Polymyositis tends to become evident in adulthood, presenting with bilateral proximal muscle weakness often noted in the upper legs due to early fatigue while walking. Sometimes the weakness presents itself as an inability to rise from a seated position without help or an inability to raise one's arms above one's head. The weakness is generally progressive, accompanied by lymphocytic inflammation (mainly cytotoxic T lymphocytes).

Polymyositis, like dermatomyositis, strikes females with greater frequency than males. The skin involvement of dermatomyositis is absent in polymyositis.
Another concern is Interstitial lung disease.

Based on the conclusion of the paper "Interstitial lung disease (ILD) in Polymyositis and dermatomyositis" by Maryann Fathi and Ingrid E Lundberg published 12/13/2005:

Investigations to detect interstitial lung disease should be performed during the initial evaluation as well as during follow-up of patients with myositis, because ILD is a frequent manifestation in patients with polymyositis or dermatomyositis and because ILD is associated with increased morbidity and mortality. This evaluation should include chest radiograph, HRCT of lungs, pulmonary function tests including diffusing capacity, and serum levels of anti-Jo1 antibodies. In the patients with ILD, clinical or subclinical, treatment with high doses of corticosteroids in combination with other immunosuppressive therapy should be initiated. Some histopathologic features including DAD, UIP, neutrophil alveolitis, digital infarcts showing microangiopathy in dermatomyositis, and amyopathic dermatomyositis have all been reported as risk factors for poor outcome. Presence of these factors is an indication for the use of aggressive immunosuppressive therapy (e.g., Methotrexate) as well as careful monitoring of lung function.

The cause is unknown but seems to be related to autoimmune factors,[2] genetics, and perhaps viruses. In rare cases, the cause is known to be infectious, associated with the pathogens that cause Lyme disease, toxoplasmosis, and others.

It is hypothesized that an initial injury causes release of muscle auto antigen, which is subsequently taken up by macrophages and presented to CD4+ TH cells. Activated TH cells synthesize IFN-¦Ã that stimulate further macrophages and further inflammatory mediator release like IL-1 and TNF-¦Á

Another important event in the pathogenesis of Polymyositis is the increased expression of MHC proteins by m/s cells. Auto-Ag is presented in association with MHC-I molecules on the surface of Myocytes and is recognized by CD8 cytotoxic T cells that subsequently initiate m/s destruction.