The document discusses the anatomy of the orbital apex, superior orbital fissure, optic foramen and canal. It describes the structures that pass through each location and clinical presentations of orbital apex syndrome which involves damage to cranial nerves II-VI with optic nerve dysfunction. Common causes include trauma, infection, inflammation and tumors. Examination focuses on visual acuity, eye movements, pupil response and assessment for complications like optic neuropathy.

1. ORBITAL APEX SYNDROME
Dr. Reshma Peter

2. APEX OF ORBIT
• Posterior most end of pyramid shaped orbit
• 4 orbital walls converge here at craniofacial junction
• Complex association b/w bony, neural, and vascular elements
• Has 2 orifices situated in the sphenoid bone
 Optic foramen
 Superior orbital fissure

3. SOF
• bony cleft at orbital apex
•Lies b/w lateral wall and the roof of the orbit with optic strut at its
superomedial margin
•bounded by greater and lesser wing of sphenoid
•the largest communication between orbit and middle cranial
cavity
•It is situated lateral to optic foramen

4. •pear-shaped with a broad base
•long axis extends upward at an angle of 45° from the base
medially to the apex directed superotemporally.
•SOF is divided at the spina recti lateralis by the annulus of
Zinn, the common tendinous origin of the recti muscles.
DIMENSIONS
Length: around 22 mm
Width : 2-3 mm at the apex
7-8 mm at the base

5. • Annulus of zinn encircles the optic foramen and central part of
SOF,dividing it into upper,middle and lower part
• The superior part contains
Trochlear nerve (IV)
Frontal and lacrimal branches
Of the ophthalmic division
Of the trigeminal nerve (V1)
Superior branch of ophthalmic vein
Recurrent branch of the lacrimal
artery(occasionally)

6. The middle part
confined within the tendinous ring
more susceptible to shearing injury during craniofacial trauma
contains
 Superior and inferior branches
of the oculomotor nerve (III)
 Nasociliary nerves (V1)
 Abducens nerve (VI)
 Inferior branch of ophthalmic
vein
 Fibers from the internal carotid
sympathetic plexus

7. Lower part:
• Inferior ophthalmic vein
The inferior venous compartment is given by the confluence
of the SOV and IOV which drain into the cavernous sinus

8. Radiographic enlargement of the superior orbital fissure
may accompany pathologic processes such as
Aneurysms, Meningioma, Choroidoma,pituitary
adenoma and Tumors of the orbital apex

9. •Located within the lesser wing of sphenoid
• It connects the orbit to the middle cranial fossa
•From an anterior view, the entrance to the optic canal is the
most superior and medial structure in the apex.
• Attains adult dimensions by age 3 and is symmetric in most
persons
Optic Foramen

10. • 2 bony roots that connect the lesser wing of the sphenoid
with the body of the sphenoid form the optic canal.
• The inferior root separates the optic canal from SOF and
also is referred to as the optic strut.
• The superior root forms the roof of the optic canal and
separates it from the anterior cranial fossa.
• The body of the sphenoid forms the medial wall of the canal.

11. Optic canal
Optic foramen:
Vertically : 6-6.5mm
horizontally: 4.5-5mm
>7mm : Abnormal
(enlarges in optic nerve
gliomas, Meningiomas)
Optic canal:
length : 8 to 10 mm
width : 5 to 7 mm
lateral wall is shortest
medial wall is longest
Structures passing through it
•Optic nerve and its meningeal
covering
•Ophthalmic artery
•Sympathetic nerves

12. • Each optic canal passes posteromedially at an angle of
approximately 35° to the sagittal
• opens posteriorly into the chiasmatic groove (which
terminates posteriorly at the tuberculum sellae).
• The canal has an intimate relationship to the sphenoid
sinus, and with extensive sinus pneumatization, the optic
canal may become completely surrounded by a posterior
ethmoidal Onodi air cell, the sphenoid sinus, or an aerated
anterior clinoid process.

13. •Throughout its intraorbital and intracanalicular course, the optic
nerve is surrounded by pia mater, arachnoid, and dura mater,
giving the nerve a sheath.
•Thus, optic nerve is a white matter tract of the brain and carries
with it meningeal coverings.
•Within the orbit, the optic nerve is quite mobile however, within
the canal, the optic nerve sheath remains adherent to the
sphenoid periosteum and thus is fixed.
•Optic nerve glioma or Meningioma may lead to unilateral
enlargement of Optic canal, seen on Xrays

14. Inferior orbital fissure
 20-mm bony defect
 Lies between lateral wall and floor of the orbit
 bounded by the :
• sphenoid
• zygomatic
• maxillary
• palatine bones
 Communicates orbit with inf temporal fossa and pterygopalatine
fossa

15. Structures passing through it:
Zygomatic nerve (V2)
 Infraorbital nerve (V2)
Infraorbital artery
 Infraorbital vein
 br from Inferior ophthalmic vein
leading to pterygoid plexus
Max division of trigeminal Nerve
Parasympathetics to lacrimal gland
Orbital Br from pterygopalatine
ganglion

16. Superior orbital fissure syndrome applies to lesions located
immediately anterior to the orbital apex, including the structures
exiting the annulus of Zinn and often those external to the annulus
as multiple cranial nerve palsies may be seen in the absence of
optic nerve pathology.
Features
• ophthalmoplegia,
• upper eyelid ptosis
• nonreactive dilated pupil
• anesthesia over the ipsilateral forehead,
• loss of corneal sensation (and hence loss of corneal reflex
• orbital pain
• Axial proptosis.
• neurotrophic keratopathy]

17. Syndrome Definition
Orbital apex syndrome involves damage to
oculomotor nerve (III)
trochlear nerve (IV)
abducens nerve (VI)
ophthalmic branch of the trigeminal nerve (V1)
with optic nerve (II) dysfunction
The orbital apex syndrome is a SOF syndrome with loss of
vision.
Cavernous sinus syndrome (CSS) may include the features of an
OAS with added involvement of the
maxillary branch of the trigeminal nerve (V2)
oculo-sympathetic fibers
more commonly bilateral

18. Cavernous sinus syndrome
(involvement of cranial nerves III, IV, V1, V2, VI, and periarterial
sympathetic plexus)
•sensory deficits in the maxillary branch of the trigeminal nerve orbital
sympathetic innervation involvement
•Traumatic carotid-cavernous fistula may be present.
•vascular congestion
• proptosis
•Chemosis
•Ophthalmoplegia
•elevated intraocular pressure (IOP)
•vascular bruit
CSF rhinorrhea  in fracture involving the sphenoid sinus, fovea
ethmoidalis, or cribriform plate.

19. • Traumatic optic neuropathy (involvement of cranial
nerve II): The intracanalicular optic nerve may be
damaged by sphenoid fractures
• The firm attachment of the dural sheath to the optic
nerve may make the intracanalicular nerve particularly
susceptible to acceleration or deceleration injuries.

20. • The superior orbital fissure, orbital apex, and cavernous
sinus are all contiguous, and although these terms
define the precise anatomic locations of a disease
process, the etiologies of these syndromes are similar.
• In some instances, patients who have features of a SOFS
may subsequently develop orbital apex and cavernous
sinus pathology.

21. Anterior Syndromes: Total Ophthalmoplegia

22. Posterior Syndromes: Trigeminal Involvement

23. Inflammatory (OID)
1. Thyroid orbitopathy
2. Sarcoidosis
3. Wegeners granulomatosis
4. Giant cell arteritis
5. Orbital inflammatory pseudo tumor
6. Tolosa hunt syndrome
Vascular
1. Carotid cavernous aneurysm
2. Carotid cavernous fistula
3. Cavernous sinus thrombosis
4. Sickle cell anemia
Etiology of Orbital Apex Syndrome

24. Infectious
1. Fungi: Aspergillosis, Mucormycosis
2. Bacteria: Streptococcus spp., Staphylococcus spp.,
Actinomyces spp., Gram-negative bacilli, anaerobes,
Mycobacterium tuberculosis
3. Spirochetes: Treponema pallidum
4. Viruses: Herpes zoster
Traumatic
1. Penetrating injury
2. Non penetrating injury
3. Orbital apex fracture
4. Retained foreign body

25. Iatrogenic
1. Sinonasal surgery
2. Orbital/facial surgery
Neoplastic
1. Head and neck tumors: nasopharyngeal carcinoma, adenoid
cystic carcinoma, squamous cell carcinoma
2. Neural tumors: neurofibroma, meningioma, ciliary neurinoma,
schwannoma, gliomas
3. Metastatic lesions: lung, breast, renal cell, malignant
melanoma
4. Hematologic: Burkitt lymphoma, non-Hodgkin lymphoma,
leukemia
5. Perineural invasion of cutaneous malignancy
Etiology of Orbital Apex Syndrome

26. Clinical Presentation
• Vision Loss
• Uniocular Diplopia
• Ophthalmoplegia
• Periorbital/Facial Pain
• Axial Proptosis
• Ptosis
• Ocular Deviation
• Headache
• Loss of sensations over the face

27. History taking
• h/o blunt orbital trauma
• h/o visual loss- whether at the time of injury or subsequently.
Progressive decrease in vision suggests optic neuropathy due to
hemorrhage into the optic nerve sheath, retrobulbar hematoma,
compression by a bony fragment, or possibly arachnoiditis at the site
of fracture.
• h/o diplopia  binocular misalignment. Diplopia will be worse in the
field of gaze of the paretic muscle.
• h/o ptosis
• Past ophthalmic history- antecedent spectacles, decreased
vision, amblyopia, strabismus, and previous ocular surgery.
• h/o Sensory disturbances in the distribution of V1 and V2

28. Examination
• Initial management in facial injuries assessing the airway
security,hemodynamic stability, and cervical spine integrity.
• An assessment of neurologic status must be made, and head
injuries must be excluded.
• Additional soft tissue and bony injuries of the head and neck
must be sought.
• In patients with suspected orbital apex fractures, the
examination should focus on an assessment for the presence
of following that may demand acute intervention
 an optic neuropathy
 an evolving orbital compartment syndrome, or
 ruptured globe

29. • Visual acuity :including pinhole vision and colour vision of
Each eye must be recorded.
• Confrontation visual fields may be performed at the bedside
prior to more formal perimetric assessment.
• Assessment of pupil responses:
The direct and consensual light responses
An absolute or relative afferent pupil defect or an efferent pupil
defect (as seen in third nerve palsy, ciliary ganglion injury,
and traumatic mydriasis) is recorded.

30. • Assessment of ocular motility:
• Volitional movements are examined at the bedside
• forced ductions and force generation examinations are
undertaken with appropriate topical anesthesia and patient
cooperation.
These assessments help differentiate between ocular motility
disturbance caused by entrapped muscles, intramuscular
hematoma, and nerve damage.
• Assessment of integrity of cranial nerve V: Sensory
disturbances should be sought in the territories of branches of
V1 and V2.

31. Orbital inspection, palpation, and assessment of globe position
•Periocular ecchymosis, edema, and proptosis in trauma
•Orbital hematoma, intraorbital emphysema, and orbital volume
changes with orbital wall fractures all alter the globe position.
•Axial displacement of the globe should be assessed by
exophthalmometry.
•Increased resistance to globe retropulsion is seen with orbital
hemorrhage.

32. • subcutaneous or intraorbital emphysema.-due to Disruption of
the mucosal integrity of the maxillary or ethmoidal sinus
• Orbital rim fractures
• Traumatic telecanthus is seen in naso-orbito-ethmoid (NOE)
fractures and lateral canthal dystopia is seen in displaced
zygomaxillary complex (ZMC) fractures.
• exclude a coexistent globe rupture or injury.
• IOP is recorded.

33. • Anterior segment trauma including corneal injury, hyphema,
iridodialysis, lens dislocation, and posterior segment trauma
including retinal commotio, retinal detachment, choroidal
rupture, and scleral rupture.
• Pharmacologic pupil dilation for fundus examination to
assess optic nerve head perfusion, disc swelling, and
peripapillary hemorrhages.
• In patients with head injuries, pharmacological pupil dilation
should only be undertaken after neurosurgical consultation

34. CT scanning
• In facial trauma and suspected fractures, noncontrast CT
scans - most appropriate initial imaging technique.
• Associated intracranial injury, associated facial fractures, and
intraorbital hematoma may be assessed.
• Axial and coronal views 3-mm cuts review the orbit, and 1-mm
axial cuts may be used to assess the optic canal.

35. • Coexistent cervical injury may preclude direct coronal
projections.
• Reconstructed coronal views may be needed in patients
with neck injury.
• Best images of relationship between the bone and soft
tissues
• Metallic orbital foreign bodies

36. Plain radiography
The orbital apex may be visualized with 2 radiographic projections
AP view for the superior orbital fissure
oblique view for the optic foramen

37. MRI
• The poor resolution of bone on MRI significantly limits its
role in general orbital trauma.
• However, better soft tissue differentiation may be
obtained.
• MRI reveals the abnormal signal indicative of recent
hemorrhage in optic nerve sheath hematoma.
• Associated neurological damage
• Wooden foreign bodies

38. • The best resolution of orbital structures is presently obtained by MRI
using standard T1w or T2w TSE pulse sequences.
• Fat appears hyperintense (bright) on T1w and T2w images, and other
structures, such as vessels, nerves, and muscles, appear darker
(hypointense) than orbital fat.
• Gd-DTPA enhances vascular structures, such as cavernous sinus or
the venous plexus surrounding Meckel’s cave and the hypophysis.
• Fat suppression techniques like STIR with or without contrast
enhancement are especially useful for the diagnosis of retrobulbar
optic neuritis and intraorbital meningiomas.
Townsend ,Clinical application of MRI in ophthalmology., NMR Biomed

39. Newer functional MRI (fMRI) with blood-oxygenation-level-
dependent (BOLD) techniques and fNMR MRI can evaluate retinal
physiology and oxygenation. PET, SPECT, MRS with NAA, DSA
and MRA/MVA with MOTSA can aid in diagnosis.
Although MRI and magnetic resonance angiography may be
helpful in diagnosing intracranial aneurysms or shunts at the
cavernous sinus, the “gold standard” for intracranial vascular
disease is catheter angiography and super selective vessel
exploration.

40. Angiography
Angiography may be considered in patients with
 orbital apex fractures
 with clinical features consistent with a carotid artery
injury, revealing
 carotid artery dissection
 carotid artery spasm
 carotid-cavernous fistula

41. Visual field assessment
• Automated static threshold perimetry (eg, Humphrey
Visual Field analysis) or
• Kinetic perimetry (eg, Goldmann perimetry)
• used in patients with adequate cooperation and fixation
to document visual field disturbance with optic
neuropathy.
• No specific visual field loss pattern is pathognomonic for
traumatic optic neuropathy.

42. Formal color testing
• Dyschromatopsia is expected in optic neuropathy
• It may be formally documented with use of the
Farnsworth-Munsell 100 hue test or the Farnsworth
panel D-15.
• These tests require patient cooperation and may not be
appropriate in the acute setting.

43. Visual-evoked potentials
(VEP)
• may assess the integrity of the visual pathway
• Able to compare pathways from each eye.
• They are a consideration in patients with altered level of
consciousness or in whom bilateral optic neuropathy is
suspected

44. Beta-2 transferrin
a definitive test for CSF rhinorrhea

45. Infections/DM/Tuberculosis/Syphilis/TAO/NSOI/GCA
Vasculitis including SLE, RA, Wegners Granulomatosis,
Sarcoidosis, Anemia Evaluation
Infections, Tuberculosis, HSV, Sarcoidosis, LGBS,
Invasive Aspergillosis, Lymphoproliferative disorders
Granulomas, Mass Lesions, Fractures
Confirmation of Diagnosis

46. Flowchart for OAS Assessment

48. Management of
OAS
Observation
Medical
Management
Surgical
Management
• Infectious:
 Antibiotics
 Antifungals
 Antivirals
• Non Infectious:
 Corticosteroids
 Immunosuppressant
• Spontaneous
resolution under
4 weeks e.g.:
OID, TAO etc.
• Orbitotomies
• Endoscopic
decompression
• Tumor removal/
debulking surgery

49. THANK YOU