was a co-author of the original research report.[145]

Physical treatments

Studies have found exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia.[146] Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy, massage, or acupuncture may find them beneficial.[147] Most patients find exercise, even low intensity exercise to be extremely helpful.[148] Osteopathic manipulative therapy can also temporarily relieve pain due to fibromyalgia.[149]

Psychological/behavioural therapies

Cognitive behavioural therapy has been shown to alleviate fibromyalgic symptoms, although it is not curative. The greatest benefit occurs when CBT is used along with exercise.[12][150] Self-management techniques such as pacing and stress management may also be helpful for some patients.[citation needed] Because the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic.[151] Accordingly, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.[152]


Although neither degenerative nor fatal, the chronic pain of fibromyalgia is pervasive and persistent. Most fibromyalgia patients report that their symptoms do not change over time. An evaluation of 332 consecutive new fibromyalgia patients found that, out of 15 factors, pain levels, self-assessed inability to work, psychological distress, pending litigation, helplessness, level of education, and coping ability had a significant and independent association with symptom severity and function.[153] Of those diagnosed with fibromyalgia, 10% to 30% report being work-impaired, and patients often need accommodations to fully participate in their education or remain active in their careers.[citation needed]


Fibromyalgia is seen in about 2% of the general population[154] and affects more females than males, with a ratio of 9:1 by ACR criteria.[155] It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.

[edit] History

Fibromyalgia has been studied since the early 1800s and referred to by a variety of former names, including muscular rheumatism and fibrositis.[156] The term fibromyalgia was coined in 1976 to more accurately describe the symptoms, from the Latin fibra (fiber)[157] and the Greek words myo (muscle)[158] and algos (pain).[159]

Dr. Muhammad B. Yunus, considered the father of the modern view of fibromyalgia, published the first clinical, controlled study of the characteristics of fibromyalgia syndrome in 1981.[160][161] Yunus' work validated the known symptoms and tender points that characterise the condition, and proposed data-based criteria for diagnosis. In 1984, Yunus proposed the interconnection between fibromyalgia syndrome and other similar conditions, and in 1986 demonstrated the effectiveness of serotonergic and norepinephric drugs.[162] Yunus later emphasized the "biopsychosocial perspective" of fibromyalgia, which synthesized the contributions of genes, personal and medical history, stress, posttraumatic and mood disorders, coping skills, self-efficacy of pain management and social support towards the functioning and dysfunctioning of the central nervous system in relation to pain and fatigue.[160][161]

Fibromyalgia was recognized by the American Medical Association as an illness and a cause of disability in 1987.[citation needed] In an article the same year, the Journal of the American Medical Association also called the disorder fibromyalgia.[163] The American College of Rheumatology (ACR) published criteria for fibromyalgia in 1990 and developed neurohormonal mechanisms with central sensitization in the 1990s.[162]

[edit] Controversies

Several controversial issues exist with regard to fibromyalgia that range from questions regarding the validity of the disorder as a clinical entity, to issues regarding primary pathophysiology and the potential existence of fibromyalgia sub-types. Dr. Frederick Wolfe, the lead author of the 1990 paper that first defined the classification criteria for fibromyalgia, has been since quoted as saying he has become cynical and discouraged about the diagnosis and that he now considers the condition a physical response to stress, depression, and economic and social anxiety.[164] Opponents of the fibromyalgia concept argue that fibromyalgia represents a ‘non-disease’ and that giving it a label simply legitimizes patients' sickness behavior.[10]

In contrast, findings from the London Fibromyalgia Epidemiology Study, which comprised a 36 month prospective, within-group comparison of 100 individuals identified as having fibromyalgia (72 of whom were newly diagnosed with the disorder), demonstrated that although physical functioning decreased slightly over time, there was also a statistically significant improvement in satisfaction with health, and newly diagnosed fibromyalgia cases reported fewer symptoms and major symptoms over the long term. No other differences in clinical status or health service use occurred over time.[165] The authors of the study concluded that the ‘fibromyalgia label’ does not have a meaningful adverse affect on clinical outcome over the long term. It is however possible that these results can be accounted for by Regression toward the mean.

The validity of fibromyalgia as a unique clinical entity is also a matter of some contention among researchers in the field. Contradictory findings from clinical research, compounded by differences in psychological and autonomic profiles among affected individuals, have been interpreted by different groups to indicate the existence of fibromyalgia sub-types.[166][167] There is also considerable overlap between fibromyalgia and other clinical disorders, which are frequently referred to collectively as "functional somatic syndromes" (e.g. irritable bowel syndrome, chronic fatigue syndrome).[168] Others have proposed that the clinical phenomena that fall under the label ‘fibromyalgia syndrome' might actually comprise several clinical entities, ranging from mild, idiopathic inflammatory processes in some individuals, to somatoform disorders resulting from neuropsychiatric processes in others, with probable overlaps in between.[166]