SearchBrowseServicesOpen researchInstitution LoginSearchMenu linksBrowseSubjects Subjects (A-D) Subjects (E-K) Subjects (L-O) Subjects (P-Z)Open accessAll open access publishingJournalsExploreOpen accessCollectionsBooksExploreCollections Collections (cont.)ElementsExploreSubjects (A-E) Subjects (F-O) Subjects (P-Z)TextbooksExploreCollectionsBook collections Book collections (cont.)Journal collectionsSeriesPartnersPartners Partners (cont.)ServicesAboutAbout Cambridge CoreEnvironment and sustainabilityGuidesHelpAgentsServices for agentsAuthorsJournalsJournals (cont.)Journals (cont.)BooksCorporatesCorporatesEditorsInformationResourcesLibrariansInformationProductsToolsResourcesPeer reviewPeer reviewPublishing ethicsJournals Journals (cont.)BooksBooks (cont.)Publishing partnersPublishing partnersPublishing partners (cont.)Open researchOpen access policiesOpen access policiesJournalsBooks and ElementsOpen access publishingAbout open accessOpen access resourcesOpen research initiativesResearch transparencyJournal flipsFlip it OpenOpen access fundingOpen access funding Cambridge Open Engage Cambridge Open Engage, Sarró et al 1 report that in patients with schizophrenia, tardive dyskinesia is associated with widespread deficits in the amount of cerebral grey matter, most prominently in the basal ganglia and thalamus, but also in frontal and temporal cortex. The word ‘tardive’, denoting delayed onset following initiation of antipsychotic treatment, implies that antipsychotic medication plays a , Tardive dyskinesia is primarily linked to the long-term use of medications that block dopamine receptors in the brain. Antipsychotic drugs, particularly older first-generation antipsychotics, are the most common cause because they interfere with dopamine signaling, a neurotransmitter crucial for movement regulation..