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dc.contributor.authorVaddadi K.en
dc.contributor.authorWaddington J.en
dc.contributor.authorClifford J.en
dc.contributor.authorHakansson K.en
dc.date.accessioned2021-05-14T10:53:29Zen
dc.date.available2021-05-14T10:53:29Zen
dc.date.copyright2006en
dc.date.created20060612en
dc.date.issued2012-10-17en
dc.identifier.citationInternational Review of Psychiatry. 18 (2) (pp 133-143), 2006. Date of Publication: April 2006.en
dc.identifier.issn0954-0261en
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/32167en
dc.description.abstractTardive dyskinesia (TD) is a movement disorder described in individuals who have been treated with anti-dopaminergic agents. The pathophysiology of this condition remains to be fully elucidated. Several mechanisms like dopaminergic supersensitivity, dysfunction of striatonigral, GABAergic neurons and disturbed balance between dopaminergic and cholinergic systems have been described. Essential fatty acids (EFAs) are important components of neuronal membrane and the EFA content of these membranes can significantly influence neuronal functioning. Lower levels of EFAs have been reported in red blood cells (RBC) and plasma of individuals with moderate to severe TD. Supplementation with EFAs (omega-3 and omega-6 and ethyl-EPA) have been tried to alleviate TD in open and double-blind clinical trials and in some animal models of TD. In addition, antioxidants (Vitamin E) and melatonin have been tried. However, smaller numbers of patients and shortened length of clinical studies make it difficult to draw any definitive conclusions. Large multi-centre studies with sound methodology of both EFAs and antioxidants are needed. © Institute of Psychiatry.en
dc.languageEnglishen
dc.languageenen
dc.publisherInforma Healthcare (69-77 Paul Street, London EC2A 4LQ, United Kingdom)en
dc.titleTardive dyskinesia and essential fatty acids.en
dc.typeReviewen
dc.type.studyortrialReview article (e.g. literature review, narrative review)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1080/09540260600583114en
dc.publisher.placeUnited Kingdomen
dc.identifier.pubmedid16777667 [http://www.ncbi.nlm.nih.gov/pubmed/?term=16777667]en
dc.identifier.source43791676en
dc.identifier.institution(Vaddadi) Department of Psychological Medicine, Monash Medical Centre, Clayton, Vic., Australia (Hakansson) Department of Neuroscience, Karolinska Institute, Stockholm, Sweden (Hakansson, Clifford, Waddington) Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin, Ireland (Clifford) Institute of Technology, Tralee, Co. Kells, Ireland (Vaddadi) Department of Psychological Medicine, Monash Medical Centre, 270 Clayton road, Clayton, Vic. 3168, Australiaen
dc.description.addressK. Vaddadi, Department of Psychological Medicine, Monash Medical Centre, 270 Clayton road, Clayton, Vic. 3168, Australia. E-mail: vaddadik@hotmail.comen
dc.description.publicationstatusEmbaseen
dc.rights.statementCopyright 2012 Elsevier B.V., All rights reserved.en
dc.identifier.authoremailVaddadi K.; vaddadik@hotmail.comen
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.openairetypeReview-
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