Case Presentation: A 54-year-old female with history of hypothyroidism, surgically treated lumbar radiculopathy and neck sarcoma status post resection and radiochemotherapy was brought to the emergency department (ED) by the police. She was unwilling to speak and history was initially obtained from her son. He states that she has been acting oddly for a year, she quit her job unexpectedly, stopped talking and eating well, and has been homeless for two months after eviction from her home. She nodded to having constipation, denied family members except her son, refused to eat and take oral medications.Her vital signs were stable. On physical exam she was unkempt, cachectic, mute, with mild bradycardia, dry mucosal membranes and skin, brittle hair and flat affect,, otherwise normal. A complete blood count (CBC), complete metabolic panel (CMP), creatine kinase (CK), urinalysis, urine toxicology screen, thyroid stimulating hormone (TSH) with free T4 (fT4), and random cortisol levels revealed an elevated creatinine 2.55 mg/dl, CK 3050 unit/L, TSH 163.67 mcU/ml, fT4 0.1 ng/dl, normal cortisol level, a negative drug screen, and mild electrolyte abnormalities suggesting dehydration. A CT head showed no intracranial abnormalities. She was given intravenous (IV) levothyroxine 100mcg and 50mg IV hydrocortisone. She showed mild improvement on day 2 of hospitalization and was able to respond with one-word answers. Levothyroxine was reduced to 75mcg IV for the following 3 days with dramatic improvement in her symptoms. By day 4, she was able to speak in full sentences and her affect had improved significantly. Repeat fT4 was 0.4 ng/dl and the patient was transitioned to 88mcg oral levothyroxine and discharged 3 days later with 100mcg oral levothyroxine daily.
Discussion: Hypothyroidism is a common endocrine disorder that can often present with neuropsychiatric manifestations, mostly mood disorders, but rarely psychosis in 5-15% of cases. Hypothyroidism is among the most common organic causes of mental disorders. When we are presented with a psychotic patient, ruling out an organic cause is the first step. The literature describes very few cases of severe hypothyroidism presenting with psychosis, known as “Myxedema Madness”, term first used in 1949, by Asher, R. Shlykov, MA et al reported a case in 2016 of an elderly hypothyroid female with psychosis, paranoia, catatonic features and Capgras syndrome, some features similar to our patient. Our patient presented with prolonged mutism and apathy with a very elevated TSH, secondary to medication non-compliance. We observed rapid improvement within 24 hours of resuming levothyroxine along with a steady increase in fT4 levels, without initiating antipsychotics.
Conclusions: Psychiatric disorders have been well associated with thyroid disease, but the mechanism behind this has not yet been elucidated. Further research is necessary to explain the association, though some suggest it could be attributed to the level of thyroid hormone, which plays an important role in cerebral processes or the level of antibodies involved in autoimmune dysthyroidism, such as Hashimoto’s thyroiditis. It is of utmost importance to consider thyroid disorders in patients who present with psychosis, especially because it can be easily diagnosed and treated. In multiple cases reported in the literature, psychotic symptoms in severe hypothyroidism resolve with hormone replacement, regardless of antipsychotic use, suggesting that antipsychotics don’t play the most important role in recovery.