Vascular Neurosurgery Flashcards
Vascular distribution during embryology to the CoW
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
Def: Fetal PComm
If the PComm remains larger than the ipsilateral P1
What proportion of individuals have a fetal PComm?
25%
What are other anatomical CoW variants?
PComm hypoplasia or absence
A1 hypoplasia
AComm absence
What are some embryonic connections between the carotid and basilar arteries?
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
Persistent primitive trigeminal artery
Connects ICA to the basilar
What happens to pial vessels?
Surrounded by CSF, form penetrating arterioles.
What are Virchow Robin spaces
A small extension of the subarachnoid space surrounding pial vessels which become encased by astrocytic end-feet.
What are the layers of cerebral arteries?
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)
Features of cerebral veins
Thin wall
No valves
Minimal smooth muscle
Less closely follow the arterial system
Level of carotid bifurcation
C4
Carotid sinus with associated carotid sinus
What does the carotid bulb sense?
Baroreceptor
What does the carotid sinus sense?
Chemoreceptor, influences respiratory pattern
Classification of the ICA
Bouthillier
Cervical
Petrous (horizontal)
Lacerum
Cavernous
Clinoid
Ophthlamic (supraclinoid)
Communicating
Number of branches of the cervical carotid
0
Under which ligament does the laceral segment of the ICA pass before entering the cavernous sinus?
Petrolingual ligament
Branches of the petrous portion of the ICA?
Caroticotympanic
Mandibulovidian
What are the two important branches of the intracavernous ICA?
Meningohypophyseal trunk
Inferolateral trunk
Branches of the meningohypophyseal trunk
Inferior hypophyseal artery-> posterior pituitary lobe
Dorsal meningeal artery
Tentorial artery (artery of Bernasconi and Cassinari)-> tentorium
Clinoid portion of the ICA
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
What is the clinical significance of the distal dural ring?
Differentiates between the pathology caused by ICA aneurysms- caroticocavernous fistula vs SAH,
Access to aneurysms near the origin of the ophthalmic artery will require?
Anterior clinoidecomy
Lateral region between the proximal and distal dural rings
Extradural and extracavernous
What is the cavernous cave?
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
What is the origin of the ophthalmic artery?
Just beyond the distal dural ring, inferior to the optic nerve and anterior clinoid process.
What are the branches of the ophthalmic segment of the ICA?
Ophthalmic
Superior hypophyseal arteries
What is meant by the term paraophthalmic aneurysms?
Used to describe aneurysms of the ophthalmic portion of the ICA which may be radiologically difficult to localise
What are two important ophthalmic artery variants
Can arise from the extradural clinoid portion of the ICA
Can rarely arise from the ECA
Meningo-ophthalmic artery
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.
Extent of the communicating segment of the ICA
From the PComA origin to the ICA bifurcation.
Length of PComm
Around 1cm
Posterolaterally projecting PCommA cause a?
Surgical CN3 palsy
Perforators from PCom
Small branches are given off supplying the genu of the internal capsule and the thalamus
The largest branch is the premamillary artery (anterior thalamoperforator)
Where is the anterior choroidal artery given off
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
Consequence of anterior choroidal ligation
Hemiparesis
Hemianaesthesia
Hemianopia
Divisions of the anterior choroidal
Cisternal
Intraventricular segment
Cisternal segment of the anterior choroidal
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
Structures supplied by the anterior choroidal?
Optic pathways
Posterior limb of the internal capsule
Basal ganglia
Choroid plexus of the temporal horn of the lateral ventricle
What is the best angiographic view of the ICA bifurcation
Oblique
Where do blister aneurysms typically arise?
Dorsomedial wall of non-branching parts of the ICA
What separates the ACA into A1 and A2 segments?
The AComm
A1= precommunicating
Relationship of A1 to the optic nerve?
Crosses over the optic tract anteromedially
Variants of the A1 segment
Maybe hypoplastic with supply from the contralateral A1 via the AComm
Unpaired or azygos ACA
Duplicated or fenestrated AComm segments.
Where do medial lenticulostriate branches of the ACA typically arise and what do they supply?
From the inferoposterior aspect of the A1 segment and supply the GP and medial putamen through the anterior perforated substance
Where does the A2 end?
With the formation of the callosomarginal and pericallosal arteries at the genu of the corpus callosum
What is the first cortical branch of the ACA?
The orbitofrontal artery
Supplies the inferior part of the frontal lobe
What are the 2 main branches of the A2 segment of the ACA?
Orbitofrontal artery (Inferior part of frontal lobe)
Frontopolar artery (anterior part of the superior frontal gyrus)
Location of the AComm
Lies in the cistern of the lamina terminalis
Classification of AComm branches
Subcallosal
Hypothalamic
Chiasmatic
What is the largest of the perforating branches of the ACA?
Recurrent artery of Heubner
Location of the recurrent artery of Heubner?
Arises from the proximal A2 segment near the A1/2 junction but can also arise from the A1
Structures supplied by the recurrent artery of Heubner
Anterior limb of internal capsule
Caudate nucleus
GP
Pericallosal artery
Considered a continuation of the ACA and closely follows the corpus callosum
In what proportion of patients is a callosomarginal artery present?
50%
Structures supplied by the pericallosal artery
Corpus callosum and its splenium
Septum pellucidum
Fornix
Precuneus cortex
Structures supplied by the callosomarginal artery?
Superior frontal gyrus through various branches
Takes a course through the cingulate sulcus
Terminates as the paracentral artery supplying the paracentral lobule
Where does the M1 end
At the MCA bifurcation as the distal M2
Location of the M1
Runs laterally in the anterior compartment or sphenoidal compartment of the deep component of the Sylvian fissure between the frontal and temporal lobes
From where do the lateral striate (lenticulostriate) arteries arise?
Form the posteroinferior part of the M1, travelling backwards along its course to penetrate the lateral portion of the anterior perforated substance
Structures supplied by the lateral striate arteries?
Basal ganglia
Internal capsule
Caudate nculeus
Passage of the M1
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.
In what proportion of individuals does PICA arise below the foramen magnum?
15%
Anatomical variations in PICA
Hypoplastic (there is often an increase in AICA calibre)
One vertebral artery may form the PICA directly.
How many MCA segments are there?
4
M1 segment
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.
M2 segment
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.
M3 segment
Opercular segment
Origin at the circular sulcus of the insula
Courses along the frontoparietal operculum
Terminates at the external surface of the operculum
M4 segment
Cortical segment
Originates at the external/top surface of the Sylvian fissure
Courses superiorly on the lateral convexity
Terminates at their final cortical territory
Segments of the PICA
Anterior medullary
Lateral medullary
Tonsillomedullary
Telovelotonsillar
Cortical (suboccipital surface)
Which nerve is closesly related to PICA at its anterior medullary segment
Hypoglossal
Which segment of the PICA forms the caudal loop?
Tonsillomedullary
Which number is PICA?
4 (caudal loop of tonsillomedullary segment followed by cranial loop)
Which PICA segment forms the cranial loop?
Telovelotonsillar segment
Which structures are supplied by the PICA?
Lateral medulla
Fourth ventricle choroid plexus
Inferior and posterior cerebellum
The general pattern of arterial supply to the midbrain, pons, medulla
Via short and long perforators to the anterior and posterolateral parts with long circumflex branches travelling over the lateral surface.
Where do the AICAs typically arise?
Near to the abducens nerve
Passage of the ACIA
Traverses the CPA closely related to the facial and vestibulocochlear nerves to supply the anterior and inferior cerebellum.
Whence does the labyrinthine artery arise?
Either from AICA or from the basilar
Passes with the vestibulcoochlear nerve to supply the inner ear
The origin of the SCA is close to which cranial nerve?
3
Structures supplied by the SCA
Superior cerebellar hemispheres
Peduncles
Vermis
Segments of AICA
Anterior pontine
Lateral pontomedullary
Flocculonodular
Cortical (petrosal surface)
Segments of SCA
Anterior pontomesencephalic
Lateral pontomesencephalic
Cerebellomesencephalic
Cortical
What are Rhoton’s three neurovascular complexes in the posterior fossa?
Upper
Middle
Lower
Upper neurovascular complex
Vessel
Brainstem region
Fissure
CNs
Cerebellar peduncle
Cerebellar surface
SCA
Midbrain
Cerebellomesencephalic
III, IV, V
Superior
Tentorial surface
MIddle neurovascular complex
Vessel
Brainstem region
Fissure
CNs
Cerebellar peduncle
Cerebellar surface
AICA
Pons
Cerebellopontine
VI, VII, VIII
MIddle
Petrosal
Lower neurovascular complex
Vessel
Brainstem region
Fissure
CNs
Cerebellar peduncle
Cerebellar surface
PICA
Medulla
Cerebellomedullary
IX, X, XI, XII
Inferior
Suboccipital
Location of P1
Horizontal segment, sits within the interpeduncular fossa before anastomosing with PComA
What is the artery of Percheron
Single large thalamoperforate branch that can supply both thalami and the midbrain
The manifestation of artery of Percheron occlusion?
Paramedian thalamic syndrome
Altered conscious state
Vertical gaze palsy
Impaired memory.
P2 segment of PCA
Distal to PCommA
Traverses around the oculomotor nerve in the ambient cistern to sit above the tentorium
Divided into the P2A and P2P segments
What demarcates P2A from P2P segments
Junction at most lateral aspect of the cerebral peduncle
Branches of the P2 segment
Multiple perforating branches including the thalamogeniculate and lateral and posterior choroidal arteries.
How does the lateral posterior choroidal artery enter the lateral ventricle?
Adjacent to the LGN via the choroid fissure
Passage of the medial posterior choroidal artery?
Passes beneath the splenium to enter the roof of the third ventricle in the velum interpositum.
Principle anastomoses between ECA and ICA
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
Which arteries supply the posterior fossa dura?
Ascending pharyngeal and occipital
Which arteries supply the supratentorial dura?
MMA and accessory meningeal branches of maxillary
Into what does the superficial middle cerebral vein drain?
Into the cavernous or the sphenoparietal sinus
Superficial middle cerebral vein
Into what does the vein of Trolard drain?
Into the SSS
Into what does the vein of Labbe drain?
Labbe drains into the transverse sinus
What is the reciprocal arrangement of the two superficial anastomotic veins?
Labbe larger in dominant hemisphere and Trolard in non-dominant
Location of the great cerebral vein of Galen
Found below the splenium of the corpus callosum
What forms the Great vein of Galen
Joining of the two internal cerebral veins
Two basal veins of Rosenthal
Occipital veins draining the medial and inferior occipital lobes
Which structures form the straight sinus?
Great vein of Galen and ISS
Passage of the basal veins of Rosenthal
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
Structures drained by basal vein of Rosenthal?
Hypothalamus
Midbrain
Medial and inferior portions of the frontal and temporal lobes including the operculum and insula
Location of the internal cerebral veins
Located in the velum interpositum
Velum interpositum
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.
What form the internal cerebral veins
Choroidal veins and thalamostriate veins
What veins drain into the thalamostriate?
Transverse caudate veins
Anterior terminal vein
Septal vein
Passage of the SSS
Crista galli-> torcular Herophili
Etymology Torcula
Wine press
Transverse sinus dominance
Often asymmetric with dominant right receiving the majority of blood from the SSS
At what point do the transverse sinuses become the sigmoid?
At the posterior petrosal edge
What structures drain into the cavernous sinus?
Superficial middle cerebral veins
Ophthalmic veins
Sphenoparietal sinus
Outflow of cavernous sinus
Superior and inferior petrosal sinuses
Superior petrosal sinus connects to?
Sigmoid sinus
Occipital sinus
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
Venous drainage of the cerebellum
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
Drainage of the brainstem
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)
Dandy’s vein
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.
Cerebellar vein
Unpaired vein running posterior to the cerebellum
Draining into the superior vermian vein or great vein of Galen
What is the anatomical signficance of the cerebellar vein
inferior aspects marks the upper border of the fourth ventricle
What are the anatomical considerations for large AVMs straddling more than one lobe?
Naturally will be supplied by multiple arterial territories as well as watershed regions.
Anatomical divisions of lateral hemisphere AVMs
Frontal, temporal, parietal, occipital, peri-Sylvian
What is a surgical consideration for AVMs extending towards the superior frontal lobe or frontal pole
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.
Drainage of lateral hemisphere AVMs
Drain via superficial veins into the SSS or the transverse sinus
Those more centrally located may involve the veins of Trollard or Labbe
Temporal AVMs extending onto the tentorial surface may drain into?
vein of Rosenthal
Arterial supply of medial hemisphere AVMs
Anteriorly by the callosomarginal artery or pericallosal.
Disruption of medial hemispheric artery supply may result in ?
Transient SMA syndrome
Which arteries should be preserved in medial hemisphere AVM surgery?
A3 and 4 (distal pericallosal) arteries to the paracentral lobule.
Venous drainage of medial hemisphere AVMs
SSS
Vein of Galen
Arterial supply of deep supratentorial AVMs?
Subcortical deep extensions recruit deep perforator feeders such as lenticulostriate from the MCA, A1 perforators and the recurrent Arteries of Heubner
Consideration for deep supratentorial AVMs
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
How can intraventricular AVM extension be demonstrated angiographically?
By demonstrating supply from the choroidal arteries angiographically.
Suboccipital and paravermian AVMs likely fed by
PICA branches beyond the tonsillar loop and with fourth ventricular extension also its choridal branches
Suboccipital and tentorial surface AVMs fed by?
SCA
AVMs on the petrosal cerebellar surface may have feeders from?
AICA
CO required by the brain?
14%
When does irreversible ischaemic brain damage occur?
4 minutes (if global)
CPP=
MAP-(ICP+CVP)
MAP=
2/3(DBP) + 1/3(SBP)
Def: Cerebral autoregulation
Is the ability of the brain to regulate its blood flow despite changes in systemic blood pressure
Significance of CVP in CPPP
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
What is the consequence of increasing intracranial volume beyond the critical volume?
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
Draw the intracranial pressure-volume curve
CBF volume/minute
700ml/inute
around 50ml per 100g
At what CBF are EEG changes seen
CBF <20ml/min
At what CBF are ischaemic changes seen
<10ml/minute
Draw the CBF autoregulatory curve
What are the 3 mechanisms of cerebral autoregulation
Myogenic
Neurogenic
Metabolic
Myogenic regulation of CBF
Thought to involve the myogenic response of cerebral smooth muscle in vessel walls.
Neurogenic control of CBF
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.
What is the significance of neuromodulation of the autoregulatory curve?
Represents a protective physiological mechanism preventing significant CBF rises and BBB break down with acute surges in BP.
Draw the CBF PaO2 curve
Draw the CBF PaCO2 curve
CO2 and cerebral blood flow
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.
O2 and cerebral blood flow
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.
Mannitol and cerebral blood flow
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.
Def: aneurysm
Pathological acquired dilatation of a vessel >50% of its diameter involving all layers of its wall
What proportion of intracranial aneurysms are saccular / Berry?
80-90%
Prevalence of intracranial aneurysms
Found in 1-5% of adult population at autopsy
What proportion of spontaneous SAH is aneurysmal?
80-85%
Epidemiology of SAH
5th decade
F: M 3:2
Factors contributing to the pathophysiology of aneurysms
Vessel wall
Genetic
Haemodynamic
Environmental
Aneurysm pathophysiology
Vessel wall biology
Intracranial aneurysms are found at bifurcation where there are more collagen than elastic fibres and the muscular wall is less well developed.
Aneurysm pathophysiology
Genetic factors associated with aneurysm formation
Autosomal dominant PKD
Ehlers-Danlos
Marfan’s
NF1
Pseudoxanthoma elasticum
Aneurysm pathophysiology
Haemodynamics
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.
Aneurysm pathophysiology
Environmental factors
Cigarette smoker
HTN
Hazard ratio
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.
Rhoton’s rules on intracranial aneurysms
- Arise at branching sites of the parent artery (e.g. PComm, MCA bifurcation, basilar bifurcation)
- Arise from a turn or curve of the artery
- Dome lays in the direction of maximal haemodynamic flow
Distribution of aneurysms
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
Classification of aneurysms based on size
Small <10mm
Large 11-25mm
Giant >25mm
Size cut off for giant aneurysm
>25mm
Anatomical components of aneurysm
Neck
Fundus
Def: wide-neck aneurysm
>4mm neck
What are the important morphological features affecting endovascular treament
Neck width
Neck:dome
What morphological factors feed into the risk of rupture
Aneurysm angle
Aspect ratio (cranio-caudal dimension divided by transverse diameter).
What is the significance of blebs
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.
Increased risk of IA in relatives in patients with IAs +/- aSAH?
15 fold
Indications for familial screening in IAs?
When >30y/o if two or more relatives affected by SAH/IA
ADPKD and IAs
Cererbral aneurysms found in 25%
Increases risk of IA by 10-20 fold dependent on FHx of IAs
Screening for IA in ADPKD
Patients with PKD and FHx of IAs
or
ADPKD and HTN
What is the added significance of connective tissues disease in the context of aneurysmal SAH
They are at increased risk of complications from intravascular diagnostic and therapeutic treatment of intracranial aneurysms
Ehler’s Danlos Collagen
Type IV
Marfan’s Syndrome caused by?
Fibrillin abnormality
Aortic coarctation and IA
Found in 10.3%
Fibromuscular dysplasia
Idiopathic segmental, non-atherosclerotic, non-inflammatory vascular disease that mainly affects renal, extracranial carotid and vertebral arteries.
Risk factors for aneurysm growth
Age >50
Female
Smoking
Non-saccular
Risk of ruptiure in growing IA
3.1% vs 0.1% per year for stable IAs.
Traumatic aneurysms
Account for <1% of all IAs
Second most common type in children (5-15%).
Can be true or pseudo
Most common sites of traumatic aneuryssms
ICA 46%
MCA 25%
ACA 22%
Natural Hx of traumatic aneurysms
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.
Surgeries in which iatrogenic traumatic aneurysms have been reported?
Trans-sphenoidal
Craniotomy for tumour and vascular lesions
EVD
In what layers of the vessel is the tear in dissection?
Intima and internal elastic lamina
Most common site of intracranial dissection?
V4 segment of the vertebral
Possible presentations of dissecting intracranial vessels
Asymptomatic
Ischaemia
Headache
Frank haemorrhage (including SAH)
Def: Blister-like aneurysms
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
Challenge of blister-like aneurysms
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.
Def: Fusiform aneurysm
Dilatation of the arterial wall which involves at least 270 deg of the vessel wall.
Dolioectatic aneurysm
Characterised by uniform pathological dilatation of an entire vessel with associated tortuosity of the vessel itself
Natural Hx of fusiform aneurysms
Can be incidental and then have a fairly benign natural Hx
Can also present with ischaemic symptoms, symptoms related to mass effect and haemorrhage.
Def: Mycotic aneurysm
Implies the presence of infection with vessel wall estruction
Treatment of mycotic aneurysms
Identify source
Appropriate Abx
4-6/52 of therapy at least.
Can be managed endovascularly or surgically in specfici situations
Rate of multiple intracranial aneurysms in SAH
Up to 35% in IUSIA
Minimum age for screening in IAs
<10y from time of ictus for family member
Management of incidental IAs
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.
Rate of aneurysm causing spontaneous SAH
85%
What proportion of non-aneurysmal spontaneous SAH is perimesencephalic?
60%
Causes of non-aneurysmal SAH
pial AVM
Tumours
Anticoagulants
Vascular dissections
Vasculitides
Location of haemorrhage in peri-mesencephalic SAH
Prepontine
Perimesencephalic cisterns with some extension into the adjacent cisterns
No blood in ventricles, Sylvian fissure of interhemispherically.
Peri-mesencephalic SAH
Complications of SAH
Intracranial:
Rebleed
Hydrocephalus
Delayed ischaemia
Seizures
Haematoma
Extracranial:
Hyponatraemia
Sepsis
Neurogenic stunned myocardium
Neurogenic pulmonary oedema
Clinical hx in SAH
Sudden onset headache
Meningism
Altered sensorium
Coma
Pathophysiology of acute SAH
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.
Subsequent pathophysiology post ictus in SAH
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
Rate of HCP on presentation in SAH
Up to 20%
What proportion of pateints presenting with HCP in context of SAH will show reduced consciousness
Up to 50%
What proportion of patients with SAH presenting with HCP may require shunt?
Up to 50%
Pathophysiology of acute HCP in SAH
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
Considerations for Mx of acute HCP in SAH
EVD, higher pressure in unsecured aneurysms due to risk of precipitating rebleed.
Serial lumbar punctures or lumbar drain
Intra-operative measurements to reduce HCP in aneurysm clipping
CSF toilet
ETB
Incidence of SAH
6-11/100,000 per annum.
Key findings in ISUIA
Small (<7mm) anteiror ciruclation aneurysms have a low rupture rates as do small type 1 aneurysms of the posterior circulation
Type 2 IAs
Aneurysms in the context of previous SAH or multiple intracranial aneurysms.
Confer increased risk of rupture
Risk score for aneurysm rutprure
PHASES
Components of PHASES score
Population (Japanese or Finnish)
HTN
Age >70
Size
Earlier SAH
Site (anatomical)
Outcome in vasospasm
Death in up to 7%
Cerebal infarction in 26%
Clinical manifestation of vasospasm
Narrowed arterial calibre demonstrated on vascular imaging resulting in delayed ischaemic neurological deficits.
Rate of radiological vs clinical vasospasm
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.
Pathophysiology of vasospasm
Not understood.
Vascular smooth muscle contraction
Endothelial cell lose NO synthesis
Proinflammatory cascade results in vessel ECM remodelling.
Incidence of DNID in SAH
30-40%
Risk factors for DNID
Increase risk with increased subarachnodi blood volume
Fisher grade correlates with risk of vasospasm.
Higher WFNS
Increasing age
HTN
HCP
Timecoure of DNID
Rarely seen <3d post ictus
Peaks 6-8/7 post SAH
Can be as late as the third week.
Clinical presentation of vasospasm
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.
ACA DNID
Clinical presentation
Most common
Frontaal lobe
Confusion or agitation
Somnolence
Abulia
Urinary incontinence.
LL weakness
MCA DNID
Clinical presentation
Aphasia
Hemiparesis
Monoparesis
Apraxias
VB DNID
Reduced LOC
Ix in ?vasospasm
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
TCD in vasospasm
Operator dependent and will only detect spasm in large anterior circulation arteries.
Flow velocity of >150cm/s is considered indicative of vasospasm in MCA
What is the Lindegard ratio?
Ratio of MCA mean flow velocity to extracranial ICA flow
(as flow velocity is dependent on CO)
LR >3 designates vasospasm
What ist the most sensitive methodology for detecting vasospasm?
DSA
Prevention of vasospasm
Adequate fluids (3L per day)
Avoid hypotension
Nimodipine
Targets for hypervolaemia in SAH
CVP up to 8-10mmHg
Additional methods to treat vasospasm
Intra-arterial nimodipine or verapamil
Transluminal balloon angioplasty
Early aneurysm treatment and then surgical toilet
Lumbar drainage may draw spasmogens into the lumbar cistern.
What proportion of aSAH die before reaching medical care?
25%
Risk of rebleeding on day one
4%
Risk of aneurysm rebeleeding after day one
1.5% per day
What proportion of unsecured aneurysms will re-rupture in the first 2 weeks
20%
What proportion of aneurysms will re rupture in the first 6 months?
50%
What is the late mortality rate of rebleeds in aSAH
60%
Annual rebleed rate of unsecured IA in SAH
3% per annum after the first 6/12.
Rate of death from early rebleeding?
70-90%
Outcomes in SAH
1/3rd die
1/3rd survive disabled
1/3rd survive independent
Neurogenic stunned myocardium
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.
ECG showing T wave inversions and widely splayed T waves (cerebral T waves) in a patient with a subarachnoid haemorrhage.
Rate of cerebral infarction post SAH
Up to 26% post ictus
What proportion of patients who undergo successful aneurysm clipping return to their pre-morbid life?
2/3rds never return to premorbifd life
Factors associated with worse prognosis in SAH
Higher WFNS grade
Higher H+H grade
Higher Fisher grade
>70y/o have significantly higher mortality rate
Rate of seizures after SAH
3%
Risk factors for seizrue post SAH
Younger age
MCA
IC haematoma
SDH
Poor grade
Surgical treatment
Causes of non-traumatic SAH
aSAH (most common)
Dural AVF
AVM
Leptomeningeal metastasis
Call-Fleming Syndrome
pmSAH
Amyloid
Dx of RCVS
Exclude other pathology (CT, LP, MR)
Diagnosed by identifying diffuse reversible cerebral vasoconstriction (either with MR/CT or invasive angiography)
Symptomology of SAH
Thunerclap headache
Nausea
Vomiting
Meningism
Photophobia
Obtunded
Clinical signs of SAH
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
Grade 1 Hunt and Hess
Asymptomatic patient or slight clinical manifestations (nuchal rigidity or minimal headache)
Hunt and Hess Grade:
Asymptomatic patient or slight clinical manifestations (nuchal rigidity or minimal haeadche)
1
Grade 2
Hunt and Hess
Moderate symptoms with no neurological deficit apart from cranial neuropathy
Hunt and Hess Grade
Moderate symptoms with no neurological deficit apart from cranial neuropathy
2
Grade 3 Hunt and Hess
Mild LOC with focal neurological deficit
Hunt and Hess Grade
Stupor, deep focal deficit or early stages of a vegetative disturbance
4
Hunt and Hess Grade 4
Stupor, deep focal deficit or early stages of a vegetative disturbance
Deep coma or decerebrate
Hunt and Hess Grade
5
Hunt and Hess Grade 5
Deep coma or decerebrate
t
What confounding factor must be accounted for with clinical grading of SAH
Grade should be determined once any acute HCP is treated
WFNS 1
15 no motor deficit
WFNS 2
GCS 13-14
No motor deficit
WFNS 3
GCS 14-13
Motor deficit
WFNS 4
GCS 12-7
WFNS V
GCS 6-3
Sensitivity of CTH for SAH in first 24h
>95%
Sensitivity of CTH for SAH after 48h?
70%
Confounders for xanthochromia in CSF?
High bilirubin levels
High protein levels
Traumatic tap
Characteristic haemorrhage for AComm?
Intraparenchymal haemorrhage in the frontal lobe
IVH
SAH
Management of unsecured aneurysm
HDU
SBP >140
Bed rest
ECG +/ Echo
What are two possible pattenrs of non-aneurysmal SAH
Peri-mesencephalic
Diffuse
Pattern of blood in perimesencephalic SAH?
Blood confined to basal cisterns surrounding the midbrain and constrained by Liliequist’s membrane (can include the proximal part of the Sylvian fissure
Lillequist Membrane
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.
Ix for ?non-aneurysmal SAH
Initial then interval imaging (6/52 post ictus)
Indications for aneurysm coil ebmolisation
Neck to dome ratio of 2:1
Neck size <5mm favourable
Close relationship to the neighbouring artery (unfavourable)
Vertebrobasilar aneurysms
Age
Indications for Balloon- assisted coilining
Wide necked aneurysms
Small aneurysms
Bifurcation aneurysms
Aneurysms with branches from the neck
Complications of endobascular coil ebmolisation
4-5% risk of stroke
7% risk of intraprocedural rupture
Coil migration
Incomplete aneurysm obliteration
Aneurysm recurrence (20%)
Aneurysm rebleeding
Contrast nephropathy
Groin haematoma
Who clipped the first intracranial aneursym?
Dandy in 1937
Which aneurysms can be accessed through pterional craniotomy?
Majority of anterior circulation aneurysms
AComm
PComm
MCA bifurcation aneurysms.
Surgical approach to aneurysms from the A2 and beyond?
Bifrontal craniotomy and interhemispheric approach
Approach for aneurysms of the upper basilar trunk?
Pterional craniotomy with additional removal of the orbitozygomatic unit to allow fot he wide trans-Sylvian dessection
Approach to PIC aneurysm
Far lateral craniotomy
Approach to VB junction aneuryms
Retrosigmoid
What has happened?
There has been intraprocedural rupture of the basilar tip aneurysm
General principle of selecting craniotomy type for aneurysm
Adequate line of sight to aneurysm whilst minimising brain retractoin
Patient positioning for pterional craniotomy
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.
Incision for pterional
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
Why should the temporalis fascia not be entered during pterional craniotomy?
It contains the frontalis branch of the facial nerve
Incision of the temporalis muscle in pterional craniotomy?
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.
When has adequate bone been removed during pterional craniotomy?
When there is a flat surface over the orbit connecting the anterior and middle cranial fossa.
What is the use of the brinfrontal craniotomy for vascular neurosurgery?
Facilitates interhemispheric approach to distal anterior cerebral artery aneuryssms e.g. pericallosal
What is the benefit of the bifrontal approach for ACA aneurysms?
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
Positioning for the bifrontal craniotomy
Supine with head in neutral or for more distal aneurysms the head can be placed in a lateral position with a 45-degree tilt.
Incision in bifrontal craniotomy
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
Scalp flap in bifrontal; craniotomy
Scalp pulled forward to expose the supraorbital frontal bone from the ipsilateral superior temporal line to the contralateral glabella.
Temporalis muscle undisturbed
Craniotomy in bifrontal
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
Dural incision in bifrontal craniotomy
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.
What are the benefits of the orbitozygomatic craniotomy for trans-Sylvian approach
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,
Use of the far lateral craniotomy in aneurysm surgery
Provides an excellent corridor to access most PICA aneurysms
Patient position for far lateral craniotomy?
Modified park bench or three-quarter prone position with the lesion side upward
The dependent arm hangs in a paddled sling.
Head position in far lateral craniotomy
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.
Incision in the far lateral craniotomy?
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.
Bony access in far lateral craniotomy
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
Action after initial craniotomy in far lateral approach?
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.
What defines the anterior extent of the condylar resection
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.
Dural incision in far lateral craniotomy?
Curves from the cervical midline, across the circular sinus to the lateral edge of the cranitomy.
The technique for subarachnoid dissection?
Cutting with microscissors
Spreading with bipolar forceps
Probing with a slightly curved blunt dissector
Rhoton microdissectors
Sequential approach to aneurysm exposure
Expose afferent, efferent arteries and aneurysm neck.
Identify perforating arteries.
Purpose of temporary clipping of aneurysm?
Can give more confidence in final dissection.
Soften aneurysm dome
Allow for better identification of perforating arteries
What can be used to minimise ischaemic injury from temproary clipping?
Barbiturate burst suppression.
Raising systemic blood pressure.
Different types of clipping
Simple clipping
Multiple intersecting clips
Stacked clipping
Overlapping clips
Tandem clipping
Tandem clipping
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.
Technical response to intraoperative aneurysm rupture?
Tamponade (cotton placed over rupture site)
Suction
Proximal control with temporary clipping.
Permanent aneurysm clipping.
What can be used intraoperatively to determine post-clipping blood flow?
Indocyanine green video angiography
Key steps in AComm aneurysm clipping
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.
Dissection of anteriorly projecting AComm aneurysm
Outer border of the ipsilateral A1 and ipsilateral A2
Then contralateral A1 and A2
Dissection of posteriorly facing ACom aneurysm
Ipsilateral A1 and A2 then contralateral A2 as the contralateral A1 is obscured by the aneurysm dome.
Disseciton of superiorly projecting AComm aneurysm
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.
Positioning for posteriorly projecting ICAA fundus
Greater degree of head rotation is required to reveal the neck of the aneurysm behind the ICA.
Approach to laterally projecting ICAA?
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.
When is it most important to presrve the PComm?
In fetal configuration
An important step in ICA bifurcation aneurysm clipping?
Careful identification and dissection of the medial and lateral lenticulostriate perforators is required to avoid incorporation into the aneurysm clip
Why is extensive dissection of the entire MCAA fundus important?
Variation in the number of M2 branches ins common.
Why are pericallsoal aneurysms challenging?
The aneurysm fundus will be encountered before the parent vessels are identified and controlled.
Possible definitions of complex aneurysms
>10mm
Those with intraluminal thrombosis
Previously coiled
Heavily calcified
Fusiform or true blister morphology.
What is the use of intracrnail stent to assist coiling
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.
What is a consideration with the use of endovascular stents?
Increased risk of thromboembolic complications and as such DAPT may be required.
Flow diverters
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.
What is the main limitation to flow-divertters
Associated with perofrator artery ischaemia
