Evidence-Based Reviews

Identifying hyperthyroidism’s psychiatric presentations

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References

“They all made me stupid,” she complained.

Zolpidem, 20 mg at night, helped temporarily as a hypnotic, but insomnia recurred within weeks. Diazepam was effective at high dosages but also dulled her cognition. The psychiatrist did not suspect a thyroid abnormality and did not perform a pituitary-thyroid laboratory evaluation.

Ms. B consulted a gynecologist, who prescribed estrogen for borderline low estradiol levels and with the hope that Ms. B’s symptoms represented early menopause. This partially ameliorated her irritability, possibly because estradiol binding of circulating T4 reduced free thyroid hormone levels.

Ms. B tried to continue working and exercising, but within 4 years her symptoms progressed to severe depression with frequent crying spells, feelings of general malaise, excessive sweating, occasional panic attacks, fatigue, sleepiness, deteriorating vision, and cognitive impairment. She struggled to read printed words and eventually took sick leave while consulting with physicians.

Finally, a routine thyroid screen before minor surgery revealed an undetectable TSH concentration. Further testing showed elevated thyroxine consistent with thyrotoxicosis. Graves’ disease was diagnosed, and euthyroidism was established with antithyroid medication.

Residual mood and anxiety symptoms persisted 1 year after euthyroidism was restored, and Ms. B sought psychiatric consultation.

Discussion. Hyperthyroidism can trigger or present as a hypomania or manic-like state, characterized by increased energy, hyperactivity, racing thoughts, hair-trigger verbal explosiveness, and decreased need for sleep.

Hypertalkativeness is common, even without pressured speech, as is irritability. Mood may be elevated, depressed, mixed, or cycling. A hyperthyroidism-related mixed syndrome of depression and hypomania can be confounding.

Mr. C: Occult hyperthyroidism

Mr. C, age 26, was apparently healthy when he was admitted into a neuroendocrine research protocol as a volunteer. His job performance was excellent, and his interactions with others were good; he was in good general health and taking no medication.

Formal psychiatric screening found no history of psychiatric disorders in Mr. C nor his family. His mental status was within normal limits. Physical exam revealed no significant abnormality. He was afebrile, normotensive, and had a resting pulse of 81 bpm.

His neurologic status was unremarkable, and laboratory screening tests showed normal CBC, liver and renal profiles, glucose, platelets and clotting times. Tests during the study, however, showed frankly elevated T4, free thyroxine (FT4), and T3 concentrations, along with undetectable TSH. Mr. C was informed of these results and referred to an endocrinologist.

Graves’ disease was diagnosed, and Mr. C received partial thyroid ablation therapy. He later reported that he had never felt better. In retrospect, he realized he had been anxious before he was treated for hyperthyroidism because he felt much more relaxed and able to concentrate after treatment.

Discussion. Subjective well-being in a patient with occult biochemical thyrotoxicosis can be misleading. Mr. C was much less anxious and able to concentrate after his return to euthyroidism.

Treatment

Refer your hyperthyroid patients to an endocrinologist for further workup and, in most cases, management. Hyperthyroidism is usually easy to treat using a form of ablation (antithyroid drugs, radioactive iodine, or partial thyroidectomy).

Remain involved in the patient’s care when psychiatric symptoms are prominent, however, as they are likely to persist even after thyrotoxicosis is corrected.6 Reasonable interventions include:

  • control of acute thyrotoxic symptoms such as palpitations and tremulousness with propranolol, 20 to 40 mg as needed, or a 20-mg bolus of prednisone (especially if thyroiditis is present)
  • address mood cycling, depression, edginess, anxiety, lability, insomnia, and/or irritability with lithium3
  • oversee smoking cessation in patients with Graves’ disease (smoking exacerbates the autoimmune pathology).

Address and correct hyperthyroidism that is artifactual (caused by overuse or secret use by a patient) or iatrogenic (related to excessive prescribed hormone dosages).

Subclinical hyperthyroidism can be transient and resolve without treatment. Lithium can be helpful when a mood disorder coexists with sub clinical hyperthyroidism. Start with 300 to 600 mg every evening with dinner. If the mood disorder is mild, even as little as 300 to 450 mg of lithium may elevate a depressed mood and remove edginess and irritability.

Lithium is antithyroid, decreases thyroid hormone output, and increases serum TSH within 24 hours of initiation, but it can provoke autoimmune hyperthyroidism in some individuals.21

Related resources

  • For comprehensive tables of hyperthyroidism’s causes, refer to Pearce EN. Diagnosis and management of thyrotoxicosis. BMJ 2006;332:1369-73, or Lazarus JH. Hyperthyroidism. Lancet 1997;349:339-43.
  • Geracioti TD Jr. Identifying hypothyroidism’s psychiatric presentations. Current Psychiatry 2006;5(11):98-117.
  • Bauer M, Heinz A, Whybrow PC. Thyroid hormones, serotonin and mood: of synergy and significance in the adult brain. Molecular Psychiatry 2002;7:140-56.

Drug brand names

  • Fluvoxamine • Luvox
  • Lithium • Lithobid, others
  • Levothyroxine • Synthroid, others
  • Prednisone • Various brands
  • Propranolol • Inderal
  • Zolpidem • Ambien

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