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Gene discovery has expanded epilepsy\u2010dyskinesia syndromes (EDS) from classic associations such as stereotypies in Rett syndrome to PRRT2\u2010related infantile seizures with paroxysmal dyskinesia and crouched gait in SCN1A\u2010associated Dravet syndrome.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>To outline the movement disorders spectrum in EDS, propose a pragmatic syndrome\u2010based clinical framework, group implicated genes into mechanistic categories, highlight selected genotype\u2013phenotype correlations, and summarize symptomatic and precision therapeutic options.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>A non\u2010systematic, structured literature review identified monogenic disorders reported with EDS, grouping publications into four tiers: multi\u2010etiology cohorts; small series and narrative\/systematic reviews; single\u2010gene or pathway\u2010focused reports; and mechanistic\/therapeutic studies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Eight cohort studies and multiple tier 2\u20133 series and reviews yielded 245 single\u2010gene associations, most mapping to ion channel and synaptic signaling pathways. Across DEE cohorts, movement disorders occurred in roughly one\u2010quarter to over one\u2010half of patients, were often hyperkinetic (notably dystonia and stereotypies), and frequently combined multiple phenomenologies. We grouped clinical presentations into early and late infantile\u2010onset EDS, Rett and Rett\u2010like syndromes, paroxysmal\/episodic and relapsing\u2013remitting disorders, disorders with severe acute motor exacerbations, and hypokinetic\/progressive phenotypes. Treatments are guided by gene\u2010 and mechanism\u2010informed strategies including sodium\u2010channel blockers, glutamatergic modulators, ketogenic diet, agents for paroxysmal dyskinesias, and deep brain stimulation in life\u2010threatening crises.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Movement disorders are common, often severe, and genetically heterogeneous across EDS. A syndrome\u2010based approach integrating clinical features, neuroimaging, and broad genetic testing (including copy number variants and repeat expansions) can guide symptomatic management and emerging precision therapies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mdc3.70641","type":"journal-article","created":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T06:45:51Z","timestamp":1777704351000},"page":"2328-2340","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Movement Disorders in Developmental and Epileptic Encephalopathies"],"prefix":"10.1002","volume":"13","author":[{"given":"Shekeeb","family":"Mohammad","sequence":"first","affiliation":[{"name":"Faculty of Medicine and Health, Sydney Medical School The University of Sydney  Sydney NSW Australia"},{"name":"Kids Neuroscience Centre, TY Nelson Department of Neurology and Neurosurgery The Children's Hospital at Westmead  Westmead NSW Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Darius","family":"Ebrahimi\u2010Fakhari","sequence":"additional","affiliation":[{"name":"Movement Disorders Program, Department of Neurology &amp; F.M. 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