40 A multi-speciality conundrum: neuropsychiatric sequelae of thyrotoxicosis

Abstract

A 51 year old man with bipolar affective disorder and an extensive forensic history was admitted informally to the forensic low secure inpatient unit for alcohol detoxification and to establish more effective long-term community management. 3 weeks into the admission his presentation abruptly changed. He would have prolonged periods of unresponsiveness, lasting hours to days, where he would lie in bed or stand rigidly with no vocal response to commands or questions. These were interspersed by periods where he would become agitated, pacing the wards, urinating and defecating in public spaces. This could last several hours and required rapid tranquilisation regularly. On examination in his stupor, he was seen to be lying in bed with his eyes closed, opening them a fraction to voice. He was sometimes able to follow simple commands but this was slow and inconsistent. He was unable to communicate through head movements or blinking and stared with a fixed expression. There was waxy flexibility of his limbs and arching on the back at regular intervals. Power was normal with flexor plantars. There were no ictal signs (i.e. no nystagmus/gaze deviation/twitching/dystonia). When agitated he was seen to have echopraxia. He consistently had hyperhydrosis and tachycardia. Bloods showed an elevated T4 (22.7) with a suppressed TSH ( It was felt that the patient had developed catatonia secondary to thyrotoxicosis due to his underlying neuropsychiatric susceptibility. He was treated effectively with high dose lorazepam as per the Maudsley Guidelines along with olanzapine (20 mg) and sodium valproate, which was used as an alternative to lithium. The thyrotoxicosis was effectively treated with carbimazole and the patient made a good recovery. Hyperthyroidism is a rare but recognised cause of psychosis and multiple case reports have demonstrated an association between thyrotoxicosis and catatonic states. In this case report, it is probable that the patient’s underlying bipolar affective disorder made him more susceptible to developing neuropsychiatric features as a consequence of his thyrotoxicosis. However, this is particularly pertinent given that lithium, the most evidence-based treatment for bipolar affective disorder, has potential to disrupt thyroid function.