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McArdle’s disease is an autosomal recessive disorder of glycogen metabolism, which occurs due to deficiency of myophosphorylase, an enzyme required for conversion of glycogen to glucose-1-phosphate in the muscle [1]. It is also known as Glycogen Storage Disease Type V or Glycogenosis Type V. This syndrome typically presents in the first two decades of life with exercise intolerance, muscle pain, cramps, rhabdomyolysis and myoglobinuria. Patients notice stiffness after exercise and a second-wind phenomenon during exercise [2]. It can present in infancy with progressive weakness, hypotonia, respiratory distress and early death. In the adult onset form, the findings are atypical with symmetric progressive limb-girdle weakness and delayed onset wasting [3]. Heart and liver have a different isomer of the phosphorylase, and are thus not affected. An ischemic exercise test can be used to screen for this condition. In a diseased person, there is absence of increase in serum lactate with an increase in ammonia production.

Atypical McArdle’s disease with asymmetric weakness and Atrophy