Severe Akathisia Research Articles

Electroconvulsive Therapy and Akathisia: A Comprehensive Literature Review of Case Reports.

This review aimed to investigate the effects of electroconvulsive therapy (ECT) on akathisia. We systematically searched MEDLINE and Embase and included case reports on akathisia caused by or treated with ECT. We identified and included 9 articles. Seven articles, representing 10 cases, reported that akathisia improved after ECT. Most cases (7 cases) were diagnosed with a mood disorder, and all 10 cases were treated with antipsychotics. Akathisia was regarded as tardive (3 cases) and severe (4 cases). Although treatments for akathisia, such as adjusting antipsychotics and adding medication for akathisia, were tried before ECT, ultimately none were effective. In all 10 cases, akathisia showed significant improvement after ECT, and nonantipsychotic psychotropics or low-dose antipsychotics were administered as post-ECT treatment. Two articles (5 cases) reported that akathisia occurred after ECT. Three of these cases were diagnosed with a mood disorder, and all 5 cases were treated with perphenazine and tricyclic antidepressants. Akathisia occurred multiple times after ECT, but it was transient. Despite attempts to manage the akathisia, including discontinuation of psychotropics, addition of medication for akathisia, and adjustment of stimulation electrode positions, the outcomes of the interventions were inconsistent. Nonetheless, no persistent akathisia was observed after the end of the ECT course. Although the effects of ECT on akathisia remain unclear because of the paucity of high-quality studies, ECT could be considered particularly for treatment-resistant, tardive, and/or severe akathisia comorbid with mood disorders. Conversely, clinicians should keep in mind that transient akathisia can develop following ECT.

The Possibility of the Second Generation Antipsychotic-Olanzapine to Cause Severe Akathisia in a Drug Naive Patient -A Case Report

Here we are presenting this case of 26 years old gentleman with no past psychiatric history who presented initially to the emergency department with anxiety and depressive symptoms in the context of ongoing stressors, diagnosed as a case of severe anxiety and started on neuroleptic medication. A few days later, it was reported by the family that the patient was moving around and only sit for a few minutes before starting to move again in response to an urge to keep moving. Barnes Akathisia-Rating Scale was administered and indicated severe akathisia. The patient started on Mirtazapine 15 mg and Propranolol 20 mg twice daily, and he dramatically improved in a few days.

Depressive symptoms in Chinese male inpatients with schizophrenia: Prevalence and clinical correlates

Depression is common in patients with schizophrenia and associated with serious consequences. However, previous studies have mixed findings on characteristics of depression in schizophrenia, partly because of the use of depressive symptom scales that are not specific to schizophrenia. This study examined the prevalence and correlates of depressive symptoms in Chinese patients with schizophrenia. A consecutive sample of 349 male inpatients with schizophrenia was recruited from the largest psychiatric specialty hospital in south-central China. Depressive symptoms and psychopathology of patients were assessed with the Calgary Depression Scale for Schizophrenia and the Positive and Negative Symptom Scale, respectively. Extrapyramidal side effects (EPSs) were assessed with the Simpson Angus Scale, the Barnes Akathisia Rating Scale, and the Abnormal Involuntary Movement Scale. Demographic and other clinical data were also collected. Depressive symptoms were present in 41.8% of male schizophrenia inpatients. Multiple logistic regression analysis revealed that early age at onset (OR [95%CI] = 1.12 [1.01,1.27], p = 0.049), more severe negative symptoms (OR [95%CI] = 1.05 [1.01,1.09], p = 0.034), more severe general psychopathological symptoms (OR [95%CI] = 1.06 [1.01,1.12], p = 0.041), akathisia (OR [95%CI] = 2.87 [1.45,5.69], p = 0.003), and dyskinesia (OR [95%CI] = 3.93 [1.36,11.33], p = 0.011) were significantly associated with depression. Appropriate antipsychotic medication treatment and reducing EPSs of antipsychotics may help prevent or relieve depression of patients with schizophrenia.

Use of combinatorial pharmacogenomic testing in two cases from community psychiatry.

This report describes two cases in which pharmacogenomic testing was utilized to guide medication selection for difficult to treat patients. The first patient is a 29-year old male with bipolar disorder who had severe akathisia due to his long acting injectable antipsychotic. The second patient is a 59-year old female with major depressive disorder who was not responding to her medication. In both cases, a proprietary combinatorial pharmacogenomic test was used to inform medication changes and improve patient outcomes. The first patient was switched to a long acting injectable that was not affected by his genetic profile and his adverse effects abated. The second patient had her medications discontinued due to the results of the genetic testing and more intense psychotherapy initiated. While pharmacogenomic testing may be helpful in cases such as these presented here, it should never serve as a proxy for a comprehensive biopsychosocial approach. The pharmacogenomic information may be selectively added to this comprehensive approach to support medication treatment.

Increased Anxiety, Akathisia, and Suicidal Thoughts in Patients with Mood Disorder on Aripiprazole and Lamotrigine.

Introduction. Akathisia affects around 18% of patients with bipolar disorder treated with aripiprazole and may worsen when aripiprazole is combined with lamotrigine and antidepressants. Case. This paper reports on two clinical cases involving patients with a diagnosis of mood disorder who developed severe akathisia, anxiety, and suicidal ideation while using a combination of aripiprazole, antidepressants, and lamotrigine. Discussion. We recommend that patients with a mood disorder taking multiple drugs should begin aripiprazole therapy with low doses and be monitored for the development of akathisia, increased anxiety, or suicidal thoughts. The appearance of these limiting side effects requires discontinuation of the drug.

Acute Dystonia, Akathisia, and Parkinsonism Induced by Ziprasidone

Ziprasidone is a second-generation antipsychotic with a lower propensity to cause extrapyramidal adverse effects that are seen at higher doses. We report a patient who developed acute dystonia, parkinsonism, and severe akathisia with ziprasidone 80 mg/d. These adverse effects subsided after dose reduction and specific treatment for akathisia and parkinsonism.

Gabapentin pharmacotherapy for antipsychotic-induced akathisia: single-patient experiment and case report

This clinical study reports upon the efficacy of gabapentin (Neurontin) for treating severe akathisia (3 on the Barnes Akathisia Rating Scale) in two patients receiving quetiapine (Seroquel), one of whom also received olanzapine (Zyprexa) for a short period. The first patient participated in an open-label experiment in which the bedtime dose of gabapentin was discontinued three times at intervals 1 week apart, resulting in severe akathisia which was quickly terminated by taking his usual 1200 mg gabapentin dose. This patient was also taking high doses of two benzodiazepines and a beta blocker, without therapeutic effect upon his akathisia; only gabapentin was efficacious. The second case is a report of a woman taking a high dose of quetiapine for anxiety who experienced severe akathisia which was relieved by taking 1200 mg of gabapentin. Possible mechanisms of action of gabapentin are discussed. Particular attention is drawn to the difference between neuroleptic-induced akathisia and the neurological condition of restless legs syndrome.

A Case of Akathisia induced by Escitalopram: Case Report & Review of Literature

Although cases of Selective Serotonin Reuptake Inhibitor (SSRI) induced akathisia have often been reported in literature, this adverse effect has not adequately been mentioned in major pharmacology textbooks. As a result, SSRIinduced akathisia is very frequently under-recognized. A review of literature showed that almost all frequently used SSRIs such as Fluvoxamine, Fluoxetine, Sertraline, Citalopram have been reported to be causing akathisia. SSRI-induced restless legs syndrome and movement disorders have also been reported. However, Escitalopram-induced akathisia is rare. In our review of literature, we could find only one single case of Escitalopram-induced severe akathisia. And this specific SSRI drug has rarely been implicated with occurrence of restless legs syndrome and extra-pyramidal side-effects like dytonia etc. Here, we present a case of Escitalopram-induced severe akathisia - a 53year old female, who had developed severe akathisia after taking Escitalopram for a few days. According to the Barnes Akathisia Rating Scale (BARS), her Global Clinical Assessment of Akathisia Score was 5 i.e. severe akathisia. As per Naronjo Adverse Drug Reaction Scale the probability of association of this adverse reaction with Escitalopram was 7 (i.e. probable). Her symptoms continued in spite of prompt discontinuation of the drug. But, she improved rapidly with the use of Propranolol and Clonazepam. On the last follow-up, she was free from any symptoms. As new generation antidepressants are rarely associated with extra-pyramidal symptoms, the recognition of such adverse effects requires a high index of suspicion. Early recognition of the symptoms and discontinuation of the offending agent along with supportive therapy like a short course of benzodiazepines, beta-adrenergic antagonists or anticholinergics may rapidly relieve the patient from this distressing symptom.

A Case of Severe Akathisia with Atomoxetine

A Case of Severe Akathisia with Atomoxetine

Reversal of Aripiprazole-Induced Tardive Akathisia by Addition of Pregabalin

Reversal of Aripiprazole-Induced Tardive Akathisia by Addition of Pregabalin

Persistent akathisia masquerading as agitated depression after use of ziprasidone in the treatment of bipolar depression

There has been increasing recognition that the second-generation antipsychotic drugs can produce extrapyramidal side effects. This case reports the development of severe akathisia in a patient being treated with ziprasidone for bipolar depression. The case illustrates that this symptom can be easily mistaken for worsening agitated depression. Akathisia may produce considerable distress and elevate suicide risk. Such symptoms may persist for weeks and be refractory to discontinuation of the offending agent or to pharmacological interventions commonly used to mitigate this reaction.

Escitalopram-Induced Severe Akathisia

To the Editor: Akathisia, which is a distressing adverse reaction, is usually underdiagnosed or misdiagnosed in patients who are treated with selective serotonin reuptake inhibitors (SSRIs). Although cases of fluoxetine-, paroxetine-, sertraline-, fluvoxamine-, and citalopram-induced akathisia are reported in the literature, to our knowledge, escitalopram-induced akathisia has not yet been reported.1 Here, we report a case of escitalopram-induced akathisia that remitted completely after diazepam treatment. Case report. Mr A, a 52-year-old man, consulted to our clinic in 2010 on referral by the neurology department with the complaints of feeling restless and having difficulty remaining still while seated and lying down. Initially, he was admitted to the neurology department with the complaint of headache; he was diagnosed as having tension type headache and was started on escitalopram 10 mg/d. Two days after receiving the first dose, he began complaining of severe motor restlessness and an unbearable state of never being able to sit still. Results of routine blood sample tests were within the normal range. Brain magnetic resonance imaging (MRI) revealed no abnormality in the brain. He had no remarkable neurologic findings. He did not have any personal or familial history of akathisia, psychiatric illness, movement disorder, or drug abuse. After other possible disorders were excluded, the diagnosis of severe akathisia, possibly induced by escitalopram, was made. On the Barnes Akathisia Rating Scale (BARS),2 his global score was 5 (severe akathisia). Subsequently, escitalopram treatment was gradually stopped. Akathisia was not resolved 3 days after the permanent withdrawal of the offending medication. He still scored 5 on the BARS. Therefore, treatment with diazepam 5 mg/d was started. At the second day of diazepam treatment, akathisia was fully resolved. His score on the BARS was 0. Diazepam was gradually stopped within 1 week. Three weeks after stopping diazepam, there was no reemergence of akathisia or other extrapyramidal side effects. The patient was scheduled for a follow-up appointment by the psychiatry and neurology outpatient clinic. Although akathisia is commonly attributed to antipsychotic medication and considered as an extrapyramidal symptom, the reports in the literature suggest varying underlying pathways.1 Deficiency of dopamine in the nigrostriatal pathway is considered to be responsible for extrapyramidal symptoms; however, serotonergic-induced inhibition of dopamine in the mesocorticolimbic pathway projecting from the ventral tegmental area (VTA) of the brain to the prefrontal cortex is thought to be responsible for the arising of akathisia. Like serotonin, norepinephrine acts similarly to inhibit dopamine in the VTA. Consequently, drugs that increase the stimulation of serotonergic or noradrenergic receptors in the mesocorticolimbic pathway theoretically could be responsible for inducing akathisia.3,4 Escitalopram is the single isomer that inhibits the serotonin reuptake produced by the racemic SSRI antidepressant citalopram. By elimination of the R-enantiomer, escitalopram would be expected to be more potent than citalopram.5 In the literature, there is only 1 citalopram-induced akathisia case, which was reported by Seedat et al.6 However, there are no literature data addressing escitalopram-induced akathisia. This may be due to the shorter half-life or the relatively recent introduction of escitalopram into the market. In our case, the possible factors that could be associated with arising akathisia are initiation of treatment with a high dose, the low affinity of escitalopram for anticholinergic receptors, and the high potency of escitalopram. To our knowledge, this is the first case report of escitalopram-induced akathisia. Akathisia is not a mild side effect, and it has even been reported that it may be associated with suicidality.1,7 Therefore, akathisia should be considered carefully in patients who are treated with SSRIs and certainly managed acutely.

Severe akathisia as a side effect of metoclopramide

Case description A case of severe metoclopramide-induced akathisia in a breast cancer patient being treated with chemotherapy is presented, eventually culminating in hospital admission. In retrospect, this adverse effect was not recognized for several weeks because the prescription had not been properly recorded in the chart, the patient initially denied using the drug, and extensive psychological adjustment difficulties were also present. Conclusion Movement disorders as an adverse effect of metoclopramide have been described on a regular basis over the past decades. Case reports such as this confirm there is under-recognition of adverse effects and emphasize the need to take a comprehensive medication history and recognize well known side effects of medications such as metoclopramide.

Akathisia after mild traumatic head injury

The authors describe the case of a 13-year-old boy who exhibited progressive disabling motor restlessness, torticollis, urinary symptoms, and confusion following a fall from a bicycle. The differential diagnosis of this striking symptom complex in this clinical context can be problematic. In this case, the symptoms ultimately appeared most consistent with severe akathisia resulting from a single administration of haloperidol used at an outside hospital to sedate the patient prior to a head CT scan. The literature on akathisia in pediatric patients, and especially in patients following acute head injury, is reviewed, with suggestions for an approach to these symptoms in this clinical setting.

Akathisia Induced by Mirtazapine After 20 Years of Continuous Treatment

Mirtazapine is an antidepressant blocking presynaptic alpha2-adrenergic receptors and an antagonist of 5-hydroxytryptamine 2A/2C, 5-hydroxytryptamine 3, and histaminergic (H) postsynaptic receptor. Acute dystonia restless legs syndrome (RLS) and manic syndromes are adverse effects of mirtazapine, whereas only few cases of acute akathisia, after the first doses of mirtazapine, are referred. Instead, mirtazapine is used to treat akathisia probably because of its antagonistic property at H1 postsynaptic receptors and dopaminergic action in the frontal cortex. A 72-year-old woman with depression, on mirtazapine treatment for almost 20 years, was admitted to an outpatient neurology clinic, with 1-week history of 3-kg weight loss and progressive intense "inner restlessness," constant movements of the legs and feet, remarkable distress, insomnia, and pacing up and down. Neurological examination had normal results, no deterioration of the depression was present, a magnetic resonance scan of the brain was unremarkable, and biochemical tests were within reference ranges. The disorder eventually resolved after the permanent withdrawal of the offending medication. After excluding other possible disorders, the diagnosis of severe akathisia, possibly induced by mirtazapine, was made. The reappearance of the symptoms after the patient had been rechallenged with mirtazapine ascertained the diagnosis of akathisia induced by mirtazapine. This report relates akathisia with mirtazapine intake after such a long period of treatment. It illustrates the importance of being alert to any movement disorder emerging in patients treated with mirtazapine, even after many years of treatment.

Perinatal Akathisia: Implications for Pharmacokinetic Changes During Pregnancy

Back to table of contents Previous article Next article Letters to the EditorFull AccessPerinatal Akathisia: Implications for Pharmacokinetic Changes During PregnancyMATTHEW L. PROWLER M.D.DEBORAH R. KIM M.D.,MATTHEW L. PROWLER M.D.Search for more papers by this authorDEBORAH R. KIM M.D.Search for more papers by this author,Published Online:1 Nov 2009https://doi.org/10.1176/appi.ajp.2009.09060823AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the editor: Although physiological changes during pregnancy significantly affect drug pharmacokinetics, no evidence-based heuristic exists for peripartum dosing (1) . To illustrate this concept, we present the case of a patient with Tourette’s syndrome who experienced severe postpartum akathisia, ameliorated by medication dose reduction. “Ms. HP” was a 29-year-old 3-weeks-postpartum Indian female (gravida 2 para 2), who presented with acute anxiety to the emergency room. Although she had experienced vocal and motor tics since childhood, she had never been treated for these symptoms. Her symptoms became more severe during her second pregnancy. Self-inflicted hitting and face scratching led to a detached retina in the second month of this pregnancy. During the fifth gestational month, her obstetrician started her on pimozide, 4 mg daily. She then reported a prompt and marked reduction in her symptoms, stating that the tics were “almost completely gone,” and she tolerated the medication without side effects throughout the pregnancy.Ms. HP had an uncomplicated delivery of a healthy female infant. Within 1 week, she reported low energy and restlessness at night, which progressed to near-constant symptoms in the second postpartum week. She described a “weird feeling” in her stomach and legs and that she “had to walk.” In her third postpartum week, she presented to the emergency room. She paced the unit hallways and was unable to remain still.The patient was emergently treated with lorazepam and benztropine, and her acute symptoms subsided. Upon discharge, pimozide was reduced to 2 mg daily, and follow-up evaluation at a community psychiatry clinic occurred within 1 week postdischarge. At that time, her akathisia had fully remitted. Her Tourette"s syndrome symptoms were present but remained diminished. At 2 months postpartum, her tics were under good control and she remained free of extrapyramidal symptoms. Several physiological factors could explain this patient’s postpartum akathisia. Pimozide is metabolized by hepatic cytochrome P450 3A and 2D6 pathways. It has been shown that drug metabolism by these isoenzymes increases during pregnancy (2) . Similarly, there is an approximate increase of 5 to 8 liters in total body water during pregnancy, in addition to 30%–50% of plasma volume (1 , 3) . This may result in a higher volume of drug distribution. During pregnancy, a decreased concentration of albumin may lead to decreased peak serum concentrations of protein-bound drugs, such as pimozide (4) . Other studies have suggested that higher drug doses may be needed to compensate for these changes during late pregnancy, with subsequent postpartum dose tapering as liver metabolism and fluid volumes return to baseline levels (5) . The present case adds to a limited clinical database and highlights the need for a broader evidence base regarding pharmacokinetic changes during pregnancy and their effects on drug dosing.Philadelphia, Pa.Dr. Kim has received research support from Neuronetics, Inc. Dr. Prowler reports no financial relationships with commercial interests.This letter (doi: 10.1176/appi.ajp.2009.09060823) was accepted for publication in July 2009.

Subsyndromal Depressive Symptoms in Middle-Aged and Older Persons with Schizophrenia

The objectives are to delineate the nature of subsyndromal depressive symptoms (SSD) in midlife and older patients with schizophrenia and schizoaffective disorder by: 1) describing the relationship of SSD with a number of other clinical features; and 2) examining which specific depressive symptoms are increased in patients broadly defined as having SSD. A total of 204 participants with schizophrenia or schizoaffective disorder and SSD who entered a federally funded intervention study at the University of California San Diego (UCSD) and University of Cincinnati were matched with schizophrenic and schizoaffective participants from the Geriatric Research Center at UCSD who had minimal or no depressive symptoms. The SSD and no depression groups were compared on a variety of clinical features including general psychopathology, positive and negative symptoms, medical and mental functioning, cognition, movement abnormalities, and specific depressive symptomatology. SSD was associated with increases in overall psychopathology; positive and negative symptoms; severity of general medical conditions; impaired physical and mental functioning; possibly more severe akathisia; and more depressive symptoms throughout the spectrum of symptom clusters measured by the Hamilton Depression Rating Scale, including anxiety and suicidality. SSD in middle aged and older patients with schizophrenia is an important clinical dimension that appears to be associated with substantial morbidity and distress. The findings suggest that is important for clinicians to look for and assess subsyndromal depressive symptoms in patients with chronic schizophrenia.

Clozapine-Induced Tardive Dystonia (Blepharospasm)

Back to table of contents Previous article Next article LETTERFull AccessClozapine-Induced Tardive Dystonia (Blepharospasm)Harpreet S. Duggal M.D., D.P.M,D.N. Mendhekar M.D., D.P.M,Harpreet S. Duggal M.D., D.P.MSearch for more papers by this author,D.N. Mendhekar M.D., D.P.MSearch for more papers by this author,Published Online:1 Jan 2007AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail SIR: Tardive dystonia is a type of “tardive” movement disorder induced by antipsychotics and is characterized by involuntary muscle contraction, which may be tonic, spasmodic, patterned, or repetitive. 1 Blepharospasm is a type of focal tardive dystonia characterized by chronic intermittent or persistent closure of the eyelids. Although there are rare reports of tardive dystonia induced by atypical antipsychotics, such as olanzapine, 2 clozapine, in contrast, has been reported to ameliorate tardive dystonia. 3 Contrary to existing literature, we report a case of a patient developing blepharospasm with clozapine. Case Report“Mrs. F,” a 46-year-old woman, presented with one month of suspiciousness, mumbling to herself, and disturbed biological functions, and she was diagnosed with schizophreniform disorder. Past and family history revealed no psychiatric or neurological illness. Initially, she was treated with trifluoperazine (15mg/day) for 4 months, which was replaced with clozapine due to severe akathisia. The dose of clozapine was increased from 25mg to 100mg/day over a period of 2 weeks after performing hematological investigations, and she was maintained on the same dose for 4 months.While being treated with clozapine, Mrs. F developed frequent and forceful blinking of her eyelids. She would blink her eyes about 40 times in a minute when exacerbated by bright light. An ophthalmological consultation was unremarkable for any eye pathology contributing to this presentation and the neurological exam did not reveal any abnormal movements, except for the blepharospasm. The patient had no prior personal or family history of blepharospasm or other movement disorders.Five months later, clozapine was tapered and stopped, but Mrs. F continued to have blepharospasm even 4 weeks after discontinuing clozapine. Subsequently, clonazepam (1mg/day) was started and the blepharospasm disappeared a month after its initiation. Two years later, the patient had a second episode of psychotic illness and was again treated with clozapine, titrated up to 75mg/day. Five weeks later, she exhibited a similar form of blepharospasm, though it was not as severe. Again, clozapine was discontinued and Mrs. F had a complete resolution of the blepharospasm with clonazepam.Comment The reappearance of blepharospasm with the administration of clozapine strongly implicates this drug in this dystonic reaction. Blepharospasm is classified as a type of focal dystonia and has been reported to occur with atypical antipsychotics. In contrast to other atypicals, such as olanzapine, which have been anecdotally reported to cause tardive dystonia, 2 clozapine has been used in treating tardive dystonia, including blepharospasm. 3 , 4 However, in rare instances, clozapine has been reported to induce tardive dystonia as well. 5 In the above case, the patient developed cervical dystonia 2 years after clozapine was started. Given the rarity of reports of clozapine-induced tardive dystonia, our patient may have developed an idiosyncratic reaction to this drug. This is further supported by the observations that this patient did not develop tardive dystonia with trifluoperazine, which is a more potent D 2 receptor antagonist than clozapine, and that the proposed mechanism of drug-induced tardive dystonia is the sensitization of dopamine receptors following their blockade. 6 Another issue highlighted by this report and the existing literature is that clonazepam is an effective treatment of tardive dystonia, 3 and may be considered before more invasive procedures, such as botulinum toxin, are tried. Herrick Memorial Hospital, Tecumseh, Mich.Delhi, India

Sudden Akathisia After a Ziprasidone Dose Reduction

Back to table of contents Previous article Next article Letter to the EditorFull AccessSudden Akathisia After a Ziprasidone Dose ReductionE. TIMUCIN ORAL, M.D., KURSAT ALTINBAS, M.D., and SIMDEN DEMIRKIRAN, M.D., E. TIMUCIN ORALSearch for more papers by this author, M.D., KURSAT ALTINBASSearch for more papers by this author, M.D., and SIMDEN DEMIRKIRANSearch for more papers by this author, M.D., Istanbul, TurkeyPublished Online:1 Mar 2006https://doi.org/10.1176/appi.ajp.163.3.546AboutSectionsPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack Citations ShareShare onFacebookTwitterLinked InEmail To the Editor:We report five cases of akathisia in female patients with bipolar disorder (who were treated with 80–160 mg/day of ziprasidone) that appeared to occur dramatically after a dose reduction. All of the patients had subjective feelings of motor restlessness. They displayed an irresistible urge to walk or move their legs, and they were evaluated with Barnes Rating Scale for Drug-Induced Akathisia (1). None of these patients had any significant medical conditions related to akathisia.Ms. A was a 27-year-old woman receiving carbamazepine. Because of a mixed episode, 120 mg b.i.d. of ziprasidone was added. After 2 months, ziprasidone was tapered to 80 mg b.i.d., and akathisia developed, with a Barnes rating scale score of 6. Ziprasidone was accordingly discontinued, and 40 mg b.i.d. of propranolol, 20 mg b.i.d. of diazepam, and 4 mg b.i.d. of biperiden were added to her treatment regimen.Ms. B, who had been receiving 200 mg b.i.d. of lamotrigine when psychotic symptoms appeared, was also 27 years old. She did not respond to 3 weeks of ziprasidone, 120 mg b.i.d., and during the tapering process, a sudden and severe akathisia developed, with a Barnes rating scale score of 14. Ziprasidone was discontinued, and the already-mentioned protocol for the treatment of akathisia was applied.Ms. C, a 46-year-old woman had her last manic episode treated with ziprasidone, 160 mg/day. After 4 weeks, her mania disappeared, but depressive symptoms emerged. Decreasing her ziprasidone dose to 120 mg/day was followed by abrupt akathisia, with a Barnes rating scale score of 9. Forty mg b.i.d. of propranolol, 30 mg b.i.d. of diazepam, and 4 mg b.i.d. of biperiden were added to her drug regimen for akathisia.A rapid-cycling bipolar patient, Ms. D, age 61, was the eldest of our five cases. She had been given valproate and ziprasidone until she complained about sedation. Her ziprasidone dose was reduced to 120 mg/day from 160 mg/day, which was also followed by sudden akathisia with a Barnes rating scale score of 14 that responded only to clonazepam, 6 mg/day.Ms. E, who had responded well to lithium prophylaxis but discontinued it because of polyuria, polydipsia, and urinary incontinence, was 48 years old. She refused to take valproate and olanzapine because she experienced hair loss and weight gain. Finally, she agreed to take 40 mg/day of ziprasidone for prophylaxis. But because of the appearance of depressive symptoms, it was also discontinued. This resulted in sudden akathisia with a score on the Barnes rating scale of 12. Her akathisia disappeared totally after treatment with 40 mg/day of propranolol, 4 mg/day of biperiden, and 2 mg/day of alprazolam. Although unexpected, akathisia after ziprasidone dose reduction in our cases was not persistent. Gradual or complete resolution of akathisia with 75% to 100% reduction in Barnes rating scale scores was observed within 7–10 days in all cases.The patients described here remind clinicians of unexpected side effects with second-generation antipsychotics and to consider extrapyramidal syndrome in patients while they are taking or discontinuing their drugs (2).

Rate of metoclopramide infusion affects the severity and incidence of akathisia

Objective: To investigate the effect of the rate of metoclopramide infusion on akathisia incidence, severity, onset of symptoms, and duration in patients with headache, and/or nausea/vomiting in the emergency department...