Version May 2024
INTRODUCTION — Hyperthyroidism is a common medical condition in the general population. The most common cause of hyperthyroidism is Graves' disease, but elevated thyroid hormone levels may occur due to a destructive thyroiditis, toxic adenoma or toxic multinodular goiter, or excess thyroid hormone supplementation.
Common systemic features of hyperthyroidism include palpitations, heat intolerance, and weight loss. A number of central and peripheral nervous system manifestations may also occur in patients with hyperthyroidism (table 1). In many cases, the neurologic manifestations occur in conjunction with the systemic features of the disease, but these may be the presenting symptom in some patients.
This topic reviews the neurologic manifestations of hyperthyroidism. Other clinical features of hyperthyroidism are discussed separately (see "Overview of the clinical manifestations of hyperthyroidism in adults" and "Clinical manifestations and diagnosis of Graves disease in children and adolescents"). The diagnosis of hyperthyroidism is also discussed separately. (See "Diagnosis of hyperthyroidism".)
NEUROLOGIC MANIFESTATIONS OF HYPERTHYROIDISM
Encephalopathy — Cognitive impairment is common in hyperthyroidism and may present as one or more different syndromes. In a cross-sectional study of older hospitalized patients, dementia and confusion were found in 33 percent and 18 percent of patients with hyperthyroidism [1]. Studies in younger individuals with newly diagnosed or induced hyperthyroidism have found lower cognitive scores compared with controls [2].
The mechanism of cognitive and behavioral dysfunction in hyperthyroidism is not known. Improvement of some clinical features (attention and concentration) with beta-blocker therapy suggests a role for a hyperthyroid-induced hyperactive adrenergic system, possibly disrupting the adrenergic pathways between the locus ceruleus and frontal lobe that subserve attention and vigilance [3].
●Clinical features – Patients with hyperthyroidism may experience behavioral and personality changes, such as psychosis, agitation, and depression. Less overt manifestations that are more common in less severe hyperthyroidism include anxiety, restlessness, irritability, and emotional lability [4]. Insomnia is also common. Older adult patients may have a less activated presentation with depression and lethargy, so-called apathetic thyrotoxicosis [1]. These behavioral manifestations are accompanied by cognitive impairments, particularly impaired concentration, confusion, poor orientation and immediate recall, amnesia, and constructional difficulties.
In severe hyperthyroidism, a condition frequently referred to as "thyroid storm," seizures may accompany the encephalopathy of acute thyrotoxicosis and occasionally are the presenting clinical feature [5]. They may be focal or generalized and may include status epilepticus [5-10]. In patients with thyroid storm, the neurologic presentation is more fulminant, progressing, if untreated, through an agitated delirium to somnolence and ultimately to coma [11]. Tremor and hyperreflexia with other pyramidal tract signs are also common features of the neurologic examination [12] (see 'Tremor' below and 'Motor neuron manifestations' below). In many of these cases there is an underlying stressor, such as sepsis, trauma, or a recent surgical procedure. Other clinical features of thyroid storm, such as tachycardia, fever, and gastrointestinal symptoms, are commonly present (table 2). Thyroid storm is discussed separately. (See "Thyroid storm".)
The presentation of cognitive dysfunction in hyperthyroidism is usually acute or subacute; however, a more protracted course similar to a degenerative dementia has also been described in a handful of case reports [3]. In one patient, single-photon emission computed tomography (SPECT) demonstrated diffusely reduced cerebral uptake with an accentuation in the temporoparietal regions bilaterally, which improved following resolution of the hyperthyroid state. The possible association of subclinical hyperthyroidism and dementia risk is discussed separately. (See "Subclinical hyperthyroidism in nonpregnant adults", section on 'Dementia'.)
●Electroencephalography – Nonspecific electroencephalography (EEG) abnormalities have been reported in 43 percent of patients with hyperthyroid encephalopathy [13]. EEG may demonstrate diffuse slowing, bitemporal sharp waves, or polyspike and slow-wave discharges, or may be normal [5,8]. In addition, an unusually high voltage with prolonged photic response and triphasic waves has been described in individual patients, but is not typical [5,10,14]. EEG may normalize with treatment, although persistence of EEG abnormalities despite a return to a euthyroid state has also been described in isolated cases, without clear prognostic implications regarding either seizure recurrence or persistence of the encephalopathy [15].
●Treatment – Treatment of hyperthyroidism typically leads to improvement in cognitive and behavioral impairments. Agitation, inattention, and frontal lobe impairment may improve more rapidly than other cognitive functions [1]. While treatment of hyperthyroidism leads to improvement in cognitive and behavioral impairments, cognitive dysfunction may persist despite a return to a euthyroid state [1,3]. Treatment of thyroid storm and Graves' hyperthyroidism is presented separately. (See "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment" and "Thyroid storm".)
Seizures in thyrotoxicosis are ultimately treated by reducing thyroid hormone concentrations; however, antiseizure medications are often used as a temporizing measure until euthyroidism is achieved. There is no evidence that any specific antiseizure medication is more effective than others in this setting [10] (see "Evaluation and management of the first seizure in adults", section on 'Management'). Recurrence of both generalized tonic-clonic seizures and encephalopathy coinciding with recurrence of the hyperthyroid state has been described [8]. Unprovoked seizures are unusual, and long-term treatment with antiseizure medications is not typically required [10].
Movement disorders
Tremor — Tremor is common in patients with thyrotoxicosis. In one small series of patients with a new diagnosis of hyperthyroidism, tremor was observed in 76 percent [16].
The tremor is typically high frequency and low amplitude and is primarily seen with action. It can involve the face and head but is usually most prominent in the upper extremities [17]. It is more usual for the tremor to be incidental to other manifestations of hyperthyroidism; however, at times a disabling tremor is the presenting complaint.
The tremor of hyperthyroidism resembles an exaggerated physiologic tremor; it is indistinguishable from anxiety-associated tremor [17]. These characteristics and its responsiveness to propranolol suggest that the pathogenesis is mediated by a heightened beta-adrenergic state [18,19] (see "Overview of tremor", section on 'Physiologic tremor'). Others have suggested a role for increased metabolism of dopamine in the etiology of hyperthyroid tremor.
Chorea — Chorea is a rare complication of hyperthyroidism, occurring in less than 2 percent of patients [20]. Chorea usually occurs in the context of other features of hyperthyroidism, but it may be a presenting symptom of a thyrotoxic state. In most cases, the onset of chorea is gradual, but a sudden onset of unilateral chorea has been described [21]. Chorea may be unilateral, bilateral, or multifocal and involves the extremities predominantly and less often the trunk or facial muscles. It may be continuous or occur in paroxysms that are spontaneous or precipitated by sudden movements [22-24]. Magnetic resonance imaging (MRI) and SPECT studies are normal, with no significant structural abnormality or abnormal cerebral perfusion [20,21].
Occurring in nonautoimmune thyroid disease as well as Graves' disease, chorea is believed to represent a direct effect of hyperthyroidism on the central nervous system. Hyperthyroidism may induce a reversible functional alteration in the dopamine turnover or receptor site response to dopamine in the corpus striatum. Studies have shown a reduction in the production and turnover of the level of homovanillic acid (HVA), a metabolite of dopamine, in the cerebrospinal fluid in hyperthyroid patients [25]. This would be an expected result of an increased sensitivity of dopamine receptors and a resulting decrease in dopamine turnover.
Chorea may improve or resolve with correction of thyroid hormone levels. In some patients, this occurs rapidly; in others, it may be delayed for several weeks or more after achieving a euthyroid state [26]. Recurrence of chorea coincident with an increase in thyroid hormone levels has been reported [20,27]. Persistence of the chorea, even for decades following treatment of hyperthyroidism, has also been described [28].
In addition to reducing thyroid hormone levels, symptomatic treatment of disabling or persistent chorea may be required. Some patients may respond to beta blockers; other pharmacologic treatments of chorea are described separately. (See "Overview of chorea", section on 'Management of chorea'.)
Other movement disorders — Myoclonus occurs rarely in hyperthyroidism. Isolated cases of unusual myoclonus affecting the trunk muscles or the platysma have been reported [29,30].
Ballism accompanying chorea has also been described [20].
Myopathy — Muscle weakness with or without atrophy and myalgias occurs in 60 to 80 percent of patients with untreated hyperthyroidism [16,31,32]. However, it is uncommon for a patient with hyperthyroidism to present with muscle weakness as the chief complaint. Patients with hyperthyroidism tend to develop muscle involvement more frequently after the age of 40. The likelihood of developing weakness, but not its degree, is correlated with the duration of the hyperthyroid state.
●Pathogenesis – The pathogenesis of myopathy in hyperthyroidism is unknown. The rapid response to thyroid-lowering treatment, at least in some patients, and a partial improvement with propranolol suggest that the muscle dysfunction is at least partly physiologic [16,33]. Contributing features may include increased cellular metabolism and energy utilization, increased catabolism and protein degradation, and inefficient energy utilization [34-37]. A significant reduction in muscle carnitine was identified in patients with hyperthyroid myopathy compared with controls [38], and it is possible that this reduction contributes to myopathy.
●Clinical presentation – As with the underlying thyroid disorder, the clinical presentation of myopathy may be acute or chronic.
•Acute thyrotoxic myopathy may present with more severe proximal and distal weakness, and rarely quadriplegia with bulbar and respiratory muscle involvement [39,40]. Rhabdomyolysis has been described in this setting [41-43].
•Chronic thyrotoxic myopathy is more common. Approximately two-thirds of patients with hyperthyroid myopathy report proximal weakness that usually begins several weeks to several months after the onset of hyperthyroidism. Hip flexors and quadriceps are predominantly affected [16]. The remainder usually has distal as well as proximal muscle involvement, although one series reported predominantly distal extremity weakness in 20 percent of patients [44]. The myopathy may be associated with myalgias.
In both presentations, muscle atrophy is usually absent. However, several cases with atrophy of shoulder muscles have been described. Isolated dysphagia has also been reported [39,45]. Deep tendon reflexes are usually normal or increased, an unusual finding in a myopathic disorder, with a shortened relaxation phase [16,44]. Paresthesias due to coexisting polyneuropathy may be present. Cramps are less common than with hypothyroidism [16]. Bulbar and respiratory muscle dysfunction occurs rarely [44,46]. Weakness is sometimes the sole manifestation of the endocrinopathy [32,44].
●Evaluation – When a patient with hyperthyroidism presents with acute weakness or has prominent bulbar muscle involvement, myasthenia gravis (MG) is more likely than muscle disease and should be carefully ruled out in these settings. (See 'Myasthenia gravis' below.)
Laboratory studies are unremarkable apart from abnormal thyroid function tests. Serum creatine kinase is generally normal, except in thyrotoxic crisis, but elevated aldolase occurs in approximately 30 percent of patients [16,44].
Electromyography (EMG) may be normal but sometimes demonstrates myopathic findings of increased polyphasic, low-amplitude motor unit potentials [32,44,47]. One study found "myopathic" changes in only 10 percent of 21 patients, while 24 percent had "neuropathic" changes [16]. Spontaneous activity is atypical. Abnormal EMG has been described in hyperthyroid individuals without clinical weakness. Muscle biopsy is rarely performed, but may be normal or may show nonspecific findings. Rarely, inflammation occurs [48].
●Treatment – Treatment of the hyperthyroid condition is usually sufficient to treat the myopathy. Symptoms may improve over a few to several months following return to euthyroid state [16,49]. Adrenergic blocking agents may be of benefit as well [50].
Peripheral neuropathy
Sensory polyneuropathy — A sensory polyneuropathy may occur with hyperthyroidism. A symmetric distal sensory disturbance and reduced Achilles reflexes are the most common features. Electrodiagnostic testing with nerve conduction studies and EMG is abnormal in up to 24 percent of thyrotoxic patients and is usually consistent with an axonal pathology [16,51-53].
Treatment of hyperthyroidism with return to a euthyroid state leads to improvement of symptoms. In one small case series, resolution of sensory complaints occurred in all patients over a seven-month period [16].
Carpal tunnel syndrome — Hyperthyroidism is an uncertain risk factor for carpal tunnel syndrome (CTS). In a prospective study of 150 patients with CTS, two patients were found with a past history of hyperthyroidism [54].
Prospective studies have identified CTS in 5 to 9 percent of patients with hyperthyroidism, although other potential contributing factors, such as diabetes, were not excluded [55,56]. This seems only marginally increased over the prevalence in the general population of 3 to 5 percent. However, the simultaneous onset of CTS symptoms and hyperthyroidism, and their remittance with treatment of hyperthyroidism, suggests a possible relationship. The pathophysiologic mechanism is not known.
The symptoms of CTS in patients with hyperthyroidism are indistinguishable from those with idiopathic CTS, with pain, sensory loss, or paresthesias in the hand in the median nerve distribution. (See "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)
Unusual neuropathies — The term "Basedow paraplegia" has been used to describe an acute development of severe leg weakness and areflexia, which occurs in the setting of severe hyperthyroidism or thyroid storm [52,57]. The arms are usually also weak, but are less severely affected. Patients recover with treatment of hyperthyroidism. Guillain-Barré syndrome (GBS) should be considered as an alternative diagnosis in patients with this presentation; GBS has been reported to be associated with Graves' disease. (See 'Disease associations' below.)
Motor neuron manifestations — Clinical features in patients with hyperthyroidism may include upper motor neuron signs related to pyramidal tract dysfunction as well as lower motor neuron signs related to a peripheral neuropathy, which may overlap with those of amyotrophic lateral sclerosis (ALS) [51,52,58,59]. There is no evidence of an association between hyperthyroidism and motor neuron disease [60].
One literature review identified 19 reported cases of hyperthyroidism with clinical features of upper and lower motor neuron involvement, similar to ALS; 16 of these patients improved with treatment of hyperthyroidism [61]. In one case series of patients with hyperthyroidism, generalized hyperreflexia was seen in 38 percent of patients [16]. In rare cases, there is also corticobulbar involvement with pseudobulbar speech [51].
Thyrotoxic periodic paralysis — Thyrotoxic periodic paralysis (PP) represents an acquired form of hypokalemic PP, in which attacks of generalized weakness occur, often precipitated by rest after strenuous exercise or a high carbohydrate load. Thyrotoxic PP is more prevalent in East Asian than in other populations and in males than in females. Any cause of hyperthyroidism can be associated with thyrotoxic PP.
This disorder is discussed in detail separately. (See "Thyrotoxic periodic paralysis".)
Headache — Hyperthyroidism has also been shown to be associated with headaches. In two studies, hyperthyroidism was found to be more common in female patients with migraine headaches [62,63]. Additionally, several cases have been reported of patients with new-onset daily persistent headaches and newly diagnosed hyperthyroidism whose headaches remitted with treatment of the hyperthyroid state [64-66].
Seizures — Hyperthyroidism is not generally associated with epilepsy; however, elevated thyroxine levels have also been associated with precipitating seizures in two patients with previously well-controlled juvenile myoclonic epilepsy [67].
Seizures are also a feature of the acute encephalopathy that can occur as a manifestation of thyroid storm. (See 'Encephalopathy' above.)
DISEASE ASSOCIATIONS — Certain neurologic conditions are associated with hyperthyroidism or Graves' disease but are not direct clinical manifestations of thyrotoxicosis.
Myasthenia gravis — It is generally recognized that there is an association between myasthenia gravis (MG) and hyperthyroidism, particularly Graves' disease. The reported prevalence of hyperthyroidism in series of patients with MG ranges between 2 to 17 percent, compared with a 1 in 10,000 prevalence in the general population [68-70].
The relationship between the two disorders is likely a shared autoimmune pathogenesis. Some, but not all, case series and case control studies have reported higher prevalence of antithyroid antibodies among patients with MG [69-71].
A closer association between the two disorders is also suggested by the following observations:
●In 44 of 51 of patients with MG and hyperthyroidism in one series, hyperthyroidism occurred simultaneously with or prior to the development of MG [68]. More than half of the patients demonstrated parallel disease activity with worsening of both diseases over a similar period of time.
●The clinical manifestations of MG patients may be influenced by comorbid autoimmune thyroid disease. In one study, MG associated with autoimmune thyroid disease was found to have a higher proportion of ocular MG compared with patients with MG without thyroid disease (41 versus 21 percent), as well as a lower frequency of thymic disease (27 versus 60 percent) and acetylcholine receptor antibodies (36 versus 57 percent) [72]. The association between ocular MG and Graves' disease may reflect immunologic cross-reactivity against common autoimmune targets in the eye muscle [73]. However, in another case series, generalized MG predominated in two-thirds of 56 patients with hyperthyroidism and MG [68].
●There may also be common genetic susceptibility in the two disorders. In one case series, all five patients with both MG and Graves' disease had in common the human leukocyte antigen (HLA) type, HLA-DQ3 [74].
Ocular MG and Graves' ophthalmopathy have overlapping symptoms but can generally be distinguished. Ptosis and orbicularis oculi weakness suggest ocular MG, while proptosis, lid retraction, lid lag, periorbital edema, and restricted eye movement with forced ductions suggest Graves' ophthalmopathy. (See "Ocular myasthenia gravis", section on 'Differential diagnosis' and "Clinical features and diagnosis of thyroid eye disease", section on 'Differential diagnosis'.)
The treatment and prognosis of MG are similar in patients with and without hyperthyroidism and consist of acetylcholinesterase inhibitors, immunosuppressive therapy, and thymectomy [69,75]. (See "Overview of the treatment of myasthenia gravis".)
Treatment of hyperthyroidism alone does not usually affect MG, although both improvement and worsening of MG symptoms with thyroid lowering have been described [76,77]. When the thyroid disorder is due to autoimmunity, immunosuppressive medications may lead to remission of both disorders [68]. Thymectomy appears to have no influence on hyperthyroidism.
Thymic enlargement due to hyperplasia is a common manifestation of Graves' disease and responds to its treatment. (See "Overview of the clinical manifestations of hyperthyroidism in adults", section on 'Thymic enlargement'.)
Stroke — Ischemic cerebrovascular disease is a rare complication of hyperthyroidism. In a prospective cohort study, 3176 patients aged 18 to 44 years with hyperthyroidism were followed for five years after the initial diagnosis; the cumulative incidence of ischemic stroke was 1.0 percent compared with 0.6 percent in a control group (hazard ratio [HR] 1.44, 95% CI 1.02-2.12) [78].
However, except for cardiogenic embolism in the setting of hyperthyroid-induced atrial fibrillation (AF), associations of hyperthyroidism with other stroke subtypes remain somewhat speculative. A systematic review and meta-analysis found no evidence to support an increased risk for stroke associated with subclinical hyperthyroidism (HR 1.17, 95% CI 0.87-1.34) [79].
Cardiogenic embolism — Cerebral infarction related to hyperthyroidism most commonly occurs as a result of a cardiogenic embolism in patients with hyperthyroid-induced AF [80]. AF occurs in 10 to 15 percent of individuals with hyperthyroidism and can be the presenting symptom. AF is more common in men than women, and its prevalence increases with age. Subclinical as well as overt hyperthyroidism is a risk factor for AF. However, hyperthyroidism causes a small percentage (<1 percent) of AF cases. (See "Overview of the clinical manifestations of hyperthyroidism in adults", section on 'Cardiovascular'.)
Some studies suggest that stroke in the setting of thyrotoxic AF is more frequent than in nonthyrotoxic AF, but others find no difference in arterial embolism rates [80-82]. (See "Atrial fibrillation in adults: Selection of candidates for anticoagulation", section on 'Hyperthyroidism'.)
In a Korean database study of over 1 million patients with AF, patients with hyperthyroidism had a higher risk of ischemic stroke and systemic embolism than those without hyperthyroidism (1.83 versus 1.62 per 100 person-years, HR 1.13, 95% CI 1.07-1.19) [83]. This risk decreased in patients treated for hyperthyroidism (HR 0.64, 95% CI 0.58-0.70).
Anticoagulation is recommended for secondary prevention of cerebrovascular events in the setting of thyrotoxic AF. Anticoagulation is more controversial for primary prevention. This topic is discussed separately. (See "Cardiovascular effects of hyperthyroidism", section on 'Treatment' and "Atrial fibrillation in adults: Use of oral anticoagulants".)
Cerebral venous thrombosis — Cerebral venous thrombosis (CVT) is a rare thrombotic cerebrovascular disorder with potential for morbidity and mortality, often occurring in association with dehydration, central nervous system infection, or hypercoagulable states; approximately 25 percent of CVTs are idiopathic [80]. An association between CVT and hyperthyroidism has been suggested by reports of several patients who developed CVT simultaneously with Graves' disease and who had no other risk factors for CVT [84-87]. The number of reported cases is reported to be higher than that expected by chance alone, given the low incidence of each condition [80,85].
The mechanism of CVT in hyperthyroidism may be related to an induced hypercoagulable state, possibly from increased factor VIII clotting activity, documented in at least two cases [80,85]. In other patients, elevated plasma fibrinogen, decreased protein C activity, and increased factors IX and XI may have contributed to a thrombotic state [87,88]. Other possible contributors include altered hemodynamics or dehydration induced by hyperthyroidism, and venous stasis due to compressive effects of a thyroid goiter on cervical veins [80,86].
The clinical manifestations and diagnosis of CVT are discussed separately. (See "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis".)
Other stroke syndromes — Thyroid hormone may also directly affect vascular smooth muscle and endothelium and alter vascular reactivity. These changes may predispose patients to cerebrovascular complications:
●Two cases of fatal stroke and bilateral carotid artery dissection have been reported in individuals with poorly controlled Graves' disease [89]. Pathologic examination of the carotid arteries revealed a segmental mediolytic arteriopathy, an idiopathic noninflammatory vasculopathy that predisposes to dissection and aneurysm formation in cerebral and systemic blood vessels. A small case control study found that autoimmune thyroid disease (both autoimmune thyroiditis as well as Graves' disease) was associated with spontaneous carotid dissection [90].
●Multiple intracranial stenoses, similar to those seen in moyamoya disease, have been described in several patients with Graves' disease [80,91,92]. Predominantly female, these patients had symptoms at a young age (mean 31 years). Clinical manifestations included transient ischemic attack and intracerebral hemorrhage. Proposed pathophysiologic mechanisms include an autoimmune process affecting the cerebral arteries or a vasculopathy produced by chronic thyrotoxic activation of the sympathetic nervous system [91,93]. In one series, the disease appeared to stabilize after treatment of hyperthyroidism [92]. (See "Moyamoya disease and moyamoya syndrome: Etiology, clinical features, and diagnosis".)
●Coincident autoimmune disorders may contribute to an increased risk of antiphospholipid syndrome, giant cell arteritis, antithrombin III deficiency, and Takayasu arteritis in patients with hyperthyroidism due to Graves' disease. However, as such cases are largely individually reported, an association between these disorders and Graves' disease is unproven [94-99]. One case control study did not find an association between giant cell arteritis and hyperthyroidism [100].
Graves' ophthalmopathy — Graves' ophthalmopathy, an autoimmune, inflammatory disease of the retroorbital tissues, occurs in 20 to 25 percent of patients with Graves' disease. Clinical symptoms include bilateral proptosis, restricted eye movements, and periorbital edema. This topic is discussed separately. (See "Clinical features and diagnosis of thyroid eye disease" and "Treatment of thyroid eye disease".)
In the absence of Graves' ophthalmopathy, patients may demonstrate other ophthalmic signs: widened palpebral fissures, infrequent blinking, and the appearance of lid retraction. These are believed to result from heightened sensitivity of receptors to sympathetic nervous system activity.
Uncommon associations — Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyneuropathy have also been described in patients with hyperthyroidism, probably reflecting an underlying predisposition to autoimmune disease [101,102].
An enlarged thyroid gland may compress the recurrent laryngeal nerve, producing vocal cord paralysis, dysphonia, and even respiratory stridor [103,104]. A Horner syndrome may also result from compression of the sympathetic chain.
New-onset Graves' disease has been reported in 20 to 30 percent of patients treated with alemtuzumab for multiple sclerosis. (See "Drug interactions with thyroid hormones", section on 'Drugs that cause hyperthyroidism'.)
SUMMARY
●Severe hyperthyroidism – Patients with severe hyperthyroidism (thyroid storm) can present with an encephalopathy characterized by behavioral and personality changes, such as psychosis, agitation, and depression, often with seizures. These symptoms are typically accompanied by hyperpyrexia and cardiovascular dysfunction (eg, tachycardia and heart failure). (See 'Encephalopathy' above.)
●Other neurologic manifestations of hyperthyroidism – Other common neurologic manifestations of hyperthyroidism include tremor, hyperreflexia, and myopathy. Less common manifestations include chorea, polyneuropathy, and headache. (See 'Tremor' above and 'Motor neuron manifestations' above and 'Myopathy' above.)
●Management and clinical course – Treatment of hyperthyroidism typically leads to improvement in cognitive and behavioral impairments and other neurologic manifestations. Long-term treatment with antiseizure medications and other neurologic treatments are typically not required. (See "Graves' hyperthyroidism in nonpregnant adults: Overview of treatment" and "Thyroid storm", section on 'Initial management'.)
●Neurologic associations with Graves' disease – Patients with Graves' disease may have a higher than expected incidence of other neurologic disorders; some (eg, myasthenia gravis [MG]) co-occur presumably because of their shared autoimmune pathogenesis. (See 'Disease associations' above.)
●Association with ischemic stroke – Ischemic stroke is associated with hyperthyroidism through a variety of mechanisms including hyperthyroid-induced atrial fibrillation (AF), a possible hypercoagulable state, and/or other autoimmune mechanisms. (See 'Stroke' above.)
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