The other significant factor affecting prognosis is the presence of a comorbid genetic condition or brain anomaly. Mortality rates from DWM are roughly 15%. In a study of Dandy–Walker variant (DWV), a mortality rate of 12.5% was observed. The most common cause of death is complications from hydrocephalus or its treatment. Untreated hydrocephalus can lead to increased intracranial pressure and brain damage. Shunts used to treat DWM have a moderate-to-good success rate, but they have a higher-than-average failure rate, which can result in failure to reduce the intracranial pressure or in infection, such as meningitis. Complications from overdrainage such as subdural haematomas are also possible and can lead to mortality. Shunts in the fourth ventricle (cystoperitoneal shunts, or CP shunts) have a generally high rate of successful cyst and ventricle size reduction, especially in the cyst (at least 80%). With a shunt in the lateral ventricles (ventriculoperitoneal shunt, or VP shunt), studies have generally found a roughly 50% successful cyst size reduction rate, with successful ventricle size reduction roughly two thirds of the time. Other systemic or genetic conditions are often present with DWM, and each have their own significant effect on prognosis. The prevalence of DWM is estimated at between 1 in 25,000 to 1 in 50,000. DWM is the cause of around 4.3% of cases of congenital hydrocephalus and 2.5% of all cases of hydrocephalus. A 2017 review found that most patients (65%) were diagnosed with either "Dandy–Walker malformation" or "Dandy–Walker syndrome", while 20% were diagnosed with "Dandy–Walker variant" and 1.1% with "mega cisterna magna". The malformation was first described in 1887 by English surgeon John Bland-Sutton as hypoplasia of the cerebellar vermis, an enlarged posterior fossa and hydrocephalus. In 1914, American neurosurgeon Walter Dandy and American paediatrician Kenneth Blackfan described the malformation as partial or complete absence of the cerebellar vermis, an enlarged fourth ventricle and hydrocephalus. In 1942, American physician John K. Taggart and Canadian–American neurosurgeon Arthur Earl Walker detailed the phenomenon extensively, ascribing the potential cause as underdevelopment of the foramina of Luschka and Magendie, now no longer believed to be significant.