Cariprazine for treating coprophagia and organic psychosis in a young woman with acquired brain injury

Discussion

On follow-up at 6 months, our patient remained free of coprophagia on cariprazine, with minimal side effects.

To the best of our knowledge, our patient represents the first reported case of use of cariprazine to treat coprophagia associated with organic psychosis. There remains a possibility of coincidental onset of psychotic illness like schizophrenia with brain injury as the patient was in her late 20s. This could have been her first episode of psychosis if she were genetically predisposed to schizophrenia, as she had a maternal history of psychotic illness.6 Brain imaging did not show any radiological evidence of a genetic predisposition to psychosis such as reductions in the anterior cingulate, the superior temporal gyrus or cerebellum, which other studies show can be interpreted as markers of a first onset of psychotic illness.7 MRI neuroimaging in our patient showed generalised cerebral atrophy with no focal lesions.

No treatment guidelines have yet been published for the management of coprophagia and therefore no universal approach has been adopted. A case-by-case analysis has enabled us to gain a general overview of the trialled treatment options and their respective efficacy. Specifically, these can be categorised into behavioural education, psychotherapy, pharmacotherapy and electroconvulsive therapy.2 4–9 Given the diversity of aetiologies, compliance and patient insight, treatment is tailored to individual circumstances with a particular intervention being successful in one case but futile in another. With regard to pharmacotherapy, a large arsenal of drugs have been used, although with varying degrees of success. Certain drug classes—namely tricyclic antidepressants, selective serotonin reuptake inhibitors (SSRIs) and anticonvulsants—have shown favourable outcomes but only in a very limited number of cases. Significant disparities in treatment response rates are observed even in the most successful class of drugs for the management of coprophagia, that is, antipsychotics. While olanzapine, risperidone and aripiprazole were not effective when used alone in a woman with catatonic schizophrenia presenting with coprophagia,10 olanzapine proved efficacious in the context of alcohol-related brain damage.8 Haloperidol is the drug most widely reported to have therapeutic benefit, with the elimination of coprophagia by using a dose of 1–3 mg a day. Impressively, a Mayo Clinic database analysis3 revealed that haloperidol was efficacious in treating coprophagia in patients with neurodegenerative dementia, developmental delay, seizures, steroid psychosis, a frontal lobe tumour and schizoaffective disorder, demonstrating its utility in a wide range of conditions. In our patient, a dose of 3 mg of haloperidol resulted in complete elimination of coprophagia and associated psychotic symptoms. Treatment augmentation with SSRIs proved ineffective. Venlafaxine helped to improve her depressive symptoms. Persistent auditory hallucinations with secondary amenorrhoea prompted us to slowly wean the patient off haloperidol in order to replace it with an alternative antipsychotic. Every such attempt, however, was met with a return of coprophagia symptoms and tolerance to the previous effective dose of haloperidol. Olanzapine, risperidone, asenapine and aripiprazole were all trialled as single antipsychotic agents without success, resulting in relapses of coprophagia and worsening of psychotic symptoms. Clozapine, which has previously been reported to be successful in the literature,11 12 was offered but declined by the patient due to its side effect profile, namely weight gain and also the need for close monitoring. Following each cycle of failed weaning, the patient was retitrated to an increasing dose of oral haloperidol, in her last relapse reaching a peak of 18 mg/day with no reduction in her coprophagia symptoms. Consequently, the decision to trial the second-generation antipsychotic, cariprazine, was made with a positive response. Compared with other antipsychotics, cariprazine appears to have a favourable side effect profile with minimal likelihood of metabolic syndrome and hyperprolactinaemia.13

As psychosis was the principal cause of our patient’s coprophagia symptoms, we suggest that the response to cariprazine may be generalised to treatment of coprophagia associated with psychotic symptoms. Various psychotropic drugs have been used to treat coprophagia; however, in this case, we have chosen cariprazine due to the predominance of psychotic symptoms.

We recognise the limitations of our case report as it is observation based on a single patient, and thus reproducibility remains to be explored. In addition, the patient’s coprophagia was underpinned by psychosis and thus antipsychotics proved effective. However, in patients whose coprophagia is precipitated by other reasons, antipsychotics may have a limited role. Finally, although cariprazine seems to be beneficial in our patient, enabling her return to the community with control of coprophagia for at least 6 months, the long-term outcomes are yet to be explored. Whether tolerance to cariprazine will also develop in due course is yet to be seen and thus we must be cautious when extrapolating our findings as a long-term success.