Risperidone as an effective choice for obsessive–compulsive symptoms and tardive dyskinesia in an Indian quadragenarian with schizo-obsessive disorder

Abstract

Tardive dyskinesia (TD) is a chronic, stigmatizing side effect of typical and atypical antipsychotics that is often debilitating for the patient and resistant to treatment. Obsessive–compulsive symptoms (OCS) may arise at any stage of schizophrenia ranging from prodrome to posttreatment and carry a poor prognosis. Management of both the conditions is a challenging and often fatiguing task for the treating physician. We report a case of schizo-obsessive disorder in an Indian quadragenarian who had developed TD with olanzapine and had failed to show improvement with clozapine and quetiapine. The patient improved dramatically with risperidone. Our findings corroborate with previous literature which has shown risperidone to be effective in treatment of TD and obsessive symptoms, possibly due to its action on the serotonergic system. The authors conclude that risperidone is an effective choice to treat TD and comorbid OCS in patients with schizophrenia.

INTRODUCTION

Tardive dyskinesia (TD) is a debilitating and socially stigmatizing side effect of neuroleptics that befalls roughly 20% of schizophrenia patients.[1] It is a known fact that first-generation neuroleptics are more prone to develop TD, but it is also being increasingly reported with second-generation antipsychotics. Schizo-obsessive disorder is listed in literature as a type of schizophrenia with comorbid obsessive–compulsive disorder (OCD) or obsessive–compulsive symptoms (OCS). Over the past 3 decades, investigators have reported prevalence rates of clinically significant OCS in the schizophrenia population of 10%–52%.[2] However, recent observations of the emergence of de novo OCD with atypical antipsychotic treatment of schizophrenia raise the possibility that some of these comorbid OCD cases were medication induced.[3] Whatever may be the origin, such patients have been shown to have more impairment in cognition and social functioning and are more resistant to treatment.[4] Management of both TD and schizo-obsessive disorder is an uphill task and faces various challenges. Improvement expectation is also modest at best. Risperidone's role in resistant schizophrenia and TD has been suggested based on its mechanism of action, especially when it is difficult to adjust the dose of neuroleptics. Risperidone has also been shown to be effective in refractory OCD. We present a case where risperidone was used to treat both, an exacerbation of schizo-obsessive disorder and TD, effectively.

CASE REPORT

A 43-year-old male patient, Mr. R, had been suffering from schizophrenia for the past 20 years. He had been previously given olanzapine 20 mg and valproate 1000 mg, on which he developed TD. Despite best efforts and change of medications to quetiapine or clozapine, there was no improvement in TD. The current exacerbation of illness was in the form of increased aggressive behavior, auditory hallucinations, delusion of grandiosity, and muttering to self. He also had obsessive symptoms in the form of checking behavior, counting compulsions, and ritualistic behavior. On examination, the patient was conscious, oriented, disinterested in the interview, muttering, and gesticulating to self. He also had TD in the form of involuntary movement of lower jaw and grinding of teeth. His neurological and other systemic examination was otherwise uneventful. The patient had been prescribed quetiapine 100 mg and tetrabenazine 25 mg, which he was taking erratically. On admission, all of patients’ blood investigations were done which included a complete hemogram, serum electrolytes, fasting blood sugar, chest roentgenogram, magnetic resonance imaging brain, and electrocardiogram, all of which were normal. The patient was initially given injectable lorazepam to manage his aggression and was restarted on quetiapine 25 mg and tetrabenazine 25 mg. However, as the patient had minimum improvement, a course of electroconvulsive therapy was given. The patient's improvement was limited and it eventually plateaued. A neurology referral was made in view of the oromandibular TD and tetrabenazine was increased to 50 mg. As patient's improvement was minimal (<20%), he was started on risperidone 2 mg, which was gradually increased to 6 mg. It was observed that patient's dyskinetic movements stopped almost completely and his psychotic symptoms and obsessive symptoms also showed considerable improvement (80% reduction). Quetiapine was slowly tapered off and the patient was maintained on risperidone 6 mg and tetrabenazine 50 mg.

DISCUSSION

Risperidone, a benzisoxazole derivative, has been heralded as a major breakthrough in the treatment of schizophrenia. Its vast pharmacological effects in the brain include D2/5HT2A antagonism, α₁ and α₂ receptor antagonism, and antihistaminic action, among others.[5] This not only makes it a versatile molecule but also increases its uses in psychiatry as well. In patients with schizophrenia, it has been documented that risperidone may reduce negative symptoms as well as dyskinetic movements.[6] One of the most troublesome side effect of antipsychotic use is TD. It is a potentially irreversible long-term adverse effect of treatment with first-generation antipsychotic medications that has been linked with poor quality of life and increased medical morbidity and mortality.[7] Dopamine receptor hypersensitivity, gamma-aminobutyric acid insufficiency, and/or structural abnormalities are some the hypotheses suggested to explain the pathophysiology of TD. A variety of suppressive agents have been tried for it with limited success. No treatment strategy for TD has emerged that is clearly superior or even successful in most patients.

We report a patient with chronic schizo-obsessive disorder (a subtype of schizophrenia with prominent obsessive symptoms), who developed TD on olanzapine and did not show improvement with clozapine or quetiapine but improved with risperidone. His dyskinetic movements reduced by 90% and his obsessive symptoms improved by 80%. The present report shows that risperidone is a wise choice in patients who have comorbid obsessive and psychotic symptoms with TD. This is opposed to many literature reviews, which have highlighted the fact that atypical antipsychotics cause obsessive symptoms and TD as well. We suggest that this may be case specific and it is worthwhile to give a trial of risperidone in such patients. Multiple open-label reports have suggested that risperidone is effective in patients with resistant OCD as well as OCD with comorbid tic disorder.[8] However, none is available on risperidone's efficacy in OCS in patients with schizophrenia, especially with coexisting TD. To the best of the authors’ knowledge, this is the first report of such a case. The exact mechanism which may have contributed to our patient's improvement is unclear, but the authors conjecture that it is related to the drug's potent 5-HT2A antagonism in addition to D2 blockade. Risperidone's affinity in vitro is 20 times higher for 5-HT2A than for D2 receptors; in vivo it occupies 5-HT2A receptors at a dose 10 times lower than it does to D2 receptors.[9] Risperidone has also been shown to dose-dependently increase extracellular concentrations of serotonin in rat frontal cortex, which may contribute to this therapeutic effect seen in our patient in both obsessive symptoms as well as TD.[10] 5-HT2A blockade leads to increase in dopamine levels which improves the dyskinetic movements. Risperidone merely could have suppressed the TD rather than treat it, but this ameliorating effect was clinically significant nonetheless. It is also possible that it is the combination of tetrabenazine and risperidone that worked, but as tetrabenazine had minimal effect before administration of risperidone, it is likely that risperidone had a greater contribution in the combination. Thus, the authors conclude that risperidone is an effective choice for patients of schizophrenia with comorbid OCS and those who develop TD in due course of treatment.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.