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IBM is characterized by weakness in the knee extensor and deep finger flexor muscles due to muscle atrophy and fibroadipose replacement. Dynamometry and manual muscle testing are commonly used to assess patient muscle strength, while magnetic resonance imaging and electromyography studies identify the patterns of muscle atrophy and motor unit potentials. Although the underlying pathophysiological mechanisms of IBM are still unknown, common histopathological markers include rimmed vacuoles and inclusions. The immune system is also largely implicated in pathogenesis, as skeletal muscle in IBM overexpresses major histocompatibility complex I (MHC-I), and cluster of differentiation (CD) 8+ T-cells, and features endomysial inflammation. Antibodies to the cytosolic 5\u2032-nucleotidase 1A (cN1A) protein have been associated with IBM but have low sensitivity and specificity. 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