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Muscle biopsies are typically normal
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MYOPATHIES ASSOCIATED WITH MALIGNANCY
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Patients with malignancies frequently develop generalized weakness, although most do not have a true paraneoplastic syndrome Muscle weakness in patients with cancer are much more likely related to impaired nutrition, increased catabolic state induced by the tumor, disuse atrophy, and perhaps toxic effects of chemotherapeutic agents There are a few well-de ned paraneoplastic syndromes, including sensory neuronopathies or sensorimotor neuropathies (eg, anti-Hu syndrome as discussed in 17) and Lambert-Eaton syndrome (see 23), resulting in generalized weakness In ammatory and necrotizing myopathies can occur in the setting of cancer (as discussed in more detail in 30) Rarely, patients with malignancy can have spread of the tumor into a region of muscle109,110 Any muscle group can be invaded by resulting in pain, swelling, and weakness in the local region EMG of the affected muscles may reveal membrane instability and MUAPs with short duration and low amplitudes Muscle biopsy can demonstrate evidence of tumor emboli
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Pathogenesis
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Hyperkalemia causes a prolonged depolarization of the muscle membrane that in turn inactivates the sodium channel inactivation reduces the excitability of the muscle membrane
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Treatment
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Muscle strength returns with correction of hyperkalemia The underlying cause of the hyperkalemia must be elucidated and treated
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Muscle weakness secondary to hypercalcemia and hypocalcemia was discussed in the section regarding parathyroid myopathies
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DISORDERS OF PHOSPHATE Hypophosphatemia
Hypophosphatemia can occur in diabetic ketoacidosis, acute alcohol intoxication, hyperalimentation with phosphate-poor preparations, severe diarrhea, and in patients taking phosphate-binding antacids Serum phosphate levels less than 04 mM/L may lead to generalized muscle weakness, rhabdomyolysis, and myoglobinuria107 Some patients develop paresthesiae and diminished muscle stretch re exes Detailed electrophysiological studies or histopathologic descriptions are lacking in hypophosphatemia-induced muscle weakness Symptoms resolve with correction of the serum phosphate levels
OTHER MYOPATHIES SECONDARY TO SYSTEMIC DISEASE
AMYLOID MYOPATHY Clinical Features
Amyloid myopathy usually occurs in the setting of primary amyolidosis (light-chain amyloidosis)111 118 and is less frequent with familial amyloidosis119,120 Amyloid myopathy does not occur in secondary amyloidosis (AA) With primary and familial amyloidosis, cardiac muscle, peripheral nerves, skin, kidneys, and other organs
SECTION II
SPECIFIC DISORDERS
can also be affected in addition to skeletal muscle In fact, most patients present with non-muscle related symptoms Approximately 20% of patients have a coexistent generalized peripheral neuropathy; mononeuropathies such as carpal tunnel syndrome and ulnar neuropathy also occur116 Amyloid myopathy usually manifests with an insidious onset of progressive proximal weakness, although distal muscles can also be affected116,118 The distal muscle weakness may be inpart related to a superimposed amyloid myopathy Hypertrophy of involved muscle groups can be appreciated; the tongue is often involved with notable macroglossia However, other patients develop atrophic muscles; again this could be related to the associated neuropathy Ventilatory failure can occur due to involvement of the diaphragm muscle and phrenic nerves Muscle induration, stiffness, and pain are also variably present
paraspinal and proximal extremity muscles111,113 118,121 Complex repetitive discharges and myotonic discharges may also be appreciated Early recruitment of short duration, low amplitude, polyphasic MUAPs is present in weak proximal muscles In addition, patients with superimposed amyloid neuropathy often have decreased recruitment of long duration, large-amplitude potentials MUAPs in distal muscles
Histopathology
Muscle biopsies demonstrate variability in ber size with an admixture of hypertrophic and atrophic bers116 Scattered necrotic and regenerating bers, and increased internalized nuclei may be seen Group atrophy related to denervation may be appreciated Amyloid deposition is best visualized using rhodamine optics on Congo-red stained section (Fig 31 3)116 After employing this technique in the routine evaluation of all muscle specimens, the Mayo Clinic demonstrated a 10-fold increase in the diagnosis of amyloid myopathy, suggesting it is probably an underdiagnosed entity116 The amyloid deposits are best appreciated surrounding small arterioles and venules In addition, muscle bers are also partially or completely encased by amyloid deposits In primary amyloidosis, immunohistochemical studies reveal that the amyloid deposits are composed of or light chains116 Immunohistochemistry employing antibodies directed against gelsolin and transthyretin are useful in excluded familial amyloidosis Membrane attack complex may co-localize with amyloid deposition ApoE was deposited in all patients regardless of the type to systemic amyloidosis in one large series of patients116 EM con rms the deposition of short,
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