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RISPERDAL® (risperidone)

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RISPERDAL Dosing - Abrupt Discontinuation/Withdrawal

Last Updated: 10/18/2024

Summary

RISPERDAL was discontinued at the end of clinical trials without a downward titration period.¹ No obvious untoward effects were observed due to abrupt withdrawal. However, due to limited clinical experience, caution should be exercised when abruptly discontinuing risperidone.
Please refer to the RISPERDAL Prescribing Information to view the Boxed Warning regarding Increased Mortality in Elderly Patients with Dementia-Related Psychosis. Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. RISPERDAL is not approved for the treatment of patients with dementia-related psychosis. [See Warnings and Precautions (5.1)].²
Neuroleptic withdrawal studies have been conducted in patients with Alzheimer’s disease and dementia examining risk of relapse³^,⁴, cognitive decline⁵, sleep/wake activity⁶ and neuropsychiatric symptom outcomes.⁵^,⁶

CLINICAL STUDIES

Neuroleptic Withdrawal Studies

Author(s)/Study Design	Summary
Devanand et al (2012)³ assessed the relapse risk following discontinuation of RIS in 110 Alzheimer's patients. *Study Design/Methods: In phase A* of the study, 180 Alzheimer's patients, experiencing psychosis (NPI ≥4, psychosis score) or agitation/aggression (NPI ≥4, agitation score) and an MMSE score 5-26 for outpatients and 2-26 for nursing home residents, received OL, flexible-dose RIS (mean dose: 0.97 mg/day) for 16-wks. Of the 112 patients who responded to treatment, 110 entered *phase B* and were randomly assigned, in a DB fashion, to 1 of 3 regimens: Group 1: continued RIS therapy for 32 wks Group 2: continued RIS therapy for 16 wks followed by PBO for 16 wks Group 3: PBO for 32 wks *Outcome Parameters - Phase B*: Primary outcome was the time to relapse (≥30% increase in NPI core score or a 5-point increase in the end of phase A score and a CGI-C score of 6 or 7) during wks 0-16. Secondary outcomes included time to relapse during wks 17-32, assessment of EPS (SAS; AIMS), somatic symptoms (TESS); cognition (MMSE; ADAS) and physical function (PSMS).	*Relapse Outcomes - Phase B: From wks 0-16, patients in Group 3 (PBO) experienced an increased risk of relapse vs Groups 1 and 2 receiving RIS (Group 3: 60%, n=24/60 vs Group 1 and 2: 33%, n=23/70, P=0.004; PBO HR: 1.94, 95% CI: 1.09-3.45; P=0.02, stratified Cox analysis). From wks 17-32, patients in Group 2 who switched to PBO, had an increased risk of relapse compared to patients in Group 1 who continued RIS (Group 2: 48%, n=13/27 vs Group 1: 15%, n=2/13; PBO HR: 4.88, 95% CI: 1.08-21.98; P=0.02, stratified Cox analysis). Safety Outcomes - Phase B: No significant differences in adverse events between patients receiving RIS (Groups 1 and 2) vs PBO (Group 3) during the first 16 wks of phase B. Likewise, from wks 17-32, there were no significant differences in such adverse events between patients in Group 2 who switched to PBO, compared to patients in Group 1 who continued RIS. The same results held true when comparing patients who continuously received RIS or PBO for 32 wks. 3 deaths occurred during phase B (RIS, n=2; PBO, n=1). Post Hoc Analysis* Patel (2017)⁴ conducted a post hoc analysis to examine the associations between neuropsychiatric symptoms at baseline, immediately after RIS treatment and the likelihood of relapse following continued treatment with RIS or discontinuation to placebo. When the NPI domain scores were classified as absent (0), mild/moderate (1-6) and severe (7-12) symptoms, there was a significant association between phase A baseline hallucinations and relapse at week 32 [16 wks into phase B randomization]; (P=0.005). Severe hallucinations increased risk of relapse in comparison with the group with no hallucinations (HR=2.70, 95% CI=1.19, 6.12, P<0.02). Auditory hallucinations significantly predicted relapse (HR=2.36, 95% CI=1.18, 4.71, P<0.02), whereas visual hallucinations did not predict relapse. Significantly more patients with phase A baseline hallucinations who switched to placebo relapsed vs those who continued RIS (76.5% [13/17] vs 38.5% [10/26], respectively; RR=1.99, 95% CI=1.14, 3.46, P<0.03). This difference remained significant for severe vs mild hallucinations (77.8% vs 36%; RR=2.88, 95% CI=1.16, 7.18, P<0.03).
Ballard et al (2008)⁵ conducted a 12-mo, DB, randomized, treatment discontinuation study assessing global cognitive decline and neuropsychiatric symptom outcomes in patients with Alzheimer’s dementia who continued antipsychotic treatment (n=83) or switched to PBO (n=82; mean age: 84.9 yrs, 76% women). *Inclusion: Patients used chlorpromazine, HAL, RIS, thioridazine, or trifluoperazine for ≥3 months, were taking ≥10 mg chlorpromazine equivalents of an antipsychotic or 0.5 mg/day of RIS and had a MMSE score >6 point or SIB score >30 points; 51 patients per arm were analyzed for the primary outcome. At baseline, the majority of patients were receiving RIS/PBO RIS (n=101) or HAL/PBO HAL (n=43). Doses: Antipsychotics were dosed according to very low, low, or high treatment categories and best matched to the patient’s pre-study dose. Fixed doses of antipsychotics or PBO were maintained throughout the 12 months of treatment. RIS: Very Low (0.5 mg/day); Low (0.5 mg twice daily); High (1 mg twice daily) Chlorpromazine: Very Low (12.5 mg/day); Low (12.5 mg twice daily); High (25 mg twice daily) Trifluoperazine: Very Low (0.5 mg/day); Low (0.5 mg twice daily); High (1 mg twice daily) HAL*: Very Low (0.75 mg/day); Low (0.75 mg twice daily); High (1.5 mg twice daily)	*SIB: Mean change, baseline to month 6: no significant difference observed for continued treatment vs PBO (-6.2 points vs -5.7 points, respectively; estimated mean difference, favoring PBO: -0.4, adjusted for baseline; P=0.9). Mean change, month 12: no significant difference for continued treatment (n=28; -16.5 points) vs PBO (n=27; -8.5 points). However, there was a clinically important numerical advantage favoring PBO (estimated mean difference in deterioration: -8.4, adjusted for baseline; P=0.1). NPI*: Mean change, baseline to month 6: no significant difference for continued treatment (n=56) vs PBO (n=53). Estimated mean change, baseline to month 12: significant difference for continued treatment (n=28; -1.4 points) vs PBO (n=31; -11.4 points). Estimated mean difference in deterioration, favoring continued treatment: -10.9, adjusted for baseline; P=0.02). No significant differences between continued treatment and PBO with regard to change in SMMSE, BADLS, STALD, FAST, or CGI-C from baseline to month 6. From baseline to month 6 there was a 0.6 point improvement and a 3.2 point deterioration in FAS totals for patients receiving PBO (n=31) vs continued treatment (n=34). For M-UPDRS scores, there was a 0.8 point deterioration and 0.4 point improvement, from baseline to mo 6, for patients receiving continued treatment (n=41) vs PBO (n=43).
Ruths et al (2004)⁶ conducted a 4-week, double-blind, placebo-controlled, randomized trial evaluating the effect of antipsychotic withdrawal on the sleep/wake activity and behavioral and psychological symptoms of dementia (BPSD) in 30 nursing home patients (mean age 83.5 years). Following a 2-week baseline period, participants currently receiving RIS (n=22), OLA (n=4), or HAL (n=4) were randomly assigned to withdraw (intervention group; n=15) or continue (reference group; n=15) antipsychotic treatment for 4 weeks. Baseline antipsychotic medications were prescribed for emerging symptoms during the study and were identified as a restart of medication in the intervention group or an increased dosage in the reference group. The Neuropsychiatric Inventory Questionnaire (NPI-Q) was administered to assess BPSD. Actigraphy was used to record sleep/wake activity during the baseline (2 weeks) and study (4 weeks) periods.	Median daily doses of antipsychotics were as follows: risperidone 0.5 mg, olanzapine 5 mg, and haloperidol 0.75 mg. Behavioral scores remained stable or improved in 11 of 15 patients following antipsychotic withdrawal. The remaining four patients (RIS=1) were noted to have an increase in agitation/aggression, anxiety, and apathy symptom scores. Sleep efficiency decreased from 86% to 75% in patients abruptly discontinuing their antipsychotics (P=0.029). An increase in 24-hour daytime and nighttime activity was observed in some patients from both groups. Sedative use did not correlate with measured actigraphy sleep efficiency or with NPI-Q assessed sleep problems.
Abbreviations: ADAS, Alzheimer's Disease Assessment Scale; AIMS, Abnormal Involuntary Movement Scale; BADLS, Bristol Activities of Daily Living Scale; CAEs, cerebrovascular adverse events; CGI-C, Clinical Global Impression of Change; CI, confidence interval; DB, double-blind; FAST, Functional Assessment Staging; EPS, extrapyramidal symptoms; HAL, haloperidol; HR, hazard ratio; (S)MMSE, (standardized) Mini Mental State Examination; M-UPDRS, Modified Unified Parkinson's disease Rating Scale; NPI, Neuropsychiatric Inventory Questionnaire; OLA, olanzapine; PBO, placebo; PSMS, Physical Self-Maintenance Scale: RIS, risperidone; SAS, Simpson-Angus Scale; SIB, Severe Impairment Battery; STALD, Sheffield Test for Acquired Language Disorders.

Case Reports

Case Reports Related to Abrupt Discontinuation/Withdrawal of Risperidone - Adults & Pediatric

Reference	Summary/Outcome
**Adult Patients**
Curran et al (2023)⁷ A female in her early 60s with a diagnosis of paranoid schizophrenia was first treated with risperidone and clonazepam.	From 2005 to 2008, the patient was prescribed risperidone 4 mg at night and a fluctuating dose of clonazepam between 250 µg once daily and 250 µg 3 times a day to treat movement disorder. The patient experienced mild orofacial dyskinesia, which worsened with reduced clonazepam dosage. The patient was re-referred by her general practitioner in 2015 to reduce the dosage of risperidone to 2 mg at night and clonazepam to 500 µg daily. Between 2016 and 2022, the dosage of risperidone was increased to 3 mg at night, and procyclidine 2.5 mg 3 times a day was added. In early 2022, the patient developed a new movement disorder after discontinuation of risperidone and procyclidine for 3 months. The patient discontinued her medications due to an auditory hallucination. Subsequently, the patient was hospitalized and diagnosed with tardive dyskinesia and dystonia, with a recommendation to restart risperidone and procyclidine. She was initiated on quetiapine 150 mg prolonged-release formulation for one week; later, the dose was increased to 300 mg. The patient then experienced a significant improvement in the symptoms, although some tardive tics and dystonia persisted. After a period of treatment, the severity of movement disorders was reduced, and the patient opted to maintain treatment with quetiapine prolonged-release formulation.
Giourou et al (2022)⁸ A 46-year-old female with schizophrenia diagnosed at the age of 22 was treated with risperidone.	The patient presented with a relapse of psychotic symptoms due to discontinuation of risperidone. The symptoms persisted after reinitiating risperidone, so it was replaced with clozapine, which led to complete remission. An increase in eosinophil count was observed with a gradual decrease in the risperidone dosage. Eosinophil count normalized after complete risperidone discontinuation. Other potential causes of eosinophilia were ruled out.
Alblowi et al (2015)⁹ A 32-year-old female was treated with risperidone 2 mg/day for a psychotic episode without mood symptoms.	After one year, the dose was decreased to risperidone 1 mg/day. Patient experienced an enlarged and protruding tongue causing difficulty in swallowing, nasal speech and hypersalivation becoming worse after discontinuation of risperidone. The patient was evaluated by several specialists before a diagnosis of risperidone withdrawal-induced tardive dyskinesia was made. Treatment was initiated with amantadine 50 mg/day and increased after 4 days to 100 mg/day. The patient responded well and the dose was increased to 100 mg twice daily with 80% improvement. The patient remained on amantadine with the intent to discontinue it in time.
Yang et al (2011)¹⁰ A 62-year-old female with a 32-year history of schizophrenia was stable on risperidone 2 mg/day.	While participating in an open-label trial of paliperidone 3 mg/day in which treatment with risperidone was ended, the patient exhibited worsening manic symptoms including euphoria, distractibility, racing thoughts, reduced need for sleep, hyperactivity and pressured speech. Treatment with paliperidone was discontinued after 10 days. Risperidone 2 mg/day was restarted and titrated to 4 mg/day over the next 4 days. Sodium valproate 1,000 mg/day was also added to the regimen. Over the next 3 weeks, the patient experienced full remission of her manic symptoms, and the sodium valproate was gradually discontinued. The patient retained a stable condition over the next year and the dose of risperidone decreased to 1 mg/day. Paliperidone is the major metabolite of risperidone, however there are pharmacodynamic and pharmacokinetic differences between the two. In this case, the rapid switch from risperidone to paliperidone predisposed the patient to manic symptoms. The author suggested that cross-titration should be considered when switching patients from risperidone to paliperidone.
Mendhekar et al (2010)¹¹ A 64-year-old female with a 12-year history of schizophrenia, previously treated with trifluoperazine, chlorpromazine and thioridazine, presented with a relapse.	The patient was started on risperidone 2 mg/day and was increased to 4 mg/day over 4 weeks. In addition, trifluoperazine 2 mg/day was added to the regimen. The patient remained stable for 3 months. The patient discontinued risperidone and trifluoperazine due to a viral fever and within 36 hours experienced bucco-lingual dyskinetic movements with involuntary movements of the respiratory muscles, grunting, and irregular breathing patterns. No abnormal movements occurred during sleep or in any other part of her body. Trials of trihexyphenidyl, clonazepam and clozapine failed. Risperidone 2 mg/day was restarted and increased to 4 mg/day over 10 days. The involuntary movements disappeared, however after 12 weeks of treatment she developed dyskinetic movements of both hands. Risperidone was discontinued and once again respiratory dyskinesia occurred. Clozapine 25 mg/day was initiated and increased to 250 mg/day over 3 weeks. After 6 weeks of treatment with clozapine there was improvement in all symptoms and the involuntary movements disappeared. The authors referenced three prior case reports of withdrawal-emergent respiratory dyskinesia associated with risperidone.
Catena Dell’osso et al (2007)¹² A 50-year-old female with bipolar I disorder received risperidone 4 mg/day. Concomitant medications included lithium, gabapentin, lorazepam and citalopram.	Due to a shuffling gait, moderate drooling and cog wheeling rigidity, risperidone was decreased to 1 mg/day, for one day, then completely discontinued. EPS resolved. Trazodone was initiated and the lithium dose was adjusted. Ten days following risperidone discontinuation the patient was diagnosed with risperidone withdrawal emergent rabbit syndrome (fine, rhythmic and rapid movements of the mouth along with vertical axis without lingual involvement). Risperidone was restarted at 1.5 mg/day. Following the first few hours of risperidone reinitiation, rabbit syndrome symptoms decreased then resolved after 3 days of therapy. No extrapyramidal symptoms were observed.
Urbano et al (2007)¹³ Patient 1: 22-year-old male with bipolar disorder and psychotic symptoms receiving risperidone 2 mg/day. Concomitant medications included valproic acid. Patient 2: 52-year-old female with recurrent major depression and anxiety disorder (not otherwise specified) receiving risperidone 2 mg/day.	Patient 1: Following the control of psychotic symptoms with risperidone, the patient became increasingly depressed and was switched from valproic acid to lamotrigine. During the next 2 years, risperidone was tapered off, over a 3-month period, then restarted due to the return of psychotic symptoms. Withdrawal dyskinesia was not observed during this time. Following an additional 18 months of therapy risperidone was again tapered and discontinued without the return of psychotic symptoms. During a follow-up appointment, 6-8 months after the discontinuation of risperidone, the patient reported a mild lingual dyskinesia (“tongue tripping”; “tongue twitching”) experienced immediately following risperidone discontinuation. Patient's medical history was negative for tardive dyskinesia. The dyskinesia was reduced to an occasional speech interference (1-2 episodes/day) at the time of report.
	Patient 2: Risperidone was added to venlafaxine therapy to control anxiety resistant to benzodiazepines. After 3.5 years of therapy, and no signs of tardive dyskinesia, risperidone was slowly tapered off due to improvements in depressive and anxious symptoms. The patient reported lingual dyskinesia with significant tongue irritation, verbal dysarthria and jaw clicking two months following the discontinuation of risperidone. The lingual dyskinesia continued one month later, in addition to, verbal dysarthria (present 25% of the time), jaw pain from chewing movements, and mouth discomfort from gum biting. Following an unsuccessful trial of quetiapine, (100 mg/day x 4 weeks then 300 mg/day x 5 weeks), the patient was restarted on risperidone 1 mg/day and quetiapine was continued. One week following the reinitiation of risperidone only minor lingual movements and dysarthric speech remained.
Ehrt et al (2005)¹⁴ An 84-year-old female with dementia with Lewy bodies received risperidone 2 mg/day and donepezil 10 mg/day for 3 months.	Risperidone was withdrawn over a 1-week period due to upper limb rigidity with cogwheel phenomenon observed during examination. Quetiapine was initiated at 25 mg/day and increased to 50 mg/day. Three days following risperidone withdrawal the patient displayed bouts of anxiety and hyperventilation. Examination revealed involuntary movements of the respiratory musculature. Respiratory dyskinesia was diagnosed, and risperidone was restarted at 2 mg/day. Respiratory dyskinesia resolved immediately following the re-institution of risperidone. Over the next 3 months risperidone was withdrawn in 0.5 mg increments. Less severe respiratory symptoms, without discomfort, were subjectively reported by the patient. The quetiapine dose remained unchanged. No respiratory dyskinesia symptoms were observed 6 months after the initial observation.
Komatsu et al (2005)¹⁵ An 84-year-old female with mixed dementia received risperidone initiated at 1 mg/day, increased to 2 mg/day after 1 week and then abruptly discontinued after 5 months.	Risperidone was added to a regimen of tiapride (50-95 mg/day) for control of delusions and delirium. Biperiden (1 mg/day) was continued to prevent EPS. Several weeks after the initiation of risperidone the patient experienced orofacial dyskinesia, stepping movements of the lower limbs, and staggered walking. Due to marked staggering observed 5 months after initiation of risperidone, treatment was abruptly discontinued. Tiapride was continued at a dose of 50 mg/day. Ten days later, the patient experienced involuntary movements of the trunk (mainly thorax), limbs (standing only), and oral/perioral area. Truncal movements occurred at a rate of 50/minute and were accompanied by forced breathing (respiratory dyskinesia). Clonazepam 1.5 mg/day was insufficient in controlling these symptoms. Hospitalization occurred 3 weeks following risperidone discontinuation. Tiapride was discontinued, haloperidol (0.5 mg/day) was initiated, and biperiden was increased to 3 mg/day. Respiratory dyskinesia improved 1 month after hospitalization. Biperiden, haloperidol, and clonazepam were tapered off. Limb dyskinesia subsided 6 weeks after hospitalization while orofacial dyskinesia persisted. Hospital discharge occurred 3-5 months after admission. Patient was medication free. All involuntary movements completely resolved 1 month after discharge.
Nishimura et al (2001)¹⁶ A 38-year-old female with schizophrenia received risperidone 2 mg/day.	Patient started on haloperidol and trihexyphenidyl for symptoms of acute anxiety, auditory hallucinations, and delusions of persecution. Haloperidol was changed to risperidone after patient developed EPS. Trihexyphenidyl was discontinued 2 months later. The risperidone dose was reduced to 1 mg/day after approximately 6-7 months. Three weeks later, the patient developed involuntary movements of the upper lip. Movements tended to increase with stress and tension and were accompanied by a feeling of tongue stiffness and gustatory dullness. No other EPS were present. The patient was diagnosed with having rabbit syndrome. Trihexyphenidyl (4 mg/day) was restarted, while risperidone was continued. Movements reduced by third day and disappeared completely by tenth day. Risperidone was discontinued after about 3 months and trihexyphenidyl was withdrawn 4 weeks later.
Miller (2000)¹⁷ An 82-year-old female with Alzheimer's dementia and major depression received risperidone 2 mg twice daily for approximately 3 months.	Patient admitted to geriatric psychiatry unit for worsening depression and increasing anxiety. Risperidone and citalopram were discontinued abruptly upon admission. Patient experienced increased anxiety and symptoms of Withdrawal-emergent dyskinesia (involuntary choreiform chewing, lip smacking, tongue thrusting and rolling) evident after 5 days. Clonazepam started at 0.25 mg bid and vitamin E added at 1200 U/d. Anxiety and depression responded to increased dosages of clonazepam 0.5 mg bid and nortriptyline 35 mg at bedtime. Dyskinesias persisted throughout admission, but noticeably diminished. Occasional lip smacking and tongue rolling remained. Patient discharged with medication regimen of nortriptyline, vitamin E, and clonazepam.
**Pediatric/Adolescent Patients**
Faisal et al (2021)¹⁸ A 13-year-old female with moderate intellectual disability and autism spectrum disorder (ASD) exhibited catatonic symptoms 8 weeks after discontinuation of risperidone 0.25 mg for 18 months.	The patient was admitted to a pediatric high-dependence unit after progressive mutism and prominent psychomotor retardation. Lorazepam 0.5 mg TID was initiated and titrated to 3 mg TID over a 12-day period before a positive response was observed. Lorazepam gradually increased to 4 mg TID over an additional 10-day period at which time the core features of catatonia had resolved. Over the next 10 days, lorazepam was reduced to 2 mg TID. However, the patient experienced sleep disturbance, overactivity, impulsive behavior, and elation. The authors postulated that the reduction of lorazepam most likely unmasked an underlying mood disorder. Aripiprazole 2 mg was initiated and titrated to a dose of 7.5 mg once daily. The patient was discharged on lorazepam 2 mg TID and aripiprazole 7.5 mg once daily.
Soundarrajan et al (2019)¹⁹ A 17-year-old female with bipolar affective disorder was switched from aripiprazole to risperidone 4 mg once daily.	Patient previously maintained on aripiprazole and carbamazepine since the age of 13 years. Six months prior, the patient’s psychotic symptoms became uncontrolled; she was switched from aripiprazole to risperidone. Patient experienced significant weight gain as well as menstrual irregularities leading to discontinuation of risperidone and reintroduction of aripiprazole. Over the next 2 days, the patient complained of inner restlessness and inability to sit in one place. She also exhibited swaying and positive Romberg’s sign. Risperidone 4 mg once daily was reintroduced, and symptoms subsided within a week. After one month, risperidone was tapered and discontinued with no reoccurrence of withdrawal symptoms.
Kumar et al (2018)²⁰ A 9-year-old male with ASD and attention deficit hyperactivity disorder (ADHD) received risperidone 1 mg daily since age 5 and gradually increased to 4 mg daily.	Patient was also treated with dexmethylphenidate extended release 20 mg daily, dexmethylphenidate 7.5 mg daily in divided doses, and clonidine 0.2 mg daily for ADHD. Patient received these medications in combination with risperidone for 2 years. At which point, he developed hyperprolactinemia associated with galactorrhea. Risperidone 4 mg was tapered and discontinued for 4 days. Within 5 days, the patient developed abnormal lip smacking, eye blinking, body rocking, shakes, and writhing movements of the neck. Patient was unresponsive to benztropine, lorazepam, and diphenhydramine. Results from a complete medical work up were negative. Patient was started on 1 mg risperidone twice daily; within 24 hours, he showed a substantial improvement in abnormal movements. Patient continued to clinically improve and was discharged on risperidone 1 mg twice daily. Over the next 8 months, the risperidone was gradually tapered and discontinued. Following this discontinuation, there was no reoccurrence of withdrawal dyskinesia symptoms.
Lore (2000)²¹ A 13-year-old male with ADHD, conduct disorder, and affective disorder received risperidone dosed at 1.5 mg/day, tapered by 0.5 mg every few months and then discontinued after 11 months.	Patient with history of psychotic features (auditory hallucinations, paranoid ideation) was treated with lithium, valproic acid, and risperidone. When psychotic symptoms resolved, risperidone was tapered and discontinued. Approximately 2 weeks after discontinuation of risperidone, patient developed withdrawal dyskinesia manifested by mild mouth movements, neck twisting, and intermittent upward gaze. Patient was started on low-dose quetiapine, titrated up to 100 mg bid. The dyskinesias resolved.

OTHER RELEVANT LITERATURE

Additional citations and those published prior to January 2000 are included in the References section for your review.²²^-²⁹

LITERATURE SEARCH

A literature search of MEDLINE^®, Embase^®, BIOSIS Previews^®, and Derwent Drug File (and/or other resources, including internal/external databases) pertaining to this topic was conducted on 26 August 2024.

References

Show

1	Data on File. RISPERDAL Clinical Trials, Janssen Pharmaceuticals, Inc.
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3	Devanand DP, Jacobo M, Schultz SK, et al. Relapse risk after discontinuation of risperidone in Alzheimer’s disease. N Engl J Med. 2012;367(16):1497-1507.
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