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Relevant bibliographies by topics / Dyskinesia, Drug-Induced

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Academic literature on the topic 'Dyskinesia, Drug-Induced'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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

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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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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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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Dissertations / Theses on the topic "Dyskinesia, Drug-Induced"

1

Klintenberg, Rebecka. "Levodopa- and Neuroleptic-Induced Dyskinesias : Studies on Pharmacological Modification and Processing of Opioid Neuropeptides." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3331.

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Books on the topic "Dyskinesia, Drug-Induced"

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D, Sethi Kapil, ed. Drug-induced movement disorders. New York: Marcel Dekker, 2004.

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1956-, Factor Stewart A., Lang Anthony E, and Weiner William J, eds. Drug induced movement disorders. 2nd ed. Malden, Mass: Blackwell Futura, 2005.

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3

Eckart, Rüther, and Hippius Hanns, eds. Tardive dyskinesia. Seattle: Hogrefe & Huber, 1992.

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E, Lang Anthony, and Weiner William J, eds. Drug-induced movement disorders. Mt. Kisco, NY: Futura Pub. Co., 1992.

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5

American Psychiatric Association. Task Force on Tardive Dyskinesia. Tardive dyskinesia: A task force report of the American Psychiatric Association. Washington, DC: The Association, 1992.

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6

B, Joseph Anthony, and Young Robert R. 1934-, eds. Movement disorders in neurology and neuropsychiatry. 2nd ed. Malden, MA: Blackwell Science, 1999.

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B, Joseph Anthony, and Young Robert R. 1934-, eds. Movement disorders in neurology and neuropsychiatry. Boston: Blackwell Scientific Publications, 1992.

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8

Lemieux, Sarah. The influence of drug-induced dyskinesias on manual tracking in Parkinson's disease. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2005.

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9

Ghassemi, Mehrdad Marco. The impact of drug-induced dyskinesias on rapid alternating movements in patients with Parkinson's disease. St. Catharines, Ont: Brock University, Faculty of Applied Health Sciences, 2005.

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10

Sethi, Kapil D. Drug-Induced Movement Disorders. Taylor & Francis Group, 2004.

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Book chapters on the topic "Dyskinesia, Drug-Induced"

1

Jain, Kewal K. "Tardive Dyskinesia." In Drug-induced Neurological Disorders, 347–61. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-73503-6_21.

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2

Fisher, H., G. C. Wagner, L. Kozell, S. K. Johnson, and R. Sandyk. "Tryptophan in the amelioration of drug-induced tardive dyskinesia." In Amino Acids, 386–90. Dordrecht: Springer Netherlands, 1990. http://dx.doi.org/10.1007/978-94-011-2262-7_45.

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3

Gershanik, Oscar S. "Other Drug-Induced Dyskinesias." In Therapeutics of Parkinson's Disease and Other Movement Disorders, 389–403. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470713990.ch26.

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4

Das, Shyamal, and Amar Mishra. "Drug Induced Dyskinesia." In Movement Disorders: A Clinical and Therapeutic Approach, 378. Jaypee Brothers Medical Publishers (P) Ltd., 2009. http://dx.doi.org/10.5005/jp/books/10538_32.

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"The Epidemiology of Tardive Dyskinesia." In Drug-Induced Movement Disorders, 54–77. CRC Press, 2004. http://dx.doi.org/10.1201/9780203913611-7.

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Segman, Ronnen H., and Bernard Lerer. "Genetic factors underlying drug-induced tardive dyskinesia." In Pharmacogenetics of Psychotropic Drugs, 245–66. Cambridge University Press, 2002. http://dx.doi.org/10.1017/cbo9780511543944.011.

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"Clinical Features and Management of Classic Tardive Dyskinesia, Tardive Myoclonus, Tardive Tremor, and Tardive Tourettism." In Drug-Induced Movement Disorders, 94–127. CRC Press, 2004. http://dx.doi.org/10.1201/9780203913611-9.

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8

Shibasaki, Hiroshi, Mark Hallett, Kailash P. Bhatia, Stephen G. Reich, and Bettina Balint. "Dyskinesia, Motor Stereotypies, and Tics." In Involuntary Movements, 137–54. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190865047.003.0006.

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Dyskinesia is characterized by complex, irregular involuntary movements involving lips, tongue, extremities, and/or trunk. The term “dyskinesia” is often used to encompass complex involuntary movements that do not fit into another category of involuntary movements. Focal dyskinesia is commonly seen in the lips and tongue (orolingual dyskinesia or oral dyskinesia). Drug side effects are the most common cause of generalized dyskinesia, usually those that influence dopamine such as L-dopa and neuroleptics (drug-induced dyskinesia, tardive dyskinesia). Motor stereotypies are repetitive occurrences of the same movements; movements commonly encountered in this condition range from simple movements like shaking arms and nodding to complex movements. Motor stereotypies are commonly observed in children with Asperger syndrome, Rett syndrome and other automatisms, and mental retardation. In adults, stereotyped movements are seen in cases of severe infectious encephalitis, autoimmune encephalitis (e.g., limbic encephalitis), cerebrovascular diseases involving the frontal lobe, and neurodegenerative diseases like frontotemporal lobar degeneration. Tics are irregular, typically brisk movements ranging from shock-like simple movements resembling myoclonus (simple tic) to complex movements (complex tic). Patients with tics tend to repeat certain movements like blinking or grimacing, but in the patients with Gilles de la Tourette syndrome, tics appear as a variety of movements including vocalization (vocal tic). These patients can stop the movements for several seconds, but it is often followed by rebound; they often feel an urge to move before a bout of tics and feel release after the bout.

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Bajorek, Tomasz, and Jonathan Hafferty. "Adverse reactions to medication." In Oxford Textbook of Inpatient Psychiatry, edited by Alvaro Barrera, Caroline Attard, and Rob Chaplin, 103–14. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198794257.003.0012.

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Adverse reactions to medication represent a major issue in inpatient psychiatry. This chapter systematically explores the most relevant, concerning, and problematic adverse effects routinely encountered in an inpatient setting. It describes the typical presentation, pathophysiology, incidence, and practical management of these problems. Extrapyramidal side effects including acute dystonia, drug-induced parkinsonism, akathisia, and tardive dyskinesia are considered before the chapter explores the rare but potentially life-threatening condition of neuroleptic malignant syndrome. Other adverse effects common to antipsychotics that are described include hyperprolactinaemia and psychotropic-induced arrhythmias including QTc prolongation. Sexual dysfunction is an under-recognized and undertreated adverse effect common to several classes of psychotropic medication and is also considered. Focusing on antidepressants, the chapter reviews the frequently encountered issue of hyponatraemia as well as serotonin syndrome and selective serotonin reuptake inhibitor-induced bleeding risk. Finally, the chapter addresses perinatal considerations for psychotropic drugs.

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Meltzer, Herbert Y., and William V. Bobo. "Antipsychotic and anticholinergic drugs." In New Oxford Textbook of Psychiatry, edited by John R. Geddes, Nancy C. Andreasen, and Guy M. Goodwin, 639–67. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198713005.003.0064.

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Antipsychotic drugs are utilized for far more than the treatment of psychosis in schizophrenia, their first indication. They now find wide use in a variety of psychotic disorders, mood disorders, developmental disorders, and drug-induced disorders. The classification of drugs as typical or atypical is based on their differences in extra-pyramidal side effects (EPS). This chapter emphasizes the greater diversity, efficacy, and safety of the atypical drugs, and the risk of tardive dyskinesia of the typical drugs. The atypical drug action may produce improvement in cognitive function and negative symptoms, as well as psychosis and mood in some patients. This diversity includes atypical drugs which produce minimal weight gain. Long-acting injectable formulations are recommended for non-adherent patients. The exceptional ability of clozapine to reduce the risk for suicide and to decrease mortality in schizophrenia is discussed. Anticholinergic and other drugs to treat EPS are also discussed.

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Conference papers on the topic "Dyskinesia, Drug-Induced"

1

Farah, Pedro Felisberto Nogueira Viana, Felipe dos Santos Souza, Felipe Oliveira Costa, Mariana Bastos Rodrigues dos Santos, and Yasmim Evelyn Lisboa Barbosa. "L-dopa: main drug induced dyskinesia." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.111.

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Introduction: 3,4-dihydroxy-L-phenylalanine (L-dopa) is the gold standard drug for the treatment of Parkinson’s disease (PD). This disease causes degeneration of dopaminergic cells, L-dopa supplies the lack of dopamine, being effective in its treatment. The average time for the onset of this hyperkinetic disorder is usually 6.5 years and the young age at the beginning of the disease. This pathology may present with chorea, dystonia, myoclonus and stereotypes. Diskinesia-inducing L-dopa (LID) remains one of the most challenging unmet needs in the treatment of PD and other neurodegenerative diseases. Methodology: This is an integrative review, using the MedLine, Cochrane and PubMed databases with the descriptors “drug induced”, “dyskinesia” and “L- dopa”. Articles published in the last 10 years; in English; clinical trial articles and original articles were included. Results: The prevalence for the development of LID was 50% for those who started PD at 40-59 years of age, compared to 16% at 70 years of age. The incidence of LID is about 90% after 9 years, but the main cause is related to the dose of levodopa and the duration of the disease. The risk factors for the development of LID are modifiable (levoodopa dose and body weight) and non- modifiable (age, sex, duration, progress and severity of the disease). Conclusion: With this, it can be concluded that doctors who deal with PD need to be aware of the risk factors for LID and know how to manage it.

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2

Rao, Anusha S., Robert E. Bodenheimer, Thomas L. Davis, Rui Li, Cissy Voight, and Benoit M. Dawant. "Quantifying drug induced dyskinesia in Parkinson's disease patients using standardized videos." In 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4649520.

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3

Silva, Thais Ellen de Ramos, Diego Rodrigues Castelhano, Cintia Anchieta, and Bruna Kuhn de Freitas Silva. "Benefits of using cannabidiol in the treatment of dyskinesias in patients with Parkinson’s." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.301.

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Introduction: Parkinson’s disease (PD) is a neurological, chronic, and progressive disease that causes the death of brain cells, especially in the area responsible for the production of dopamine, which, among other functions, controls body movements. The first signs of PD are usually hand tremors, muscle stiffness, pain, dizziness, sleep disturbances, respiratory and urinary systems. In this context, cannabidiol (CBD) has been a source of research to improve institutional motor disorders. Objectives: Compile scientific evidence on the use of cannabidiol to improve dyskinesias in patients with Parkinson’s. Methodology: This is an integrative literature review, through the selection of scientific articles, available in the virtual databases: PubMed, Scielo, and Google academic, published between the years 2018 to 2021. Results: CBD has a positive effect, bradykinesia, tremors, stiffness and psychotic, mood and sleep disorders, quality of life, its adverse effects are observed with low frequency. In addition, there seems to be a beneficial drug interaction between CBD and levodopa (l-DOPA), the drug of choice for the treatment of this disease. The prolonged use of this drug causes a type of dyskinesia, known as DOPA- induced dyskinesias (LIDs). Thus, modulation of the endocannabinoid system through CBD presents itself as a possible promising therapy for the control of PD and LIDs. Conclusion: Studies induced expressive results regarding the use of CBD to treat PD. However, as there is still no consensus, specific studies are carried out to assess the safety of using CBD in patients with long-term PD and its possible beneficial interaction with antiparkinsonian drugs.

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Souza, Felipe dos Santos, Matheus Furlan Chaves, and Antonio Marcos da Silva Catharino. "Rabbit syndrome induced by the use of Risperidone: a case report." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.013.

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Context: Risperidone is a selective monoaminergic antagonist, its main action as an antipsychotic is attributed to its affinity to dopamine D2 receptors. However, intervention in dopaminergic transmission by this medication can affect the motor control performed by the striatum, generating the so-called extrapyramidal syndromes. Among these syndromes, we have the rabbit syndrome (SC), which is manifested by the chronic use of antipsychotics and causes involuntary movements of the muscles of the jaw and tongue. Case report: E. B. L., a 89- year-old woman undergoing neurological follow-up due to dementia. He started using risperidone 1mg at night to treat behavioral changes and aggressions. However, 4 months after the start of the medication, he started to have a tremor of the chin and stiffness in the upper limbs. These symptoms improved after switching from risperidone to olanzapine 5mg at night. Conclusions: The present study emphasizes the importance of recognizing Rabbit Syndrome and the clinical repercussions of symptomatic variants, such as tardive dyskinesia, nocturnal bruxism and altered tongue motricity, in the differential diagnosis of drug-induced movement disorders. In this sense, neurological assessment includes an elucidating clinical history and targeted physical examination.

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