|Year : 2019 | Volume
| Issue : 4 | Page : 499-501
Risperidone-induced tardive akathisia: A rare antipsychotic side effect with management issues
Biswa Ranjan Mishra, Rajeev Ranjan, Debadatta Mohapatra, Santanu Nath
Department of Psychiatry, All India Institute of Medical Sciences, Bhubaneswar, Odisha, India
|Date of Submission||11-Mar-2018|
|Date of Acceptance||22-Mar-2018|
|Date of Web Publication||25-Oct-2019|
Dr. Rajeev Ranjan
Department of Psychiatry, Room No. 411, Academic Block, All India Institute of Medical Sciences, Bhubaneswar . 751 019, Odisha
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Akathisia is a movement disorder, a common extrapyramidal side effect that has been reported to occur primarily with antipsychotics and some neurological conditions. It is manifested by a subjective feeling of inner restlessness along with objective evidence of motoric restlessness. Tardive akathisia (TA) is rare, and there is very sparse literature available as regards to its phenomenology and management. We report a case of TA that occurred after 10 months of starting atypical antipsychotic, risperidone, and challenges faced in management.
Keywords: Akathisia, antipsychotic, extrapyramidal symptoms, risperidone, tardive akathisia
|How to cite this article:|
Mishra BR, Ranjan R, Mohapatra D, Nath S. Risperidone-induced tardive akathisia: A rare antipsychotic side effect with management issues. Ann Indian Acad Neurol 2019;22:499-501
|How to cite this URL:|
Mishra BR, Ranjan R, Mohapatra D, Nath S. Risperidone-induced tardive akathisia: A rare antipsychotic side effect with management issues. Ann Indian Acad Neurol [serial online] 2019 [cited 2020 Jan 22];22:499-501. Available from: http://www.annalsofian.org/text.asp?2019/22/4/499/249700
| Introduction|| |
Akathisia is a movement disorder characterized by a sense of restlessness and inability to keep still, associated with a dysphoric feeling or a compulsion to move about. Typically, symptoms of akathisia appear 5–6 days after initiating dopamine blockers or increasing the dose or at times being delayed for up to a month., Tardive akathisia (TA) is a rare variant of akathisia, which is symptomatically similar to acute akathisia, but appears gradually, generally after few months or after a year of chronic treatment with dopamine blockers. The treatment with regard to medication-induced acute akathisia is established. However, there are anecdotal reports in relation to treatment approach for TA.,
We are reporting a case with late-onset paraphrenia (persistent delusional disorder) who manifested with TA after 10 months of therapy with risperidone, with highlights on the management approaches in such rare presentations.
| Case Report|| |
A 57-year-old woman presented with a 4-year history of continuous illness featured by infidelity for husband, self-muttering, irritability, and insomnia. Her mental status examination revealed irritable affect, delusion of infidelity and persecution, impaired judgment, and Grade 1 insight. She was diagnosed as late-onset paraphrenia. In view of late onset, organic causes were evaluated including blood investigations and neuroimaging (magnetic resonance imaging [MRI] brain) which were unremarkable. Risperidone was prescribed, and she was maintaining well on risperidone 8 mg/day without any extrapyramidal symptoms for 10 months. In the last follow-up, she presented with restlessness and inability to sit still since last few days accompanied with psychic restlessness, along with worsening of her psychopathology. Barnes Akathisia Rating Scale was applied which yielded a total score of 9 and the global clinical assessment of akathisia score of 5, which was suggestive of “severe akathisia.” In view of the onset after more than 10 months of risperidone use, a diagnosis of TA was considered and risperidone was stopped. In view of lack of literature with regard to treatment approaches in TA, we initially conceptualized this entity being similar to other tardive syndromes (i.e., tardive dyskinesias), and owing to the aggravation in psychopathology, amisulpride, a medium D2 receptor binder atypical antipsychotic, was started and increased over 1 week to 200 mg/day, along with tetrabenazine 50 mg/day, with which there was worsening of akathisia. We revised our treatment in lines of the management of acute akathisia. All antipsychotics were discontinued. Propranolol 40 mg/day was started, along with lorazepam 4 mg/day, with which there was dramatic improvement in next 3–4 days. In view of persisting paraphrenia, the patient was started on aripiprazole 10 mg/day, which was gradually hiked up to 20 mg/day over next 20 days. Propranolol and lorazepam were tapered and stopped in next 10 days. Interestingly, there was a significant reduction in preoccupation related to the delusions with aripiprazole 20 mg/day, without any evidence of any other extrapyramidal symptoms, in the next two follow-ups in 3 months.
| Discussion|| |
Akathisia is a neuroleptic-induced side effect in which the patient has observable component, which is called “motoric akathisia.” Coupled with this, many also experience a “cognitive” or “psychic” akathisia manifested by restless thoughts crowding the mind like “ping pong balls.”, It has been classified based on its onset and duration into various types, namely, “acute,” “tardive,” “withdrawal,” and the “chronic” variety, among which acute variety is commonly seen. TA has an onset usually after 3 months of starting an antipsychotic or any change in its dose. The patient described had an onset of akathisia after more than 10 months of risperidone use. The risk factors for akathisia are neuroleptic use (high potency, higher dose, and rapid titration), female sex, iron deficiency, affective psychosis, negative symptoms, and neurocognitive deficits. This case had few risk factors for akathisia, such as female gender and the use of high-potency neuroleptic risperidone. The description of worsening of psychopathology with the evolution of akathisia was very much evident in the patient. However, the psychopathology reduced only after the reduction in severity of akathisia, following withdrawal of antipsychotics. This suggests an overlap between “psychic akathisia” and “psychopathology,” which needs careful delineation and management.
In context to akathisia, there is an abundance of literature related to acute akathisia, with paucity of information about TA. Although acute akathisia can be caused by both neuroleptic and nonneuroleptic drugs (selective serotonin reuptake inhibitors, noradrenergic and specific serotonergic antidepressant, antiemetics, etc.),, no reports of TA ascribed to nonneuroleptics are there in the literature. TA has been reported with both typical antipsychotics such as haloperidol, perphenazine, molindone, loxapine, and thioridazine, and atypical antipsychotics such as olanzapine, amisulpride, clozapine, risperidone, and levomepromazine. This case is probably one of the few cases to report risperidone as the causative agent of TA.
The pathophysiology of TA remains obscure such as acute akathisia. Akathisia has been proposed to result from generalized reduction in dopamine tone in the brain which triggers a compensatory noradrenergic activity. These noradrenergic fibers are thought to innervate the shell portion of the nucleus accumbens more than the core portion which results in a mismatch, thus culminating into the restless semi-purposeful movements and associated dysphoria. However, few researchers have conceptualized TA as one of the tardive syndromes with similar pathophysiology but variation in presentation.
The literature search did not reveal any specific guidelines for the management of TA. Pharmacological approaches for acute akathisia entails initial reduction and switching of the antipsychotic, followed by the use of agents such as beta-blocker propranolol (30–80 mg/day), mirtazapine 15 mg/day, mianserin 30 mg/day, antimuscarinics, cyproheptadine, benzodiazepines, and clonidine. For TA, a different treatment option was proposed by Burke et al. in their study which reported improvement with dopamine-depleting drugs such as tetrabenazine and reserpine in 58% and 87% of their patients having TA, respectively, with complete abatement in only 33% of patients. Initially, we conceptualized this case with TA as a tardive syndrome variant. Hence, considering the severity of patient's psychopathology, we started her on tetrabenazine but did not produce any improvement in TA or psychopathology. Therefore, we planned to manage the case in the lines of acute akathisia. Hence, antipsychotic was stopped, propranolol was started, and TA symptoms improved completely within 1 week along with reduction in preoccupation related to psychopathology. Subsequently, the patient was maintained on aripiprazole, and propranolol was tapered and stopped. The patient in her subsequent follow-ups maintained stable without evidence of any other extrapyramidal symptoms.
Therefore, we suggest that clinicians should be aware of the possibility of the evolution of TA with the use of neuroleptics at high dose. The phenomenology and management of TA is similar to that of acute akathisia.
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.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Sachdev P. The classification of akathisia. Mov Disord 1995;10:235-7.
Sachdev P, Kruk J. Clinical characteristics and predisposing factors in acute drug-induced akathisia. Arch Gen Psychiatry 1994;51:963-74.
Lohr JB, Eidt CA, Abdulrazzaq Alfaraj A, Soliman MA. The clinical challenges of akathisia. CNS Spectr 2015;20 Suppl 1:1-4.
Sachdev P. The epidemiology of drug-induced akathisia: Part II. Chronic, tardive, and withdrawal akathisias. Schizophr Bull 1995;21:451-61.
Brune M, Braunig P. Akathisia. Fortschr Neurol Psychiatr 1997;65:396-406.
Raveendranathan D, Swaminath GR. Mirtazapine induced akathisia: Understanding a complex mechanism. Indian J Psychol Med 2015;37:474-5.
] [Full text]
Burke RE, Kang UJ, Jankovic J, Miller LG, Fahn S. Tardive akathisia: An analysis of clinical features and response to open therapeutic trials. Mov Disord 1989;4:157-75.
Albayrak Y, Hashimoto K. Benefical effects of sigma-1 agonist fluvoxamine for tardive dyskinesia and tardive akathisia in patients with schizophrenia: Report of three cases. Psychiatry Investig 2013;10:417-20.
Atmaca M, Korkmaz S. Delayed-onset akathisia due to amisulpride. Indian J Pharmacol 2011;43:460-2.
] [Full text]
Kyriakos D, Bozikas VP, Garyfallos G, Lavrentiadis G, Giouzepas J, Fokas K, et al.
Tardive nocturnal akathisia due to clozapine treatment. Int J Psychiatry Med 2005;35:207-11.
Shimizu E, Watanabe H, Iyo M. Delayed-onset nocturnal akathisia due to risperidone and levomepromazine: A case report. Eur Psychiatry 2002;17:294-5.
Taylor D, Paton C, Kapur S. The Maudsley Prescribing Guidelines in Psychiatry. Chichester, West Sussex: John Wiley & Sons Inc.; 2015.