Highlights Muscle weakness after COVID-19 can be caused by critical illness myopathy. Critical illness myopathy should be suspected in patients with long ICU stay. Health systems must plan access to rehabilitative facilities after COVID-19.

Reply to 'SARS-CoV-2-associated critical ill myopathy or pure toxic myopathy?' Dear Editor,We read with great interest the letter by Finsterer and Scorza (2020) about our description of a critical illness myopathy (CIM) after coronavirus disease 2019 with a long stay in intensive care unit (ICU) (Bagnato et al., 2020).Finsterer and Scorza have doubts about the diagnosis of CIM since: (1) 'Needle electromyography (EMG) was myogenic only in a single muscle' and 'From lower limb muscle no needle EMG was recorded';(2) CIM was not associated with a critical illness polyneuropathy (CIP); and (3) no muscle biopsy, muscle magnetic resonance imaging, or repetitive nerve stimulation was performed. In fact, the statements in point 1 are incorrect, since we wrote that 'EMG indicated myopathy in the proximal muscles of the upper limbs and in the proximal and distal muscles of the lower limbs'. Moreover, in the table we specified that clearly myopathic findings ('short-duration and low-amplitude with early full recruitment' motor unit action potentials) were found in the right and left deltoid, quadriceps, and tibialis anterior (i.e. in six muscles of the upper and lower limbs). In addition, we performed a direct muscle stimulation (Rich et al., 1996), which showed muscle inexcitability in the right quadriceps and abnormal excitability in the right tibialis anterior, further confirming a diagnosis of myopathy.Regarding point 2, a diagnosis of CIM does not need a coexistent CIP, since a pure or prevalent myopathy has been reported in most patients with ICU-acquired weakness (Lefaucheur et al., 2006). In relation to the clear neurophysiological demonstration of a myopathic involvement, repetitive stimulation for neuromuscular junction evaluation was not performed (point 3). We agree with Finister and Scorza that a muscle biopsy and a muscle MRI would have strengthened a diagnosis of CIM, but we deemed clinical and neurophysiological findings adequately clear without the need to perform further and more invasive or expensive examinations.Finister and Scorza then argue that the patient may have had drug-induced toxic myopathy, rather than a CIM, and they report the potential myotoxicity of some drugs used to treat the patient. The patient did not suffer from a toxic rhabdomyolysis (e.g. from olanzapine), since her creatinine kinase level was normal. Besides, CIM defines an ICU-acquired weakness in critically ill patients not caused by a specific etiological factor, but by different risk factors, among which several drugs commonly used in ICU have been reported (Yang et al., 2018). Accordingly, it is not unusual for drugs to have contributed to the patient's CIM etiology.