Hyperthyroidism - Clinical Features

Hyperthyroidism

Clinical Features and Associated Disorders

Although new-onset adulthood seizures are rarely related to hyperthyroidism, the seizure incidence among thyrotoxic patients ranges from 1 to 9 percent. Movement disorders, such as tremor (usually enhanced physiological tremor) and choreoathetosis, as well as upper motor neuron signs, including spasticity, hyperreflexia, clonus, and Babinski's signs, may also be observed.

Peripheral neurological features include cranial and peripheral neuropathies, as well as neuromuscular junction and muscle disturbances . Ocular features include lid lag, stare, widened palpebral fissures, extraocular muscle dysfunction with diplopia, and optic nerve compression with visual impairment.
Eyelid retraction manifests in several ways: (1) Stellwag's sign, a staring expression with infrequent blinking; (2) Dalrymple's sign, a widened palpebral fissure due to retraction of both the upper and lower lids; (3) von Graefe's sign, a larger than normal portion of visible sclera with downward eye movement; (4) Joffroy's sign, a lack of frontalis muscle contraction with upgaze; and (5) Moaubius' sign, sympathetic overactivity-induced exophthalmos with resultant limited convergence.

Although reports of a distal sensorimotor polyneuropathy in thyrotoxic patients are rare, improvement of the neuropathic features with attainment of the euthyroid state indicates that these features are manifestations of hyperthyroidism. Myasthenia gravis (MG) can be associated with hyperthyroidism, although some of the reported cases may have been secondary to coincident MG. Also, when bulbar weakness responds to treatment of the hyperthyroid state, it is more likely related to hyperthyroidism. When MG co-exists with thyrotoxic myopathy, the clinical findings do not differ from those in euthyroid patients, although the patients may be weaker due to the co-existence of two motor disorders. Thyrotoxic myopathy is characterized by the gradual onset of proximal limb weakness, which may be accompanied by myalgias, easy fatigability, and prominent atrophy. Although the muscular atrophy may be severe, most patients remain ambulatory. Shoulder girdle muscles can be more severely affected than the hip girdle muscles, with prominent atrophy and scapular winging. Distal limb muscles are also affected, the facial muscles may be affected, and, rarely, bulbar and ocular muscles are involved.

Thyroid-associated ophthalmopathy refers to the exophthalmos and ocular muscle dysfunction associated with thyroid disease. It is seen in most patients with Graves' disease but is also seen in 5 percent of patients with Hashimoto's thyroiditis. It is not correlated with the onset of Graves' disease, having been reported to precede (rarely), occur concomitantly with, or develop after its treatment. It also does not correlate with the level of circulating thyroid hormone and may occur in euthyroid patients or in patients with hypothyroid Graves' disease. When it is prominent, thyroid-associated ophthalmopathy may cause exposure keratopathy (due to marked proptosis), as well as optic nerve compression. Thyrotoxic periodic paralysis refers to recurrent attacks of flaccid paralysis of the limbs and trunk (the oculobulbar muscles are usually spared or involved to a lesser degree) due to secondary hypokalemia.

Differential Diagnosis.

The differential diagnosis of thyrotoxicosis includes other hypermetabolic disorders, euthyroid hyperthyroxinemia, and nonthyroidal causes. Occasionally, recognition that myopathic features are due to thyrotoxicosis can be difficult, especially if the myopathy is the presenting feature (rare), when exophthalmos is minimal, or when an apathetic state is present. When it is present, the observation of hyperreflexia is helpful, because this feature is not observed in other metabolic myopathies. Thyrotoxic myopathy with pronounced muscular atrophy should be differentiated from progressive muscular atrophy by the presence of fasciculations and more profound weakness in the latter. When thyrotoxic myopathy involves the ocular and bulbar musculature, it must be differentiated from MG. In thyrotoxic myopathy, rapid muscle fatigue and recovery with rest is not appreciated, a response to anticholinesterases is not observed, and decrement is not apparent on EMG; in MG, ocular and bulbar muscle involvement is more pronounced and atrophy is not present. Polymyositis should also be considered and is differentiated by EMG and muscle biopsy.

Evaluation.

TFTs can confirm thyrotoxicosis, typically demonstrating an elevated free T4 , total T4 , T3 RU, free thyroxine index (FTI), free T3 , total T3 , and a suppressed (usually undetectable) TSH. A normal or elevated TSH in the face of unequivocal clinical thyrotoxicosis should raise suspicion for a TSH-secreting pituitary adenoma. Other laboratory features may include anemia, hypokalemia, hypercalcemia, and an elevated erythrocyte sedimentation rate. Roughly half of hyperthyroid patients demonstrate EEG changes, most commonly generalized slowing or excessive fast activity, both of which resolve with attainment of the euthyroid state. Magnetic resonance imaging (MRI) with gadolinium may demonstrate the characteristic features of thyroid ophthalmopathy including multiple extraocular muscle (EOM) involvement, smooth margins gradually tapering into the tendon insertions, and uniform enhancement when contrast is administered. These features are readily displayed with fat saturation techniques that de-emphasize intraocular fat. Optic nerve impingement may also be visualized with a similar approach. MRI may also be useful in ruling out orbital pseudotumor, Tolosa-Hunt syndrome, orbital lymphoma, Wegener's granulomatosis, and orbital aspergillosis.

When co-existent MG is considered, acetylcholine receptor antibodies in response to edrophonium (Tensilon) may be helpful in its evaluation. Although the Tensilon test may be normal in MG (false-negative result) and may lead to improvement of dysthyroid orbitopathy (false-positive result), patients with thyrotoxic bulbar features typically do not have immunological, electrophysiological, or pharmacological evidence of MG.

Management.

Almost all of the clinical features of thyroid dysfunction, with the exception of thyroid-associated ophthalmopathy, resolve once the euthyroid state is achieved. , Medical treatment of thyrotoxicosis includes the use of beta blockers; antithyroid, anti-inflammatory, and immunosuppressive drugs; radioactive iodine-131; and iodine-containing compounds. Beta blockers, in addition to decreasing the beta adrenergic-mediated features of thyrotoxicosis, may decrease the peripheral conversion of T4 to T3 . Beta blockers are also useful in the prophylactic treatment of TPP while attainment of the euthyroid state is awaited. A typical dosage regimen is propranolol, 40 mg four times daily. In hyperthyroid patients with co-existent MG, beta blockers should be used cautiously because of their neuromuscular blocking properties. Higher grade orbital features typically require either systemic corticosteroids (with or without cyclosporine), irradiation, or orbital decompression, yet some believe surgery is rarely indicated because the dysthyroid orbitopathy usually spontaneously arrests before a serious degree of ophthalmopathy has been reached. One of the most frequent complications of thyroid surgery is recurrent laryngeal nerve paralysis. A more limited surgery involving partial lid suturing may be required to protect the cornea.

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