Graves’ Disease and the Manifestations of Thyrotoxicosis
DeGroot LJ.
ncbi.nlm.nih.gov/books/NBK2...
MUSCLES
The muscular symptoms vary from mild myasthenia to profound muscular weakness and atrophy, especially of proximal muscle groups. This weakness forms the basis of a useful clinical test. If a thyrotoxic patient seated in a chair is asked to hold one leg out straight and in a horizontal position, he or she may be able to do so for 25 - 30 seconds only; normal persons can maintain such a position for 60 - 120 seconds. Toe standing and step climbing may also bring out muscle weakness that is otherwise not so apparent. In the more extreme forms of muscular involvement, there is not only weakness but also atrophy. Wasting of the temporals and interossei may be noted in a considerable number of patients, and in a few, wasting of all skeletal muscles. This wasting may go so far as to bear a close resemblance to progressive muscular atrophy; occasionally the myopathy may shade into the picture of a polymyositis. Muscle cell necrosis and lymphocyte infiltration may be visible histologically, but usually are not found even when the symptoms of weakness are severe [175]. Tremor, which is usually present, is ascribed to altered neural function. Fasciculations are unusual.
The speed of both tension development [290] and relaxation of the muscles is increased, so that the reflex time is shortened. The electromyogram is normal in most instances but may occasionally resemble that of muscular dystrophy [291]. Work efficiency, measured in terms of the calories of heat produced while performing a given amount of work, has been reported to be both decreased [292] and normal. The question of metabolic efficiency of hyperthyroid muscle has been revisited by Erkintalo et al, using phosphorus-31 MRI spectroscopy, finding that toxic muscle required more energy to function than normal, presumably because of additional ATP-consuming mechanisms [293]. Creatine excretion is increased. The muscles have decreased ability to take up creatine, produced in the liver, from the blood [294-295]. Creatinine excretion is initially increased by the general catabolism of hyperthyroidism, but as muscle mass diminishes, creatinine excretion in the urine is depressed.
Myasthenia gravis may simulate thyrotoxicosis, and vice versa [296]. It has been reported that neostigmine both strengthens the muscles in thyrotoxic myopathies and is without effect. Certainly, the response is small in comparison with the immediate and striking correction of weakness seen in myasthenia gravis. Thyrotoxicosis may rarely ameliorate myasthenia gravis, but typically it is accentuated by thyrotoxicosis and is also worsened by myxedema. The close relationship between these two diseases is apparent in the observation that thyrotoxicosis occurs in 3% of patients with myasthenia gravis. The pathogenic anti-acetylcholine receptor antibodies that occur in myasthenia gravis are clearly comparable to the anti-TSH receptor antibodies found in Graves' disease. In addition, it has been found that TG and acetyl- cholinesterase share epitopes recognized by B cells. It is, however, uncertain that this plays any role in the pathogenesis of muscle disease in Graves' patients.
Periodic paralysis is precipitated and worsened by thyrotoxicosis [297]. This relationship has been extensively studied in Japan, where it is a familiar syndrome, particularly in men. The paralysis is usually associated with and due to hypokalemia. While the exact mechanism is not known, the hypokalemia is believed to be caused by a shift to the intracellular compartment. It has been demonstrated that thyrotoxicosis augments K+ uptake and release from cells. Experimental T4 treatment augments synthesis of membrane Na+-K+ activated ATPase. The episodes of paralysis tend to be infrequent and sporadic, but most commonly occur after a meal, following exercise, or start during sleep, and can be induced by administration of glucose and insulin. The onset following meals or exercise presumably relates to rapid K+ uptake by cells. Episodes last from minutes to hours, usually involving peripheral muscles, but can cause paralysis of the diaphragm and affect the heart. Serious episodes can be associated with extensive muscle cell damage and necrosis, EKG abnormalities such as ST and T wave changes, PVCs, first degree heart block, prolonged Q, T intervals, and even ventricular fibrillation [298].
Potassium treatment has some protective effect, and quickens recovery from attacks. Propranolol, for reasons not entirely clear, has prophylactic action. Therapy of the thyrotoxicosis almost always causes the rapid and permanent disappearance of the syndrome.
Myotonia congenita and myotonia dystrophic do not occur with increased frequency with thyrotoxicosis.
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