AANS2000AANS2000AANS2000Internet Outline of

Neurosurgery

E. R. Flotte MD, 2009

 

Please send comments and corrections to admin@flotte2.com

www.outlineofneurosurgery.com

 

Vascular

 

 

 

Neurovascular Anatomy

 

 

Radiology

Blood on MRI: (T1/T2) <24h (oxyhemoglobin): iso/iso. 1-3d (DeoxyHgb): iso/hypo. 3-14d (intracellular metHgb): hyper/hypo. >14d (extracellular metHgb): hyper/hyper.  hemosiderin: hypo/hypo

Angiogram: 0.5% risk of stroke, 7% w/atherosclerosis

 

 

Cerebral Aneurysms

·         Berry aneurysms: Saccular.

·         Predispoition for braching points on arteries (e.g. circle of Willis)

·         False aneurysms (lack media, defects in internal elastic lamina).

·         Other types of aneurysms:

o    Oncotic aneurysms: most common with left atrial myxoma, choriocarcinoma

o    Fusiform (nonsaccular)

o    Dissecting

o    Mycotic (infectious)

o    Pseudoaneurysms: encapsulated hematoma from vessel injury. Often traumatic or iatrogenic.

·         Prevalence 1-6%: 1% overall, 1% in young, 4% in elderly. 20-30% multiple.

·         Locations: Pcom (35%) > Acom (30%) > MCA (20%) > basilar tip (5%).

·         Risk factors: age, smoking (3-10x), heavy alcohol use, HTN (3x), ?hormones

·         Predisposing factors: Aortic coarctation, AD polycystic kidney disease, fibromuscular dysplasia, Marfans, Ehlers-Danlos, homocystinuria, NF1, AVMs

·         Aneurysm growth rates: unclear if linear or episodic (Koffijberg H JN8/08editorial Britz G)

·         Rupture risk:

o    International Study of Unruptured Intracranial Aneurysms (ISUIA) (NEJM 12/10/1998): Retrospective.

§  Risk for aneurysms <10mm = 0.05%/yr. (0.5%/yr in those with previous rupture from another aneurysm). For >10mm = 1%/yr.

§  Other studies refute this (rupture rate 1-2%/yr) (Juvela, Mocco, Rinkel).  Some feel ISUIA selected for low-risk lesions since high-risk lesions were treated and withdrawn.

o    ISUIA Part 2 Wiebers DO Lancet 7/12/2003: Prospective: <7mm, 7–12mm, 13–24mm, and >25mm yearly rupture rates were 0.15%, 1.2%, 3.1%, and 8.6%.  (<7mm with previous SAH was 0.4%)

§  5-year rupture rates for anterior circulation: 0, 2.6, 14.5, and 40%, posterior circulation: 2.5, 14, 18.4, and 50% (no history of SAH).

·         Rupture risk increased with: Large size (no critical size), high dome/neck ratio, high aspect (aneurysm depth:neck width), slow flow.

o    Smaller aneurysms produce more extensive SAH (Russell SM JN8/03).

·         If two or more family members have aneurysms, others should be screened by MRA or CTA (5-10% positive). Frequency is debated (every 6mos to 5yrs) (Kim DH N8/03)

·         Presentation:

o    Incidental unruptured

o    Symptomatic unruptured: seizures, mass-effect (e.g. CN3 plasy from pcom)

o    Ruptured: usually cause subarachnoid hemorrhage (SAH), occasionally ICH, IVH, SDH

 

Aneurysmal Subarachnoid Hemorrhage (SAH)

·         Spontaneous SAH Diagnosis:

o    Presentation:

§  Sudden onset (“thunder-clap”) headache, back pain.

§  Loss of consciousness, new neurologic deficits.

§  Meningismus (nuchal rigidity; Kernig’s, Brudzinski’s signs)

§  Subhyaloid, vitreous, or retinal hemorrhages on fundoscopy

§  Mass-effect: CN3 palsy (pcom or basilar tip)

o    CT

o    CT Angio: Sensitivity/specificity >95% for aneurysms >7mm. Look for neck calcification or plaques. Especially beneficial for emergent ICH evacuation.

§  With SAH: If aneurysm seen it is reliable. Perform angio to confirm (-) CTA.

§  No SAH: If (+) consider angio to confirm small aneurysms. If (-) then probably reliable.

o    MRI/MR angio: False-positive and false-negative rates 10%. Also consider MRI with gradient echo sequence

§  Superficial siderosis (hemosiderin staining of leptomeninges) may be seen with recurrent SAH on T2/GRE MRI (more often non-aneurysmal)

o    LP: Performed if CT/CTA is negative – although efficacy with (-) combined CT/CTA unclear.

§  CT negative in 5% of SAH.

§  LP reported to cause neurologic worsening in 13% of SAH patients

§  Xanthochromia becomes apparent after 4 hours.

§  “Bloody Tap” – local hemorrhage during LP. May mimic SAH. Xanthochromia is absent. Blood clots in tube (as opposed to SAH which won’t).

§  If CT/CTA and LP negative but clinical suspicion high then some consider angio (LP may be negative with loculated blood), but efficacy unclear

o    Cerebral angiogram: 4 vessel - gold standard.

§  Risk of hemorrhage 3% with SAH.

§  Must see both PICA origins to be adequate

§  May need carotid compression to visualize flow through Acom from both ACAs

§  Alcock test: vertebral injection with carotid compressions – test circle of Willis patency

§  Size: ICA 6mm, MCA 4mm (average)

§  3D-angiography

·          “Angiogram-negative” SAH (or “Occult” SAH)

o    10% of SAH. Most common cause is non-visualized aneurysm due to aneurysm thrombosis or inadequate study.

o    Other causes: Perimesencephalic SAH, spinal or cerebral AVM, sickle cell, pituitary apoplexy, cocaine, arterial dissection, “SAH of truly unknown cause”

·         Spontaneous thrombosis of aneurysms may occur (10% of autopsy series); however they may reappear and rupture years later.

·         Cannot diagnose “benign” SAH in presence of vasospasm

o    Acom is most common location.

o    Hemorrhage rate is 0.5%/year (lower than angiogram (+) SAH). Other SAH complications occur (vasospasm may be less likely).

o    Consider repeat angiogram at 10-14 days. Overall 2-25% positive yield on repeat angiogram, but up to 70% with interhemispheric SAH.

o    Surgical exploration has been advocated by some, especially if re-bleeding occurs or if the SAH is in a typical aneurysm location (interhemispheric, Sylvian fissure)

o    Isolated convexity SAH rarely due to aneurysm – more commonly due to posterior reversible encephalopathy, venous sinus thrombosis, vasculitis, etc (Refai D JN12/08)

·         SAH Complications:

o    Rerupture: 4% 24hr, 20% 2wks, 50% 6mos, then 3%/yr.

o    Vasospasm: See below.

o    Hydrocephalus: 10% require shunting.

§  If placing EVD before securing aneurysm, drain at 15cmH2O to avoid detamponading aneurysm

§  No difference in shunt placement between gradual and rapid EVD weaning (Klopfenstein JD JN2/04)

§  Rammos S JN12/08 suggest EVD can be converted to VP shunt at the same site, and CSF RBC and protein have no effect on shunt survival

o    Effect of increased ICP on outcome unclear Heuer JC JN9/04

o    Seizures:

§  Seizure incidence after SAH is 5 to 8% Rosengart AJ JN8/07

§  Based on meta-analysis of 4 RCTs, prophylactic AED usage after SAH was significantly associated with worse outcome at 3 months, development of cerebral vasospasm, neurological deterioration, and cerebral infarction as well as elevated temperature during hospitalization. Use may be justified in high risk patients (cortical injury, unsecured aneurysms) Rosengart AJ JN8/07

o    Cardiac: elevated cardiac enzymes and EKG changes common. MI.

 

Aneurysm Treatment

·         Unruptured:

o    Reviews: Neurosurgical Focus 11/04 (Spetzler, Dacey et al), Journal of Neurosurgery 1/02 Special Section (Winn, Weir et. al.)

o    International Study of Unruptured Intracranial Aneurysms (ISUIA) (NEJM 12/10/1998): <10mm = 0.05%/yr rupture rate does not justify surgery.

§  Advocated by AHA Stroke Council (2000)

§  Other studies refute this (rupture rate 1-2%/yr).  Most aneurysms with SAH are <10mm. Median size of rupture 7.5mm.

o    Komotar RJ N1/08: Symptomatic unruptured aneurysms generally should be treated; incidental aneurysms < 5 mm should be managed conservatively; aneurysms > 5 mm in patients younger than 60 years of age should be seriously considered for treatment; incidental aneurysms > 10 mm should be treated in nearly all patients younger than 70 years of age

o    Growth (>1mm), shape (multilobulated, “tits”), genetic conditions, previous SAH from another aneurysm may increase rupture rate and warrant treatment

·         With ICH: Higher rebleed rates than pure SAH. Clot evacuation alone mortality 75-100%. Must secure aneurysm. Consider coiling then evacuation.

·         E-ACA (ε-aminocaproic acid, Amicar): Inhibits plasminogen→plasmin (digests fibrin). Rebleeds decreased from 20% to 12%, but vasospasm increased from 23% to 32%, hydrocephalus increased, mortality unchanged. Consider in non-surgical patients.

·         Poor Grade (Hunt-Hess IV or V) controversial. Some favor early treatment because a subset (up to 30%) will have good outcome (Laidlaw JD N12/03, Komotar RJ N2/09)

·         Seizures with unruptured aneurysm usually treated with clipping and removal of aneurysm without extensive cortical resection. Not clear if coiling improves seizures.

·         Ruptured: Airway and hemodynamic stabilization, control BP, ventriculostomy/LD for hydrocephalus, Nimodipine, analgesics, consider AEDs (until secured - see above)

 

Aneurysm Surgery

o    Timing: earlier (1 to 3 days post-hemorrhage) generally favored in H/H I-III, but late has some advantages, e.g. less brain swelling.

§  International Cooperative Study on the Timing of Aneurysm Surgery (ICSTAS) concluded “early surgery was neither more hazardous nor beneficial than delayed surgery”  (Kassell NF JN7/90Part 1, Part 2)

§  Netherlands observational study showed no difference in timing – Nieuwkamp DJ AN8/05

§  Reviews:  deGans K N2/02 (meta-analysis)

o    Consider: mannitol, CSF drainage, mild hypothermia (33-36º), SBP <140 until clip placed.

o    Hypothermia: IHAST study showed no benefit, increase in bacteremia (Todd MM NEJM 1/13/05)

o    Some routinely fenestrate the lamina terminalis to prevent hydrocephalus, particularly for acoms (Komotar RJ N12/02, Andaluz N N11/04), others show no benefit (Komotar RJ N1/08)

o    Some achieve burst suppression on EEG on all aneurysm patients (Spetzler RF N10/01)

o    Consider microdoppler, MEPs (more sensitive than SSEPs).

o    Previously coiled aneurysms: do not remove coils if placed >3mos previously. <6mos removal is controversial.

o    Obtain proximal control.

§  For ICA aneurysms, access carotid in neck (or petrous) or have endovascular balloon in place

o    Options for angiography include: routine intraoperative, selective intraoperative, and routine postoperative. 

§  Intraoperative angiogram: Estimated to avert serious complications in 2-10% of patients. Complications 0.5-2.5%. (Chiang VL JN6/02, Tang G JN6/02editorial Heros RC, Klopfenstein JD JN2/04, Kivisarri RP N11/04)

§  Indocyanine green video angiography also an option.

o    Temporary occlusion:

§  Raise BP – normotension to mild hypertension.

§  Etomidate (0.3mg/kg) or propofol to burst suppression (Barbs cause hypotension, but pentobarb is used).

§  Less likely to be tolerated w/MCA aneurysm (26% infarction, versus 9% with ICA, 16% with Acom) (less risk distal to lenticulostriates).

§  Always clamp proximal first (clamping distally first would increase transmural pressure and possible rupture)

§  Released every 10-15min.

§  Overall about 10% stroke rate.

o    Aneurysmorraphy: opening of aneurysm (after temporary clipping) to evacuate thrombus

o    Complications: intraoperative rupture, stroke

§  Intraop Rupture: Tamponade dome with cottonoid, lower BP, consider burst suppression, temporary occlusion (remember to occlude branching vessels – pcom, anterior choroidal, etc)

§  Neck avulsion: wrap with cotton then apply clip (Lanzino G JN11/03)

o    Remember to consider: nimodipine, BP control, AEDs, lumbar drain, microdoppler, MEPs, EEG, intraop angio, ICA access in neck

·         Audio: Advanced Strategies for the Treatment of Intracranial Aneurysms – Giannotta SL, Cerebral Aneurysms: Effect of New Knowledge and Technology on Current Practice – Heros RC

 

Aneurysm Endovascular Treatments (Coiling & Stenting)

o    Neuroendovascular Devices

o    Cranial nerves deficits usually improve post-coiling.

o    Timing of coiling does not affect procedural morbidity or outcome.

o    Measure dome-to-neck ratio

o    Coil types: 3-D, complex fill, biologically active.

§  Matrix (bioactive coated): similar morbidity to bare platinum. Recanalization rate 25%. Pierot L N11/08 (French Matrix Registry)

·          “Clearly, the Matrix coil is not better than bare platinum in the current generation that was assessed. The cost differential between the bare platinum and Matrix coils certainly indicates that the use of Matrix coils in their current form is not cost-effective, and I would not recommend its use at this time, as it has clearly shown no benefit.” - Rosenwasser RH,comment on Pierot L N11/08

o    Adjuncts:

§  Balloon remodeling: for wide-necked aneurysms.

§  Stent-assisted coiling: for wide-neck & fusiform aneurysm.

§  Stenting alone:  

·         Most stents have 6-9% metal surface coverage, except PED which has 30-35%

·         Wingspan (Yavuz K JN9/08)

·         Pipeline Embolization Device: results in flow reduction and progressive occlusion over months, requires dual antiplatelet therapy – not for acute SAH (Lylyk P N4/09)

·         Intracranial Stents

o    Surgical remnants may be treated with coiling (Bendok BR N9/02)

o    Follow-up angiography varies, commonly done at 6 months, 3 years (safe time for end of follow-up is unknown)

§  Role of CTA, MRA unclear.

·         3D TOF or contrast-enhanced MRA follow-up: Gauvrit JY JN3/08

§  Risk of permanent major morbidity from  surveillance angiography after coiling is 0.04% (other series 0.3-2.3%) (Ringer AJ N11/08)

o    Complications

§  5-10% morbidity, 2% mortality. Ischemia 9%, hemorrhage 3%.

§  Recurrence 10-15%.

§  Rupture during coiling:

1.     Complete coiling

2.     Reverse heparin

3.     Consider EVD

4.     Stat CT

5.     Treat as for SAH

 

Coiling vs Clipping

o    Factors: aneurysm location, size, shape, neck:dome ratio, luminal thromus, calcification, collateral supply, parent vessel morphology; patient age, clinical status, preference; vasospasm

o    International Subarachnoid Aneurysm Trial (ISAT) (Molyneux A Lancet 10/26/02):

§  1yr neurologic outcome better with SAH (unruptured not studied) for CE. 7% risk reduction CE vs SC. (Only 2 pts from US). For equivalent treatment.

§  Only 20% of eligible patients randomized – most of rest were clipped. Most centers outside of US. Operator experience not reported. Patient characteristics atypical (higher H/HI-II, anterior circulation, <10mm)

§  Mitchell P JN3/08: “Could late rebleeding overturn the superiority of cranial aneurysm coil embolization over clip ligation seen in the International Subarachnoid Aneurysm Trial”. “The advantage of coil embolization over clip ligation cannot be assumed for patients < 40 years old” Editorials: Mocco J, Heros RC

o    Others:

§  Johnston SC Stroke 3/01: California database. Mortality CE 0.5%, SC 3.5%. Poor outcome CE 9%, SC 22%.

§  Raftopoulos C N6/03: Unruptured. Occlusion rates: Total: CE 56%, SC 93%. Subtotal: CE 15%, SC 2%. Fail: CE 29% (60% were MCA), SC 5%. Complications: temporary CE 10% SC 16% permanent CE 8% SC 2%. Recommendation: coil only for DNR >2.5.

§  Barrow Ruptured Aneurysm Trial

o    No RCT for unruptured aneurysms

o    No difference in shunt-dependent hydrocephalus between the two groups (except patients with IVH – higher with coiling) (Dehdashti AR JN9/04)

o    No difference in vasospasm (Hoh BL N10/04)

o    Clipping may have a better chance of improving CN3 palsy (Chen PR N6/06)

 

Specific aneurysms

o    Cavernous ICA:

§  Unruptured may cause ophthalmoplegia (usually without dilated pupil, cf. pcom), headache, eye pain

§  Ruptured, may cause:

·         Carotid-Cavernous Fistula

·         SAH, if it expands through carotid ring into subarachnoid space

·         Epistaxis, from rupture into sphenoid sinus

·         Emboli

§  Treatment

·         Generally for symptoms (especially visual problems), giant aneurysms (especially subarachnoid extension)

·         Incidentally usually followed – low risk of CCF

·         Coiling or trapping. May reduce mass effect. See CCF.

·         Cavernous aneurysm with carotid stenosis requiring treatment is controversial, but each generally treated separately on own merits

 

o    Proximal ICA/Paraclinoidal: Aka carotidophthalmic / paraophthalmic. May cause blindness. 

§  No radiographic way to determine if they are intradural or extradural (Iihara K JN8/03). 

§  Subtypes:

·         Carotid Cave (C3): usually point medial. Mostly extradural but may be intradural.  Coiling favored

·         Ophthalmic artery aneurysm: points superiorly. May compress optic nerve/chiasm

·         Superior hypophyseal: points inferiorly or medially

§  If anterior wall (aka superior hypophyseal) or true ophthalmic (off C2) consider surgery. If carotid cave (C3) or pointing inferiorly, consider coiling.

§  Endovascular treatment generally favored if feasible

§  Surgical:

o    Clipping if feasible – pterional approach. If not ICA occlusion ± EC-IC bypass

o    Proximal control: Expose cervical ICA or have endovascular balloon in place

o    Usually requires drilling anterior clinoid (possible removal of optic strut and sectioning of falciform ligament)

o    Safe to clip ophthalmic a. or superior hypophyseal a. if necessary

o    Bilateral ophthalmic a. aneurysms may be approached from one side usually.

§   Case Series: Fulkerson DH N2/09

§   Reviews: Giannotta SL N3/02 (Operative Nuances); Iihara K JN8/03 – comment Heros RC

§  Videos: Giannotta SL N3/02

 

o    Posterior Communicating (Pcom):

§  Approach: Pterional

§  Arise distal to pcom.  If no CN3 palsy more likely to be adherent to temporal lobe – avoid retraction.

§  More likely to cause subdural hematoma with SAH

§  Complete CN3 palsy (or pupil only, often painful): pcom OR basilar apex aneurysms.

o    Versus Pupil sparing CN3 palsy (10-20% involve pupil, may be painful): DM, HTN. 

§  Look for fetal PCA on angio.

§  Clipping:

o    Avoid temporal lobe retraction

o    Ensure patency of anterior choroidal & thalamoperforators after clipping.

o    Pcom may be sacrificed if not fetal.

o    CN3 palsy: evacuate fundus, do not dissect off CN3. 

o    Small: clip perpendicular to ICA. Large: fenestrated Sundt encircling clip around & parallel to ICA (prevents kinking).

o    May need to temporarily clip proximal and distal ICA and PcomA (can result in anterior choroidal infarct).

 

o    Anterior Choroidal:

§  Approach: Pterional.

§  Anterior choroidal artery: 16% stroke rate with clipping. 25% arise from MCA or Pcom. Supplies internal capsule, optic tract, lentiform nucleus, amygdala.

·         Anterior choroidal injury (pcom or achor): Hemiplegia, hemihypesthesia, homonymous hemianopsia (cognition unimpaired).

 

o    ICA bifurcation (Carotid Terminus): 

§  May cause ICH (resembling putaminal ICH).

§  Know whether acom & A2s fill from contralateral A1 – if so can sacrifice ipsilateral A1 if necessary.

§  Open medial sylvian fissure distal to proximal after exposing ICA.

§  Watch for anterior choroidal & lenticulostriates (off ACA & MCA). Must see back side to avoid perforators. Clip parallel to M1.

 

o    MCA bifurcation:

§  Cause ICH, SDH. Higher risk with temporary occlusion. More often multiple (up to 45%).

§  Treatment: generally favors clipping.

§  Early bifurcation may imply more lenticulostriates off M1/M2 – must be spared.

§  Approaches:

o    1) Pterional:  Exposes ICA for proximal control, then follow to MCA bifurcation.

o    2) Transsylvian: Splits Sylvian fissure. Follow M2s to aneurysm. (Yasargil & Fox)

o    3) Superior Temporal Gyrus: Better if ICH present. (Heros)

§  When clip placement not possible consider STA-MCA bypass (spare STA in dissection) or arterial reimplantation (threatened M2 grafted end-to-side to other M2)

§  Reviews: Chyatte D N2/01 (Operative Nuances), Heros RC N4/01 (Operative Nuances)

§  Videos: Chyatte D N2/01, Heros RC N4/01

 

o    Anterior Communicating (Acom):

§  Look for ACA and aneurysm filling from each side.

§  Approach: Pterional.

o    Consider morphology, A1 dominance (for proximal control), language dominance. Right generally favored.

§  Surgery: Consider resecting gyrus rectus. Identify both A1s & A2s. Avoid perforators from posterior Acom and recurrent artery of Heubner (86% off A2)

§  Reviews: Solomon RA N1/01 (Operative Nuances), Riina HA N10/02 (Operative Nuances), Sekhar LN ON11/07 (Operative Nuances)

§  Videos: Solomon RN N1/01, Riina HA N10/02, Sekhar LN ON11/07

 

o    Distal ACA: Note if aneurysm is supracallosal (above genu) or infracallosal (may require anterior corpus callosotomy), azygous ACA (7-16%). Pterional/ subfrontal used for low A2, interhemispheric for others

 

 

Posterior Circulation Aneurysms

o    General

§  Partially thrombosed giant posterior circulation aneurysms (Iihara K N11/08)Figure 1 Management Algorithm

§  Books: Drake CG et al, Surgery of Vertebrobasilar Aneurysms, Springer 1996

 

o    PCA:

o    P2: Pterional, subtemporal, or occipital interhemispheric approach. See Terasaka S N8/00

 

o    Basilar apex:

§  Delayed (non-emergent) surgery preferred, especially if complex

§  Must preserve thalamoperforators – damage causes irreversible coma.

·         Use shortest possible clip

§  Approaches:

o    Pterional (Yasargil) or Orbitozygomatic: Consider COZ or zygomotomy for high bifurcation. Subtemporal craniectomy (for temporal retraction). Wide dissection of Sylvian Fissure. Generally go between ICA & CN3 – more perforators in opticocarotid window. Mobilize anterior choroidal a. off temporal lobe. Resect uncus. Follow Pcom through Lillequist’s membrane. Consider sharply ligating Pcom (if not fetal).

§  Advantages: Less temporal retraction, less CN3 manipulation, better for high bifurcation. Disadvantages: Deep field, poor proximal control.

§   Reviews: Hsu FPK (Spetzler RF) ON1/05 (Operative Nuances)

o    Subtemporal (Drake): Better for low bifurcation, posterior projection.

§  Advantages: Short working distance, lateral view of aneurysms and perforators. Disadvantages: Temporal retraction, CN3 & CN4 injury.

o    Combined (Heros): Combined pterional/subtemporal craniotomy. Uncus mobilized superolaterally out of incisura.

o    Temporopolar (Sano)

o    Extended Lateral Transsylvian (Batjer) (Bendok BR N7/04Video)

 

o    Vertebrobasilar junction: Far lateral, Transpetrosal.

 

o    AICA: Approaches: Retrosigmoid, Far lateral, Transpetrosal - see Gonzalez LF N11/04

 

o    PICA: May cause 4th ventricle IVH.

§  Retrosigmoid or Far lateral (less risk CN palsies). Can include CN12 fibers in clip. Spare brainstem perforators. (DAmbrosio AL N7/04)

·         May be approached via contralateral far-lateral (Bragg TF NF12/08)

§  Proximal PICA: Must spare perforators. See below as for fusiform aneurysms.

§  Distal PICA: Rare. Distal to perforators: May clip aneurysm, clip PICA proximal to lesion, or trap

§  Case Series:  Al-khayat H (Samson D) N1/05

 

o    Giant aneurysms: >25mm. Higher rate of rupture.

§  Most common locations: cavernous/ophthalmic, MCA, basilar tip

§  Consider clipping, trapping, bypass & clipping, hunterian ligation

§  Consider using skull-base approaches – e.g. orbitozygomatic

§   Giant Serpentine aneurysm: > 25 mm in diameter that is partially thrombosed with a residual serpiginous vascular channel (Christano LD NF5/09)

§  Review: Spetzler RF N10/01 (Operative Nuances)

§  Video: Spetzler RF N10/01

 

o    Infundibulum: Triangular diverticulum <3mm at take-off of vessel (eg pcom). Bleeding reported but felt to be extremely low.  Consider wrapping if doing surgery for another aneurysm.

o    Unclippable aneurysms: Options include carotid ligation

o    Blood-blister aneurysms: thin-walled, no neck, fragile, rupture during surgery.  On nonbranching supraclinoid ICA (usually dorsal wall). More common in young women? (Sim SY JN9/06)

§  Treatment Options:

·         Surgical clipping/wrapping/ICA sacrifice: Preop ICA Balloon Test Occlusion.  Prep for STA-MCA bypass. Consider wrapping (sliastic sling), bypass

·         Endovascular stenting (covered or stent-within-stent advocated – Lee JH JN3/09), coiling (stent-assisted), ICA sacrifice

 

·         Subarachoid Hemorrhage grading

o    Hunt-Hess:

o    Grade 1-3 operated (some will manage grade 3 until they improve to grade 2).

o    Grades 4&5: Clipping/Coiling may decrease rupture rate and enable aggressive medical management– 35% favorable outcome (44% in Grade 4, 13% in Grade 5), 31% death. (Suzuki S JN11/06)

§  Generally 4/5 previously managed non-operatively, but “recent published data show that early or ultra-early aggressive surgical treatment followed by NICU management may improve the risks of morbidity and mortality in these patients.” Controversial. (Suzuki S JN11/06)

§   Patients with Grade 4/5 and an intracerebral hematoma may benefit from surgical evacuation (with prior coiling or concomitant clipping) (comment by Heros RC JN11/06)

o    Over 90% or Grade 4/5 patients dead or disabled with no treatment

o    WFNS:

                 

o    40% of Grade 4/5 patients independent at 3mos – argues for aggressive treatment.

o    Glascow Coma Scale (GCS) may be more predictive than Hunt-Hess or WFNS (St Julien J N8/08Table 1 comparison of systems)

o    Fisher: CT grading. 1=none; 2 = <1mm thick; 3 = >1mm, clot; 4=ICH, IVH. (Table 1 Kramer JH JN8/08 – Fisher, Modified Fisher, and Classen Scores comparison)

§  Grades 1, 2, 4 had minimal vasospasm. Grade 3 had 96% incidence of vasospasm.

 

Vasospasm

·         #1 cause of morbidity after SAH

·         Incidence: Angiographic 50-70%, symptomatic 30%.

o    Correlated with Fisher grade on CT (Grade 3 is highest).

o    Cigarette smoking is a risk factor.

o    Review of risk factors – Harrod CG N4/05

·         Peak 7-10d. Range 3-14 days.  If it develops, may last for weeks.

·         Symptoms: new focal deficits, worsened headache, AMS

o    ACA spasm gives frontal lobe syndrome.

·         Detection:

o    Transcranial Doppler Ultrasound (TCDs): Mild: 120-200cm/s, MCA:ICA ratio 3-6; Severe: >200 cm/s, ratio >6.

o    Consider DWI or perfusion MRI/CT

o    Confirm with Angiogram (possibly CTA/MRA)

o    For new deficits STAT CT to rule out hemorrhage, etc.

Treatment:

·         Triple-H Therapy (HHH):

o    IVF + colloid, vasopressors

o    Targets: CVP > 10, PCWP 14-18, HCT 30-35 prophylactically. SBP 160-220

o    Unclipped aneurysm: CVP & PCWP 6-10, SBP <160.

o    For deficit raise SBP >200.

o    Can use low-dose vasopressin/ddAVP to counteract diuresis.

o    75% of deficits reversed, No RPT.

o    Avoid with cerebral edema or massive infarct

o    Increasing CO, MAP effective (not CVP) (Kim DH N11/03)

·         Nimodipine: improves outcome by 40%, reduces stroke by 34% and clinical vasospasm from 30% to 20%, no change in mortality or angiographic vasospasm. 60mg po q4hr for 21 days

·         Endovascular vasospasm treatment

o    Angioplasty: Repeat CT first to rule out ICH.

o    Papavarine: Intraarterial papavarine’s efficacy is inconclusive. Half-life is less than 24hrs, vasospasm recurs in 24-48hrs. Can increase ICP, cause transient deficits, blindness, seizures, thrombocytopenia and paradoxical exacerbation of vasospasm.

o    Review: Eddleman CS NF3/09

·         Lumbar drainage reported in retrospective trial to decrease vasospasm from 50% to 20% (Klimo P JN2/04)

·         Lovenox showed no benefit in prevention.

·         Cisternal thrombolytic therapy with inflow/outflow catheters or “head shaking” have had mixed results. RCT showed no overall difference in vasospasm with intraoperative cisternal injection of rt-PA, but did show 56% decrease in patients with thick subarachnoid clot.

·         Audio: Scientific Basis of Cerebral Vasospasm – Dacey RG

 

Perimesencephalic SAH

·         aka Perimesencephalic Nonaneurysmal SAH (PNSAH)

·         May be due to rupture of small perimesencephalic vessels.

·         Young males, can occur during exercise.

·         May have similar presentation to SAH (headache, meningismus), but Hunt-Hess is 1-2.

·         All are angiogram-negative. CT/MRI shows SAH only in interpeduncular/ ambient/ prepontine cisterns.

o    3% of basilar tip aneurysms mimic BPS, so some feel angiogram is mandatory.

o    Some suggest CT-angiography alone may be sufficient (N10/06).

o    Some perform brain and spinal MRI to rule out dural fistula or spinal AVM.

o    Cannot diagnose PNSAH in presence of vasospasm – must repeat angio

·         Repeat angiography/CTA is controversial.  Most perform at 1-2 weeks and some at 2-6 mos.

·         Rebleeding and vasospasm in true BPS have not been reported.

o    Nimodipine is controversial.

·         “SAH of truly unknown cause”: SAH outside perimesencephalic/prepontine cistern. May be occult aneurysm. Higher complications.

 

Mycotic aneurysms

·         18% have SAH

·         10% of patients with endocarditis (SBE) develop mycotic aneurysms.

o    SBE Risk factors: IV drug use, immunosuppresion

o    SBE symptoms: fever, heart murmur, Roth’s spots (retinal hemorrhages), Janeway’s lesions (macules on palms/soles), Osler’s nodes (cutaneous nodules)

o    Check echocardiogram to r/o SBE

·         Most common in distal MCA. 20% multiple.

·         Staph aureus, bhemolytic Strep (viridans) most common organisms.

·         Treatment: Resolves w/in 6 wks w/antibiotics. Follow with serial imaging (angiography).

o    Clipping controversial, consider for:  SAH, growth on antibiotics, or failure to decrease after 4-6 week of antibiotics.

§  Difficult to find – use stereotaxy or have endovascularist place coil nearby.

o    Coiling is an option

o    Cardiac surgery (valve replacement) with anticoagulation relatively safe (but risk must be discussed). Bioprosthetic valve preferred over biomechanical valve to reduce need for anticoagulation.

 

Traumatic Aneurysms

·         Most are pseudoaneurysms from ruptured/lacerated vessel wall

·         Most are peripheral (MCA, ACA branches) or at skull base (petrous or cavernous ICA or VA)

·         High rate of rupture

·         Suspect with delayed hemorrhage – SAH or ICH

·         Diagnosis: MRA, CTA, angio

·         Treatment: endovascular coiling/trapping/stenting (Cohen JE N9/08) or surgical clipping usually recommended

o    Extracranial carotid pseudoaneurysms: May expand. May be stented (covered or uncovered) or managed conservatively.

 

Fusiform Aneurysms

·         AKA dolichoectatic aneurysm, nonsaccular intracranial aneurysm, giant serpentine aneurysm, dissecting aneurysm

·         Terminology is not standardized & may lead to confusion

·         Also defined as a spectrum: dolichoectasia, fusiform, transitional, giant serpentine

·         Considered a different entity than acute dissecting aneurysms (dissection)

·         Vertebrobasilar > carotid.

·         Most often due to atherosclerosis – chronic, stable or variably progressive

·         May also occur with collagen vascular disease, fibromuscular dysplasia

·         Presentation:

1.     Mass effect: on brainstem, cranial nerves

2.     Ischemia: TIA, stroke

·         Due to local perforating vessel thrombosis or distal thromboembolism

·         Cerebral ischemia and BA thrombosis are the most common causes of death

·         New onset ischemic symptoms may herald impending rupture (Flemming KD JN7/04)

3.     Rupture/SAH: 1-2%/year risk. After SAH 30% rebleed rate, highest in first 24hrs. (Flemming KD JN7/04)

·         56% 5-year mortality rate if aneurysm is enlarging (4% if stable). About 50% will enlarge. (Mangrum WI JN1/05)

Treatment:

·         Indications:

  • Incidental: Consider following with imaging at 6mos then yearly to look for growth; MRA is adequate (Mangrum WI JN1/05)
  • Ischemic symptoms: treated with anticoagulation/antiplatelets, although increases risk with rupture
  • Enlarging: consider endovascular/surgical treatment. (Mangrum WI JN1/05)
  • Compression: see below
  • SAH: early endovascular/surgical treatment is warranted because of high rebleed rate

·         Surgical/endovascular Options:

1)     Proximal (Hunterian) ligation or trapping:

·         Endovascular is favored treatment. Done with Balloon, GDC coils.

·         May also be done with surgical ligation

·         Balloon test occlusion (BTO) necessary first (20 minutes).

·         Based on location:

·         VA Involving PICA takeoff: coil proximal to PICA/aneurysm

·         VA Proximal to PICA: trap (clip proximal and distal)

·         VA Distal to PICA: clip/coil distal to PICA, proximal to aneurysm

·         Basilar: staged bilateral vertebral occlusion if pcoms adequate. (Axionnat R N8/03)

·         If patient does not tolerate BTO combine with bypass: contralateral PICA bypass, VA-PICA anastamosis (with radial artery graft), occipital a. bypass.

·         Others feel that clipping proximally only does not guarantee against re-bleeding and all VA aneurysms must be trapped with PICA revascularization if patient doesn’t tolerate BTO or aneurysm involves PICA (Hamada J JN12/03)

·         Risk of permanent deficits: 14% basilar, higher with hypoplastic pcoms. Note if vert is dominant, or contralateral vasospasm exists. May not cause resolution, occasional rebleed.

2)     Endovascular stenting ± coling (stent-assisted)

·         Case Series: Greenberg E JN7/07, Coert BA JN5/07

·         Reviews: Hanel RA JN2/05

3)     Wrapping: Unproven efficacy.

4)     Clipping/Reconstruction

·         Case Series: Mangrum WI JN1/05, Flemming KD JN7/04, Flemming KD JN3/00, Vishteh AC JN8/99, Drake CG JN 1997 (largest series)

 

Symptomatic Vertebrobasilar Dolichoectasia

·         Vertebrobasilar ectasia may cause brainstem or cranial nerve compression

·         Treatment:  for significant, progressive symptoms

·         Pexy: Sling (e.g. Goretex) around artery sutured to petrous/clival dura.  Usually via far lateral approach.

·         Microvascular decompression: placement of Teflon felt, usually for cranial nerves (e.g. CN6) (De Ridder D JN12/07)

·         Case Reports: Ubogu EE JN1/02

 

MCA fusiform aneurysms

·         Occur in children, young patients (<40yo).

·         Lower bleed rate than VA & ICA fusiform aneurysms.

·         Small aneurysms present with SAH, large ones with ischemia or mass effect.

·         May be due to atherosclerosis or dissection.

·         May be stenotic or dilated on angio, but MRI/MRA shows external dilation.

·         Treatment:

·         Indications: SAH, very large aneurysms, or symptomatic from chronic ischemia or mass effect (acute ischemia treat as for stroke).

·         Proximal occlusion and distal bypass (saphenous or arterial interposition if M1, otherwise can use STA).

·         Cannot trap and excise M1 due to lenticulostriates (will thrombose with proximal occlusion).

·         Partial clipping is ineffective

·         Reviews: Day AL JN8/03

 

 

Vascular Dissection

·         Terminology varies: disruption between intima & media  or media & adventitia (also called dissecting aneurysm)

·      Pseudoaneurysm: encapsulated hematoma around vessel, usually traumatic

·         Extracranial or intracranial

·         Spontaneous or post-traumatic

o    Spontaneous: Risks: OCPs, collagen vascular disease (RA, SLE), fibromuscular dysplasia (“string of beads”), inherited (Marfan’s, Ehler-Danlos IV),  migraines, HTN. Delivery, Pharyngeal infections

o    Post-traumatic: Suspect with evidence of blunt trauma to the neck

o    Iatrogenic: during endovascular procedures

·         Causes TIA/CVA (occlusion, thrombosis, or emboli) or SAH (if intracranial, less common)

o    Extracranial: sub-intimal, rupture rare. Intracranial: lacks external elastic membrane, rupture (SAH) more common.

·         Angio, CTA, MRA patterns:

o    String sign (luminal stenosis)

o    Pearl and string sign (fusiform dilation with adjacent stenosis - higher re-bleed rate?) (Figure 1 Chamoun RB JN:P8/08)

o    Intimal flap / Double lumen

o    Fusiform dilation.

o    T1 MRI: ↑T1 (mural hematoma) around narrow flow void

o    CTA or MRA generally obtained first, angiogram if CTA/MRA negative but high clinical suspicion

o    May also be diagnosed by ultrasound

Extracranial Dissection

·         Hemorrhage is rare

·         Carotid: Usually 2cm above bifurcation below skull base.

·         Symptoms: Facial/eye pain, carotidynia (neck pain), pseudo-Horner’s (no anhydrosis), cervical bruit

·         Vertebral: Between skull base & C2 or C6. Occipital HA.

·         Symptoms: occipital pain/headache (after trauma); brainstem signs (e.g. Wallenberg’s)

·         Treatment:

  • Observation for asymptomatic traumatic VA dissection (per cervical trauma guidelines)
  • Anticoagulation 6-12 wks (heparin 7-14d then coumadin) or until >50% re-canalized on MRA/angio then antiplatelets.
    • Serial imaging until resolution.
    • Do not use if SAH present – surgical or endovascular
    • No randomized trials of effectiveness of anticoagulants or antiplatelets
    • Consider antiplatelets initially if high bleeding risk (large CVA).
    • Consider adding antiplatelets to anticoagulation for clinical progression.
    • For significant stenosis after healing of dissection, angioplasty ± stenting considered (no randomized trials)

Intracranial Dissection

·         May occur on ACA (A2), MCA, PCA, Vertebrobasilar

·         Treatment:

·         Endovascular angioplasty ± stenting

·         Endovascular proximal occlusion (coils, balloons)

·         Vertebrobasilar: options as for fusiform aneurysm above (trapping, proximal occlusion)

·         Case Series: Anxionnat R N8/03 (intracranial)

 

 

AVM – Arteriovenous Malformations

·         Hemorrhage rate: 3-4%/yr. Rehemorrhage: 6% @ 6-12mos then 3%/yr. (Ondra SL JN9/90, Hernesniemi JA N11/08)

o    Risk of death from ruptured AVM: 1%/yr. Mortality from hemorrhage: 15%. Lifetime risk: 1-0.3life expectancy, or 105-age. 

o    For deep AVMs (basal ganglia, thalamus, brainstem) risk is 10%/year.

o    Higher rupture rate: previous hemorrhage, small size, deep drainage.

o    No increased risk if symptomatic (HA, seizures, etc).

o    No known increase with pregnancy if non-ruptured, but rehemorrhage rate may be higher (26%) if ruptured during pregnancy - controversial. Generally managed expectantly until delivery. C-section vs vaginal delivery is controversial.

·         15% have associated aneurysms (examine imaging closely).

·         Vasospasm occurs in 1%.

·         Presentation: hemorrhage 50%, seizure 25%, deficit (2º to steal) 25%, headaches (migraine-like, more common w/occipital AVM). Younger presentation than aneurysms.

·         Often wedge-shaped, apex at ventricle.

·         Audio: Cerebral AVMs: Changing Concepts in Treatment Alternatives – Heros RC

Treatment

·         Based on age, grade (location, size, drainage), symptoms.

·         Asymptomatic: 55yo used as general cutoff for treatment

o    New York Islands AVM Study suggested conservative treatment if asymptomatic, but study was problematic. (Stapf C Stroke 5/03)

o    “A randomized trial of unruptured brain arteriovenous malformations (ARUBA)” is a currently ongoing RCT of observation versus any treatment

·         Ruptured AVMs: usually treated electively after 2-4weeks. Emergent ICH evacuation can be done with or without AVM resection.

·         Spetzler-Martin Grade: Spetzler RF JN86

o    Grade I-II: generally treated surgically

·         Some feel embolization should not be performed for most Grade I or II AVMs, because they can be resected with low risk of morbidity.

o    Grade III: treatment individualized

·         Lawton’s revisions to grade III: Grade III- (S1VD1E1; low grade - resectable), Grade III (S2VD1E0; intermediate – ± resectable), Grade III+ (S2VD0E1; high-grade – conservative management), and Grade III* (S3VD0E0; rare). Lawton MT N4/03

·         Medium-sized Grade III AVMs in eloquent regions can be embolized to reduce surgical risk, but lesions in noneloquent brain regions generally can be excised without embolization

o    Grade IV-V: managed conservatively unless repeated hemorrhages leads to deterioration

·         Barrow Neurological Institute’s Grades IV and V AVMs showed a 1% annual bleeding rate in patients treated conservatively compared with a 10.4% rate in patients whose AVMs were treated partially or palliatively; they recommend conservative treatment without embolization for most Grades IV and V AVMs. (Citation pending)

o    Large-volume AVMs: embolization, embolization followed by radiosurgery, radiosurgery with low radiation doses and planned repeat radiosurgery for the expected residual, staged-volume radiosurgery, and fractionated radiation therapy.

·         Surgery

o    Wait 3-30 days (e.g. 1 week) after embolization

o    Consider pretreatment with propanolol to minimize NPPB

o    Wide exposure. Circumferential dissection, preserving draining veins.

·         For intraop bleeding: can use controlled hypotension. Check for venous compression by retractors.

o    Postop/intraop angio. Residual may have higher rupture risk – excise.

o    Complications: Postop ICH or severe edema in 3-12%.

o    Normal Perfusion Pressure Breakthrough (NPPB): Postop swelling or hemorrhage. Hyperemia detected with Perfusion MRI. Control BP.

o    Reviews: Hashimoto N N6/01, Clatterbuck RE ON7/05 (Operative Nuances), Hashimoto N N7/07S, Natarajan SK N6/08

o    Videos: Hashimoto N N6/01, Clatterbuck RE ON7/05, Hashimoto N N7/07S, Natarajan SK N6/08

·         Embolization:

o    NBCA (N-butyl cyanoacrylate), polyvinyl alcohol particles, coils.

o    Almost always adjunctive, not primary treatment (cure rates 5-40%).

o    Some recommend 24-72 hrs ICU monitoring.

o    Hopkins recommends not embolizing >50% at one time if multiple feeders, use local/propofol, pedicles tested with amobarbital. (N12/03 p1259)

o    Risks: ICH 1-4%. AVM may recanalize after successful embolization.

o    Staged endovascular embolization may result in reduction of NPPB with very large high-flow AVMs. Generally staged at days to weeks intervals, 20-30% per stage.

o    Valavanis and Yasargil reported a 39% cure rate in 387 embolized AVMs. For AVMs that were embolized with curative intent, they reported a 75% cure rate.

o    Large AVMs in eloquent areas with progressive neurological deficit, palliative embolization can improve or stabilize the neurological deficit in more than 90% of cases

o    Adjunctive:

o    Wait 3-30 days before performing surgery

·         Embolization can be used to obliterate deep arterial pedicles (such as the lenticulostriates and thalamoperforators) that are inaccessible during the early surgical exposure.

o    Previous embolization is a negative predictor of successful AVM radiosurgery, and some consider its use to be contraindicated prior to radiosurgery (Andrade-Souza YM N3/07)

·         Not recommended before SRS, but if performed wait 30 days before SRS then repeat angio.

·         Embolization has been used pre-SRS in AVMs larger than 3 cm to reduce size and AVMs with angioarchitectural abnormalities that predict a high risk of hemorrhage during the latency period – i.e. intranidal and venous aneurysms or those associated with a large arteriovenous fistula (AVF).

·         Radiosurgery:

o    Recommended for AVMs smaller than 3 cm (volume <10cc) in diameter when surgery carries a high risk of morbidity

o    The 3 cm size cut-off is supported by anecdotal case series and nonrandomized cohort studies.

o    Radiosurgery AVM score – Pollock/Flickinger (Pollock BE JN1/02) Modified System – Pollock BE N8/08

o    Bleeding risk unchanged for 2-3yr latency (controversial – some studies report lower or higher rates) (Marayuma K NEJM1/13/05)

o    Margin doses: Small AVMs 23Gy (no benefit from higher doses). Large, risky location: 16-18Gy. (<15Gy ineffective).

o    Use MRI (Or CTA) with (or without) angio for targeting.

o    2yr obliteration: >4cm3 = 40-60%, <4cm3 = 85-100%. Overall 75% (Pollock BE N6/03)

o    Factors reducing success: size, location, age, prior embolization (Andrade-Souza YM N3/07)

o    Size: >15cm3 consider staged SRS at 6mo intervals.

o    Hypofractionated Conformal Stereotactic Radiotherapy has also been used (Lindvall P N11/03)

o    Hematoma may compress vessels, may targeting difficult. Perform SRS 2-3mos after hemorrhage.

o    Complications: cyst formation (2%, may occur between 5 and 20 years post-treatment), edema (10% symptomatic, 4% need surgery), necrosis 3-6%.

o    Follow-up: Repeat angio not performed until 3yrs, then consider retreatment, repeat SRS. 

o    If early draining vein but no nidus, consider it treated.

o    Follow-up MRI has 100% positive and 85% negative predictive values – some get only MRI only for follow-up.

o    Persistent AVM may be treated with repeat SRS or surgery

·         Some feel SRS make subsequent surgery easier in many cases (Sanchez-Mejia RO N2/09)

Deep (Brainstem/Thalamic) AVMs

·         Rupture rate basal ganglia/thalamus AVMs is 10%/year (Fleetwood IG JN4/03)

·         Basal Ganglia/Thalamus: see Gross B N9/08

·         Radiosurgery: 66% success, 10% permanent deficits. Risk higher in tectum. Higher doses (20Gy) preferred. (Pollock BE JN2/04, Maruyama K JN3/04, Andrade-Souza YM N1/05)

AVM-associated aneurysms

·         10% of aneurysms have associated by AVMs

·         Classifications: terminology varies.

1.     Intranidal aneurysms: increased risk of rebleeding (10%/year); can be targeted by embolization.

2.     Pedicle (flow-related distal) aneurysms: some report higher risk of bleeding

3.     (Flow-related) Proximal aneurysms: on circle of Willis vessels feeding AVM.

§  Rupture risk unclear but reported to be at least that of isolated aneurysm. 

§  Obliteration of AVM may reportedly increase risk of rupture.

4.     Incidental:  unrelated circle of Willis

o    Drake Classification: see Chart (Cunha e Sa MJ JN1992)

·         Treatment (flow-related): Controversial

o    Some recommended treating the AVM suggesting flow-related aneurysms will regress afterwards (Meisel HJ N4/00)

o    Others recommend treating lesion that probably bled 1st or both simultaneously. If its not clear which bled, presume it’s the aneurysm. (Cunha e Sa MJ JN1992)

§  “The late Charles Drake taught that the aneurysm should be considered to have bled whenever bleeding associated with an AVM and an aneurysm is observed” – Fox AJ, comment on Meisel HJ N4/00

o    Others recommend always treating the aneurysm first (or both simultaneously), as treatment of the AVM may increase the risk of rupture (Thompson RC N8/98)

 

Dural Arteriovenous Fistulas (AVFs)

·         Acquired, due to venous sinus thrombosis, fed from ECA (dural or transosseous) or less commonly ICA (dural – tentorial, orbital or cavernous sinus).

·         May present with local symptoms (e.g. tinnitus) or SAH/ICH

·         Cortical venous drainage (CVD) (aka retrograde leptomeningeal venous drainage - RVLD) is #1 SAH risk – 10% mortality.

·         Locations:

o    Transverse/ sigmoid: most common.

·         Symptoms: Pulsatile tinnitus (also caused by aberrant ICA, glomus tympanicum.), occipital bruit.

·         Less SAH risk.

·         Parallel venous channel may be the recipient pouch near the transverse sinus (Caragine LP N12/03)

o    Cavernous sinus (CCF): see below

o    Tentorial apex (ICA/ECA to deep cortical veins): increased SAH risk

o    Orbital/ anterior fossa: increased SAH risk. Can’t treat ophthalmic/ethmoidal feeders endovascularly

o    Others

·         Diagnosis:

o    MRI/MRA: multiple flow-voids in enlarged, enhancing transverse sinus

·         Cortical drainage involvement may mimic neoplasm

o    Angiogram: ECA or ICA feeders to venous sinus

·         Borden and Cognard classifications (see right – from Strom RG N2/09)

·         Treatment:

o    “Aggressive”:  Cortical or retrograde venous drainage, ICH/SAH, seizures, progressive neurologic deficit: requires urgent treatment.

o    “Benign”: Anterograde drainage: can treat symptomatically.

o    Options for surgery or embolization are disconnection of cortical venous drainage vs. complete obliteration

o    Endovascular embolization: transarterial (higher recurrence) or transvenous (riskier)

·         Anterior fossa lesions with feeders via ethmoidals/ ophthalmic a. are treated surgically, not endovascularly

o    Surgery:

·         Single leptomeningeal draining vein can be treated with vein ligation.

·         Alternative: excision and packing of sinus.   Potential for high blood loss early.

o    SRS: 68% obliteration, 24% regression. Considered for “benign” DAVFs (Soderman M JN6/06 – editorials by Heros RC, Sheehan J)

Carotid-cavernous fistula

·         Barrow Classification (A-D)