Relevant bibliographies by topics / Syndrome tardif

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Syndrome tardif'

Author: Grafiati
Published: 4 June 2021
Last updated: 4 February 2022

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Journal articles on the topic "Syndrome tardif"

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Amouri, M., A. Masmoudi, T. J. Meziou, et al. "Syndrome d’Olmsted de début tardif." Annales de Dermatologie et de Vénéréologie 138, no. 12 (2011): A222. http://dx.doi.org/10.1016/j.annder.2011.10.236.

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Manckoundia, P., P. Khau Van Kien, J. M. Petit, L. Faivre, and G. Vaillant. "Diagnostic tardif d'un syndrome de Di George." La Revue de Médecine Interne 22 (December 2001): 570s. http://dx.doi.org/10.1016/s0248-8663(01)80309-x.

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Pruna, L., K. Angioi-Duprez, J. L. Rigon, and P. Kaminsky. "Diagnostic tardif d’un syndrome de Gronblad-Strandberg-Touraine." La Revue de Médecine Interne 31 (June 2010): S185. http://dx.doi.org/10.1016/j.revmed.2010.03.322.

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Khensal, S., S. Rezgui, K. Benmohammed, et al. "Challenges du diagnostic tardif du syndrome de Turner." Annales d'Endocrinologie 78, no. 4 (2017): 381. http://dx.doi.org/10.1016/j.ando.2017.07.537.

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Lasry, F., S. Ait Khouya, M. Oumlil, H. Hadj Khalifa, and M. Fehri. "« Prune belly syndrome » : un mode de révélation inhabituel et tardif." Archives de Pédiatrie 11, no. 3 (2004): 259. http://dx.doi.org/10.1016/j.arcped.2003.12.014.

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Kalafate, N., and F. Chentli. "Syndrome de Wolfram : diagnostic souvent tardif malgré un début précoce." Annales d'Endocrinologie 73, no. 4 (2012): 394–95. http://dx.doi.org/10.1016/j.ando.2012.07.974.

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Benabdelaziz, Ines, Emna Sansa, Ibrahim Omri, et al. "Le syndrome de Rasmussen à début tardif : à propos d’un cas." Revue Neurologique 175 (April 2019): S19. http://dx.doi.org/10.1016/j.neurol.2019.01.077.

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Jaillon-Riviere, V., S. Dupont, Françoise Bertran, et al. "Le syndrome de Rasmussen à début tardif : caractéristiques cliniques et thérapeutiques." Revue Neurologique 163, no. 5 (2007): 573–80. http://dx.doi.org/10.1016/s0035-3787(07)90463-4.

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Diyane, K., G. Elmghari, and N. Elansari. "P139 Syndrome de Wolfram : diagnostic souvent tardif malgré un début précoce." Diabetes & Metabolism 40 (March 2014): A62. http://dx.doi.org/10.1016/s1262-3636(14)72431-0.

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Thévenot, T., O. Sitbon, R. Dhôte, et al. "Syndrome de Reynolds et hypertension artérielle pulmonaire : un diagnostic trop tardif." La Revue de Médecine Interne 19 (January 1998): 446. http://dx.doi.org/10.1016/s0248-8663(98)90156-4.

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Dissertations / Theses on the topic "Syndrome tardif"

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Bednarek, Nathalie. "Spasmes infantiles a debut tardif (apres un an)." Reims, 1994. http://www.theses.fr/1994REIMM025.

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Maillier, Bruno. "Interet des potentiels tardifs ventriculaires dans le syndrome d'apnees du sommeil." Reims, 1993. http://www.theses.fr/1993REIMM061.

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STAMM, DIDIER. "Pneumopathies interstitielles du syndrome tardif de la rubeole congenitale : evolution du taux des complexes immuns circulants : a propos de 2 observations." Lyon 1, 1988. http://www.theses.fr/1988LYO1M166.

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Samyn, Isabelle. "LA QUESTION DES AUTISMES :L'AUTISME, SYNDROME OU SYMPTOME ?" Phd thesis, Université Lumière - Lyon II, 2005. http://tel.archives-ouvertes.fr/tel-00089457.

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Cette étude sur le développement précoce de l'Autisme Infantile est un travail de
recherche de quatre ans.
A partir d'une réflexion heuristique sur la diversité du syndrome autistique nous abordons
la question des autismes et plus précisément du développement du trouble autistique au
sein d'un éventail relativement étendu de pathologies.
Ce travail présente, dans un premier temps, les problèmes de délimitation nosographique
entre le normal et le pathologique, puis, dans un second temps, les difficultés à poser un
diagnostic d'autisme.
Ces réflexions théorico-cliniques s'inspirent, d'une part, de rencontres cliniques, et
d'autre part, d'une revue historique des grands travaux de recherche sur le trouble
autistique.
Ce parcours heuristique conduit à notre étude clinique qui s'appuie sur la question du
développement précoce de sujets atteints d'Autisme Infantile Précoce selon leur âge
d'entrée dans la pathologie. Deux sous-groupes sont étudiés : les Autistes Précoces et les
Autistes à Début Tardif.
La confirmation d'une différenciation intragroupale et la découverte des particularités
développementales de ces deux sous-groupes nous permettent d'aborder plus précisément
le rôle du trouble autistique au sein de l'Autisme Infantile Précoce et de pathologies à
troubles autistiques associés, telle que la névrose obsessionnelle.
Nos résultats et notre discussion nous amènent à la conclusion suivante : la caractéristique
principale de la pathologie autistique – l'autisme des sujets – serait la conséquence d'un
mode défensif pathologique dont le rôle, la fonction, l'intensité et l'évolution dépendent
de troubles sous-jacents propres à chacun. La pathologie s'insérerait alors dans une
catégorie déterminée par l'âge auquel les sujets la développent et par les moyens à leur
disposition pour se défendre contre leurs troubles précoces, leur fragilité originelle et
contre les obstacles environnementaux qu'ils vont rencontrer.
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Ndiaye, Bakhao. "Facteurs de risque de l'accès tardif aux soins et de la perte de vue chez les patients infectés par le VIH suivis à Bruxelles et dans la région Nord Pas-de-Calais." Lille 2, 2009. http://www.theses.fr/2009LIL2S046.

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Mewton, Nathan. "Imagerie cardiaque par résonance magnétique à la phase aigüe de l'infarctus du myocarde : de la physiopathologie à l'évaluation des nouvelles thérapeutiques de reperfusion." Thesis, Lyon 1, 2009. http://www.theses.fr/2009LYO10293.

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La première partie de cette thèse porte sur l'étude du no-reflow ou obstruction microvasculaire en IRM cardiaque. Dans une première étude, nous avons mesuré l'incidence du no-reflow dans une population de 25 patients pris en charge pour infarctus du myocarde sans sus-décalage du segment ST. Nous avons trouvé que 32% de ces patients présentaient un no-reflow et que la présence de no-reflow était associée à une taille d'infarctus significativement plus importante ainsi qu'une élévation plus importante des enzymes cardiaques. Dans une deuxième étude nous avons comparé la performance diagnostique du myocardial blush grade (MBG) pour le diagnostic du no-reflow avec l'IRM cardiaque sur les séquences de rehaussement tardif post-gadolinium. Cette étude a été réalisée dans une population de 39 patients pris en charge pour un premier épisode de STEMI. Nous avons trouvé que le MBG sous-estimait la présence de no-reflow à la phase aiguë de l'infarctus après reperfusion optimale en comparaison avec l'IRM. La deuxième partie de cette thèse concerne la quantification de l'infarctus du myocarde en IRM cardiaque de rehaussement tardif post-gadolinium. Nous avons comparé une technique d'évaluation semi-quantitative visuelle rapide avec la planimétrie manuelle classique sur une population de 103 patients pris en charge pour syndrome coronarien aigu. La taille de l'infarctus était évaluée par ces deux méthodes en IRM cardiaque réalisée 4 jours après admission. Nous avons trouvé une excellente corrélation et un bon niveau de concordance entre les deux méthodes d'évaluation de la taille d'infarctus, avec des temps de posttraitements beaucoup plus courts pour l'analyse visuelle rapide. Enfin, la troisième partie de cette thèse aborde le sujet de l'utilisation de l'IRM cardiaque comme outil de mesure dans les essais thérapeutiques sur la reperfusion myocardique. Nous avons utilisé l'IRM cardiaque pour évaluer l'efficacité de l'utilisation de la cyclosporine A à la phase aigüe de l'infarctus reperfusé et son effet sur remodelage ventriculaire à 6 mois. Dans cette étude 28 patients ont été étudiés en IRM cardiaque 5 jours et 6 mois après un infarctus du myocarde. Nous avons trouvé une persistance de la réduction significative de 23% de taille de l'infarctus à 6 mois dans le groupe traité par cyclosporine par rapport au groupe contrôle. Il n'y avait pas d'effet négatif de la cyclosporine A sur le processus de remodelage ventriculaire gauche
We assessed the presence and extent of microvascular obstruction (MVO) and its relationship with infarct size and left ventricular (LV) functional parameters after acute non-ST elevated myocardial infarction (NSTEMI). 25 patients with first acute NSTEMI underwent a complete cardio magnetic resonance (CMR) study 72 hours after admission. MO was detected in 32% of patients and was significantly associated with a larger infarct size. There were no significant difference between both groups for the LV functional parameters but patients with MO showed a higher troponin-I and CK release. We studied the relation between Myocardial Blush Grade (MBG) and gadolinium-enhanced CMR for the assessment of MVO in 39 patients with acute ST elevated myocardial infarction (STEMI) treated by primary PCI. No statistical relation was found between MBG and MVO extent at CMR (p=0.63). MBG underestimates MVO after an optimal revascularization in AMI compared to CMR.We compared the performance and post-processing time of a global visual scoring method to standard quantitative planimetry and we compared both methods to the peak values of myocardial biomarkers. 103 patients admitted with reperfused AMI to our intensive care unit had a complete CMR study 4±2 days after admission. There was an excellent correlation between quantitative planimetry and visual global scoring for the hyperenhancement extent’s measurement (r=0.94; y=1.093x+0.87; SEE=1.2; P<0.001) and there was also a good concordance between the two approaches with significantly shorter mean post-processing time for the visual scoring method. There was also significant levels of correlation between the enzymatic peak values and the visual global scoring method. The visual global scoring method allows a rapid and accurate assessment of the myocardial global delayed enhancement. This study examined the effect of a single dose of cyclosporine A used at the time of reperfusion, on LV remodeling and function by cardiac magnetic resonance (CMR) in the early days and 6 months after AMI.28 patients of the original cyclosporine A study had an acute (day 5) and a follow-up (6 months) CMR study. There was a persistent 23% reduction of the absolute infarct size at 6 months without any dementrial effect in the cyclosporine A group compared with the control group of patients. Cyclosporine A used at the moment of AMI reperfusion persistently reduces infarct size and does not have a detrimental effect on LV remodeling
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Wion-Barbot, Nelly. "Trouble de l'hormonogenèse surrénalienne à révélation tardive et dystrophie ovarienne micropolykystique." Angers, 1988. http://www.theses.fr/1988ANGE1099.

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MACQUART, DE TERLINE PATRICE. "Revue bibliographique de la maladie de leber-coats : a propos d'une forme de survenue tardive." Nantes, 1989. http://www.theses.fr/1989NANT096M.

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Lepelletier, Eric. "Une hypoparathyroidie de decouverte tardive : manifestations neurologiques et cardiovasculaires : a propos d'un cas." Université Louis Pasteur (Strasbourg) (1971-2008), 1990. http://www.theses.fr/1990STR1M218.

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Lima, Daniela Paoli de Almeida. "Trauma craniencefálico leve: avaliação tardia da qualidade de vida e alterações neuropsicológicas." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5152/tde-17022009-114757/.

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Trauma de crânio leve (TCE leve) é definido como um déficit neurológico transitório que ocorre após um trauma incluindo história de náuseas, vômitos, cefaléia ou tontura acompanhada de alteração ou perda da consciência com duração inferior a 15 minutos, amnésia pós traumática e Escala de Coma de Glasgow entre 13 e 15. Apesar da alta taxa de sobrevida, pode cursar com alguma morbidade, principalmente nos três primeiros meses posteriores ao trauma e cerca de 18 % dos pacientes desenvolvem pelo menos uma síndrome psiquiátrica no primeiro ano após o acidente. O diagnóstico ainda é um desafio no sentido de minimizar-se gastos desnecessários com exames subsidiários entretanto, intervenções precoces podem evitar seqüelas. Nosso objetivo foi verificar o impacto do TCE leve na qualidade de vida de suas vítimas e diagnosticar as várias alterações neuropsicológicas que podem advir deste trauma. Esses alterações podem ser verificadas através de instrumentos de pesquisa. Inicialmente, foram avaliadas cinqüenta vítimas com TCE leve, atendidas no Hospital João XXIII, em Belo Horizonte - MG, as quais foram submetidas a dosagem de proteína S100B e tomografia de crânio (TCC) na admissão. Nessa fase, verificou-se que a proteína S100B tem valor preditivo negativo de 100%. Dezoito meses após o trauma, esses pacientes foram procurados em suas residências, quando foi lhes solicitado para que respondessem a quatro instrumentos de pesquisa [dois para diagnóstico de qualidade de vida (World Health Organization WHOQOL-100), e o Short Form-36 (SF-36), um para análise da presença de ansiedade e depressão (Escala Hospitalar de Ansiedade e Depressão (EHAD) e o Questionário de Sinais e Sintomas (QSS), baseado no Post Concussion Questionnaire] com o objetivo de pesquisar a presença de sinais e sintomas da síndrome pós-concussão. Também foram pesquisados aspectos sociodemográficos, como idade, escolaridade, estado civil, renda pessoal e origem desta renda. Os mesmos questionários foram preenchidos por um grupo de controle composto, necessariamente, por coabitantes dos pacientes, sem história de trauma craniano de qualquer gravidade e com idade a mais próxima possível da do paciente. Na avaliação pelo WHOQOL-100, pacientes apresentaram qualidade de vida inferior nos domínios nível de independência, ambiente e no total de domínios (p< 0,05). Na avaliação do SF-36, pacientes revelaram qualidade de vida inferior nos domínios capacidade funcional, vitalidade, saúde mental (p<0,001), dor, estado geral de saúde e aspectos mentais (p<0,05). Pacientes apresentaram mais ansiedade e estavam uma classe acima de seus controles pela EHAD. Pacientes referem ainda número maior de sinais e sintomas da síndrome pós-concussão do que seus respectivos controles. Não verificamos correlação entre a qualidade de vida, classificação na EHAD ou número de sinais e sintomas da SPC com as dosagens de proteína S100B ou com a presença de lesão na TCC realizadas na admissão
Mild head trauma (MHT) is defined as a transitory neurological deficit that happens after the trauma and includes a history of nausea, vomiting, headache or dizziness and loss or alteration of consciousness (less than 15 minutes), post-trauma amnesia, and Glasgow Coma Scale (GCS) at admission between 13 and 15. Despite the high survival rates, some morbidity has been observed in the three month period after this trauma. Approximately 18% of head trauma patients develop at least one psychiatric syndrome in the first year after the accident. The diagnostics difficulty and the risks of complications after the MHT continue to be a relevant problem at the emergency departments around the world. Limitations of active participation in daily life are alterations that influence life quality. Several of these alterations may be diagnosed through Interview Instruments. Our study was divided in two phases. In the first phase, 50 MHT patients admitted at Hospital João XXIII, Belo Horizonte-MG, Brazil, had protein S100B dosing and head CT taken at admission. Concentration values of S100B lower than 0.01 g/l were considered negative once this was the lowest value found in patients who did not show brain injuty signs in the CT scan. In that study it was found that protein S100B has 100% negative predictive value. In this second phase of the study, 18 months after the trauma, these patients were contacted at their homes and asked to answer four self- assessment questionnaires: two for quality of life diagnostic - World Health Organizations WHOQOL-100 and the Short Form-36 (SF36); one for the analysis of anxiety and depression - Hospital anxiety and depression scale-HADS; and one instrument developed by the author based on the Rivermead Post Concussion Questionnaire to evaluate the presence of post-concussion syndrome signs and symptoms. Several socio-demographic aspects were also analyzed, including income, source of income, means of transportation used, etc. The same questionnaires were filled by a control group formed necessarily by patients co-inhabitants, with no history of head trauma of any severity, and with closest age as possible to the patients. In the WHOQOL assessment patients showed a lower quality of life in the independence, environment, as well as in the total domains (p< 0,05). In the SF 36 assessment patients showed a lower quality of life in the functional capacity, vitality, and mental health domains (p<0,001); and also in pain, general health situation, and mental aspects (p<0,05). Patients showed more anxiety and, in the HADS Scale, showed at least a level higher, on average, than their controls. Patients also showed a higher number of post-concussion signs and symptoms than their respective controls. We did not find correlation between the later quality of life and protein S100B dosing at admission. We were not able to find correlation between the protein concentrations with the presence of brain lesions in the CCT scans taken at patients admission in the emergency department
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Books on the topic "Syndrome tardif"

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Morton, Walker, ed. The yeast syndrome. Bantam Books, 1986.

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Trowbridge, John Parks. The yeast syndrome. Bantam Books, 1989.

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Akathisia and restless legs. Cambridge University Press, 1995.

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Fox, Susan H. Delayed and Often Persistent. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190607555.003.0021.

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Tardive syndromes are drug-induced hyperkinetic movement disorders that occur as a consequence of dopamine D2 receptor antagonism/blockade. There are several types, including classical tardive dyskinesia, tardive dystonia, tardive tics, tardive myoclonus, and tardive tremor, and it is important to the management of these disorders that the type of movement disorder induced is identified. Tardive syndromes can occur with all antipsychotic drugs, including so-called atypical drugs. Patients taking these drugs should be evaluated frequently for side effects. Evaluating the nature of the movement (i.e., chorea or dystonia) is important because treatment options can differ according to the type of dyskinesia present.
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Maksimowski, Michael, and Rajesh Tampi. Treatment of Neuropsychiatric Disorders. Edited by Shirshendu Sinha. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190265557.003.0011.

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In this chapter different issues associated with the treatment of neuropsychiatric disorders will be reviewed including neuropharmacokinetics, neuropharmacodynamics, drug interactions, antiparkinsonians, nootropics, treatment of tardive dyskinesia, treatment of neuroleptic malignant syndrome, neurosurgical approaches and pain management
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Sybert, Virginia P. Metabolic Disease. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195397666.003.0011.

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Porphyrias – Congenital Erythropoietic Porphyria – Erythropoietic Protoporphyria – Hereditary Coproporphyria – Porphyria Cutanea Tarda – Variegate Porphyria – Mucopolysaccharidoses – Hunter Syndrome – Other Metabolic Disorders – Acrodermatitis Enteropathica – Alkaptonuria – Biotinidase Deficiency – Familial Cutaneous Amyloidosis – Prolidase Deficiency
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Sybert, Virginia P. Metabolic Disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190276478.003.0011.

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Chapter 11 covers Porphyrias (Congenital Erythropoietic Porphyria, Erythropoietic Protoporphyria, Hereditary Coproporphyria, Porphyria Cutanea Tarda, and Variegate Porphyria), Mucopolysaccharidoses (Hunter Syndrome), and Other Metabolic Disorders (Acrodermatitis Enteropathica, Alkaptonuria, Biotinidase Deficiency, Familial Cutaneous Amyloidosis, and Prolidase Deficiency). Each condition is discussed in detail, including dermatologic features, associated anomalies, histopathology, basic defect, treatment, mode of inheritance, prenatal diagnosis, and differential diagnosis.
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Sachdev, Perminder. Akathisia and Restless Legs. Cambridge University Press, 2006.

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Stewart, Jessica Ann, L. Mark Russakoff, and Jonathan W. Stewart. Pharmacotherapy, ECT, and TMS. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199326075.003.0016.

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Physicians’ attention to patients’ concerns and attitudes about taking medication will engender adherence, as will close monitoring of potentially disconcerting side effects. The primary indication for antipsychotic medications is the treatment of psychotic disorders and mania, even in the absence of psychosis. The more troublesome side effects of antipsychotic medications include increased appetite and weight gain; extrapyramidal side effects, tardive dyskinesia, and neuroleptic malignant syndrome. Antidepressants are effective for treating depressive illness, including major depression, persistent depressive disorder (dysthymia) and premenstrual dysphoric disorder. They are also often used effectively in the treatment of anxiety disorders, obsessive-compulsive disorder, bulimia nervosa, and somatic symptom disorders. Selective serotonin reuptake inhibitors (SSRIs) are generally well tolerated. Other important categories of medications include mood stabilizers and anxiolytics.
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Trowbridge, John P., and Morton Walker. The Yeast Syndrome: How to Help Your Doctor Identify & Treat the Real Cause of Your Yeast-Related Illness. Bantam, 1986.

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Book chapters on the topic "Syndrome tardif"

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Casey, D. E., and G. A. Keepers. "Neuroleptic Side Effects: Acute Extrapyramidal Syndromes and Tardive Dyskinesia." In Psychopharmacology: Current Trends. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73280-5_7.

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Hofmann, R., J. Braun, and H. J. Vogt. "Differentialdiagnose von Klinefelter-Syndrom und Pubertas tarda mit Hilfe des transrektalen Ultraschalls." In Verhandlungsbericht der Deutschen Gesellschaft für Urologie. Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-83170-6_321.

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Wolf Gilbert, R., and C. Waters. "Tardive Syndromes." In Encyclopedia of Movement Disorders. Elsevier, 2010. http://dx.doi.org/10.1016/b978-0-12-374105-9.00078-2.

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Fahn, Stanley, Joseph Jankovic, and Mark Hallett. "The tardive syndromes." In Principles and Practice of Movement Disorders. Elsevier, 2011. http://dx.doi.org/10.1016/b978-1-4377-2369-4.00019-6.

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Jankovic, Joseph, Mark Hallett, Michael S. Okun, Cynthia Comella, Stanley Fahn, and Jennifer Goldman. "The tardive syndromes." In Principles and Practice of Movement Disorders. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-323-31071-0.00017-2.

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Spranger, Jürgen W., Paula W. Brill, Christine Hall, Gen Nishimura, Andrea Superti-Furga, and Sheila Unger. "Spondylo-Epi-Metaphyseal and Spondylo-Metaphyseal Dysplasias." In Bone Dysplasias. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190626655.003.0007.

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This chapter further discusses bone dysplasias and explores achondrogenesis type 1A, odontochondrodysplasia, Schneckenbecken dysplasia, opsismodysplasia, spondylometaphyseal dysplasia (Sedaghatian type), spondyloenchondrodysplasia, SEMD (PAPSS2 type) and brachyolmia (autosomal recessive type), Dyggve-Melchior-Clausen dysplasia, spondylometaepiphyseal dysplasia (short limb-abnormal calcification type), spondylometaphyseal dysplasia with cone-rod dystrophy, dyssegmental dysplasia, Schwartz-Jampel syndrome, spondyloepiphyseal dysplasia tarda (X-linked), aggrecan-associated skeletal dysplasias, Wolcott-Rallison syndrome, Schimke immunoosseous dysplasia, progressive pseudorheumatoid chondrodysplasia, spondylometaphyseal dysplasia (corner fracture type), sponastrime dysplasia, CODAS syndrome, N-acetyl-neuraminic acid synthase (NANS) deficiency, and spondylo-epi-metaphyseal dysplasia with immune deficiency and developmental disability (EXTL3-deficient type). Each discussion includes major radiographic features, major clinical findings, genetics, major differential diagnoses, and a bibliography.
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Singh, BK. "Spectrum of Tardive Syndromes: Clinical Recognition and Management." In Textbook of Postgraduate Psychiatry (2 Volumes). Jaypee Brothers Medical Publishers (P) Ltd., 2018. http://dx.doi.org/10.5005/jp/books/14227_75.

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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. 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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Shibasaki, Hiroshi, Mark Hallett, Kailash P. Bhatia, Stephen G. Reich, and Bettina Balint. "Dyskinesia, Motor Stereotypies, and Tics." In Involuntary Movements. 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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Sienaert, Pascal, Peter van Harten, and Didi Rhebergen. "The psychopharmacology of catatonia, neuroleptic malignant syndrome, akathisia, tardive dyskinesia, and dystonia." In Psychopharmacology of Neurologic Disease. Elsevier, 2019. http://dx.doi.org/10.1016/b978-0-444-64012-3.00025-3.

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Conference papers on the topic "Syndrome tardif"

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Song, Seung Yun, Yinan Pei, Jiahui Liang, and Elizabeth T. Hsiao-Wecksler. "Design of a Portable Position, Velocity, and Resistance Meter (PVRM) for Convenient Clinical Evaluation of Spasticity or Rigidity." In 2017 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/dmd2017-3503.

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Spasticity is a common consequence of the upper motor neuron syndrome and usually associated with brain lesion, stroke, cerebral palsy, spinal cord injury, and etc. On the other hand, rigidity is a neuromuscular disorder often found in Parkinson’s disease patients. Both of spasticity and rigidity are characterized by abnormal hypertonic muscle behaviors that will cause discomfort and hinder daily activities. Worldwide, the estimated affected population of spasticity is around 12 million [1], and rigidity affects more than 10 million people [2]. Clinical evaluation of spasticity or rigidity involves personal assessment using qualitative scales, such as the Modified Ashworth Scale (MAS) or Modified Tardieu Scale (MTS) for spasticity and Unified Parkinson’s Disease Rating Scale (UPDRS) for rigidity. However, this evaluation method heavily relies on the rater’s personal experience/interpretation and usually results in poor consistency and low reliability. The goal of this design was to develop a quantitative measurement device that can be used to assist clinical evaluation of spasticity or rigidity. This portable device, the Position, Velocity, and Resistance Meter (PVRM), can be strapped around a patient’s limb to measure angular position, angular velocity and muscle resistance of a given joint while the patient’s limb is passively stretched by the clinician. Acquiring this quantitative data from patients will not only allow clinicians to make more reliable assessments but also help researchers gain additional insights into the quantification of spasticity and rigidity.
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