Corticosteroid-Induced Myopathy Follow-up

Updated: Jun 12, 2023
  • Author: Patrick M Foye, MD; Chief Editor: Stephen Kishner, MD, MHA  more...
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Consider the judicious use of steroids.



Although prior studies have reported full motor recovery, some patients may be left with varying degrees of residual weakness.



In chronic (classic) steroid myopathy, recovery from weakness may take weeks to months following discontinuation or dose reduction of the corticosteroid.

In acute steroid myopathy, recovery may be prolonged (>6 mo). The course can be relatively mild, with an insidious onset and a fair prognosis, or it can be severe and life-threatening. However, even the less severe course can be followed by chronic and irreversible changes if steroids are continued. [5]


Patient Education

Inform patients of the potential of development of myopathy when starting high-dose or long-term corticosteroid therapy.


Medicolegal Diagnostic Concerns

The main potential pitfall in diagnosing steroid myopathy relates to patients with polymyositis/dermatomyositis, which typically is treated with corticosteroids. The main symptom of polymyositis/dermatomyositis is proximal upper and lower extremity weakness. When these patients, while being treated with corticosteroids, develop increasing weakness, it can be difficult to determine whether the weakness is secondary to the polymyositis or to steroid myopathy.

Laboratory studies can aid in differentiating between the 2 conditions. Creatine kinase typically is elevated significantly in polymyositis/dermatomyositis. In steroid myopathy, it typically has been described that, although there is elevated urinary creatinine excretion, the serum creatine kinase is not significantly elevated. [1, 24] However, some studies have reported elevations of creatine kinase in some cases of the previously described acute form of steroid myopathy.

On electrodiagnostic study, polymyositis typically demonstrates normal NCS results, as, commonly, does steroid myopathy. On EMG study, however, polymyositis demonstrates abnormal spontaneous activity and increased polyphasic waveforms with short durations. The classic form of steroid myopathy has been described as not demonstrating significantly abnormal EMG findings. Again, some studies have described an acute form of steroid myopathy that can demonstrate abnormal spontaneous activity, an early recruitment pattern, and small, polyphasic waveforms. [22, 24]

The initial recommendation is to decrease or discontinue the use of the corticosteroid. [10] If the weakness improves, then steroid myopathy is the most likely diagnosis. If the weakness persists or worsens, then the most likely diagnosis is worsening of the polymyositis.

Overall, when reading the published medical literature, there are significant challenges when trying to assess whether various steroid treatments are actually associated with steroid myopathy and how frequently this occurs. For example, in patients with asthma, long-term steroid based therapy reportedly causes a side effect of steroid-induced myopathy in some patients. 

However, Wu et al, in a systematic review of nine studies, looked at whether steroid treatments cause myopathy in asthmatic persons and concluded that standardized methods used to establish the diagnosis of myopathy are lacking, as is a clear definition of myopathy in functional terms. The investigators highlighted a need to ascertain myopathy side-effect rates for fluorinated versus non fluorinated steroids and for different administration routes and dosages. [33]