Why Myositis is hard to diagnose

According to the Sydney Medical School - The University of Sydney - all of these conditions have proximal muscle weakness which may be why it took so long to diagnose me with polymyositis:

*Denervating conditions: spinal muscular atrophies, amyotrophic lateral sclerosis
*Neuromuscular junction disorder: Eaton-Lambert syndrome, myasthenia gravis
*The genetic muscular dystophies: Duchenne's fascioscapulohumeral, limb girdle, Becker's, Emery-Dreifuss type, distal, ocular
*Myotonic diseases: dystrophia myotonica, myotonia congenita
*Congenital myopathies: nemaline, mitoctondrial, centronuclear, central core
*Glycogen storage diseases: adult onset acid maltase deficiency, McArdle's disease
*Lipid storage myopathies: carnitine deficiency, carnitine palmityltransferase deficiency
*The periodic paralyses
*Myositis ossificans: generalized and local
*Endocrine myopathies: hypothyroidism, hyperthyroidism, acromegaly, Cushing's disease, Addison's disease, hyperparathyroidism, hypoparathyroidism, vitamin D deficiency myopathy, hypokalemia, hypocalcemia
*Metabolic myopathies: uremia, hepatic failure
Toxic myopathies: acute and chronic alcoholism, drugs including penicillamine, clofibrate, chloroquine, emetine
*Nutritional myopathies: vitamin E deficiency, malabsorption
*Carcinomatous neuromyopathy: carcinomatous cachexia
*Acute rhabdomyolysis'
*Proximal neuropathies: Guillain-Barre syndrome, acute intermittent porphyria,chronic autoimmune polyneuropathy
*Microembolization by atheroma or carcinoma
*Polymyalgia rheumatica
*Other collagen vascular diseases: rheumatoid arthritis, sclerocerma, systemic lupus erythematosus, polyarteritis nodosa
*Infections: acute viral, including influenza, mononucleosis, rickettsia, coxsackie virus, rubella and rubella vaccination, acute bacterial including typhoid
*Parasites: including toxoplasma, trichinisla, schistosoma, cysticerci, sarcosporidia
*Septic myositis: including staphylococcus, streptococcus, clostridium welchft, and leprosy
Myasthenia gravis is the prototypical disorder of the neuromuscular junction, in which weakness often affects the extraocular and bulbar muscles and becomes worse with repetitive contraction. A similar pattern of activity-increased weakness is found in Eaton-Lambert syndrome. Both of these diseases can cause proximal muscle weakness, but can be separated from polymyositis/dermatomyositis by their characteristic electromyographic patterns as well as absence of serum muscle enzyme elevation.
Glycogen storage diseases result from enzyme deficiencies involving the glycolytic pathway. McArdle's disease, or myophosphorylase deficiency, is caused by failure to degrade glycogen for energy under anaerobic conditions. Disorders of muscle lipid metabolism may mimic polymyositis. Carnitine deficiency results in inability to transport long-chain fatty acids into mitochondria for oxidation, leading to lipid accumulation in muscle fibers and a chronic proximal myopathy.
Other causes of proximal myopathy include vitamin D deficiency, adrenal insufficiency, hypophosphatemia, hyperthyroidism, carcinomatous neuromyopathy and exposures to various toxic substances. A variety of drugs are capable of producing inflammatory or noninflammatory myopathy include: chloroquine, cimetidine, clofibrate, colchicine, corticosteroids, cyclosporin. Ethanol, heroine, ipecac, levadopa, lovastatin, penicillamine,phenytoin, nicotinic acid, vincristine, zidovudine."
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