Cavernous sinus anatomy Paired sinus located on either side of the sella turcica in middle cranial fossa and upper part of the sphenoid bone It is divided by septa into small ‘caves’ – from which it gets its name. Walls of veins are extremely thin Extent- anteriorly (superior orbital fissure) to posteriorly (apex of petrous temporal bone)
Boundaries The borders of the cavernous sinus are as follows: Anterior – superior orbital fissure Posterior – petrous part of the temporal bone. Medial – body of the sphenoid bone. Lateral – meningeal layer of the dura mater running from the roof to the floor of the middle cranial fossa. Roof – meningeal layer of the dura mater that attaches to the anterior and middle clinoid processes of the sphenoid bone. Floor – endosteal layer of dura mater that overlies the base of the greater wing of the sphenoid bone.
2 main branches Meningohypophyseal trunk Arises from the posterior genu Dorsal meningeal artery Inferior hypophyseal artery Tentorial artery of Bernasconi-Cassinari Inferolateral trunk Arises from the horizontal segment Marginal tentorial artery
Other branches Mcconnell’s capsular artery Ophthalmic artery Persistent trigeminal artery
Venous connections of Cavernous sinus Orbit – Superior and Inferior ophthalmic Vein Cerebral hemispheres – Middle and Inferior cerebral veins Retina – Central Retinal vein Transverse sinus – SPS Jugular bulb – IPS Dura – Middle meningeal veins Pterygoid venous plexus – emissary veins Facial vein – ophthalmic vein
Intercavernous sinuses Named based on ralationship with pituitary Ant Intercavernous sinus(larger) Post Intercavernous sinus Ant + Post – Circular sinus
Neural relationships 3rd, 4th, V1, V2 & 6 th 6th N is adherent to the lateral surface of the ICA medially Laterally with V1 3rd N pierces the roof in the occulomotor Triangle 4th nerve enters the dura at the posterior edge Of the triangle Occulomotor and trochlear cisterns
Travels through cavernous sinus: Travels through lateral wall of cavernous sinus: Abducens nerve (CN VI) Carotid plexus (post-ganglionic sympathetic nerve fibres ) Internal carotid artery (cavernous portion) Oculomotor nerve (CN III) Trochlear nerve (CN IV) Ophthalmic (V1) and maxillary (V2) branches of the trigeminal nerve
Clinical significance of VascularRelations • Lesion of surgical importance affecting ICA range from aneurysm to carotid-cavernous fistulae. • After removal of anterior clinoid process, mobilization of anterior loop ofICA can be done for clipping of aneurysm. • Treatment of aneurysm ranges from simple observation to balloonocclusion and trapping of the lesion with or without bypass.
Conditions affecting Cavernous sinusand its contents • Midbrain Infection • Cavernous Sinus Thrombosis • Orbital Fracture • Petrous Bone Fracture (Temporal bone Fracture ) • Internal Carotid Artery Aneurysm • Mastoiditis • Increased Intracranial Pressure
Clinical and applied aspects • It is the only anatomic location in the body in which an artery travelscompletely through a venous structure. If the internal carotid arteryruptures within the cavernous sinus, an atriovenousfistula iscreated . • Cavernous sinus syndrome may result from mass effect from atumour or CST and cause opthalmoplegia from compression of theoculomotor nerve, trochlear nerve, and abducens nerve, ophthalmicsensory loss from compression of the ophthalmic nerve, andmaxillary sensory loss from compression of the maxillary nerve. • Cavernous sinus thrombosis is the formation of a blood clot withinthe cavernous sinus.
DEVELOPMENT Padget (1956) Cavernous sinus Plexiform extension of prootic sinus and ventral myelencephalic vein Superior ophthalmic v Primitive maxillary v as it drains into the prootic sinus, and develops into the superior ophthalmic vein which drains directly into the cavernous sinus. 23
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Knosp (1987) 20% of fetal skull bases- SMCV drains into the cavernous sinus 60% of fetal skull bases- SPS and cavernous sinus show a connection Hence developmental basis for varied pattern of venous tributaries and drainage 25
Dangerous area of face Flow of blood in all tributaries & communication are reversible as they possess no valve Spread of infection can lead to thrombosis of Cavernous sinus The cavernous communicate with dangerous area of Face through 2 routes Superior opthalmic vein Deep facial veins , pterygoid plexus of vein, Emissary vein.
Spread of infection to cavernous sinus 1. Infection of the upper lip, vestibule of the nose and eyelids spread by way of the angular, supraorbital and supratrochlear veins to the ophthalmic veins. Commonest route of infection. 2. Intranasal operations on the septum, turbinates or ethmoid / sphenoid sinus infection through the ethmoidal veins.
Spread of infection to cavernous sinus 3. Operations on the tonsil, peritonsillar abscess, surgery or Osteomyelitis of the maxilla, dental extraction and deep Cervical abscess spread by pterygoid plexus or by direct Extension to the internal jugular vein. 4. Involvement of the middle ear and mastoid with lateral sinus Phlebitis or thrombosis retrograde spread through the Petrosal sinuses to the cavernous sinus.
Systemic and local conditions increasing the risk of cerebral venous thrombosis Transient risk factors Infection Central nervous system Ear, sinus, mouth, face, and neck Systemic infectious disease Pregnancy and puerperium Dehydration Mechanical precipitants Head injury Lumbar puncture Neurosurgical procedures Jugular catheter occlusion Drugs Oral contraceptives Hormone replacement therapy Androgens Asparaginase Tamoxifen Glucocorticoids
Systemic and local conditions increasing the risk of cerebral venous thrombosis
Septic cavernous sinus thrombosis Most commonly results from contiguous spread of infection from the nose (50%), sphenoidal or ethmoidal sinuses (30%) and dental infections (10%). • Staphylococcus aureus is the most common - found in 70% of the cases. • Streptococcus is the second leading cause. • Gram-negative rods and anaerobes may also lead to cavernous sinus t hrombosis . • Rarely aspergillus fumigatus and mucormycosis .
Cavernous Sinus thrombosis Characterized by multiple cranial neuropathies Clinical feature - G eneral feature of infection – fever , rigors ,malaise, and severe frontal & Periorbital pain. Unilateral or bilateral exopthalmos & tender eye ball Oedema of eyelid & chemosis of conjuctiva Oculomotor feature – external opthalmoplegia Ptosis Slight exopthalmos Dilated pupil with loss of accomdation reflex
Cavernous Sinus thrombosis • Impairment of ocular motor nerves, horner’s syndrome and Sensory loss of the first or second divisions of the trigeminal n erve in various combination • The pupil may be involved or spared or may appear spared w ith concomitant oculosympathetic involvement.
Occular manifestation of cavernous sinus thrombosis SIGN INVOLVED STRUCTURES Ptosis Edema of upper eye lid, Sympathetic plexus, III cranial nerve Chemosis Thrombosis of superior and inferior ophthalamic vein Proptosis Venous engorgement Sensory loss/ Periorbital pain V cranial nerve Corneal ulcers Corneal exposure due to proptosis Lateral rectus palsy VI cranial nerve Complete ophthalmoplegia CN II, IV, VI Decreased visual acuity or blindness Central retinal artery/ vein occlusion secondary to ICA arteritis, septic emboli, ischemic optic neuropathy
Complication of Cavernous Sinus thrombosis • Intracranial extension of infection may result in meningitis, encephalitis, brain abscess, pituitary infection, and epidural and subdural empyema. • Cortical vein thrombosis can result in hemorrhagic infarction. • Extension of the thrombus to other sinuses can occur.
Imaging of cavernous sinus Cavernous sinus on CT Head
Cavernous sinus on MRI Brain
Cavernous sinus on MRI Brain
Ethmoid and sphenoid sinusitis complicated by cavernous sinus thrombosis and ischemic infarction
Tolosa -Hunt syndrome The tolosa -hunt syndrome is caused by an inflammatory process of unknown etiology . Diagnostic criteria — the specific diagnostic criteria recommended by the international headache society are summarized: ●Unilateral headache, and ●Granulomatous inflammation of the cavernous sinus, superior orbital fissure or orbit, demonstrated by MRI or biopsy, and ●Paresis of one or more of the ipsilateral third, fourth, and/or sixth cranial nerves, and evidence of causation demonstrated by both of the following: •Headache has preceded oculomotor paresis by ≤2 weeks or developed with it •Headache is ipsilateral to the granulomatous inflammation ●Symptoms not better accounted for by an alternative diagnosis
Carotid-cavernous fistulas Acquired rather than congenital vascular malformations, carotid-cavernous fistulas (CCF) may arise spontaneously or from secondary causes
CLASSIFICATION CCFs may be high- or low-flow lesions: ●High-flow CCFs result from a direct connection between the intracavernous carotid artery and the surrounding cavernous sinus. ●Low-flow ccfs represent a subtype of dural fistula resulting from indirect communication between the cavernous sinus and branches of the internal or external carotid artery within the adjacent dura . These are often referred to as cavernous dural fistulas or dural ccfs .
Barrow classification of CCF Type A fistulas are characterized by direct shunting of blood flow from the ICA into the cavernous sinus. Type B and C fistulas are shunts to the cavernous sinus from branches of the ICA and ECA, respectively. Type D fistulas have shunts from both the ICA and ECA simultaneously.