The current case report describes a 30-35-year-old African American male with no past psychiatric history who presented with psychotic-like symptoms and was ultimately found to have psychosis disorder due to hyperthyroidism. The hyperthyroidism was treated with surgical removal, but uniquely, the psychotic symptoms persisted post-operatively even with evidence of euthyroid, normal PTH and calcium levels. The symptoms were significant enough to lead to multiple-day inpatient psychiatric hospitalization. Ultimately, the patient was treated with a second-generation antipsychotic Olanzapine, resolving the psychotic symptoms.
A. Psychiatric Condition and Beta-Adrenergic Activation in Hyperthyroidism
Although the overlap between symptoms of hyperthyroidism and psychiatric conditions is significant, vital signs and physical exam abnormalities often can distinguish between the two. Persistent tachycardia can distinguish between psychiatric conditions such as mania or psychosis and hyperthyroidism. However, one must use caution to use those objective measures, as tachycardia can often exist in co-morbid psychiatric conditions such as anxiety, substance use, or several other medical conditions (6; 9). In hyperthyroidism, there is an overactivation of beta-adrenergic receptor mediation of catecholamines, which could cause agitation, aggression, and tachycardia (3). In our case, the patient had benign initial vital sign parameters initially, with no tachycardia, but developed tachycardia which led to thyroid testing, so vital signs were useful in formulating the differential diagnosis.
B. Comparison of Current Case to Past Cases of Psychosis Secondary to Thyrotoxicosis
Previous case reports have shown that psychosis secondary to thyrotoxicosis have multiple primary psychiatric etiologies including depression and mania (5). Our patient had unknown etiology of psychosis, but our leading differentials were related to medical condition (thyrotoxicosis), primary thought disorder such as unspecified schizophrenia spectrum or other psychotic disorder or due to substance-induced psychotic disorder secondary to cannabis use. Interestingly, for psychosis secondary to thyrotoxicosis, most case reports have a majority of non-primary thought disorders as etiology (5).
C. Pathogenesis of Thyrotoxicosis-Induced Psychosis
There is a prevalence of data that suggests beta-adrenergic activation would help explain the similarity of thyrotoxicosis to symptoms such as mania, aggression or anxiety (6;9). However, the connection of thyrotoxicosis to psychosis is less clear. It is thought that, in Graves Disease, the increase in TSH receptor (TSHR) antibodies activates TSH receptors in the hippocampus and cerebrum, producing neuropsychiatric symptoms (14). In addition, studies have shown altered glucose metabolism in limbic structures in patients with hyperthyroid disease states implicating the limbic system in the manifestation of psychiatric symptoms (14, 15). Psychosis brain imaging studies indicate that the frontal lobe and limbic lobe are impacted in schizophrenia perhaps further explaining the link (5, 9, 10).
D. Treatment
Treating thyrotoxicosis-induced psychosis typically involves a combination of medical and psychiatric treatment. The primary goal is to reduce the thyroid hormone levels to normal ranges with antithyroid medications such as Methimazole and Propyluracil, but those effects may not be seen for several weeks. Therefore, more invasive treatments could be necessary such as thyroidectomy or radioactive iodine ablation (7). Symptomatically, beta-blockers have a unique role in treatment of thyrotoxicosis induced psychosis as they are indicated for thyrotoxicosis treatment but also indicated for treatment of anxiety, a psychiatric illness. They provide a dual role in their indication. Psychiatric evaluation is recommended in these patients to rule out organic psychiatric illness like bipolar disorder or anxiety or panic attacks. In terms of psychiatric medications, if psychotic symptoms persist, second generation antipsychotics such as Risperidone or Olanzapine may be indicated. First generation antipsychotic could help but there are case reports of Haldol causing dystonia and even thyroid storm in some patients (16). Lithium is a unique medication in that it is approved by the U.S Food and Drug Administration for treatment of acute mania and has well-known antithyroid properties. Ultimately, patients should have psychiatric and medical outpatient follow ups to monitor for signs of psychosis and thyroid levels.
E. Significance
This case presentation is one of many reports displaying psychosis due to hyperthyroidism. However, there are few reports of patients having two instances of acute psychosis in one hospital admission with one instance of psychosis being POD6 of a thyroidectomy (5; 7; 9). In terms of medication, olanzapine's mechanism of action of antagonizing dopamine D2 receptors in the mesolimbic pathway could explain the decrease in delusions and disorganized behavior once this medication was started (12).
When patients present to the ED with psychosis, it is important to have hyperthyroidism on the differential and to order TSH/triiodothyronine (T3)/fT4 labs. Thyrotoxicosis’ high mortality rate of 8-25% increases the urgency of immediate treatment with antithyroid medications. On physical examination, persistent tachycardia and thyromegaly are typical findings guiding workup toward thyrotoxicosis-induced psychosis. One must use caution in using objective measures alone, as tachycardia can often exist in co-morbid psychiatric conditions such as anxiety and substance use, displaying the importance of ordering thyroid labs.
This case’s acute psychosis after thyroidectomy is not fully understood, and more research on Graves’ Disease complications post-thyroidectomy needs to be performed to understand the etiology of this rebound acute psychosis. However, this case displays the importance of medication compliance with antithyroid medication in Graves Disease patients. This patient’s ED presentation could have been averted if he was compliant with the prescribed Methimazole. This case demonstrates the need for extended monitoring of Graves Disease patients post-thyroidectomy. This patient was asymptomatic POD1-4, but POD5, the patient redeveloped delusional thinking and combativeness. The patient could have developed these neuropsychiatric issues at home with the inability to adhere to his Synthroid and Olanzapine medications. Close follow-ups are needed in these patients to monitor TSH/T3/fT4 labs and assess instances of psychosis or psychiatric abnormalities.
F. Limitations and Future Studies
Limitations of this case include lack of long-term follow up to see how long the symptoms of psychosis persisted and if the anti-psychotic effectively treated those symptoms. It is unclear if the patient has an underlying primary thought disorder that was the actual etiology of the psychotic symptoms after removal of the thyroid. Due to the diagnostic time frame and clinical course of primary thought disorders like schizophrenia and schizoaffective disorder, it can often take years before an accurate diagnosis can be achieved. Future studies can explore the true prevalence of psychosis due to thyrotoxicosis or discover the true incidence of psychosis persisting even after treatment of medical conditions that cause psychosis.