Journal articles: 'Tardivel'

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Marquis, Dominique. "Un homme et son journal : comment Jules-Paul Tardivel « domestiqua » La Vérité." Mens 13, no. 2 (July 23, 2014): 35–57. http://dx.doi.org/10.7202/1025982ar.

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En 1881, Jules-Paul Tardivel lance à Québec La Vérité, un journal de combat ultramontain. Tardivel porte ce journal à bout de bras, mais il n'est pas seul : il est soutenu par un réseau ultramontain encore très actif à cette époque. En 1890, Tardivel fait face à des difficultés matérielles telles que la survie du journal est sérieusement mise en péril. Les amis ultramontains de Tardivel sont alors mis à contribution pour trouver une solution. Plusieurs propositions sont évoquées, mais Tardivel, ne voulant pas partager la direction du journal, trouvera finalement une solution lui permettant de demeurer le seul maître à bord. Cette incursion dans l'histoire de ce journal, rendue possible grâce à une volumineuse correspondance, permet de comprendre un aspect du rôle du réseau ultramontain dans la construction de La Vérité.

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Lagrée, Michel. "De Veuillot à Tardivel, ou les ambiguïtés de la haine de la modernité." Articles 67 (December 14, 2011): 251–59. http://dx.doi.org/10.7202/1006778ar.

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Dans l’ultramontanisme québécois, Jules-Paul Tardivel est souvent présenté comme le disciple le plus zélé de Louis Veuillot. Cependant, si l’on envisage la modernité du double point de vue du changement sociotechnique et du changement démocratique, la confrontation de Veuillot et Tardivel révèle une double ambiguïté. Le premier affiche une technophobie provocante là où le second, en bon Américain, cultive la science-fiction. Veuillot est un monarchiste, nostalgique du corpus christianum médiéval; Tardivel est un nationaliste, donc vecteur d’une idéologie moderne en dernière instance

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Marquis, Dominique. "Amitiés et communautés d’opinion. Le réseau de Jules-Paul Tardivel au service de La Vérité." Articles 84, no. 1-2 (October 1, 2018): 5–24. http://dx.doi.org/10.7202/1051528ar.

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Cet article jette un premier regard sur le réseau ultramontain de Jules-Paul Tardivel à deux moments de l’histoire professionnelle du journaliste : les années 1884-1886 et 1889-1891. Cette exploration a été menée à partir d’une analyse des correspondances entre Tardivel et ses collègues, ainsi qu’une analyse de son journal personnel. Elle montre une évolution dans la constitution du réseau ultramontain du dernier quart du XIXe siècle. L’analyse permet aussi de mesurer l’influence et le soutien du réseau dans la construction de La Vérité, journal de combat ultramontain dirigé par Tardivel.

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Marquis, Dominique. "« Procurer à mes lecteurs quelques heures de délassement » : Les Mélanges, les Notes de voyage et le roman Pour la patrie de Jules-Paul Tardivel." Journal of the Canadian Historical Association 23, no. 1 (May 22, 2013): 157–78. http://dx.doi.org/10.7202/1015731ar.

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Jules-Paul Tardivel a été propriétaire et rédacteur principal du journal La Vérité de 1881 à 1905, date de son décès. Ardent défenseur des principes ultramontains, il utilise son journal comme une arme de combat contre toutes les idées qui s’éloignent de l’orthodoxie catholique et qu’il juge trop libérales. Tardivel n’a cependant pas uniquement publié son journal : on compte aussi plusieurs livres et brochures à son actif. Les idées véhiculées par Tardivel dans La Vérité ont été abondamment analysées, mais l’historiographie est demeurée plus discrète sur ses autres publications. Cet article s’intéresse à quelques-uns de ces livres, plus particulièrement aux Mélanges, aux Notes de voyage et au roman Pour la patrie. Grâce à une analyse croisée des livres, du journal et de la correspondance de Tardivel, nous découvrirons quelles ont été les stratégies déployées par le journaliste et son réseau pour assurer la diffusion de ces oeuvres qui ont participé au même combat que le journal. Si ces publications n’ont pas connu le succès souhaité, elles s’ajoutent néanmoins à l’arsenal varié de publications ultramontaines recensées durant la seconde moitié du XIXe siècle.

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Pleau, Jean-Christian. "Les lectures honnêtes de Jules-Paul Tardivel." Dossier 32, no. 3 (October 11, 2007): 75–87. http://dx.doi.org/10.7202/016579ar.

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Résumé Le roman publié en 1895 par Jules-Paul Tardivel, Pour la patrie. Roman du xxe siècle, est souvent considéré comme une curiosité de l’histoire littéraire québécoise et n’a reçu que peu d’attention de la part de l’institution universitaire. Ce roman paraît à première vue inclassable et totalement coupé des grands courants de la littérature française aussi bien que québécoise. Un examen plus attentif montre toutefois que Tardivel était en fait bien informé de l’actualité littéraire européenne, voire qu’il connaissait certaines oeuvres avant-gardistes. L’inventaire de ces modèles permet de mieux cerner la part d’originalité de Pour la patrie, mais il permet surtout d’atténuer l’image caricaturale qu’on se fait souvent de Tardivel et de mieux comprendre le rapport ambigu que celui-ci entretenait avec la littérature.

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Pitzer, Martina, Guido Engelmann, and Thomas Stammschulte. "Antipsychotika-induzierte tardive Bewegungsstörungen – Fallbeispiel einer tardiven Dystonie unter Aripiprazol und Literaturübersicht." Zeitschrift für Kinder- und Jugendpsychiatrie und Psychotherapie 45, no. 4 (July 1, 2017): 325–34. http://dx.doi.org/10.1024/1422-4917/a000460.

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Zusammenfassung. Extrapyramidalmotorische Nebenwirkungen (EPMS) werden im Vergleich zu Antipsychotika der ersten Generation (FGA) unter Antipsychotika der zweiten Generation (SGA) seltener beschrieben. Dies scheint bei Erwachsenen auch tardive Dyskinesien (TDs) einzuschließen, jedoch nicht tardive Dystonien (TDts). Bei Kindern und Jugendlichen wurde unter FGA eine TD seltener beobachtet als bei Erwachsenen. Zur TDt existieren keine Daten. Unter SGA finden sich zu tardiven Bewegungsstörungen bei Kindern und Jugendlichen nur wenige und widersprüchliche Angaben. SGA unterscheiden sich in ihrem Nebenwirkungsprofil. Dabei verursacht Aripiprazol zwar weniger metabolische und kardiale Nebenwirkungen, verglichen mit anderen SGA bei Kindern und Jugendlichen jedoch relativ häufig EPMS. Bisher wurden TDs oder TDts unter Aripiprazol nur bei Erwachsenen beschrieben. Anhand des Fallberichts einer TDt unter Aripiprazol bei einer 13-jährigen Patientin werden Symptomatik, Differentialdiagnostik, Pathophysiologie, Prävalenz und Therapie tardiver Dystonien dargestellt. Unter Medikation mit SGA sollte das mögliche Auftreten von EPMS einschließlich tardiver Bewegungsstörungen berücksichtigt und klinisch regelmäßig überprüft werden.

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Chartier, Daniel. "Les origines de l’écriture migrante. L’immigration littéraire au Québec au cours des deux derniers siècles." Études 27, no. 2 (December 15, 2006): 303–16. http://dx.doi.org/10.7202/290058ar.

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Résumé Au cours des deux derniers siècles, plus de cinq cents écrivains ont émigré au Québec dans des conditions et des circonstances variées. L’apport de ces écrivains à la vie littéraire du Québec est considérable: on constate que la part d'étrangers parmi les écrivains est deux fois plus importante que parmi la population en général. Quelquefois en marge des courants littéraires, parfois au coeur de la construction imaginaire nationale, les écrivains émigrés ont des parcours différents selon l'époque de leur arrivée, leur origine, leur langue et leur statut professionnel. De l'arrivée d'intellectuels révolutionnaires et de religieux ultramontains au XIXe siècle (Napoléon Aubin, Jules-Paul Tardivel), des grands voyageurs et exilés du début du XXe siècle (Marie Le Franc, Louis Hémon). de la première vague d'immigration européenne de l'après-guerre (Monique Bosco, Marco Micone) à la diversification continentale de la fin du siècle (Ying Chen, Sergio Kokis, Tecia Werbowski), l'histoire de l'immigration littéraire incite à une relecture de toutes les frontières et des constituantes de l'histoire culturelle du Québec.

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ROBERT, LUCIE. "ANGÉLINE DE MONTBRUN OU LA DISSOLUTION DE L’UTOPIE ULTRAMONTAINE." Dossier 44, no. 1 (February 22, 2019): 51–61. http://dx.doi.org/10.7202/1056363ar.

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Dans Formation de l’imaginaire littéraire au Québec, 1764-1867, Maurice Lemire notait que « les structures de redoublement de miniaturisation » dominent le monde du roman au xixe siècle. Cette miniaturisation se lit dans la création d’une société en miniature (précisément), isolée du reste du monde, un « enclos » (le mot est de Lemire) où le monde est réduit à la parenté et au voisinage et à l’intérieur duquel « tout est euphémisé » (ibid). Nous croyons que ces miniatures correspondent à des utopies. Nous suggérons donc de relire le roman de Laure Conan comme présentant à travers la création de Valriant une de ces miniatures et de mettre en valeur l’utopie que le roman propose, qui se révélera une utopie ultramontaine. À la différence des utopies libérales que sont celles sur lesquelles se terminent par exemple Charles Guérin de Chauveau et Jean Rivard d’Antoine Gérin-Lajoie, et qui sont aussi une projection dans un avenir imaginaire, les utopies ultramontaines (que l’on retrouvera dans la finale de Pour la patrie de Tardivel) sont des univers sans avenir possible, destinés à disparaître avec la/le protagoniste. Reste la question de savoir ce qu’est une utopie ultramontaine au féminin et on observera comment Valriant se construit contre l’image du cloître, qui sera pourtant celle qui survivra au xxe siècle.

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Mashevs’kyi, Oleg, and Myroslav Baraboi. "Anglo-Canadian Historiography Genesis of the French Canadian Nationalism." European Historical Studies, no. 7 (2017): 64–83. http://dx.doi.org/10.17721/2524-048x.2017.07.64-83.

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The article investigates the genesis of the French-Canadian nationalism in the Anglo-Canadian historiography. The essence of debate that arose among English-Canadian historians about the conquest of New France (Quebec) by Great Britain as one of the main causes of the French-Canadian problem is analyzed. In particular, as opposed to the pro-British point of view, which considers this conquest as a progress and benefit for the residents of French Canada, its opponents considered the issue as a tragedy for the French Canadians. Particularly the attention is drawn to the changes of the historiographical paradigm after the Second World War, when even pro-British historians had to reconsider their attitude to conquest Canada by Great Britain and recognize its consequences for the French Canadians. Special attention is paid to the reflection of the Anglo-Canadian historiography upon the uprising in 1837-1838 in Quebec on as one of the first manifestations of the radical French-Canadian nationalism. The basic approach in the Anglo-Canadian historiography about members of radical and liberal leaders of French-Canadian nationalism (H. Bourassa, L. Groulx, J. P Tardivel, H. Mercier), which contributed to the institutionalization and politicization of French-Canadian nationalism have been disclosed. The article also clarifies the position of the Anglo-Canadian historiography about the genesis of the “Quiet revolution” in Quebec as of the highest expression of French-Canadian nationalism.

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Pardis, Parnian, Gary Remington, Roshni Panda, Milan Lemez, and Ofer Agid. "Clozapine and tardive dyskinesia in patients with schizophrenia: A systematic review." Journal of Psychopharmacology 33, no. 10 (July 26, 2019): 1187–98. http://dx.doi.org/10.1177/0269881119862535.

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Background: It is commonly recommended that a switch to clozapine be implemented in the face of tardive dyskinesia, even if current treatment involves another “atypical” agent. However, reports do indicate clozapine carries a liability for tardive dyskinesia. Aims: This review sought to evaluate clozapine in relation to tardive dyskinesia in the context of available evidence. Methods: Medline, Embase, and PsycINFO databases were searched for studies published in English, using the keywords: clozapine AND tardive dyskinesia OR TD. References from major review articles were searched for additional relevant publications. Studies were included if they investigated: tardive dyskinesia in clozapine-treated patients diagnosed with schizophrenia spectrum disorders, and reported on two or more assessments of tardive dyskinesia severity measured by the Abnormal Involuntary Movement Scale; or clozapine’s tardive dyskinesia liability. Results: In total, 513 unique citations were identified and 29 reports met the inclusion criteria. Thirteen studies suggest clozapine reduces dyskinetic symptoms over time ( n=905 clozapine-treated participants); however, the minimum required dose and effect of withdrawal requires further investigation. The majority of reports which address clozapine’s liability for tardive dyskinesia are case studies (11 of 14 reports, 79%), and clozapine was only the first-line treatment in one of the remaining three studies reporting treatment-emergent dyskinetic symptoms with clozapine in 12% of patients. No significant between-drug differences were identified comparing clozapine’s risk to other atypical antipsychotics. Conclusions: Research to date supports switching to clozapine for the purpose of reducing tardive dyskinesia risk and/or treating existing tardive dyskinesia, but prospective randomized controlled trials are necessary if we are to substantiate existing recommendations.

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Sarró, Salvador, Edith Pomarol-Clotet, Erick J. Canales-Rodríguez, Raymond Salvador, Jesús J. Gomar, Jordi Ortiz-Gil, Ramón Landín-Romero, Fidel Vila-Rodríguez, Josep Blanch, and Peter J. McKenna. "Structural brain changes associated with tardive dyskinesia in schizophrenia." British Journal of Psychiatry 203, no. 1 (July 2013): 51–57. http://dx.doi.org/10.1192/bjp.bp.112.114538.

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BackgroundThe pathological basis of tardive dyskinesia is unknown. Although its clinical features implicate the basal ganglia, imaging studies have not found clear evidence that it is associated with volume changes in these or other brain structures.AimsTo determine, using voxel-based structural imaging, whether there are regions of grey matter volume change in people with schizophrenia who also have tardive dyskinesia compared with those without tardive dyskinesia.MethodA total of 81 people with chronic schizophrenia, 32 with tardive dyskinesia and 49 without, were examined using magnetic resonance imaging (MRI) and whole-brain, optimised voxel-based morphometry. A comparison group of 61 healthy controls was also examined.ResultsCompared with those without tardive dyskinesia, patients with tardive dyskinesia showed a pattern of volume reductions in predominantly subcortical regions, including the basal ganglia and the thalamus. Within the basal ganglia, volume reductions were seen in the caudate nucleus, to a lesser extent in the putamen, and only marginally in the globus pallidus. The patients with tardive dyskinesia, but not those without, showed significant volume reductions in the basal ganglia compared with the healthy controls but both groups had smaller volumes than controls in other affected areas.ConclusionsThe pathological process or processes that underlie the development of tardive dyskinesia are not just neurochemical in nature, but affect brain structure.

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Myslobodsky, M. S. "Anosognosia in Tardive Dyskinesia: "Tardive Dysmentia" or "Tardive Dementia"?" Schizophrenia Bulletin 12, no. 1 (January 1, 1986): 1–6. http://dx.doi.org/10.1093/schbul/12.1.1.

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Davis, R. Jeffrey, Jeffrey L. Cummings, and Robert W. Hierholzer. "Tardive Dystonia: Clinical Spectrum and Novel Manifestations." Behavioural Neurology 1, no. 1 (1988): 41–47. http://dx.doi.org/10.1155/1988/362502.

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Tardive dystonia was identified in 25 patients: involvement of the face and neck was most common; truncal and limb dystonia were also observed. There were 3 cases of laryngospasm and 2 of spasmodic dysphonia. The latter has not been previously reported as a manifestation of tardive dystonia. In all cases, movements typical of classic tardive dyskinesia could be demonstrated. This group illustrates the variety of dystonic disorders that may occur in conjunction with tardive dyskinesia.

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Kornetova, Ye G., A. V. Semke, Ye G. Dmitrieva, Yu N. Borodyuk, and A. S. Boyko. "CLINICAL AND SOCIAL RISK FACTORS OF TARDIVE DYSKINESIA IN PATIENTS WITH SCHIZOPHRENIA DURING ANTIPSYCHOTIC TREATMENT." Bulletin of Siberian Medicine 14, no. 1 (February 28, 2015): 32–39. http://dx.doi.org/10.20538/1682-0363-2015-1-32-39.

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The purpose of the present work was to study the clinical features and risk factors of tardive dyskinesia among the schizophrenia patients who durably receive the antipsychotic therapy. 180 of the 18 to 65 age bracket schizophrenia patients, who were treated in a residential psychiatric treatment facility, were examined with the use of the Positive and Negative Syndrome Scale (PANSS), Abnormal Involuntary Movement Scale (AIMS), and the basic chart of formalized sociodemographic and clinico-dynamic features developed at the Tomsk Mental Health Research Institute. The acquired data were processed by the Mann–Whitney U-Test and χ2. The average age of the tardive dyskinesia patients turned out to be conclusively older than that of the patients without this derangement. People who have tardive dyskinesia statistically often happen to be single in comparison with other variants of marital status. It was found out that women happen to have tardive dyskinesia more often, which allows us to see the female gender as a risk factor. The tardive dyskinesia patients had certain negative symptoms. The patients were arranged into groups according to the prepotency of symptom-complexes over the subgroups: with orofacial, thoracolumbar and combined tardive dyskinesia. The average age of the orofacial dyskinesia patients turned out to be conclusively older than that of the patients without tardive dyskinesia. The negative symptoms level in the subgroup was conclusively higher than among those without tardive dyskinesia. The average age of the thoracolumbar dyskinesia patients was conclusively older than that of the patients without tardive dyskinesia. The average age of the combined dyskinesia patients was conclusively older than the patients without the tardive dyskinesia. The patients having schizophrenia for longer than 10 years prevailed in the combined dyskinesia group. Such characteristics as education level and social status, age of when the medical problem started, dominance of the positive symptoms, duration of antipsychotic agents administration, somatic condition, use of psychoactive substances, suicidal and hetero-aggressive behaviors make no contribution to the risk of tardive dyskinesia development in the presence of schizophrenia, and they are not protective factors either.

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Youssef, Hanafy. "Serum immunoglobulins in tardive dyskinesia — implication for pathogenesis of the syndrome." Irish Journal of Psychological Medicine 7, no. 2 (September 1990): 145–46. http://dx.doi.org/10.1017/s0790966700016761.

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AbstractLevels of immunoglobulins were measured in 32 schizophrenic patients with tardive dyskinesia and 34 schizophrenic patients without tardive dyskinesia. The duration of neuroleptic treatment in years was similar in the two groups. The serum immunoglobulin concentrations (mg%) were found to be significantly different in the two groups; IGA and IGM levels were higher in patients with tardive dyskinesia. The present results may be explained on the basis of dysfunction of the immunological system in tardive dyskinesia.

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Rosenheck, Robert A. "Evaluating the cost-effectiveness of reduced tardive dyskinesia with second-generation antipsychotics." British Journal of Psychiatry 191, no. 3 (September 2007): 238–45. http://dx.doi.org/10.1192/bjp.bp.106.035063.

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BackgroundSecond-generation antipsychotics may have few advantages over older, cheaper drugs, except for possibly reduced risk of tardive dyskinesia.AimsTo evaluate the cost-effectiveness of second-generation antipsychotics with regard to reducing tardive dyskinesia.MethodLiterature was reviewed on risk of tardive dyskinesia with second-generation antipsychotics; on severity duration and impairment of tardive dyskinesia; and on the relationship of this disorder to quality of life and quality-adjusted life-years (QALYs). Diverse cost and benefit assumptions and of 1-year and 5-year planning horizons were examined in a deterministic sensitivity analysis.ResultsEstimating 0.143 QALYs lost per case of severe tardive dyskinesia, 1-year cost-effectiveness estimates for second-generation antipsychotics ranged from $185 000 ($370 000) to $850 000 ($1.7 million) per QALY, and 5-year cumulative estimates ranged from $74 000 ($ 149 000) to $342 000 ($683 000) per QALY, all above the conventional policy threshold of $25 000 ($50 000).ConclusionsReduction of tardive dyskinesia with second-generation antipsychotics appears unlikely to meet standards for cost-effectiveness.

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Chiu, Helen, Joseph Lau, Linda Lam, and Patrick Shum. "Association of Negative Symptoms with Tardive Dyskinesia in Schizophrenic Patients." Australian & New Zealand Journal of Psychiatry 27, no. 2 (June 1993): 228–32. http://dx.doi.org/10.1080/00048679309075771.

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In recent years, great deal of interest has been focused on the association between negative symptoms of schizophrenia and tardive dyskinesia, but the literature is far from conclusive. Thirty-six schizophrenic patients with tardive dyskinesia and 76 without were surveyed using the Scale for Assessment of Negative Symptoms. On univariate analysis, the composite score and scores of certain subscales were associated with tardive dyskinesia, but this association was lost on multivariate analysis. After adjusting for confounding variables like age, education and antipsychotic dose, no association of negative symptoms and tardive dyskinesia was found.

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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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Bhavsar, Vishal. "What is the evidence on cholinergic medication for tardive dyskinesia?" BJPsych Advances 24, no. 5 (August 13, 2018): 289–94. http://dx.doi.org/10.1192/bja.2018.35.

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SUMMARYAntipsychotic drugs are associated with movement disorders, especially with long-term use. Tardive dyskinesia, a condition characterised by repetitive involuntary muscle activity, is considered to be the most chronic, distressing and disabling of antipsychotic-associated movement disorders. There is theoretical justification for the use of cholinergic drugs in tardive dyskinesia, and they are used in clinical practice. A Cochrane systematic review synthesised randomised controlled trial data evaluating the effectiveness of cholinergic drugs for tardive dyskinesia, and for a range of secondary outcomes, including quality of life. In line with the authors of the review, this Commentary concludes that much higher-quality evidence on the use of cholinergic drugs in tardive dyskinesia is necessary, and that a patient with tardive dyskinesia should be offered the opportunity to try a newer cholinergic drug, ideally in the context of a well-conducted and reported clinical trial. At the same time, given uncertainty regarding clinical effectiveness, and in view of their accepted adverse effects, it would be understandable if a person with tardive dyskinesia decided to avoid cholinergic drugs.DECLARATION OF INTERESTNone.

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Ricciardi, Lucia, Tamara Pringsheim, Thomas R. E. Barnes, Davide Martino, David Gardner, Gary Remington, Donald Addington, et al. "Treatment Recommendations for Tardive Dyskinesia." Canadian Journal of Psychiatry 64, no. 6 (February 21, 2019): 388–99. http://dx.doi.org/10.1177/0706743719828968.

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Background: Tardive dyskinesia is a movement disorder characterised by irregular, stereotyped, and choreiform movements associated with the use of antipsychotic medication. We aim to provide recommendations on the treatment of tardive dyskinesia. Methods: We performed a systematic review of studies of the treatment of tardive dyskinesia. Studies were rated for methodological quality using the American Academy of Neurology Risk of Bias Classification system. Overall level of evidence classifications and grades of recommendation were made using the Scottish Intercollegiate Guidelines Network framework. Results: Preventing tardive dyskinesia is of primary importance, and clinicians should follow best practice for prescribing antipsychotic medication, including limiting the prescription for specific indications, using the minimum effective dose, and minimising the duration of therapy. The first-line management of tardive dyskinesia is the withdrawal of antipsychotic medication if clinically feasible. Yet, for many patients with serious mental illness, the discontinuation of antipsychotics is not possible due to disease relapse. Switching from a first-generation to a second-generation antipsychotic with a lower D2 affinity, such as clozapine or quetiapine, may be effective in reducing tardive dyskinesia symptoms. The strongest evidence for a suitable co-intervention to treat tardive dyskinesia comes from tests with the new VMAT inhibitors, deutetrabenazine and valbenazine. These medications have not been approved for use in Canada. Conclusion: Data on tardive dyskinesia treatment are limited, and the best management strategy remains prevention. More long-term safety and efficacy data are needed for deutetrabenazine and valbenazine, and their routine availability to patients outside of the USA remains in question.

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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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Mould, Anna, and Jerzy Strukowski. "Multifactorial Tardive Dyskinesia: a case study." Journal of Prescribing Practice 3, no. 2 (February 2, 2021): 82–86. http://dx.doi.org/10.12968/jprp.2021.3.2.82.

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This article is a case review of an older lady presenting with Tardive Dyskinesia, a rare phenomenon in modern times. This case is interesting, as the typical causative factor of this presentation was absent. The authors discuss the risk factors for developing Tardive Dyskinesia, as well as medication likely contributing to this lady's case. The paper also discusses treatment, prognosis and how the mechanism of Tardive Dyskinesia can be multifactorial. The authors hope this case review will provide an update to prescribers both within the mental health field and in other medical specialties, as Tardive Dyskinesia is seen less often in practice.

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Haile, Kibrom, and Halima Umer. "The use of clozapine and clonazepam co-administration in the treatment of a severe tardive dyskinesia: A case report." SAGE Open Medical Case Reports 7 (January 2019): 2050313X1983325. http://dx.doi.org/10.1177/2050313x19833254.

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This is a case report of a patient who was treated with clozapine and clonazepam after he developed neuroleptic-induced tardive dyskinesia following treatment for schizophrenia. There are reports of clozapine treatment itself causing tardive dyskinesia; however, more reports have shown clozapine’s benefit for patients with neuroleptic-induced tardive dyskinesia. This is a case report of a patient with neuroleptic-induced tardive dyskinesia who benefitted from clozapine treatment with adjuvant use of clonazepam – the first such case report from Ethiopia. A 43-year-old male patient developed severe involuntary abnormal body movements mainly involving the trunk after he received chlorpromazine for 8 years for the diagnosis of schizophrenia. When the movement disorder became intolerable and disabling, the diagnosis of severe neuroleptic-induced tardive dyskinesia was established and the patient was started on clozapine with adjuvant clonazepam treatment. Following such management, the patient responded well and the dyskinetic movements were fully controlled, and the patient was able to work. Patients with severe and disabling neuroleptic-induced tardive dyskinesia can be treated and be productive if they receive treatment with clozapine, with adjuvant use of clonazepam.

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Kanzaki, Akinori, Hidetoshi Tada, Akihito Otsuka, and Tadashi Nakamura. "Severe tardive dyskinesia induced by domperidone in presenile and non-dementia type 2 diabetes man with alcohol misuse showing albuminocytological dissociation and white matter hyperintensity." BMJ Case Reports 12, no. 5 (May 2019): e228789. http://dx.doi.org/10.1136/bcr-2018-228789.

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Domperidone has difficulty passing the blood–brain barrier, thus rarely causes tardive dyskinesia. Furthermore, its symptoms in adults are generally mild. Although both alcohol and diabetes are thought to increase the risk of development of tardive dyskinesia, their impact remains controversial, especially diabetes, and factors related to worsened tardive dyskinesia have not been clearly elucidated. A 59-year-old man with type 2 diabetes and history of alcohol misuse, who had been chronically prescribed domperidone at 15 mg/day, showed severe tardive dyskinesia, which was remitted within several days by stopping the drug. In our case, albuminocytological dissociation and white matter hyperintensity on MRI were confirmed, which were thought to be related to blood–brain barrier dysfunction. This present findings indicate that alcohol misuse and type 2 diabetes, as well as albuminocytological dissociation and white matter hyperintensity may result in severe tardive dyskinesia, even in individuals receiving domperidone.

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Giménez-Roldán, S., D. Mateo, and P. Bartolomé. "Tardive dystonia and severe tardive dyskinesia." Acta Psychiatrica Scandinavica 71, no. 5 (May 1985): 488–94. http://dx.doi.org/10.1111/j.1600-0447.1985.tb05061.x.

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Peckham, Alyssa M., and Jessica A. Nicewonder. "VMAT2 Inhibitors for Tardive Dyskinesia—Practice Implications." Journal of Pharmacy Practice 32, no. 4 (February 18, 2018): 450–57. http://dx.doi.org/10.1177/0897190018756512.

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Tardive dyskinesia is a potentially irreversible, debilitating, hyperkinetic movement disorder that can result from dopamine receptor antagonists. Prompt recognition and resolution of symptoms are instrumental in preventing disease irreversibility, though current treatment options have fallen short of robust, effective, and long-term symptom control. In April 2017, the Food and Drug Administration (FDA) approved 2 new vesicular monoamine transporter 2 (VMAT2) inhibitors, deutetrabenazine and valbenazine, for chorea related to Huntington’s disease and tardive dyskinesia, respectively. These agents were pharmacologically modified from tetrabenazine, a VMAT2 inhibitor used off-label in the treatment of tardive dyskinesia. Despite FDA-labeled indications of deutetrabenazine and valbenazine, each agent was explored as a treatment option for those with tardive dyskinesia. In this study, the pharmacologic modifications of the 2 new VMAT2 inhibitors are described, with detailed explanation as to how these may impact clinical practice. The associated case series, observational studies, and clinical trials exploring their use in the treatment of tardive dyskinesia are reported with expert opinion on practice implication.

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Emmanuel, Thanos. "Remission of treatment-resistant depression with tardive akathisia with electroconvulsive therapy." BMJ Case Reports 12, no. 9 (September 2019): e229714. http://dx.doi.org/10.1136/bcr-2019-229714.

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This report presents a case of drug-induced severe tardive akathisia developing after the combination of a selective serotonin reuptake inhibitor and an antipsychotic, in a woman with severe major depression. The trial and combination of multiple medications is common practice in treatment-resistant patients with depression. With the increase in the prevalence of treatment-resistant depression, adverse effects of medication such as tardive akathisia are becoming more common. Tardive akathisia persists even after the withdrawal of the causative agent and is very challenging to treat. The patient did not respond to any standard medications indicated for drug-induced akathisia. As a result, the patient became suicidal and extremely distressed with all treatment options exhausted. Guidelines on the management of drug-induced tardive akathisia are non-existent. This reflects the importance of this case study, which reveals the complete remission of both tardive akathisia and all the patient’s depressive symptoms after electroconvulsive therapy . This report provides evidence of an established treatment intervention used in a new situation.

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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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Dinan, Timothy G., and Dora Kohen. "Tardive Dyskinesia in Bipolar Affective Disorder: Relationship to Lithium Therapy." British Journal of Psychiatry 155, no. 1 (July 1989): 55–57. http://dx.doi.org/10.1192/bjp.155.1.55.

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Forty patients under the age of 60 years with a DSM–III diagnosis of bipolar affective disorder were examined for the presence of tardive dyskinesia. The overall prevalence was 22.5%, with an age-related increase. Patients with and without tardive dyskinesia did not differ in terms of duration of affective illness or exposure to neuroleptics, but those patients with tardive dyskinesia had significantly more psychiatric admissions and were on lithium for significantly greater lengths of time.

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Ivanova, Svetlana A., Anton JM Loonen, P. Roberto Bakker, Maxim B. Freidin, Nienke J. ter Woerds, Asmar FY Al Hadithy, Arkadiy V. Semke, et al. "Likelihood of mechanistic roles for dopaminergic, serotonergic and glutamatergic receptors in tardive dyskinesia: A comparison of genetic variants in two independent patient populations." SAGE Open Medicine 4 (January 1, 2016): 205031211664367. http://dx.doi.org/10.1177/2050312116643673.

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Objectives: An established theory for the pathogenesis of tardive dyskinesia is disturbed dopaminergic receptor sensitivity and/or dopaminergic intracellular signaling. We examined associations between genetic variants of neurotransmitter receptors and tardive dyskinesia. Methods: We assessed tardive dyskinesia in Caucasian psychiatric inpatients from Siberia (N = 431) and a long-stay population from the Netherlands (N = 168). These patients were genotyped for 43 tag single nucleotide polymorphisms in five neurotransmitter receptor genes, and the results for the two populations were compared. Results: Several significant associations with tardive dyskinesia were identified, but only GRIN2A (rs1345423) was found in both patient populations. This lack of agreement was probably due to the small effect size of the associations, the multiple testing and the small sample size of the Dutch patient population. After reviewing the literature, we propose that the constitutive stimulatory activity of serotonergic type 2 receptors may be relevant. Conclusions: Inactivity of the serotonergic, type 2C receptor or blockade of these receptors by atypical antipsychotic drugs may decrease the vulnerability to develop tardive dyskinesia.

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Beasley, Charles M., Mary Anne Dellva, Roy N. Tamura, Hal Morgenstern, William M. Glazer, Kevin Ferguson, and Gary D. Tollefson. "Randomised double-blind comparison of the incidence of tardive dyskinesia in patients with schizophrenia during long-term treatment with olanzapine or haloperidol." British Journal of Psychiatry 174, no. 1 (January 1999): 23–30. http://dx.doi.org/10.1192/bjp.174.1.23.

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BackgroundTardive dyskinesia is important in the side-effect profile of antipsychotic medication.AimsThe development of tardive dyskinesia was evaluated in patients treated with double-blind, randomly assigned olanzapine or haloperidol for up to 2.6 years.MethodsTardive dyskinesia was assessed by the Abnormal Involuntary Movement Scale (AIMS) and Research Diagnostic Criteria for Tardive Dyskinesia (RD-TD); it was defined as meeting RD-TD criteria at two consecutive assessments. The risk of tardive dyskinesia, the relative risk, incidence rate, and incidence rate ratio were estimated.ResultsThe relative risk of tardive dyskinesia for the overall follow-up period for haloperidol (n=522) v. olanzapine (n=1192) was 2.66 (95% CI=1.50–4.70). Based on data following the initial six weeks of observation (during which patients underwent medication change and AIMS assessments as frequently as every three days), the one-year risk was 0.52% with olanzapine (n=513) and 7.45% with haloperidol (n=114). The relative risk throughout this follow-up period was 11.37 (95% Cl=2.21–58.60).ConclusionOur results indicated a significantly lower risk of tardive dyskinesia with olanzapine than with haloperidol.

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Shrestha, Resha, Takaomi Taira, Pranaya Shrestha, Pravesh Rajbhanari, Sudan Dhakal, Samir Acharya, and Basant Pant. "Surgical Treatment of Tardive Dystonia in Nepal: A Case Report." Nepal Journal of Neuroscience 12, no. 2 (October 8, 2016): 81–84. http://dx.doi.org/10.3126/njn.v12i2.15899.

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Tardive dystonia is a subtype of dystonia which is seen in patients receiving antipsychotic treatment for long period. Medical treatment of tardive dystonia is very complex and many cases do not respond well to currently available treatment and sometimes can be irreversible. Surgical treatments like pallidotomy and Deep Brain Stimulation (DBS) have shown some promising results. We report this case of Tardive Dystonia who benefitted from Pallidotomy. We believe this is the first case in Nepal.Nepal Journal of Neuroscience 12:81-84, 2015

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WOLF, DWIGHT V., and KAREN DINEEN WAGNER. "Tardive Dyskinesia, Tardive Dystonia, and Tardive Tourette's Syndrome in Children and Adolescents." Journal of Child and Adolescent Psychopharmacology 3, no. 4 (January 1993): 175–98. http://dx.doi.org/10.1089/cap.1993.3.175.

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Eisenthal, Sherman, and William E. Falk. "Medication Decisions and the Risk of Tardive Dyskinesia." Psychological Reports 62, no. 2 (April 1988): 467–72. http://dx.doi.org/10.2466/pr0.1988.62.2.467.

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A random sample of one-third or 338 of the psychiatrists from the Massachusetts Psychiatric Society were surveyed. 48% or 162 completed a questionnaire composed of 10 vignettes, all describing the initial contact with an adult male schizophrenic outpatient who had been receiving chlorpromazine treatment and who showed no signs of tardive dyskinesia. The vignettes depicted varying durations of treatment, symptoms and courses of illness during prior treatment. Instructions focussed on the effect of the potential for developing tardive dyskinesia on decisions to continue to use chlorpromazine. We found that the primary consideration in medication decisions was to control active psychotic symptoms; a secondary one was to minimize the risk of tardive dyskinesia. When the psychosis was in remission, avoiding tardive dyskinesia was given higher priority than seeking to maintain the remission.

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Heitzmann, Edwige, Hervé Javelot, Luisa Weiner, and Bruno Michel. "A Case of Aripiprazole-Induced Tardive Dyskinesia with Dramatic Evolution." Case Reports in Psychiatry 2016 (2016): 1–3. http://dx.doi.org/10.1155/2016/7031245.

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Aripiprazole is reported to be a good clinical safety profile antipsychotic. However, recent data suggest that the risk of tardive dyskinesia could be higher than initially thought. We report the case of aripiprazole-induced tardive dyskinesia with dramatic evolution in a patient with several risk factors, including older age and exposure to antipsychotic over a period longer than six months. This case and its dramatic evolution, associated with other cases recently published, suggest reconsidering the real risk of tardive dyskinesia associated with aripiprazole, particularly in the elderly.

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Cooper, S. J., M. M. Doherty, and D. J. King. "Tardive Dystonia." British Journal of Psychiatry 155, no. 1 (July 1989): 113–15. http://dx.doi.org/10.1192/bjp.155.1.113.

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Tardive dystonia is a rare movement disorder. We outline the development of tardive dystonia in a young schizopohrenic, and demonstrate the importance of applying a double-blind, placebo-controlled, crossover trial of any putative successful treatment.

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Falk, WilliamE, JoanneD Wojick, and AlanJ Gelenberg. "DILTIAZEM FOR TARDIVE DYSKINESIA AND TARDIVE DYSTONIA." Lancet 331, no. 8589 (April 1988): 824–25. http://dx.doi.org/10.1016/s0140-6736(88)91684-4.

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Waddington, John L., Eadbhard O'Callaghan, Peter Buckley, Cathy Madigan, Oonagh Redmond, John P. Stack, Anthony Kinsella, Conall Larkin, and Joseph T. Ennis. "Tardive Dyskinesia in Schizophrenia: Relationship to Minor Physical Anomalies, Frontal Lobe Dysfunction and Cerebral Structure on Magnetic Resonance Imaging." British Journal of Psychiatry 167, no. 1 (July 1995): 41–44. http://dx.doi.org/10.1192/bjp.167.1.41.

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BackgroundIt was hypothesised that schizophrenic patients with tardive dyskinesia show an excess of neurodevelopmental disturbance, particularly minor physical anomalies, in association with cognitive dysfunction and abnormalities of cerebral structure.MethodForty-seven out-patients with a DSM–III diagnosis of schizophrenia were examined for tardive dyskinesia using the Abnormal Involuntary Movement Scale; they were examined also for minor physical anomalies and neuropsychological test performance. Cortical atrophy, signal hyperintensities and lateral ventricular volume were determined on magnetic resonance imaging.ResultsPatients with and without tardive dyskinesia could not be distinguished by age, gender distribution or a number of clinical measures; however, patients with tardive dyskinesia sorted fewer categories on the Wisconsin Card Sorting Test (P = 0.04). Cerebral structure in patients with and without tardive dyskinesia could not be distinguished on magnetic resonance imaging but those with dyskinesia, all of whom showed involvement of the orofacial region, showed more evident minor physical anomalies of the head relative to those of the periphery (P = 0.02).ConclusionsTardive orofacial dyskinesia in schizophrenia appears to be associated particularly with poorer frontal lobe function, while predominance of craniofacial dysmorphogenesis may constitute a vulnerability factor that is related to the early origins of the disease process.

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Godeiro-Junior, Clecio, Andre C. Felício, Patrícia de Carvalho Aguiar, Vanderci Borges, Sonia M. A. Silva, and Henrique B. Ferraz. "Neuroleptic-Induced Tardive Cervical Dystonia: Clinical Series of 20 Patients." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 36, no. 2 (March 2009): 222–26. http://dx.doi.org/10.1017/s0317167100006582.

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Background:Cervical dystonia (CD) may be classified according to the underlying cause into primary or secondary CD. Previous exposure to neuroleptics is one of the main causes of adult-onset secondary dystonia. There are few reports that characterize the clinical features of primary CD and secondary neuroleptic-induced CD. Herein our aim was to investigate a series of patients with neuroleptic induced tardive CD and to describe their clinical and demographic features.Patients and Methods:We retrospectively evaluated 20 patients with neuroleptic-induced tardive CD and compared clinical, demographic and therapeutic characteristics to another 77 patients with primary CD. All patients underwent Botulinum toxin type-A therapy.Results:We did not identify any relevant clinical and demographic characteristics in our group of patients that could be used to distinguish tardive and primary CD.Conclusion:Patients with tardive CD presented demographic characteristics and disease course similar to those with primary CD.

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Adityanjee, S. K., Jayaswal, T. M. Chan, and M. Subramaniam. "Temporary Remission of Tardive Dystonia Following Electroconvulsive Therapy." British Journal of Psychiatry 156, no. 3 (March 1990): 433–35. http://dx.doi.org/10.1192/bjp.156.3.433.

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An improvement in tardive dystonia in a patient who had received ECT for a schizophrenic psychosis is reported. The improvement suggests that the pathophysiology of tardive dystonia may involve neurotransmitter receptor changes similar to those seen in schizophrenia.

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Rowley, Anthony. "Vendanges tardives." Commentaire Numéro108, no. 4 (2004): 1076. http://dx.doi.org/10.3917/comm.108.1076.

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Chaplin, Robert, and Mark Potter. "Tardive dyskinesia: screening and risk disclosure." Psychiatric Bulletin 20, no. 12 (December 1996): 714–16. http://dx.doi.org/10.1192/pb.20.12.714.

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A questionnaire was sent to a random sample of 339 psychiatrists on the Royal College mailing list, enquiring about their practice of screening and risk disclosure in patients at risk of tardive dyskinesia. The response rate was 70%. There was wide variation in the rate of informing patients of the risk. Over half of the respondents felt that knowledge about tardive dyskinesia would reduce compliance, a view which predicted a low rate of informing patients. There was support for the issuing of clinical practice guidelines by the College. Psychiatrists need further education about tardive dyskinesia.

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Dean, Charles E., and Paul D. Thuras. "Mortality and tardive dyskinesia: long-term study using the US National Death Index." British Journal of Psychiatry 194, no. 4 (April 2009): 360–64. http://dx.doi.org/10.1192/bjp.bp.108.049395.

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BackgroundWhether the development of tardive dyskinesia leads to an increase in mortality is still unclear.AimsTo explore the relationship between tardive dyskinesia and mortality over a 10-year period, using the National Death Index.MethodDeath certificates were obtained from the National Death Index on 1621 people repeatedly assessed for tardive dyskinesia by trained raters. Variables with the potential for influencing survival time were also investigated.ResultsTardive dyskinesia was significantly associated with an increase in mortality (P<0.001), but this association became non-significant when drug course and age were entered in the regression analysis. Those who had taken only conventional antipsychotics were twice as likely to die compared with those taking atypical agents (P<0.02). For those aged 53–65 years, conventional agents were associated with a sevenfold increase in mortality.ConclusionsOlder individuals with tardive dyskinesia treated with conventional antipsychotics appear to have a shortened survival time.

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McCreadie, Robin G., Lesley J. Robertson, and David H. Wiles. "The Nithsdale Schizophrenia Surveys. IX: Akathisia, Parkinsonism, Tardive Dyskinesia and Plasma Neuroleptic Levels." British Journal of Psychiatry 160, no. 6 (June 1992): 793–99. http://dx.doi.org/10.1192/bjp.160.6.793.

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Of all known schizophrenics living in Nithsdale, south-west Scotland, 146 (88%) were examined for the presence of the three principal movement disorders secondary to antipsychotic medication, namely akathisia, tardive dyskinesia and Parkinsonism. Of these, 18% had akathisia, 5% pseudoakathisia, 29% tardive dyskinesia, 8% persistent tardive dyskinesia, and 27% Parkinsonism. No movement disorder was seen in 44%, 36% had one and 20% had more than one movement disorder. Plasma neuroleptic levels at the time of clinical assessment were measured by the radioreceptor technique. Correlations between dose and plasma level were low; the ratio of mean plasma concentration to mean dose was greatest with fluphenazine decanoate and lowest for sulpiride. The concentration:dose ratio was higher in the elderly. There was no relationship between neuroleptic levels and akathisia, Parkinsonism or tardive dyskinesia. Additional psychotropic medication influenced neuroleptic levels. In 9% of patients receiving oral antipsychotic medication, no drug was detected in plasma.

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Brown, Keith W., Thomas White, J. M. Wardlaw, Nicholas Walker, and D. Foley. "Caudate Nucleus Morphology in Tardive Dyskinesia." British Journal of Psychiatry 169, no. 5 (November 1996): 631–36. http://dx.doi.org/10.1192/bjp.169.5.631.

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ObjectiveThe objective of this project was to test whether there are differences in the size of the caudate nucleus in schizophrenic in-patients with and without tardive dyskinesia.MethodThe study was cross-sectional in design, examining group differences between institutionalised schizophrenic patients with and without tardive dyskinesia, using non-enhanced computerised tomography scans of the brain. The group comprised 15 schizophrenic patients with persistent tardive dyskinesia and 21 in-patient schizophrenic controls who were group-matched for demographic variables.ResultsThe dyskinetic subjects had a significantly larger left caudate nucleus and tended to have a larger right caudate nucleus than the controls. There were no differences between the groups on any of the measures of cerebral atrophy.ConclusionsThe findings can be understood within the context of models of neostriatal function. It is possible that a larger caudate nucleus could be used to identify patients at risk of developing tardive dyskinesia.

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Chaplin, Robert, and Clive Timehin. "Informing Patients About Tardive Dyskinesia: Four-Year Follow Up of a Trial of Patient Education." Australian & New Zealand Journal of Psychiatry 36, no. 1 (February 2002): 99–103. http://dx.doi.org/10.1046/j.1440-1614.2002.00979.x.

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Objective: This paper evaluates the effects of an educational intervention about tardive dyskinesia on knowledge and clinical stability at long-term follow up. Method: Fifty-six patients receiving antipsychotic maintenance completed a questionnaire assessing their knowledge about tardive dyskinesia. After random allocation to either educational intervention or control group, their knowledge, clinical stability and rates of tardive dyskinesia were reassessed after four years. Results: Seventy per cent of patients completed the study. The patients in the educational group retained significantly more knowledge at follow up than at baseline but this knowledge was not significantly greater than that of the control group. There were no significant differences in the clinical outcomes between the groups. Conclusion: Patients can retain a small but significant amount of information with a low risk of noncompliance. Discussion about tardive dyskinesia is necessary in the process of obtaining informed consent to treatment.

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Robinson, A. D. T., and R. G. McCreadie. "The Nithsdale Schizophrenia Survey V. Follow-up of Tardive Dyskinesia at3-1/2 years." British Journal of Psychiatry 149, no. 5 (November 1986): 621–23. http://dx.doi.org/10.1192/bjp.149.5.621.

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The point-prevalence of tardive dyskinesia in schizophrenics from a discrete geographical area (Nithsdale, in Dumfries and Galloway Region) in 1981, 1982, and 1984 was 31%, 27%, and 30% respectively. This suggests that the prevalence of tardive dyskinesia in a community of schizophrenics has reached a plateau. In 12% of patients there was persistent dyskinesia, i.e. abnormal involuntary movements were present at all three assessments. Persistent dyskinesia was more common in older patients. The severity of tardive dyskinesia fluctuated between assessments in 41 % of patients, indicating that it is only a transient feature in some cases.

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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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Adams, James David. "Tardive Dyskinesia and Dopamine Oxidation, Cumulative Effects." J 2, no. 2 (March 31, 2019): 138–41. http://dx.doi.org/10.3390/j2020011.

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It is likely that tardive dyskinsesia is caused by the oxidation of dopamine in dopaminergic neurons. This oxidation produces oxygen radicals that damage neurons. Damage accumulates until tardive dyskinesia occurs. The use of dopamine D2 receptor inhibitors should be limited to the lowest doses for the shortest duration possible.

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Chiu, Helen F. K., and Sing Lee. "Tardive Dystonia." Australian & New Zealand Journal of Psychiatry 23, no. 4 (December 1989): 566–70. http://dx.doi.org/10.3109/00048678909062626.

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Unlike tardive dyskinesia (TD) which is much better known by clinicians, tardivedystonia is a more recently recognised complication of neuroleptic use. It refers to chronic dystonia related to the use of neuroleptic drugs and may be an even more disabling condition than TD. This article reviews its epidemiology, clinical features and treatment aspects, and suggests that it should be separated from TD as a distinct entity.

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Journal articles on the topic 'Tardivel'

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