Steroid-induced myopathy emg findings

If the neurologic examination is unrevealing, a more general physical examination, searching for extramuscular signs, is warranted ( Table 6 5 , 7 – 15 , 17 , 18 , 21 , 24 – 27 , 34 , 36 , 38 ) . Mental status testing may reveal changes suggestive of a myopathy-inducing electrolyte disorder (calcium or magnesium) or an arrest of mental development as occurs in genetic myopathies. 25 , 29 The cardiovascular assessment may elicit changes consistent with a cardiomyopathy—a nonspecific consequence of many myopathy-inducing disorders—or a pericarditis, as occurs with some of the infectious and rheumatologic causes of muscle weakness. 5 , 7 , 8 , 9 , 18 , 21 , 24 , 25 , 29 , 36 , 38

Although the normal starting dose of One-Alpha is - micrograms/kg/day (and subsequent adjustment is by careful titration), in severe cases doses of up to 2 microgram/kg/day may be required. Whilst ionised serum calcium levels may provide a guide to response, measurement of plasma alkaline phosphatase activity may be more useful. Levels of alkaline phosphatase may be markedly raised in the pre-term low birthweight infant. Whilst levels of 5 times the normal adult laboratory value may be usual in this group, alkaline phosphatase levels above times the adult range indicate active disease. A dose of microgram/kg/day has proved effective as prophylaxis against early neonatal hypocalcaemia in premature neonates.

Myopathy due to steroids can be acute or chronic [3] and in some instances may involve the respiratory muscles [9]. The chronic form occurs after prolonged use with a more insidious onset whereas the acute presentation, if present, may be associated with rhabdomyolysis and abrupt onset [9]. Myopathy secondary to steroid may predispose patients to osteoporosis and sedentary life style which exposes to risks of contractures, deep venous thrombosis (DVT) and pressure sores. Stopping the administration of steroids results in insidious response; however, complete recovery may take weeks to months [11]. The laboratory findings are generally non specific [11, 12]. Creatinine kinase (CK) and lactate dehydrogenase (LDH) levels may be within normal limits; however, before development of myopathy the urinary creatinine excretion may specifically rise [3]. Acute myopathy shows increased CK levels with myoglobinuria which is absent in cases of chronic use of steroids [9]. EMG and NCS remains normal in chronic phases but some case reports of acute onset have indicated abnormal spontaneous activity (positive sharp waves and fibrillation potentials) [9]. There is no definite treatment for reversing steroid-induced myopathy; however, stopping the administration of steroids or, in cases where it is essential to be given, administer low doses on alternate days or offering non-fluorinated forms may minimize the risk with improvement in weeks to months. Our patient sufficently showed improvement on withdrawal of steroids and had been ambulatory in the ward three to four weeks after appropriate dose reduction.

A few cases of worsening of myasthenic symptoms have been observed with the use of ampicillin 53 and other penicillins. Bacitracin may also worsen myasthenia, but the literature is confounded by the concomitant use of other antibiotics. 47 Polymyxins are considered to act both pre-and post-synaptically to produce or exacerbate myasthenia gravis. 25 Their action is reversed by the administration of diaminopyridine only. 47 Tetracycline and its analogues are reported to have weak neuromuscular blocking effects which usually are reversed by calcium, 47 and are thought to exacerbate myasthenia gravis. 23 , 25 There have been reports of worsening of myasthenia with the use of imipenem/cilastatin, 54 and with infusion of vancomycin. 55 The mechanism of action of these at the neuromuscular junction is not known.

Steroid-induced myopathy emg findings

steroid-induced myopathy emg findings

A few cases of worsening of myasthenic symptoms have been observed with the use of ampicillin 53 and other penicillins. Bacitracin may also worsen myasthenia, but the literature is confounded by the concomitant use of other antibiotics. 47 Polymyxins are considered to act both pre-and post-synaptically to produce or exacerbate myasthenia gravis. 25 Their action is reversed by the administration of diaminopyridine only. 47 Tetracycline and its analogues are reported to have weak neuromuscular blocking effects which usually are reversed by calcium, 47 and are thought to exacerbate myasthenia gravis. 23 , 25 There have been reports of worsening of myasthenia with the use of imipenem/cilastatin, 54 and with infusion of vancomycin. 55 The mechanism of action of these at the neuromuscular junction is not known.

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