Elevated sed rate and muscle weakness
by Nathan Wei, MD, FACP, FACR
Nathan Wei is a nationally known board-certified rheumatologist and author of the Second Opinion Arthritis Treatment Kit. It's available exclusively at this website... not available in stores.
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Many different diseases can cause this syndrome complex.
Information from the American College of Rheumatology
Muscle weakness and muscle achiness often go hand in hand. Myopathy refers to muscle injury and myalgia as muscle pain.
Also, with muscle weakness one must differentiate muscle weakness that is due to damage to nerves (neuropathy) and weakness that is due to muscles (myopathy).
When there is muscle weakness, a second distinction must be made. Are the muscles weak because of true damage to the muscle (myopathy) or are the muscles weak because of deconditioning?
Let’s start out with a disorder that may present with weakness and achiness.
Polymyalgia rheumatica (PMR) is a disorder that is associated with severe muscle pain and stiffness in the neck, shoulder, and hip area. Stiffness is most apparent in the morning. This disorder can develop rapidly--in some patients, overnight. In other people, polymyalgia rheumatica develops more gradually. The cause of polymyalgia rheumatica is not known. The fact that polymyalgia rheumatica is rare in people under the age of 50 suggests it may be linked to aging.
Symptoms of polymyalgia rheumatica are quickly controlled with treatment, but relapse occurs if treatment is tapered or stopped too early.
Giant cell arteritis, also known as temporal arteritis, is a disorder that stems from inflammation of arteries in the head (most often the temporal arteries, which are located on the temples on each side of the head), neck, and arms. This causes the arteries to narrow, reducing blood flow. Early treatment is critical.
It is unclear how or why polymyalgia rheumatica and giant cell arteritis are related, but approximately 15 percent of people with polymyalgia rheumatica also develop giant cell arteritis. Patients can develop giant cell arteritis either at the same time as polymyalgia rheumatica or after the polymyalgia symptoms disappear. About half of the people affected by giant cell arteritis also have polymyalgia rheumatica.
When a person is diagnosed with polymyalgia rheumatica, the doctor also should look for symptoms of giant cell arteritis because of the risk of blindness. Untreated, giant cell arteritis can lead to serious complications including permanent vision loss and stroke.
White women over the age of 50 are most at risk of developing polymyalgia rheumatica and giant cell arteritis. Women are twice as likely as men to develop the conditions. Both conditions almost exclusively affect people over the age of 50. The average age at onset is 70 years. Polymyalgia rheumatica and giant cell arteritis are common. In the United States, it is estimated that 700 per 100,000 people in the general population over 50 years of age develop polymyalgia rheumatica. An estimated 200 per 100,000 people over the age of 50 develop giant cell arteritis.
The primary symptoms of polymyalgia rheumatica are moderate to severe stiffness and muscle pain near the neck, shoulders, or hips. The stiffness is more severe in the morning or after a period of inactivity, and lasts longer than 30 minutes. People with this condition also tend to have flu-like symptoms, such as fever, weakness, and weight loss.
Early symptoms of giant cell arteritis also may resemble the flu. People experience headaches, pain in the temples, and blurred or double vision. Pain may also affect the jaw and tongue.
To diagnose the condition, a physician considers the patient's symptoms and results of laboratory tests.
The most typical laboratory finding in people with polymyalgia rheumatica is an elevated erythrocyte sedimentation rate, commonly referred to as the sed rate. This test measures how quickly red blood cells fall to the bottom of a test tube of unclotted blood. Rapidly descending cells (an elevated sed rate) indicate inflammation. Before making a diagnosis of polymyalgia rheumatica, additional tests to rule out other conditions, such as rheumatoid arthritis are usually done.
The doctor may recommend a test for rheumatoid factor (RF). People with rheumatoid arthritis are likely to have RF in their blood, but most people with polymyalgia rheumatica do not.
Severe headaches, jaw pain, and vision problems are typical symptoms of giant cell arteritis. Physical examination may reveal a temporal artery that is tender to the touch, inflamed, and has a reduced pulse. A temporal artery biopsy is recommended if there is any suspicion of giant cell arteritis.
In a person with giant cell arteritis, the biopsy will show abnormal cells in the artery walls. Some patients showing symptoms of giant cell arteritis will have negative biopsy results. In those cases a second biopsy may be needed. Some suggest biopsying both temporal arteries.
With treatment, symptoms disappear quickly, usually in 24 to 48 hours. If there is no improvement, other possible diagnoses should be considered.
The treatment of choice is prednisone. Polymyalgia rheumatica responds to a low daily dose of prednisone. Once symptoms disappear, the dosage can be reduced slowly. The amount of time that treatment is needed is different for each patient. Most patients can discontinue medication after 6 months to 2 years. If symptoms recur, prednisone treatment is required again.
Giant cell arteritis carries a risk of blindness. The blindness is permanent once it happens. A high dose of prednisone is needed to prevent blindness and should be started as soon as possible, sometimes even before the diagnosis is confirmed with a temporal artery biopsy. Symptoms quickly disappear with treatment. Typically, people with giant cell arteritis must continue taking a high dose of prednisone for several months. Once symptoms disappear and the sed rate has normalized and there is no longer a risk of blindness, the steroids can be tapered.
The duration of drug treatment differs by patient. Once treatment is discontinued, polymyalgia may recur; but once again, symptoms respond rapidly to prednisone.
Another disease that can cause elevated sed rate and muscle weakness is Sjogren’s disease. Neuromuscular manifestations occur in 10-20% of patients.
The criteria for diagnosis of Sjogren's disease would be the following:
1.Primary Sjogren's symptoms and objective signs of ocular dryness with positive Schirmer's test and positive Rose-Bengal or fluorescein staining of cornea and conjunctiva.
2.Symptoms of objective signs of dry mouth with decreased parotid flow rate and abnormal biopsy of salivary gland, with elevated rheumatoid factor and presence of anti-SSA (Ro) or anti-SSB (La).
In secondary Sjogren's syndrome, one would have signs and symptoms of Sjogren's disease plus clinical features consistent with a diagnosis of rheumatoid arthritis, systemic lupus erythematosus, polymyositis, or scleroderma. It’s important to exclude other conditions such as sarcoidosis, pre- existing lymphoma, acquired immunodeficiency disease, and other known causes of dry eyes or enlargement of the salivary glands.
Twenty-five per cent of patients with rheumatoid arthritis have Sjogren's syndrome; 50% of patients with Sjogren's have rheumatoid arthritis.
Patients with Sjogren's may have fever, fatigue, joint and muscle aches and pains, or swollen lymph nodes. Weakness is more proximal than distal. Weakness can occur in those with kidney problems and low potassium levels. Muscle biopsy may show muscle inflammation.
When Sjogren's syndrome is suspected in muscle, a sed rate and electromyography should be performed, and muscle and nerve biopsy should be considered. Muscle involvement has been reported to include myositis, muscle fiber death, and elevated muscle enzymes in the blood.
Neuropathies (damage to nerves) are characterized by numbness and tingling or burning.
Symptoms mimicking disc abnormalities with nerve root pain and weakness in a nerve root distribution can occur.
Therapy is directed towards the blood vessel inflammation (vasculitis) associated with the neurological problems. These can include corticosteroids, azathioprine, cyclophosphamide, and IVIG.
Malignancy can produce neurologic symptoms. Neurologic weakness can also be associated with malignancy. This is called paraneoplastic neuropathy. Chemotherapy can cause a drug-induced myopathy (eg. cyclosporine).
Muscle weakness can be due to muscle damage from hypothyroidism, hyperthyroidism, Cushing's disease, dermatomyositis, and polymyositis.
Damage to multiple nerves- called a polyneuropathy- may be due to rheumatoid arthritis, systemic lupus erythematosis, polyarteritis nodosa or cryoglobulinemia.
An elevated sed rate suggests polymyositis, dermatomyositis or systemic lupus erythematosis or even infection.
Lumbosacral plexopathy is an immune based problem that affects the large nerves leading from the low back to the legs.
It comes on in older patients and is characterized by pain, lower extremity weakness, and a progressive course. EMG tests show nerve damage in the legs and spinal muscles. Nerve biopsy reveals inflammatory cells around small blood vessels. An elevated sed rate is seen. Treatment consists of steroids an immune globulin.
Another cause of elevated sed rate and muscle weakness is a rare condition called microscopic polyangiitis (MPA.)
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