Habitat : Rubus canadensis is native to central and eastern Canada (from Newfoundland to Ontario) and the eastern United States (New England, the Great Lakes region, and the Appalachian Mountains.It grows on thickets, woods and clearings.
Rubus canadensis is a deciduous rhizomatous shrub forms thickets up to 2 to 3 meters (7-10 feet) tall. The leaves are alternately arranged, each measuring 10 to 20 centimeters (4-8 inches) long. The inflorescence is a cluster of up to 25 flowers. The fruit is an aggregate of many small drupes, each of which contains a tiny nutlet. The plant reproduces by seed, by sprouting up from the rhizome, and by layering. The stems can grow one meter (40 inches) in height in under two months. CLICK & SEE THE PICTURES
It is in flower in July. The flowers are hermaphrodite (have both male and female organs) and are pollinated by Apomictic.Suitable for: light (sandy), medium (loamy) and heavy (clay) soils and prefers well-drained soil. Suitable pH: acid, neutral and basic (alkaline) soils. It can grow in semi-shade (light woodland) or no shade. It prefers moist soil. Cultivation:
Easily grown in a good well-drained loamy soil in sun or semi-shade. This species is a blackberry with biennial stems, it produces a number of new stems each year from the perennial rootstock, these stems fruit in their second year and then die. The stems are free from prickles. The plant produces apomictic flowers, these produce fruit and viable seed without fertilization, each seedling is a genetic copy of the parent. Plants in this genus are notably susceptible to honey fungus. Propagation:
Seed – requires stratification and is best sown in early autumn in a cold frame. Stored seed requires one month stratification at about 3°c and is best sown as early as possible in the year. Prick out the seedlings when they are large enough to handle and grow on in a cold frame. Plant them out into their permanent positions in late spring of the following year. Cuttings of half-ripe wood, July/August in a frame. Tip layering in July. Plant out in autumn. Division in early spring or just before leaf-fall in the autumn.
Fruit – raw or cooked in pies, jams etc. Sweet, juicy and richly flavoured, it is generally preferred to most other species of blackberries. The fruit can be pressed into cakes and then dried for later use. The fruit can be up to 25mm long. Medicinal Uses:
The stems and the fruit have been used in the treatment of dysentery. A decoction of the root has been used in the treatment of dysentery.
Other Uses:…Dye…..A purple to dull blue dye is obtained from the fruit.
Disclaimer : The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplement, it is always advisable to consult with your own health care provider.
Inflammation is the response of body tissues to injury or irritation; characterized by pain, swelling, redness and heat. Kinesiology is the science of human movement and it focuses on how the body functions and moves.
Belly fat is particularly dangerous because it produces inflammatory molecules that enter the bloodstream and increase the risk of heart disease and diabetes, he said.
Woods and his colleagues examined the effects of diet and exercise on the inflammation of visceral or belly fat tissue in mice. A high-fat diet was first used to induce obesity in the animals.
After six weeks, mice were assigned to either a sedentary group, an exercise group, a low-fat diet group, or a group that combined a low-fat diet with exercise for six or twelve weeks so the scientists could compare the effects in both the short and long term, said an Illinois release.
“The surprise was that the combination of diet and exercise didn’t yield dramatically different and better results than diet or exercise alone,” said Vicki Vieira, study co-author.
Woods said that it is a promising finding. “The benefits of exercise were apparent even if the animals were still eating a high-fat diet. That tells me that exercise could decrease or prevent these life-threatening diseases by reducing inflammation even when obesity is still present.”
“The good news is that this was a very modest exercise programme. The mice ran on a treadmill only about one-fourth of a mile five days a week. For humans, that would probably translate into walking 30 to 45 minutes a day five days a week,” he noted.
Definition: Pseudogout is a form of arthritis that occurs when a particular type of calcium crystal accumulates in the joints. As more of these crystals are deposited in the affected joint, they can cause a reaction that leads to severe pain and swelling. The swelling can be either short-term or long-term and occurs most frequently in the knee, although it can also affect the wrist, shoulder, ankle, elbow, or hand. The pain caused by pseudogout is sometimes so excruciating that it can incapacitate someone for days.
It is a type of arthritis that, as the name implies, can cause symptoms similar to gout, but in reaction to a different type of crystal deposit.
As its name suggests, the symptoms of pseudogout are similar to those of gout (see “Gout“). Pseudogout can also resemble osteoarthritis or rheumatoid arthritis. A correct diagnosis is vital, as untreated pseudogout can lead to joint degeneration and osteoarthritis. Pseudogout is most common in the elderly, occurring in about 3% of people in their 60s and as many as half of people in their 90s.
The cause of this condition is unknown. Because risk increases significantly with age, it is possible that the physical and chemical changes that accompany aging increase susceptibility to pseudogout.
Pseudogout develops when deposits of calcium pyrophosphate crystals accumulate in a joint. Crystals deposit first in the cartilage and can damage the cartilage. The crystals also can cause a reaction with inflammation that leads to joint pain and swelling. In most cases it is not known why the crystals form, although crystal deposits clearly increase with age. Because the condition sometimes runs in families, genetic factors are suspected of contributing to the disorder as can a severely underactive thyroid (hypothyroidism), excess iron storage (hemochromatosis), low magnesium levels in blood, an overactive parathyroid gland, and other causes of excessive calcium in the blood (hypercalcemia).
Pseudogout also can be triggered by joint injury, such as joint surgery or a sprain, or the stress of a medical illness. If the underlying condition causing pseudogout can be identified and treated, it may be possible to prevent future attacks. Frequently, however, there is no identifiable trigger; in those cases there is no way to prevent pseudogout from recurring.
Who gets pseudogou
The calcium crystal deposits seen in pseudogout affect about 3 percent of people in their 60s and as many as 50 percent of people in their 90s. Any kind of insult to the joint can trigger the release of the calcium crystals, inducing a painful inflammatory response. Attacks of pseudogout also can develop following joint surgery or other surgery. However, not everyone will experience severe attacks.
Symptoms: * pain, swelling, and stiffness around a single joint
* occasionally, more then one joint affected at a time
* fever, usually low-grade
It may be difficult to diagnose pseudogout because it shares so many symptoms with gout, infection, and other causes of joint inflammation. In fact, pseudogout often occurs in people with other joint problems, such as osteoarthritis. Therefore, even when pseudogout is correctly identified, it is important to investigate whether there are other conditions present as well.
Diagnosis is to be done on the basis of symptoms and medical tests. The physician will use a needle to take fluid from a swollen or painful joint to determine whether calcium pyrophosphate crystals are present.This is done with a needle, after applying a numbing medication to the joint.This joint fluid is then analyzed for evidence of calcium crystals, inflammation, or infection. Your doctor may also order tests for other conditions that can trigger pseudogout, including tests of calcium and thyroid function.
An X-ray of the joint may be taken to determine whether calcium-containing deposits are present, creating a condition known as chondrocalcinosis. Other potential causes of symptoms, such as gout, rheumatoid arthritis, or infection, must be ruled out. Pseudogout often is present in people who have osteoarthritis.
To combat joint pain and swelling, your doctor may prescribe NSAIDs such as indomethacin and naproxen, or may give you glucocorticoid injections to keep the swelling down (see “Corticosteroid injections”). Your doctor may also remove fluid from the inflamed joint, a procedure called aspiration, as this may help to ease the pressure and inflammation.
The combination of joint aspiration and medication usually eliminates symptoms within a few days, although the doctor may also recommend treatment with oral corticosteroids over a short period of time. Daily use of a low-dose NSAID or colchicine, a medicine that is also used in the treatment of gout, may help to prevent further attacks. Unfortunately, there is no treatment available that can dissolve the calcium crystal deposits, although the joint degeneration that often goes along with pseudogout may be slowed by treatments that decrease joint swelling. Occasionally, people with recurrent or chronic pseudogout may develop osteoarthritis. In this case, surgery (such as joint replacement) may be the only effective treatment.
It is not known how to prevent pseudogout. If the condition has developed because of some other medical conditions, such as hemochromatosis (too much iron stored in the body), or parathyroid problems, treatment of that condition may prevent progression of other features of that potentially dangerous illness and may, in some cases, slow the development of pseudogout.
Points to Remember:
When a patient complains of joint pain, physicians often do not consider pseudogout because it can be confused with gout and other types of arthritis. Diagnosis is confirmed by microscopic identification of calcium pyrophosphate crystals. Anti-inflammatory agents can help lessen symptoms but there is currently no way to eliminate the crystals themselves.
The rheumatologist’s role in the treatment of pseudogout
Rheumatologists are actively engaged in research into the causes of pseudogout to better prevent and treat this form of arthritis. Because people with pseudogout tend to be older and more susceptible to side effects from anti-inflammatory medications, they benefit from seeing rheumatologists, who offer valuable expertise in using such drugs.
Rheumatologists are experts at diagnosing pseudogout and direct a team approach to the chronic, degenerative consequences of crystal deposits. This is important because the patient may need advice about surgery or may require additional information and support from physical and occupational therapists and nurses.
To find a rheumatologist
For a listing of rheumatologists in your area, click here.
For more information
The American College of Rheumatology has compiled this list to give you a starting point for your own additional research. The ACR does not endorse or maintain these Web sites, and is not responsible for any information or claims provided on them. It is always best to talk with your rheumatologist for more information and before making any decisions about your care.
National Institute of Arthritis and Musculoskeletal and Skin Diseases Information Clearinghouse www.niams.nih.gov
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.
Fibromyalgia is a chronic condition characterized by widespread pain in your muscles, ligaments and tendons, as well as fatigue and multiple tender points — places on body where slight pressure causes pain. Fibromyalgia is more common in women than in men. Previously, fibromyalgia was known by other names such as fibrositis, chronic muscle pain syndrome, psychogenic rheumatism and tension myalgias.
It is a disorder classified by the presence of chronic widespread pain and tactile allodynia. 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”. It is not contagious, and recent studies suggest that people with fibromyalgia may be genetically predisposed. The disorder is not directly life-threatening. The degree of symptoms may vary greatly from day to day with periods of flares (severe worsening of symptoms) or remission; however, the disorder is generally perceived as non-progressive.
Although the intensity of symptoms may vary, they’ll probably never disappear completely. It may be reassuring to know, however, that fibromyalgia isn’t progressive or life-threatening. Treatments and self-care steps can improve fibromyalgia symptoms and general health.
Incidence: It affects more females than males, with a ratio of 9:1 by American College of Rheumatology (ACR) criteria. Fibromyalgia is seen in about 2% of the general population. It is most commonly diagnosed in individuals between the ages of 20 and 50, though onset can occur in childhood.
Signs and symptoms:-
The defining symptoms of fibromyalgia are chronic, widespread pain and tenderness to light touch. There is also typically moderate to severe fatigue. Those affected may also experience heightened sensitivity of the skin (also called allodynia), tingling of the skin (often needle-like), achiness in the muscle tissues, prolonged muscle spasms, weakness in the limbs, and nerve pain. Chronic sleep disturbances are also characteristic of fibromyalgia. Indeed, studies suggest that sleep disturbances are related to a phenomenon called alpha-delta sleep, a condition in which deep sleep (associated with delta EEG waves) is frequently interrupted by bursts of brain activity similar to wakefulness (i.e. alpha waves). Deeper stages of sleep (stages 3 & 4) are often dramatically reduced.
click & see Eighteen sites (nine pairs) or tender points seen in patients with fybromyalgia
.Signs and symptoms of fibromyalgia can vary, depending on the weather, stress, physical activity or even the time of day. Common signs and symptoms include:
* Widespread pain. Fibromyalgia is characterized by pain in specific areas of your body when pressure is applied, including the back of your head, upper back and neck, upper chest, elbows, hips and knees. The pain generally persists for months at a time and is often accompanied by stiffness.
* Fatigue and sleep disturbances. People with fibromyalgia often wake up tired and unrefreshed even though they seem to get plenty of sleep. Some studies suggest that this sleep problem is the result of a sleep disorder called alpha wave interrupted sleep pattern, a condition in which deep sleep is frequently interrupted by bursts of brain activity similar to wakefulness. So people with fibromyalgia miss the deep restorative stage of sleep. Nighttime muscle spasms in your legs and restless legs syndrome also may be associated with fibromyalgia.
* Irritable bowel syndrome (IBS). The constipation, diarrhea, abdominal pain and bloating associated with IBS are common in people with fibromyalgia.
* Headaches and facial pain. Many people who have fibromyalgia also have headaches and facial pain that may be related to tenderness or stiffness in their neck and shoulders. Temporomandibular joint (TMJ) dysfunction, which affects the jaw joints and surrounding muscles, also is common in people with fibromyalgia.
* Heightened sensitivity. It’s common for people with fibromyalgia to report being sensitive to odors, noises, bright lights and touch.
* Numbness or tingling sensations in the hands and feet (paresthesia)
* Difficulty concentrating
* Mood changes
* Chest pain
* Dry eyes, skin and mouth
* Painful menstrual periods
The cause of fibromyalgia is unknown. Fibromyalgia can, but does not always, start as a result of some trauma such as a traffic accident, major surgery, or disease. Some evidence shows that Lyme Disease may be a trigger of fibromyalgia symptoms. Another study suggests that more than one clinical entity may be involved, ranging from a mild, idiopathic inflammatory process to clinical depression Genetics
By using self-reported “Chronic Widespread Pain” (CWP) as a surrogate marker for fibromyalgia, the Swedish Twin Registry found that a modest genetic contribution may exist:
* Monozygotic twins with CWP have a 15% chance that their twin sibling has CWP
* Dizygotic twins with CWP have a 7% chance that their twin sibling has CWP
Studies have shown that stress is a significant precipitating factor in the development of fibromyalgia, and that PTSD is linked with fibromyalgia.The Amital study found that 49% of PTSD patients fulfilled the criteria for FMS, compared with none of the controls.
A non-mainstream hypothesis that fibromyalgia may be a psychosomatic illness has been described by John E. Sarno’s “tension myositis syndrome”. He believes many cases of chronic pain result from changes in the body caused by the mind’s subconscious strategy of distracting painful or dangerous emotions. Education, attitude change, and, in some cases, psychotherapy are treatments proposed to stop the brain from using that strategy. Dopamine abnormality
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 , which is a common co-morbid condition in patients with fibromyalgia. 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 , 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. Interestingly, patients with restless legs syndrome have also been demonstrated to have hyperalgesia to static mechanical stimulation.
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. It was therefore 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). This conclusion was based on three key observations: (1) fibromyalgia is associated with stress; (2) chronic exposure to stress results in a disruption of dopamine-related neurotransmission; and (3) dopamine plays a critical role in modulating pain perception and central analgesia in such areas as the basal ganglia including the nucleus accumbens, insular cortex, anterior cingulate cortex, thalamus, periaqueductal gray, and spinal cord.
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.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), fibromyalgia patients fail to release dopamine in response to pain and, in some cases, actually have a reduction in dopamine levels during painful stimulation. 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 legs syndrome. Trials of other dopamine agonists are currently ongoing. Serotonin
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 may explain (in part) many of the symptoms associated with the disorder. This hypothesis is derived in part by the observation of decreased serotonin metabolites in patient plasma and cerebrospinal fluid. 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. 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. Eli Lilly and Company, the manufacturer of duloxetine has submitted a supplementary new drug application (sNDA) to the FDA for approval of it use in the treatment of FM. The relevance of dysregulated serotonin metabolism to the pathophysiology is a matter of debate. Ironically, 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.
Electroencephalography studies have shown that people with fibromyalgia lack slow-wave sleep and circumstances that interfere with stage four sleep (pain, depression, serotonin deficiency, certain medications or anxiety) may cause or worsen the condition. According to the sleep disturbance hypothesis, an event such as a trauma or illness causes sleep disturbance and possibly initial chronic pain that may initiate the disorder. The hypothesis supposes that stage 4 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 to 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.
The sleep disturbance/substance P hypothesis could explain “tender points” that are characteristic of fibromyalgia but which are otherwise enigmatic, since their positions don’t correspond to any particular set of nerve junctions or other obvious body structures. The hypothesis proposes that these locations are more sensitive because the sensory nerves that serve them are positioned in the spinal cord to be most strongly affected by substance P. This hypothesis could also explain some of more general neurological features of fibromyalgia, since substance P is active in many other areas of the nervous system. The sleep disturbance hypothesis could also provide a possible connection between fibromyalgia, chronic fatigue syndrome (CFS) and post-polio syndrome through damage to the ascending reticular activating system of the reticular formation. This area of the brain, in addition to apparently controlling the sensation of fatigue, is known to control sleep behaviors and is also believed to produce some neuropeptides, and thus injury or imbalance in this area could cause both CFS and sleep-related fibromyalgia.
Critics of the hypothesis argue that it does not explain slow-onset fibromyalgia, fibromyalgia present without tender points, or patients without heightened pain symptoms, and a number of the non-pain symptoms present in the disorder.
Human growth hormone
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. Most patients with FM with low IGF-I levels failed to secrete HGH after stimulation with clonidine and l-dopa.
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, In addition, treatment with exogenous HGH or growth hormone secretagogue reduces fibromyalgia related pain and restores slow wave sleep though there is disagreement about the proposition. Deposition disease
The ‘deposition hypothesis of fibromyaglia’ posits fibromyalgia is due to intracellular phosphate and calcium accumulations that eventually reaches levels sufficient to impede the ATP process, possibly caused by a kidney defect or missing enzyme that prevents the removal of excess phosphates from the blood stream. Accordingly, proponents of this hypothesis suggest that fibromyalgia may be an inherited disorder, and that phosphate build-up in cells is gradual but can be accelerated by trauma or illness. Calcium is required for the excess phosphate to enter the cells.The additional phosphate slows down the ATP process; however the excess calcium prods the cell to continue producing ATP.
Diagnosis is made with a specialized technique called mapping, a gentle palpitation of the muscles to detect lumps and areas of spasm thought to be caused by an excess of calcium in the cytosol of the cells. The mapping technique is notably different from the manual tenderpoint examination upon which a diagnosis of fibromyalgia depends and is purportedly different from the detection of trigger points that characterize the myofascial pain syndrome.
While this hypothesis does not identify the causative mechanism in the kidneys, it proposes a treatment known as guaifenesin therapy. This treatment involves administering the drug guaifenesin to a patient’s individual dosage, avoiding salicylic acid in medications or on the skin. Often products for salicylate sensitivity are very helpful. If the patient is also hypoglycemic, a diet is designed to keep insulin levels low.
The phosphate build-up hypothesis explains many of the symptoms present in fibromyalgia and proposes an underlying cause. The guaifenesin treatment, based on this hypothesis, has received mixed reviews, with some practitioners claiming many near-universal successes and others reporting no success. Of note, guaifenesin is also a central acting muscle relaxant used in veterinary anaesthesia that is structurally related to methocarbamol, a property that might explain its utility in some fibromyalgia patients. A controlled trial of guaifenesin for the treatment of fibromyalgia demonstrated no evidence for efficacy of this medication. However, this study has been criticized by the chief proponent of the deposition hypothesis for not limiting salicylic acid exposure in patients, and for studying the effectiveness of only guaifenesin, not the entire treatment method.As of 2005, further studies to test the protocol’s effectiveness are in the planning stages, with funding for independent studies largely collected from groups which advocate the hypothesis. It should be noted that nothing in the scientific literature supports the proposition that fibromyalgia patients have excessive levels of phosphate in their tissues.
Other hypotheses have been proposed related to various toxins from the patient’s environment, viral causes such as the Epstein-Barr Virus, growth hormone deficiencies possibly related to an underlying (maybe autoimmune) disease affecting the hypothalamus gland, an aberrant immune response to intestinal bacteria, neurotransmitter disruptions in the central nervous system, and erosion of the protective chemical coating around sensory nerves. A 2001 study suggested an increase in fibromyalgia among women with extracapsular silicone gel leakage, compared to women whose implants were not broken or leaking outside the capsule. This association has not repeated in a number of related studies, and the US-FDA concluded “the weight of the epidemiological evidence published in the literature does not support an association between fibromyalgia and breast implants.” Due to the multi-systemic nature of illnesses such as fibromyalgia and chronic fatigue syndrome (CFS/ME), an emerging branch of medical science called psychoneuroimmunology (PNI) is looking into how the various hypotheses fit together.
Another hypothesis on the cause of symptoms in fibromyalgia states that patients suffer from vasomotor dysregulation causing improper vascularflow and hypoperfusion (decreased blood flow to a given tissue or organ).
Always a comorbid disease?
Cutting across several of the above hypotheses is the proposition that fibromyalgia is almost always a comorbid disorder, occurring in combination with some other disorder that likely served to “trigger” the fibromyalgia in the first place. Two possible triggers are gluten sensitivity and/or irritable bowel. Irritable bowel is found at high frequency in fibromyalgia, and a large coeliac support group survey of adult celiacs revealed that 7% had fibromyalgia and also has a co-occurrence with chronic fatique.
According to this hypothesis, some other disorder (or trauma) occurs first, and fibromyalgia follows as a result. In some cases, the original disorder abates on its own or is separately treated and cured, but the fibromyalgia remains. This is especially apparent when fibromyalgia seems triggered by major surgery. In other cases the two disorders coexist.
Risk factors for fibromyalgia include:
* Your sex. Fibromyalgia occurs more often in women than in men.
* Age. Fibromyalgia tends to develop during early and middle adulthood. But it can also occur in children and older adults.
* Disturbed sleep patterns. It’s unclear whether sleeping difficulties are a cause or a result of fibromyalgia — but people with sleep disorders, such as nighttime muscle spasms in the legs, restless legs syndrome or sleep apnea, can also develop fibromyalgia.
* Family history. You may be more likely to develop fibromyalgia if a relative also has the condition.
* Rheumatic disease. If you have a rheumatic disease, such as rheumatoid arthritis, lupus or ankylosing spondylitis, you may be more likely to have fibromyalgia.
As with many other syndromes, there is no universally accepted cure for fibromyalgia, though some physicians claim to have found cures.However, a steady interest in the disorder on the part of academic researchers as well as pharmaceutical interests has led to improvements in its treatment, which ranges from symptomatic prescription medication to alternative and complementary medicine.
The European League Against Rheumatism (EULAR) issued the first guidelines for the treatment of fibromyalgia syndrome (FMS) and published them in the September 17th On-line First issue of the Annals of the Rheumatic Diseases.
Many medications are used to treat specific symptoms of fibromyalgia, such as muscle pain and insomnia.
A number of pain relievers have been prescribed for fibromyalgia. This includes NSAID medications over the counter, COX-2 inhibitors, and tramadol in prescription form for more advanced cases. Recently, pregabalin (marketed as Lyrica) has been given FDA approval for the treatment of diagnosed Fibromyalgia.
Muscle relaxants, such as cyclobenzaprine (Flexeril) or tizanidine (Zanaflex), may be used to treat the muscle pain associated with the disorder.
Tricyclic antidepressants (TCAs)
Traditionally, low doses of sedating antidepressants (e.g. amitriptyline and trazodone) have been used to reduce the sleep disturbances that are associated with fibromyalgia and are believed by some practitioners to alleviate the symptoms of the disorder. Because depression often accompanies chronic illness, these antidepressants may provide additional benefits to patients suffering from depression. Amitriptyline is often favoured as it can also have the effect of providing relief from neuralgenic or neuropathic pain. It is to be noted that Fibromyalgia is not considered a depressive disorder; antidepressants are used for their sedating effect to aid in sleep.
Selective serotonin reuptake inhibitors (SSRIs)
Research data consistently contradict the utility of agents with specificity as serotonin reuptake inhibitors for the treatment of core symptoms of fibromyalgia. Moreover, SSRIs are known to aggravate many of the comorbidities that commonly affect patients with fibromyalgia including restless legs syndrome and sleep bruxism.
Anti-seizure drugs are also sometimes used, such as gabapentin and pregabalin (Lyrica). Pregabalin, originally used for the nerve pain suffered by diabetics, has been approved by the American Food and Drug Administration for treatment of fibromyalgia. A randomized controlled trial of pregabalin 450 mg/day found that a number needed to treat of 6 patients for one patient to have 50% reduction in pain.
Dopamine agonists (e.g. pramipexole (Mirapex) and ropinirole(ReQuip)) have been studied for use in the treatment of fibromyalgia with good results. A trial of transdermal rotigotine is currently on going .
A controlled clinical trial of amitriptyline and fluoxetine demonstrated utility when used in combination.
Central Nervous System (CNS) Stimulants
Cognitive dysfunction in fibromyalgia, often referred to as “brain fog,” may be treated with low doses of central nervous system (CNS) stimulants such as Modafinil, Adderall, Provigil, Methylphenidate (Ritalin, Ritalin SR, Methylin, Methylin ER.) These non-amphetamine stimulants are also used to treat the chronic fatigue that is characteristic of fibromyalgia.
Stimulants may be habit forming and can have other serious side effects, so it is important to note that other treatments may be effective. Care should be taken with any prescription, as people with fibromyalgia are known to be sensitive to medications.
Cannabis and cannabinoids
Fibromyalgia patients frequently self-report using cannabis therapeutically to treat symptoms of the disorder. Writing in the July 2006 issue of the journal Current Medical Research and Opinion, investigators at Germany’s University of Heidelberg evaluated the analgesic effects of oral THC (?9-tetrahydrocannabinol) in nine patients with fibromyalgia over a 3-month period. Subjects in the trial were administered daily doses of 2.5 to 15 mg of THC, but received no other pain medication during the trial. Among those participants who completed the trial, all reported a significant reduction in daily recorded pain and electronically induced pain.Previous clinical and preclinical trials have shown that both naturally occurring and endogenous cannabinoids hold analgesic qualities,particularly in the treatment of cancer pain and neuropathic pain, 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 such as fibromyalgia, and they propose that the disorder may be associated with an underlying clinical deficiency of the endocannabinoid system.
Users of Epsom Salts in the gel form (Magnesium Sulfate), have reported significant and lasting relief from pain associated with fibromyalgia. Epsom Salts have long been touted for their ability to reduce pain and swelling.
Studies have found exercise improves fitness and sleep and may reduce pain and fatigue in some people with fibromyalgia. Many patients find temporary relief by applying heat to painful areas. Those with access to physical therapy, massage, or acupuncture may find them beneficial. Most patients find exercise, even low intensity exercise to be extremely helpful. Osteopathic manipulative therapy can also temporarily relieve pain due to fibromyalgia.
A holistic approach—including managing diet, sleep, stress, activity, and pain—is used by many patients. Dietary supplements, massage, chiropractic care, managing blood sugar levels, and avoiding known triggers when possible means living as well as it is in the patient’s power to do.
As the nature of fibromyalgia is not well understood, some physicians believe that it may be psychosomatic or psychogenic.Although there is no universally accepted cure, some doctors have claimed to have successfully treated fibromyalgia when a psychological cause is accepted.
Cognitive behavioral therapy has been shown to improve quality of life and coping in fibromyalgia patients and other sufferers of chronic pain. Neurofeedback has also shown to provide temporary and long-term relief.
Biofeedback and self-management techniques such as pacing and stress management may be helpful for some patients. The use of medication to improve sleep helps some patients, as does supplementation with folic acid and ginkgo biloba.
In a 2001 review of four case studies, symptom alleviation was found by minimizing consumption of monosodium glutamate.
Milnacipran, a serotonin-norepinephrine reuptake inhibitor (SNRI), is available in parts of Europe where it has been safely prescribed for other disorders. On May 22nd, 2007, a Phase III study demonstrated statistically significant therapeutic effects of Milnacipran as a treatment of fibromyalgia syndrome. At this time, only initial top-line results are available and further analyses will be completed in the coming weeks. If ultimately approved by the FDA, Milnacipran could be distributed in the United States as early as summer, 2008.
Among the more controversial therapies involves the use of guaifenesin; called St. Amand’s protocol or the guaifenesin protocol 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, and the lead researcher has suggested that the annecdotaly reported benefits where due to placebo suggestion. The results of the study have since been contested by Dr St. Amand, who was a co-author or the original research report.
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; however, there are no controlled trials of safety or efficacy in clinical use.
Living with fibromyalgia:-
Fibromyalgia can affect every aspect of a person’s life. While neither degenerative nor fatal, the chronic pain associated with fibromyalgia is pervasive and persistent. FMS can severely curtail social activity and recreation, and as many as 30% of those diagnosed with fibromyalgia are unable to maintain full-time employment. Like others with disabilities, individuals with FMS often need accommodations to fully participate in their education or remain active in their careers.
In the United States, those who are unable to maintain a full-time job due to the condition may apply for Social Security Disability benefits. Although fibromyalgia has been recognized as a genuine, severe medical condition by the government, applicants are often denied benefits, since there are no formal diagnostic criteria or medically provable symptoms. Because of this, if an applicant does have a medically verifiable condition that would justify disability benefits in addition to fibromyalgia, it is recommended that they not list fibromyalgia in their claim. However, most are awarded benefits at the judicial level; the entire process often takes two to four years.
In the United Kingdom, the Department for Work and Pensions recognizes fibromyalgia as a condition for the purpose of claiming benefits and assistanc.
Fibromyalgia is often referred to as an “invisible” illness or disability due to the fact that generally there are no outward indications of the illness or its resulting disabilities. The invisible nature of the illness, as well as its relative rarity and the lack of understanding about its pathology, often has psychosocial complications for those that have the disorder. Individuals suffering from invisible illnesses in general often face disbelief or accusations of malingering or laziness from others that are unfamiliar with the disorder.
There are a variety of support groups on the Web that cater to fibromyalgia sufferers.
The validity of fibromyalgia as a unique clinical entity is a matter of some contention among researchers in the field. For example, it has been proposed that the pathophysiology responsible for the symptoms that are collectively classified as representing “fibromyalgia” is poorly understood, thereby suggesting that the fibromyalgia phenotype which is the difference between an individual’s heredity and what that heredity produces, may result from several different disease processes that have global hyperalgesia – an increased sensitivity to pain – and allodynia in common, an observation that has led to the proposition that current diagnostic criteria are insufficient to differentiate patient groups from each other. Alternatively, there is evidence for the existence of differing pathophysiological – which is the study of the disturbance of normal mechanical, physical, and biochemical functions of the body – within the greater fibromyalgia construct[, which may be interpreted to represent evidence for the existence of biologically distinct “sub-types” of the disorder akin to conditions such as epilepsy, schizophrenia and major depressive disorder. In a January 14, 2008 article in the New York Times, the controversy of the reality of the disease and its proposed cures are discussed, while citing that the American College of Rheumatology, the Food and Drug Administration and insurers recognize fibromyalgia as a diagnosable disease. Drug companies are aggressively pursuing fibromyalgia treatments, seeing the potential for a major new market.
Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose
A three-year study of nearly 500 participants was the first to compare two treatment targets for LDL (“bad”) cholesterol and systolic blood pressure levels in people with diabetes.
To assess the impact of treatments on the participants’ cardiovascular health, researchers used ultrasound to measure the thickness of their carotid (neck) arteries. Ultrasound was also used to measure the size and function of the left ventricle, which is the heart’s main pumping chamber. Among participants who were given aggressive treatment, carotid artery thickness measurements were significantly lower.