Etiology:
- congenital (97%) = “berry aneurysm” in 2% of population (in 20% multiple); associated with aortic coarctation and adult polycystic kidney disease
- infectious ( 3%) = mycotic aneurysm
- arteriosclerotic: fusiform shape
- traumatic
- neoplastic
- fibromuscular disease
Risk factors:
- Family history for aneurysms in 1st- / 2nd-degree relatives
- Female gender
- Oral contraceptives / pregnancy
- Advanced age >50 years
- Hypertension
- Cigarette smoking
- Cerebral arteriovenous malformation
- Vasculitis
- Connective tissue disorder: Marfan syndrome, Ehlers-Danlos syndrome type IV, autosomal dominant polycystic renal disease, pseudoxanthoma elasticum, neurofibromatosis type 1
- Asymmetry of circle of Willis
Pathogenesis: arterial wall deficient in tunica media + external elastic lamina (natural occurrence with advancing age)
Aneurysm by shape:
- Saccular
= berry- / bleb-like outpouching - Cause: hemodynamic stress + repeated endothelial damage ← turbulent blood flow
Site: circle of Willis (COW) in 90–95%, arterial bifurcation in 5–10%
Location: anterior circulation (90%), posterior circulation (10%), distal to COW (5%)
Size: 2–3 mm small to giant >2.5 cm - Fusiform
= circumferential involvement of wall
Cause: predominantly atherosclerotic degeneration
Location: posterior circulation- Serpentine
= partly thrombosed containing tortuous vascular channels
Cause: recurrent cycles of thrombosis + recanalization within fusiform aneurysm
- Serpentine
Location of aneurysm:
- by autopsy:
- circle of Willis (85%): aCom (25%), pCom (18%), MCA bifurcation (25%), distal ACA (5%), ICA at bifurcation (4%), ophthalmic a. (4%), anterior choroidal a. (4%)
- posterior fossa (15%): basilar bifurcation (7%), basilar trunk (3%), vertebral-PICA (3%), PCA (2%)
- by CT: detection rate of aneurysms at pCom (40%), aCom / MCA, basilar artery (80%)
- by angiography (= symptomatic aneurysms): pCom (38%) >aCom (36%) >MCA bifurcation (21%) >ICA bifurcation >tip of basilar artery (2.8%)
- by risk of bleeding: 1–2% per year aCom (70% bleed), pCom (2nd highest risk)
◊Aneurysms at bifurcations / branching points are at greatest risk for rupture!
NECT:
- well-delineated round / lobulated slightly hyperdense extra-axial mass
- calcium deposit common in atherosclerotic fusiform aneurysm
CECT:
- enhancing lumen of partially thrombosed aneurysm
- rim-enhancement in completely thrombosed aneurysm
CTA: 95% positive detection rate
MR:
- mass:
- iso- / hyperintense on T1WI
- hypointense on T2WI (DDx to primary brain tumor)
- patent aneurysm with internal signal / flow void ← rapid internal blood flow:
- flow void on T2WI = CLASSIC feature
- flow void on T1WI in 50% (DDx: aerated anterior clinoid / supraorbital cell)
- partially / completely thrombosed aneurysm:
- well-demarcated round para- / intrasellar lesion
- internal T1-hyperintensity + CHARACTERISTIC heterogeneous T2-hypointensity ← blood clot
- laminated layers of variable SI if thrombosed
- hypointense rim of hemosiderin
- high SI in sulci + cisterns on FLAIR = sign of rupture
CEMR (T1WI):
- enhancing slow flow in patent lumen
- increased phase artifact in patent aneurysm
MRA (3D TOF): detects aneurysm >3 mm in diameter
Angio (all 4 cerebral vessels):
- contrast outpouching
- <2 mm infundibuli typically occur at pCom / anterior choroidal a. origin
- mass effect in thrombosed aneurysm
- 2nd arteriogram within 1–2 weeks detects aneurysm in 10–20% following negative 1st angiogram!
Purpose: confirm aneurysm and host vessel, detect multiple aneurysms, define neck, identify perforating arteries, assess potential for collateral circulation
Prognosis:
- Death in 10% within 24 hours from concomitant intracerebral hemorrhage, extensive brain herniation, massive infarcts + hemorrhage within brainstem
Mortality: 45% within 30 days (25% prior to admission) - Complete recovery in 58% of survivors
- Cerebral ischemia + infarction
- Rebleeding rate: 12–20% within 2 weeks, 11–22% within 30 days, up to 50% within 6 months (increased mortality); thereafter 1–2–4% risk/year
Cx: subdural hematoma
Rx: clipping; endovascular coiling
Surgical mortality rate: 50% (1–3%) for ruptured (unruptured) aneurysm
Age: 20–70 years, peak 5th–6th decade; F >>M
Cause: sinus thrombophlebitis
- progressive visual impairment
- cavernous sinus syndrome: trigeminal nerve pain, oculomotor nerve paralysis
Site: extradural portion of cavernous sinus ICA
- undercutting of anterior clinoid process
- erosion of lateral half of sella
- erosion of posterior clinoid process
- invasion of middle cranial fossa
- enlargement of superior orbital fissure
- erosion of tip of petrous pyramid
- rimlike calcification (33%)
- displacement of thin bony margins without sclerosis
Rx: often inoperable; balloon embolization ± parent artery occlusion
= aneurysm >25 mm in diameter, usually presenting with intracranial mass effect
- Risk of rupture increases proportionally with size!
Incidence: 5% of all intracranial aneurysms
Age: 5th–7th decade; M<F
- visual disturbance; cranial nerve palsy; seizure
- TIA / infarct ← thromboemboli from aneurysm
Type: saccular >>fusiform
Location: (arise from arteries at the base of the brain)
- middle fossa: cavernous segment of ICA (43%), supraclinoid segment of ICA, terminal bifurcation of ICA, middle cerebral artery
- posterior fossa: at tip of basilar artery, AICA, vertebral a.
Skull film:
- predominantly peripheral curvilinear calcification (22%)
- mass effect:
- bone erosion (44%)
- pressure changes on sella turcica (18%)
CT:
- well-delineated, round / lobulated, slightly hyperattenuating extraaxial mass
- often peripheral intramural / luminal calcified thrombus
CECT:
- “target” sign = centrally opacified vessel lumen + ring of thrombus + enhancing fibrous outer wall
- simple ring-blush (75%) of fibrous outer wall with total thrombosis
- little / no surrounding edema
MR:
- mixed heterogeneous signal intensity of laminated appearance (= combination of subacute + chronic hemorrhage, calcification)
Cx: 6% annual risk of rupture; subarachnoid hemorrhage in >50%
Mortality for untreated giant aneurysm:
68% at 2 years, 80% at 5 years
DDx: partially thrombosed giant aneurysm may mimic slowly growing solid destructive tumor → MR / conventional angiography prior to biopsy!
Incidence: 28,000 cases/year = 10 cases/10,000 persons/year
Age: 50–60 years of age; M÷F = 1÷2
Rupture size: 5–15 mm
- “worst headache of one's life” ± meningismus
- neck stiffness, nausea, vomiting
- history of warning leak / sentinel hemorrhage hours to days earlier; sudden loss of consciousness (in up to 45%)
Clues for which aneurysm is bleeding:
- the largest aneurysm (87%)
- anterior communicating artery (70%)
- contralateral side of all visualized aneurysms (60%), nonvisualization due to spasm
mnemonic: BISH
- Biggest
- Irregular contour
- Spasm (adjacent)
- Hematoma location
Location of blood suggesting accurately in 70% the site of the ruptured aneurysm:
- according to location of subarachnoid hemorrhage:
- Anterior chiasmatic cistern: aCom
- Septum pellucidum: aCom
- Interhemispheric fissure: aCom
- Intraventricular: aCom, ICA, MCA
- Sylvian fissure: MCA, ICA, pCom
- Anterior pericallosal cistern: ACA, aCom
- Prepontine cistern: basilar a.
- Foramen magnum: PICA
- Symmetric distribution in subarachnoid space: ACA + basilar a.
- according to location of cerebral hematoma:
- Inferomedial frontal lobe: aCom
- Temporal lobe: MCA
- Corpus callosum: pericallosal a.
- intraventricular hemorrhage:
from aneurysms at aCom, MCA, pericallosal artery
CAVE: blood may have entered in retrograde manner from subarachnoid location
Cause: congenital in 20–30%, mycotic in 22%
mnemonic: FECAL P
- Fibromuscular dysplasia
- Ehlers-Danlos syndrome
- Coarctation
- Arteriovenous malformation
- Lupus erythematosus
- Polycystic kidney disease (adult)
- 35% of patients with one MCA aneurysm have one on the contralateral side (= mirror image aneurysms)!
- Simultaneous aneurysm + AVM in 4–15%
= 3% of all intracranial aneurysms; multiple in 20%
Source: subacute bacterial endocarditis (65%), acute bacterial endocarditis (9%), meningitis (9%), septic thrombophlebitis (9%), myxoma
Location: distal to first bifurcation of major vessel (64%); often located near surface of brain, especially over convexities
- suprasellar cistern = circle of Willis
- inferolateral sylvian fissure = MCA trifurcation
- genu of corpus callosum = origin of callosomarginal artery
- bottom of 3rd ventricle = pericallosal a.
NECT:
- aneurysm rarely visualized; indirect evidence from focal hematoma after rupture
- zone of increased density / calcification
- increased density in subarachnoid, intraventricular, intracerebral spaces ← extravasated blood
- focal / diffuse lucency of brain ← edema / infarction / vasospasm
CECT:
- intense homogeneous enhancement within round / oval mass contiguous with vessel
- incomplete opacification with mural thrombus
Cx: recurrent bleeding (more frequent than with congenital aneurysm)
= 38% of intracranial aneurysms
Site:
- at origin of pCom (65%)
- at bifurcation of internal carotid artery (23%)
- at origin of ophthalmic artery (12%) medial to anterior clinoid process → most likely to become giant aneurysm
Presentation: bitemporal hemianopia ← extrinsic compression on chiasm
- calcifications rare (DDx: frequent in atherosclerotic cavernous sinus aneurysm)