Abstract
Caffeine is a very widely consumed psychoactive substance that is implicated in multiple psychiatric manifestations ranging from anxiety to psychosis [1]. It is also known to worsen psychosis in patients with pre-existing schizophrenia [2]. Excessive coffee consumption in psychiatric patients is not uncommon. We present an interesting case of chronic schizophrenia with psychotic exacerbation following excessive coffee consumption.
A 52-year-old man lives in a supported residential facility (SRF). He has a long-standing history of paranoid schizophrenia that has been relatively stable with mild residual positive symptoms over the last few years. He was being managed with parenteral risperidone 100 mg intramuscular injection fortnightly.
He presented with two weeks’ history of psychotic relapse characterized by predominant delusions of persecution and reference of people following him in order to rape him. He acted on his delusions by scratching his face to disguise himself from these rapists. His sleep was disturbed and he was noted to be markedly agitated on admission. This acute psychotic episode was preceded by excessive coffee consumption daily of 20 to 25 cups for the last few weeks. The SRF staff corroborated this information.
He was admitted to our inpatient unit and was started on olanzapine 20 mg/day to control his agitation and psychotic symptoms. Parenteral risperidone was continued as before. Four weeks of inpatient stay in the open ward did not ameliorate his acute symptoms. His coffee intake was significant but difficult to monitor and control in the open ward. He was subsequently transferred to the closed ward with strict monitoring and restriction of his coffee intake. His acute psychotic symptoms settled within ten days of closed ward admission without any changes to his regular psychotropic prescription. He was discharged to his SRF with recommendations to monitor and manage his coffee intake.
The patient represented after two months with similar acute psychotic symptoms in the background of increasing coffee consumption. There was no evidence to suggest non-compliance with medication. He was admitted directly to the closed ward and his coffee intake was restricted. He improved in the next two weeks with no change to his maintenance medication regime.
Although it is difficult to conclusively demonstrate caffeine as the etiological factor in this patient's acute psychotic relapse, there is enough evidence to draw a temporal correlation between the worsening of his positive symptoms and his caffeine intake.
Caffeine is a methylxanthine that exerts its primary actions by antagonism of the adenosine receptors [3,4]. Dopaminergic activity in the mesolimbic pathway can be increased by the effects of caffeine which has been postulated to be responsible for its behavioural effects [3]. Caffeine is also known to increase the serum levels of olanzapine and clozapine by competitively inhibiting the CYP1A2 isoenzyme [5]. However, it should not influence the levels of risperidone as it is metabolized by CYP2D6 and CYP3A [5]. The rapid resolution of psychotic symptoms without additional drug therapy and with the restriction of caffeine intake would suggest that increased dopaminergic activity was the primary mechanism to explain the acute worsening of the patient's psychosis.
This knowledge has potential implications on controlling the indiscriminate use of caffeine in psychiatric facilities. Previous research looking at the use of decaffeinated drinks has not found the benefits to be conclusive [6–8]. There are reports to suggest that excessive caffeine intake with or without dependence can cause psychosis, exacerbate chronic psychosis or be a contributing factor in certain cases of treatment refractory psychosis [1,2,9,10]. Our case report offers further evidence to back the recommendations by other authors [10] that the screening of caffeine consumption can be of importance in a certain group of vulnerable psychotic patients. In DSM-IV, caffeine-related disorders include caffeine intoxication, caffeine-induced anxiety disorder and caffeine-induced sleep disorder. Based on the available literature and this case report, we propose that disorders related to caffeine use be expanded further in future classificatory systems.