Vascular Neurosurgery Flashcards
Aneurysmal rebleed rate
0-24 h: 4%
0-2 wk: 20 %
0-6 mo: 50%
> 6 mo: 3%
Associated pathologies with aneurysmal formation
Hypertension
Endocarditis
Poly cystic kidney
Ehler-Donlas
Marfan syndrome
Moyamoya
Pseudoxanthoma elasticum
Aortic coarctation
AVM
Fibromuscular dysplasia
Vasculitis
NF1
ISUIA 1 (1 year rupture risk with unruptured aneurysm)
No previous bleed vs. previous bleed
0-10 mm: 0.05% vs 0.5%
10-24 mm: <1 % vs <1%
>24 mm: 6%
ISUIA 2 (Five-year rupture risk who is unruptured aneurysm)
CAVERNOUS ICA
<7 mm: 0%
7-12 mm: 0%
13-24 mm: 3%
>24 mm: 6.4%
ISUIA 2 (Five-year rupture risk who is unruptured aneurysm)
ANTERIOR CIRCULATION
<7 mm: 0% (1.5% if previous bleed)
7-12 mm: 2.6%
12-24 mm: 14.5%
>24 mm: 40%
ISUIA 2 (Five-year rupture risk who is unruptured aneurysm)
POSTERIOR CIRCULATION
<7 mm: 2.5% (3.5% if previous bleed)
7-12 mm: 14.5%
13-24 mm: 18.4%
>24 mm: 50%
% of aneurysm locations
30% Acom
25% Pcom
20% MCA bifurcation
8% ICA bifurcation
17% other locations
Imaging sensitivity CTA vs. MRI for aneurysm
> 5 mm : 95-100% vs 85-100%
<5 mm : 64-83% vs 56%
Fisher’s grade and vasospasm risk
Grade 1- No bleed (21%)
Grade 2- Diffuse or vertical layer < 1 mm thick (25 %)
Grade 3- Localized clot or vertical layer >1 mm thick (37 %)
Grade 4- ICH or IVH (31%)
Modified Fisher’s and Vasospasm risk
Grade 1: Focal or diffuse THIN SAH (24%)
Grade 2: Grade 1 + IVH (33%)
Grade 3: Focal of diffuse THICK SAH (33 %)
Grade 4: Grade 3 + IVH (40%)
What is Lindegaard’s ratio?
Velocity MCA:ICA
<3 : No vasospasm
3-6: Mild/moderate vasospasm
>6: Severe vasospasm
Mean MCA Velocity
<120 cm/s : No vasospasm
120-200 cm/s: Mild/moderate vasospasm
>200 cm/s: Severe vasospasm
Triple H therapy
Hypervolemia: CVP 10 cmH2O, P wedge 18 mmHg.
Hemodilution: Hct 30%
Hypertension: SBP up to 220 (in secured aneurysm)
ISAT trial primary outcome
Coiling is superior to clipping
At 1 year 24% of coiling patients were dependent/dead vs. 31% in clipping group (mRS 3-6)
Surgical options for fusiform aneurysm
- Wrapping
- Clip reconstruction
- Trapping (+/- distal revascularization)
How do you use PAPAVERINE for vessels in spasms.
Dip cottonoid with 30 mg in 9 ml saline, then place it on artery for 2 minutes.
What is Paine’s point
Used to do ventriculostomy to relax brain during aneurysmal clipping.
From sphenoid ridge: 2.5 cm up + 2.5 cm anterior.
4.5 cm deep
What is management of mycotic aneurysm
Antibiotics: IV for 6 wks then PO for 6 wks.
What is most common organism in mycotic aneurysm
Streptococcus viridan (44%)
Staph aureus (18%) : classic in endocarditis
AHA/ASA guidelines for spontaneous ICH
1.Hemostasis: correct coagulopathy.
2. DVT prophylaxis: intermittent pneumatic compression.
3. SBP< 140
4. Seizure control: patient with clinical seizures, patient with mental status change + seizures findings on EEG.
STICH 1
Inclusion criteria
Spontaneous ICH
-Arisen within 72 h
-At least 2 cm on CT scan
-GCS >=5/15
-No obvious underlying causes
Conclusion
Depends on ICH depth from cortical surface
>1cm or GCS <=8: surgical patients tend to do worse
<=1 cm: tend toward better outcomes but not significant.
STICH 2
Inclusion criteria
-ICH with 1 cm from cortical surface.
-ICH volume 10-100 ml
-Best GCS motor score 5-6 and eye score >= 2
-No IVH
-No obvious underlying cause.
-Presentation with 48h
Conclusion:
Possible survival advantage in early surgery (within 12 h) especially with GCS 9-12/5
Indications of stenting in carotid stenosis
-Contralateral ICA occlusion
-Hostile neck
-tandem lesion
-above C2
-medical comorbidities eg congestive heart failure, and stable, angina, recent myocardial infarction
Anterior choroidal artery stroke symptoms
3 H’s
Homonymous hemianopia
Hemianesthesia
Hemiparesis
Heubner artery stroke
Territory: Caudate + putamen, Anterior limb of IC
Symptoms: Aphasia, mild hemiparesis of face and arm
PICA stroke
Territory: lateral part of medulla
Symptoms: WALLENBERG SYNDROME
-Ipsilateral horner (descending sympathetic)
-Ipsilateral cerebellar signs (Inf cerebellar peduncle)
-Ipsilateral face sensory loss of pain and temperature (Spinal trigeminal nucleus and tract)
-Contralateral body sensory loss of pain and temperature (lateral spinothalamic tract)
-Dysphagia (Nucleus ambiguous)
-Vomiting, vertigo, nystagmus (Vestibular nuclei)
Basilar artery bifurcation or PCA
Territory: midbrain infarction
Weber’s syndrome
-Ipsilateral CN III palsy
-Contralateral hemiparesis
Symptoms of vertebral insufficiency
5 D’s
Dizziness
Decreased vision
Diplopia
Dysarthria
Drop attack
Contraindications for tPA in stroke
-Improving symptoms
-Heparin infusion within 48h
-GI or GU hemorrhage within past 21 days.
-Major surgery with past 14 days.
-ICH on CT/hx of ICH.
-Stroke or serious head injury in past 3 months.
-Arterial puncture at noncompressible in the previous 21 days.
-Thrombin inhibitors or Factor Xa inhibitors in the past 2 days.
-Sustained SBP > 185.
-Sustained DBP > 110.
-Serum glucose < 50 mg/dl or >400 mg/dl
Moyamoya disease presentation
Pediatric present with ISCHEMIC STROKE or TIA (80%)
Young adult present with HEMORRHAGE (60%)
Headache
Seizures
Neurological deficits or cognitive decline
Involvement of heart and kidney
What is findings of Moyamoya disease in DSA/MRI/CT
DSA: puff of smoke
MRI: Multiple flow-void in basal ganglia
CT: multiple punctate dots in basal ganglia
Suzuki stages of Moyamoya disease
I: bilateral stenosis of suprasellar ICA.
II: dilation of ACA, MCA, PCA, collateral vessels at brain base.
III: progression of ICA stenosis and moyamoya vessels.
IV: progressive occlusion of circle of Willis and PCA, reduction of moyamoya vessels, presence of extracranial collateral.
V: Worsening of stage IV:
VI: no major cerebral artery or moyamoya vessels, extensive collateral from ECA.
What are indications of surgical management in Moyamoya disease?
-Presence of mass effect from clot
-Suzuki stage II-IV
-Patients with recurrent or progressive ischemic events in good neurological condition
What is surgical treatment of choice in moyamoya disease
STA-MCA bypass (direct revascularization)
Timing of surgery for Moyamoya disease
> 2 m after the most recent symptomatic event
AVM risk of rupture/ year
2-4%
ARUBA trial
Superiority of medical management over surgical management at follow up of 33.3 months
What is “Normal pressure breakthrough”?
Failure of autoregulation in chronically dilated vessels of ischemic regions of brain. The increase in global perfusion pressure to normal level after resection of AVM is thought to result repressurization of previously hypotensive brain and cerebral hyperemia, swelling, or hemorrhaging
American/English/French classification of spinal AVM
Type I: dural AVM, Loc fistula at dura (IA single feeder, IB >1 feeders)
Type II: glomus, Loc in spinal cord
Type III: Juvenile, Loc anywhere, causing scoliosis
Type IV: pial, Loc fistula on pia
Merland’s sub classification of Type IV spinal AV fistula
I: Single thin ASA, small single AVF, slow venous drainage
II: multiple dilated ASA and PSA, multiple medium AVF, slow venous drainage.
III: multiple dilated ASA and PSA, single giant AVF, giant venous ectasia with rapid drainage
Borden’s classification of dural AVF
1: Drainage into sinus only or meningeal vein
2: drainage into sinus and leptomeningeal vein
3: drainage into only leptomeningeal vein
Cognard classification of DAVF
I: anterograde drainage to sinus
IIa: drainage into sinus with retrograde flow.
IIb: drainage into sinus with retrograde flow into cortical veins
IIa+b: drainage into sinus with retrograde flow to sinus and cortical veins.
III: Direct drainage to cortical veins without ectasia
IV: direct drainage to cortical veins with ectasia
V: Direct drainage to spinal perimedullary veins
Barrow classification of CCF
A: direct, high flow = direct connection between ICA and cavernous sinus.
B: indirect, low flow = connection between ICA branches and cavernous sinus.
C: indirect, low flow = connection between ECA branches and cavernous sinus.
D: indirect, low flow = connection between ICA and ECA branches and the cavernous sinus
Treatment of CCF
Type A (high flow): Transarterial ballon OR sacrifice ICA if patient tolerates
Types B,C,D (low flow):
Observe (50% resolve spontaneously) if: Normal CN and IOP < 25 mmHg OTHERWISE transvenous embolizatiom
Images finding of cerebral arterial dissection
Angiogram: double lumen sign/ string sign
MRI: crescent sign
Risk of seizures after SAH
20 %
Types of ocular hemorrhage associated with SAH
- Subhyaloid (periretinal) hemorrhage
- intraretinal hemorrhage
- Hemorrhage with vitrous humor (Terson Syndrome)
Risk of acute HCP in SAH
21%
Criteria of infundibulum
- Triangular
- Widest portion < 3mm
- Vessels at apex
Risk factors for post-SAH seizures
Age > 65
MCA aneurysm
Volume of SAH
Associated with ICH or SDH
Poor neurological grade
Rebleeding
Vasospasm
Hyponatremia
HCP
HTN
Infarction
Time of vasospasm
Start at day 3
Peak day 6-8
Mean time of risk 3-14 days
Follow up schedule for treated aneurysm
Coiled: 6 mo, 1.5 y, 3.5, y, every 5-10 years
Clipped: 1 y, 5 y, every 10 y thereafter
Most common location of mycotic aneurysm
Distal MCA branches (75-80%)
Causes of cortical SAH
Trauma (most common)
Pial AVM
DAVF
CVAD
Venous thrombosis
Vasculitis
RCVS
PRES
Cerebral amyloid angiography
Coagulopathy
Brain tumors
Perimesencephalic SAH criteria
1.CT or MRI done < 2 days meeting the following:
-Epicenter of hemorrhage immediately anterior to brainstem.
-there may be extention to ant part of ambient cis or basal part of sylvian fissure.
-absence of complete filling of anterior interhemispheric fissure.
-no more than minute amount of blood in lateral portion of sylvian fissure.
-absence of frank IVH
- Negative 4 vessels cerebral angiogram
3.Appropriate clinical picture: no LOC, no H/A, SAH grade 1 or 2 (H&H or WFNS) and no drug use
AVM presentation
Hemorrhage- 58%
Seizures-34 %
Reminders - 8% : mass effect, headache, ischemia, bruit, increased ICP
Hemorrhage location with IVM
ICH - 82%
IVH : usually accompanied with ICH, pure IVH indicated intraventricular AVM
SAH
SDH
% Of aneurysm in AVM patients
7%
AVM surgery basics
- Wide exposure
- Isolate and occlude feeding arteries before draining veins.
- Excision of whole nidus is necessary to prevent rebleeding.
- Identify and spare vessels of passage and adjacent arteries.
- Dissect directly on nidus, work on sulci and fissures whenever possible
- Consider pre op embolization in high flow lesions
- Lesions with supply from multiple vascular territories may require staging
Cause of Delayed post op deterioration after AVM resection
- Normal perfusion pressure breakthrough.
- Occlusive hyperemia: due to obstruction outflow from adjacent normal brain.
- Rebleeding from retained nidus.
- Seizures
What are the most common regions for DVA
- Area supplied by MCA.
- Region of VOG
Presentation of cavernous malformations
Seizures (50%)
Hemorrhage (25%)
Focal neurological deficits (25%)
Subtypes of cavernous malformations
CMM1:
Locus: 7q11-q22 - Gene: KRIT1
CMM2
Locus: 7p15-13 - Gene: MGC4607
CMM3
Locus: 3q25.2-q27 - Gene: PDCD10
Risk of hemorrhage in cavernous malformations
-CMs initially presented with hge
-Brainstem CMs
-Familial CMs
-Multiple CMs
Risk of seizures in cavernous malformations
5-year risk of first time seizure
6% in CM presenting with symptoms
4% in incidental CMs
MRI sequences and finding in cavernous malformations
Gradient-echo T2WI
SWI
Findings
Mixed signal core with low signal rim, sometimes described as “popcorn appearance”.
Indications of surgery in cavernous malformations
-Solitary asymptomatic CMs if easily accessible and not in eloquent area to prevent hemorrhage
-Early CM resection < 6 weeks from hemorrhage in patients with seizures.
-symptomatic easily accessible CMs.
-Deep CMs if symptomatic or after prior hemorrhage.
-after a second symptomatic bleed in a brainstem CMs.
Overall risk of death or nonfatal stroke after resection of incidental CM
6%
Most common location for DAVF
Transverse/sigmoid sinus (63%)
Theories of DAVF formation
- Venous sinus occlusion awakens dominant embryonic dural arteriovenous channels.
- venous hypertension/thrombosis promotes local angiogenesis and the de novo formation of the DAVF.
- The DAVF may arise first and itself result in venous sinus thrombosis.
Presentation of DAVF
Pulsatile tinnitus (92%)
occipital bruit. (89%)
headache (41%)
Visual impairment (33%)
Papilledema (26%)
Indications for intervention in DAVF
- Presence of cortical venous drainage.
- Neurologic dysfunction.
- Hemorrhage.
- Orbital venous congestion
- Refractory symptoms.
What are the 2 locations are more favorable for surgery in DAVF
- Anterior fossa/ethmoidal
- Tentorial DAVFs
True VOG malformations fed from which arteries
Medial and lateral choroidal
Circumferential
Mesencephalic
Anterior choroidal
Percallosal
Meningeal
Yasargil Classification of VOGM
I - Pure internal fistula: single or multiple.
II - Fistula between thalamoperforator and the VOG
III -Mixed form: the most common
IV - Plexiform AVM
Lasjaunias et al classification of VOMG
- Choroidal type (Yasargil I,II,III)
- Mural type (Yasargil IV)
VOGM common presentation depending on age
Prenatal: cardiac decompensation and/or hydrops
Neonates: congestive heart failure
Infants: cyanotic heart failure, seizures, encephalomalacia
Late childhood: HCP, seizures, developmental delay, dilated facial veins
Collateral circulation for ICA stenosis
- Flow through the circle of Willis.
- Retrograde flow through ophthalmic artery.
- Proximal maxillary artery.
- Cortical cortical anastomosis
- Dural leptomeningeal anastomosis
Collateral circulation for vertebral artery stenosis
- ECA through occipital artery
- Thyroxervical trunk
- Contralateral VA
Collateral circulation for basilar artery occlusion
- Posterior communicating artery
- Anastomosis between PCA and PICA
PCA occlusion syndrome
- Unilateral occipital loop infarction.
- Balint syndrome.
- Cortical blindness (anton syndrome)
- Weber syndrome.
- Alexia without agraphia.
- Thalamic pain syndrome.
What branch of PCA supplies thalamus and midbrain.
Artery of Percheron
Criteria for clinical diagnosis of VBI
2 or more of the following:
-Motor or sensory symptoms or both occurring bilaterally in the same event.
-Diplopia: ischemia of upper brainstem (midbrain) near ocular nuclei.
-Dysarthria: ischemia of lower brainstem.
-homonymous hemianopsia: ischemia of occipital cortex.
Appearance of thrombosed sinuses on MRI at various stages
Acute (0-7d): T1 iso T2 hypo
Subacute: T1 hyper T2 hyper
Late: T1 Black (flow void) T2 black (flow void)
The yearly risk of rupture of cavernous malformation
0.5-1% it
Ottawa SAH rule
Age > 40 years
Neck pain or stiffness
witnessed loss of consciousness
Onset during exertion
Thunderclap headache
Limited neck flexion on exam
H&H grade mortality
1 : 11%
2 : 26%
3 : 37%
4 : 71%
5 : 100%
Risk of vasospasm in H&H
1: 22%
2: 33%
3: 52%
4: 53%
5: 74%
Spetzler Ponce classification of AVM
Class A
- Spetzler-Martin score 1 or 2.
- Microsurgical resection is preferred treatment.
- 8% chance on postoperative deficit (95 % CI= 6-10).
Class B
- Spetzler-Martin score 3
- Multimodality treatment
- 18 % chance on postoperative deficit (95 % CI= 15-22)
Class C
- Spetzler-Martin score 4-5
- No treatment, with exception of recurrent hemorrhages, progressive
neurological deficits, steal-related symptoms, and AVM-related aneurysm
-32 % chance on postoperative deficit (95 % CI = 27-38)
