As well as glands, the seminal vesicles contain smooth muscle and connective tissue. This fibrous and muscular tissue surrounds the glands, helping to expel their contents. The outer surface of the glands is covered in peritoneum. Function
The seminal vesicles secrete a significant proportion of the fluid that ultimately becomes semen. Fluid is secreted from the ejaculatory ducts of the vesicles into the vas deferens, where it becomes part of semen. This then passes through the urethra, where it is ejaculated during a male sexual response.About 70-85% of the seminal fluid in humans originates from the seminal vesicles. The fluid consists of nutrients including fructose and citric acid, prostaglandins, and fibrinogen. Nutrients help support sperm until fertilisation occurs; prostaglandins may also assist by softening mucous of the cervix, and by causing reverse contractions of parts of the female reproductive tract such as the fallopian tubes, to ensure that sperm are less likely to be expelled. Clinical significance
Disease
Diseases of the Seminal vesicles as opposed to that of prostate gland are extremely rare and are infrequently reported in the medical literature.Congenital anomalies associated with the seminal vesicles include failure to develop, either completely (agenesis) or partially (hypoplasia), and cysts. Failure of the vesicles to form is often associated with absent vas deferens, or an abnormal connection between the vas deferens and the ureter. The seminal vesicles may also be affected by cysts, amyloidosis, and stones.
Andermann syndrome, also known as agenesis of corpus callosum with neuronopathy (ACCPN) and Charlevoix disease, among other names, is a very rare neurodegenerative genetic disorder that damages the nerves used to control muscles and related to sensation and is often associated with agenesis of the corpus collosum.It was first described by Eva Andermann et al. in 1972. Symptoms and signs
Symptoms begin in infancy and include:
hypotonia
areflexia
amyotrophy
variable degrees of dysgenesis of the corpus callosum
mild to severe intellectual and developmental delay
psychiatric problems including paranoid delusions, depression, hallucinations and autistic-like behavior

Genetics
The inheritance pattern is autosomal recessive. Several genes have been associated with the disorder, including SLC12A6. Neuropathology
Autopsy examination of 8 cases has shown both developmental and degenerative neuropathologic features in this disease, consistent with clinical duality as both a neurodevelopmental and neurodegenerative disorder.In the central nervous system, accompanying the hypotonia at birth is hypoplasia of the corticospinal tracts. Another developmental feature is seen in the corpus callosum, which varies from absent to hypoplastic. The anterior commissure is almost always absent, but occasionally hypoplastic. A bundle of Probst can be found running antero-posterior rather than crossing the midline. The axonal damage due to the channel deficiency can cause a reactive axonal overgrowth leading to small tumor-like growths, or tumorlets, called axonomas, or balls of aberrant axons. Damaged axons can also show a sign of inhibition of axonal transport, forming axonal spheroids.