Neurosurgery Flashcards

Question 1

Q

What are the bones forming the cranium

Answer

A

8 pieces:

1) Frontal bone
2) Parietal bone x 2
3) Occipital bone
4) Temporal bone x 2
5) Sphenoid bone
6) Ethmoidal bone

Question 2

Q

What are the skull sutures?

Answer

A

*1) Coronal sutures**
divide frontal bone from parietal bone
*2) Sagittal suture**
divide parietal bones in midline
*3) Lambdoid suture**
divide parietal bone/temporal bone from occipital bone
*4) Squamosal suture**
divide temporal bone from parietal and sphenoidal bone
*5) Metopic suture**
divide the frontal bone in midline
completely fuses before 1yo, and will be replaced by bone tissue thus usually not found in adults

Question 3

Q

What are the brain fontanelles?

Answer

A

Brain fontanelles are “soft spots” between the refused cranial bones in infancy. It allow deformity of the skull during birth. Including:

*1) Anterior fontanelle**
diamond shaped, at the junction of coronal and sagittal sutures
closed around 1-2yo
known as “bregma” after closure
*2) Posterior fontanelle**
triangular, at the junction of sagittal and lambdoid sutures
closed around 2-3 months

Question 4

Q

What are the layers of meninges?

Answer

A

Meninges have 3 layers:

*1) Dura mater**
an outer endosteal layer, inner meningeal layer
attached to skull at the cranial sutures
2 layers separate to form dural venous sinuses
*2) Arachnoid mater**
thin, loose layer of meninges
arachnoid granulations (projection of arachnoid at the superior sagittal sinus) reabsorbs CSF
the subarachnoid space extends down the spinal canal terminating at sacrum; contains CSF and major blood vessels
*3) Pia mater**
thin layer of meninges closely related to cortical surface, conforming to the contours of sulci and gyri (except in cerebellum)

Question 5

Q

What are the dural folds?

Answer

A

The cranial vault is divided by 3 reflections of the dura mater (“dural folds”):

*1) Falx Cerebri**
divides the two cerebral hemispheres
attach anteriorly to crista galli, posteriorly to tentorium cerebelli
*2) Tentorium cerebelli**
attach to the anteriorly to the anterior and posterior clinoid processes
separates cerebellum from cerebral hemispheres
*3) Falx cerebelli**
divides the cerebellum along the sagittal plane

Question 6

Q

What are the different cranial fossa?

Answer

A

*1) Anterior cranial fossa**
(Superior view) floor is formed by frontal bone’s orbital plate, the ethmoid bone, and the sphenoid bone
Anterior and lateral boundary: Frontal bone
Posterior boundary: Sphenoidal bone:
sella turcica’s tubercle i.e. tuberculum sellae (medial)
anterior clinoid process
Posterior margin of the lesser wing (lateral)
*2) Middle Cranial Fossa**
(Superior view): floor is formed by the body and greater wing of the sphenoid bone, the squamous part of the temporal bone
Anterior boundary (see posterior boundary of anterior fossa)
Posterior boundary:
sella turcica’s dorsum sellae
crest of the petrous temporal bone
*3) Posterior Cranial Fossa:**
Floor is formed mainly by the occipital bone, with petrous part of temporal bone
Anterior margin: Clivus medially, and petrous part of temporal bone laterally

Question 7

Q

What is the Crista Galli

Answer

A

It is a raise portion of the ethmoid bone (medially located, at the anterior cranial fossa)

It is the anterior attachment of the falx cerebri

Question 8

Q

Foramina of cranial base - Superior view

Answer

A

眼超超圓橢圓轉轉
爛耳Jer
舌大

Two diagonal rows:

*0) Cribiform plate**
olfactory nerve (CN I)
*1) Optic canal**
optic nerve (CN II)
opthalmic artery
*2) Superior orbital fissure (LFT SOV NASO2)**
Superior and inferior opthalmic vein
oculomotor nerve (CN III)
Trochlear nerve (CN IV)
abducens nerve (CN VI)
Lacrimal, frontal, nasociliary branches of opthalmic nerve (V1)
Sympathetic fibres
*3) Foramen rotundum**
Maxillary branch of trigeminal nerve (CN V2)
*4) Foramen ovale (mandy access smallstone)**
Mandibular branch of trigeminal nerve (CN V3)
Accessory meningeal artery
Lesser petrosal nerve
Otic ganglion
Emissary vein
*5) Foramen spinosum (MM,MM)**
Middle Meningeal Artery
Meningeal branch of mandibular nerve (CN V3)
*6) Foramen Lacerum -> Carotid Canal**
Greater petrosal nerve
Internal carotid artery
*7) Internal acoustic meatus**
Facial nerve (CN VII)
Vestibulocochlear nerve (CN VIII)
Labyrinthine arteries
*8) Jugular foramen**
CN IX - XI
Sigmoid sinus
Inferior petrosal sinus
Posterior meningeal artery
*9) Hypoglossal canal**
CN XII
*10) Foramen Magnum**
Medulla oblongata
Meninges
Vertebral arteries
Spinal roots of accessory nerves

Question 9

Q

Foramina of cranial base - inferior view

Answer

A

Difference from superior view:

start with Ovale
Lacerum splits into lacerum and carotid canal
add Stylomastoid foramen
*1) Greater palatine foramen**
greater palatine nerve and vessels
*2) Lesser palatine foramen**
lesser palatine nerve and vessels
*3) Foramen ovale (Mandy access smallstone)**
Mandibular branch of trigeminal nerve (CN V3)
Accessory meningeal nerve
Lesser petrosal nerve
*4) Foramen spinosum**
Middle meningeal artery
Meningeal branch of mandibular nerve (CN V3)
*5) Foramen Lacerum**
Greater petrosal nerve
*6) Carotid canal**
Internal carotid artery, carotid autonomic plexus
*7) Stylomastoid foramen**
facial nerve (CN VII)
*8) Jugular fossa**
CN IX - XI
internal jugular vein
*9) Mastoid foramen**
Posterior meningral artery
*10) Foramen magnum**
Medulla oblongata
Verbetral arteries
Spinal roots of accessory nerves (CN XI)

Question 10

Q

Course of middle meningea artery

What is its clinical significance?

Answer

A

MMA is a branch of maxilary artery (from ECA)
Enters the middle cranial fossa through foramen spinosum
Forms a groove in the inner aspect of temporal bone as it goes up to supply the meninges
*Clinical significance**: Common cause of Extradural Haematoma due to:
Pterion fracture (injury to the anterior division of MMA)
Temporal bone fracture

Question 11

Q

Where is the pterion?

What is the clinical significance?

Answer

A

The pterion is made up of the frontal, temporal, sphenoid, parietal bones, it is where these bones meet. Clinical significance being:

1) the weakest point of the skull
2) Fracture can cause injury of anterior division of MMA, thus extradural haematoma

Question 12

Q

Where is the superior orbital fissure?

What is its contents?

Answer

A

Superior orbital fissure is between the greater and lesser wings of the sphenoidal bone. It contains:

Superior and inferior opthalmic vein
- oculomotor nerve (CN III)
Trochlear nerve (CN IV)
abducens nerve (CN VI)
Lacrimal, frontal, nasociliary branches of opthalmic nerve (V1)
Sympathetic fibres

Arrangements from superior to inferior:
LFT SOV NASO2

Question 13

Q

What structures pass through the foramen rotundum and foramen ovale?

Answer

A

Foramen rotundum:
1) maxillary division of trigeminal nerve (CN V2).

Foramen ovale (Mandy Access smallstone, OVALE)

1) Mandibular division of the trigeminal nerve (CN V3)
2) Accessory meningeal artery
3) Lesser petrosal nerve
4) Otic ganglion
5) Emissary vein

Question 14

Q

What structures run through the jugular foramen?

Answer

A

1) Cranial nerve IX to XI
2) Internal jugular vein
3) Sigmoid sinus, Inferior petrosal sinus

Question 15

Q

Cranial Nerve PE

Answer

A

*CN1**
ask about change in smell
test with coffee, soap etc
*CN2**
Use spectacles
Visual acuity with Snellen’s chart & Finger
Visual field by confrontation test
Pupillary light reflex (if palsy, no direct & consensual with stimulating affected side)
*CN3, 4, 6**
Test pupillary reflex & accomodation reflex; PERRLA (pupils equal, round and reactive to light and accommodation)? Anisocoria?
Any ptosis or nystagmus
Test eye movements
*CN5**
Corneal reflex
Facial sensation (ophthalmic, maxillary, mandibular) ^OMM
Clench teeth to palpate masseter & temporalis
Open jaw to look for ipsilateral jaw deviation (pterygoids)
Jaw jerk (if UMN lesion)
*CN7**
Inspection for facial asymmetry, nasolabial folds
Look up for forehead wrinkles (Frontalis; temporal)
Shut eyes to resist opening (Obicularis oculi; zygomatic)
Show teeth (Levator anguli oris, Zygomatic major and minor, Depressor anguli oris, Buccinator, Risorius)
Puff up chin (Buccinator, obicularis oris)
Clench teeth & depress mouth angle (platysma)
(sensory by taste of anterior 2/3 of tongue)
*CN8**
Occlude one ear and whisper numbers, patient repeats
Rinne’s Test, Weber’s test
*CN9, 10**
Say AHH & observe soft palate (deviates to normal side)
Test for gag reflex
*CN11**
Shrug shoulders to resist force (Trapezius)
Test right SCM by asking patient to turn neck left, vice versa
*CN12**
Look for tongue fasiculation & wasting
Stick out tongue (deviates to lesion side)
Test tongue power through cheek

Question 16

Q

Olfactory nerve

Function and course

Answer

A

Function: special sensory of smell

*Course:**
exits the cranium through cribiform plate of ethmoid bone
nerve endings (olfactory bulbs) lie on epithelial surface

Question 17

Q

Optic nerve

Function and course

Answer

A

Optic nerve (CN II):

Function: Purely special sensory: vision

*Course:**
arises from retina
enters cranium through the optic canal (also passes opthalmic artery and central vein of retina)
two optic nerves meet at optic chiasm in middle cranial fossa
becomes optic tracts and terminates at the lateral geniculate body in the thalamus

Question 18

Q

Match lesion with visual field defect

Answer

A

1 - @ optic nerve
= Monocular loss of vision

2 - @ optic chiasma
= bitemporal hemianopia

3 - @ optic tract
= contralateral homonymous hemianopia

4 - @ temporal lobe optic radiation
= contra upper quadrantic homo hemianopia

5 - @ parietal lobe optic radiation
= contra lower quadrantic homo hemianopia

6 - @ occipital lobe (PCA infarct)
= contra homo hemianopia with macular sparing

7 - @ macula, retina
= Central scotoma

Question 19

Q

Occulomotor nerve

Function and course

Answer

A

Occulomotor nerve

Function:

*1) Somatic Motor**
superior, medial and inferior rectus muscles, inferior oblique muscle, Levator palpebrae superiorus
*2) Parasympathetic**
via ciliary ganglion to supply sphincter pupillae (pupil constriction) and ciliary muscles (lens accomodation)

Course:
- Exits cranium via superior orbital fissure

Question 20

Q

Trochlear nerve and Abducens nerve

(function and course)

Answer

A

Function: Both somatic motor

Trochlear nerve: supply superior oblique (abduct, depress)
Abducens: supply lateral rectus muscle

Course:
- Both exits cranium from superior orbital fissure

Question 21

Q

Ocular motility nerve palsy presentations

Answer

A

Depends on which nerve:

*3rd nerve palsy**
i) down and out (unopposed lateral rectus & superior oblique)
ii) ptosis (dysfunctional levator palpebrae superioris)
iii) mydriasis (dysfunctional pupillary constrictor) -> more common in surgical CN III palsy
*4th nerve palsy (opposite of CN III)**
i) “nasal upshoot”
ii) Dysfunctional depression & abduction (function of superior oblique)
iii) Compensate by “chin down” (for unopposed elevation) & contralateral head tile (unopposed extorsion)
*6th nerve palsy**
i) Esotropia (worse for distance than near) with limited abduction
ii) Compensate by “face turn” to the affected side

Question 22

Q

Occulomotor nerve palsy DDx

Answer

A

Should divide into medical & surgical:

Medical CN3 palsy (pupil sparred)

*1) Microvascular infarction**
e.g. DM, HTN, atherosclerosis

Surgical CN3 palsy (fixed dilated pupils)

*1) PComm artery aneurysm**
compression arising from aneurysm from posterior communicating artery

2) Uncal herniation (temporal lobe)

3) Cavernous sinus syndrome, orbital apex syndrome

*4) Brainstem lesion** (rare)
affecting the oculomotor nuclei and EW nuclei
e.g. midbrain vascular syndromes, multiple sclerosis and tumours

Question 23

Q

Explain pupil involvement in CN III palsy

Answer

A

In occulomotor nerve palsy:

*1) If Isolated pupil involvement (dilated)**
more likely surgical cause (esp compressive lesions)
The fibres of the oculomotor nerve innervating the pupillary constrictor muscle are located superomedially near the nerve surface, thus more prone to nerve damage
*2) If pupil sparring**
more likely medical cause (microvascular infarct)
central fibres of the oculomotor nerve are more vulnerable to microvascular infarction

Question 24

Q

Trochlear nerve palsy DDx

Answer

A

1) Microvascular infarction (e.g. DM, HTN)

2) Congenital anomaly

3) Closed head trauma

4) Cavernous sinus syndrome, orbital apex syndrome

Question 25

Q

Abducens nerve palsy DDx

Answer

A

1) Microvascular infarction (DM, HTN)

*2) Raised ICP e.g. SOL, trauma**
false localising sign, thus ALWAYS check for papilloedema & raised ICP signs

3) Cavernous sinus syndrome, orbital apex syndrome

Question 26

Q

Which cranial nerve most susceptible to damage in closed head injury?

Answer

A

Abducens nerve (CN VI), because:

1) Greatest intra-cranial length
- thus prone to streching

2) The only nerve exiting from the dorsal brainstem
3) Compression against the petrous ligament or the ridge of the petrous temporal bone

Question 27

Q

Trigeminal nerve

Foramen
Function
Branches

Answer

A

Trigeminal nerve has 3 branches (OMM) -> sensation and motor

1) Ophthalmic Branch (V1)

*Foramen**: superior orbital fissure
*Function:**
sensation to skin of forehead, scalp, eyelid, nose, cornea
*Branches:**
suprorbital, supratrochlear, lacrimal, infratrochlear, ethmoidal nerves

2) Maxillary Branch (V2)

*Foramen**: Foramen rotundum
*Function:**
sensation to skin of maxilla, upper lip, maxillary teeth and sinus

3) Mandibular Branch (V3)

*Foramen**: foramen ovale
*Function:**
sensation to skin over lower lip, mandible, anterior 2/3 of tongue
motor function of:
muscles of mastication
anterior belly of digastric, mylohyoid
tensor tympani
tensor veli palatini

Branches: buccal, auriculotemporal, lingual, inferior alveolar nerves

Question 28

Q

Facial Nerve

Function and Course

Answer

A

CN VII

Function:

*1) Motor**
muscle of facial expression (see photo)
posterior belly of digastric, stylohyoid
stapedius
*2) Sensory**
Skin around external auditory meatus, tympanic membrane
sensation to soft palate
taste from anterior 2/3 of tongue
*3) Parasympathetic**
lacrimal glands, nasal glands
submandibular and sublingual glands

Course:

from pons at cerebellopointine angle
enters middle ear via internal auditory meatus; gives 3 branches:
Greater Petrosal Nerve (para to lacrimal -> via pterygopalatine ganglion)
Chorda Tympani (taste to ant 2/3, para to saliva -> via submandibular ganglion)
Nerve to Stapedius
travel along facial canel in petrous temporal bone
then exits via the stylomastoid foramen
enters parotid gland (most superficial) for terminal devisions:
Temporal
Zygomatic
Buccal
Marginal Mandibular
Cervical

Question 29

Q

Unilateral facial weakness (upper face spared)

Answer

A

UMN Lesion (supranuclear lesion or facial nucleus affected):

1) MCA cerebral infarction
2) AICA syndrome (lateral pontine syndrome)
3) Cerebral haemorrhage
4) Lacunar infarction, posterior limb internal capsule
5) Mass lesion

Question 30

Q

Unilateral facial weakness (upper face & lower face)

Answer

A

LMN lesion (i.e. facial nerve palsy):

*Common**
1) Bell’s palsy (idiopathic)

2) Trauma

*Rare**
3) Tumour (e.g. acoustic schwannoma, cholesteatoma)

4) Diabetic mononeuropathy/ microvascular infarction
5) Ramsay Hunt syndrome (type II, caused by HZV in geniculate nucleus)
6) Lyme Disease
7) HIV
8) Sarcoidosis

Question 31

Q

Vesticulocochlear nerve:

1) Function and course
2) what bony fracture may cause this to be damaged?

Answer

A

CN VIII

Function: purely sensory

*1) Vestibular portion**: sensory for orientation and motion.
*2) Cochlear portion**: sensory for hearing

Course:

arises from the cerebellopontine angle
enters the ear via internal auditory meatus
then separates into vesticular and cochlear portions

A fracture of the temporal bone may lead to injury of this nerve

Question 32

Q

How to assess hearing loss?

Answer

A

1) Physical Exam - Rinne and Weber tests
- can be used as screening for unilateral deafness to distinguish between sensorineural and conduction hearing deficits.

2) Formal audiometry should subsequently be performed if there is clinical concern

Question 33

Q

Glossopharyngeal nerve

Function, Course

Answer

A

CN IX

Function:

*1) Motor**
stylopharyngeus, lifting and opening pharynx
*2) Sensory**
Taste and sensation to posterior 1/3 of tongue
Sensation to palate, pharynx (afferent of gag reflex)
*3) Parasympathetic**
Parotid gland (via the otic ganglion)

Course:
- exits via the jugular foramen

Question 34

Q

Vagus nerve

Function and course

Answer

A

Function

*1) Motor**
pallatoglossis of tongue
pharynx, larynx, upper esophagus, palate
*2) Sensation**
skin behind auricle
pharynx, larynx
trachea, bronchi
heart
esophagus, stomach, intestines
*3) Parasympathetic**
smooth muscles of thoracic and abdominal organs

Course:

arises from medulla
exits via jugular foramen
joined by cranial accessory nerve
pass down within carotid sheath, behind and between IJV and common carotid
at the neck, give rise to right RLN that hooks around right subclavian artery
at the thorax, give rise to left RLN that hooks around the aortic arch, also cardiac branches
then travel at left and right of esophagus, enters abdomen via esophageal hiatis (T10)
left vagus nerve becomes anterior vagal trunk, right becomes posterior

Question 35

Q

Accessory nerve

Answer

A

CN XI

*1) Spinal root**
function: purely motor, SCM and trapezius
course: originate from cervical plexus, enter cranium via foramen magnum, leave through jugular foramen
*2) Cranial root**
function: joins the vagus nerve
course: originate from medulla, exits cranium via jugular foramen

Question 36

Q

Hypoglossal nerve

Answer

A

CN XII

*Function: pure motor**
supplies all intrinsic and extrinsic muscles of the tongue, except palatoglossus (PG)
*Course:**
originate from medulla
exits through hypoglossal canal

Question 37

Q

Cluster of cranial nerve signs DDx

Answer

A

1) Brainstem lesions

*2) Orbital Apex Syndrome**
CN II, III, IV, V1, VI
*3) Cavernous sinus syndrome**
CN III, IV, V1, V2, VI
*4) Cerebellopontine angle tumour**
CN V, VII, VIII (+ jugular foramen IX, X, XI)

Question 38

Q

Where do the common carotid arteries originate from?

Answer

A

The right is a branch of the brachiocephalic trunk

The left comes directly off of the aortic arch

Question 39

Q

Course of internal carotid artery

Answer

A

A. Course in Neck:

starts at the bifurcation of common carotid artery (level C4)
origin is dilated, forming the carotid sinus
initially lateral to ECA, then becomes medial and posterior to it
continue travel up with IJV in the carotid sheath
passes under posterior belly of digastric muscle and parotid gland to enter base of skull
no branches in neck

B. Course in Skull

enters cranium via carotid canal (in petrous temporal bone)
tortuous course with six bends (to relieve pressure effect on the delicate cerebral tissue)
enters cavernous sinus (lies in the medial wall), after which it turns back on itself to pass medial to the anterior clinoid process (of the sphenoid bone).
give rise to branches:
Opthalmic artery (forst branch after ICA emerge from cavernous sinus, exits via optic canal) -> supratrochlear and supraorbital branches, central retinal artery
Anterior cerebral artery
Middle cerebral artery
Posterior communicating artery

Question 40

Q

Role of carotid sinus and body

Answer

A

Carotid sinus is the dilated origin of the internal carotid artery at the bifurcation (C4 level). It is richly innervated by the glossopharyngeal nerve (CN IX). Carotid body is the chemoreceptor at the carotid sinus.

Acts as a baroreceptor and chemoreceptor:

if high BP, then vagal mediate to decrease HR, peripheral vasodilation
if high CO2 or low O2, then vagal mediate to increase respiratory rate

Question 41

Q

Course and branches of vertebral artery

Answer

A

Vertebral artery:

originates from the subclavian artery
crosses the apex of the lung
enters the transverse foramina of vertebrae C1-6
enters the cranium via foramen magnum, piercing the dura mater
runs on anterolateral surface of medulla to join with the contralateral vertebral artery
form basilar artery into the circle of Willis

Important branches (actually Basilar artery branches):

1) Anterior spinal artery
2) Posterior spinal artery
3) Anterior and posterior inferior cerebellar artery
4) Superior cerebellar artery
5) Pontine branches
6) Posterior cerebral artery
7) Basilar artery

-> inferior cerebellar arteries also gives off the labyrinthine arteries that supply the inner ear via the internal acoustic meatus

Question 42

Q

What is the course of basilar artery?

Answer

A

Formed from the union of the two vertebral arteries.

It lies on the clivus (part of the cranium at the base of the skull).

Question 43

Q

Draw the circle of Willis.

What is it? Where is it located?

Answer

A

Circle of Willis = anastomosis between the internal carotid arteries anteriorly and the vertebral arteries posteriorly, located within the cranium and forming the major blood supply to the brain.

It is found at the base of the brain in the region of the optic chiasma and the pituitary stalk

Question 44

Q

What is contained within the sella turcica?

Answer

A

The pituitary stalk gives rise to the pituitary gland which sits in the sella turcica in the middle cranial fossa. Note that this is surgically accessible through a transphenoidal approach via the sphenoid sinus

Question 45

Q

Where do berry aneurysms classically form?

Answer

A

At the point at which a cerebral artery branches off the circle of Willis. They can rupture and bleed. They are associated with polycystic kidney disease.

Question 46

Q

Drainage pathway of the brain

Answer

A

2 drainage systems:

*1) Dural sinuses**
drains superficial structures (e.g. cerebral or cerebellar cortex)
*2) Internal cerebral vein**
choroid vein (drains choroid plexus) and thalamostriate vein joins to form internal cerebral vein at the interventricular foramen

Question 47

Q

What are the dural venous sinuses?

Answer

A

These are areas where the outer periosteal layer of the dura mater becomes separated from the inner meningeal layers. These contain venous blood and are lined with endothelium. Examples:

*1) Superior sagittal sinus**
begins anteriorly at the crista galli, then along superior part of falx cerebri
ends in the right transverse sinus
connects many venous lakes with the archnoid granulation (thus filter CSF back to blood)
*2) Inferior saggital sinus**
lies in free margin of falx cerebri
ends into straight sinus to left transverse sinus
*3) Straight sinus**
runs in the junction of the falx cerebri and the tentorium cerebelli
formed by junction of great cerebral vein and inferior saggital sinus
continues into left transverse sinus
*4) Transverse sinus**
in lateral part of tentorium cerebelli, start at internal occipital protuberance
on reaching mastoid temporal bone, it forms the sigmoid sinus
*5) Sigmoid sinus**
emerge through the jugular foramen as IJV

6) Petrosal sinus

7) Cavernous sinus

Question 48

Q

What drains into the right and left transverse sinuses?

Answer

A

The superior sagittal sinus drains into the right transverse sinus.
The inferior sagittal sinus drains into the straight sinus to continue as the left transverse sinus.
The superior petrosal sinus drains into the transverse sinuses, connecting the cavernous sinus

Question 49

Q

Sagittal sinus thrombosus causes

Answer

A

Sagittal sinus thrombosis may arise from:

Skull, nose, face, scalp infections, via diploic or emissary vein connections

Question 50

Q

Are there valves within the dural venous sinuses?

What is the clinical significance?

Answer

A

There are no valves in the sinuses or in the veins which connect to them.

This makes them vulnerable to infection, as bidirectional blood flow is possible.

Question 51

Q

What is petrosal sinus?

Answer

A

There is a superior petrosal sinus and an inferior petrosal sinus. The superior sinus runs in the edge of the tentorium cerebelli and connects the cavernous sinus with the transverse sinus.

The inferior petrosal sinus runs between the occipital bone and the temporal bone, connecting the cavernous sinus and the internal jugular vein.

Question 52

Q

What is the cavernous sinus?

What are the borders of cavernous sinus?

Answer

A

Cavernous sinus is a paired structure found lateral to the body of the sphenoid bone (at the sella turcica)

It has a cavern-like appearance filled with blood. It drains from the superficial middle cerebral, superior and inferior ophthalmic veins and the sphenoparietal sinuses.

Borders:

1) Medial: Sphenoid bone / sphenoid sinus
2) Superior (Roof) and Lateral: Meningeal layer of Dura
3) Inferior (Floor): Endo-osteal layer of Dura
4) Anterior: Superior orbital fissure
5) Posterior: Petrous temporal bone

Question 53

Q

What are the relations (Content, drainage) of cavernous sinus?

Answer

A

Running through it:

1) ICA and CN 6 traverse the sinus
2) CN 3, 4, V1, V2 runs in the lateral wall

*aka “OTOM CAT”**
Lateral (sup to inf): Occulomotor, Trochlear, Opthalmic, Maxillary
Superior (med to lat): Internal Carotid, Abducens

Receives:

*1) Opthalmic veins** (which links pterygoid venous plexus and anterior facial vein)
*2) Superficial Middle Cerebral Vein** (Brain venous drainage)
*3) Sphenoparietal sinus** (dura drainage)

Connection:

*1) Superior petrosal sinus** to Right transverse sinus
*2) Inferior petrosal sinus** to Internal jugular vein

Question 54

Q

What is found in the lateral wall of the cavernous sinus?

Answer

A

The occulomotor nerve (CN III), trochlear nerve (CN IV), the ophthalmic and maxillary branches of the trigeminal nerve (CN V1 and CN V2)

“OTOM CAT”

Question 55

Q

Why can facial infections result in cavernous sinus thrombosis?

Answer

A

*1) Facial infections**
infection may spread through the facial vein
a triangle formed by the upper lip, nose, medial cheek and medial eye that is drained via the inferior ophthalmic vein to the cavernous sinus

2) Deep infection via pterygoid venous plexus around the pterygoid muscles

Question 56

Q

What are the layers of the scalp from superficial to deep?

Answer

A

Skin

Connective tissue (dense)

Aponeurotic layer

Loose areolar connective tissue

Periosteum

Question 57

Q

How does the internal jugular vein form?

Answer

A

From the inferior petrosal sinus and the sigmoid sinus forming the internal jugular vein, this exits the skull through the jugular foramen.

The transverse sinuses drain into the sigmoid sinus which forms an S-shape to pass to the jugular foramen. The inferior petrosal sinus connects and drains the cavernous sinus into the internal jugular vein.

Question 58

Q

Cerebral cortex and lobes

Answer

A

Cerebral cortex is divided into four lobes by 2 major sulci and 2 imaginary lines:

Central sulcus (Rolandic fissure): frontal from parietal
Lateral sulcus (Sylvian fissure): frontal from temporal
Line from parieto-occipital sulcus to pre-occipital notch: parietal from occipital
Line horizontally from posterior end of sylvian fissure: parietal from posterior temporal

Lobes being:

1) Frontal
2) Parietal
3) Temporal
4) Occipital

Question 59

Q

Function of each cerebral lobes

Answer

A

Frontal Lobe

intellectual activity
emotion
voluntary movements (Primary motor cortex at pre-central gyrus)
speech (Broca’s area at inferior frontal gyrus of dominant hemisphere)

Parietal lobe

somatic sensation (primary sensory cortex at post-central gyrus)
integration of sensory stimuli with other information (parietal association cortex)

Temporal Lobe

Hearing (primary auditory cortex at superior temporal gyrus)
Integration of auditory stimuli with other sensory information (temporal association region)

Occipital Lobe
- Vision (visual cortex)

Question 60

Q

What is the corpus callosum?

Answer

A

It is a massive band of white matter that connects the left and right cerebral hemispheres, spanning the length of the longitudinal fissure of the brain

Question 61

Q

Signs of cerebellar dysfunction

Answer

A

1) Ataxia
2) Nystagmus
3) Dysdiadochokinesia
4) Intention tremor

Question 62

Q

How is the cerebellum connected to the brainstem?

Answer

A

Cerebellum connected to brainstem via 3 pairs of cerebellar peduncles:

*1) Superior cerebellar peduncles**
to midbrain
transmits efferent fibres to midbrain and thalamus
*2) Middle cerebellar peduncles**
to pons
relays input from higher centres via pontine nucleus
*3) Inferior cerebellar peduncles**
to medulla
relays input from vesticular nucleus, spinal cord, and inferior olivary nuclei

Question 63

Q

What is the basal ganglia consist of?

What is its physiology and function?

Answer

A

Basal Ganglion:

1) Putamen, globus pallidus (lentiform nucleus)
2) Caudate nucleus
3) Claustrum

Function:

caudate nucleus and putamen receive afferent from cerebral cortex and thalamus
send efferent to globus pallidus
globus pallidus send efferent to thalmus, red nuclei, substantia nigra, reticular formation
for planning and regulation of complex voluntary movements, and learning of motor skills

Question 64

Q

What are the parts of the brainstem?

Answer

A

*1) Midbrain**
formed by two parts: tectum and the paired cerebral peduncles
Internally they are separated by the substantia nigra into the crus cerebri and tegmentum
CN III (from interpeduncular fossa), CN IV
Pineal gland located at dorsal surface, secretes melantonin
*2) Pons**
CN V, CN VI (arises from ventral surface), CN VII, CN VIII
*3) Medulla oblongata**
CN IX, CN X, CN XI, CN XII

Answer 65

A

The midbrain is associated with the accommodation and pupillary light reflexes:

1) Light reflexes

Retina sends signal to optic nerve. Fibres from optic tract enters superior colliculus and syncapse on the pretectal nucleus (no need go through occipital visual cortex)
Fibres pass bilaterally towards the Edinger–Westphal nuclei
parasympathetic fibres (via CN3) then head to the ciliary ganglion and, subsequently, the constrictor pupillae.

2) Accommodation reflex

light on each retina is taken to the occipital lobe via the optic nerve -> optic tract -> optic radiation
Cortico-tectal fibres travel through the superior colliculus and synapse on the pretectal nucleus
Fibres pass bilaterally towards the Edinger–Westphal nuclei
parasympathetic fibres (via CN3) then head to the ciliary ganglion and, subsequently, the ciliary muscles, constrictor pupillae

Answer 66

A

This contains the descending motor fibres i.e. corticospinal and corticobulbar fibres

which control movement through the cranial nerves and in the peripheral nervous system

Answer 67

A

4th ventricle

Answer 68

A

Corneal reflex = involuntary blinking of the eyelids elicited by stimulation of the cornea:

1) Sensory afferents: from the ophthalmic division of the trigeminal nerve (CN V1)
2) It synapse in the trigeminal sensory nucleus in the pons
3) Fibres then travel to the ipsilateral facial motor nucleus in the pons
4) Motor efferents: sent via facial nerve to orbicularis oculi (zygomatic branches)

Answer 69

A

*Descending motor**: The lateral corticospinal (pyramidal) tract decussates at the medullary pyramids.
> controls peripheral muscles (limbs)
*Ascending sensory**: The dorsal column–medial lemniscus pathway
> fine touch, vibration, two-point discrimination, and proprioception

Answer 70

A

The area postrema.

> the permeability allows it to act as the chemoreceptor trigger zone (CTZ) for vomiting
> contact time for blood-borne hormones to interact with neuronal receptors involved in regulation of blood pressure, body fluids

Answer 71

A

Gag reflex:

1) Sensory Afferents: from the pharynx travel in the glossopharyngeal nerve (CN IX)
2) Travels to the nucleus solitarius of the medulla
3) Connections to the nucleus ambiguus of the vagus nerve at medulla
4) Motor efferents: sent via the vagus nerve to the pharyngeal muscles and soft palate.

Answer 72

A

Reticular formation

Answer 73

A

There are four interconnected ventricles.

There is a left and right lateral ventricle (one for each hemisphere), the third ventricle and the fourth ventricle.

Interventricular foramina (of Monro) connects the lateral ventricles to the third ventricle.

Cerebral aqueduct (of Sylvius) connects the third ventricle to the fourth ventricle

Answer 74

A

1) Lateral Ventricles

largest ventricles, lie deep in cerebral hemispheres
Consists of frontal horn, body, occipital horn, temporal horn
Foramen of Monro is inferior to the frontal horns

2) 3rd Ventricle

thin, slit like ventricle
bound laterally by thalamus, inferiorly by hypothalamus

3) 4th Ventricle

diamond shaped ventricle
Anterior wall = pons and medulla
Superior roof = cerebellar hemispheres, superior and inferior medullary vela

Answer 75

A

The foramen of Luschka

Answer 76

A

1) Mechanical shock absorption as cushion

*2) Suspension of brain in fluid**
to reduce effective weight of the brain
prevent curshing of lower portion of brain under its own weight
protection from sudden pressure change
*3) Nutrition & elimination of waste**
delivers glucose to brain
*4) Biochemical homeostasis**
regular ion composition and pH
*5) Immunological**
circulating immunological factors

Answer 77

A

Composition:
Normally crystal clear, containing:

*1) Water
2) Protein, glucose** (less than plasma)
*3) Small amount of white cells
4) Electrolytes**
More Na, Cl and H+ ions than plasma
Less Ca, K than plasma

Volume: around 150ml

Answer 78

A

*Production:**
Around 500ml per day
70% from Choroid plexuses of the lateral, 3rd & 4th ventricles - 30% from directly from vessels lining the ventricular wall
*Circulation:**
lateral to 3rd ventricle via foramina of Monro (interventricular foramina)
3rd to 4th ventricle via aqueduct of Sylvius
4th to subarachnoid space of spinal cord via foramen of Magendie (medial) & 2 foramina of Luschka (lateral)
After going around the spinal cord, it enters the cranial cavity through the foramen magnum, and flows around the brain within the sub-arachnoid space.
*Re-Absorption:**
80% re-absorbed by arachnoid granulations at dural venous sinuses, passively under CSF pressure
20% is absorbed at the spinal nerve roots

Answer 79

A

Blood -brain barrier controls the entry of substances into the extra-cellular fluids of the CNS and the rate of entry. It is formed by:

1) Tight junctions (zona occludens) between the endothelial cells of the cerebral capillaries.

2) Astrocytic foot processes applied to the basal membranes of the cerebral capillaries

Fat crosses easily, with fat soluble drugs (opiate, anaesthetics)
Glucose can also cross
Hydrogen ion do not usually cross

Answer 80

A

It is absent in a few areas:

*1) Median eminence of hypothalamus**
where hypothalamic neurons release hormones into the portal system, in order to act on the anterior pituitary
*2) Posterior pituitary (Neurohypophysis**)
ADH and oxytocin are released by neurons directly into the blood
*3) Circumventricular organs** adjacent to 3rd and 4th ventricles
the area is adjacent to the chemotrigger zone
such as the supraoptic crest, the area postrema and tuber cinerium

Answer 81

A

BBB integrity is affected by: infection, tumours, trauma, and ischaemia.

Answer 82

A

Classified based on communicating or not, and aetiology

COMMUNICATING:

*1) Congenital**
arnold chiari malformation
encephalocele
*2) Acquired**
normal pressure hydrocephalus (60% no known aetiology)
Infective (e.g. meningitis or post-meningitis)
SAH or IVH
Cenous hypertension, sinus thrombosis
Hydrocephalus ex vacuo (due to post stroke volume loss)
over-production e.g. choroid plexus papilloma

NON-COMMUNICATING:

*1) Congenital**
Aqueduct stenosis
Dandy Walker malformation (atresia of foramen of Magendi and Luschka)
Vascular malformation
*2) Acquired**
tumours (e.g. at 3rd ventricle, posterior fossa, pineal region)
aqueductal haematoma
abscess
ventricular scarring

Answer 83

A

Depends on neonate vs adults

Neonates:

Bulging fontanelles
Prominent scalp veins
Sunset eyes (due to CSF pressure over midbrain tectum)
Papilloedema
Disproportionate head growth
Irritability, developmental delay

Adults:

Raised ICP symptoms: headache, nausea, vomiting, drowsiness, papilloedema
Loss of upward gaze
Cognitive impairment, poor concentration

Answer 84

A

Classical triad symptoms of:

1) Dementia
2) Gait ataxia
3) Urinary incontinence

Causes:

1) Mostly idiopathic (60%)
2) Arise insidiously after SAH
3) Arise insidiously after meningitis

Answer 85

A

*1) CT, MRI** to look for:
periventricular oedema
enlargement of temporal horns (>2mm), lateral ventricles, and 3rd ventricles
obliteration of basal cistern and cortical sulci
*2) Cranial USG** in infant
if fontanelles are open

Answer 86

A

Definitive management is by:

A. External Drainage of CSF

*1) Lumbar puncture and lumbar drain**
as temporary CSF drainage until normal circularion/resorption
only be considered in communicating hydrocephalus
avoid over-drainage -> may lead to SDH or cerebellar tonsillar herniation
*2) External Ventricular Drainage (EVD)**
used in acute setting (e.g. SAH) when hydrocephalus is trasient, in order to avoid permanent shunt
used as temporaizing measure if high particulate content of CSF increase risk of early shunt blockage (e.g. protein in post-meningitis, or blood in IVH)
can use to administer intrathecal medication for treatment of ventriculitis

B. Permanent Shunting

*1) VP Shunt (ventriculo peritoneal)**
commonest shunt, from proximal catheter at lateral ventricle, to distal catheter tunneled to the abdomen which is inserted to peritoneal cavity
*2) VA Shunt (ventriculo atrial)**
if VP shunt not preferred (e.g. extensive abd surgery, peritonitis, morbid obesity)
distal catheter inserted via jugular vein to SVC
*3) LP Shunt (lumbo peritoneal)**
only for communicating hydrocephalus

C. Ventriculostomy
1) Endoscopic third ventriculostomy

D. Medical Treatment (only in selected circumstances for temporalizing)

*1) Osmotic diuretics (e.g. mannitol)**
as temporizing measure in acute setting e.g. blocked shunt
*2) Acetazolamide (carbonic anhydrase inhibitor)**
inhibits CSF production
often used in benign intracranial hypertension in neonates, as temporizing measure while the child gains weight prior to shunt procedure

Answer 87

A

1) Obstruction / Blockage
2) Dislodgement / Breakage / Erosion
3) Infection
4) Seizure
5) Overshunting, may cause subdural haematoma

Ventriculo-peritoneal shunt (for hydrocephalus):
6) Abdominal complications e.g. pseudo-cyst

Ventriculo-atrial shunt:

6) Shunt embolism
7) Short catheter length (requires repeated lengthening in growing child)
8) Perforation
9) Pulmonary HTN

Answer 88

A

Adult: normally 10 -15 mmHg

Raised ICP: Elevation of mean CSF pressure above 15mmHg when measured in lateral decubitus position

Answer 89

A

Intracranial content = blood + CSF + Brain

In case of increasing ICP, compensated in this order:

i) venous blood
ii) CSF
iii) brain

Answer 90

A

1) Reduced venous blood volume in brain

2) Decreased CSF volume

+) Infant: separation of sutures, bulging fontanelles

3) Long term: skull bone erosion, brain atrophy

Answer 91

A

This shows the changing nature of the compliance of the intracranial contents with increases in the ICP.

Initially, due to a higher intracranial compliance, a small rise in the volume leads to little rise in the ICP.

At a higher volume, there is an exponential rise in the ICP owing to the contents becoming ‘stiffer’ due to volume overload. The volume at which this ICP decompensation occurs differs among individuals.

Answer 92

A

Cerebral Perfusion Pressure

= Mean arterial pressure - intracranial pressure
= MAP - ICP

Answer 93

A

CBF = CPP/CVR

where CPP = cerebral perfusion pressure

CVR = cerebrovascular resistance (Radius⁴; Length; Viscosity)

Answer 94

A

Between systolic pressures of 50–150mmHg, the cerebral blood flow remains constant owing to local autoregulation of flow.

Auto-regulation achieved by:

*􏲹1) Myogenic response** of the arteriolar smooth muscle cells:
MAP increases -> increase wall tension
> stimulate reactive contraction of the cells
> thus increase cerebral vascular resistance
*2) Vasodilator “Washout”**
if blood flow is increased due to increased MAP
> locally produced vasodilators are washed out
> thus decreased vasodilation
> thus increased cerebral vascular resistance

Factors affecting cerebral blood flow:

*1) Systemic arterial pressure
2) CO2:**
hypercarbia increases CBF due to increase H+
hypocarbia leads to cerebral vasoconstriction
*3) Hypoxia**: causes vasodilation
*4) 􏲹Sympathetic innervation of cerebral vessels**: this has a minor effect on the cerebral flow

Answer 95

A

This is mixed vagal and sympathetic stimulation that occurs in response to an elevated ICP. It leads to the Cushing’s triad:

*1) Hypertension** -> to ensure an adequate cerebral perfusion pressure
*2) Reflex bradycardia
3) Irregular respiration**

Answer 96

A

Initial symptoms:

*1) Headache** worse in morning (meningeal stretching)
*2) Nausea, Vomiting** (brainstem distortion)
*3) Confusion, impaired consciousness**
as ICP increases, there is decreased cerebral blood flow

Signs:

*4) Decrease GCS
5) Cushing’s Reflex at a later stage**
Hypertension
Bradycardia
Irregular respiration
*6) Papilloedema
7) Cranial nerve palsy:**
Unilateral mydriasis (dilated pupils from CN III lesion)
Diplopia (CN VI lesion)

if untreated
- Cerebral ischemia
- Coma
- Brain herniation
- Brainstem compression
- Respiratory arrest
- Certain Death

Answer 97

A

This occurs in raised ICP because the occulomotor nerve is pushed against the free edge of the tentorium and is a sign of impending tentorial herniation (coning).

The fibres that are damaged are the parasympathetics that travel with the third nerve from the Edinger–Westphal nucleus in the midbrain to supply sphincter pupillae, leading to unopposed sympathetic dilatation of the pupil.

Without a CT, in a suspected extradural haematoma, a burr hole would be drilled on the same side as the pupil. However, in some cases the opposite side can be dilated (false localizing sign).

Answer 98

A

Practically, consider the reversible causes first:

Fever
Seizure
Infection
Inadequate sedation
Electrolyte disturbances
Hypercapnia

Based on Monro-Kellie Doctrine:

A. Increased CSF

*1) Hydrocephalus** (obstructive vs communicating, congenital vs acquired)
see hydrocephalus DDx

B. Increased Blood

*2) Intra-cranial bleeding**
Extra-dural, subdural, subarachnoid, intracerebral, intraventricular

3) Hyperaemia

*4) Venous sinus obstruction**
cerebral venous thrombosis
Trauma with fractures overlying sinus

C. Increased Brain

*5) Mass lesions**
Tumour
Infection (cerebral abscess, empyema, tuberculoma, hydatid cyst)
*6) Brain Swelling (Cerebral oedema)**
Cerebral Contusion, Diffuse Axonal Injury
Vasogenic (e.g, SAH, cerebral inschemia)
Metabolic i.e. hyponatremia
Cytotoxic (e.g. encephalitis, meningitis)
Hydrocephalic

Answer 99

A

1) Obliteration of the cortical sulci / basal cistern

2) Midline shift / cerebral herniation from pressure effect

*3) Features of hydrocephalus**
enlargement of the temporal horn >2mm
enlargement of the 3rd ventricle
periventricular oedema

Answer 100

A

1) BP/P, Saturation, respiratory rate, ABG, urine output
2) GCS monitoring if conscious
3) ICP monitoring if unconscious
4) Transcranial Doppler
5) Study of metabolism

Answer 101

A

*Indicated in head trauma patient if:**
No reliable clinical monitoring (e.g. sedation & coma)
GCS less than 8
Abnormal CT
Normal CT, but presence of >2 risk factors
Age >40
SBP <90
Focal neurological deficit (unilateral or bilateral motor posturing)
*Contraindication**
Conscious patient
Coagulopathy

Answer 102

A

A. Invasive methods

*1) Ventricular monitoring (Gold Standard)**
External ventricular drain (EVD) or ventriculostomy
passed into the anterior horn of the lateral ventricle via usually a frontal burr hole
*2) Brain parenchymal ICP transducer (“microsensor”)**
through a cranial access device (usually referred to as ‘a bolt’)
Use when ventricle is too difficult to puncture e.g. too small or having bleeding tendency

3) Subdural catheter: little used now and has been shown to correlate poorly with ‘actual’ ICP

4) Palpation of a craniotomy flap when the bone is left out (obviously not very accurate but can be a useful sign if there is no ICP monitor in situ).

Non-invasive methods
5) Not well validated but transcranial Doppler (TCD) can be used to measure velocities in the middle cerebral artery and derive a ‘pulsatility index’ that may correlate with ICP.

6) Jugular venous O2

Answer 103

A

Two main reasons:

1) A high ICP can lead to cerebral herniation
- may lead to rapid onset of coma, respiratory failure, and death.

􏲹2) A high ICP causes a reduction of the cerebral perfusion pressure (CCP = MAP - ICP)

Answer 104

A

Initial management (to buy time)

*1) Resuscitation (ABC)**
intubation if airway not protected
consider inotropes to maintain MAP to increase CPP (if not traumatic)
*2) Look for reversible causes**, i.e.
fever
seizure (if sedated may need EEG)
infection
hypercapnia
inadequate sedation
*3) Enhanced venous drainage**
avoid neck rotation, remove neck collar (if not indicated)
Head elevation (~30-40º)
*4) Diuretics**
IV 20% mannitol (200ml)
can also consider frusemide
*5) Controlled hyperventilation**
decreases PaCO₂ to ~4.5 kPa, thus causing certain vasoconstriction of cerebral arteries
*6) Controlled hypothermia**
reduce basal metabolic rate
*7) Sedation (Barbiturate coma)**
with phenobarbitol, thiopentone
Decreases Neuronal activities & cerebral metabolism, thus lowering cerebral blood flow and ICP
Monitor EEG
*±8) Dexamethasone**
Reduce cerebral edema for tumour and infection only

Emergency Surgical Managment:

*1) CSF drainage** if hydrocephalus
EVD

2) Decompressive craniectomy
+/-􏰇 evacuation of mass lesions, evacuation of clot

±3) Lobectomy for intractably raised ICP

Answer 105

A

PaCO₂ should be kept around 4.5 kPa

if too low, vasoconstriction will be too pronounced, causing an increase in Cerebrovascular Resistance (CVR), which then greatly decreases the Cerebral Blood Flow, causing greater neurological deficits

Answer 106

A

Note that traumatic brain injury might destroy vasoreactivity:

While normally increasing MAP will reduces ICP while keeping CBF relatively constant;

With vasoreactivity gone, raised MAP will increase CBF and increases the ICP -> therefore don’t raise the MAP!

Answer 107

A

2 classes:

A. Supratentorial Herniation

*1) Transtenorial**:
usually uncal herniation: the uncus of the temporal lobe passes through the tentorial hiatus
but can also be central herniation
*2) Subfalcine / Cingulate**
where the cingulate gyrus herniates beneath the falx cerebri
*3) Transcalvarial** (Fungus)
*4) Tectal**

B. Infra-tentorial Herniation

*5) Reverse transtentorial
6) Tonsillar herniation** (i.e. Coning)
leading to displacement of the medulla and the cerebellar tonsils through foramen magnum. Compression of the respiratory centre leads to respiratory depression

1) Subfalcine/ supra-callosal / Cingulate
4) cerebellar tonsil herniation (coning)
5) transcalvarial/ fungus
6) Central

Answer 108

A

i.e. Transtentorial herniation of uncus of temporal lobe, which will compress the following:

*1) Ipsilateral CN III**
ipsilateral mydriasis
downward outward eye
*2) CN I and retinal vein**
papilloedema
*3) Posterior cerebral artery**
> ipsilateral occipital cortex infarction -> cortical blindness

4) Aqueduct of sylvius -> hydrocephalus

5) Midbrain and pontine infarction and haemorrhage (loss of consciousness, bradycardia, respiration changes, hypertension, may even cause decorticate & decerebrate postures)

6) Contralateral hemiplegia

*7) Kernohan’s notch**
contralateral cerebral peduncle pushed against tentorium -> ipsilateral hemiplegia (false localising sign)

Answer 109

A

i.e. Downward displacement of diencephalon trans-tentorially, causing:

1) Bilateral miosis

2) Cheyne-Stokes respiration

3) Loss of consciousness

Answer 110

A

Displacement of cerebellar tonsils through foramen magnum (aka coneing), causing:

1) Cardiorespiratory arrest (from medulla distortion)

2) Impaired consciousness

3) Decorticate posture (flexed; above red nucleus) –> decerebrate posture (extended, below red nucleus)

Answer 111

A

*1) CN VI Palsy**
long intra-cranial route
may be compressed against the petrous ligament on the ridge of the petrous temporal bone
*2) CN III Palsy**
transtentorial uncal herniation may compress CN III against free edge of tentorium
*3) Kernohan’s notch**
transtentorial uncal herniation may compress contralateral cerebral peduncle pushed against tentorium
thus ipsilateral hemiparersis

Answer 112

A

Motor, Verbal, Eye

M6 = obey command
M5 = localise pain
M4 = withdraw to pain
M3 = abnormal flexion to pain
M2 = extend to pain
M1 = no movement

V5 = Oriented to TPP
V4 = Confused speech
V3 = Inappropriate words
V2 = Incomprehensible sounds
V1 = no speech

E4 = spontaneous eye movement
E3 = open to command
E2 = open to pain
E1 = not open

Answer 113

A

Based on GCS (“3, 4, 5”)

Mild head injury (GCS 13-15)

Moderate head injury (GCS 9-12)

Severe head injury (GCS 3-8)

Answer 114

A

Depends on sensorium:

If orientated = 1 in 6000

If disorientated = 1 in 120

Answer 115

A

*1) Mechanism and timing of trauma**
any safety equipments (e.g. seatbelt, helmet)
*2) Consciousness**
any LOC, any confusion

3) Any Seizure

4) Symptoms of elevated ICP (headache, N, V)

5) Neurological deficits

Answer 116

A

Low threshold in head trauma:

1) Any drop in GCS
2) Seizure, focal neurological deficits
3) Penetrating skull injury, skull fracture
4) Known coagulopathy

Answer 117

A

A. ATLS, stablisation of patient

*1) ABC, primary survey**
may require intubation and ventilation
*2) Secondary survey**

B. Evaluation and investigations

*3) Bloods tests and CT Brain** for severity of primary brain injury
low threshold for repeated imaging

C. Temporary management of any high ICP

*4) Mechanical method**, look for reversible causes
*5) Hyperventilation
6) Hypothermia
7) Diuretics, barbituate coma**

D. Other managment

*8) Seizure prophylaxis
9) Stress ulcer prophylaxis
10) Optimise nutrition
11) Manage hyperthermia**
due to hypothalamic dysfunction or infection
*12) Manage hyponatremia** with careful fluid and electrolyte balance
HypoNa is common due to SIADH, stress response to trauma with Na & water retention, and overhydration

D. Early liasion with neurosurgical unit and ICU

E. Definitive surgical management if needed

Answer 118

A

A. Acute / Short term

*1) Scalp laceration
2) Skull fracture, base of skull fracture
3) Brain contusion, diffuse axonal injury
4) ICH** (EDH, SDH, SAH)
*5)􏲸 Meningitis and brain abscess**: if there is an open communication

􏲹B. Chronic / Longer term
1) Epilepsy: especially common in the situation of a depressed fracture, intracranial haematoma or prolonged amnesia

2) Hydrocephalus: caused by obstruction from an intraventricular haemorrhage

3) Chronic subdural haematoma: may cause symptoms from a chronic elevation of the ICP, and managed by surgical evacuation

*􏲸4) Cognitive symptoms**:
post traumatic amnesia
post concussion syndrome e.g. persisting headaches, dizziness and poor concentration

Answer 119

A

*Presentation:**
Usually post head injury
Classical lucid interval
Symptoms of raised ICP
*Anatomy:**
break of the temporal bone -> bleeding from the middle meningeal artery
not necessarily associated with cortical damage if evacuated in a timely manner
*CT findings:**
Convex, len-shaped haematoma
Does not cross sutures (because EDH strip pericranial dura away from skull), can cross tentorium
Often associated skull fracture
Coup lesion, may have countrecoup subdural
Midline shift if large

Answer 120

A

*0) Management of traumatic head injury** first
ATLS, resuscitation
management of raised ICP

Definitive treatment:

*1) Acute craniotomy + Clot evacuation**
not necessarily associated with cortical damage if evacuated in a timely manner

Answer 121

A

SDH:

*Presentation:**
usually post traumatic injury
*Anatomy:**
due to tearing of dural bridging veins; thus especially in elderly with brain atrophy
indicates underlying cortical damage (mass effect increases ICP)

CT findings:
- crescentic haematoma
- can cross suture lines, does not cross tentorium
- flattens the sulci
- mass effect, midline shift, significant oedema
- Density depends on timing:
> swirling lucency if active bleeding
> hyperdense if acute (<1 week)
> isodense if sub-acute (1-3 week)
> hypodense if chronic (>3 weeks)

Answer 122

A

*0) Management of traumatic head injury first**
ATLS, resuscitation
management of raised ICP

Definitive treatment:

*1) Acute craniotomy + Clot evacuation**
if acute SDH and midline shift >1cm

2) Burrhole if chronic SDH

Answer 123

A

Brain Contusion

*1) Presentation**
from traumatic head injury
delayed drop in GCS due to evolution of haematoma
raised ICP Sx
*2) Mechanism**:
mechanism often from rapid deceleration of the brain against the inside of the cranium
*3) CT findings**:
coup countre-coup is common
Bifrontal contusions is common
Initial CT: maybe normal, under-estimate the eventual size of contusion
24-48 hour CT: new and larging lesion, “salt and pepper” appearance

==> therefore repeat CT is low threshold

Answer 124

A

Diffuse axonal injury

*Mechanism:**
high energy impact/deceleration
> causing shearing of the white matter against the grey matter, thus significant fibre disruption
> parenchymal disruption, thus generalised cerebral oedema, increased ICP
*Presentation**
after traumatic head injury (usually high energy)
may have prolonged coma
poor prognosis
*Radiological Findings:**
CT often initially normal
Need MRI to note petechial haemorrhage

Answer 125

A

1) Battle’s sign, haemotympanum

2) CSF otorrhoea

*3) CSF rhinorrhoea**
due to mastoid fracture, but intact eardrum therefore CSF flow to nose through Eustachian tube
*4) Racoon eyes**
indicates skull fracture over anterior cranial fossa
NEVER put in a Ryle’s tube through nose, or else go to brainstem

Answer 126

A

1) CN palsy: 1, 2, 6, 7, 8

2) CSF leakage, meningitis

3) Traumatic aneurysm

4) Carotid-cavernous fistula (delayed presentation, swollen red eye)

Answer 127

A

*1) Conservative management**
Bedrest for 5-7 days
CSF leak usually spontaneously resolve within 2 weeks

2) Consider prophylactic antibiotics in some units

3) Operative repair in some cases

Answer 128

A

Burr holes are used for procedures that require limited intracranial access:

*1) Immediate Relief of acute EDH or SDH**
before performing a formal craniotomt + clot evacuation

2) Treatment of chronic SDH

*3) Placement of ventriculostomy catheter**
e.g. external ventricular drain

4) Placement of intra-parenchymal ICP monitor

5) Access for some stereotactic neurosurgery, including brain biopsy for tumour pathology

Answer 129

A

Principles of burr hole placement:

i) away from major venous sinuses
ii) away from air sinuses
iii) not overlying eloquent brain.

The following are common sites for placement:

*1) Frontal**
midpupillary line
1 inch behind anterior hair line
to avoid the primary motor cortex
*2) Parietal**
overlying the parietal eminence
*3) Temporal**
1 inch anterior and superior to external auditory meatus
commonly used in the case of an acute extradural haematoma

4) Occipital

Answer 130

A

Classical technique being:

1) Position patient on horseshoe head cushion
2) Check side on CT, which must be displayed in theatre
3) Shave scalp and prepare it with alcohol solution
4) Prepare skin and drape having marked midline and incision. Drape as if for a craniotomy. Plan incision so that trauma flap could be raised if necessary.
5) Incision down to bone approximately 4 cm in length
6) Use periosteal elevator to scrape back periosteum
7) Insert small self-retaining retractor – this should stop all skin edge and galeal bleeding
8) Use the perforator attached to a Hudson brace to perforate the outer table of the skull. Continue using the instrument until the inner table has just been perforated and a small amount of shiny dura can be seen. A conical hole should be the result (in the case of an extradural, at this stage dark clot and altered blood should be expressed)
9) Swap the perforator for the burr and widen the hole to its base without damaging the underlying dura
10) If subdural access is needed, score the dura with a no. 15 blade and pick up with a dural hook. Cut onto the dural hook to fashion a cruciate opening of the dura
11) Use monopolar diathermy to coagulate dural leaves
12) Closure: 2/0 Vicryl to galea and clips or 3/0 nylon to skin.

Answer 131

A

*1) Bleeding**
Extradural bleeding
Scalp bleeding
*2) Infection**
ventriculitis
subdural empyema
wound infection

3) ‘Plunging’ and damage of underlying structures

4) Venous sinus damage and possible air embolism

5) CSF leak possible if dura opened.

Answer 132

A

*Presentation PE:**
1) “Worst headache of my life”
2) Sudden, transient loss of consciousness
3) Vomiting (common).
4) Meningism (nuchal rigidity, photophobia, Kernig)
5) Retinal hemorrhages
*Ix:**
1) CT shows blood in basal cistern (star of David sign)
2) LP showing Xanthochromia (yellow color from RBC lysis); sometimes blood in CSF
3) Cerebral angiogram (DSA CTA MRA) confirming

Answer 133

A

Symptoms:

*1) Thunderclap headache**
sudden severe
*2) Altered consciousness level
3) Meningism**
neck stiffness
photophibia, phonophobia

Signs:

1) Decreased GCS
2) Neck stiffness, Kernig sign
3) Focal neurological signs

Answer 134

A

Most common two causes:
1) Traumatic SAH

2) Ruptured saccular (berry) aneurysms (associated with PCKD)

Others:

*3) AVM
4) Brain tumour bleeding
5) Paramesencephalic SAH**
blood is purely located around the midbrain with unknown origin

Answer 135

A

Associated with PCKD; found @ bifurcations of Circle of Willis:

1) A Comm artery & Ant cerebral artery
2) P Comm artery & internal carotid artery
3) Bifurcation of MCA

Answer 136

A

*1) Routine Bloods**
esp CBC, clotting profile

2) CT Brain, consider CT angiogram

*3) Lumbar puncture for Xanthochromia**
if CTB negative, but still clinically suspicious
due to breakdown products of Hb in the CSF
*4) Consider a formal catheter digital subtraction angiogram (DSA)**
both diagnostic and therapeutic

Answer 137

A

*0) Supportive managment**
if traumatic then ABC, ATLS
admit to acute stroke unit, neurosurgical unit
close monitoring, regular neuro obs

1) Flat bed rest

*2) Triple H therapy**
hypertension
hypervolemia (3L IVF over 24 hours)
haemodilution
*3) Ca channel blocker (nimodipine)**
60mg Q4H for 21 days
if aneurysmal SAH, in order to prevent vasospasm

4) Prophylactic anti-convulsants

*5) Early neurosurgery** if aneurysm bleeding
microsurgical clipping
endovascular coiling
endovascular stenting with Flow-diverters

Answer 138

A

1) Re-rupture and re-bleeding

*2) Vasospasm** (Peaks Day 7-10)
presents with altered neurological and new neurological Sx and signs
causing delayed cerebral ischemia

3) Hydrocephalus (secondary from blockade by hematoma)

4) Seizure

5) SIADH

Answer 139

A

“SAH”

1) Nimodipine ^{<span>S</span>ea = fish = nimo}

2) Angioplasty & intra-arterial papaverine

*3) Triple H therapy**
Hypervolemia
Hypertension -> may require vasopressor to induce SBP >180
Hemodilution

Answer 140

A

*World Federation of Neurological Surgeons (NFNS) Grades**
based on GCS and focal neurological signs

1 = GCS 15, no focal neurological deficits

2 = GCS 13-14, no focal neurological deficits

3 = GCS 13-14, focal neurological deficits

4 = GCS 7-12, yes or no focal neurological deficits

5 = GCS <7, yes or no focal neurological deficits

*Fisher Grading**
based on CT appearance

1: no evidence of SAH
2: <1mm thick
3: >1mm thick
4: any thickness, but with IVH or parenchymal extension

Answer 141

A

1) Rupture, causing SAH

*2) Mass effect**
Oculomotor palsy (P Com Aneurysm)
Visual loss (Opthalmic artery aneurysm)

3) Thrombo-embolism

Answer 142

A

The most common causes being:

*1) Hypertension & Atherosclerotic disease**
giving rise to Charcot-Couchard aneurysms at smaller terminal arteries

Others:

3) Aneurysm
4) AVM
5) Brain tumour bleeding
6) Trauma
7) Coagulopathy
8) Amyloid angiopathy

Answer 143

A

*1) Basal ganglia** (66%)
Putamen (dilated pupils)
*2) Pons** (10%)
pinpoint pupils

3) Cerebellum (10%)

4) Other areas
* *- brainstem
- thalamus** (poorly reactive pupils)
* *- lobar or cortical**

Answer 144

A

Meningism indicates menigeal irritation, presentation with:

1) Headache
2) Nuchal rigidity
3) Photophobia

DDx:

*1) Meningitis
2) Subarachnoid haemorrhage**

Answer 145

A

*0) Supportive management, ABC**
admission to acute stroke unit, ABC, etc…
NPO, IV fluid
treat fever, correct hypergly with insulin
Neuro-obs
*1) Management of HTN**
IV calcium channel blockers (eg, nicardipine) and β-blockers (eg, labetalol)
*2) Reversal of coagulopathy**
IV vitamin K1 10mg (if warfarin)
Consider prothrombin complex concentrates (PCC); if not available then give FFP

3) Management of raised ICP if any

±Neurosurgical Intervention (depends)

4) Urgent surgical evacuation in:

Cerebellar ICH, due to high morbidity from rapid development of brainstem compression
Selected large lobar ICH or temporal lobe ICH

5) Conservative treatment in:

thalamic or brainstem ICH, due to high mortality with no survival benefit
Most supratentorial ICH, due to no benefit

Answer 146

A

Based on locations:
1) Leptomeninges: meningitis

2) Brain parenchyma: encephalitis
3) Spinal cord: myelitis
4) Pus inside: Brain abscess, Spinal cord abscess
5) Pus outside: Epidural empyema, subdural empyema

Answer 147

A

1) Neurons don’t regenerate - permanent neurological dysfunction
2) Little space in cranium -> mass effect & cerebral oedema prominently cause damage & herniation
3) Meninges damage will lead to hydrocephalus
4) Antibiotics penetration against BBB is often low

Answer 148

A

*1) CNS infection Symptoms & Signs**
meningism (photophobia, nuchal rigidity, headache)
encephalitis signs (altered consciousness, seizures)
raised ICP (morning headache, nausea & vomiting)
other focal neurological signs e.g. sensory, motor disturbances, seizures
*2) Previous or current symptoms suggestive of other foci of infection**
skin rash (purpuric rash if meningococcal)
URTI & diarrhoea common if meningococcal
pneumonia, sinusitis
infective endocarditis
*3) Past medical history**
any chronic infection esp TB
any immunization
any connective tissue disorders
*4) TOCC**
travel history
occupational risk with pigs -> strep suis
mosquito bite (Dengue fever, Zika virus, Japanese B encephalitis)

Answer 149

A

Blood Investigations:

*1) CBC for leukocytosis, ESR
2) LFT, RFT, blood glucose for baseline
3) Clotting profile** to guide LP
*4) Blood culture x2**
for smear & culture, viral serology, PCR
before initiating antibiotics (start antibiotics ± dexamethasone after taking blood)

CNS investigations:

*4) CT head** to r/o mass effect, note hydrocephalus
*5) Lumbar puncture**
for CSF gram smear and culture, antigen detection
CSF analysis
note opening pressure

6) EEG if seizure

Septic workup:

*7) CXR, Echocardiogram, ENT exam
8) Skull X-ray, sinus, mastoid**if suspect mastoiditis etc.
*9) Sputum, NPA, throat swab, urine, stool** for culture & viral studies

Answer 150

A

1) Pyogenic Meningitis

*- Neisseia meningitidis
Streptococcus pneumoniae (esp in elderly)**
(Strep suis if pigs)
(E coli, GBS, HI in neonates)
(HI, NM, SP in children)

2) Chronic Meningitis

*- Tuberculosis
Cryptococcal neoformans**

Answer 151

A

*1) Local transmissino from nearby structures**
nasopharyngeal infection, middle ear, sinusitis
osteomyelitis
*2) Penetrating wound**
Direct spread via skull or meningeal defect (e.g. open skull fracture)
Iatrogenic post-neurosurgery
*3) Hematogenous spread in septicemia**
e.g. IE, lung abscess, pneumonia

Answer 152

A

Acute or insidious onset of:

1) Fever, chills & rigor
2) Headache, N+V+
3) Meningism: Photophobia,*Nuchal rigidity
4) Confusion, decrease GCS
5) Focal neurological deficits
*±) If Meningococcal**
purpuric rash
prodrome of URTI, diarrhoea
*±) If Streptococcal Suis**
pig and pork product contact
early permanent deafness from cochlear damage

Answer 153

A

*1) General Examination**
fever
purpuric rash?
*2) Neurological exam**
focal neurological signs as Cx of meningitis
*3) Meningism signs** (See pic)
Kernig sign: cannot full passive extension of knee when hip knee flexed 90-90
Brudzinski sign: passive neck flexion will cause hip knee flexion
*4) Fundoscopy**
for papilloedema in case of raised ICP

Answer 154

A

Mainly in pyogenic and chronic meningitis:

*1) Basal meningeal adhesions** (esp in TB), causing:
obliterate subarachnoid space thus hydrocephalus, raised ICP
*2) Cranial nerve palsy** due to entrapment by fibrosis
usu CN 3, 4, 6 (EOM nerves)
CN 8 damage tends to persist

3) Cerebral infarct & stroke due to thrombosis

4) Seizure

5) Complicates into cerebritis, cerebral abscess, subdural effusion, empyema

6) SIADH

if meningococcemia

*7) Spetic shock, DIC
8) Adrenal haemorrhage** (Friederichsen Waterhouse syndrome)

Answer 155

A

1) Mycobacterium tuberculosis

2) Cryptococcus neoformans
- high in pigeon faeces
- usually patients are immuno compromised
_______
less common:
3) Treponema pallidum (syphilis)

4) Lyme’s disease - ticks*
5) Candida*

Answer 156

A

0) LP for CSF gram smear & culture, antigen detection
- after exclusion of SOL by CT/MRI

1) Empirical Antibiotics ASAP (IV, high dose, good BBB pentration)
- IV Ceftriaxone + IV Vancomycin 📘
± Ampicillin if anticipate Listeria (pregnant, elderly, immunocompromised)

*±2) adjunctive** dexamethasone
before/with first dose of antibiotics to decrease inflammatory complications
if suspect pneumococcal

±3) elevation of head by 30 degrees and anticonvulsant for ICP symptoms relief

Answer 157

A

All good BBB penetration:

*1) Ceftriaxone**
covers most meningitis bugs except Listeria
*2) Vancomycin**
covers cephalosporin resistant streptococcus
*±3) Ampicillin**
covers Listeria
added if high risk e.g. pregnancy, elderly

Answer 158

A

1) Chemoprophylaxis with rifampicin before HIB or Neisseria meningitidis contact (Not for pregnant mothers however)
2) active immunisation eg HIB vaccination, meningococcus vaccination, pneumococcal vaccination

Answer 159

A

Usually presented over days/weeks as a cerebral mass lesion with little evidence of infection:

1) Raised ICP

2) Seizures

3) Focal neurological signs

Thus may be difficult to distinguish from cerebral mass lesion e.g. tumour

Answer 160

A

1) Local extension

Frontal lobe from:
paranasal sinus, mastoid, teeth
Strep viridans, anaerobes
Temporal lobe, cerebellum from:
middle ear, sphenoid sinus, mastoid
Strep, pseudomonas, enterobacteriaceae
Cavernous sinus
Orbit
*2) Direct from penetrating wound**
open skull fracture, iatrogenic after surgery
*3) Haematological from distant focus**
e.g. infective endocarditis

Answer 161

A

NEVER.

As brain abscess is a SOL, therefore LP is contra-indicated

Answer 162

A

*1) Empirical Antibiotics (IV, at least 6 weeks)**
Pencillin G
Cefotaxime
Metronidazole

2) Steroid

3) Anti-epileptic prophylaxis

*4) Clinical radiological monitoring**
serial CT head to monitor progress
*5) Consider surgical drainage**
stereotactic/US guided aspiration
craniotomy and excision of abscess cavity

Answer 163

A

• Skin
• Subcutaneous tissue
• Fat
• Supraspinous ligament
• Interspinous ligament
• Ligamentum flavum
• Epidural fat
• Dura mater
• Arachnoid mater
-> into subarachnoid space

Answer 164

A

1) Left lateral postion, back & knees flexed
2) Aseptic technique
3) Inject LA to skin

4) Insert LP needle at cranial angle of 10-20 degrees at:

**between spinous processes of L3/4, L4/5, or L5/S1
i.e. below the level at which the spinal cord ends (L1 in an adult, but lower in a child as a result of differential growth**

5) ‘Pop’ is often felt as the ligamentum flavum is traversed
6) Remove stylet to allow CSF to drip out (do not aspirate)
7) Note appearance & measure opening pressure
8) Remove spinal needle
9) Patient should remain flat for at least 30 min to prevent a low pressure headache.

Answer 165

A

*1) Raised ICP & space occupying lesion**
based on CT (unequal pressures between supra- and infra-tentorial compartments)
clinical signs of papilloedema, false localising signs

2) Bleeding tendency

3) Local infection @ area of needle insertion

±4) Local anatomical disturbance e.g. severe kyphoscoliosis

Answer 166

A

Lumbar puncture may cause:

1) headache

2) dry tap

3) subdural hematoma

4) aneurysmal subarachnoid hemorrhage

*5) brain herniation**
if SOL exists in the brain

Answer 167

A

Brain tumours can be classified into:

A. Brain metastasis (most common)

B. Primary Intrinsic tumours (i.e. Neuroectodermal tumour)

*1) Glioma**
astrocytoma, glioblastoma multiforme
*2) Tumours from Neurons and primitive cells**
neuroblastoma, medulloblastoma

C. Extrinsic tumours
1) Meningioma

2) Pituitary tumour

3) Vestibular Schwannoma

Answer 168

A

1) Lung (40%)

2) Breast (20%)

3) Malignant Melanoma (10%)

4) Genitourinary (esp Kidney)
5) Gastrointestinal

Answer 169

A

Depends on the grading:

Low grade
I - pilocytic astrocytoma
II - astrocytoma

diffuse, slow growing
resection can be curative

High grade
III - anaplastic astrocytoma
IV - glioblastoma multiforme

Rapidly growing, high malignancy
Very poor prognosis

Answer 170

A

*1) Supportive medical treatment**
Dexamethasone to decrease cerebral oedema
Anticonvulsants

2) Biopsy

Definitive plan depends on grading:

if low grade
3) Surgical craniotomy for curative resection

if high grade
3) Maximal safe resection if possible, consider surgical debulking

*4) Chemo-RT**
tele-radiotherapy
oral temozolomide

5) Anti-angiogenesis agents e.g. bevacizumab

*6) Rehabilitation**
PT, OT, speech
clin psy

Answer 171

A

Meningioma:

slow growing, benign tumour; may undergo malignant change in 1-2%
arises from arachnoid granulations
causes reactive hyperostosis and may invade adjacent bone

Answer 172

A

*1) Skull radiograph:**
boney hyperostosis with sunray effect and calcification
*2) CT**
well demarcated homogenous lesion
may be calcified with surrounding oedema
*3) MRI**
Iso-intense on T1W image
striking enhancement with gadolinium contrast
*4) Angiogram**
very vascular lesions

Answer 173

A

1) Corticosteroid

2) Anti-epileptics

*3) Surgical resection**
with the aim of complete resection of tumour and the meningeal origin
recurrence depends on the completeness of tumour resection

Answer 174

A

Schwannoma of CN VIII, might be part of NF2 esp if bilateral

*Clinical Feature:**
unilateral progressive sensorineural hearing loss
vertigo and tinnitus is rare (due to slow growth, thus allows compensation)
hydrocephalus from obstruction of 4th ventricle

Ix: MRI

Management:

*1) Conservative management** w/ serial imaging
if small and asymptomatic, as it is a slow growing tumour
*2) Surgical excision
3) Stereostatic radiosurgery**

Answer 175

A

*1) Schwannoma**
“acoustic neuroma”
other CN (not I or II) schwannoma
spinal schwannoma
peripheral nerve schwannoma
*2) Other nervous system tumours**
meningiomas
ependymomas
astrocytoma
*3) Eye signs**
Cataract (early onset)
Retinal harmatoma
Optic nerve meningioma
*4) Very little Skin involvement**
less than 6 cafe au lait spots
cutaneous schwannomas (plaque lesions)

Answer 176

A

1) Pituitary adenoma (in adults)

2) Pituitary Carcinoma (very rare; secondary more common than primary tumour)

(in children: craniopharyngioma, CNS germ cell tumour)

Answer 177

A

*Based on Endocrinology**
functional (secreting, ~80%)
non-functional (non-secreting)
*Based on Size:**
Microadenomas < 10 mm (observe if non-secreting)
Macroadenomas > 10 mm (surgery mostly)

*Functional putuitary adenoma:**
Prolactinoma (most common)
GH producing tumour
ACTH producing tumour
Glycoprotein secreting tumours (TSH, FSH, LH, α, β- subunits)

Answer 178

A

*1) Local symptoms**
visual loss (bitemporal hemianopia from optic chiasm)
hydrocephalus (3rd ventricle), raised ICP Sx

2a) Usually hypopituitarism from mass effect

GH: growth retardation, central obesity, round face
FSH, LH: hypogonadism, infertility, amenorrhoea
ACTH: adrenal insufficiency e.g. weight loss, orthostatic hypotension, hypoglycemia, hyponatremia, but NO hyperpigmentation like Addison’s)
TSH: hypothyroidism

2b) Symptoms of pituitary hormone hyper-secretion if functional adenoma:

Prolactin: galactorrhoea, amenorrhoea, impotence
GH: gigantism in children, acromegaly in adult
ACTH: Cushing’s disease
TSH: rarely, 2º hyperthyroidism

3) Incidental radiological finding on skull X-ray, CT scan or MRI

Answer 179

A

*1) Radiology**
MRI (preferred)
CT (better visualisation of calcification)

2) Blood test for screening of functional pituitary adenoma (which might be asymptomatic):

a) Prolactinoma
- increased serum prolactin (>10x increase, beware of false negative hook effect)
- 50%+ size shrinkage with dopamine agonist

b) GH-producing tumour
- serum GH or IGF1 (insulin like growth factor) increased (difficult coz short t_1/2)
- Stimulation test with Insulin tolerance test or arginine infusion test
- Supression test e.g. OGTT showing non-suppressible serum GH

Answer 180

A

*1) Medical therapy for secreting pituitary adenoma**
a) Prolactinoma
dopamine agonists i.e. bromocriptine, carbegoline
first line

b) GH/TSH secreting tumour
- somatostatin analogues e.g. Octreotide, Lanreotide
- adjunct to surgery & RT

*2) Surgical resection** (usu trans-sphenoidal)
for macroadenoma
for secreting tumour (e.g. ACTH, GH)
when medical therapy for prolactinoma failed
*3) Radiotherapy** (tele-radiotherapy or radiosurgery e.g. Gamma knife, X-knife)
if unfit for surgery
Macroadenoma, esp macroprolactinoma
as adjunct, esp in persistent hormonal hyperfunction despite surgical intervention

Answer 181

A

1) Transphenoidal -> route of choice

2) Transfrontal -> for very large suprasellar extension, esp with severe chiasmal compression

Answer 182

A

1) Mortality – very rare
2) Endocrine - diabetes insipidus, hypopituitarism
3) Visual loss
4) CSF leakage & meningitis
5) Vascular injury & CVA
6) ENT symptoms
7) Intracranial haemorrhages etc

Answer 183

A

Hemorrhagic infarction of pituitary tumour

*Presentation:**
Variable onset of severe headache
Meningism
Vertigo
Visual defects e.g. bitemporal hemianopia
Altered consciousness

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Neurosurgery Flashcards

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