There are also connections with the pterygoid plexus of veins via inferior ophthalmic vein, deep facial vein and emissary veins. Contents
Apart from the blood which passes through a venous sinus, several anatomical structures, including some cranial nerves and their branches, also pass through the sinus.Structures within the outer (lateral) wall of the compartment from superior to inferior:
Oculomotor nerve
Trochlear nerve
Ophthalmic and maxillary branches of the trigeminal nerveStructures passing through the midline (medial) wall:
Abducens nerve
Internal carotid artery accompanied by the internal carotid plexusThese nerves, with the exception of CN V2, pass through the cavernous sinus to enter the orbital apex through the superior orbital fissure. The maxillary nerve, division V2 of the trigeminal nerve travels through the lower portion of the sinus and exits via the foramen rotundum. The maxillary branch passes external to, but immediately adjacent to, the lateral wall of the sinus.The optic nerve lies just above and outside the cavernous sinus, superior and lateral to the pituitary gland on each side, and enters the orbital apex via the optic canal. Function
Venous drainage
As a venous sinus, the cavernous sinus receives blood from the superior and inferior ophthalmic veins and from superficial cortical veins, and is connected to the basilar plexus of veins posteriorly. The cavernous sinus drains by two larger channels, the superior and inferior petrosal sinuses, ultimately into the internal jugular vein via the sigmoid sinus, also draining with emissary vein to pterygoid plexus. Clinical significance
It is the only anatomic location in the body in which an artery travels completely through a venous structure.
Salla disease (SD) is an autosomal recessive lysosomal storage disease characterized by early physical impairment and intellectual disability. It was first described in 1979, after Salla, a municipality in Finnish Lapland. Salla disease is one of 40 Finnish heritage diseases and affects approximately 130 individuals, mainly from Finland and Sweden. Presentation
Individuals with Salla disease may present with nystagmus in the first months of life as well as hypotonia, reduced muscle tone and strength, and cognitive impairment. The most severely impaired children do not walk or acquire language, but the typical patient learns to walk and speak and has normal life expectancy. The MRI shows arrested or delayed myelination. Genetics
SD is caused by a mutation in the SLC17A5 gene, located at human chromosome 6q14-15. This gene codes for sialin, a lysosomal membrane protein that transports the charged sugar, N-acetylneuraminic acid (sialic acid), out of lysosomes. The mutation causes sialic acid to build up in the cells.The disease is inherited in an autosomal recessive manner. This means the defective gene responsible for the disorder is located on an autosome (chromosome 6 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Diagnosis
A diagnosis of this disorder can be made by measuring urine to look for elevated levels of free sialic acid.