Varying degrees of sensory deficit corresponding to each of the five senses have been described as an effect of thyrotoxicosis and its treatment, or related to accompanying disease states. Visual disturbances in thyrotoxicosis occur primarily as a complication of Graves’ ophthalmopathy due to optic nerve compression at the apex of the orbit, diplopia related to extraocular muscle dysfunction, or rarely, damage to the cornea. Sensorineural hearing loss while common in hypothyroidism, occurs rarely in thyrotoxicosis, and has been attributed to an adverse drug effect of the thionamides (4,5). Olfactory toxicity has also been ascribed to methimazole use in laboratory animals, but similar data has not been published in humans. An altered sense of smell may occur as a complication of orbital decompression surgery in patients with Graves’ ophthalmopathy (6). Disorders of taste have been described in both hypothyroidism and hyperthyroidism (7). Peripheral neuropathy occurs in association with thyrotoxicosis, including symmetric distal sensory neuropathy (8), carpal tunnel syndrome (9), and due to coexistence of vitamin B12 deficiency (10).

Tremor associated with thyrotoxicosis is most evident in the hands, but can occur elsewhere, such as in the tongue, trunk, and lower extremities. It is believed to be due to beta-adrenergic stimulation and responds dramatically to beta-adrenergic blocking agents. Chorea, which is a rapid, non-repetitive, random movement of the extremities or less commonly the facial muscles or trunk, has been described in thyrotoxic patients and resolves following successful treatment of the patient’s thyroid condition (11).

Myopathy occurs to some degree in the majority of patients with overt thyrotoxicosis. It is frequently proximal in location, and most commonly involves the pelvic girdle and shoulder muscles. In one prospective cohort, muscle complaints occurred in 67% of thyrotoxic patients, most of whom had demonstrable weakness by dynamometric testing in four or more muscle groups (8). Muscular weakness in this study correlated with serum-free T₄ concentrations, and was not associated with creatine kinase enzyme elevations; it resolved an average of 3.6 months following therapy.

Myasthenia gravis occurs infrequently (less than 1%) in patients with Graves’ disease (12,13), but conversely, autoimmune thyroid disease occurs frequently in patients with myasthenia gravis. A retrospective review found that 7.7% of myasthenia gravis patients carried a diagnosis of Graves’ disease, and another 4.2% had a history of Hashimoto’s thyroiditis (14). Myasthenia gravis occurring in the setting of Graves’ disease in this study occurred at a younger age and was more likely to be associated with thymic hyperplasia.

Thyrotoxic periodic paralysis occurs as a result of an intracellular shift of potassium in a genetically and clinically susceptible patient. Occurring most frequently in Asian males,
patients with this disorder present with episodic paralysis following an episode of carbohydrate ingestion or intense physical exercise, and are noted to have clinical and laboratory evidence of thyrotoxicosis. Total body stores of potassium are normal in these individuals, but serum potassium during an episode of paralysis may be <1.5 mEq/L. Initial judicious therapy with intravenous potassium is often required, taking care to avoid rebound hyperkalemia. The addition of beta-adrenergic blocking agents reduces the frequency of repeat attacks while awaiting a return to euthyroidism. Interestingly, mutations within Kir2.6, an inward rectifier potassium channel, have recently been implicated in the susceptibility of at least one-third of thyrotoxic periodic paralysis patients (15).

Seizures are a well-recognized component of thyroid storm (16), but are only seen in a minority (<1%) of patients with moderate thyrotoxicosis. In a recent series of six patients with first seizures occurring in association with thyrotoxicosis, the subtype was generalized tonic–clonic in four patients, complex partial seizures with secondary generalized tonic–clonic seizures in two patients, and a focal seizure in one patient (17). Although the exact mechanism through which thyroid hormone elevation contributes to seizures is unknown, both seizures and electroencephalogram abnormalities resolve with correction of thyroid hormone levels in affected patients, and recur with subsequent episodes of thyrotoxicosis (17).

Embolic and ischemic cerebrovascular events have both been described in patients with overt thyrotoxicosis, although the former, resulting from atrial fibrillation, is more common (18,19).