Neurological Manifestations of Thyroid Disease

Updated: Jun 27, 2023
Author: Gabriel Bucurescu, MD, MS, FACNS; Chief Editor: Nicholas Lorenzo, MD, CPE, MHCM, FAAPL 



The thyroid gland plays an important role in tissue metabolism and development. It secretes thyroxine (3,5,3'5'-tetraiodothyronine), which is abbreviated as T4, and small amounts of 3,5,3'-triiodothyronine, abbreviated T3. Both have systemic effects. Abnormal thyroid hormone levels lead to hypothyroid and hyperthyroid states. Inadequate thyroid hormone during development leads to congenital hypothyroidism (also known as cretinism) with associated irreversible brain damage.


Thyroid hormones regulate protein synthesis by affecting gene transcription and mRNA stabilization.


In hyperthyroidism (ie, thyrotoxicosis) increased thyroid function leads to increased cardiac output at rest and after exercise but to decreased muscle bulk and function.[1, 2]

Muscle activity shows altered electrical responses, altered energy metabolism, and increased sensitivity to beta-adrenergic stimuli. In a clinical study of experimental thyrotoxicosis, the activity of oxidative and glycolytic enzymes in skeletal muscle decreased by 21–37%. Lean body mass decreases and rate of whole body protein breakdown is enhanced. Thyroid hormones have profound effects on mitochondrial oxidative activity, synthesis and degradation of proteins, sensitivity of tissues to catecholamines, differentiation of muscle fibers, capillary growth, and levels of antioxidant enzymes and compounds. Muscles show contraction weakness and lack of normal contraction potentiation. Patients have lower levels of carnitine.

The central effects of hyperthyroidism are most pronounced in development. Cerebral circulation and oxygen consumption elevate. Studies on rat brain mitochondria show minimal effects. Measurements from rats suggest well-preserved brain iodothyronine homeostasis despite high thyroid hormone levels. Brain T4 and T3 concentrations and brain T3 production and turnover rates do not change significantly. levels of glutamate dehydrogenase and pyruvate dehydrogenase activity in the brain are reduced. Beta-adrenergic binding sites in the cerebral cortex are increased and gamma-aminobutyric acid (GABA) binding sites are decreased. Brain levels of serotonin, 5-hydroxyindoleacetic acid, and substance P are altered. Native pain sensitivity and number of opiate receptors are increased. Thyroid hormones affect myelination, therefore increased levels lead to oxidative damage to the myelin membrane and/or the oligodendroglial cells.


In hypothyroidism, muscle contraction and relaxation are slowed while duration is prolonged.

The amount of myosin ATPase decreases. Slowing of release and reaccumulation of calcium in the endoplasmic reticulum may decrease relaxation. In peripheral nerves, segmental demyelination has been observed with decreased nerve conduction velocities. Patients develop polyneuropathy with loss of reflexes and weakness. Decreases in vibration, joint-position, and touch-pressure sensations also are seen.

Thyroid deficiency can impair hippocampal neurogenesis, differentiation, and maturation in developmental and adult rat brains, suggesting a similar mechanism in humans. Hypothyroidism changes synaptic transmission and plasticity in area CA1 of the hippocampus, which, in turn, may be the mechanism that leads to impairment in learning and memory.[3]



Thyroid disease is common in adults. An estimated 20 million Americans have some form of thyroid disease. According to the American Thyroid Association, more than 12% of the US population will develop a thyroid condition during their lifetime.[4]

Women are five to eight times more likely than men to have thyroid problems.[4]  One survey found the prevalence of hypothyroidism to be 1.4% in adult females and 0.1% in adult males. The prevalence of Graves disease, a hyperthyroid condition, is 1.9% in females and about 0.19% in males. Peak age incidence is in the range of 30-50 years. Congenital disease occurs in 1 per 4000 neonates in North America and Western Europe. This is seen more frequently in areas of iodine deficiency.

About 1 billion people are at risk for iodine deficiency disorders. Endemic goiter is most the common manifestation and has a varying prevalence. In communities with severe iodine deficiency, prevalence is 5–15% but can reach 100%. This situation occurs in developing countries.

Race-, sex-, and age-related demographics

No race predilection is known.

Thyroid disease is more common in women, but men also are affected.[4]

Thyroid disease is most common in adults aged 30–50 years, but all age groups are affected. Cretinism and neonatal myxedema manifest in the intrauterine/perinatal period.


Prognosis is generally good, since most symptoms are reversible with correction of the underlying problem. Neurologic complications are seldom fatal.

Congenital complications of iodine deficiency lead to cretinism and neonatal myxedema.

Untreated myxedema may lead to myxedema coma and eventually to death in children and adults.

Severity of symptoms of thyroid disease varies with the degree and duration of the deficiency.

Some degree of myopathy is found in about 50% of thyrotoxic patients.

Thyroid storm is an emergency requiring rapid therapy to prevent death.

Although now uncommon, postoperative thyroid disease can be seen.




Presenting symptoms depend on whether thyroid hormone levels are increased or decreased. Symptoms are generalized initially. Neurologic signs appear after months to years. The brain, peripheral nerves, and muscular systems can be affected.


Hypothyroidism occurs when T4 and T3 levels fall below physiologically required levels. Severe hypothyroidism results in myxedema, which results from accumulation of hydrophilic mucopolysaccharides in subcutaneous tissues. The term myxedema can be synonymous with hypothyroidism. However some reserve myxedema for severe hypothyroidism only. Common symptoms include the following:

  • Weakness, fatigue, lethargy, and somnolence

  • Cold intolerance, decreased sweating

  • Dry, coarse skin

  • Headache - In children, subclinical hypothyroidism has been associated with exacerbation of migraine headaches[5]

  • Swelling of the face and extremities

  • Impaired memory and cognition, poor concentration

  • Mild weight gain (with anorexia)

  • Coarseness of voice and impaired hearing

  • Paresthesias and arthralgias

  • Muscle cramps

  • Constipation


Hyperthyroidism results from excessive levels of T4 and T3. Symptoms include the following:

  • Confusion

  • Seizures - Prognosis is good if patients become euthyroid[6]

  • Nervousness and tremor, emotional lability

  • Muscle weakness

  • Heat intolerance

  • Weight loss (with increased appetite)

  • Palpitations



In infants this results in cretinism, which manifests as delayed physical and mental development. Affected infants have enlarged tongues, a coarse cry, thickened subcutaneous tissues, potbelly, umbilical hernia, hearing defects, and speech defects.

Other findings are slowness and masking or disinhibition of facial expression.

Strabismus may be noted.

Some develop thalamic posturing, with severe motor deficits and a characteristic posture.

When the patient is laid on one side, the undermost limb extends and the uppermost limb flexes.

Other signs include microcephaly; inability to sit, stand, or walk; prominent primitive facial reflexes (especially the visual suck reflex); blepharospasm; and a prominent glabellar reflex.

Patients appear autistic (ie, total disregard of surroundings and absence of purposeful activity).

Other signs include the following:

  • Hypotonia

  • Cerebellar signs manifesting with ataxia, tremor, and dysmetria

  • Polyneuropathy

  • Cranial nerve deficits

  • Entrapment neuropathy (eg, carpal tunnel syndrome)

  • Slowing of voluntary movements

  • Myopathic weakness, which can be subdivided into 4 subtypes: Kocher-Debre-Semelaigne syndrome, Hoffmann syndrome,[7] atrophic form, and myasthenic form. Muscle hypertrophy is very rare in hypothyroid patients.

  • Neuropsychiatric signs: Dementia, apathy, mental dullness, irritability, sleepiness.

  • Hashimoto encephalopathy (HE), a rare, sometimes controversial classification of neurologic syndromes occurring in patients with steroid-responsive autoimmune thyroid disease[8, 9] : It was first described in 1966 and was associated with serum anti-thyroid antibodies. A single case report linked Hashimoto encephalopathy with painful legs and moving toes syndrome.[10] Other case reports of miscarriages, focal seizures, and palatal tremor associated with Hashimoto encephalopathy have also been made. Rare cases of primary demyelination and encephalopathy have also been reported. There have also been reports of the encephalopathy mimicking vascular occlusion of the middle cerebral artery.[11]


Hyperthyroidism manifests systemically, affecting primarily muscle function and the central nervous system.

It is associated with neuropsychiatric and neurologic syndromes and myopathy (eg, chronic thyrotoxic myopathy, exophthalmic ophthalmoplegia/infiltrative ophthalmopathy/Graves ophthalmopathy), thyrotoxic periodic paralysis, and myasthenia gravis.

Patients may manifest irritability, nervousness, tremulousness, apprehension, emotional lability, and agitation.

Major depression, anxiety, hypomania or mania, schizophreniform disorder, and delirium also may occur. Milder deficits in memory, complex problem solving, and attention may be present.

Psychosis (visual and auditory hallucinations) is infrequent.

The clinical picture is seldom clear. The onset of symptoms is insidious, and often patients are referred to psychiatrists before the diagnosis is made. This is especially true for older patients, in whom dementia or depression is suspected. The presence of such symptoms may be related to the premorbid personality, but no definitive studies exist to support this theory.

One of the difficulties in establishing the contribution of a premorbid personality is the inability of precisely determining the onset of thyroid dysfunction.

Psychiatric symptoms have no direct relationship to the severity of the hyperthyroidism; once thyroid hormone levels are back to normal, the symptoms may resolve over months.

Neurologic syndromes include chorea, ballism, embolic stroke secondary to tachycardia-induced atrial fibrillation, status epilepticus, and coma (which may occur in thyrotoxic crises).[12] A case report describes a triad of acute ataxia, Graves disease, and stiff person syndrome.[13]

A single case of reversible and unilateral corticospinal tract disease was reported recently. It was thought to be secondary to autoimmune free T3-thyrotoxicosis, and improved significantly with carbimazole 10 mg daily. The patient had low TSH, high T3 , normal T4 and very high antithyroid peroxidase antibody.[14]

Chronic thyrotoxic myopathy is a common complication. This myopathy is characterized by progressive weakness and wasting of skeletal musculature. Goiter of the nodular type is often present (and sometimes exophthalmos). More than 50% of thyrotoxic patients have some degree of myopathy. The myopathy is slowly progressive; the pelvic girdle and thigh muscles are affected preferentially.

Exophthalmic ophthalmoplegia also is known as Graves ophthalmopathy and infiltrative ophthalmopathy. This refers to weakness of external ocular muscles and exophthalmos from Graves disease. Strabismus and diplopia may be present, as well as pain and lid retraction. The term infiltrative ophthalmopathy refers to ocular muscle histology that suggests an autoimmune process: prominent fibroblastic tissue, degenerated fibers, and infiltration of lymphocytes, mononuclear leukocytes, and lipocytes.

Thyrotoxic periodic paralysis resembles familial periodic paralysis and manifests with attacks of mild to severe weakness, during which serum potassium levels are generally low.

Thyrotoxic neuropathy was also reported. Both the clinical and electrophysiological abnormalities resolved with treatment of the thyrotoxicosis.

Myasthenia gravis may be associated with hyperthyroidism. Hyperthyroidism is seen in 5% of patients with myasthenia gravis. Conversely, incidence of myasthenia gravis is 20-30 times higher in hyperthyroid patients than in the general population. Weakness and muscle atrophy from hyperthyroid myopathy can coexist with other abnormalities secondary to myasthenia gravis.

Graves disease has been associated with intracranial arterial stenosis/occlusion (moyamoya syndrome). The exact mechanism is unknown; it is believed that thyroid hormones may augment vascular sensitivity to the sympathetic nervous system and induce pathological changes in the arterial walls.[15]

Subclinical hyperthyroidism has been linked to sudden unexpected death in epilepsy (SUDEP). The mechanism is hypothesized to be facilitation of cardiovascular abnormalities. Subclinical hyperthyroidism has been reported to increase heart rate, left ventricular mass, and cardiac contractility, which, in turn, could lead to diastolic dysfunction and impaired ventricular ejection fraction response to exercise and atrial arrhythmias.[16]


Clinicians must be able to identify characteristic neurologic deficits of thyroid disease so as to predict and possibly prevent neurologic complications. These include drug effects, which can suppress thyroid-stimulating hormone (TSH) secretion, inhibit thyroid hormone release or synthesis, decrease hormone-protein binding, or inhibit conversion of T4 to T3.

Drugs affecting the thyroid are as follows:

  • Dopamine, L-dopa

  • Glucocorticoid excess

  • Iodide

  • Lithium carbonate

  • Sulfonylureas

  • Phenylbutazone

  • Phenytoin

  • Salicylates

  • Fenclofenac

  • Furosemide

  • Propylthiouracil

  • Propranolol

  • Amiodarone

  • Iopanoic acid (Telepaque), iopodate (Oragrafin)

Causes of hyperthyroidism are as follows:

  • Graves disease

  • Toxic multinodular goiter

  • Toxic adenoma

  • Iodide-induced hyperthyroidism

  • Subacute thyroiditis

  • Factitious (exogenous) thyroiditis

  • Neonatal thyrotoxicosis (eg, pregnant mother with Graves disease)

  • TSH-secreting pituitary tumor

  • Nontumorigenic pituitary-induced hyperthyroidism

  • Choriocarcinoma (uterine or testicular origin) or hydatidiform mole

  • Struma ovarii

  • Hyperfunctioning thyroid carcinoma (usually metastatic)

Hypothyroidism can be primary, secondary, or due to tissue resistance to thyroid hormone.

Primary causes of hypothyroidism are as follows:

  • Destructive lesions such as Hashimoto thyroiditis

  • Idiopathic myxedema

  • Radioactive iodine therapy for hyperthyroidism

  • Subtotal thyroidectomy (eg, surgery for Graves disease)

  • Neck irradiation for other diseases

  • Following acute thyroiditis (can be transient)

  • Cystinosis

  • Defects in enzymes that are necessary for thyroid hormone synthesis (congenital goiter)

  • Endemic goiter (iodine deficiency)

  • Iodine excess (>6 mg/d)

  • Drug-induced thyroid agenesis

  • Thyroid dysgenesis or ectopy

  • Maternal iodide

  • Antithyroid drugs

Secondary causes of hypothyroidism are as follows:

  • Hypothalamic dysfunction due to neoplasm

  • Eosinophilic granuloma or therapeutic irradiation

  • Pituitary dysfunction due to neoplasm

  • Pituitary surgery or irradiation

  • Idiopathic hypopituitarism

  • Sheehan syndrome (ie, postpartum pituitary necrosis)

  • Dopamine infusion

  • Severe illness

  • Heatstroke[17]

  • Traumatic brain injury





Laboratory Studies

Blood levels of thyroid hormone and serum thyrotropin (ie, TSH) are the most important diagnostic tests. levels of free T4 and free T3 in serum provide a better assessment of the thyroid status than total T4 and T3. The levels of T4 and T3 are decreased in hypothyroidism, and they are increased in hyperthyroidism.

Serum TSH levels range from 0.5 to 5.0 microunits per milliliter. TSH is increased in hypothyroidism, and as thyroid function becomes autonomous, it decreases. It is a useful marker for the efficacy of therapy. The TSH-immunometric assay (TSH-IMA) can discriminate directly between normal TSH and reduced levels without requiring the use of the thyrotropin-releasing hormone (TRH) infusion test. If TSH levels remain high in cases of treated hypothyroidism, the possibility of a TSH-secreting pituitary adenoma should be considered.

TRH infusion test can be performed by infusing TRH intravenously and measuring TSH in serum to determine the presence of TSH in the pituitary. TSH is reduced in hyperthyroidism in autonomous thyroid production and hypothalamic pituitary disease. This test has been superseded by the TSH-IMA.

Thyroid hormone-binding ratio (known previously as T4 and T3 uptake) and transthyretin levels are rarely useful for common clinical purposes.

Radioactive iodine (RAI) uptake can differentiate causes of hyperthyroidism: subacute thyroiditis (low uptake) versus Graves disease (high uptake).

Antithyroid antibodies, the most important being thyroid microsomal antibody (TMAb), are seen in 95% of patients with Hashimoto thyroiditis but in only 10% of adults with no disease. In Graves disease, 55% of patients have circulating TMAbs. Recently, in a small study, antithyroid antibodies were found to be the most common abnormality in a group of patients with autoimmune manifestations and atypical neurologic features.

Antithyroperoxidase antibodies from patients with Hashimoto encephalopathy were found to bind to cerebellar cells expressing glial fibrillary acid protein.[18]

Thyroglobulin antibodies (TGAbs) are present in the serum of 60% of patients with Hashimoto disease.

Interestingly, increased levels of thyroglobulin antibodies and/or antithyroid peroxidase antibodies have been found in patients with aquaporin-4 (AQP4) antibody–positive CNS autoimmunity and multiple sclerosis, both in pediatric and adult age groups. AQP4 antibody plays an important role in the pathophysiology of neuromyelitis optica (NMO) spectrum disorders, and such patients have a high frequency of autoimmune thyroid disease.[19]

Antibodies against thyroid TSH receptor (TRAbs) are seen in the serum of patients with Graves disease.

Serum thyroglobulin is most useful in follow-up of metastatic thyroid carcinoma after thyroidectomy.

Creatine kinase (CK) levels may be elevated.

Cerebrospinal fluid (CSF) protein may be increased.

Imaging Studies

Imaging studies such as MRI or CT scan are of limited use in thyroid disease. Pituitary or hypothalamic tumors can be seen, as can metastatic lesions of thyroid carcinoma, which are usually solitary. In cases of severe exophthalmic ophthalmoplegia, extraocular muscle swelling can be observed on both MRI and CT scans (sometimes impinging on the optic nerve). Brains of adults with congenital hypothyroidism may show atrophy, especially of the brain stem and perisylvian regions (with cerebellum sparing). Patients with antibodies against thyroid antigens may show nonspecific MRI changes, probably due to demyelination.

Thyroid scan (which involves either radioactive iodine 123 or iodine 131) correlates thyroid function and structure. It can diagnose the functional state of a thyroid nodule or search for thyroid tissue in neck masses.

Thyroid ultrasound can assess whether a thyroid mass is solid or cystic. It is used usually to help in diagnosing a single thyroid nodule; cystic lesions may be simple cysts or benign follicular tumors, which could be managed medically, sparing the patient the need for surgery. However, follicular carcinoma also can become cystic, in which case tissue biopsy would be required. Solid masses suggest a possible tumor, in which case the treating physician would be inclined to proceed to surgery.

Other Tests

Electroencephalography in hyperthyroidism

EEG may support the suspicion of CNS involvement. Alpha rhythm is accelerated, and rolandic mu rhythm may be augmented.

Some have reported paroxysmal bursts and clinical seizures (eg, grand mal). Patients with epilepsy and thyroid dysfunction may respond poorly to anticonvulsants until the underlying endocrine problem is treated. Thyroxine can produce epileptic activity. In thyrotoxic crises with encephalopathy, EEG abnormalities are characterized by marked slowing with superimposed fast activity. Triphasic waves are reported rarely.

Electroencephalography in hypothyroidism

EEG is characterized by an excess of low-voltage activity with a poor or absent alpha-blocking response. In myxedematous coma, slow, low-voltage activity predominates. Generalized periodic sharp wave discharges, mimicking Jakob-Creutzfeldt encephalopathy, have been reported in one case. EEG abnormalities tend to resolve as thyroid abnormalities are treated. In myxedematous infants, delay in EEG development (especially of sleep spindle) can occur. Generally, EEG shows excessive low-voltage slowing.


EMG generally provides limited information. Proximal muscles are more likely to show an abnormal pattern than distal muscles. In hyperthyroid patients, abnormalities include reduced duration of mean action potentials and increased mean percentage of polyphasic potentials. Large action potentials may be seen in thyrotoxic myopathy but are not associated histologically with neuropathic change and are not believed to indicate denervation. In hypothyroidism, EMG changes include polyphasic action potentials, hyperirritability, repetitive discharges after reflex motion, and low-voltage, short-duration motor unit potentials. Changes usually resolve as thyroid function normalizes.

Nerve conduction studies

Nerve conduction velocities (NCV) are decreased in hypothyroid patients with polyneuropathy. Patients show diffuse sensory neuropathy due to axonal degeneration and not, as previously thought, to segmental demyelination. Amplitude of sensory compound nerve action potentials (CNAP) is reduced and NCVs are slowed. In carpal tunnel syndrome, typical nerve conduction abnormalities are seen.

One case was reported of severe hyperthyroidism with motor-sensory neuropathy, moderately slow NCVs, absent sural CNAP, and low sural sensory NCV. Thyrotoxic neuropathy (also known as Basedow paraplegia) is very rare.

Evoked potential studies 

Generally these are not useful in thyroid disease. Visual evoked potentials show increased latencies in hyperthyroidism with no change after patients become euthyroid.[20, 21, 22, 23]

In hypothyroid patients, amplitudes are decreased and latencies are prolonged. Latencies and amplitudes improved inconsistently among some patients as thyroid function normalized. Brainstem evoked responses are marginally useful, with some studies showing abnormalities. Patients who had been hyperthyroid for longer than 6 months showed increased N19-P23 amplitudes in median somatosensory evoked potentials with the latency unaffected.


The following procedures may be needed:

  • Thyroidectomy

  • Fine-needle biopsy

  • Muscle or peripheral nerve biopsy: This can confirm diagnosis or differentiate diagnoses. Both hyperthyroid and hypothyroid patients may have disturbed levels of carnitine but by separate mechanisms.[24]

Histologic Findings


Sural nerve biopsies reveal axonal degeneration.

Electron microscopy reveals the following:

  • Focal microfibrillar disorganization, sometimes with nemaline rods

  • Mitochondrial accumulation

  • Occasional basophilic degeneration: In cardiac and skeletal muscle, basophilic degeneration is due to deposits of polysaccharide material.

  • No definite abnormalities in muscle from individuals with congenital hypothyroidism

Muscle histology reveals the following:

  • Type I fiber excess

  • Atrophy of type I and II fibers

  • Altered oxidative enzyme activity, abnormal collection of glycogen, peripheral crescents, and distention of cytoplasmic reticulum

  • Vacuolar myopathy

  • Increased central nuclear counts

  • Central cores with oxidative activity in type I fibers

  • Impaired myelin formation


Sural nerve biopsies reveal the following:

  • Excessive axonal branching

  • Degenerative changes of preterminal axons

  • Edematous protein infiltration of endoneurium and perineurium

  • Segmental demyelination in teased fiber preparation

Electron microscopy reveals the following:

  • Increased glycogen, acid mucopolysaccharides, and aggregates of glycogen and cytoplasmic laminar bodies in Schwann cells

  • In brain, small neuronal cell bodies with increased cell packing density, decreased neurophil, decreased myelin, and gliosis (especially in the substantia nigra and globus pallidus)

Muscle histology reveals the following:

  • Few pathologic changes in hyperthyroidism

  • Mild atrophy, infiltration of fat cells, nonspecific focal myofibrillar degeneration, mitochondrial hypertrophy, and focal dilatation of transverse tubular system



Approach Considerations

Neurologic manifestations in thyroid diseases are manageable on an outpatient basis. Therapy is maintained for months (if not years). In most cases, neurologic abnormalities slowly resolve.

Thyroid storm and myxedema coma are exceptions. Both are emergencies that require aggressive treatment in the ICU. The mortality rate of thyroid storm can be as high as 20–40%. The symptoms usually are exaggerated manifestations of the symptoms seen in hyperthyroidism; a superimposed infection and the stress associated with it would exacerbate the symptoms. Fever, abdominal pain, delirium, and psychosis can occur. The patient may become obtunded. Thyroid storm should be suspected in any patient with severe hyperpyrexia, tachycardia, and a goiter.

Medical Care

Neurologic manifestations in thyroid disease generally develop slowly. They are diagnosed months or years after initial endocrine problems. Patients seek care after developing characteristic systemic signs and symptoms.

Polyneuropathy is rarely the initial manifestation of undetected hypothyroidism. Metastatic thyroid carcinoma rarely presents as an initial brain metastatic lesion.

Chorea-ballism has been reported sporadically. Chorea has been associated with elevated levels of antithyroid antibodies, with the symptoms responding to oral steroid treatment.

Interestingly, one study reports that mild hypothyroidism is associated with better survival of ambulatory elderly patients after acute stroke.[25]

Several reports of intracranial vascular disease (arterial occlusion, superior sagittal sinus thrombosis, cerebral vein thrombosis) have been reported associated with both hypothyroidism and hyperthyroidism. However, the patients had multiple pathologies, and a clear correlation with thyroid disease is difficult to establish.[26, 27, 28]

Pregnant patients require follow-up at least monthly. Closely observe these newborns for thyroid disease.

Surgical Care

Surgery is indicated in the treatment of thyroid masses and large goiters.


The following consultations may be warranted:

  • Internal medicine/endocrinologist

  • Head and neck surgeon

  • Nuclear medicine specialist

  • Radiation oncologist

  • Pathologist


Iodine deficiency is not widespread in the United States, although immigrants from areas of endemic deficiency may require dietary consultation. Pregnant women may require more careful screening.



Medication Summary

The goal is to establish a euthyroid state. In hypothyroidism, this involves thyroid replacement, which is attained readily. In hyperthyroidism, elevated thyroid hormone is treated with surgery, which causes hypothyroidism and requires thyroid replacement, or with drugs and radioactive iodine.

Symptoms that are associated with abnormal thyroid states are treatable.

Thiourea derivatives

Class Summary

These medications are preferred for suppressing thyroid function.

Propylthiouracil (PTU)

Propylthiouracil is a derivative of thiourea that inhibits organification of iodine by the thyroid gland. It also inhibits the conversion of T4 to T3, which is advantage over other agents.

Methimazole (Tapazole)

Methimazole suppresses thyroid function and has a mechanism similar to that of PTU; it does not inhibit peripheral conversion of T4 to T3. Methimazole is fifteen times as potent as PTU. PTU-equivalent dosing can be used, divided thrice daily.

Beta-adrenergic blocking agents

Class Summary

These agents are used to treat symptomatic hyperthyroidism.

Propranolol (Inderal)

This nonselective, beta-adrenergic blocking agent treats symptomatic tachycardia. Propranolol has membrane-stabilizing activity and decreases the automaticity of contractions.

Thyroid hormones

Class Summary

These agents are used in thyroid hormone replacement.

Levothyroxine (Synthroid, Levoxyl)

Levothyroxine is synthetic, but it is identical to natural T4; in its active form, levothyroxine influences the growth and maturation of tissues; it is involved in normal growth, metabolism, and development.


Class Summary

These agents replace depleted electrolytes.

Potassium chloride (K-DUR)

Potassium chloride is essential for the transmission of nerve impulses, maintenance of intracellular tonicity, and maintenance of normal renal function. It is also vital for skeletal and smooth muscles. Potassium chloride replaces potassium lost in thyrotoxic periodic paralysis.


Class Summary

These agents provide immunosuppressive therapy for Graves ophthalmopathy, especially in cases of severe exophthalmos.

Prednisone (Deltasone, Sterapred, Orasone)

Prednisone is a widely used glucocorticoid that suppresses inflammatory processes by reversing increased capillary permeability and suppressing PMN activity; it is used to treat allergic, inflammatory, and autoimmune disorders.

Tricyclic antidepressants

Class Summary

These agents may help relieve painful polyneuropathy.

Amitriptyline (Elavil)

By inhibiting the reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, amitriptyline may increase the synaptic concentration of these neurotransmitters in the CNS; it is useful as an analgesic for certain chronic and neuropathic pain.

Antiepileptic agents

Class Summary

These agents are useful in treating neuropathic pain.

Gabapentin (Neurontin)

Gabapentin's exact mechanism is unknown. It is structurally related to GABA and is useful in some pain syndromes.