What is the difference between polymyalgia rheumatica and polymyositis

It rarely affects people under This condition is related to another inflammatory condition called giant cell arteritis. Giant cell arteritis can cause headaches, vision difficulties, jaw pain and scalp tenderness. It's possible to have both conditions together. The signs and symptoms of polymyalgia rheumatica usually occur on both sides of the body and might include:. The exact cause of polymyalgia rheumatica is unknown. Two factors appear to be involved in the development of this condition:.

Polymyalgia rheumatica and another disease known as giant cell arteritis share many similarities. Many people who have one of these diseases also have symptoms of the other. Giant cell arteritis results in inflammation in the lining of the arteries, most often the arteries in the temples. Signs and symptoms include headaches, jaw pain, vision problems and scalp tenderness.

If left untreated, this condition can lead to stroke or blindness. Symptoms of polymyalgia rheumatica can greatly affect your ability to perform everyday activities, such as:. These difficulties can affect your health, social interactions, physical activity, sleep and general well-being. Our patients tell us that the quality of their interactions, our attention to detail and the efficiency of their visits mean health care like they've never experienced. Understand the similarities and differences between polymyalgia and fibromyalgia.

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When placing the hands for manual muscle testing, it is important to take into consideration regions of joint instability or pain, areas of painful rash, thin skin and regions of calcinosis. For a complete exam, bilateral proximal and distal muscle groups should be tested e. Testing for sensory loss and testing reflexes should also be performed as these factors are usually, but not always, spared in patients with myopathy. If a patient is complaining of weakness or fatigue but has a normal MMT, this may suggest that the patient has asthenia.

However, if there is a large size differential between the patient and the examiner, the physician may not be able to pick up some changes in strength. For example, a patient that used to bench press pounds, but can now only bench press pounds would have a significant decrease in strength that may not be picked up on MMT by examiners with a smaller stature.

If the patient has true weakness on physical exam, or if the patient provides history that is convincing for true weakness, the timing of the weakness can be an important clue into the differential diagnosis. If a patient complains of weakness that is episodic as opposed to persistent, this may suggest a metabolic myopathy, transient ischemic attacks, myasthenia gravis, electrolyte abnormalities, or periodic paralysis syndromes. Most inflammatory myopathy causes persistent weakness.

In addition to diseases of muscle, weakness can be caused by disorders of upper motor neurons, lower motor neurons, and the neuromuscular junction. The pattern of weakness may give a clue as to which is affected. One-sided weakness hemiparesis is highly suggestive of upper motor neuron diseases including ischemic stroke, intracranial hemorrhage, or brain or spinal cord tumors. But, it is important to remember that upper motor neuron disease, such as ALS, can also cause weakness in either just one extremity or both arms, both legs, all four extremities.

Language or cognitive abnormalities, or cranial nerve abnormalities may be important clues to suggest upper motor neuron disease. Lower motor neuron disease may be suggested by the presence of hyporeflexia, muscle twitching fasciculations , distal more than proximal weakness, or rapid muscle atrophy. Weakness in only one extremity is usually caused by lower motor neuron disease such as with compression of a nerve root, peripheral nerve, or nerve plexus.

In these cases, the weakness may be accompanied by neuropathic pain or numbness or both. However, lower motor neuron disease, such as multiple sclerosis, can also cause weakness in both arms, both legs, or all four extremities; in these cases, the presence of lower motor neuron signs may help distinguish the etiology. Myopathy often causes persistent symmetric proximal muscle weakness, sparing the facial muscles. However, there are many exceptions. Intermittent weakness may suggest a disease of the neuromuscular junction such as myasthenia gravis — especially if the patient has facial involvement such as ptosis, diplopia or dysarthria.

Involvement of the face and scapular winging suggests facioscapulohumeral dystrophy. In an older patient, asymmetric weakness involving both proximal and distal muscles such as the finger flexors may suggest inclusion body myositis.

The physical exam can be used to confirm the presence of weakness and to establish the pattern of weakness. Just as the pattern of joints involved can give insight into the type of arthritis present, the pattern of muscle involvement can give insight into the type of underlying muscle disorder. The differential diagnosis of weakness is extensive, and the signs and symptoms of inflammatory myopathy have significant overlap with other myopathies. Therefore, there will be times when the diagnosis remains elusive despite a thorough work-up.

However, the accurate diagnosis of inflammatory myopathy is essential in order to initiate early and aggressive immunosuppressive therapy. These issues may lead to situations where patients who have non-inflammatory myopathies are treated with immunosuppressives or where patients who have inflammatory myopathies are not treated.

Usually, a careful history and physical exam combined with appropriate diagnostic testing can distinguish among the myopathies.

The following entities may be confused with idiopathic inflammatory myopathy. Hypo- and hyperthyroidism, hypo- and hyperparathyroidism, Cushing syndrome and acromegaly can all be associated with proximal muscle weakness. Of these, hypothyroidism is the most likely to cause elevated muscle enzymes. Thyroid and parathyroid abnormalities can be easily diagnosed by testing thyroid hormone levels, parathyroid hormone levels, calcium and phosphorus.

Weakness associated with Cushing syndrome and acromegaly usually occurs at a time when the other distinguishing clinical features are evident. Viruses, bacteria, and parasites all can cause inflammation of muscle. Viruses may induce diffuse weakness, myalgia, or elevated CPK. These cases are usually self-limited and associated with other signs and symptoms of infection.

Bacterial infections of muscle are often due to staphylococcus or streptococcus, are usually focal, and may be associated with abscess formation pyomyositis. Trichinosis and toxoplasma can cause a polymyositis-like illness.

These entities may be associated with elevated serum antibodies to the organisms and the organisms may be observed on muscle biopsy. Statin drugs are a frequent cause of toxic myopathy. Statin myopathy may manifest as myalgia, weakness, elevated muscle enzymes or all three. Severe cases may be associated with rhabdomyolysis. Recently, it has been reported that some patients may have an inflammatory myopathy triggered by the statin.

The myopathic effects of the statin drugs appear to be dose dependent, and exercise may worsen symptoms. When starting a statin, testing CPK is recommended only for those with myopathic symptoms at baseline, patients with renal or hepatic dysfunction or in those patients taking medications known to interact with statins.

During therapy, monitoring CPK is recommended only for those presenting with muscle symptoms. Severe symptoms should prompt discontinuation of the drug, while mild symptoms may necessitate close monitoring or lowing of the dose. In patients who have already been diagnosed with inflammatory myopathy, it is unclear whether lipid lowering agents worsen the condition, however it seems reasonable to avoid use of these agents, if possible.

Many other drugs and toxins can also cause myopathy, including fibric acid derivatives particularly when used in combination with statins , cimetidine, colchicine, hydroxychloroquine, labetalol, AZT, amiodarone, hydroxyurea, rifampin, phenytoin, corticosteroids, cocaine, heroin and ethanol.

In most cases, stopping the offending agent leads to a resolution of symptoms, but the duration that symptoms remain following withdrawal is variable and may take months. Therefore, it is important to take a detailed history of medication, alcohol and recreational drug use.

Metabolic myopathies are a large, heterogeneous group of disorders in which patients have genetic defects in the pathways of carbohydrate breakdown the muscle glycogenoses , in lipid metabolism, or in mitochondrial DNA. These defects affect the ability of skeletal muscle to use energy. The symptoms of these diseases usually begin in childhood or as a young adult but may also occur well into adulthood. The clinical features of metabolic myopathies may be indistinguishable from idiopathic inflammatory myopathy progressive, persistent, proximal muscle weakness but will often present as episodic fatigue, muscle aches or cramps following activity.

In addition, muscle enzymes may be elevated and, occasionally, rhabdomyolysis follows strenuous activity. Many other muscle glycogenoses exist although they typically do not cause proximal muscle weakness.

Disorders of lipid metabolism include primary carnitine deficiency and carnitine palmitoyltransferase deficiency. Because these entities may be inherited, patients may report a family history of muscle weakness or fatigability after exercise.

Thus, a careful family history can aide in the diagnosis. The forearm lactate-ammonia exercise test may be used to screen for some of the inborn errors of glycogen metabolism but often yields false positive results. Of note, this test does not need to be performed under ischemic conditions as it may precipitate rhabdomyolysis. Inflammation is not usually observed on MRI of involved muscle group, which can help differentiate from IIM but certainly can be present during a time of muscle injury.

Ultimately, muscle biopsy with analysis of the tissue using histochemistry, biochemistry or electron microscopy is the most useful for making the diagnosis of these entities. The muscular dystrophies are a large group of genetic disorders in which there are mutations in the genes of structural sarcolemmal proteins and glycoproteins.

Dystrophin and dysferlin are included in this protein complex, but there are many other associated proteins and glycoproteins which may be mutated and associated with disease states. These disorders include Becker muscular dystrophy, facioscapulohumeral dystrophy, limb-girdle muscular dystrophy, myotonic dystrophies, and the distal myopathies.

Although the clinical presentation may indistinguishable from inflammatory myopathy, clinical features may help distinguish between the two. Muscular dystrophies are associated with presentation in childhood or adolescence, a slowly progressive course, early muscle atrophy, involvement of the facial muscles, a family history of muscle weakness, calf atrophy or hypertrophy, and early distal muscle weakness.

In muscle biopsies, abnormal staining for the dystrophin complex can distinguish the muscular dystrophies from other forms of myopathy.

Genetic testing is also available for some of the muscular dystrophies, but it is expensive. Because inflammatory myopathy may, at times, present with muscle pain or tenderness, fibromyalgia and polymyalgia rheumatica may be confused with inflammatory myopathy.

The muscle pain and tenderness, which is characteristic of these disorders, may confound the ability to perform accurate manual muscle testing. Because, in fibromyalgia, there is no inflammation and no muscle injury, the ESR, CRP and muscle enzymes should be normal.

Although polymyalgia rheumatica is a systemic inflammatory disease and the ESR and CRP are usually elevated, muscle enzymes are normal. Diseases of the neuromuscular junction including myasthenia gravis and Eaton-Lambert syndrome result from the production of autoantibodies that interfere transmission of signal at the neuromuscular junction.

They may present as symmetric proximal muscle weakness, but weakness usually gets worse with repetitive muscle use, facial muscles may be involved, and muscle enzymes are usually normal. Testing for serum muscle enzymes is an indirect marker of muscle damage. CPK is the most commonly used, but it is not the only one that is useful. Serum CPK may not be elevated in some patients with muscle disease because of decreased muscle mass or the presence of an antibody that binds to the enzyme and interferes with detection.

In this situation, the other muscle enzymes may be useful. This has the potential to cause confusion, and lead the physician to suspect liver damage. Testing the gamma glutamyl transpeptidase GGT level, which is specific to liver, can help resolve this question and prevent an unnecessary liver biopsy in a patient with muscle disease.

This issue is of particular importance to those patients on known hepatotoxic drugs, such as methotrexate. The anti-synthetase antibodies are usually associated with either dermatomyositis or polymyositis but rarely may be found in patients with inclusion body myositis. Anti-SRP antibodies identify a syndrome of severe and rapidly progressive proximal muscle weakness, markedly elevated levels of serum CK, an association with cardiac involvement and poor response to steroid therapy.

Anti-Mi-2 antibodies are associated with dermatomyositis that responds well to therapy. EMG can differentiate neuropathic from myopathic causes of weakness in cases where the etiology is unclear. The test involves placing needle electrodes in various muscle groups and measuring the muscle potentials. Myopathies will cause characteristic abnormal potentials, but it is frequently not possible to distinguish between myopathies.

The results are operator dependent, and therefore it is important to refer to someone who is experienced with the technique. Also, the test can be quite painful, so it is a good idea to warn the patient beforehand. MRI is useful in the evaluation of inflammatory myopathy patients. In T1 weighted images, muscle normally has a low to intermediate signal grey or dark. Scarring and fatty replacement of muscle, which may be seen with in advanced inflammatory myopathy, appears bright.