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Journal articles on the topic 'Dyskinesia, Drug-Induced'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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1

Romaniuk, Małgorzata, Konrad Suswał, Aleksandra Skałecka, Maria Gromek, Martyna Kozłowska, and Paweł Krukow. "Drug-induced dyskinesias, can they be prevented?" Current Problems of Psychiatry 21, no. 2 (June 1, 2020): 95–101. http://dx.doi.org/10.2478/cpp-2020-0009.

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AbstractIntroduction: Dyskinesia is a symptom complex in the form of involuntary, repetitive movements of lips, lower jaw, tongue, less often the trunk and limbs. Despite the use of newer drugs in treatment neuroleptics, dyskinesia has not ceased to be a clinical problem.Method: The work is based on a research review for which the Google Scholar database was used as well PubMed. The search range was limited to 2008-2020. We have included descriptive publications tardive dyskinesia only as a consequence of antipsychotic medications.Material: We present the use of tetrabenazine analogues, deep brain stimulation, neuroleptics, benzodiazepines and botulinum toxin in late-suffering patients drug-induced dyskinesias, which may indicate an improvement in your health.Discussion: The first method of treating tardive dyskinesia are withdrawal antipsychotic medications, but for many patients this is impossible. Valbenazine and Deep Brain Stimulation are the most effective in treating Tardive Dyskinesia.Conclusions: There are not enough studies with the highest reliability to create unequivocal recommendations in the treatment of drug-induced tardive dyskinesia.

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2

Marianto, Marianto, Hartono Kosim, and I. Made Wedastra. "Drug-Induced Tardive Dyskinesia." International Journal of Research and Review 8, no. 9 (September 23, 2021): 413–22. http://dx.doi.org/10.52403/ijrr.20210953.

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Drug-induced movement disorders could be classified into acute, subacute, and chronic based on the time of occurrence. Tardive dyskinesia (TD) is one of the most frequent long-term drug-induced movement disorders. Delay in treatment often caused TD to be irreversible. In this review, we will discuss TD in-depth to enhance clinician knowledge regarding the diagnosis, prevention, and comprehensive management of patients with TD. Keywords: tardive dyskinesia, movement, disorder, antipsychotic.

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3

Kondo, Tomoyoshi, and Hiroshi Ishiguchi. "3. Drug Induced Dyskinesia." Nihon Naika Gakkai Zasshi 96, no. 8 (2007): 1621–26. http://dx.doi.org/10.2169/naika.96.1621.

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4

Ostroumova, T. M., V. A. Tolmacheva, O. D. Ostroumova, and V. A. Parfenov. "Drug-induced tardive dyskinesia." Neurology, Neuropsychiatry, Psychosomatics 12, no. 1 (February 21, 2020): 81–86. http://dx.doi.org/10.14412/2074-2711-2020-1-81-86.

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5

MONTENEGRO, M. AUGUSTA, ANNA ELISA SCOTONI, and FERNANDO CENDES. "Dyskinesia induced by phenytoin." Arquivos de Neuro-Psiquiatria 57, no. 2B (June 1999): 356–60. http://dx.doi.org/10.1590/s0004-282x1999000300002.

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Phenytoin is an effective antiepileptic drug, although, it can be associated with many side effects, including dyskinesia. OBJECTIVE: To describe the clinical characteristics of phenytoin induced dyskinesia. METHODS: We investigated the occurrence of involuntary movements in patients followed at our adult and pediatric epilepsy clinics during the period of one year. RESULTS: Three patients presented with phenytoin-induced dyskinesia: one adult with axial and orofacial dyskinesia, and two children with choreoathetosis. They did not have other signs of phenytoin intoxication and had complete recovery after phenytoin withdrawal. CONCLUSION: Phenytoin induced dyskinesia may occur during either chronic or initial treatment and with normal serum phenytoin levels. However, it occurs most often in patients on polytherapy, usually after increasing dosage and with toxic serum levels. Other signs of phenytoin intoxication may be present in these patients, but often the dyskinesia is the only side effect, which may delay the diagnosis and treatment. The clinical characteristics of the involuntary movements vary and may be focal or generalized, most often characterized by choreoathetosis and dyskinesias. These may last for hours, days or even years, but frequently disappear completely after phenytoin withdrawal.

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6

Gopika S Kumar, Divya V Nair, Remya Raghu, and Arun K. "Antipsychotic Drug Induced Tardive Dyskinesia." International Journal of Research in Pharmaceutical Sciences 11, no. 4 (December 24, 2020): 7383–85. http://dx.doi.org/10.26452/ijrps.v11i4.3922.

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A typical antipsychotics are at a lower risk of developing extra-pyramidal symptoms (EPS). But now, atypical antipsychotics are increasingly being associated with neurological side effects such as tardive dyskinesia, tardive dystonia, akinesia, parkinsonism, akathisia, bradykinesia, tremor etc. in which one of the major cases reported is Olanzapine induced tardive dyskinesia (TD). Schooler and Kane criteria is used for diagnosing tardive dyskinesia. Many cases have been published on this particular drug-induced side effect. In many instances tardive dyskinesia is misdiagnosed as tardive dystonia. Here we report the case of tardive dyskinesia associated with the use of antipsychotic drugs in a 50-year-old adult male suffering from persistent delusional disorder in a tertiary health care centre in India. The patient was on Olanzapine therapy for more than 2 years. Upon recurrent episodes of somatic delusions, Olanzapine dose was increased. When the patient developed symptoms of TD, the dose of Olanzapine was de-escalated. Even though the drug dose was reduced, the symptoms persisted which lead to the diagnosis of olanzapine induced TD. Based on this, Olanzapine was stopped and Clozapine treatment was initiated. On follow up, the patient was found to be relieved of the symptoms and complete recovery was achieved after 2 months of clozapine treatment.

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7

Vijayakumar, Dhanya, and Joseph Jankovic. "Drug-Induced Dyskinesia, Part 1: Treatment of Levodopa-Induced Dyskinesia." Drugs 76, no. 7 (April 18, 2016): 759–77. http://dx.doi.org/10.1007/s40265-016-0566-3.

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8

Brown, Keith W., and Thomas White. "The Psychological Consequences of Tardive Dyskinesia the Effect of Drug-Induced Parkinsonism and the Topography of the Dyskinetic Movements." British Journal of Psychiatry 159, no. 3 (September 1991): 399–403. http://dx.doi.org/10.1192/bjp.159.3.399.

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The effect of drug-induced Parkinsonism and of the topography of the dyskinetic movements on the psychological consequences of tardive dyskinesia was assessed in 20 schizophrenic subjects and 20 non-dyskinetic schizophrenic controls matched for age, sex, the presence of anticholinergic medication, and the presence and severity of drug-induced Parkinsonism. Limb–truncal subscale scores but not orofacial scores had a significant correlation with cognitive impairment and with negative symptoms. Drug-induced Parkinsonism was found to be a powerful confounding variable.

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9

Vijayakumar, Dhanya, and Joseph Jankovic. "Drug-Induced Dyskinesia, Part 2: Treatment of Tardive Dyskinesia." Drugs 76, no. 7 (April 18, 2016): 779–87. http://dx.doi.org/10.1007/s40265-016-0568-1.

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10

Chen, Jack J. "Drug-induced movement disorders." Mental Health Clinician 1, no. 7 (January 1, 2012): 167–73. http://dx.doi.org/10.9740/mhc.n90206.

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This comprehensive review covers approaches for both the recognition and management of drug-induced movement disorders. Pharmacotherapeutic approaches for treating akathisia, dystonia, Parkinsonism and tardive dyskinesia are explored. The importance of early detection via periodic assessment is discussed.

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11

Sachdev, Perminder. "Drug-Induced Movement Disorders in Institutionalised Adults with Mental Retardation: Clinical Characteristics and Risk Factors." Australian & New Zealand Journal of Psychiatry 26, no. 2 (June 1992): 242–48. http://dx.doi.org/10.1177/000486749202600208.

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Fifty-three institutionalised adults with mental retardation, the majority (73.5%) moderate to severe, were examined for drug-induced movement disorders. Using a global AIMS score of 2 or more, 16 (34%) of the 47 subjects who had been exposed to neuroleptics had tardive dyskinesia (TD). Three of these had developed the dyskinesia upon withdrawal of neuroleptics. The dyskinetic movements were mainly seen in the lingual, perioral and other facial muscles. Two (33%) out of 6 subjects with no history of exposure to neuroleptics also had similar dyskinetic movements. The total neuroleptic dose significantly, and age marginally, but not sex, brain damage or level of mental retardation, emerged as risk factors for TD. Two (3.7%) subjects had definite akathisia and 16 (30.8 %) significant extrapyramidal side effects. This study supports the findings of previous studies of considerable neurological adverse effects of neuroleptics in this patient group and cautions against their injudicious use. It provides further evidence for some putative risk factors for TD and is noteworthy for its lack of support for the contentious issue of brain damage as a risk factor.

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12

Loonen, Anton J. M., and Svetlana A. Ivanova. "New insights into the mechanism of drug-induced dyskinesia." CNS Spectrums 18, no. 1 (December 20, 2012): 15–20. http://dx.doi.org/10.1017/s1092852912000752.

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Dyskinesia is an extrapyramidal movement disorder characterized by involuntary, repetitive, irregular motions that affect the mouth and face and/or the limbs and trunk. Tardive dyskinesia (TD) is a well-known complication of long-term treatment with antipsychotic drugs. Dyskinesia is also induced with levodopa, a treatment for Parkinson's disease, and it occurs spontaneously as a symptom of Huntington's disease. Research on the pathogenesis of TD has focused on a dysfunction of either the dopaminergic or serotonergic system. However, recent evidence has suggested that we should focus on the possible damage of GABAergic medium spiny neurons (MSNs). MSNs are the first station in the cortico-striato-thalamo-cortical circuit that regulates the amplitude and velocity of movements. Two pathways can be distinguished in this circuit: a direct pathway, which increases movements (hyperkinesia), and an indirect pathway, which decreases movements (hypokinesia). Both pathways are activated by glutamatergic corticostriatal neurons. Here, we discuss some evidence that supports the hypothesis that indirect pathway MSNs are damaged in dyskinesia.

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13

Hutny, Michał, Jagoda Hofman, Aleksandra Klimkowicz-Mrowiec, and Agnieszka Gorzkowska. "Current Knowledge on the Background, Pathophysiology and Treatment of Levodopa-Induced Dyskinesia—Literature Review." Journal of Clinical Medicine 10, no. 19 (September 25, 2021): 4377. http://dx.doi.org/10.3390/jcm10194377.

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Levodopa remains the primary drug for controlling motor symptoms in Parkinson’s disease through the whole course, but over time, complications develop in the form of dyskinesias, which gradually become more frequent and severe. These abnormal, involuntary, hyperkinetic movements are mainly characteristic of the ON phase and are triggered by excess exogenous levodopa. They may also occur during the OFF phase, or in both phases. Over the past 10 years, the issue of levodopa-induced dyskinesia has been the subject of research into both the substrate of this pathology and potential remedial strategies. The purpose of the present study was to review the results of recent research on the background and treatment of dyskinesia. To this end, databases were reviewed using a search strategy that included both relevant keywords related to the topic and appropriate filters to limit results to English language literature published since 2010. Based on the selected papers, the current state of knowledge on the morphological, functional, genetic and clinical features of levodopa-induced dyskinesia, as well as pharmacological, genetic treatment and other therapies such as deep brain stimulation, are described.

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14

Lobo, A. J., and R. J. Dickinson. "Drug points: Cricopharyngeal dyskinesia induced by prochlorperazine." BMJ 295, no. 6593 (August 1, 1987): 333. http://dx.doi.org/10.1136/bmj.295.6593.333.

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15

Abida, I., I. Baati, S. Omri, R. Sallemi, and J. Masmoudi. "Drug-induced tardive dyskinesia: A case report." European Psychiatry 33, S1 (March 2016): S610—S611. http://dx.doi.org/10.1016/j.eurpsy.2016.01.2282.

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IntroductionTardive dyskinesia (TD) is a serious medical condition that affects a significant proportion of patients treated with antipsychotic agents.ObjectiveTo report a patient who developed tardive dyskinesia after initiation of antipsychotic and antidepressant treatment.Case reportMiss H. is 24-year-old Tunisian woman who had been diagnosed with bipolar disorder 6 years ago. She received various drugs: olanzapine, haloperidol, amisulpride, sertraline, paroxetine, etc. On November 2013, she first complained of hand tremor and then developed severe dystonia of the trunk and chorea. A series of laboratory tests was performed after the onset of these involuntary movements. It included complete blood count, liver, renal, and thyroid function tests, blood prolactin level, blood glucose level, blood copper level and ceruloplasmin level. A brain MRI was also performed. These examinations showed no specific findings. The diagnosis of TD was presumed. The patient was first treated with amisulpride, lorazepam, avlocardyl and piracetam until May 2014. Then, amisulpride was substituted by olanzapine until August 2015. The luck of improvement led to her admission. We stopped antipsychotic treatments and prescribed her vitamin E (900 mg/day), clonazepam (6 mg/day) and vitamin B6. The follow-up led to the decline of the Abnormal Involuntary Movement Scale (AIMS) score of 7 points over 6 weeks.ConclusionTD remains a serious side effect that worsens the prognosis and affects the quality of life of patients. Cluster randomised trial should be done in order to develop practice recommendations for prevention and management of TD.Disclosure of interestThe authors have not supplied their declaration of competing interest.

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16

Vaiman, E. E., N. A. Shnayder, N. G. Neznanov, and R. F. Nasyrova. "Candidate genes involved in the development of antipsychotic-induced tardive dyskinesia in patients with schizophrenia." Neuromuscular Diseases 10, no. 3 (December 6, 2020): 10–26. http://dx.doi.org/10.17650/2222-8721-2020-10-3-10-26.

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Introduction. Drug-induced dyskinesia is an iatrogenic undesirable side reaction from the extrapyramidal system that occurs during the administration of drugs, most often antipsychotics in patients with schizophrenia. At the end of the 20 th century, studies were conducted on the search for candidate genes and the carriage of single nucleotide variants of antipsychotics-induced tardive dyskinesia. Purpose of the study – to analyze research results reflecting candidate genes and their single nucleotide variants associated with antipsychotic-induced tardive dyskinesia. Materials and methods. We searched for full-text publications in Russian and English in the eLIBRARY, PubMed, Web of Science, Springer databases using keywords (tardive dyskinesia, drug-induced tardive dyskinesia, antipsychotics, antipsychotics, typical antipsychotics, atypical antipsychotics, genes, polymorphisms) and combined searches for words over the past decade. Results. The lecture discusses candidate genes encoding proteins/enzymes involved in the pharmacodynamics and pharmacokinetics of antipsychotics Conclusion. Timely identification of individual genetic characteristics of the patient can contribute to the development of diagnostic test systems and in the future selection of the safest and most effective antipsychotic therapy.

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17

Casey, Daniel E. "Neuroleptic drug-induced extrapyramidal syndromes and tardive dyskinesia." Schizophrenia Research 4, no. 2 (March 1991): 109–20. http://dx.doi.org/10.1016/0920-9964(91)90029-q.

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18

Lang, Anthony E. "Clinical Differences Between Metoclopramide- and Antipsychotic-Induced Tardive Dyskinesias." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 2 (May 1990): 137–39. http://dx.doi.org/10.1017/s031716710003033x.

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ABSTRACT:A patient with tardive dyskinesia dominated by pelvic thrusting movements is described. A retrospective review of the clinical features documented in patients with metoclopramide- and antipsychotic-induced tardive dyskinesias seen over a six year period demonstrated that the occurrence of pronounced pelvic thrusting and respiratory dyskinesias were significantly more common in the metoclopramide treated group. The occurrence of bucco-linguomasticatory movements, limb stereotypies or chorea, and mild truncal or abdominal rocking were not significantly different between the two groups. None of the tardive dystonia patients had metoclopramide as the causative agent. These findings will require confirmation in larger, better matched patient populations. Whether the differences relate to different pharmacologic profiles of drug action, patient populations exposed, or other factors, remains to be elucidated.

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19

Ross, R. T. "Drug-Induced Parkinsonism and Other Movement Disorders." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 17, no. 2 (May 1990): 155–62. http://dx.doi.org/10.1017/s0317167100030389.

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ABSTRACT:This is a review of reserpine, haloperidol, and various phenothiazines that produce parkinsonism and other movement disorders. The by-products of illicit meperidine synthesis, MPTP and its more sinister companion, MPP, are also discussed. Movement disorders, transient or fixed, frank parkinsonism and/or dyskinesia, due to a variety of other medications and toxic agents are included. These are methanol, lithium, methyldopa, antimetabolites, antidepressants, sympathomimetic anorexiants, some types of antihistamines, and various combinations of agricultural chemicals.

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20

Claxton, Katherine L., Jack J. Chen, and David M. Swope. "Drug-Induced Movement Disorders." Journal of Pharmacy Practice 20, no. 6 (December 2007): 415–29. http://dx.doi.org/10.1177/0897190007310514.

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Drug-induced movement disorders (DIMDs) pose a significant burden to patients, often resulting in nonadherence, disease relapse, and decreased quality of life. Dopamine-receptor blocking agents such as conventional antipsychotics (eg, haloperidol and chlorpromazine) and antiemetics (eg, metoclopramide and prochlorperazine) are most commonly implicated. DIMDs can be categorized by the onset of symptoms: acute reactions occurring hours to days after exposure, subacute DIMDs appearing within weeks, and tardive occurring months to years after drug exposure. The DIMDs of akathisia, tardive dyskinesia, dystonia, and parkinsonism are reviewed. Their epidemiology, mechanism, clinical presentation and differential diagnosis, risk factors, morbidity and mortality, and prevention and management are discussed. For many of these disorders, treatment inconsistently provides benefit, and therefore, primary prevention is essential. Clinicians and other healthcare professionals play a key role in the identification of patients with DIMDs, or those at risk, and in implementing prevention and treatment plans.

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21

Asmal, Laila. "Tardive dyskinesia on clozapine: A case report." South African Journal of Psychiatry 15, no. 1 (March 1, 2009): 2. http://dx.doi.org/10.4102/sajpsychiatry.v15i1.169.

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Antipsychotic-induced tardive dyskinesia is a potentially irremediable and debilitating condition with the onset most commonly associated with the use of first-generation antipsychotics. The development of tardive dyskinesia on clozapine, a second-generation antipsychotic, is uncommon, and the drug is therefore a treatment option for those patients who develop the syndrome following treatment with first- generation agents. I report on the case of a 27-year-old man who developed severe tardive dyskinesia following initiation of clozapine treatment. To the best of my knowledge, this is the first case of tardive dyskinesia associated with clozapine use reported in South Africa.

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22

Fisk, G. G., and S. M. York. "The Effect of Sodium Valproate on Tardive Dyskinesia - Revisited." British Journal of Psychiatry 150, no. 4 (April 1987): 542–46. http://dx.doi.org/10.1192/bjp.150.4.542.

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As a treatment for tardive dyskinesia, sodium valproate was tested in a double-blind placebo-controlled parallel group trial, with 6-week base-line observation period followed by 6 weeks of treatment. Sodium valproate was not found to be an effective treatment for either tardive dyskinesia or drug-induced Parkinsonism, and did not affect mental state or behaviour.

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23

Rupniak, N. M. J., S. J. Tye, and S. D. Iversen. "Drug-induced purposeless chewing: animal model of dyskinesia or nausea?" Psychopharmacology 102, no. 3 (November 1990): 325–28. http://dx.doi.org/10.1007/bf02244098.

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24

Tamtè, Martin, Ivani Brys, Ulrike Richter, Nedjeljka Ivica, Pär Halje, and Per Petersson. "Systems-level neurophysiological state characteristics for drug evaluation in an animal model of levodopa-induced dyskinesia." Journal of Neurophysiology 115, no. 3 (March 1, 2016): 1713–29. http://dx.doi.org/10.1152/jn.00868.2015.

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Disorders affecting the central nervous system have proven particularly hard to treat, and disappointingly few novel therapies have reached the clinics in recent decades. A better understanding of the physiological processes in the brain underlying various symptoms could therefore greatly improve the rate of progress in this field. We here show how systems-level descriptions of different brain states reliably can be obtained through a newly developed method based on large-scale recordings in distributed neural networks encompassing several different brain structures. Using this technology, we characterize the neurophysiological states associated with parkinsonism and levodopa-induced dyskinesia in a rodent model of Parkinson's disease together with pharmacological interventions aimed at reducing dyskinetic symptoms. Our results show that the obtained electrophysiological data add significant information to conventional behavioral evaluations and hereby elucidate the underlying effects of treatments in greater detail. Taken together, these results potentially open up for studies of neurophysiological mechanisms underlying symptoms in a wide range of neurological and psychiatric conditions that until now have been very hard to investigate in animal models of disease.

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25

Kumar, Gaurav. "A Review and Case Study of the Action of Chlorpromazine on Dopaminergic Pathways and its Associated Extrapyramidal Disturbances." International Journal for Research in Applied Science and Engineering Technology 10, no. 4 (April 30, 2022): 3163–67. http://dx.doi.org/10.22214/ijraset.2022.42012.

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Abstract: As a first-line antipsychotic, Chlorpromazine is an excellent blocking agent of the D2 receptor. Dopamine pathways are predominantly affected by the use of this medicine in schizophrenia therapy, leading to the development of drug-induced Parkinsonism (DIP). Extrapyramidal symptoms (EPS) include motor rigidity, tremors, restlessness, dystonia, stumbling, nervousness, improper posture, Tardive dyskinesia, Akathisia, and many other side effects. In seniors over 70 suffering from schizophrenia, DIP has become very common and is the second most common cause of Parkinsonism behind Parkinson's disease (PD). A concise review of the actual mechanism of blockade by chlorpromazine is presented in this article, with a particular focus on EPS and other adverse effects. Keywords: Drug-induced Parkinsonism, Extrapyramidal symptoms, Schizophrenia, Tardive dyskinesia, Chlorpromazine.

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Madani, Nadine, Jennifer A. O’Malley, Brenda E. Porter, and Fiona M. Baumer. "Lacosamide-Induced Dyskinesia in Children With Intractable Epilepsy." Journal of Child Neurology 35, no. 10 (June 11, 2020): 662–66. http://dx.doi.org/10.1177/0883073820926634.

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Lacosamide, an antiepileptic drug prescribed for children with refractory focal epilepsy, is generally well tolerated, with dose-dependent adverse effects. We describe 4 children who developed a movement disorder in conjunction with the initiation and/or uptitration of lacosamide. Three patients developed dyskinesias involving the face or upper extremity whereas the fourth had substantial worsening of chronic facial tics. The patients all had histories suggestive of opercular dysfunction: 3 had seizure semiologies including hypersalivation, facial and upper extremity clonus while the fourth underwent resection of polymicrogyria involving the opercula. Onset, severity, and resolution of dyskinesias correlated with lacosamide dosing. These cases suggest that pediatric patients with dysfunction of the opercular cortex are at increased risk for developing drug-induced dyskinesias on high-dose lacosamide therapy. Practitioners should be aware of this potential side effect and consider weaning lacosamide or video electroencephalography (EEG) for differential diagnosis, particularly in pediatric patients with underlying opercular dysfunction.

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Doval, Nimisha, Soumitra Das, and Vikas Moun. "Aripiprazole in Tardive Dyskinesia: Is it a Safe Choice?" Journal of Neurosciences in Rural Practice 08, no. 02 (April 2017): 294–95. http://dx.doi.org/10.4103/jnrp.jnrp_359_16.

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ABSTRACTTardive dyskinesia (TD) is a potentially irreversible drug-induced movement disorder associated with prolonged administration of antipsychotics. Conventionally, first generation antipsychotics were the agents thought to have a higher risk of TD as compared to second and third generation antipsychotics. Aripiprazole is a third generation antipsychotic with a novel mechanism of action, and until recently, cases of drug-induced movement disorders were less well known with it. But off late, several cases of TD with aripiprazole have been reported. We present here a case of middle-aged women with preexisting tardive movements, which exacerbated with aripiprazole use and reduced in frequency and intensity on withdrawal of the drug.

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Purvis, Tara L. "Are extrapyramidal symptoms less recognized? Case report of modern practitioners' unfamiliarity with first generation antipsychotics." Mental Health Clinician 1, no. 7 (January 1, 2012): 164–66. http://dx.doi.org/10.9740/mhc.n91689.

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A case is presented where initial suspicion of lithium toxicity was mistaken. Drug-induced Parkinsonism and tardive dyskinesia were present, underscoring the need to improve training of movement disorder assessment.

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29

Sandyk, Reuven, and Stanley R. Kay. "Neuroradiological Covariates of Drug-Induced Parkinsonism and Tardive Dyskinesia in Schizophrenia." International Journal of Neuroscience 58, no. 1-2 (January 1991): 7–53. http://dx.doi.org/10.3109/00207459108987181.

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30

Lee, Sang-hwa, Hee-yeon Shin, Jeong-hwa Kim, Yeon-jin Kim, Seung-yeon Cho, Jung-mi Park, Chang-nam Ko, and Seong-uk Park. "A Case of Drug-Induced Acute Dyskinesia Treated with Korean Medicine." Journal of Internal Korean Medicine 38, no. 5 (October 30, 2017): 853–61. http://dx.doi.org/10.22246/jikm.2017.38.5.853.

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31

Hansen, Thomas E., William L. Brown, Ronald M. Weigel, and Daniel E. Casey. "Underrecognition of tardive dyskinesia and drug-induced parkinsonism by psychiatric residents." General Hospital Psychiatry 14, no. 5 (September 1992): 340–44. http://dx.doi.org/10.1016/0163-8343(92)90069-m.

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32

Buck, Kerstin, and Boris Ferger. "l-DOPA-induced dyskinesia in Parkinson's disease: a drug discovery perspective." Drug Discovery Today 15, no. 19-20 (October 2010): 867–75. http://dx.doi.org/10.1016/j.drudis.2010.08.014.

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33

Nevet, Alon, Genela Morris, Guy Saban, Nina Fainstein, and Hagai Bergman. "Discharge Rate of Substantia Nigra Pars Reticulata Neurons Is Reduced In Non-Parkinsonian Monkeys With Apomorphine-Induced Orofacial Dyskinesia." Journal of Neurophysiology 92, no. 4 (October 2004): 1973–81. http://dx.doi.org/10.1152/jn.01036.2003.

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Involuntary movements (dyskinesia) are a common symptom of dopamine-replacement therapy in parkinsonian patients, neuroleptic drug treatment of mental patients, and tic disorders. Levodopa-induced dyskinesia has been shown to be associated with substantial reduction of firing rate in the internal part of the globus pallidus. This study characterizes the changes that occur in the activity of the substantia nigra pars reticulata (SNr) of non-parkinsonian (normal) monkeys with apomorphine (APO)-induced orofacial dyskinesia. We conducted extracellular recordings of SNr neurons of two monkeys before and after induction of orofacial dyskinesia by systemic administration of APO. Involuntary orofacial movements appeared a few minutes after the injections and lasted 20–40 min. Almost all recorded neurons changed their firing rate after APO injection (96%), and most declined (70%). The mean amplitude of decreases was also larger than that of increases (40 vs. 21% of the control rate). Changes in firing pattern were not significant on average. Pairs of SNr neurons were uncorrelated before APO injection, similar to the normal pallidum. However, unlike the increased correlations in the pallidum that accompany parkinsonism, orofacilal dyskinesia in non-parkinsonian monkeys was not associated with changes in correlation between SNr neurons. We conclude that normal monkeys treated with APO can model orofacial dyskinesia and tic disorders that are a consequence of dopaminergic over-activity. These symptoms appear to be more related to reduced firing rate of SNr neurons and thus to disinhibition of their targets, than to changes in pattern and synchronization.

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Vayman, E. E., N. A. Shnayder, N. G. Neznanov, and R. F. Nasyrova. "Pathophysiological mechanisms underlying antipsychotic-induced tardive dyskinesia." Bulletin of Siberian Medicine 18, no. 4 (January 14, 2020): 169–84. http://dx.doi.org/10.20538/1682-0363-2019-4-169-184.

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Purpose. To analyze the results of classical and modern studies reflecting the pathophysiological mechanisms of antipsychotic-induced tardive dyskinesia.Materials and methods. We searched for full-text publications in Russian and English in the databases of E-Library, PubMed, Web of Science and Springer published over the past decade, using keywords (tardive dyskinesia (TD), drug-induced tardive dyskinesia, antipsychotics (AP), neuroleptics, typical antipsychotics, atypical antipsychotics, pathophysiology, etiology and combinations of these words). In addition, the review included earlier publications of historical interest.Results. The lecture proposed theories of development of AP-induced TD, examining its effect on dopaminergic receptors, dopaminergic neurons, neurons of the basal ganglia, and other theories: activation of estrogen receptors, disorders of melatonin metabolism, disorders of the endogenous opioid system, oxidative stress with predominant oxidation processes, blockade of 5-HT2-receptors, a decrease in the pyridoxine level, genetic predisposition, interaction of AP with the brain trace element – iron, carbonyl stress and immune inflammation and the role of the neurotrophic factor.Conclusion. The disclosure of the mechanisms of AP-induced TD will allow the development of a strategy for personalized prevention and therapy of the considered neurological complication of the AP-therapy for schizophrenia in real clinical practice.

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Gerber, Patricia E., and Larry D. Lynd. "Selective Serotonin-Reuptake Inhibitor–Induced Movement Disorders." Annals of Pharmacotherapy 32, no. 6 (June 1998): 692–98. http://dx.doi.org/10.1345/aph.17302.

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OBJECTIVE: To compile and evaluate all available data suggesting an association between selective serotonin-reuptake inhibitor (SSRI) administration and the occurrence of movement disorders, and to characterize these reactions in terms of onset, duration, treatment and outcome, and potential predisposing factors. METHODOLOGY: Reports of movement disorders were identified by conducting a comprehensive literature search that included tertiary adverse drug reaction resources, MEDLINE, EmBASE, Biological Abstracts, Current Contents, Reactions, ClinAlert, and International Pharmaceutical Abstracts. In addition, reports were solicited from the Canadian proprietary manufacturers of SSRIs, and from the Therapeutic Products Program of Health Canada. Each case was then classified according to the description of the movement disorder, based on predefined diagnostic criteria. RESULTS: A total of 127 published reports of SSRI-induced movement disorders were identified involving akathisia (n = 30), dystonia (19), dyskinesia (12), tardive dyskinesia (6), parkinsonism (25), and 15 cases of mixed disorders. Ten isolated cases of bruxism were identified. Ten additional reports could not be classified. Manufacturers of SSRIs provided 49 reports of akathisia, 44 of dystonia, 208 of dyskinesia, 76 of tardive dyskinesia, 516 of parkinsonism, and 60 of bruxism. Treatment strategies included discontinuation of the SSRI; dosage reduction; or the addition of a benzodiazepine, β-blocker, or anticholinergic agent. CONCLUSIONS: SSRI use appears to be associated with the development of movement disorders, as either a direct result of the drug or exacerbation of an underlying condition. Predisposing factors may include the use of neuroleptics, existing neurologic diagnoses, or preexisting movement disorders. Clinicians should be cognizant of the potential for these reactions, as prompt recognition and management is essential in preventing potentially significant patient morbidity.

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Pourcher, Emmanuelle, Philippe Baruch, Roch Hugo Bouchard, Marie-Josée Filteau, and Danielle Bergeron. "Neuroleptic Associated Tardive Dyskinesias in Young People with Psychoses." British Journal of Psychiatry 166, no. 6 (June 1995): 768–72. http://dx.doi.org/10.1192/bjp.166.6.768.

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BackgroundApart from ageing, the factors associated with vulnerability to the emergence of tardive dyskinesia are poorly defined.MethodRisk factors associated with the presence of a chronic choreic or dystonic disorder were assessed in a cross-sectional comparison of anamnestic and clinical data in a homogeneous group of 64 young psychotic patients (under 40 years of age) on chronic low to moderate doses of neuroleptics.ResultsDyskinetic subjects presented more indirect indicators of occult brain damage, such as a perinatal event or traumatic brain injuries in infancy and early childhood; neurological examination showed more anomalies in dyskinetic patients than in non-dyskinetics, with a higher prevalence of facial release reflexes.ConclusionThese data may support the hypothesis that occult acquired brain damage is important in the genesis of this ‘drug-induced’ disorder.

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Rissardo, Jamir Pitton, and Ana Letícia Fornari Caprara. "The Link Between Amitriptyline and Movement Disorders: Clinical Profile and Outcome." Annals of the Academy of Medicine, Singapore 49, no. 4 (April 30, 2020): 236–51. http://dx.doi.org/10.47102/annals-acadmed.sg.202023.

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Introduction: Amitriptyline (AMT) is a tricyclic antidepressant. In this review, we evaluate the clinical and epidemiological profile, pathological mechanisms and management of AMT-associated movement disorders. Materials and Methods: A search for relevant reports in 6 databases was performed. Studies that reported patients developed only ataxia or tremor after AMT use were excluded. Results: A total of 48 reports on 200 cases were found. AMT-associated movement disorders included myoclonus (n = 26), dyskinesia (n = 11), dystonia (n = 8), stutter (n = 5), akathisia (n = 3) and restless legs syndrome (n = 1). For less well-defined cases, 99 patients had dyskinesia, 19 had psychomotor disturbances, 3 had myoclonus, 11 had dystonia, 12 had Parkinsonism and 1 each had akathisia and extrapyramidal symptoms. Mean and standard deviation (SD) and median ages were 45.40 years (SD 16.78) and 40 years (range 3.7–82 years), respectively. Over half were women (58.13%) and the most common indication was depression. Mean and median AMT doses were 126 mg (SD 128.76) and 75 mg (range 15–800 mg), respectively. In 68% of patients, onset of movement disorders was <1 month; time from AMT withdrawal to complete recovery was <1 month in 70% of cases. A weak negative linear correlation (r = −0.0904) was found between onset of movement disorders and AMT dose. AMT withdrawal was the most common treatment. Conclusion: Amitriptyline is associated with various movement disorders, particularly myoclonus, dystonia and dyskinesias. Stutters and restless legs syndrome are some of the less common associations. Ann Acad Med Singapore 2020;49:236–51 Key words: Akathisia, Drug-induced, Dyskinesia, Dystonia, Myoclonus

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Lata, Paul F., and Denise L. Walbrandt Pigarelli. "Chronic Metoclopramide Therapy for Diabetic Gastroparesis." Annals of Pharmacotherapy 37, no. 1 (January 2003): 122–26. http://dx.doi.org/10.1345/aph.1c118.

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OBJECTIVE To review the safety and efficacy of chronic metoclopramide for diabetic gastroparesis. DATA SOURCES Medical literature was accessed through MEDLINE (1965 to October 2002) and PubMed (1965 to October 2002). Key search terms included metoclopramide; diabetic gastroparesis; and dyskinesia, drug induced. DATA SYNTHESIS Metoclopramide is often used for diabetic gastroparesis, despite the risk of tardive dyskinesia. Published information is limited regarding long-term efficacy and toxicity of metoclopramide. The literature was assessed concerning these topics. CONCLUSIONS Limited data do not provide sufficient evidence to conclude whether metoclopramide is efficacious for chronic use. Routine monitoring may mitigate the risk associated with metoclopramide therapy.

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Shin, Eunju, Elisabetta Tronci, and Manolo Carta. "Role of Serotonin Neurons in L-DOPA- and Graft-Induced Dyskinesia in a Rat Model of Parkinson's Disease." Parkinson's Disease 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/370190.

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L-DOPA, the most effective drug to treat motor symptoms of Parkinson's disease, causes abnormal involuntary movements, limiting its use in advanced stages of the disease. An increasing body of evidence points to the serotonin system as a key player in the appearance of L-DOPA-induced dyskinesia (LID). In fact, exogenously administered L-DOPA can be taken up by serotonin neurons, converted to dopamine and released as a false transmitter, contributing to pulsatile stimulation of striatal dopamine receptors. Accordingly, destruction of serotonin fibers or silencing serotonin neurons by serotonin agonists could counteract LID in animal models. Recent clinical work has also shown that serotonin neurons are present in the caudate/putamen of patients grafted with embryonic ventral mesencephalic cells, producing intense serotonin hyperinnervation. These patients experience graft-induced dyskinesia (GID), a type of dyskinesia phenotypically similar to the one induced by L-DOPA but independent from its administration. Interestingly, the 5-HT1Areceptor agonist buspirone has been shown to suppress GID in these patients, suggesting that serotonin neurons might be involved in the etiology of GID as for LID. In this paper we will discuss the experimental and clinical evidence supporting the involvement of the serotonin system in both LID and GID.

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Mokarian, Faezeh, Hamidreza Famitafreshi, and Mahsa Hadipour Jahromy. "Berberis vulgaris alleviates Levodopa-induced dyskinesia in male mice." Herba Polonica 64, no. 4 (December 1, 2018): 44–49. http://dx.doi.org/10.2478/hepo-2018-0023.

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Summary Introduction: Parkinson’s disease is a chronic debilitating disease and many patients use Levodopa as a major treatment. However, this drug in long-term use causes a serious condition that is known as Levodopa-induced dyskinesia (LID). Berberis vulgaris (BV) has been known to be a good potential medication for neurologic diseases such as movement disorders. The aim of this study is to investigate the usefulness of BV for LID in mice. Material and methods: In this study, 48 adult male mice were randomly divided into six groups: 1) saline group, 2) MPTP + LID, 3) MPTP + LID + BV (5 mg/kg), 4) MPTP + LID + BV (10 mg/kg), 5) MPTP + LID + BV (20 mg/kg). MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) (30 mg/kg/day/i.p.) was used to induce Parkinson’s disease and Levodopa (50 mg/kg/day/i.p.) was used to induce LID. After induction of LID, mice received intraperitoneally (i.p.) different dosages of BV for 25 days. To investigate movement disorder improvement (dyskinesia), AIMS (Abnormal Involuntary Movement Scale) and cylinder tests were used. Results: Mice that received BV at dosages of 10 and 20 mg/kg/day showed improvement in AIMS and the cylinder test. Conclusion: BV is a useful drug for treating LID. So, parkinsonian disease patients may get a beneficial effect after treatment with BV for LID.

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van Harten, P. N., and H. W. Hoek. "Recognition of Movement Disorders in Psychiatry: Video Fragments." European Psychiatry 24, S1 (January 2009): 1. http://dx.doi.org/10.1016/s0924-9338(09)70347-5.

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Movement disorders in psychiatry can be divided in those related to an underlying neurological or other somatic disease, related to a psychiatric syndrome, drug induced and psychogenic. In this workshop the typical clinical aspects of each of these movement disorders will be discussed and shown on video with the focus on drug induced. Drug induced can be divided in acute and tardive movement disorders. Acute movement disorders such as acute dystonia, akathisia, parkinsonism and mycoclonus, start short after taking dopamine receptor blocking agents, often an antipsychotic. Once recognized they are relatively easy to treat. Tardive movement disorders such as tardive dyskinesia and tardive dystonia start months or years after using dopamine receptor blocking agents. Treatment is often disappointing, therefore prevention is needed.

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Raveendranathan, Dhanya, and Swaminath Rao. "Sertraline induced acute mandibular dystonia." Journal of Neurosciences in Rural Practice 06, no. 04 (October 2015): 586–87. http://dx.doi.org/10.4103/0976-3147.169804.

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ABSTRACTSpecific serotonin reuptake inhibitors have been linked with the occurrence of drug-induced parkinsonism, dystonia, dyskinesia, and akathisia. Here, we describe a patient with a diagnosis of emotionally unstable personality disorder and depression who developed severe mandibular dystonia with sertraline in the absence of concurrent prescription of medications, which have potential action on the dopaminergic system. This case highlights the need for clinicians to be aware of this alarming acute adverse effect with sertraline, which is conventionally considered to be well-tolerated and safe.

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Thavarajah, Rooban, ArunachalamM Anusa, Dinesh Nayak, Elizabeth Joshua, UmadeviKrishnamohan Rao, and Kannan Ranganathan. "A Study on Drug-Induced Tardive Dyskinesia: Orofacial Musculature Involvement and Patient’s Awareness." Journal of Orofacial Sciences 10, no. 2 (2018): 86. http://dx.doi.org/10.4103/jofs.jofs_82_18.

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Clark, Glenn T., and Saravanan Ram. "Four Oral Motor Disorders: Bruxism, Dystonia, Dyskinesia and Drug-Induced Dystonic Extrapyramidal Reactions." Dental Clinics of North America 51, no. 1 (January 2007): 225–43. http://dx.doi.org/10.1016/j.cden.2006.09.002.

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Hong, Jin Yong, Mun Kyung Sunwoo, Jung Han Yoon, Suk Yun Kang, Young H. Sohn, Phil Hyu Lee, and Seo Hyun Kim. "Rapid drug increase and early onset of levodopa-induced dyskinesia in Parkinson’s disease." PLOS ONE 15, no. 8 (August 20, 2020): e0237472. http://dx.doi.org/10.1371/journal.pone.0237472.

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Tyurnikov, V. M., D. M. Nizametdinova, A. O. Gushcha, E. Yu Fedotova, V. V. Poleshchuk, S. L. Timerbaeva, and A. S. Sedov. "Unilateral posteroventral pallidotomy in the treatment of drug-induced dyskinesia in Parkinson's disease." Voprosy neirokhirurgii imeni N.N. Burdenko 81, no. 5 (2017): 69. http://dx.doi.org/10.17116/neiro201781569-74.

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Lenders, M. W. P. M. "Long term results of unilateral posteroventral pallidotomy for antipsychotic drug induced tardive dyskinesia." Journal of Neurology, Neurosurgery & Psychiatry 76, no. 7 (July 1, 2005): 1039. http://dx.doi.org/10.1136/jnnp.2004.044438.

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Gardos, G., D. E. Casey, A. Perenyi, J. D. Cole, E. Kocsis, J. A. Samson, and W. Wycoff. "A fifteen year follow-up study of tardive dyskinesia and drug induced Parkinsonism." European Neuropsychopharmacology 6 (June 1996): 131–32. http://dx.doi.org/10.1016/0924-977x(96)87911-9.

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Bédard, Paul J., Baltazar Gomez Mancilla, Pierre Blanchette, Céline Gagnon, and Thérèse Di Paolo. "Levodopa-Induced Dyskinesia: Facts and Fancy. What Does the MPTP Monkey Model Tell Us?" Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 19, S1 (February 1992): 134–37. http://dx.doi.org/10.1017/s0317167100041500.

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ABSTRACT:Levodopa-induced dyskinesia, one of the most frequent long-term side effects of antiparkinsonian therapy, is often attributed to denervation supersensitivity of dopamine receptors and perhaps more specifically the D-1 receptor. The available evidence based not only on clinico-pathological studies in patients but also on results of experiments performed on methyl-phenyl-tetrahydropyridine (MPTP)-treated monkeys suggests that the mechanisms may be more complex than heretofore believed. Thus it appears that no single receptor is the sole culprit, that some form of denervation supersensitivity is probably involved but not in the form of increased density of dopamine receptors. Moreover, other neurotransmitter systems must be considered such as GABA, excitatory aminoacids and peptides. The MPTP monkey model remains very useful for predicting the potential of new drugs for inducing dyskinesia. Such trials however must be performed in drug-naive animals.

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Jadapalle, Sree Latha Krishna, Edwin McCray, John Azat Masoud, and Michael W. Kortz. "Methylphenidate-Induced Chorea Due to Possible Cytochrome P450 Metabolism Heterogeneity - A Rare Case." CNS Spectrums 26, no. 2 (April 2021): 176–77. http://dx.doi.org/10.1017/s1092852920002898.

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AbstractBackgroundChorea is defined as a hyperactive movement disorder associated with involuntary, quick, and unpredictable muscle contractions of the limbs, face, and trunk. The unpredictable nature of these movements includes variation in speed, timing, and direction of movement. A wide variety of medications, medical conditions and illicit drugs have been associated with movement disorders. Examples include a multitude of antipsychotic induced movement disorders and dyskinesia related to dopaminergic agents, like levodopa and metoclopramide. Dyskinesias have been associated with psycho-stimulant use, such as methylphenidate. However, most cases reported were associated with large doses or chronic use. Aside from dyskinesia, methylphenidate is known to be associated with tic disorder, tremor, and muscle spasm. However, this case reported is unlike any of the above described and involved the development of chorea after only 2 days of moderate doses of methylphenidate, in a patient on chronic methadone maintenance treatment, with successful arrest of symptoms following discontinuation of the methylphenidate.Case PresentationA 47-year-old female was admitted to our hospital after presenting to the emergency department with 1 week of violent flailing movements. The ballistic flailing movements started acutely after 2 days of initiating methylphenidate in addition to her chronic methadone treatment and 2-week period of initiation of paroxetine. Lab work showed normal CBC, CMP, CRP, CK, and TSH. Urine drug screen, CT angiography of the head, and Huntington’s disease testing were all unremarkable, suggesting a decreased likelihood of illicit drugs, traumatic brain injury, or Huntington’s disease etiologies. Confirmation of the diagnosis was made as the chorea symptoms abruptly resolved upon discontinuation of methylphenidate and administration of intravenous Benadryl. The patient has been on methadone alone for 11 months and methylphenidate alone 2 years back with no involuntary movements or any similar presentation that shows the possibility of drug interaction through cytochrome P450 metabolism between Methylphenidate and methadone.ConclusionWe are presenting a rare case report that adds on to the scarce literature on methylphenidate-induced chorea. It also challenges the consulting psychiatrists to broaden their differential diagnosis for acute onset of choreiform movement disorders. This unique case intrigues the thought process to consider the interaction of methylphenidate in the presence of cytochrome P450 2D6 and 3A4 inhibitors like methadone.

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