abnormalities are observable on prenatal ultrasound. Brain MRI scans can reveal any brain anomalies that could be associated with the syndrome. Methods of genetic detection include whole exome sequencing and panel testing, which involves sequencing a selection of potential genes involved. Sanger sequencing can confirm the nature of the mutation. Once a family has been identified as being carriers for mutated CENPF genes, prenatal diagnosis and preimplantation genetic diagnosis can be offered for future conceptions. Treatment Treatment targets the symptoms. The intestinal atresia is usually surgically correctable in infancy with anastomosis; however, no eye surgery had been reported . Van Bever et al. recommended monitoring patients for glaucoma. A 2021 case report reported the successful use of a kidney transplant for renal failure in one late adolescent patient. Prognosis The prognosis is not yet certain. The majority of those affected have survived birth and infancy, and these individuals have continued to live through childhood and adolescence. However, a large minority with the most severe presentations have died before birth or shortly after. The oldest known people with the syndrome, Strømme's original two siblings, who had a mild-to-moderate presentation, were in their twenties and in employment . Epidemiology The prevalence of the syndrome is not yet known. , around 13 individuals had been diagnosed. History The condition was first identified in 1993, when Norwegian paediatrician Petter Strømme and his associates observed two infant siblings with microcephaly and eye abnormalities alongside apple-peel intestinal atresia at Rogaland Central Hospital in Stavanger, Norway. They proposed that it constituted a new syndrome. Later studies by Slee and Goldblatt (1996), Shanske et al. (2002), Bellini et al. (2002) and others observed other patients with similar symptoms who appeared to have the syndrome. In 2008, Van Bever et al. proposed that the syndrome be named after Strømme, after encountering another patient who seemed to have the syndrome. In 2015, Waters et al. conducted a genetic analysis on a British family in which four foetuses had miscarried with symptoms of a ciliopathy. They found that the foetuses had mutations in both copies of CENPF. They subsequently analysed a cohort of 1,000 individuals with microcephaly and found that one of them, a girl, had mutations in both of her copies of CENPF. Her learning delay was mild-to-moderate, and she did not have any other issues with her bodily systems. This confirmed for the first time that mutations in CENPF