![]() The common clinical findings of CSS are as follows:.The combination of CN VI palsy and ipsilateral Horner syndrome localizes the lesion to the cavernous sinus (Parkinson sign). Additionally, due to the postganglionic sympathetic plexus travelling on the ICA and CN VI, damage can cause an ipsilateral loss of sympathetic tone presenting as a Horner syndrome. The cavernous sinus is a fixed space limited by bony structures, so any pathology within the sinus has the ability to compress internal structures, causing ophthalmoplegia and facial sensory changes. The pathomechanism of CSS is characterized by the compression and dysfunction of the structures within the cavernous sinus. Mucormycosis, aspergillosis, actinomycosis, nocardiosis, mycobacterium, herpes zoster ![]() Intracavernous aneurysm, carotid-cavernous fistula, cavernous sinus thrombosis Meningioma, chordoma, neuroma, pituitary adenoma, metastases, lymphoma, nasopharyngeal carcinoma, chondrosarcoma, hemangioma, neuroblastomaīasal skull fracture, operative trauma to cavernous sinus after skull base surgery Table 1: Causes and clinical features of cavernous sinus syndrome Cause Specific etiologies of CSS are listed in Table 1. The thrombus can then cause damage locally or travel to the brain, causing stroke-like symptoms or encephalitis and meningitis. Due to the valveless nature of the facial veins, the sinuses are vulnerable to stagnation and poor drainage in the setting of severe infection, causing the formation of a thrombus. Septic CST is typically seen as a complication of a facial infection, such as sinusitis or cellulitis. One important infectious etiology of CSS includes cavernous sinus thrombosis (CST), which may present initially to an ophthalmologist and requires urgent management due to its life-threatening prognosis. Less common causes are vascular etiologies and infections. ![]() Other common causes of CSS include trauma and self-limited inflammatory disease. The most common cause of CSS is mass effect from tumor. EtiologyĪ CSS is caused by any pathology or lesion present within the cavernous sinus that disrupts the function of other anatomical structures. CN II does not travel within the cavernous sinus, but is closely associated superomedially. CN III, CN IV, CN V 1, and CN V 2 are all tethered to the lateral wall of the cavernous sinus, but CN VI lies freely inferolateral to the ICA and medially to the other CNs. Post-ganglionic, third-order sympathetic fibers (Horner syndrome) run on the ICA and CN VI and then CN V 1. The internal carotid artery (ICA) traverses the carotid sinuses bilaterally. The presence of important CNs and blood vessels makes the cavernous sinus a unique site for potential pathology. (Figure 1)įigure 2: Schematic of the facial venous drainage system The pituitary gland sits within the sella turcica which exists medial to the cavernous sinus, and the optic chiasm lies superior to the cavernous sinus on the midline in close proximity to the pituitary gland. ![]() Each cavernous sinus is flanked laterally by the temporal bone of the skull and inferiorly by the sphenoid bone, with close proximity to the sphenoid sinuses. The cavernous sinuses are dural venous sinuses that communicate with one another. This fact and the extensive direct and indirect vascular connections of the centrally located cavernous sinuses make them vulnerable to pathology at many sites. The dural sinuses and the cerebral and emissary veins have no valves, which allows blood to flow in either direction (anterograde or retrograde) according to venous pressure gradients in the vascular system. The venous drainage system of the head and face have a unique anatomy. Cavernous sinus syndrome (CSS) is a condition caused by any pathology involving the cavernous sinus which may present as a combination of unilateral ophthalmoplegia (cranial nerve (CN) III, IV, VI), autonomic dysfunction (Horner syndrome) or sensory CN V 1- CN V 2 loss.
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