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17.1 Skull Base
Symptoms due to hormonal
deciency—Anterior hypopitu-
itarism (growth hormone deciency, central hypogonadism,
central hypothyroidism and central hypoadrenalism) can result
from larger lesions, such as pituitary macroadenomas, which
typically have a diameter of
more than 10mm. Regardless of
size, anterior hypopituitarism
and diabetes insipidus can result
from lesions affecting the pituitary infundibulum (stalk).
Growth hormone deciency symp-
toms—This causes symptoms like late
growth in children, poor muscle
strength, irritability, weakening of bone
strength and an overall unwell feeling.
TSH deciency symptom—Low TSH
level in body causes symptoms like
fatigue, low energy, sensitivity to cold
temperatures, constipation and weight
gain.
Prolactin deciency symptoms—Low
prolactin level causes symptoms like an
inability to breastfeed after childbirth.
ACTH deciency symptoms—ACTH
deciency causes symptoms like fatigue
and low energy, low blood pressure, low
blood sugar and upset stomach.
Gonadotropins deciency symptoms—
Low levels of gonadotropins cause
symptoms like infertility, decrease in
sex drive, erectile dysfunction and irregular menstrual cycles.
Functional tumours of pitu-
itary gland (microadenoma)
Adrenocorticotropic (ACTH)
hormone secreting tumour—
ACTH secreting tumours of
pituitary present with symptoms
like
461
Accumulation of fat in the upper back and
midsection (moon face) Disproportionate
roundness of the face
Weakness and thinning of the arms and
legs
Elevated blood pressure and blood sugar
levels
Bone deterioration
Acne stretch marks
Bruises
Depression, agitation, or anxiety
Growth hormone-secreting
tumours—The symptoms
depend on a patient’s age.
In children—Excessive growth hormones
may cause the body size and height in
children to increase, which is known as
gigantism.
In adults—Adults present with acromeg-
aly and other symptoms may be exces-
sive growth of soft tissue and bones,
diabetes, hypertension, heart disease,
heavy snoring, carpel tunnel syndrome,
headache, coarse facial features, mis-
aligned teeth, joint pain and increased
body hair.
Prolactin-secreting tumours—
This clinical syndrome may not
be identied until the tumour is
large. The prolactinoma can produce too much prolactin, which
can lower normal levels of sex
hormones, such as testosterone
in men and oestrogen in women.
The prolactinoma presents differently in men and women.
462
In women—Prolactinoma might present
with irregular menstrual periods, lack of
menstrual periods and milky discharge
from the breasts.
In men—Prolactin- producing tumour may
cause male hypogonadism, erectile dysfunction, lowered sperm count, loss of
sex drive and breast growth.
Thyroid-stimulating hormonesecreting tumour—This
tumour is a rare cause of hyperthyroidism (overactive thyroid
disease). Excessive TSH production from this tumour leads
to increased production of thyroid hormone from the thyroid
gland.
Patients with TSH- producing hormone of
pituitary gland may present with weight
loss, rapid or irregular heartbeat, nervousness or irritability, frequent bowel
movements, excessive sweating, high
blood pressure and thin skin. Other
symptoms include loss or decreased
vision/diplopia/and orbitopathy.
Associated symptoms—These
symptoms may be either due to
the spread of the tumour or due
to the involvement of pituitary
gland in systemic disease.
Symptoms due to extension of
pituitary tumour to other
areas—These symptoms are
produced by the involvement of
other parts of the brain and brain
blood vessels, spinal cord and
meninges which cover the brain
and spinal cord, nearby bone,
eyes, lymph nodes, organs such
17 History andExamination ofSkull Base
as the lungs, heart, liver, pancreas, kidneys, ovaries and supra
sellar extension, i.e. vision
problem, headache, etc.
Symptoms due to secondary
involvement of the pituitary gland-
Sarcoidosis patients may exhibit
a range of skin rashes, inammation of the eyes and enlargement of the lacrimal glands.
Patients with Langerhans cell
histiocytosis may be evaluated
for lung or other solid organ
involvement, skin rashes, or
bone lesions that are either painful or asymptomatic.
Patients with pituitary-related
systemic infections may exhibit
systemic symptoms specic to
the infection, such as Whipple’s
disease or tuberculosis.
Patients with incidentally discovered sellar masses may also
be completely asymptomatic but
may have unrelated complaints
such as vertigo or H/O head
injuries.
– Symptoms of sellar lesions of
non-pituitary origin:
Clinical diabetes insipidus at
presentation is highly indicative
of a non-pituitary aetiology of a
sellar or parasellar masses.
Insidious onset and slowly
progressive visual loss—This is
a common presenting complaint
with sellar/parasellar mass of
non-pituitary origin present.
This is owing to the proximity of
the optic nerves, chiasm and
optic tracts to the sella turcica.
In children, craniopharyngiomas
may present with vision problems as a result of optic nerve
compression by the lesion.
Unilateral vision loss—This
may be a common presentation
17.1 Skull Base
463
of lesions located anterior to the
chiasm, such as meningiomas of
the optic nerve sheath.
Homonymous hemianopsia—
This is visual loss on the same
half of both eyes present in
lesions compressing the visual
system more posteriorly along
the optic tract, such as meningiomas or aneurysms.
Bitemporal eld decit—
Lesions within the sella, such as
Rathke’s cleft cysts, can produce the typical bitemporal
eld decit caused by chiasmal
compression from the inferior
side.
Meningiomas and other suprasellar lesions may manifest as
bitemporal eld cuts of the traditional superior chiasmal compression type.
Lesions involving the chiasm,
such as gliomas, may present
with more unusual visual decits such as vision loss, proptosis, nystagmus and other
symptoms, i.e. precocious
puberty.
Tumours causing obstruction of
cerebrospinal uid (CSF) ow
may lead to an increase in intracranial pressure, which may
manifest as transient visual
obscuration.
The presence of cranial nerve
neuropathy at presentation is
suggestive of a non-pituitary
aetiology for a sellar/parasellar
mass, even though the acute
onset of cranial neuropathy frequently follows apoplexy into an
adenoma. Cranial nerve abnormalities are present in 25% of
patients with non-pituitary sellar
or parasellar masses, most frequently affecting cranial nerves
ii, iii, IV, or VI.
Headache—This is often an
important complaint in patients
with large tumours that produce
ventricular dilatation. Other
causes of headache in sellar and
non-sellar lesions are intrasellar
or suprasellar cysts and inammatory disorders of sella that
causes distortion of the diaphragms or irritation of the parasellar dura.
Patients with masses compressing the deep subfrontal region,
including the septa portion of
the anterior third ventricle, may
present with personality
changes and dementia, anos-
mia due to close proximity of
the olfactory tract.
Hypothalamic tumours in children may produce the dience-
phalic syndrome manifest as
wasting, poor development
and sexual immaturity.
Hypothalamic dysfunction in
adults may lead to disruption of
the control of appetite and cause
syndromes of polyphagia and
massive obesity or severe
starvation.
• Symptoms/chief complaints of sellar
and suprasellar tumours and lesions
– Epidermoid cyst—Epidermoid
cyst is a slow-growing epithelial
inclusion cyst that typically occurs
in the fourth and fth decades,
either sellar mass or para sellar
mass. Epidermoid cysts may present with visual disturbance, hypopituitarism, diabetes insipidus and
cranial nerve abnormalities.
– Arachnoid cyst—This is a rare
cystic lesion found in the suprasellar region and may present with
visual symptoms due to compression of the optic nerves, chiasm, or
optic tracts. There may be signs of
increased intracranial pressure, for
464
17 History andExamination ofSkull Base
example, hydrocephalus secondary
to obstruction of the foramina of
Monro.
Suprasellar arachnoid cysts—
They are usually diverticula
from Lilliquist’s membrane and
present with precocious puberty,
gelastic seizure (sudden and
uncontrollable burst of laughter
or giggling) and hydrocephalus.
Sellar (infradiaphragmatic)
arachnoid cyst—It is present
later in life and presents with
visual symptoms and
hypopituitarism.
– Rathke’s cleft cyst—Rathke’s cleft
cysts, a common developmental
pathology in the sellar and suprasellar regions of adults, are rare in
children. They predominantly
affect adults, with a female-to-male
ratio of 2:1 and an average presentation age of 38years. These cysts
originate from remnants of Rathke’s
pouch’s squamous epithelium.
Although typically small, intrasellar and asymptomatic, approximately one-third of Rathke’s cleft
cysts may extend into the suprasellar region. Symptomatic cysts can
compress adjacent structures, leading to headaches and visual abnormalities, commonly visual eld
decits and anterior pituitary dysfunction. Due to stalk compression,
some patients may also exhibit
hyperprolactinemia, while others
may have diabetes insipidus.
– Craniopharyngioma—Apart from
adenomas, craniopharyngiomas are
among the most common types of
pituitary tumours. They typically
manifest at two distinct life stages:
during the rst or second decade
and then again in the fth decade.
Craniopharyngiomas originate
from embryonic squamous cell
remnants of Rathke’s cleft, which
persist after the stomodeal epithelium ascends to the upper portion
anterior lobe of the pituitary gland.
The symptoms of craniopharyngiomas vary depending on the patient’s
age, the tumour’s size and whether
the growth is predominantly intrasellar or suprasellar.
In children—The craniopharyngiomas are often present with
features of
Raised intracranial tension—
headache, nausea and vomiting.
Endocrinologic dysfunction—
Endocrine dysfunction seen in
80% of children with craniopharyngioma, presented either as
growth failure (93% of patients)
or delayed sexual development
(20% of patients).
Visual symptoms—The common visual symptoms of craniopharyngioma are loss of visual
acuity, visual eld decit, or
both.
In adults—Adults affected with
craniopharyngioma can experience various types of anterior
pituitary hormone deciencies.
Gonadotropin deciency is the
most common, although growth
hormone, pituitary-adrenal and
thyroid axes may be affected as
well. Approximately 50% of
patients might exhibit moderately increased prolactin levels
due to hypothalamic-pituitary
stalk compression. Diabetes
insipidus, present in 23% of
patients before surgery, is a signicant marker for lesions not
originating from the pituitary.
Other hypothalamic symptoms
in adults include obesity, drowsiness and either hypothermia or
hyperthermia, with visual
impairments being a more common presentation.
17.1 Skull Base
465
• Symptoms/chief complaints of
suprasellar tumours:
– Chiasmatic/hypothalamic glioma
(4–8%)—Chiasmatic gliomas most
commonly arise in the rst decade
of life and rapidly extend to the
hypothalamus. They present with
visual disturbances, spasmus
nutans (involuntary head and eye
movement in children), early-onset
puberty, diencephalic syndrome
and painless proptosis accompanied by varying levels of visual
loss. These gliomas can also appear
as a hypothalamic mass, leading to
obstructive hydrocephalus at the
level of the foramen of Monro.
– Hypothalamic hamartoma—
Hypothalamic hamartomas are usually small and asymptomatic in the
rst two decades of life. Symptoms
such as hyperphagia, behavioural
problems, gelastic seizures, autonomic dysfunction, lethargy and
precocious puberty may indicate
hyperactivity syndrome in children.
Sessile hamartomas often cause
gelastic seizures, whereas pedunculated hamartomas generally lead to
early puberty.
– PNET—Primitive neuroectoder-
mal tumour (PNET) are infratentorial, midline tumours of the
posterior fossa in children around
1year age but some time seen in the
suprasellar region.
– Suprasellar chordoma—Children
with suprasellar region chordomas,
which are uncommon, may present
with isolated left sixth nerve palsy
without any other neurological
impairment.
– Metastatic Lesions—The tumours
such as medulloblastomas, ependymomas, or germinomas can metastasise in the suprasellar area.
– Clival meningioma with supra-
sellar extension—Clival meningi-
oma with suprasellar extension is a
rare entity in children that can present with headache with intermittent
vomiting, diplopia and sixth nerve
palsy.
– Suprasellar germinoma—Germi-
noma, a tumour of germ cell origin,
frequently seen in children and
adolescents. This tumour presents
with a classical triad of diabetes
insipidus (DI), pan-hypopituitarism
and visual disturbances.
Type I: It arises from the pineal region pri-
marily and metastasises to the third ventricular oor, hypothalamus, pituitary
stalk and visual apparatus.
Type II: It originates from the suprasellar
region similar to type I, but the origin is
from the suprasellar region primarily.
Type III: It develops more inferiorly along
the hypothalamo- neurohypophysial
axis, optic apparatus, stalk and third ventricular oor. These tumours are intrasellar and displace the pituitary gland.
– Langerhans Histiocytosis—This
is presented with central DI, ataxia
and obstructive hydrocephalus.
– Neurohypophysitis—This is more
common in females especially who
have a history of Hashimoto’s thyroiditis, atrophic gastritis, or pernicious anaemia and present with DI.
– Infundibular tumours (lesion of
pituitary stalk)—Infundibular
tumours are divided into congenital, neoplasm and infection
(Table17.4).
• Presentation/chief complaints of
infra-sellar lesions
– Chordoma—Symptoms with
which chordoma presents depend
on the direction of growth of the
tumour.
466
Table 17.4 Pituitary stalk/infundibular lesions
Congenital Inammatory Neoplastic
Ectopic neurohypophysis
Rathke cleft cyst
Pituitary cyst
Neurosarcoidosis, Langerhans histiocytosis
Lymphocytic hypophysitis
Wegener hypophysitis
Neurohypophysis
17 History andExamination ofSkull Base
Craniopharyngioma, Pituitary adenoma
Metastatic lymphoma
Germinoma
Cranial neuropathy—The third,
fourth, or sixth cranial nerves
are involved by chordoma in
approximately one-third of
patients. The nerve involvement
is asymmetric, and most patients
have more than one nerve
involved.
Visual symptoms—Diplopia is
the most common presenting
symptom. Visual eld defects,
when occur, are similar to those
seen with pituitary adenoma.
Headaches—It occurs early.
Neck pain—This is one of the
common presenting complaints
of chordoma.
Symptoms of nasopharyngeal
congestion may be present.
Endocrinologic dysfunction—
The symptoms of endocrine
dysfunction are unusual, but in
some cases, there may be symptoms of anterior pituitary insufciency or mild
hyperprolactinemia may occur.
– Dermoid tumour—This tumour is
commonly found in infants, present
visual disturbance, headache, seizures and chemical meningitis.
– Optic nerve glioma—Optic nerve
gliomas, typically slow-growing
tumours, commonly affect children. About 10% of these tumours
occur within an optic nerve. Onethird of the tumours involve both
the chiasm and optic nerve, another
third mainly affects the chiasm, and
the remaining quarter primarily
involves the hypothalamus. In 55%
of cases, gliomas are multicentric.
Symptoms include afferent pupillary defect, proptosis, retroorbital
pain and progressively deteriorating vision.
– Parasellar meningioma—This is
one of the most frequent tumours in
this space.
• Presentation of infratemporal fossa
tumours
– Types of infratemporal fossa
tumours
Benign—Hemangioma, lipoma,
meningioma, nasopharyngeal
angiobroma and schwannoma
Malignant—Adenoid cystic carcinoma, adenocarcinoma, brosarcoma, hemangiopericytoma,
histiocytosis, Hodgkin’s disease,
osteosarcoma, rhabdomyosarcoma and squamous cell
carcinoma.
– Presentation of infratemporal fossa
tumours
Cheek swelling, nasal obstruction, hemifacial pain and slow
progressive trismus
Hearing loss
• Presentation/chief complaints of lat-
eral skull base tumour
– Vestibular schwannoma and other
tumours of cerebello pontine (CP)
angle—Vestibular schwannoma
usually presents with U/L progressive hearing loss (sensorineural
type), unsteadiness, tinnitus, vertigo and cerebellar symptoms.
– Glomus tumour—Glomus tumour
presents with dysphagia, dizziness,
hearing loss, hearing pulsation in
17.1 Skull Base
467
ear, hoarseness of voice and facial
palsy.
• Presentation of anterior skull base
tumour/lesions
– Aesthesioneuroblastoma (olfac-
tory neuroblastoma)-
Nasal symptoms—Unilateral
nasal mass, anosmia U/L, nasal
bleed, nasal obstruction and
nasal discharge.
Neurological symptoms—
Headache and nausea
Ophthalmological symptoms—
Proptosis, extraocular paralysis
and blindness
Facial—Swelling, pain, anaesthesia, and trismus.
– CSF rhinorrhea—The cerebrospi-
nal uid (CSF) rhinorrhoea occurs
when there is a stula between the
dura and the skull base or a connection between the nasal cavity and
subarachnoid space. It can be traumatic, occurs following head
trauma (fronto-basal skull fractures), as a result of intracranial surgery, or non-traumatic, occurs in
destruction lesions of the skull
base, congenital lesion (meningoencephalocele), spontaneously.
CSF rhinorrhoea presents with various symptoms:
Watery nasal discharge U/L or
B/L
Headache—Postural headache
is a common symptom of intracranial hypotension; it worsens
when in sitting or standing position but relieved on lying down.
H/O—Recurrent meningitis—
This is more frequent in spontaneous CSF rhinorrhoea.
Other symptoms are H/O head
or nasal trauma, diplopia (this is
due to a decrease in intracranial
pressure), anosmia, pulsatile tinnitus, neck pain, dizziness, or
vertigo.
– Juvenile nasopharyngeal angio-
broma
Nasal symptoms—Nasal mass,
epistaxis, U/L or B/L nasal
obstruction and rhinorrhea.
Facial symptoms—Cheek swelling, facial pain, facial deformity,
dropping eye or bulging eye,
change in visual acuity and
facial numbness.
Other symptoms include headache, hearing loss and sleep
apnoea.
4. Examination
(a) General/whole body examination
• Gigantism—Tall stature, macrocephaly, headache, visual changes, hypopituitarism and soft tissue hypertrophy.
• Acromegaly—Enlarged hands and
feet, enlarged facial features including facial bones, lip and nose and
tongue, thickened skin and excessive
sweating
• Proptosis—It is dened as an abnormal protrusion of the eye ball beyond
the boundaries of the bony orbit.
• Hypertension (raised BP)
(b) Systemic examination
• CNS—Sign of raised intracranial
pressure.
(c) Local examination
• Nasal examination
– Nasal mass:
U/L nasal mass arising from
anterior skull base/cribriform
area—Aesthesioneuroblastoma.
Congested/red U/L nasal mass
located posterior part of the
nasal cavity—juvenile nasopharyngeal angiobroma.
U/L nasal mass originates from
middle meatus area—inverted
papilloma.
Polypoidal mass arising from
skull base—encephalocele
– Nasal discharge
Watery—CSF rhinorrhoea
Mucoid—allergic
468
Purulent or mucopurulent—
sinusitis
– Nasal bleeding—It is a sign of JNA,
schwannoma and SCC.
• Orbital examination—papilledema,
chiasmatic/hypothalamic gliomaO/E—fundoscopy, optic pallor, or disc
oedema. Visual acuity might be
reduced, telecanthus
• Ear examination:
– Otoscopy (rising sun sign)—This is
suggestive of glomus jugulare.
– Tuning’s fork test—Type and
degree of hearing loss are noted.
The unilateral sensorineural hearing loss (SNHL) is a sign of CP
angle tumour.
– Redish hue at the centre of TM—
Glomus tympanicus.
• Examination of face
– Facial swelling—This is suggestive
of infratemporal tumour, JNA
extending to cheek.
– Swelling in zygomatic area—
Infratemporal tumour.
• Facial nerve examination—The facial
nerve is examined for its motor and
sensory functions.
• Examination of the eighth cranial
nerve—Tuning’s fork test and vestibular function test to evaluate hearing
and balance.
• Cranial nerve examination
– Paralysis or paresis of the third,
fourth and sixth cranial nerves and
the rst division of the trigeminal
nerve may occur owing to tumoural
involvement in the cavernous sinus.
– Cranial nerve 9th, 10th, 11th and
12th can be involved in
infratemporal fossa tumours and
jugular tumours.
17 History andExamination ofSkull Base
Classication of anterior cranial base
trauma (Fain etal.)
Type I: Involves only the anterior wall of
the frontal sinus.
Type II: Involves the face (craniofacial dis-
junction of the Lefort II type or crush
face) and extends upward to the cranial
base and, in occurrence, to the anterior
wall of the frontal sinus, because of the
facial retrusion.
Type III: Involves the frontal part of the
skull and extends down to the cranial
base.
Type IV: Is a combination of types II and
III.
Type V: Involves only ethmoidal or sphe-
noidal bones. CSF leak is infrequent in
types II, and transitional, if it occurs, but
it often occurs in types III, IV and V
which include in every case a dural tear.
Cavernous sinus thrombosis—cavernous
sinus thrombosis is very rare but a lifethreatening condition presents with:
Severe headache often accompanied by
tearing
Swelling, redness and irritation around one
and both eyes
Dropping eyelids
Inability to move the eye
High fever
Pain and numbness around the face and eye
Fatigue
Vision loss or double vision
Altered mental status from confusion to
coma
H/O sinus, dental and lip infection
17.1 Skull Base
469
Superior orbital ssure syndrome
Ophthalmoplegia—Due to compression
or damage to oculomotor, trochlear and
abducens nerves causes restricted movement of the eyeball.
Ptosis—This is developed due to loss of
oculomotor motor supply to the levator
palpebrae superioris and loss of sympathetic input (third-order postganglionic)
to Muller’s muscle.
Proptosis—Due to decreased tension in
the extraocular muscles with loss of
innervation
Fixed dilated pupil—Due to loss of para-
sympathetic supply to the pupil by the
oculomotor nerve.
Lacrimal hypersecretion and eyelid or
forehead anaesthesia: Due to damage
to branches of the ophthalmic division
of the trigeminal nerve.
Loss of corneal reex—Due to loss of
afferent input from the ophthalmic division of the trigeminal nerve.
Chemosis and bruits in vascular causes:
Due to altered blood ow and vascular
congestion.
Facial trauma patients may concurrent sub-
conjunctival haemorrhage, periorbital
ecchymosis and soft tissue contusion.
Extensive masses in the region of the supe-
rior orbital ssure may be marked by
proptosis, eyelid swelling and chemosis
• Orbital apex syndrome (OAS)—The
orbital apex, located at the posterior
part of the orbit where the four orbital
walls meet, includes the superior
orbital ssure and the optic canal.
The optic canal, situated medially to
the superior orbital ssure, transmits
the meningeal-covered optic nerve
and the ophthalmic artery to the cranial fossa. Both the optic canal’s contents and the middle section of the
superior orbital ssure traverse the
common tendinous ring. The superior
part of the ssure carries the troch-
lear nerve (CNIV), the superior
branch of the ophthalmic vein, the
recurrent meningeal artery, the lacri-
mal nerve (CNV1) and the frontal
nerve (CNV1). Meanwhile, the abdu-
cens nerve (CNVI), the nasociliary
nerve (CN V1) and the superior and
inferior divisions of the oculomotor
nerve pass through the middle por-
tion. The inferior portion transmits the
inferior branch of the ophthalmic vein.
• The causes of orbital apex syndrome
are as follows:
• Inammatory—Sarcoidosis, Churg-
Strauss syndrome, granulomatosis with
polyangiitis, Tolosa hunt syndrome,
giant cell arteritis, orbital inammatory
pseudotumor, thyroid orbitopathy and
IgG4-related orbital myositis.
• Infectious—Most commonly caused by
invasive fungal sinusitis or post-septal
bacterial orbital cellulitis. The causative
agents are fungi (aspergillosis and
mucormycosis), bacteria (Streptomyces,
staphylococcus, actinomycosis, gram-
negative bacilli, anaerobes and myco-
bacterium tuberculosis), spirochete
(Treponema pallidum) and virus—
Herpes zoster.
• Neoplastic—Head neck tumours (naso-
pharyngeal carcinoma (NPC), orbital
adenoid cystic CA), neural tumour (neu-
robroma, meningioma, glioma, ciliary
neurinoma and schwannoma), traumatic
(sino-nasal surgery, orbital surgery,
orbital apex fracture and penetrating
injury).
• Vascular—Carotid cavernous aneu-
rysm, carotid cavernous stula and cav-
ernous sinus thrombosis.
• Other—Mucocele, brous dysplasia
and neurobromatosis.
• Pathophysiology—The orbital apex
syndrome dysfunction of the optic
(continued)
470
17 History andExamination ofSkull Base
nerve, oculomotor (III)nerve, trochlear
(IV)nerve, abducens (VI) nerve and/or
the ophthalmic branch of the trigeminal
nerve (V1) may occur.
• Symptoms/signs—The most common
initial presentations of OAS are visual
loss and ophthalmoplegia with multiple
cranial nerves involvement. The loss of
vision is due to optic nerve, optic disc
oedema, or subsequent optic atrophy
may develop shortly.
• Other ndings are as follows:
– Corneal—Absence of corneal reex
and sensation
– Pupillary—Relative afferent pupil-
lary defect indicating involvement of
optic nerve.
– Periorbital pain, facial pain and
hypoesthesia of forehead.
– Orbital—Proptosis with or without
orbital congestion
– Conjunctival—Chemosis and con-
junctival injection
Tolosa hunt syndrome—It is described as
episodic orbital/periorbital pain associated
with paralysis of one or more of the third,
fourth and sixth cranial nerve. Tolosa hunt
syndrome is usually idiopathic and is
thought to be from non-specic inammation in the region of the cavernous sinus
and/or superior orbital ssure. However,
traumatic injury and tumours can also
cause this syndrome. It is presented as
sharp shooting, stabbing, boring, severe
and intense pain in the orbital or periorbital
area.