Pargyline reduces/prevents neuroleptic-induced acute dystonia in monkeys

1987 ◽  
Vol 93 (2) ◽  
Author(s):  
R. Heintz ◽  
D.E. Casey
Keyword(s):  
2016 ◽  
Vol 22 ◽  
pp. e78-e79
Author(s):  
Lars Wictor ◽  
Klas Wictorin ◽  
Håkan Widner ◽  
Andreas Puschmann

2002 ◽  
Vol 36 (5) ◽  
pp. 827-830 ◽  
Author(s):  
Deborah V Kelly ◽  
Lizanne C Béïque ◽  
M Ian Bowmer

OBJECTIVE: To report a case of suspected extrapyramidal symptoms (EPS) in a patient initiated on ritonavir and indinavir while taking risperidone for a tic disorder. CASE SUMMARY: A 35-year-old white man with AIDS received risperidone 2 mg twice daily for treatment of a Tourette's-like tic disorder. Ritonavir and indinavir were initiated, and 1 week later, he experienced significantly impaired swallowing, speaking, and breathing, and worsening of his existing tremors. Ritonavir and indinavir were discontinued. On the same day, the patient increased the risperidone dosage to 3 mg twice daily. Symptoms continued to worsen over the next 3 days. All investigations and laboratory parameters were unremarkable, and vital signs were stable. Risperidone was discontinued and clonazepam initiated. Three days later, the patient's symptoms were significantly improved. DISCUSSION: The symptoms described herein are consistent with neuroleptic-induced acute dystonia and potentially neuroleptic-induced parkinsonism. We believe this adverse effect occurred as a result of a drug interaction between ritonavir/indinavir and risperidone. Based on the pharmacokinetics of these medications, we hypothesize that inhibition of CYP2D6 and CYP3A4 by ritonavir and indinavir may have resulted in an accumulation of the active moiety of risperidone, which may explain the occurrence of EPS in this patient. CONCLUSIONS: This is the second published case report describing a suspected drug interaction with ritonavir, indinavir, and risperidone. Caution is warranted when risperidone is prescribed with ritonavir/indinavir, and possibly with other antiretrovirals that inhibit the same pathways.


2018 ◽  
Vol 31 (4) ◽  
pp. 396-399 ◽  
Author(s):  
Sema Baykara ◽  
Muhammed Fatih Tabara ◽  
Sevda Korkmaz ◽  
Murad Atmaca
Keyword(s):  

2016 ◽  
Vol 33 (S1) ◽  
pp. S620-S621
Author(s):  
C. Tüz

PurposeIn this article, a case who was prescribed duloxetine (30 mg capsule) upon the fibromyalgia diagnosis by a physical therapist and had acute dystonia and dyskinesia after approximately 1.5 hours from duloxetine intake shall be presented.CaseIt was learnt that a married female patient aged 38 consulted a physical therapist with the complaint of back pain and duloxetine (30 mg capsule) was prescribed. It was reported that, the patient applied to our hospital with the compliant of involuntary movements around the mouth, on the lips and neck, spasm, inability to open the mouth completely, spasm in jaw, gritting teeth, mumbling and aphasia after approximately 1.5 hours from her duloxetine intake. The patient was conscious. Her psychomotor activity was natural. As a result of cranial MR, EEG, BT examinations hemogram and the routine biochemistry examinations, any abnormality in zinc and iron levels was not detected. Complaints of the patient regressed after 1 hour from the discontinuance of duloxetine and the administration of biperiden 5 mg/mL ampoule 1000 cm3 in SF. After 72 hours, any symptoms were not found.DiscussionDopamine neurotransmission can be inhibited through the increase in serotonin and norepinephrine. Additionally, dystonia may originate from the prevailing of noradrenaline as a result of the failure of dopaminergic–noradrenergic balance.Disclosure of interestThe author has not supplied his/her declaration of competing interest.


1990 ◽  
Vol 7 (2) ◽  
pp. 141-142 ◽  
Author(s):  
R N Chithiramohan ◽  
C G Ballard ◽  
L G Measey
Keyword(s):  

AbstractWe present a case showing inducement of acute dystonia by clomipramine therapy and discuss the possible explanations. We could find no previous reports of this phenomenon.


CNS Spectrums ◽  
2020 ◽  
Vol 25 (2) ◽  
pp. 278-278
Author(s):  
Charles Haverty ◽  
Julie Niedermier ◽  
Hossam Guirgis

Abstract:We report two cases of acute dystonia in patients after receiving prochlorperazine to address nausea in the context of buprenorphine/naloxone (Suboxone) therapy. Both were admitted for opioid withdrawal and developed nausea and vomiting refractory to ondansetron on the first hospital day.Within six hours of receiving an intramuscular injection of ten milligrams of prochlorperazine, a 24-year-old Caucasian male developed buccolingual crisis (trismus and dysphagia). His symptoms resolved with repeated intramuscular doses of diphenhydramine, benztropine, and lorazepam.A 31-year-old Caucasian female developed laryngeal dystonia (stridor) and buccolingual crisis (dysphagia, grimacing, and tongue protrusion) within thirty minutes of receiving ten milligrams of prochlorperazine intramuscularly. Given respiratory impairment, emergency airway protection was initiated, and the patient responded to repeated intramuscular doses of benztropine and lorazepam.Although one patient was male and both were relatively young, they did not have other known risk factors for drug induced acute dystonic reactions including history of dystonic reactions, recent cocaine use, or low BMI. Neither patient had a history of exposure to antipsychotic medications and both had medical histories that were otherwise noncontributory. While both patients were at risk for or developing dehydration from nausea and vomiting, their electrolytes were within normal limits on admission, less than twelve hours earlier. We postulate potential etiologies that may possibly explain these events:1)The patients’ reactions are consistent with the expected number in the general population to have acute dystonia secondary to prochlorperazine use. A small study in 2000 showed that 3.9% of patients receiving prochlorperazine for nausea in an emergency room setting experienced acute dystonia.2)Could patients receiving intramuscular prochlorperazine during Suboxone therapy have increased risk for severe acute dystonic reactions? According to the European Medicines Agency, hypertonicity is a “common” side effect of Suboxone, occurring in 1% to 10% of patients.3)Could there be potential interactions between Suboxone and prochlorperazine or between prochlorperazine and substances detected (or undetectable, such as designer drugs) via routine toxicology screening?4)Could the acute dystonia be unrelated to medication interaction, but instead result from use of prochlorperazine in patients having rapid electrolyte shifts and exhibiting dehydration during acute opioid withdrawal?Given the known risk of opioids, with or without prochlorperazine, to cause respiratory depression and these case reports of acute dystonia with the potential to cause airway impairment due to prochlorperazine administration, we encourage prescribers to exercise caution when utilizing prochlorperazine for the management of nausea and vomiting in patients receiving Suboxone for acute opioid withdrawal.


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