eMedicine Specialties > Neurology > Neuromuscular Diseases

Thyroid Disease: Treatment & Medication

Author: Gabriel Bucurescu, MD, MS, Staff Neurologist, Neurology Service, Philadelphia Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Jan 29, 2009

Treatment

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.5
  • 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.6,7,8

Surgical Care

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

Consultations

  • Internal medicine/endocrinologist
  • Head and neck surgeon
  • Nuclear medicine specialist
  • Radiation oncologist
  • Pathologist

Diet

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.

Activity

No restrictions are recommended typically.

Medication

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

These medications are preferred for suppressing thyroid function.


Propylthiouracil (PTU)

Derivative of thiourea that inhibits organification of iodine by thyroid gland. Also inhibits conversion of T4 to T3, which is advantage over other agents.

Adult

300-450 mg/d PO divided tid; rarely, as much as 1600 mg/d may be required

Pediatric

Adjust dosage according to severity of disease and patient weight

Has anti-vitamin K activity and may potentiate activity of oral anticoagulants

Documented hypersensitivity; breastfeeding mothers

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May cause rash, vasculitis, and rarely, hepatocellular damage and agranulocytosis; use sparingly in pregnant patients, because drug crosses placenta


Methimazole (Tapazole)

Suppresses thyroid function and has mechanism similar to that of PTU; does not inhibit peripheral conversion of T4 to T3.
Fifteen times as potent as PTU. PTU equivalent dosing can be used, divided tid.

Adult

Mild hyperthyroidism: 15 mg/d PO; adjust to effect
Moderately severe hyperthyroidism: 20-30 mg/d PO; adjust to effect
Severe hyperthyroidism: 60 mg/d PO; adjust to effect
Maintenance dose: 5-15 mg PO qd

Pediatric

Initial dose: 0.4 mg/kg PO divided tid
Maintenance dose: Half initial dose

Has anti-vitamin K activity and may potentiate activity of oral anticoagulants

Documented hypersensitivity; breastfeeding mothers

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

May cause agranulocytosis; closely monitor patients for adverse effects; may cause hypoprothrombinemia and bleeding

Beta-adrenergic blocking agents

These agents are used to treat symptomatic hyperthyroidism.


Propranolol (Inderal)

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

Adult

20-40 mg PO q4-6h

Pediatric

2-4 mg/kg/d PO divided bid

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability, possibly reducing effects
Conversely, calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase levels, and thus toxicity or effects
May increase toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines

Documented hypersensitivity; uncompensated congestive heart failure (CHF); bronchial asthma; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in patients with renal or hepatic dysfunction (may reduce intraocular pressure); beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia
Abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely

Thyroid hormones

These agents are used in thyroid hormone replacement.


Levothyroxine (Synthroid, Levoxyl)

Synthetic, but identical to natural T4; in its active form, influences growth and maturation of tissues; is involved in normal growth, metabolism, and development.

Adult

25 mcg PO initially; increase to effect prn

Pediatric

10-15 mcg/kg/d PO initially; adjust to effect prn

Cholestyramine may decrease levothyroxine absorption; estrogens may decrease response to thyroid hormone therapy in patients with nonfunctioning thyroid gland; levothyroxine increases effect of anticoagulants; conversion of hypothyroid patient to euthyroid state may decrease activity of some beta-blockers

Documented hypersensitivity; uncorrected adrenal insufficiency; untreated thyrotoxicosis

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

Treatment of myxedema coma may require simultaneous administration of glucocorticoids; caution in patients with angina pectoris or cardiovascular disorders; monitor thyroid status periodically

Electrolytes

These agents replace depleted electrolytes.


Potassium chloride (K-DUR)

Essential for transmission of nerve impulses, maintenance of intracellular tonicity, and maintenance of normal renal function. Also vital for skeletal and smooth muscles. Replaces potassium lost in thyrotoxic periodic paralysis.

Adult

100-200 mEq PO during an attack

Pediatric

Administer as in adults

ACE inhibitors may elevate serum potassium concentrations; potassium-sparing diuretics and potassium-containing salt substitutes can produce severe hyperkalemia; hypokalemia may result in digoxin toxicity, use caution if discontinuing potassium preparation for patients who are maintained on digoxin

Hyperkalemia; renal failure and conditions in which potassium retention is present; oliguria or azotemia; crush syndrome; severe hemolytic reactions; anuria; adrenocortical insufficiency

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

High plasma concentrations of potassium may cause death due to cardiac depression, arrhythmias, or arrest; plasma levels do not necessarily reflect tissue levels
Monitor potassium replacement therapy whenever possible by continuous or serial ECG

Corticosteroids

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


Prednisone (Deltasone, Sterapred, Orasone)

Widely used glucocorticoid that suppresses inflammatory processes by reversing increased capillary permeability and suppressing PMN activity; used to treat allergic, inflammatory, and autoimmune disorders.

Adult

15-20 mg/d PO, although as much as 100 mg may be necessary; after obtaining satisfactory response, can be tapered slowly

Pediatric

Adjust dosage according to severity of symptoms (as in adult dosing)

Drugs that induce hepatic enzymes may increase clearance; estrogens may decrease clearance; may increase digitalis toxicity secondary to hypokalemia; phenobarbital, phenytoin, and rifampin may increase metabolism of glucocorticoids—in such cases, consider increasing maintenance glucocorticoid dose; diuretics may cause hypokalemia, monitor patients

Documented hypersensitivity; viral, fungal, or tubercular skin infections; peptic ulcer disease; hepatic dysfunction; connective tissue infections

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Patients are at risk for multiple complications, such as severe infections; abruptly discontinuing glucocorticoids may cause adrenal crisis; complications of glucocorticoid use include hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, infections

Tricyclic antidepressants

These agents may help relieve painful polyneuropathy.


Amitriptyline (Elavil)

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

Adult

10-100 mg PO qhs

Pediatric

<12 years: Not recommended
>12 years: Administer as in adults

Metabolized by P-450 2D6 system, so drugs that inhibit this enzyme system (eg, cimetidine, quinidine) may increase levels
Phenobarbital may decrease effects by increasing its metabolism; amitriptyline inhibits hypotensive effects of guanethidine; may interact with thyroid medications, alcohol, CNS depressants, barbiturates, and disulfiram

Documented hypersensitivity; MAOIs within past 14 d; caution in patients who have seizures, cardiac arrhythmias, glaucoma, or history of urinary retention

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Schizophrenic patients may develop increased symptoms of psychosis; caution in patients with impaired liver function; lowers seizure threshold
Common adverse effects include antimuscarinic effects such as dry mouth, sedation, and blurred vision; others include orthostatic hypotension, increased appetite, and constipation; caution in patients who have seizures, cardiac arrhythmias, glaucoma, or history of urinary retention

Antiepileptic agents

These agents are useful in treating neuropathic pain.


Gabapentin (Neurontin)

Exact mechanism unknown. Structurally related to GABA; useful in some pain syndromes.

Adult

300-1200 mg PO tid

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Antacids may reduce bioavailability significantly, so administer gabapentin at least 2 h following antacid; may increase norethindrone levels significantly

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Do not administer to patients with renal failure, since it is excreted by kidneys

More on Thyroid Disease

Overview: Thyroid Disease
Differential Diagnoses & Workup: Thyroid Disease
Treatment & Medication: Thyroid Disease
Follow-up: Thyroid Disease
References

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Further Reading

Keywords

thyroid neuropathy, thyroid myopathy, hyperthyroidism, hypothyroidism, Graves disease, myxedema, cretinism, thyrotoxicosis, Graves ophthalmopathy, thyroid eye disease, thyroid ophthalmopathy, thyroid orbitopathy, infiltrative ophthalmopathy, thyroid disease, T3, T4, thyroxine, thyroid hormones, regulation of thyroid hormones, myasthenia gravis, chronic thyrotoxic myopathy

Contributor Information and Disclosures

Author

Gabriel Bucurescu, MD, MS, Staff Neurologist, Neurology Service, Philadelphia Veterans Affairs Medical Center
Gabriel Bucurescu, MD, MS is a member of the following medical societies: American Academy of Neurology, American Clinical Neurophysiology Society, and American Epilepsy Society
Disclosure: Nothing to disclose.

Medical Editor

Thomas A Kent, MD, Professor, Department of Neurology, Baylor College of Medicine; Neurology Care Line Executive, Michael E DeBakey Veterans Affairs Medical Center
Thomas A Kent, MD is a member of the following medical societies: American Academy of Neurology, American Neurological Association, New York Academy of Sciences, Royal Society of Medicine, Sigma Xi, and Stroke Council of the American Heart Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Agapito S Lorenzo, MD, Laboratory Director, Associate Professor, Departments of Neurology, Creighton University and University of Nebraska Medical Center
Agapito S Lorenzo, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
Disclosure: Nothing to disclose.

Chief Editor

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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