Psychosis induced by hypothyroidism mistaken for brief reactive psychosis

To the Editor

Psychosis is a rare neuropsychiatric com-plication of hypothyroidism, described in the 1800s (Ord, 1888). Published reports of myxoedema psychosis describe a range of possible clinical presentations, featuring combinations of paranoia, visual hallucinations, mania, confusion and delusions. Definitive treatment constitutes thyroxine replacement and some clinicians report that adjunctive antipsychotics assist or accelerate recovery (Hynicka, 2015). Neuropsychiatric sequelae of hypothyroidism may persist despite treatment, due to irreversible damage secondary to chronic metabolic changes (Azzopardi et al., 2010).

A 32-year-old woman presented to hospital following a minor motor vehicle accident, without physical injuries. She was hypervigilant with marked psychomotor agitation, requiring intramuscular droperidol and physical restraint. This occurred in the context of new visual hallucinations, paranoia, bizarre delusions, disorganised thoughts and impulsivity for 14 days beforehand. There was no prior history of depression, mania or psychosis. She denied any physical symptoms or medical comorbidities. Physical examination and vital signs were unremarkable. She denied illicit substance use and urine drug screening returned negative.

Her psychiatric symptoms resolved spontaneously without further psychiatric intervention. An organic screen for psychosis, including brain imaging, was performed; however, thyroid function tests (TFTs) were inadvertently omitted. Her discharge diagnosis was a brief reactive psychosis.

She re-presented 1 week later, appearing perplexed with paranoid delusions and fluctuating consciousness. TFTs identified a thyroid-stimulating hormone (TSH) of 246.6 mU/L (0.30–5.00) and undetectable T4 < 5.4 pmol/L (9.1–19.6). Other organic screening tests were normal. Collateral history revealed primary hypothyroidism untreated for 20 years. Endocrinology consultation identified physical manifestations of hypothyroidism with delayed relaxation of deep tendon reflexes, cool dry skin and profound psychomotor slowing. Her thyroid was non-tender and unenlarged; her vital signs, cardiac and respiratory examinations, were unremarkable.

Twice-weekly intramuscular levothyroxine (due to refusal of oral therapy) and daily olanzapine (15 mg) were prescribed. Facial angioedema prompted a change from olanzapine to risperidone 2 mg daily. Transition to oral thyroxine occurred once appropriate. Cognitive screening using the Montreal Cognitive Assessment improved from 17/30 on day 3 to 29/30 on day 15. She was discharged on day 16 without thought disorder, perceptual disturbance, paranoia or delusions. Her TSH reduced to 0.82 mU/L and T4 increased to 9.5 pmol/L. Community monitoring by Psychiatry and Endocrinology demonstrated stability without re-emergence of neuropsychiatric symptoms, permitting cessation of risperidone.

This case highlights the importance of consistently performing a complete organic screen when approaching a ‘first-episode psychosis’. This case is an unusual report of psychosis due to hypothyroidism masquerading as a primary psychiatric disorder.