Product Code Database
The cavernous sinus within the human head is one of the dural venous sinuses creating a cavity called the lateral sellar compartment bordered by the temporal bone of the human skull and the sphenoid bone, lateral to the sella turcica.
Blood leaves the sinus via superior and inferior petrosal sinuses as well as via the emissary veins through the foramina of the skull (mostly through foramen ovale). There are also connections with the pterygoid plexus of veins via inferior ophthalmic vein, deep facial vein and emissary veins.
Structures within the outer (lateral) wall of the compartment from superior to inferior:
Structures passing through the midline (medial) wall: (2025). 9780808923718, Churchill Livingstone. ISBN 9780808923718
These 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.
The pituitary gland lies between the two paired cavernous sinuses. An abnormally growing pituitary adenoma, sitting on the bony sella turcica, will expand in the direction of least resistance and eventually invade the cavernous sinus. Cavernous sinus syndrome may result from mass effect of these tumors and cause Ophthalmoparesis (from compression of the oculomotor nerve, trochlear nerve, and abducens nerve), ophthalmic sensory loss (from compression of the ophthalmic nerve), and maxillary sensory loss (from compression of the maxillary nerve). A complete lesion of the cavernous sinus disrupts CN III, IV, and VI, causing total ophthalmoplegia, usually accompanied by a fixed, dilated pupil. Involvement of CN V (V1 and variable involvement of V2) causes sensory loss in these divisions of the trigeminal nerve. Horner's syndrome can also occur due to involvement of the carotid ocular sympathetics, but may be difficult to appreciate in the setting of a complete third nerve injury.Blumenfeld, H, Neuroanatomy through clinical cases. Sinauer Associates, Inc., 2002.
Because of its connections with the facial vein via the superior ophthalmic vein, it is possible to get infections in the cavernous sinus from an external facial injury within the danger area of the face. In patients with thrombophlebitis of the facial vein, pieces of the clot may break off and enter the cavernous sinus, forming a cavernous sinus thrombosis. From there the infection may spread to the dural venous sinuses. Infections may also be introduced by facial lacerations and by bursting pimples in the areas drained by the facial vein.Kumar, P. & Clark, M. Clinical Medicine, 6th ed. London: W.B. Saunders; 2005.
Potential causes of cavernous sinus syndrome include , direct extension of nasopharyngeal tumours, meningioma, or pituitary apoplexy, of the intracavernous carotid artery, carotid-cavernous fistula, bacterial infection causing cavernous sinus thrombosis, aseptic cavernous sinus thrombosis, idiopathic granulomatous disease (Tolosa–Hunt syndrome), and fungal infections. Cavernous sinus syndrome is a medical emergency, requiring prompt medical attention, diagnosis, and treatment.
|
|
