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Treatment
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Surgical resection of the pituitary adenoma with subsequent reduction of the growth hormone levels leads to improved muscle strength86
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PANHYPOPITUITARISM
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Pituitary failure in adults commonly leads to muscle weakness and fatigue, probably due to secondary de ciencies of thyroid and glucocorticoid hormones98 The myopathy improves with replacement of these hor-
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Pathogenesis
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Ischemic damage and secondary hemorrhagic infarction result from long-standing, diabetic vasculopathy
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TABLE 31 1 ETIOLOGIES OF SECONDARY HYPOKALEMIC AND HYPERKALEMIC PARALYSES
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Figure 31 2 Diabetic Muscle Infarct Quadriceps muscle biopsy reveals widespread necrosis and endomysial in ammatory cell in ltrate Paraf n section, stained with hematoxylin and eosin
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Treatment
The muscle pain and swelling resolves after several weeks, although symptoms may recur in the contralateral leg Treatment consists of immobilization and pain control Sometimes we give a short course of prednisone to help with the pain by reducing edema and release of cytokines However, one must closely monitor the serum glucose levels in such cases
Hypokalemic Paralysis Thyrotoxic periodic paralysis Renal tubular acidosis Villous adenoma Bartter s syndrome Hyperaldosteronism Chronic or excessive use of diuretics, corticosteroids, licorice Amphotericin B toxicity Alcoholism Toluene toxicity Barium poisoning Hyperkalemic Paralysis Addison disease Hypoaldosteronism (hyporenemic) Isolated aldosterone de ciency Excessive potassium supplementation Potassium-sparing diuretics (eg, spironolactone, triamterene) Chronic renal failure Rhabdomyolysis
weak muscles may demonstrate brillation potentials and positive sharp waves as well as early recruitment of small duration, low-amplitude MUAPs The EKG may demonstrate bradycardia, attened T waves, prolonged PR and QT intervals, and notable U waves
MYOPATHIES ASSOCIATED WITH ELECTROLYTE IMBALANCE
DISORDERS OF POTASSIUM (HYPOKALEMIA) Clinical Features
Hypokalemia is the most common electrolyte abnormality that causes muscle weakness106 Clinical, laboratory, and electrophysiological features are similar to familial hypokalemic periodic paralysis (see 29) Patients must be evaluated for other etiologies of hypokalemia (Table 31 1) before assuming a diagnosis of family hypokalemic periodic paralysis Patients usually present with symmetric proximal or generalized weakness, although asymmetric muscle weakness can be seen Weakness is often accompanied by complaints of myalgias and cramps A severe complication of hypokalemia is rhabdomyolysis with myoglobinuria and secondary renal failure
Histopathology
Biopsies of very weak muscles may demonstrate vacuoles and scattered necrotic bers
Pathogenesis
The mechanism of muscle ber destruction and weakness is not fully known Reduced extracellular potassium concentration may render the muscle membrane less excitable Hypokalemia may also diminish blood ow and suppress the synthesis and storage of glycogen in muscles
Treatment
Muscle strength returns with correction of the hypokalemia The patients need a medical work-up to elucidate the underlying cause of the hypokalemia
HYPERKALEMIA Clinical Features
Hyperkalemia can also cause generalized muscle weakness In addition, there is evidence of increased neuronal or muscle membrane excitability as manifested by the presence of Chvostek s sign or myotonic lid lag There
Laboratory Features
Usually the potassium levels need to be less than 25 mEq/l before any muscle breakdown and weakness occur Serum CK levels are usually elevated in patients with hypokalemic myopathy NCS are normal EMG of
MYOPATHIES ASSOCIATED WITH SYSTEMIC DISEASE
are a number of causes of hyperkalemia and these need to be excluded before concluding a patient has familial hyperkalemic periodic paralysis (Table 31 1)
DISORDERS OF MAGNESIUM
Hypermagnesemia most often occurs secondary to over usage of magnesium-containing laxatives, particularly if the patient has renal insuf ciency108 It can also develop during treatment of eclampsia with magnesemia sulfate Severe generalized and ventilatory muscle weakness may ensue but resolve with correction of the serum magnesium levels Muscle and nerve hyperexitability as characterized by Chovstek s and Trousseau s signs and tetany may be seen in hypomagnesemia However, hypocalcemia and other electrolyte disturbances typically accompany hypomagnesemia and therefore, it is dif cult to attribute the neuromuscular abnormality solely to the low serum magnesium levels
Laboratory Features
Most patients with severe generalized weakness have serum potassium levels greater than 7 mEq/L Renal insuf ciency and acidosis may accompany the hyperkalemia but serum CK levels are usually normal EKG may demonstrate tall, peaked T-waves Routine NCS are normal EMG may demonstrate early recruitment of small myopathic MUAPs, but brillation potentials and positive sharp waves are not typically seen Unlike, familial potassium-sensitive periodic paralysis, myotonic discharges are never seen in the acquired forms of hyperkalemic myopathy
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