The verumontanum, or mountain ridge, is a distinctive landmark in the prostatic urethra, important in the systemic division of posterior valve disorders:Type I - Most common type; due to anterior fusing of the plicae colliculi, mucosal fins extending from the bottom of the verumontanum distally along the prostatic and membranous urethra
Type II - Least common variant; vertical or longitudinal folds between the verumontanum and proximal prostatic urethra and bladder neck
Type III - Less common variant; a disc of tissue distal to verumontanum, also theorized  to be a developmental anomaly of congenital urogenital remnants in the bulbar urethraDewan has suggested that obstruction in the posterior urethra is more appropriately termed congenital obstructions of the posterior urethral membrane (COPUMs), a concept that has come from an in-depth analysis of the historical papers, and evaluation of patients with a prenatal diagnosis that has facilitated video recording of the uninstrumented obstructed urethra. The congenital obstructive lesions in the bulbar urethra, named Type III Valves by Young in 1919, have been eponymously referred to as Cobbs collar or Moormans ring. For each of the COPUM (Posterior Urethra) and Cobbs (Bulbar Urethra) lesions, the degree of obstruction can be variable, consistent with a variable expression of the embryopathy. The now nearly one hundred year old nomenclature of posterior urethral valves was based on limited radiology and primitive endoscopy, thus a change COPUM or Cobbs has been appropriate.
They derive from the nerve sheaths of the upper part of the nervus vestibularis in the region between the central and peripheral myelin (Obersteiner-Redlich-Zone) within the area of the porus acousticus, 1 cm from the brainstem. Genotype–phenotype correlation
Many people with NF2 were included in studies that were designed to compare disease type and progression with exact determination of the associated mutation. The goal of such comparisons of genotype and phenotype is to determine whether specific mutations cause respective combinations of symptoms. This would be extremely valuable for the prediction of disease progression and the planning of therapy starting at a young age. The results of such studies are the following:
In most cases the mutation in the NF2 gene causes shortened peptides. There are no mutational hot spots. People with frameshift mutations or nonsense mutations have poor prognosis. People with missense mutations have a better prognosis. In cases with mutations in the splice-acceptor-region, there is no good correlation to determine. Point mutations may have only minor effects. Cases are published in which exactly the same mutation is associated with clearly different outcomes.These results suggest that other factors (environment, other mutations) will probably determine the clinical outcome. Diagnosis
NF2 is a genetically transmitted condition. Diagnosis is most common in early adulthood (20–30 years); however, it can be diagnosed earlier. NF2 can be diagnosed due to the presence of a bilateral vestibular schwannoma, or an acoustic neuroma, which causes a hearing loss that may begin unilaterally.