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Clinical and genetic heterogeneity of PM represents a diagnostic challenge.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We performed detailed phenotypic and genomic analyses in a large cohort (n\u00a0=\u00a0169) of patients referred for PM and could establish a molecular diagnosis in 38 patients.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Pathogenic variants in <jats:italic>ASPM<\/jats:italic> and <jats:italic>WDR62<\/jats:italic> were the most frequent causes in non\u2010consanguineous patients in our cohort. In consanguineous patients, microarray and targeted gene panel analyses reached a diagnostic yield of 67%, which contrasts with a much lower rate in non\u2010consanguineous patients (9%). Our series includes 11 novel pathogenic variants and we identify novel candidate genes including <jats:italic>IGF2BP3<\/jats:italic> and <jats:italic>DNAH2<\/jats:italic>. We confirm the progression of microcephaly over time in affected children. Epilepsy was an important associated feature in our PM cohort, affecting 34% of patients with a molecular confirmation of the PM diagnosis, with various degrees of severity and seizure types.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Our findings will help to prioritize genomic investigations, accelerate molecular diagnoses, and improve the management of PM patients.<\/jats:p><\/jats:sec>","DOI":"10.1002\/mgg3.1768","type":"journal-article","created":{"date-parts":[[2021,8,17]],"date-time":"2021-08-17T08:52:35Z","timestamp":1629190355000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Phenotypes and genotypes in non\u2010consanguineous and consanguineous primary microcephaly: High incidence of 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