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251
transferrin assay is the test of choice because of
its high sensitivity and specicity. Various combinations of planar tomography and CT, contrastenhanced CT cisternography, and radionuclide
cisternography, and, more recently, MR cisternography have been used in the diagnosis of CSF
leak. MRI with NCCT is a very useful and specic diagnostic and localizing technique.
Traumatic CSF rhinorrhea is managed by conservative measures in 70–80% of cases. In cases
of iatrogenic and spontaneous leaks, it is less
likely to heal with conservative measures. It is
currently accepted that endoscopic intranasal
management of CSF rhinorrhea is the preferred
method of surgical repair, with higher success
rates and less morbidity than intracranial surgical
repair. Uncomplicated CSF stula, located at the
posterior wall of frontal sinuses can be repaired
extradurally with osteoplastic frontal sinusotomy.
Intracranial approaches should be reserved for
more complicated CSF rhinorrhea. The timing
for surgery and CSF drainage procedures must be
decided with great care and with a clear strategy.
This chapter reviewed the applied anatomy and
physiology, causes, diagnosis and treatment of
CSF leakage.
7.9.1 Applied Physiology
The total volume of CSF in adults is 90–150ml.
CSF is produced in the choroid plexus and ependyma at a rate of 0.35 ml/min (500 ml/d). It is
absorbed in arachnoid villi, total volume turned
over 3–5 times per day. CSF circulates from the
lateral ventricle to the third ventricle via the
aqueduct of Sylvius. From the third ventricle, the
uid circulates into the fourth ventricle and out
into the subarachnoid space via the foramina of
Magendie and Luschka. After circulating through
the subarachnoid space, CSF is reabsorbed via
arachnoid villi.
CSF consists of a mixture of water, electrolytes (Na+, K+, Mg2+, Ca2+, Cl−, and HCO
cose (60–80% of blood glucose), amino acids
and various proteins (22–38 mg/dL). CSF is
colourless, clear and typically devoid of cells
such as polymorphonuclear cells and mononu-
−
), glu-
3
clear cells (<5/μL). CSF represents the end product of the ultraltration of plasma across epithelial
cells in the choroid plexus lining the ventricles of
the brain. Circulation of CSF is maintained by
the hydrostatic differences between its rate of
production and its rate of absorption. Normal
CSF pressure is approximately 10–15 mmHg,
and elevated pressure constitutes an intracranial
pressure (ICP) greater than 20mmHg.
7.9.2 Applied Anatomy
The most common anatomic sites of spontaneous
cerebrospinal uid (CSF) leaks are the areas of
congenital weakness of the anterior cranial fossa
and areas related to the type of surgery performed. The lateral lamella of the cribriform
plate appears to be involved in approximately
40% of the cases, the frontal sinus in 15%
whereas sella turcica and sphenoid sinus are
involved in 15%. Common sites of injury secondary to endoscopic sinus surgery include the lateral lamella of the cribriform plate and the
posterior ethmoid roof near the anterior and
medial sphenoid wall. Rarely, the leak can originate in the middle or posterior cranial fossa and
can reach the nasal cavity by way of the middle
ear and eustachian tube. These patients typically
present with aural fullness due to a serous middle
ear effusion.
7.9.3 Classication
It is classied by Ommaya etal. (1960) [107]. It
is grossly divided into traumatic, non-traumatic
and congenital types. Both entities can be further
classied:
(A) Traumatic
(i) Non-surgical
(ii) Surgical
(B) Non-traumatic
(i) Normal pressure
(ii) High pressure
(C) Congenital
Traumatic CSF leak can be divided on the
basis of aetiology:
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P. Mittal et al.
(A) Trauma—it is the most common type and
anterior cranial fossa is the most common
site (cribriform and roof of ethmoid). It is
further classied into non-surgical and surgical. Non-surgical (accidental) accounts for
~80% of all CSF leaks result of blunt or penetrating head trauma. 2–3% of major head
trauma results in CSF leaks. CSF leak occurs
in 15–30% of cases of skull base fracture.
Leak may be either immediate (within 48h)
or delayed and in ~95% of cases of delayed
leaks occur within 3 months. Surgical
(Iatrogenic) CSF leak accounts for 16% of
CSF leaks. Endoscopic sinus surgery is the
most common cause (0.5% of ESS cases).
The most common site of injury is the lateral
lamella of the cribriform plate.
(B) Non-traumatic—it is 4% of cases of CSF rhi-
norrhea. It can be further classied into high,
normal pressure leaks. High-pressure leak is
45% of non-traumatic cases. The pathophysiology is persistent high intracranial
pressure (ICP), that leads to remodelling and
thinning of the skull base and creates communication (theorized to be due to ischemia
from compression of vessels). The causes of
high ICP are intracranial tumour growth
(typically pituitary tumours) and hydrocephalus secondary to obstruction of the normal
pathway of CSF uid drainage. Normal pressure leaks are 55% of non-traumatic cases.
The causes are true spontaneous leaks (usually seen in adults). Tumours and other
osteolytic lesions of skull base erodes the
boundary of the nasal and cranial cavity
(nasopharyngeal carcinoma, inverted papilloma, etc.)
(C) Congenital—It may be either increased ICP
or normal ICP. The reason for congenital
CSF leak is the failure of closure of the normal linings which separates the cranial and
nasal cavity. It typically involves the foramen cecum and fonticulus frontalis. The
persistent cricopharyngeal canal creates a
vertical midline defect connecting the middle cranial fossa to the sphenoid. Primary
empty sella syndrome is developed by congenital widening of the diaphragma sella.
7.9.4 Patient Evaluation
Presenting symptoms are clear, watery discharge
from the nose (more on bending forward). The
uid is non-sticky and has a salty taste in the
mouth. Patients are not able to sniff back the
uid. The other presentation is the history of
recurrent meningitis. The history should be
focused on duration, onset, associated symptoms.
History should also include the severity, laterality
and quantity of rhinorrhea. The important questions are history of trauma, symptoms of meningitis, recent sinus surgery or neurosurgery. The
physical examination includes complete ENT
examination, weight and BMI, site of leak by
banding forwards.
7.9.5 Dierential Diagnosis
Autonomic dysfunction, allergic rhinitis, CSF
oto-rhinorrhoea are the differentials for CSF
rhinorrhoea.
7.9.6 Investigations
(A) Bed Side Test
1. Halo or Ring Sign—blood will separate
out from CSF when nasal discharge is
placed on a lter paper (central blood
with clear ring). The ring sign is not specic to bloody CSF. Blood mixed with
water, saline, and other mucus will also
form a ring sign.
2. Reservoir sign—Morning rise showed
gush of CSF leak. It is because of uid
collection in paranasal sinuses.
3. A handkerchief is not stiff when soaked
with CSF uid.
(B) Laboratory Tests
1. Glucose testing—It is a rapid but highly
unreliable test. CSF glucose level is twothird of blood glucose level. Glucose oxidase paper colour is changed with
glucose concentrations of 5+ mg/dL. In
recent trauma, the presence of blood
gives false-positive results. Recent men-
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ingitis or other intracranial infections
cause a lower concentration of glucose in
CSF (false-negative). False-positive
results with lacrimal secretions or nasal
mucus. Negative glucose virtually eliminates a diagnosis of CSF uid.
2. Beta-trace protein—It is also known as
prostaglandin D synthase. It is synthesized primarily in arachnoid cells, oligodendrocytes and choroids plexus (CNS).
It is also found in human testis, heart and
serum. It is not routinely ordered as it
may be altered in many cases like renal
insufciency, multiple sclerosis, cerebral
infarctions and some CNS tumours.
Fluid with a concentration >2.0mg/L is
usually positive for CSF. Concentration
<1.5 mg/L is not likely to contain
CSF. Sensitivity and specicity are not
high as beta-2-transferrin.
3. Beta-2-transferrin—It is currently the
single best test for identifying the presence of CSF [108]. It is a protein produced by neuraminidase in CNS located
only within the CSF, perilymph and
aqueous humour. The assay has a high
sensitivity (94–100%) and specicity
(98–100%). It is rapid and is a noninvasive test and it requires only 0.5cc of
uid. It is stable at room temperature for
approximately 4h, so immediate refrigeration following collection is recommended. Specimen should not be frozen.
If assay facility is available, one can get
results within 3 h. Sensitivity is about
100% with specicity of 95%.
(C) Imaging Studies
1. High-Resolution CT Scans [109]—It is
the imaging modality of choice for identifying a skull base defect associated
with a CSF leak (Fig.7.49). It may demonstrate skull base defects resulting from
accidental or iatrogenic trauma, and
underlying anatomic or developmental
abnormality, or an erosive lesion such as
neoplasm. It should have 1mm cuts with
axial, sagittal and coronal views.
Pneumocephalus on a CT scan may indi-
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Fig. 7.49 CT PNS showing left roof of ethmoid bony
defect post-trauma
cate a dural tear. A deviated crista galli is
a radiological sign supporting primary
CSF rhinorrhea. However, it may reveal
defects in the skull base that do not leak
or are not sites of active leaking, making
the diagnosis more difcult.
2. CT Cisternography—It is more invasive, not very frequently used. Intrathecal
contrast dye is injected and a CT scan is
obtained. It is more accurate especially
those with active leaks (Fig. 7.50).
Sensitivity for detecting leaks drops from
nearly 100% with active leaks to 60%
with intermittent leaks. It may miss cribriform or ethmoid sinus defects. It can be
associated with nausea, headaches and
acute organic psychosyndromes.
3. Magnetic resonance imaging (MRI)—It
is not recommended as a rst-line imaging
modality unless an encephalocele is suspected. It demonstrates soft tissue abnormalities and pooling of CSF (high signal
intensity on T2). It is not good at dening
bony defects, unlike a CT scan. Contrast
helps in the differentiation of sinus inammation from CSF uid. It is more expensive and time-consuming.
4. MR Cisternography—Avoidance of
intrathecal injection of contrast is the key
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Fig. 7.50 CT cisternography showing left lateral lamella
of cribriform plate defect
P. Mittal et al.
I-131, Indium 111) is done and pledgets
placed at areas suspected of leak and
scintigrams of the skull are obtained.
Pledgets are then removed and measured
for radioactive tracer. The test is positive
only with active leak (70% detection
when active, 30–40% in inactive) and it
has poor localization. Radioactive isotope is absorbed into the circulatory system and deposited into normal tissues.
(D) Diagnostic Procedures
Intrathecal injection of Fluorescein dye:
It is good at locating active CSF leaks. After
lumbar puncture or drain placement, 10ml
of CSF is withdrawn and about 0.1 ml of
10% uorescein solution is mixed with
withdrawn CSF. The mixture is then reinjected into the subarachnoid space over
10 min period. In most cases, dye can be
seen without lters. Smaller defects may
require lters or black light (yellow lter on
endoscope, blue on light source). It is important to keep a low concentration of uorescein; high doses can lead to severe side
effects (500+mg) like seizure, pulmonary
edema, coma and death.
Fig. 7.51 MRI cisternography (T2 with Cg) in spontaneous CSF rhinorrhea, defect in left cribriform plate
benet of it. T2-weighted imaging can be
used to detect CSF in the sinonasal cavity
(Fig. 7.51). Pulse sequence can be
designed to enhance the detection probability. As with CT cisternography, falsenegative studies may result in intermittent
leaks. MR cisternography and HRCT of
nose PNS is the most accepted modality
to diagnose the site of leak.
5. Nuclear medicine tests (radionuclide
cisternography)—Intrathecal injection
of radioactive tracers (technetium-99,
7.9.7 Treatment
(A) Medical Therapy
1. Conservative management: It has been
advocated in immediate-onset CSF rhinorrhea following accidental trauma. It
consists of a 7–10 day trial of bed rest
with the head end elevation by 15–30
degrees. The patient should avoid coughing, sneezing, nose-blowing and heavy
weight lifting. Stool softeners should be
used to decrease the strain associated
with bowel movements. 75–80% of traumatic CSF leaks will spontaneously
resolve with this management.
2. Lumbar drain [110]: Lumber drain can
be considered if CSF leak does not resolve
after 5–7 days of conservative management, mainly in large skull defects or iat-
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255
rogenic CSF leaks. Continuous drainage
is recommended over intermittent drainage (prevents spikes in CSF pressure).
The usual rate of drain is 10–15 cc/h.
Risks involve headaches, nausea and emesis, pneumocephalus, infection, coma.
3. Antibiotics: Role is controversial. The
reason for use is to prevent intracranial
infections. Brodie et al. concluded that
there is no signicant difference in the
incidence of meningitis with prophylactic antibiotic therapy [111]. It can be used
in iatrogenic CSF leak following skull
base injuries during FESS.
4. Diuretic: It is utilized in the presence of
a CSF leak with increased ICP [112].
Acetazolamide inhibits the conversion of
water and CO
to bicarbonate and H+.
2
Loss of H+ slows the action of the Na+/
K+ ATPase enzymes that are responsible
for the production of CSF results in
decreased ICP.
(B) Surgical Therapy
1. Intracranial Approach: (mostly done
via frontal craniotomy, rarely middle or
posterior fossa)
The indications include comminuted
skull fractures with displaced fragments
requiring reduction, extensive skull base
fractures associated with intracranial
haemorrhages or contusions that require
craniotomy for treatment [113]. It is also
indicated when co-existing surgically
amenable mass lesion is laying inside the
cranium, more than 3cm cranial defect,
multiple defects, multiple failed endoscopic repairs and when site of leak is not
visible by all investigations. Dural
defects may be closed primarily with or
without the use of grafts which could be
free or pedicled periosteal or dural aps
(Fig. 7.27a), muscle plugs, mobilized
portions of the falx cerebri, fascia grafts
or many commercial grafts. It should be
reinforced with brin glue. Advantages
include direct visualization of defect,
inspection of adjacent cerebral cortex
with a better chance of patching a
defect in the face of increased ICP.
Disadvantages comprise increased morbidity, increased hospital time, injury to
the brain from retraction (haematoma,
seizures, cognitive dysfunction and risk
of permanent anosmia). It is not good for
visualization of the sphenoid sinus.
Failure rates for this approach are 40%
for the rst attempt and 10% overall.
2. Extracranial Approach: It can be fur-
ther divided into external and endoscopic types.
(a) External approach: These proce-
dures are infrequently chosen in current practice, given the high success
rates and low morbidity associated
with the endoscopic approach.
However, they should be part
of every skull base surgeon’s
armamentarium.
• External ethmoidectomy—
Begins with the tarsorrhaphy on
the ipsilateral eye. Incision is
made halfway between the medial
canthus and the midline of the
nose down to the bone. Lateral
elevation of the periosteum
exposes the anterior lacrimal
ridge and the lacrimal fossa. The
lacrimal sac is elevated and
retracted out of the fossa. The
anterior ethmoidal artery which
will be encountered 2–2.5 cm
posterior to the lacrimal crest
should be ligated. The frontoethmoid suture line marks the
level of fovea ethmoidalis (dissection should never be superior
to this line). The posterior
ethmoidal artery is found approximately 1.2 cm posterior to the
anterior ethmoidal artery in the
fronto-ethmoid suture line and
the optic nerve lies 5–6mm posterior to the posterior ethmoidal
artery. A complete dissection of
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the ethmoid labyrinth should be
done and the skull base defect is
then identied.
• Trans-ethmoidal sphenoidot-
omy—First an external ethmoidectomy is carried out as above,
the sphenoid sinus opening is
then identied and enlarged; the
anterior wall of the sinus is
removed to reach the sella region.
• Sublabial-transseptal sphe-
noidotomy—Can be carried out
using sublabial or transnasal incision with exposure of pyriform
aperture and nasal spine is made
free. Left or right septal mucoperichondrial ap is elevated laterally and inferiorly along the nasal
oor in the subperiosteal plane.
The cartilaginous septum is dislocated from the maxillary crest
and the contralateral nasal oor
mucoperiosteal ap is elevated.
The contralateral nasal septum is
not elevated off the cartilage. The
bony–cartilaginous junction is
disarticulated and the opposite
posterior ap is elevated. The
bony septum is removed to
expose the sphenoid rostrum,
which is widely removed via
osteotomies or a drill to expose
the entire sinus.
• Trans-antral approach—It
offers wide access to the anterior
sphenoid, ethmoids, pterygopalatine fossa and maxilla. A gingivobuccal sulcus incision is made to
expose the anterior wall of the
maxilla. The periosteum is elevated superiorly as far as the
infraorbital nerve and canine
fossa osteotomy performed to
enter into the maxillary sinus. The
ethmoidal bone can then be
approached medially and superiorly through the maxilloeth-
moidal angle. When needed, the
pterygopalatine fossa can be
accessed via the posterior wall of
the maxillary sinus.
• Osteoplastic ap—Indicated for
the defect in the posterior table of
the frontal sinus especially if
more than 2 cm and above the
oor and lateral to the lamina
papyracea and is approached via
coronal incision or eyebrow incision (Fig.7.52).
(b) Endoscopic Approach: It is the
most common and successful
approach (90–95% success rate)
[114]. The advantages are better
magnied visualization, angled visualization, no external incisions and
minimized intranasal mucosal injuries. It is of many types:
• Transfrontal approach (Lothrop
or Draf III procedure)—It allows
access to the oor and posterior
wall of the frontal sinus. The
main advantage is it avoids obliteration of the frontal sinus with
the osteoplastic ap. The frontal
sinus outow tract must be preserved to avoid mucocele. It is
not effective for the defects in the
most lateral or superior aspects of
the sinus. It begins by performing
a complete ethmoidectomy followed by identication and dissection of frontal recess with
removal of superior septum and
interfrontal septum.
• Transcribriform approach—
Exposes the medial anterior cranial fossa from the medial aspect
of the middle turbinate to the
olfactory groove (Fig. 7.53).
Posteriorly, it extends to the anterior aspect of the planum sphenoidale. Crita galli is exposed by
removal of the perpedicular plate
of ethmoid bone. Care should be
a
b
c
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257
Fig. 7.52 (a) Incision marking, (b) drilling the outline of
frontal sinus after marking with X-ray templet, (c) anterior frontal sinus wall is elevated, (d) view of frontal
sinus, (e) repair of dural defect with fascia lata and secured
Fig. 7.53 (a) Showing bony defect of left cribriform plate with dura exposed in spontaneous leak (black arrow), (b)
facia lata composite grafting, (c) showing brin glue/dura seal in situ
taken while doing dissection near
the olfactory groove.
• Transfovea approach—For get-
ting access to the lateral aspect of
the anterior cranial fossa. The
with suturing, (f) obliteration of frontal sinuses
(Courtesy—Dr. Hitesh Verma, Associate Professor,
AIIMS, New Delhi, India)
dissection extends from the middle turbinate to the lamina papyracea. The frontal sinus marks the
anterior limit and the sphenoid
marks the posterior limit. In some
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P. Mittal et al.
cases, the middle turbinate is
removed and the transfovea and
transcribriform approaches are
combined.
• Transplanum approach—
Allows exposure of skull base
defects along the planum sphenoidale and those with signicant
involvement of the suprasellar
region. Anterior and posterior
ethmoidectomy is performed
rst, which provides access to the
most anterior aspect of the planum. The anterior seller wall is
taken down to provide posterior
exposure.
• Trans-sellar approach—The
route of choice can be medial or
lateral to middle turbinate for
defects on the sella turcica. It is
part of extended endoscopic procedure for pituitary lesion excision. Complete ethmoidectomy is
followed by the opening of sphenoid sinus ostia. If bilateral
access is needed, the posterior
bony septum and the intersinus
septum can be removed.
• Transpterygoid approach—
First an endoscopic modied
medial maxillectomy is performed. The infraorbital nerve is
then identied and its trajectory
followed. A complete sphenoethmoidectomy is then performed. The crista ethmoidalis is
isolated and the main branch of
the sphenopalatine artery (SPA) is
identied. The pterygopalatine
ganglion which lies posterior to
the SPA should be preserved. The
fat in the pterygopalatine fossa
may be dissected or cauterized
until the pterygoid bones are identied. Anterior wall of the lateral
recess of the sphenoid sinus, pterygoid base is drilled. It is good to
access any defect in the middle
fossa oor that occurs in this
vicinity lateral to the Sternberg
canal and the foramen rotundum.
The key to endoscopic repair of a CSF leak is
good visualization and exposure of the defect. If
an encephalocele is present, it should be cauterized at its stalk with bipolar cautery prior to
reduction into the anterior cranial fossa to prevent intracranial haemorrhage. For good exposure, the surgeon should elevate the surrounding
mucosa to provide 2–5 mm of bone exposure
around the defect. Any mucosa remaining in the
defect should be removed prior to repair to avoid
poor adhesion of graft with bed and to prevent
future mucocele formation.
There are many types of grafts utilized, but it
should be noted that the graft should be roughly
30% larger than the defect to account for postoperative shrinkage. Types of grafting material utilized are cartilage, bone (septum, mastoid tip,
middle turbinate), mucoperichondrium, septal
mucosa, turbinate mucosa and/or bone, fascia
(temporalis, fascia lata), abdominal fat, and pedicled septal or turbinate aps. It should be noted
that pedicled aps tend to tint, fold and contract
when utilized.
7.9.8 Grafting Techniques
1. Overlay technique—a graft is placed directly
over the defect.
2. Underlay technique—the graft is placed
between the dura and bony defect.
3. The combined technique utilizes both under-
lay and overlay grafts.
4. Bathplug technique, where a fat plug with a
specically secured vicryl suture into the
intradural space [115].
In addition to these techniques, we may reinforce the repair with brin glue to provide an
improved seal. The placement of absorbable (gel
foam) and/or non-absorbable packing can further
improve the seal. Non-absorbable pack removal
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259
may lead to the displacement of the graft when
removed. In the face of increased ICP, it is recommended that a multilayered graft be utilized.
The size of the defect also plays a role in the
grafting technique utilized. If the defect is
<2 mm, the type of grafting technique utilized
typically does not make much difference as most
techniques will be successful in repairing the
CSF leak. If the defect is 2–5mm, one must note
whether comminuted bone segments or signicant dural injury is present. If they are not present, the use of an overlay grafting technique is
sufcient. However, if either is present, one
should utilize a composite graft or a separately
harvested bone plus mucosa grafting technique
where the bone is placed in an underlay fashion
while the mucosa is placed in an overlay fashion.
If the defect is >5mm, the repair should be performed with a composite graft or separate bone
plus mucosa grafting technique as described
above. Meningitis (0.3%), brain abscess (0.9%),
subdural haematoma (0.3%), smell disorders
(0.6%), headache (0.3%) are the complications
of endoscopic technique (much lesser than craniotomy) [116].
Postoperative care includes bed rest with the
head of the bed set at 15–30 degrees for 3–5days.
The blood pressure should be maintained at a
normal level. Stool softeners and cough suppressants to prevent straining, coughing. The patients
should be advised to avoid blowing the nose and
any heavy lifting. If a lumbar drain is utilized
postoperatively, it should be left 3–5days with a
maximum drainage of 10–15 cc/h. If nonabsorbable packing is utilized, antibiotics should
be given.
optic nerve whereas indirect optic nerve injury
occurs due to blunt impact to head or face which
further sets a shearing force damaging the optic
nerve or its blood supply. Direct and indirect
injuries both cause mechanical and ischemic
damage to the optic nerve. CT scanning helps in
delineating fractures of bones and is critical for
surgical planning. MRI is superior in delineating
soft tissue involvement. Both corticosteroids and
surgical decompression alone or in combination
helps in improving visual prognosis.
Orbital and Optic Nerve Anatomy [
117]
Optic nerve is 3–4mm in diametre, 35–50mm
in length from retina to optic chiasma. It is basically divided into four segments. The rst segment named as intraocular segment is around
1mm in length. The second segment is intraorbital with 20–30mm length, third and fourth segments are intracanalicular (5–11 mm) and
intracranial (3–16mm), respectively, as depicted
in Fig.
7.54. The optic canal is approximately
6.5 mm in diametre and 8–10 mm in length.
Figure 7.55 depicts relations of intracanalicular
part of the optic nerve. Relations of intraorbital
part of optic nerve are shown in Fig.7.56. Optic
canal contains optic nerve axons, their supportive
glia, the ophthalmic artery and branches of the
carotid sympathetic plexus of the autonomic nervous system. Axons of the optic nerve arise from
the ganglion cell layer of the retina and extend
beyond chiasma and optic tracts just before synapsing in the lateral geniculate body.
7.10 Part J: Optic Nerve Anatomy
andManagement
Orbit is pyramidal in shape with apex posteriorly
and base directed anteriorly. The optic canal rests
in the sphenoid bone and lies at the apex of the
orbit. Optic nerve injury is classically divided
into direct and indirect types. Direct optic nerve
injury is caused by penetrating injuries to the
Intracular
Intraorbital
Intracanalicula
Intracanial
Fig. 7.54 Parts of optic nerve
260
superior
opthalmi
vei
nerve
Opthalmic artery
Opthalmic nerve
Superior rectusTrochlear nerve
Lateral rectus
Optic nerve
rectus
Infratrochlear
nerve
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P. Mittal et al.
Frontal
nerve
c
n
Lateral rectus
Oculomotor
nerve
Fig. 7.55 Relationship of intracanalicular segment of optic nerve
Nasociliary
nerve
Abducens
Levator palpebrae superioris
Superior oblique
Medical rectus
Annulus of zinn
Inferior rectus
Inferior opthalmic vein
Anterior
ethmoidal
artery
and nerve
Fig. 7.56 Relationship of intraorbital part of optic nerve
The optic nerve is surrounded by pia, arachnoid and dura mater in its intraorbital and intracanalicular part which forms the optic sheath. In
the intracanalicular part, the dura is fused to
sphenoid periosteum and at the posterior end of
the optic canal, the optic nerve sheath is fused to
dura lining calvaria. Thus, intracranial part lies in
subarachnoid space. Intraocular optic nerve is
Medical
Opthalmic
artery
supplied by arterial circle of Zinn–Haller with
contributions from posterior ciliary arteries, the
pial arterial network and the peripapillary choroidal vasculature. Perforating branches derived
Posterior ethmoidal artery
and nerve
from the ophthalmic artery supplies intraorbital
part of the optic nerve and intracanalicular part is
supplied by small pial branches from ophthalmic
artery. On the other hand, intracranial part is sup-
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