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Neurosurgical Training > Vascular Neurosurgery > Flashcards

Vascular Neurosurgery Flashcards

1
Q

Vascular distribution during embryology to the CoW

A

Typically during initial embryological development the ICA supplies the ACA, MCA and PCA

Later, the PComm atrophies, with the basilar supplying most of the blood to the posterior circulation

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2
Q

Def: Fetal PComm

A

If the PComm remains larger than the ipsilateral P1

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3
Q

What proportion of individuals have a fetal PComm?

A

25%

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4
Q

What are other anatomical CoW variants?

A

PComm hypoplasia or absence

A1 hypoplasia

AComm absence

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5
Q

What are some embryonic connections between the carotid and basilar arteries?

A

Persistent primitive trigeminal artery (arising from the precavernous ICA lateral to the dorsum sellae

Persistent primitive hypoglossal artery can also connect hte ICA to the basilar, thereby representing a single artery supplying the brainstem and cerebellum.

Both variants are associated with intracranial aneursyms

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6
Q
A

Persistent primitive trigeminal artery

Connects ICA to the basilar

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7
Q

What happens to pial vessels?

A

Surrounded by CSF, form penetrating arterioles.

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8
Q

What are Virchow Robin spaces

A

A small extension of the subarachnoid space surrounding pial vessels which become encased by astrocytic end-feet.

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9
Q

What are the layers of cerebral arteries?

A

Tunica adventitia (collagen and fibroblasts)

Tunica media (smooth muscles, with larger arteries having more layers)

Tunic intima (single layer of endothelium separated from the media by a layer of elastic tissue)

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10
Q

Features of cerebral veins

A

Thin wall

No valves

Minimal smooth muscle

Less closely follow the arterial system

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11
Q

Level of carotid bifurcation

A

C4

Carotid sinus with associated carotid sinus

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12
Q

What does the carotid bulb sense?

A

Baroreceptor

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13
Q

What does the carotid sinus sense?

A

Chemoreceptor, influences respiratory pattern

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14
Q

Classification of the ICA

A

Bouthillier

Cervical

Petrous (horizontal)

Lacerum

Cavernous

Clinoid

Ophthlamic (supraclinoid)

Communicating

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15
Q

Number of branches of the cervical carotid

A

0

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16
Q

Under which ligament does the laceral segment of the ICA pass before entering the cavernous sinus?

A

Petrolingual ligament

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17
Q

Branches of the petrous portion of the ICA?

A

Caroticotympanic

Mandibulovidian

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18
Q

What are the two important branches of the intracavernous ICA?

A

Meningohypophyseal trunk

Inferolateral trunk

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19
Q

Branches of the meningohypophyseal trunk

A

Inferior hypophyseal artery-> posterior pituitary lobe

Dorsal meningeal artery

Tentorial artery (artery of Bernasconi and Cassinari)-> tentorium

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20
Q

Clinoid portion of the ICA

A

Exits the dural covering of the cavernous sinus through the proximal dural ring which forms the roof of the sinus and is in continuity with the dura covering the adjacent anterior clinoid process

It is a transitional segment between the cavernous sinus before the ICA exits through the distal ring and enters the subarachnoid space

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21
Q

What is the clinical significance of the distal dural ring?

A

Differentiates between the pathology caused by ICA aneurysms- caroticocavernous fistula vs SAH,

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22
Q

Access to aneurysms near the origin of the ophthalmic artery will require?

A

Anterior clinoidecomy

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23
Q

Lateral region between the proximal and distal dural rings

A

Extradural and extracavernous

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24
Q

What is the cavernous cave?

A

Medial space between the proximal and distal dural rings.

Usually extradural though rupture of carotid cave aneurysms extending superiorly out of the cave may result in SAH

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25
Q

What is the origin of the ophthalmic artery?

A

Just beyond the distal dural ring, inferior to the optic nerve and anterior clinoid process.

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26
Q

What are the branches of the ophthalmic segment of the ICA?

A

Ophthalmic

Superior hypophyseal arteries

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27
Q

What is meant by the term paraophthalmic aneurysms?

A

Used to describe aneurysms of the ophthalmic portion of the ICA which may be radiologically difficult to localise

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28
Q

What are two important ophthalmic artery variants

A

Can arise from the extradural clinoid portion of the ICA

Can rarely arise from the ECA

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29
Q

Meningo-ophthalmic artery

A

Rare variant with the artery arising from the MMA and entering the orbit through the SOF, which may pose a risk to sight if sacrificed during endovascular procedures.

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30
Q

Extent of the communicating segment of the ICA

A

From the PComA origin to the ICA bifurcation.

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31
Q

Length of PComm

A

Around 1cm

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32
Q

Posterolaterally projecting PCommA cause a?

A

Surgical CN3 palsy

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33
Q

Perforators from PCom

A

Small branches are given off supplying the genu of the internal capsule and the thalamus

The largest branch is the premamillary artery (anterior thalamoperforator)

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34
Q

Where is the anterior choroidal artery given off

A

1-3mm distant to the PComm usually arising from the posterior aspect of the ICA prior to its termination at the circle of Willis

Can arise as several (1-5) trunks

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35
Q

Consequence of anterior choroidal ligation

A

Hemiparesis

Hemianaesthesia

Hemianopia

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36
Q

Divisions of the anterior choroidal

A

Cisternal

Intraventricular segment

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37
Q

Cisternal segment of the anterior choroidal

A

Crosses the optic tract, running along its lateral aspect towards the medial temporal lobe, passes the cerebral peduncles to reach the LGN before entering the choroidal fissure and becoming the intraventricular segment

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38
Q

Structures supplied by the anterior choroidal?

A

Optic pathways

Posterior limb of the internal capsule

Basal ganglia

Choroid plexus of the temporal horn of the lateral ventricle

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39
Q

What is the best angiographic view of the ICA bifurcation

A

Oblique

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40
Q

Where do blister aneurysms typically arise?

A

Dorsomedial wall of non-branching parts of the ICA

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41
Q

What separates the ACA into A1 and A2 segments?

A

The AComm

A1= precommunicating

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42
Q

Relationship of A1 to the optic nerve?

A

Crosses over the optic tract anteromedially

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43
Q

Variants of the A1 segment

A

Maybe hypoplastic with supply from the contralateral A1 via the AComm

Unpaired or azygos ACA

Duplicated or fenestrated AComm segments.

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44
Q

Where do medial lenticulostriate branches of the ACA typically arise and what do they supply?

A

From the inferoposterior aspect of the A1 segment and supply the GP and medial putamen through the anterior perforated substance

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45
Q

Where does the A2 end?

A

With the formation of the callosomarginal and pericallosal arteries at the genu of the corpus callosum

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46
Q

What is the first cortical branch of the ACA?

A

The orbitofrontal artery

Supplies the inferior part of the frontal lobe

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47
Q

What are the 2 main branches of the A2 segment of the ACA?

A

Orbitofrontal artery (Inferior part of frontal lobe)

Frontopolar artery (anterior part of the superior frontal gyrus)

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48
Q

Location of the AComm

A

Lies in the cistern of the lamina terminalis

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49
Q

Classification of AComm branches

A

Subcallosal

Hypothalamic

Chiasmatic

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50
Q

What is the largest of the perforating branches of the ACA?

A

Recurrent artery of Heubner

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51
Q

Location of the recurrent artery of Heubner?

A

Arises from the proximal A2 segment near the A1/2 junction but can also arise from the A1

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52
Q

Structures supplied by the recurrent artery of Heubner

A

Anterior limb of internal capsule

Caudate nucleus

GP

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53
Q

Pericallosal artery

A

Considered a continuation of the ACA and closely follows the corpus callosum

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54
Q

In what proportion of patients is a callosomarginal artery present?

A

50%

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55
Q

Structures supplied by the pericallosal artery

A

Corpus callosum and its splenium

Septum pellucidum

Fornix

Precuneus cortex

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56
Q

Structures supplied by the callosomarginal artery?

A

Superior frontal gyrus through various branches

Takes a course through the cingulate sulcus

Terminates as the paracentral artery supplying the paracentral lobule

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57
Q

Where does the M1 end

A

At the MCA bifurcation as the distal M2

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58
Q

Location of the M1

A

Runs laterally in the anterior compartment or sphenoidal compartment of the deep component of the Sylvian fissure between the frontal and temporal lobes

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59
Q

From where do the lateral striate (lenticulostriate) arteries arise?

A

Form the posteroinferior part of the M1, travelling backwards along its course to penetrate the lateral portion of the anterior perforated substance

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60
Q

Structures supplied by the lateral striate arteries?

A

Basal ganglia

Internal capsule

Caudate nculeus

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61
Q

Passage of the M1

A

Bifurcates at its genu, turning upwards at the anteroinferior aspect of the insula.

The only large branches of the M1 are usually the anterior temporal artery and temporopolar branch.

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62
Q

In what proportion of individuals does PICA arise below the foramen magnum?

A

15%

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63
Q

Anatomical variations in PICA

A

Hypoplastic (there is often an increase in AICA calibre)

One vertebral artery may form the PICA directly.

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64
Q

How many MCA segments are there?

A

4

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65
Q

M1 segment

A

Sphenoidal segment

Origin- bifurcation of the ICA

Courses parallel to the sphenoid ridge.

Terminates at the genu adjacent to the insula or at the main bifurcation.

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66
Q

M2 segment

A

Insular segment

Originates at the limen insulae or genu

Courses posterosuperiorly in the insular cleft

Terminates at the circular sulcus of the insula where it makes a hairpin turn.

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67
Q

M3 segment

A

Opercular segment

Origin at the circular sulcus of the insula

Courses along the frontoparietal operculum

Terminates at the external surface of the operculum

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68
Q

M4 segment

A

Cortical segment

Originates at the external/top surface of the Sylvian fissure

Courses superiorly on the lateral convexity

Terminates at their final cortical territory

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69
Q

Segments of the PICA

A

Anterior medullary

Lateral medullary

Tonsillomedullary

Telovelotonsillar

Cortical (suboccipital surface)

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70
Q

Which nerve is closesly related to PICA at its anterior medullary segment

A

Hypoglossal

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71
Q

Which segment of the PICA forms the caudal loop?

A

Tonsillomedullary

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72
Q

Which number is PICA?

A

4 (caudal loop of tonsillomedullary segment followed by cranial loop)

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73
Q

Which PICA segment forms the cranial loop?

A

Telovelotonsillar segment

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74
Q

Which structures are supplied by the PICA?

A

Lateral medulla

Fourth ventricle choroid plexus

Inferior and posterior cerebellum

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75
Q

The general pattern of arterial supply to the midbrain, pons, medulla

A

Via short and long perforators to the anterior and posterolateral parts with long circumflex branches travelling over the lateral surface.

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76
Q

Where do the AICAs typically arise?

A

Near to the abducens nerve

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77
Q

Passage of the ACIA

A

Traverses the CPA closely related to the facial and vestibulocochlear nerves to supply the anterior and inferior cerebellum.

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78
Q

Whence does the labyrinthine artery arise?

A

Either from AICA or from the basilar

Passes with the vestibulcoochlear nerve to supply the inner ear

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79
Q

The origin of the SCA is close to which cranial nerve?

A

3

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80
Q

Structures supplied by the SCA

A

Superior cerebellar hemispheres

Peduncles

Vermis

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81
Q

Segments of AICA

A

Anterior pontine

Lateral pontomedullary

Flocculonodular

Cortical (petrosal surface)

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82
Q

Segments of SCA

A

Anterior pontomesencephalic

Lateral pontomesencephalic

Cerebellomesencephalic

Cortical

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83
Q

What are Rhoton’s three neurovascular complexes in the posterior fossa?

A

Upper

Middle

Lower

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84
Q

Upper neurovascular complex

Vessel

Brainstem region

Fissure

CNs

Cerebellar peduncle

Cerebellar surface

A

SCA
Midbrain

Cerebellomesencephalic

III, IV, V

Superior

Tentorial surface

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85
Q

MIddle neurovascular complex

Vessel

Brainstem region

Fissure

CNs

Cerebellar peduncle

Cerebellar surface

A

AICA

Pons

Cerebellopontine

VI, VII, VIII

MIddle

Petrosal

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86
Q

Lower neurovascular complex

Vessel

Brainstem region

Fissure

CNs

Cerebellar peduncle

Cerebellar surface

A

PICA

Medulla

Cerebellomedullary

IX, X, XI, XII

Inferior

Suboccipital

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87
Q

Location of P1

A

Horizontal segment, sits within the interpeduncular fossa before anastomosing with PComA

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88
Q

What is the artery of Percheron

A

Single large thalamoperforate branch that can supply both thalami and the midbrain

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89
Q

The manifestation of artery of Percheron occlusion?

A

Paramedian thalamic syndrome

Altered conscious state

Vertical gaze palsy

Impaired memory.

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90
Q

P2 segment of PCA

A

Distal to PCommA

Traverses around the oculomotor nerve in the ambient cistern to sit above the tentorium

Divided into the P2A and P2P segments

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91
Q

What demarcates P2A from P2P segments

A

Junction at most lateral aspect of the cerebral peduncle

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92
Q

Branches of the P2 segment

A

Multiple perforating branches including the thalamogeniculate and lateral and posterior choroidal arteries.

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93
Q

How does the lateral posterior choroidal artery enter the lateral ventricle?

A

Adjacent to the LGN via the choroid fissure

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94
Q

Passage of the medial posterior choroidal artery?

A

Passes beneath the splenium to enter the roof of the third ventricle in the velum interpositum.

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95
Q

Principle anastomoses between ECA and ICA

A

Ascending pharyngeal artery branches anastomose with cavernous ICA branches and meningeal vertebral artery branches.

Facial artery anastomoses with the ophtahlmic artery and the occipital arery with the vertebral artery branches

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96
Q

Which arteries supply the posterior fossa dura?

A

Ascending pharyngeal and occipital

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97
Q

Which arteries supply the supratentorial dura?

A

MMA and accessory meningeal branches of maxillary

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98
Q

Into what does the superficial middle cerebral vein drain?

A

Into the cavernous or the sphenoparietal sinus

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99
Q
A

Superficial middle cerebral vein

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100
Q

Into what does the vein of Trolard drain?

A

Into the SSS

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101
Q

Into what does the vein of Labbe drain?

A

Labbe drains into the transverse sinus

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102
Q

What is the reciprocal arrangement of the two superficial anastomotic veins?

A

Labbe larger in dominant hemisphere and Trolard in non-dominant

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103
Q

Location of the great cerebral vein of Galen

A

Found below the splenium of the corpus callosum

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104
Q

What forms the Great vein of Galen

A

Joining of the two internal cerebral veins

Two basal veins of Rosenthal

Occipital veins draining the medial and inferior occipital lobes

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105
Q

Which structures form the straight sinus?

A

Great vein of Galen and ISS

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106
Q

Passage of the basal veins of Rosenthal

A

Arise at the anterior perforat3ed substance on the medial aspect of the temporal lobe and run posteriorly and medially.

Travel around the mesencephalon in the ambient cistern

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107
Q

Structures drained by basal vein of Rosenthal?

A

Hypothalamus

Midbrain

Medial and inferior portions of the frontal and temporal lobes including the operculum and insula

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108
Q

Location of the internal cerebral veins

A

Located in the velum interpositum

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109
Q

Velum interpositum

A

The velum interpositum is a small membrane containing a potential space just above and anterior to the pineal gland which can become enlarged to form a cavum velum interpositum.

The velum interpositum is formed by an invagination of pia mater forming a triangular membrane the apex of which points anteriorly.

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110
Q

What form the internal cerebral veins

A

Choroidal veins and thalamostriate veins

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111
Q

What veins drain into the thalamostriate?

A

Transverse caudate veins

Anterior terminal vein

Septal vein

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112
Q

Passage of the SSS

A

Crista galli-> torcular Herophili

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113
Q

Etymology Torcula

A

Wine press

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114
Q

Transverse sinus dominance

A

Often asymmetric with dominant right receiving the majority of blood from the SSS

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115
Q

At what point do the transverse sinuses become the sigmoid?

A

At the posterior petrosal edge

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116
Q

What structures drain into the cavernous sinus?

A

Superficial middle cerebral veins

Ophthalmic veins

Sphenoparietal sinus

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117
Q

Outflow of cavernous sinus

A

Superior and inferior petrosal sinuses

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118
Q

Superior petrosal sinus connects to?

A

Sigmoid sinus

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119
Q

Occipital sinus

A

Varyingly present, more common in children

May run from the torcula in the midline to the foramen magnum and can be the source of significant bleeding in an otherwise straightforward midline posterior fossa approach

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120
Q

Venous drainage of the cerebellum

A

Superficial cerebellar hemispheres drain into the nearest of the sigmoid or transverse sinuses

Superior and inferior vermian veins run along the vermis in the midline

Anterior drain into the superior or inferior petrosal sinuses

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121
Q

Drainage of the brainstem

A

Veins are small and widespread

The lateral mesencephalic vein which is contiguous with the petrosal vein, connecting the basal vein of Rosenthal with the superior petrosal sinus

Dandy’s vein drains the anterior cerebellum, posterior medulla and ventral pons,

Anterior mesencephalic vein

Precentral (cerebellar vein)

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122
Q

Dandy’s vein

A

Superior petrosal vein

Large vein extending from the lateral surface of the pons draining into the superior petrosal sinus.

Drains a large area including the anterior cerebellum, lateral and posterior medulla and anterior pons.

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123
Q

Cerebellar vein

A

Unpaired vein running posterior to the cerebellum

Draining into the superior vermian vein or great vein of Galen

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124
Q

What is the anatomical signficance of the cerebellar vein

A

inferior aspects marks the upper border of the fourth ventricle

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125
Q

What are the anatomical considerations for large AVMs straddling more than one lobe?

A

Naturally will be supplied by multiple arterial territories as well as watershed regions.

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126
Q

Anatomical divisions of lateral hemisphere AVMs

A

Frontal, temporal, parietal, occipital, peri-Sylvian

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127
Q

What is a surgical consideration for AVMs extending towards the superior frontal lobe or frontal pole

A

Likely to attract supply from distal ACA branches such as the frontopolar artery anteriorly or the fronto-orbital artery basally.

Surgical exposure must be extended to access these vessels.

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128
Q

Drainage of lateral hemisphere AVMs

A

Drain via superficial veins into the SSS or the transverse sinus

Those more centrally located may involve the veins of Trollard or Labbe

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129
Q

Temporal AVMs extending onto the tentorial surface may drain into?

A

vein of Rosenthal

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130
Q

Arterial supply of medial hemisphere AVMs

A

Anteriorly by the callosomarginal artery or pericallosal.

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131
Q

Disruption of medial hemispheric artery supply may result in ?

A

Transient SMA syndrome

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132
Q

Which arteries should be preserved in medial hemisphere AVM surgery?

A

A3 and 4 (distal pericallosal) arteries to the paracentral lobule.

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133
Q

Venous drainage of medial hemisphere AVMs

A

SSS

Vein of Galen

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134
Q

Arterial supply of deep supratentorial AVMs?

A

Subcortical deep extensions recruit deep perforator feeders such as lenticulostriate from the MCA, A1 perforators and the recurrent Arteries of Heubner

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135
Q

Consideration for deep supratentorial AVMs

A

Frequently extend in a cone type fashion towards the ventricles and are expected to have ependymal feeders that are not identified on the preoperative angiogram

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136
Q

How can intraventricular AVM extension be demonstrated angiographically?

A

By demonstrating supply from the choroidal arteries angiographically.

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137
Q

Suboccipital and paravermian AVMs likely fed by

A

PICA branches beyond the tonsillar loop and with fourth ventricular extension also its choridal branches

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138
Q

Suboccipital and tentorial surface AVMs fed by?

A

SCA

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139
Q

AVMs on the petrosal cerebellar surface may have feeders from?

A

AICA

140
Q

CO required by the brain?

A

14%

141
Q

When does irreversible ischaemic brain damage occur?

A

4 minutes (if global)

142
Q

CPP=

A

MAP-(ICP+CVP)

143
Q

MAP=

A

2/3(DBP) + 1/3(SBP)

144
Q

Def: Cerebral autoregulation

A

Is the ability of the brain to regulate its blood flow despite changes in systemic blood pressure

145
Q

Significance of CVP in CPPP

A

ICP represents the cerebral venous outflow pressure.

The sagittal sinus pressure does not change with a range of ICP

Dural sinuses are thus rigid

CVP is therefore often omitted from the CPP formula

146
Q

What is the consequence of increasing intracranial volume beyond the critical volume?

A

Initially, compensatory mechanisms (as per MKD) are able to maintain ICP at normal or near-normal levels through the movement of CSF into the spinal canal and increased absorption.

There may be some partial compression of venous sinuses.

When these mechanisms are overcome there is an exponential change in ICP.

A pathophysiological rise in ICP is met with a reduction in CPP and CBF

147
Q

Draw the intracranial pressure-volume curve

A
148
Q

CBF volume/minute

A

700ml/inute

around 50ml per 100g

149
Q

At what CBF are EEG changes seen

A

CBF <20ml/min

150
Q

At what CBF are ischaemic changes seen

A

<10ml/minute

151
Q

Draw the CBF autoregulatory curve

A
152
Q

What are the 3 mechanisms of cerebral autoregulation

A

Myogenic

Neurogenic

Metabolic

153
Q

Myogenic regulation of CBF

A

Thought to involve the myogenic response of cerebral smooth muscle in vessel walls.

154
Q

Neurogenic control of CBF

A

Cerebral vasculature receives sympathetic innervation from the superior cervical ganglion- extra parenchymal vessels are thought to be regulated by the ANS, though not thought to play a major role in physiological regulation.

May play a role when BP rises above the normal limits of autoregulation through modulation of the normal autoregulatory curve.

155
Q

What is the significance of neuromodulation of the autoregulatory curve?

A

Represents a protective physiological mechanism preventing significant CBF rises and BBB break down with acute surges in BP.

156
Q

Draw the CBF PaO2 curve

A
157
Q

Draw the CBF PaCO2 curve

A
158
Q

CO2 and cerebral blood flow

A

CO2 has a marked and reversible effect on CBF

Hypercapnia causes significant dilation resulting in increased CBF.

Hypocapnia has the opposite effect.

Due to the curvilinear relationship, outside the physiological range of PCO2, reductions cause a marked reduction in CBF.

This does not persist past 24-48h of hypocapnia suggesting htere is physiologicaln buffering.

159
Q

O2 and cerebral blood flow

A

Hypoxia is a profound vasodilator

At levels above 8kPa changes in PaO2 has very minimal effect on CBF but below 6.7kPa CBF increases exponentially.

160
Q

Mannitol and cerebral blood flow

A

HCt and blood viscosity affect CBF.

Mannitol principally thought to create an osmotic gradient to reduce cerebral oedema.

Its speed of action is more consistent with autoregulatory cerebral vasoconstriction and reduction in intravascular volume in response to a rapid increase in peripheral intravascular volume and hence cerebral perfusion.

161
Q

Def: aneurysm

A

Pathological acquired dilatation of a vessel >50% of its diameter involving all layers of its wall

162
Q

What proportion of intracranial aneurysms are saccular / Berry?

A

80-90%

163
Q

Prevalence of intracranial aneurysms

A

Found in 1-5% of adult population at autopsy

164
Q

What proportion of spontaneous SAH is aneurysmal?

A

80-85%

165
Q

Epidemiology of SAH

A

5th decade

F: M 3:2

166
Q

Factors contributing to the pathophysiology of aneurysms

A

Vessel wall

Genetic

Haemodynamic

Environmental

167
Q

Aneurysm pathophysiology

Vessel wall biology

A

Intracranial aneurysms are found at bifurcation where there are more collagen than elastic fibres and the muscular wall is less well developed.

168
Q

Aneurysm pathophysiology

Genetic factors associated with aneurysm formation

A

Autosomal dominant PKD

Ehlers-Danlos

Marfan’s

NF1

Pseudoxanthoma elasticum

169
Q

Aneurysm pathophysiology

Haemodynamics

A

Increased risk of aneurysm formation at sites of increased haemodynamic stress (e.g. unbalanced AComm, low-pressure shunts e.g. high flow AVM and along collateral pathways after spontaneous or iatrogenic carotid occlusion.

Wall shear stress and other local haemodynamic factors implicated.

170
Q

Aneurysm pathophysiology

Environmental factors

A

Cigarette smoker

HTN

171
Q

Hazard ratio

A

n its simplest form, the hazard ratio can be interpreted as the chance of an event occurring in the treatment arm divided by the chance of the event occurring in the control arm, or vice versa, of a study.

172
Q

Rhoton’s rules on intracranial aneurysms

A
  1. Arise at branching sites of the parent artery (e.g. PComm, MCA bifurcation, basilar bifurcation)
  2. Arise from a turn or curve of the artery
  3. Dome lays in the direction of maximal haemodynamic flow
173
Q

Distribution of aneurysms

A

90% of saccular are anterior criculation

AComm (30-35%)

ICA including PComm (30-35%)

MCA (20%)

Basilar bifurcation is the most common site in the posterior circulation

174
Q

Classification of aneurysms based on size

A

Small <10mm

Large 11-25mm

Giant >25mm

175
Q

Size cut off for giant aneurysm

A

>25mm

176
Q

Anatomical components of aneurysm

A

Neck

Fundus

177
Q

Def: wide-neck aneurysm

A

>4mm neck

178
Q

What are the important morphological features affecting endovascular treament

A

Neck width

Neck:dome

179
Q

What morphological factors feed into the risk of rupture

A

Aneurysm angle

Aspect ratio (cranio-caudal dimension divided by transverse diameter).

180
Q

What is the significance of blebs

A

Often identify the point of rupture in ruptured IAs.

Presence in unruptured IAs is associated with increased rupture risk and inform the decision to treat

Most often opposite the point of maximal flow.

181
Q

Increased risk of IA in relatives in patients with IAs +/- aSAH?

A

15 fold

182
Q

Indications for familial screening in IAs?

A

When >30y/o if two or more relatives affected by SAH/IA

183
Q

ADPKD and IAs

A

Cererbral aneurysms found in 25%

Increases risk of IA by 10-20 fold dependent on FHx of IAs

184
Q

Screening for IA in ADPKD

A

Patients with PKD and FHx of IAs

or

ADPKD and HTN

185
Q

What is the added significance of connective tissues disease in the context of aneurysmal SAH

A

They are at increased risk of complications from intravascular diagnostic and therapeutic treatment of intracranial aneurysms

186
Q

Ehler’s Danlos Collagen

A

Type IV

187
Q

Marfan’s Syndrome caused by?

A

Fibrillin abnormality

188
Q

Aortic coarctation and IA

A

Found in 10.3%

189
Q

Fibromuscular dysplasia

A

Idiopathic segmental, non-atherosclerotic, non-inflammatory vascular disease that mainly affects renal, extracranial carotid and vertebral arteries.

190
Q

Risk factors for aneurysm growth

A

Age >50

Female

Smoking

Non-saccular

191
Q

Risk of ruptiure in growing IA

A

3.1% vs 0.1% per year for stable IAs.

192
Q

Traumatic aneurysms

A

Account for <1% of all IAs

Second most common type in children (5-15%).

Can be true or pseudo

193
Q

Most common sites of traumatic aneuryssms

A

ICA 46%

MCA 25%

ACA 22%

194
Q

Natural Hx of traumatic aneurysms

A

Risk of rupture can be high if progressively enlarging on repeat imaging.

Can become visible days after the trauma so if not seen on initial imaging, low threshold for repeat imaging is necessary.

195
Q

Surgeries in which iatrogenic traumatic aneurysms have been reported?

A

Trans-sphenoidal

Craniotomy for tumour and vascular lesions

EVD

196
Q

In what layers of the vessel is the tear in dissection?

A

Intima and internal elastic lamina

197
Q

Most common site of intracranial dissection?

A

V4 segment of the vertebral

198
Q

Possible presentations of dissecting intracranial vessels

A

Asymptomatic

Ischaemia

Headache

Frank haemorrhage (including SAH)

199
Q

Def: Blister-like aneurysms

A

Small dilatations, hemispherical shaped and bulging from non-branching sites of the dorsal wall of the supraclinoid ICA opposite the PComm origin and the anterior choroidal artery

200
Q

Challenge of blister-like aneurysms

A

1% of all ruptured IAs

Very fragile wall

Can be difficult to identify on the first DSA and may only be picked up on interval angiography.

201
Q

Def: Fusiform aneurysm

A

Dilatation of the arterial wall which involves at least 270 deg of the vessel wall.

202
Q

Dolioectatic aneurysm

A

Characterised by uniform pathological dilatation of an entire vessel with associated tortuosity of the vessel itself

203
Q

Natural Hx of fusiform aneurysms

A

Can be incidental and then have a fairly benign natural Hx

Can also present with ischaemic symptoms, symptoms related to mass effect and haemorrhage.

204
Q

Def: Mycotic aneurysm

A

Implies the presence of infection with vessel wall estruction

205
Q

Treatment of mycotic aneurysms

A

Identify source

Appropriate Abx

4-6/52 of therapy at least.

Can be managed endovascularly or surgically in specfici situations

206
Q

Rate of multiple intracranial aneurysms in SAH

A

Up to 35% in IUSIA

207
Q

Minimum age for screening in IAs

A

<10y from time of ictus for family member

208
Q

Management of incidental IAs

A

Those <7mm have an exceedingly small risk of rupture if incidental and asymptomatic

Location, presence of lobulations and other risk factors should be taken into account

Repeat imaging on MR 6-12 months from diagnosis and if no interval growth no further imaging may be required taking into account risk factors, age and aneurysm size.

209
Q

Rate of aneurysm causing spontaneous SAH

A

85%

210
Q

What proportion of non-aneurysmal spontaneous SAH is perimesencephalic?

A

60%

211
Q

Causes of non-aneurysmal SAH

A

pial AVM

Tumours

Anticoagulants

Vascular dissections

Vasculitides

212
Q

Location of haemorrhage in peri-mesencephalic SAH

A

Prepontine

Perimesencephalic cisterns with some extension into the adjacent cisterns

No blood in ventricles, Sylvian fissure of interhemispherically.

213
Q
A

Peri-mesencephalic SAH

214
Q

Complications of SAH

A

Intracranial:

Rebleed

Hydrocephalus

Delayed ischaemia

Seizures

Haematoma

Extracranial:

Hyponatraemia

Sepsis

Neurogenic stunned myocardium

Neurogenic pulmonary oedema

215
Q

Clinical hx in SAH

A

Sudden onset headache

Meningism

Altered sensorium

Coma

216
Q

Pathophysiology of acute SAH

A

Acute increase in ICP due to extravasation of blood into subarachnoid space.

Vasodilatory cascade

Reduction in CPP-> LOC.

Subsequent acute global ischaemia and cerebral oedema may contribute to brain injury.

A greater volume of haemorrhage and early brain injury correlate to a worse outcome

Intracerebral haemorrhage may cause focal deficit.

217
Q

Subsequent pathophysiology post ictus in SAH

A

Cell death

Cerebral vasospasm

Impaired cerebrovascular autoregulation

Electrophysiological abnormalities may result in seizures and cortical spreading depolarisation

May result in hypoperfusion-> ischaemic deficits even in the absence of vasospasm.

Microthrbombi in parenchymal vessels results from an early increase in procoagulant activity.

HCP

218
Q

Rate of HCP on presentation in SAH

A

Up to 20%

219
Q

What proportion of pateints presenting with HCP in context of SAH will show reduced consciousness

A

Up to 50%

220
Q

What proportion of patients with SAH presenting with HCP may require shunt?

A

Up to 50%

221
Q

Pathophysiology of acute HCP in SAH

A

Impairment of CSF bulk flow and absorption via normal physiological and anatomical pathways

Intraventricular blood may impair aqueductal flow.

Boood breakdown products and elevated protein may impair arachnoid villi reabsorption

222
Q

Considerations for Mx of acute HCP in SAH

A

EVD, higher pressure in unsecured aneurysms due to risk of precipitating rebleed.

Serial lumbar punctures or lumbar drain

223
Q

Intra-operative measurements to reduce HCP in aneurysm clipping

A

CSF toilet

ETB

224
Q

Incidence of SAH

A

6-11/100,000 per annum.

225
Q

Key findings in ISUIA

A

Small (<7mm) anteiror ciruclation aneurysms have a low rupture rates as do small type 1 aneurysms of the posterior circulation

226
Q

Type 2 IAs

A

Aneurysms in the context of previous SAH or multiple intracranial aneurysms.

Confer increased risk of rupture

227
Q

Risk score for aneurysm rutprure

A

PHASES

228
Q

Components of PHASES score

A

Population (Japanese or Finnish)

HTN

Age >70

Size

Earlier SAH

Site (anatomical)

229
Q

Outcome in vasospasm

A

Death in up to 7%

Cerebal infarction in 26%

230
Q

Clinical manifestation of vasospasm

A

Narrowed arterial calibre demonstrated on vascular imaging resulting in delayed ischaemic neurological deficits.

231
Q

Rate of radiological vs clinical vasospasm

A

Up to 90% of patients following SAH may have vasospasm.

Only half of these will show ischaemic deficits.

Ischaemia can be demonstrated in arterial territories not displaying radiological vasospspasm.

232
Q

Pathophysiology of vasospasm

A

Not understood.

Vascular smooth muscle contraction

Endothelial cell lose NO synthesis

Proinflammatory cascade results in vessel ECM remodelling.

233
Q

Incidence of DNID in SAH

A

30-40%

234
Q

Risk factors for DNID

A

Increase risk with increased subarachnodi blood volume

Fisher grade correlates with risk of vasospasm.

Higher WFNS

Increasing age

HTN

HCP

235
Q

Timecoure of DNID

A

Rarely seen <3d post ictus

Peaks 6-8/7 post SAH

Can be as late as the third week.

236
Q

Clinical presentation of vasospasm

A

Awake patient:

Increased headache, confusion, agitation, altered cognition, somnolence, focal neurological deficits

Signs may reflect relevant arterial territory.

Leucocytosis and pyrexia may be seen

Comatose patient:

May be difficult to detect, high level of vigilance.

237
Q

ACA DNID

Clinical presentation

A

Most common

Frontaal lobe

Confusion or agitation

Somnolence

Abulia

Urinary incontinence.

LL weakness

238
Q

MCA DNID

Clinical presentation

A

Aphasia

Hemiparesis

Monoparesis

Apraxias

239
Q

VB DNID

A

Reduced LOC

240
Q

Ix in ?vasospasm

A

Exclude other causes of neurological deterioration (electrolytes, HCP, haemorrhage)

Positive response to initial management is highly supportive of the diagnosis of vasospasm

TCD

CT perfusion studies

SPECT

DWI MR

CT angio

DSA

241
Q

TCD in vasospasm

A

Operator dependent and will only detect spasm in large anterior circulation arteries.

Flow velocity of >150cm/s is considered indicative of vasospasm in MCA

242
Q

What is the Lindegard ratio?

A

Ratio of MCA mean flow velocity to extracranial ICA flow

(as flow velocity is dependent on CO)

LR >3 designates vasospasm

243
Q

What ist the most sensitive methodology for detecting vasospasm?

A

DSA

244
Q

Prevention of vasospasm

A

Adequate fluids (3L per day)

Avoid hypotension

Nimodipine

245
Q

Targets for hypervolaemia in SAH

A

CVP up to 8-10mmHg

246
Q

Additional methods to treat vasospasm

A

Intra-arterial nimodipine or verapamil

Transluminal balloon angioplasty

Early aneurysm treatment and then surgical toilet

Lumbar drainage may draw spasmogens into the lumbar cistern.

247
Q

What proportion of aSAH die before reaching medical care?

A

25%

248
Q

Risk of rebleeding on day one

A

4%

249
Q

Risk of aneurysm rebeleeding after day one

A

1.5% per day

250
Q

What proportion of unsecured aneurysms will re-rupture in the first 2 weeks

A

20%

251
Q

What proportion of aneurysms will re rupture in the first 6 months?

A

50%

252
Q

What is the late mortality rate of rebleeds in aSAH

A

60%

253
Q

Annual rebleed rate of unsecured IA in SAH

A

3% per annum after the first 6/12.

254
Q

Rate of death from early rebleeding?

A

70-90%

255
Q

Outcomes in SAH

A

1/3rd die

1/3rd survive disabled

1/3rd survive independent

256
Q

Neurogenic stunned myocardium

A

Takotsubo type cardiomyopathy

ECG changes including dysrhythmias, ST changes and neurogenic T waves

These are postulated to be secondary to the effect of excess circulating catecholamines as a result of hypothalamic insult from SAH on the repolarisation phase of the ECG.

A degree of subendocardial ischaemia may be seen in severe cases.

257
Q
A

ECG showing T wave inversions and widely splayed T waves (cerebral T waves) in a patient with a subarachnoid haemorrhage.

258
Q

Rate of cerebral infarction post SAH

A

Up to 26% post ictus

259
Q

What proportion of patients who undergo successful aneurysm clipping return to their pre-morbid life?

A

2/3rds never return to premorbifd life

260
Q

Factors associated with worse prognosis in SAH

A

Higher WFNS grade

Higher H+H grade

Higher Fisher grade

>70y/o have significantly higher mortality rate

261
Q

Rate of seizures after SAH

A

3%

262
Q

Risk factors for seizrue post SAH

A

Younger age

MCA

IC haematoma

SDH

Poor grade

Surgical treatment

263
Q

Causes of non-traumatic SAH

A

aSAH (most common)

Dural AVF

AVM

Leptomeningeal metastasis

Call-Fleming Syndrome

pmSAH

Amyloid

264
Q

Dx of RCVS

A

Exclude other pathology (CT, LP, MR)

Diagnosed by identifying diffuse reversible cerebral vasoconstriction (either with MR/CT or invasive angiography)

265
Q

Symptomology of SAH

A

Thunerclap headache

Nausea

Vomiting

Meningism

Photophobia

Obtunded

266
Q

Clinical signs of SAH

A

Obtunded

Focal neurology may be present due to local mass effect from a giant aneurysm, parnechymal haemorrhage, SDH, large subarachnoid clot

CN3 (PComm)

CN6 (ICP)

Seizure activity

267
Q

Grade 1 Hunt and Hess

A

Asymptomatic patient or slight clinical manifestations (nuchal rigidity or minimal headache)

268
Q

Hunt and Hess Grade:

Asymptomatic patient or slight clinical manifestations (nuchal rigidity or minimal haeadche)

A

1

269
Q

Grade 2

Hunt and Hess

A

Moderate symptoms with no neurological deficit apart from cranial neuropathy

270
Q

Hunt and Hess Grade

Moderate symptoms with no neurological deficit apart from cranial neuropathy

A

2

271
Q

Grade 3 Hunt and Hess

A

Mild LOC with focal neurological deficit

272
Q

Hunt and Hess Grade

Stupor, deep focal deficit or early stages of a vegetative disturbance

A

4

273
Q

Hunt and Hess Grade 4

A

Stupor, deep focal deficit or early stages of a vegetative disturbance

274
Q

Deep coma or decerebrate

Hunt and Hess Grade

A

5

275
Q

Hunt and Hess Grade 5

A

Deep coma or decerebrate

t

276
Q

What confounding factor must be accounted for with clinical grading of SAH

A

Grade should be determined once any acute HCP is treated

277
Q

WFNS 1

A

15 no motor deficit

278
Q

WFNS 2

A

GCS 13-14

No motor deficit

279
Q

WFNS 3

A

GCS 14-13

Motor deficit

280
Q

WFNS 4

A

GCS 12-7

281
Q

WFNS V

A

GCS 6-3

282
Q

Sensitivity of CTH for SAH in first 24h

A

>95%

283
Q

Sensitivity of CTH for SAH after 48h?

A

70%

284
Q

Confounders for xanthochromia in CSF?

A

High bilirubin levels

High protein levels

Traumatic tap

285
Q

Characteristic haemorrhage for AComm?

A

Intraparenchymal haemorrhage in the frontal lobe

IVH

SAH

286
Q

Management of unsecured aneurysm

A

HDU

SBP >140

Bed rest

ECG +/ Echo

287
Q

What are two possible pattenrs of non-aneurysmal SAH

A

Peri-mesencephalic

Diffuse

288
Q

Pattern of blood in perimesencephalic SAH?

A

Blood confined to basal cisterns surrounding the midbrain and constrained by Liliequist’s membrane (can include the proximal part of the Sylvian fissure

289
Q

Lillequist Membrane

A

Liliequist membrane is an arachnoid membrane separating the chiasmatic cistern, interpeduncular cistern and prepontine cistern. It arises anteriorly from the diaphragma sellae and extends posteriorly separating into two sheets, although some authors delineate three discrete components

One extends posterosuperiorly to the posterior edge of the mammillary body (known as the diencephalic membrane); it separates the suprasellar cistern from the interpeduncular cistern 8.

The second sheet extends posteroinferiorly to the pontomesencephalic junction (known as the mesencephalic membrane); it separates the interpeduncular and prepontine cisterns 8.

Laterally it is described as being attached to the oculomotor nerve (CN III), although there is some disagreement concerning the sites of the superior attachment and its lateral border 6.

The Liliequist membrane has neurosurgical importance, especially in endoscopic and microsurgery, and historically needed to be negotiated when performing pneumoencephalography 7.

290
Q

Ix for ?non-aneurysmal SAH

A

Initial then interval imaging (6/52 post ictus)

291
Q

Indications for aneurysm coil ebmolisation

A

Neck to dome ratio of 2:1

Neck size <5mm favourable

Close relationship to the neighbouring artery (unfavourable)

Vertebrobasilar aneurysms

Age

292
Q

Indications for Balloon- assisted coilining

A

Wide necked aneurysms

Small aneurysms

Bifurcation aneurysms

Aneurysms with branches from the neck

293
Q

Complications of endobascular coil ebmolisation

A

4-5% risk of stroke

7% risk of intraprocedural rupture

Coil migration

Incomplete aneurysm obliteration

Aneurysm recurrence (20%)

Aneurysm rebleeding

Contrast nephropathy

Groin haematoma

294
Q

Who clipped the first intracranial aneursym?

A

Dandy in 1937

295
Q

Which aneurysms can be accessed through pterional craniotomy?

A

Majority of anterior circulation aneurysms

AComm

PComm

MCA bifurcation aneurysms.

296
Q

Surgical approach to aneurysms from the A2 and beyond?

A

Bifrontal craniotomy and interhemispheric approach

297
Q

Approach for aneurysms of the upper basilar trunk?

A

Pterional craniotomy with additional removal of the orbitozygomatic unit to allow fot he wide trans-Sylvian dessection

298
Q

Approach to PIC aneurysm

A

Far lateral craniotomy

299
Q

Approach to VB junction aneuryms

A

Retrosigmoid

300
Q

What has happened?

A

There has been intraprocedural rupture of the basilar tip aneurysm

301
Q

General principle of selecting craniotomy type for aneurysm

A

Adequate line of sight to aneurysm whilst minimising brain retractoin

302
Q

Patient positioning for pterional craniotomy

A

Mayfield

Rotate 15-20 degrees away from the site of the aneurysm

Head extended 20 degrees to make the malar eminence the high point of the surgical field.

Head then lift above the heart.

303
Q

Incision for pterional

A

Curvilinear beginning at the zygomatic arch 1cm anterior to the tragus and curving to the midline behind the hairline at the widow’s peak.

Scalp elevated to expose the zygomatic root postero-inferiorly and the keyhole anteriorly

304
Q

Why should the temporalis fascia not be entered during pterional craniotomy?

A

It contains the frontalis branch of the facial nerve

305
Q

Incision of the temporalis muscle in pterional craniotomy?

A

Incised from the zygomatic arch to the superior temporal line along the skin incision then anteriorly to the keyhole, running 1cm below the superior temporal line.

The temporalis is flapped anteriorly, leaving a cuff of fascia and muscle along the superior temporal line to suture the muscle to during closure for improved cosmetic outcome.

306
Q

When has adequate bone been removed during pterional craniotomy?

A

When there is a flat surface over the orbit connecting the anterior and middle cranial fossa.

307
Q

What is the use of the brinfrontal craniotomy for vascular neurosurgery?

A

Facilitates interhemispheric approach to distal anterior cerebral artery aneuryssms e.g. pericallosal

308
Q

What is the benefit of the bifrontal approach for ACA aneurysms?

A

Pericallosal aneurysms are normally in the midline but deep to the falx.

The bifrontal approach allows for sutures to retract the superior sagittal sinus allowing a direct view to the aneurysm

309
Q

Positioning for the bifrontal craniotomy

A

Supine with head in neutral or for more distal aneurysms the head can be placed in a lateral position with a 45-degree tilt.

310
Q

Incision in bifrontal craniotomy

A

For right-sided approaches

Begins at the right zygoma and ends at the contralateral superior temporal line because the craniotomy is eccentric to the right side

311
Q

Scalp flap in bifrontal; craniotomy

A

Scalp pulled forward to expose the supraorbital frontal bone from the ipsilateral superior temporal line to the contralateral glabella.

Temporalis muscle undisturbed

312
Q

Craniotomy in bifrontal

A

Rectangular craniotomy made that is two-thirds in front of the coronal suture and just across the midline to the contralateral side.

Care must be taken to strip the dura away from the skull to prevent venous sinus injury

313
Q

Dural incision in bifrontal craniotomy

A

Semicircular flap with its hinge point being the SSS.

The interhemispheric fissure is then in view and subarachnoid dissection can continue down to the aneurysm.

314
Q

What are the benefits of the orbitozygomatic craniotomy for trans-Sylvian approach

A

Dramatically enhances the standard pterional craniotomy, increasing exposure, minimising retraction and improving manoeuvrability for large, giant or complex anterior circulation aneurysms and for aneurysms of the upper basilar trunk,

315
Q

Use of the far lateral craniotomy in aneurysm surgery

A

Provides an excellent corridor to access most PICA aneurysms

316
Q

Patient position for far lateral craniotomy?

A

Modified park bench or three-quarter prone position with the lesion side upward

The dependent arm hangs in a paddled sling.

317
Q

Head position in far lateral craniotomy

A

Three manoeuvres are used

Flexion in the AP plan until the head is one finger’s breadth from the sternum

Rotation 45 degrees away from the side of the lesion, bringing the nose to the floor

Lateral flexion 30 degrees downward towards the floor.

The ipsilateral mastoid process becomes the highest point of the operative shield.

These manoeuvres put the clivus perpendicular to the floor, allowing the surgeon to look down the axis of the vertebral axis.

318
Q

Incision in the far lateral craniotomy?

A

Hockey-stick incision made beginning in the cervical midline over the C4 spinous process, extending cephalad to the inion, coursing laterally over the superior nuchal line to the mastoid bone and finishing inferiorly at the mastoid tip.

319
Q

Bony access in far lateral craniotomy

A

Myocutaneous flap opened inferolaterally to expose the occipital bone and foramen magnum.

C1 laminectomy performed laterally tot he sulcus arteriosus,

Suboccipital craniotomy is extended unilaterally from the foramen magnum up to the muscle cuff at the level of the transverse sinus and as far laterally as possible then back to the foramen magnum

320
Q

Action after initial craniotomy in far lateral approach?

A

Foramen magnum widened using rongeurs and high-speed drill.

Suboccipital craniotomy is extended past the midline.

The posteromedial two thrids of the occipital condyle are drilled away.

321
Q

What defines the anterior extent of the condylar resection

A

The condylar emissary vein or the dura that .begins to curve anteromedially.

The condylar resection allows the dural flap reflected against the condyle to be completely flat.

322
Q

Dural incision in far lateral craniotomy?

A

Curves from the cervical midline, across the circular sinus to the lateral edge of the cranitomy.

323
Q

The technique for subarachnoid dissection?

A

Cutting with microscissors

Spreading with bipolar forceps

Probing with a slightly curved blunt dissector

324
Q
A

Rhoton microdissectors

325
Q

Sequential approach to aneurysm exposure

A

Expose afferent, efferent arteries and aneurysm neck.

Identify perforating arteries.

326
Q

Purpose of temporary clipping of aneurysm?

A

Can give more confidence in final dissection.

Soften aneurysm dome

Allow for better identification of perforating arteries

327
Q

What can be used to minimise ischaemic injury from temproary clipping?

A

Barbiturate burst suppression.

Raising systemic blood pressure.

328
Q

Different types of clipping

A

Simple clipping

Multiple intersecting clips

Stacked clipping

Overlapping clips

Tandem clipping

329
Q

Tandem clipping

A

Fenestrated clip to close the distal aspect of the aneurysm neck followed by a shorter clip to close the proximal portion of the aneurysm neck can also be used.

Force of the fenestrated clip is greatest at the distal end of the clip to allow an even distribution of force across the whole aneurysm neck and prevent refilling.

330
Q

Technical response to intraoperative aneurysm rupture?

A

Tamponade (cotton placed over rupture site)

Suction

Proximal control with temporary clipping.

Permanent aneurysm clipping.

331
Q

What can be used intraoperatively to determine post-clipping blood flow?

A

Indocyanine green video angiography

332
Q

Key steps in AComm aneurysm clipping

A

Identify H of A1 2 branches to ensure that none of the branches are compromised on clip application.

Safe corridors of vascular dissection must be established around the aneurysm.

Risk of intraoperative rupture with injudicious frontal lobe retraction.

333
Q

Dissection of anteriorly projecting AComm aneurysm

A

Outer border of the ipsilateral A1 and ipsilateral A2

Then contralateral A1 and A2

334
Q

Dissection of posteriorly facing ACom aneurysm

A

Ipsilateral A1 and A2 then contralateral A2 as the contralateral A1 is obscured by the aneurysm dome.

335
Q

Disseciton of superiorly projecting AComm aneurysm

A

Ipsilateral and contralateral A1s dissected to provide proximal control before identifying both A2s.

These often require a fenestrated clip around the ipsilateral A2 to avoid leaving a neck remnant.

336
Q

Positioning for posteriorly projecting ICAA fundus

A

Greater degree of head rotation is required to reveal the neck of the aneurysm behind the ICA.

337
Q

Approach to laterally projecting ICAA?

A

Care must be taken with temporal lobe retraction as it maybe adheerent to the aneurysm

Ther anterior choroidal artery branches may be duplicated and must all be preserved.

338
Q

When is it most important to presrve the PComm?

A

In fetal configuration

339
Q

An important step in ICA bifurcation aneurysm clipping?

A

Careful identification and dissection of the medial and lateral lenticulostriate perforators is required to avoid incorporation into the aneurysm clip

340
Q

Why is extensive dissection of the entire MCAA fundus important?

A

Variation in the number of M2 branches ins common.

341
Q

Why are pericallsoal aneurysms challenging?

A

The aneurysm fundus will be encountered before the parent vessels are identified and controlled.

342
Q

Possible definitions of complex aneurysms

A

>10mm

Those with intraluminal thrombosis

Previously coiled

Heavily calcified

Fusiform or true blister morphology.

343
Q

What is the use of intracrnail stent to assist coiling

A

Can be used for wide-necked aneurysms

The coil mass can be “jailed” in the aneurysm with the stent wires preventing prolapse of coils into the patent vessel.

344
Q

What is a consideration with the use of endovascular stents?

A

Increased risk of thromboembolic complications and as such DAPT may be required.

345
Q

Flow diverters

A

Intraluminal flow is redirected to the distal parent vessel rather than into the aneurysm using a stent with a low porosity mesh weave.

Adjunctive coils may also be placed into the aneurysm to provide immediate aneurysm closure and prevent delayed haemorrhage from a ball-valve haemodynamic effect.

346
Q

What is the main limitation to flow-divertters

A

Associated with perofrator artery ischaemia

347
Q
A

Neurosurgical Training (7 decks)

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