scholarly journals Role of COMT V158M Polymorphism in the Development of Dystonia after Administration of Antipsychotic Drugs

2021 ◽  
Vol 11 (10) ◽  
pp. 1293
Author(s):  
Antonio Gennaro Nicotera ◽  
Gabriella Di Rosa ◽  
Laura Turriziani ◽  
Maria Cristina Costanzo ◽  
Emanuela Stracuzzi ◽  
...  

Antipsychotics (APDs) represent the main pharmacological strategy in the treatment of schizophrenia; however, their administration often may result in severe adverse effects, such as extrapyramidal symptoms. Typically, dystonic movements are considered the result of impaired function and/or abnormalities of dopaminergic neurotransmission/signaling in the basal ganglia. The catechol O-methyltransferase (COMT) gene is located within the 22q11.2 region, and its product is an enzyme involved in transferring a methyl group from S-adenosylmethionine to catecholamines, including dopamine. Studies showed that COMT Val158Met polymorphism modifies enzymatic activity and, consequently, synaptic dopamine concentration in specific brain areas. We identified a patient with 22q11.2 deletion syndrome presenting with cervical and trunk dystonia after paliperidone administration, which persisted even after drug discontinuation. Given the patient’s genetic condition, we hypothesized that the dopaminergic dysfunction had been aggravated by COMT involvement, thus causing dystonia. In line with this hypothesis, we carried out a study on psychiatric patients in chronic treatment with APD to evaluate the distribution of the COMT Val158Met polymorphism and its role in the onset of adverse extrapyramidal symptoms. The study included four patients with dystonia after administration of APDs compared to 17 patients who never presented adverse drug reactions. Our data suggest that the Val/Val and Met/Met polymorphisms of the COMT gene are associated with a protective effect for the development of collateral extrapyramidal symptoms in patients treated with APDs, while the Val/Met genotype could be considered a risk factor for the development of dystonia after APDs administration.

2021 ◽  
Author(s):  
Jinmeng Liu ◽  
Xia Liu ◽  
Hui Wang ◽  
Yemiao Gao

Abstract Background: Previous studies have suggested negative parenting environments, especially harsh parenting, is a specific risk factor for non-suicidal self-injury (NSSI). However, the potential mechanism between harsh parenting and NSSI has not been explored. Based on the experiential avoidance model and empirical researches, we aimed to examine if depressive symptoms are a mediator between harsh parenting and NSSI. Moreover, the catechol-O-methyltransferase (COMT) Val158Met polymorphism related to depressive symptoms may also exert a moderating effect on NSSI, thus, the interaction between harsh parenting and COMT were also considered in our study.Method:373 junior high school students were recruited for the study by using a longitudinal design. Adolescents answered self-report questionnaires and provided Saliva samples for DNA genotyping.Result:The results revealed that harsh parenting was positively associated with NSSI after 18 months, and this association was mediated by depressive symptoms. Moreover, the moderating role of COMT in the direct and indirect effect of harsh parenting on NSSI only among adolescents with two Val alleles. However, the relationship was not significant for Met carriers.Conclusion: Genetic variations of COMT Val158Met may be a critical candidate in understanding the development of depression and NSSI. We conclude that the Val homozygotes of the COMT Val158Met polymorphism play a susceptible role both in depressive symptoms and NSSI.


NeuroImage ◽  
2016 ◽  
Vol 125 ◽  
pp. 633-642 ◽  
Author(s):  
L. Forest Gruss ◽  
Taimour Langaee ◽  
Andreas Keil

2010 ◽  
Vol 6 (5) ◽  
pp. 662-668 ◽  
Author(s):  
Martin Reuter ◽  
Clemens Frenzel ◽  
Nora T. Walter ◽  
Sebastian Markett ◽  
Christian Montag

PLoS ONE ◽  
2019 ◽  
Vol 14 (4) ◽  
pp. e0211170 ◽  
Author(s):  
Gioia Mastromoro ◽  
Giulio Calcagni ◽  
Paolo Versacci ◽  
Carolina Putotto ◽  
Marcello Chinali ◽  
...  

Author(s):  
Hilga Katerberg ◽  
Danielle C. Cath ◽  
Damiaan A. J. P. Denys ◽  
Peter Heutink ◽  
Annemiek Polman ◽  
...  

2016 ◽  
Vol 90 (5) ◽  
pp. 420-427 ◽  
Author(s):  
E. Hidding ◽  
H. Swaab ◽  
L.M.J. de Sonneville ◽  
H. van Engeland ◽  
J.A.S. Vorstman

2017 ◽  
Vol 9 (2) ◽  
pp. 54-56
Author(s):  
Candace B. Borders ◽  
Amanda Suzuki ◽  
David Safani

22q11.2 deletion syndrome (22q11DS) is a risk factor for psychiatric illnesses, including schizophrenia and anxiety. Small studies have shown that several neuroleptic medications are effective in treating psychosis in this population, but are also associated with an increased risk of adverse effects - particularly, seizures. In this case, we discuss a 34-year-old patient presenting with late onset schizophrenia, which ultimately led to her diagnosis of 22q11DS. Subsequent management of the patient's psychosis with asenapine was complicated by concurrent anxiety and panic disorder; thus, we examine the role of anxiolytic therapy in conjunction with antipsychotics in this patient population.


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