J&J Medical Connect
RISPERDAL®

(risperidone)

J&J Medical Connect

Connect with us

  • Products

This information is intended for US healthcare professionals to access current scientific information about J&J Innovative Medicine products. It is prepared by Medical Information and is not intended for promotional purposes, nor to provide medical advice.

RISPERDAL Dosing - Abrupt Discontinuation/Withdrawal

Last Updated: 08/26/2026

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
  • A withdrawal study has been conducted in children and adolescents treated off label with RISPERDAL for ≥1 year.7
  • Additional citations and those published prior to January 2012 are included in the References section for your review.8-24

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.
  • Three 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 PBO.
    • 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 PBO 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, DB, PBO-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 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: RIS 0.5 mg, OLA 5 mg, and HAL 0.75 mg.
  • Behavioral scores remained stable or improved in 11 of 15 patients following antipsychotic withdrawal. The remaining 4 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; BPSD, behavioral and psychological symptoms of dementia; CGI-C, Clinical Global Impression of Change; CI, confidence interval; DB, double-blind; EPS, extrapyramidal symptoms; FAST, Functional Assessment Staging; HAL, haloperidol; HR, hazard ratio; (S)MMSE, (standardized) Mini Mental State Examination; mo, month; M-UPDRS, Modified Unified Parkinson's Disease Rating Scale; NPI-Q, Neuropsychiatric Inventory Questionnaire; OL, open label; OLA, olanzapine; PBO, placebo; PSMS, Physical Self-Maintenance Scale: RIS, risperidone; RR, relative risk; SAS, Simpson-Angus Scale; SIB, Severe Impairment Battery; STALD, Sheffield Test for Acquired Language Disorders; TESS, Treatment Emergent Symptom Scale; wk, week.

Withdrawal Study

Author(s)/Study Design
Summary
Dinnissen et al (2024)7 evaluated the continued benefits of off-label RIS for the treatment of behavioral problems in children and adolescents without intellectual disability who had been treated with RIS for ≥1 year (N=35).
Study Design/Methods:
  • Inclusion criteria: Children and adolescents 6 to 18 years of age on RIS treatment for ≥1 year and with an IQ of ≥70
  • Exclusion criteria: Psychotic disorder diagnosis based on DSM-IV-TR or RIS prescription for the treatment of tics

Intervention: Participants were randomized 1:1 to either continued RIS during 16 weeks (continuation group) or to 2 weeks of their regular dose (at study entry) followed by gradual withdrawal to placebo over a 6-week period and 8 weeks of complete placebo (discontinuation group).
Outcomes:
  • Primary outcome: D-total score on the parent-reported NCBRF-TIQ.
  • Secondary outcomes: Clinician-rated CGI-I; parent-, child-, and teacher-rated SDQ; and parent-rated R-MOAS.
Baseline Characteristics:
  • The mean (SD) age was 11.85 (2.49) years and 13.01 (2.42) years in the discontinuation (n=16) and continuation groups (n=19), respectively.
  • The groups did not differ in age, sex, total IQ, or RIS dose at baseline.
  • The discontinuation vs continuation group had a significantly higher percentage of participants with melatonin as a comedication (37.5% vs 5.3%; χ2=5.64; P=0.018) and a significantly higher percentage of participants with tic disorder (18.8% vs 0%; χ2=3.90; P=0.048).
  • Participants in the discontinuation group scored significantly higher on the parent-rated SDQ subscales of Conduct problems (t[31]=3.29; P=0.003) and Hyperactivity/inattention (t[31]=2.22; P=0.034). Participants in the discontinuation group also reported a significantly higher total SDQ score (t[31]=3.11; P=0.004) and child-reported total SDQ score (t[24]=2.11; P=0.045).

Outcomes:
  • Primary outcome: Change in the D-total score did not differ between the groups (Δ=-4.01; 95% CI, 12.48 to 4.46).
  • Secondary outcome: The clinician-rated CGI-I score indicated a significantly worsened overall functioning at follow-up in 31.3% of participants in the discontinuation group vs 6.7% of participants in the continuation group.
  • A significant increase in the verbal aggression component of the R-MOAS was observed in the discontinuation group compared with the continuation group (Δ=-5.27; 95% CI, -9.16 to 1.38).
  • The discontinuation vs continuation group reported worse behavioral outcomes in the teacher-reported SDQ on the subscales for emotional problems (Δ=2.06; 95% CI,3.54 to -0.58), conduct problems (Δ= 1.50; 95% CI, -2.96 to -0.05), and peer relationship problems (Δ=-1.44; 95% CI, 2.85 to -0.03) as well as a worse total score (Δ=-6.27; 95% CI, -10.17 to -2.38) (all P<0.05).
Abbreviations: Δ, difference in mean change from baseline to follow-up between the treatment groups; CGI-I, Clinical Global Impressions-Improvement scale; CI, confidence interval; DSM-IV-TR, Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition; D-total, total Disruptive Behavior; IQ, intelligence quotient; NCBRF-TIQ, Nisonger Child Behavior Rating Form-Typical IQ; RIS, risperidone; R-MOAS, Retrospective Modified Overt Aggression Scale; SD, standard deviation; SDQ, Strengths and Difficulties Questionnaire.

Case Reports


Case Reports Related to Abrupt Discontinuation/Withdrawal of Risperidone - Adults & Pediatric
Reference
Summary/Outcome
Adult Patients
Patel et al (2025)25
A 65-year-old female with involuntary movements was treated with risperidone.
  • The patient was admitted for involuntary movements involving the trunk (mainly the abdomen and perioral region) that had started after abruptly stopping risperidone.
  • The involuntary movements caused respiratory distress and disappeared during sleep.
  • Results of cardiorespiratory tests (ie, chest X-ray, pulmonary function test, arterial blood gas, electrocardiography, and 2D echo) were normal.
  • CSF examination, CSF autoimmune encephalitis panel, and tests for Wilson’s disease (serum ceruloplasmin, 24-hour urinary calcium, and Kayser-Fleischer ring) were negative.
  • Based on the clinical profile and exclusion of other causes, the patient was diagnosed with withdrawal-emergent dyskinesia.
  • Treatment was initiated with clonazepam, and the patient’s condition improved significantly over the next 4 weeks.
Curran et al (2023)26
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 1 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)27
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)28
A 32-year-old female was treated with risperidone 2 mg/day for a psychotic episode without mood symptoms.
  • After 1 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.
Pediatric/Adolescent Patients
Shah et al (2026)29
A 12-year-old female patient with Landau-Kleffner syndrome on long-term risperidone treatment presented with galactorrhea, visual disturbance, and frequent falls.
  • The patient had been on risperidone treatment from the age of ~5 years for aggression and self-injury.
  • At 12 years of age, she developed galactorrhea and visual disturbance and experienced frequent falls.
  • Results of laboratory tests of beta-human chorionic gonadotropin, thyroid function, and liver function were normal, whereas the serum prolactin level was high (40.2 ng/mL).
  • No pituitary enlargement or mass effect was apparent in a computed tomography examination of the brain.
  • Risperidone was discontinued, which was followed by worsening aggression, impulsivity, and self-injurious behaviors.
  • Fluoxetine and escitalopram were tried but discontinued because of inadequate response and side effects.
  • Treatment with olanzapine 2.5 mg (4 times daily) was well tolerated and led to resolution of galactorrhea and return of behavioral stability within 4 weeks.
  • Laboratory tests after medication switch showed normal LH and FSH levels.
  • The clinical findings supported a diagnosis of risperidone-induced hyperprolactinemia.
Faisal et al (2021)30
A 13-year-old female with moderate intellectual disability and 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)31
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)32
A 9-year-old male with ASD and 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.
Abbreviations: 2D, 2 dimensional; ADHD, attention deficit/hyperactivity disorder; ASD, autism spectrum disorder; BID, twice daily; CSF, cerebrospinal fluid; FSH, follicle-stimulating hormone; LH, luteinizing hormone; TID, thrice daily.

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 27 July 2026.

 

References

1 Data on File. RISPERDAL Clinical Trials, Janssen Pharmaceuticals, Inc.;  
2 RISPERDAL® (risperidone) [Prescribing Information]. Titusville, NJ: Janssen Pharmaceuticals, Inc; https://www.jnjlabels.com/package-insert/product-monograph/prescribing-information/RISPERDAL-pi.pdf
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.  
4 Patel AN, Lee S, Andrews HF, et al. Prediction of relapse after discontinuation of antipsychotic treatment in Alzheimer’s disease: the role of hallucinations. Am J Psychiatry. 2017;174(4):362-369.  
5 Ballard C, Lana MM, Theodoulou M, et al. A randomised, blinded, placebo-controlled trial in dementia patients continuing or stopping neuroleptics (The DART-AD Trial). PLoS Med. 2008;5(4):e76.  
6 Ruths S, Straand J, Nygaard HA, et al. Effect of antipsychotic withdrawal on behavior and sleep/wake activity in nursing home residents with dementia: a randomized, placebo‐controlled, double‐blinded study. The Bergen District Nursing Home Study. J Am Geriatr Soc. 2004;52(10):1737-1743.  
7 Dinnissen M, Dietrich A, Bierens M, et al. Long-term effectiveness of off-label risperidone treatment in children and adolescents: a randomized, placebo-controlled discontinuation study. J Child Adolesc Psychopharmacol. 2024;34(6):253-263.  
8 Okada, T. Convulsions induced by withdrawal of risperidone. Seishin Igaku. 1999;41(11):1205-1208.  
9 Lane HY, Chang WH. Manic and psychotic symptoms following risperidone withdrawal in a schizophrenic patient. J Clin Psychiatry. 1998;59(11):620-621.  
10 Rowan AB, Malone RP. Tics with risperidone withdrawal. J Am Acad Child Adolesc Psychiatry. 1997;36(2):162-163.  
11 Anand VS, Dewan MJ. Withdrawal-emergent dyskinesia in a patient on risperidone undergoing dosage reduction. Ann Clin Psychiatry. 1996;8(3):179-182.  
12 Krasucki CG, Mackeith JA. Severe hypertension associated with risperidone withdrawal. Psychiatr Bull. 1995;19(7):452-453.  
13 Rosebush PI, Kennedy K, Dalton B, et al. Protracted akathisia after risperidone withdrawal. Am J Psychiatry. 1997;154(3):437-438.  
14 Franks M, Macritchie K, Mahmood T, et al. Bouncing back: is the bipolar rebound phenomenon peculiar to lithium? a retrospective naturalistic study. J Psychopharmacol. 2008;22(4):452-456.  
15 Van Reekum R, Clarke D, Conn D, et al. A randomized, placebo-controlled trial of the discontinuation of long-term antipsychotics in dementia. Int Psychogeriatr. 2002;14(2):197-210.  
16 Lore C. Risperidone and withdrawal dyskinesia. J Am Acad Child Adolesc Psychiatry. 2000;39(8):941.  
17 Yang FW, Liang CS. Manic symptoms during a switch from risperidone to paliperidone: a case report. J Neuropsychiatry Clin Neurosci. 2011;23(3):E29.  
18 Mendhekar DN, Inamdar A. Withdrawal-emergent respiratory dyskinesia with risperidone treated with clozapine. J Neuropsychiatry Clin Neurosci. 2010;22(2):E24.  
19 Catena Dell’osso M, Fagiolini A, Ducci F, et al. Newer antipsychotics and the rabbit syndrome. Clin Pract Epidemiol Ment Health. 2007;3:6.  
20 Urbano M, Spiegel D, Rai A. Atypical antipsychotic withdrawal dyskinesia in 4 patients with mood disorders. J Clin Psychopharmacol. 2007;27(6):705-707.  
21 Ehrt U, Fritze F, Aarsland D. Respiratory dyskinesia as discontinuation effect of risperidone. J Clin Psychopharmacol. 2005;25(6):609.  
22 Komatsu S, Kirino E, Inoue Y, et al. Risperidone withdrawal-related respiratory dyskinesia: a case diagnosed by spirography and fibroscopy. Clin Neuropharmacol. 2005;28(2):90-93.  
23 Nishimura K, Tsuka M, Horikawa N. Withdrawal-emergent rabbit syndrome during dose reduction of risperidone. Eur Neuropsychopharmacol. 2001;11(4):323-324.  
24 Miller LJ. Withdrawal-emergent dyskinesia in a patient taking risperidone/citalopram. Ann Pharmacother. 2000;34(2):269.  
25 Patel A, Gohil A, Archana K, et al. Unusual movements with a breath of complexity: a case of respiratory dyskinesia. Abstract presented at: 32nd Annual Conference of the Indian Academy of Neurology; October 29-November 2, 2025; Varanasi, India.  
26 Curran M, Mellor E, Howarth S. Heterogeneous tardive syndromes are still treatable with quetiapine. Prog Neurol Psychiatry. 2023;27(2):17-20.  
27 Giourou E, Theodoropoulou A, Batzikosta P, et al. A case report of eosinophilia associated with risperidone withdrawl in a patient with schizophrenia. Abstract presented at: 30th European Congress of Psychiatry (EPA); June 4-5, 2022; Virtual.  
28 Alblowi MA, Alosaimi FD. Tardive dyskinesia occurring in a young woman after withdrawal of an atypical antipsychotic drug. Neurosciences (Riyadh). 2015;20(4):376-379.  
29 Shah SJ, Goradia V, Dattani AV, et al. Symptomatic hyperprolactinemia mimicking pituitary pathology in a child with Landau-Kleffner syndrome, autism spectrum disorder, and intellectual disability: a case report. J Med Case Rep. 2026.  
30 Faisal M, Pradeep V, O’Hanrahan S. Case of paediatric catatonia precipitated by antipsychotic withdrawal in a child with autism spectrum disorder. BMJ Case Rep. 2021;14(4):e240785.  
31 Soundarrajan G, Chogtu B, Krishna V, et al. Akathisia induced by abrupt withdrawal of risperidone: a case report. Psychopharmacol Bull. 2019;49(1):80-83.  
32 Kumar M, Mattison R, Baweja R. Withdrawal-emergent dyskinesia after acute discontinuation of risperidone in a child with autism spectrum disorder. J Clin Psychopharmacol. 2018;38(6):640-642.  

Would you like to clear and leave your conversation? Message history will be lost.