Abstract
Psychiatric disturbance associated with endocrine disorders is well recognized, particularly thyroid disorder [1, 2]. Acute psychosis has been reported in patients with Addison's disease where destruction of the adrenal cortex results in primary hypoadrenalism [3]. The association between hypopituitarism and psychosis, however, has been infrequently reported with cases largely of women with a history of traumatic delivery, diagnosed with Sheehan's syndrome [4, 5]. Reports of hypopituitarism and psychosis in men are rare [2]. We report on a man presenting with panhypopituitarism and psychosis in the absence of altered sensorium.
A 46-year old, unemployed male AP was admitted to hospital with his first presentation of psychosis after he barricaded himself into his neighbour's home. At admission he appeared disorganised with rambling speech and was observed responding to internal stimuli. He reported bizarre delusional beliefs of a paranoid and persecutory nature. He was slow in movement and speech. Significant aggression required initial closed ward management. He had cold intolerance and complained of occasional dizziness but denied having headaches or erectile dysfunction. Physical examination revealed cool peripheries, sparse axillary and pubic hair, and soft adult-sized testicles. Panhypopituitarism was confirmed biochemically with inappropriately subnormal thyroid-stimulating hormone (TSH) in the presence of low free thyroxine (FT4), flat cortisol response to Short Synacthen test with undetectable adrenocorticotrophin hormone (ACTH), undetectable testosterone with low lutenizing hormone (LH) and follicle-stimulating hormone (FSH), and low insulin-like growth factor (IGF-1) indicating growth hormone deficiency. Prolactin was normal whilst on risperidone. Magnetic resonance imaging (MRI) appearances of the pituitary suggested an empty sella. There was no family history or past history of psychiatric problem and no history of substance abuse.
It is unclear how long the pituitary dysfunction had existed prior to his presentation. The presence of secondary sexual characteristics would be in keeping with pituitary insufficiency developing in adulthood. No history was forthcoming to suggest previous pituitary apoplexy.
AP was commenced on oral hydrocortisone and thyroxine alongside risperidone (8 mg) with a gradual cessation of his psychotic symptoms over 3 weeks. He discontinued his endocrine medications 5 weeks after discharge resulting in a relapse of his symptoms while reporting compliance with risperidone. This was supported by the presence of demonstrable extra-pyramidal side effects. Psychomotor retardation, preoccupation and decreased mental agility were the most prominent symptoms on readmission. He reported persecutory ideas about the supervising psychiatrist in the absence of other psychotic symptoms. The persecutory ideas resolved rapidly and the psychomotor retardation improved with recommencement of thyroxine and hydrocortisone. Antipsychotic medications were tapered and ceased without worsening of his mental state.
The exact mechanism by which psychosis occurs in individuals with hypopituitarism is still obscure although it has been postulated that hypothyroidism, hypoglycaemia and hypocorticism may all have a role [4]. Some reported cases fail to distinguish what appear to be psychotic behaviours related to delirium which more aptly explains the disorientation and fluctuation of consciousness seen in those patients [5]. AP experienced neither disorientation nor altered sensorium. Psychotic symptoms may develop acutely or persist over lengthy periods of time [4] prior to being recognized as symptoms of endocrine abnormality.
Awareness of the pathognomic findings of hypopituitarism and characteristic symptom complexes associated with hypopituitarism-related psychosis (atypical onset, affective lability, thought disorganization, paranoid delusions and auditory hallucinations) may lead to increased recognition of this condition prior to the onset of delirium or coma.