2. • An intracranial aneurysm is defined as an
abnormally circumscribed dilatation of an
artery which grows and ruptures over time.
• Ant circulation 85%. post cirulation 15%.
• Ant circulation: ICA 30%. ACA 30%. MCA 25%
• Post circulation: PCA 2%. Basilar artery 10%.
• Mostly at branching sites
3.
4.
5.
6.
7.
8.
9. Saccular aneurysm
• M.c. intracranial aneurysm morphology
• arising from first- and second-order branches
in the circle of Willis
• Intracranial arteries are structurally unique in
that they lack external elastic lamina. The
disappearance of the external elastic lamina
occurs in the horizontal segment of the
cavernous portion of internal carotid arteries
10. • most significant pathogenetic factor is
considered to be the degeneration of tunica
media and internal elastic lamina at the
branching sites of intracranial arteries in
regions of chronic hemodynamic stress
11. FUSIFORM ANEURYSM
• circumferential dilatation in a segment of an
intracranial artery.
• not have a defined orifice (neck)
• The inflow and outflow of fusiform aneurysms
are longitudinally separate
• associated with atherosclerosis
• If an arterial fusiform dilatation is
accompanied by a marked elongation, it is call
a dolichoectasia
12.
13. DISSECTING ANEURYSM
• result of splitting or dissection of an arterial wall
by blood flow entering through a tear
• radiographic appearance of pearl-and-string sign
• outpouching mimicking a saccular aneurysm
(pseudoaneurysm or false saccular aneurysm), or
a fusiform segmental dilatation
• can occur spontaneously, but they are commonly
associated with trauma or an underlying
vasculopathy such as fibromuscular dysplasia
• Male predominance
14.
15.
16. • Approximately 5% of intracranial aneurysms
are associated with heritable connective
tissue disorders, the most important being
Ehlers-Danlos syndrome vascular type (type
IV), neurofibromatosis type 1, and autosomal
dominant polycystic kidney disease
17. • Familial intracranial aneurysms are defined as those
identified in two or more first-degree relatives
• increases with age
• current cigarette smoking
• Cocaine use
• coarctation of the aorta
• Pheochromocytoma
• Congenital abnormalities of the intracranial artery,
such as persistent carotid-vertebrobasilar anastomoses
• vertebro-basilar fenestrations
28. • The sensitivity of CT scan in detecting SAH
decreases with the time interval after the
hemorrhage because of the change in density
of subarachnoid blood on CT (Best in 24hrs. In
1 week sensitivity 50%. In 2 weeeks 30%)
• The characteristics of cerebrospinal fluid (CSF)
for patients with SAH include increased red
blood cell count and xanthochromia.
29. • Approximately 2 hours after the hemorrhage,
xanthochromia becomes detectable and may last
as long as several weeks.
• LP positive 100% in 12 hrs to 2 weeks. 70% after
3 weeks. 40% after 4 hrs
• Multimodal magnetic resonance imaging (MRI),
including fluid-attenuated inversion recovery
(FLAIR) and gradient echo (GRE) sequences, is
becoming an important diagnostic tool to detect
acute and chronic SAH.
38. • either conventional open surgery or endovascular
treatment should be performed as soon as
possible after the onset of SAH unless
contraindicated .
• a ruptured aneurysm in the anterior circulation
and Hunt and Hess or World Federation of
Neurosurgeons (WFNS) grades 1 to 3, surgical
treatment is usually considered.
• Surgical treatment for a patient with Hunt and
Hess or WFNS grades 4 and 5 is controversial
owing to the overall poor outcome regardless of
the surgery. Such poor-grade patients may be
good candidates for intentionally delayed surgery
or endovascular treatment.
40. • newer endovascular techniques to treat
complex-shaped aneurysms, such as stenting
and liquid embolic materials, requires
aggressive antiplatelet therapy because of the
thrombogenic nature of those materials
• their use appears to be limited to unruptured
aneurysms.
