4. Cerebral Arteries
A1-segment
Anterior cerebral artery
from carotid bifurcation to
anterior communicating
artery gives rise to the
medial lenticulostriate
arteries.
A2-segment
Part of anterior cerebral
artery distal to the anterior
communicating artery.
P1-segment
Part of the posterior
cerebral artery proximal to
the posterior
communicating artery.
The posterior
communicating artery is
between the carotid
bifurcation and the
posterior cerebral artery)
P2-segment
Part of the posterior
cerebral artery distal to the
posterior communicating
artery
5. Middle Cerebral Artery
• Horizontal M1-segment
• gives rise to the lateral lenticulostriate arteries which supply part of head and body of
caudate, globus pallidus, putamen and the posterior limb of the internal capsule.
• Notice that the medial lenticulostriate arteries arise from the A1-segment of the anterior
cerebral artery.
• Sylvian M2-segment
• Branches supply the temporal lobe and insular cortex (sensory language area of
Wernicke), parietal lobe (sensory cortical areas) and inferolateral frontal lobe
• Cortical M3-segment
• Branches supply the lateral cerebral cortex
6. Aneurysms
• They result from focal degeneration of the arterial
wall. They are the most common cause of
SAH. They are of 3 types :
• Saccular (outpouching from arterial
bifurcation) - Lacks internal elastic lamina
• Fusiform (arterial dilatation)
• Dissecting (pseudo-aneurysm)
7. SACCULAR ANEURYSM
Berry like vesel outpouching
arising from the bifurcation of the
arteries. 80% of Intracranial
aneurysms
85% - anterior
circulations 15%-
Posterior circulations.
8. FUSIFORM
ANEURYSM
• No definitive neck.
• Long course of circumferential thickness.
• Dolichoectasia .
• Vertebrobasilar systemcommonly affected.
9. DISSECTING
ANEURYSM
• May be intracranial or extra-cranial.
• Intracranial vertebralor
posterior
inferior cerebellar arteries – SAH
• Extra-cranial carotid and vertebral arteries – Stroke
(in young)
11. INCIDENCE
• General population is 0.5-5 %
• Women >> Men
• Increases with advancing age.
• Genetic Predisposition.
• Overall risk of rupture = 0.5-2 % per annum,
12. Risk Factor
of Rupture
• Daughtersac
• Multi-lobulations
• Irregular surface
• Bottle-neck shape
• Interval growth
• Increase ratio of maximum
• aneurysm diameter to
parent vessel
diameter.
13. Location
• Most cerebral aneurysms arise from the circle of
Willis and middle cerebral artery bifurcations.
• Ninety percent involve the anterior
circulation,
and
10% the posterior circulation.
16. Multiple
aneurysm
Multiple aneurysms
are found in 15% to
30% of patients,
Women: Men= 5:1
ratio,
Most frequently
involve the middle
cerebral artery.
Of the patients with
multiple cerebral
aneurysms,
75% have two,
• 15% have three 10%
have four or more.
17.
18. • Bilateral symmetrical aneurysms are called Mirror
Aneurysms, and
• most often involve the ICA or the MCA bifurcations.
• When one of multiple aneurysms ruptures and causes
subarachnoid hemorrhage, it is most often the largest, although
this is not always the case.
• For instance, Nehls and colleagues have reported the
propensity for anterior communicating aneurysms to rupture
when several are present simultaneously.
19. Etiology
Primary Causes
Atherosclerosis
• Hypertension
• Smoking
Abuse of cocaine,
methamphetamine, ephedrine,
heroin, and other drugs
that produce arteritis or
hypertension
Vascular malformations -
fibromuscular dysplasia,
spontaneous cervical
carotid or vertebral artery
dissection, Takayasu's arteritis,
neurofibromatosis I
Connective tissue disorders,
such as Marfan's syndrome and
Ehlers- Danlos syndrome
20. Secondary Causes
• Penetratingand nonpenetratingtrauma
• Dissection (posttraumatic or otherwise)
• Inflammation or mycosis due to septic
• Neoplasm
• infundibulumrepresents the residua of a
developmental vessel that has undergone incomplete
regression.
• It most commonly involves the junction of the
internal carotid artery and posterior
communicating artery and less commonly involves
the origin of the anterior choroidal artery from the
internal carotidartery.
• Infundibula are usually 3 mm or less in diameter.
21. Pathology
• Pathologically, a number of patients with cerebral
aneurysms demonstrate collagen type III
abnormalities.
• The walls of saccular cerebral aneurysms contain intima
and adventitia, but the media and internal elastic
membrane are thinned or absent.
• Neoplasm: Pitutary adenoma – Growth hormone
• Mycotic- spread of infection to vasa vasorum.
22. Features Need To Be
Assessed
• size: ideally 3 axis maximum size
measurements
• neck: maximal width of the neck of an
aneurysm
• the shape and lobulation
• orientation: the direction in which the
aneurysm points is often important in both
endovascular and surgical planning
23. Cont….
• any smaller branches in the vicinity of an
aneurysm
• any branch taking off from the aneurysm
• the presence of other aneurysms
• relevant arterial variant anatomy
(that may complicate or exclude
endovasculartreatment
26. Lumbar
Puncture
• Before CT, it was the only
method to confirm the diagnosis
of SAH but presently it is
only indicated when CT is
normal in patients with
sudden, severe headache.
• CSF is bloody not clearing
with sequential tubes,
Xanthrochromia is
present after 1-2 days of
SAH.
28. Cerebral Aneurysm
• CT examination is secondarily
important to identify cerebral
aneurysms, typically 5 mm or
larger in diameter.
• The rate of identification of cerebral
aneurysms - at least 67% for
aneurysms 3 to 5 mm in diameter and to
approach 100% for larger
aneurysms.
Giant aneurysms are most commonly identified in middle-age women; are typically
located in the extradural carotid artery, the middle cerebral artery bifurcation, or the
basilar summit; and usually manifest with mass effect
29. Cerebral
Aneurysm
• MRI is superior to CT for
• the localization of cerebral
aneurysms,
• their relationship with adjacent
structures, and
• associated changes in
neighboring brain tissue.
30. Management of
intracranial aneurysms
• The goal of preoperative management is
• to stablize the patient for aneurysm obliteration
and
• prevent the development of systemic
complications or secondary cerebral insults
such as hypotension or hypoxia.
• Ideally successful management of acutely
ruptured aneurysm begins with adequate
ventilation and oxygenation, normovolemia,
hemodynamic stability, normoglycemia and ICP
control.
31. • After initial stabilisation , a thorough
radiographic evaluation is undertaken.
• Surgical Methods:
• Current surgical options include direct
aneurysmal clippingand endovascular
exclusion -- Surgical Clipping or Coil Embolization
for the specific indications for treating an
aneurysm surgically, endovascularly, or
both).
32. Endovascular methods
• GDC COILS - Of the various endovascular options currently available, Guglielmi
detachable coils (GDCs) have had the largest influence with respect to treatment of
subarachnoid hemorrhage; GDCs are first-line therapy nowdays.
• These coils are soft, flexible, and can be contoured to the configuration of the
aneurysm.
• Sizes range from 2 to 20 mm in diameter and 2 to 30 cm in length.
• Balloon embolization is efficacious in selected patients, but it has a higher
incidence of complications than coil embolization.
33. Indications for endovascular treatment
Posterior circulation aneurysms, especially basilar apex.
Patients with poor clinical grade (ie, Hunt and Hess grades 4-5).
Patients who are medically unstable.
Symptomatic cavernous aneurysms.
Small-neck aneurysms in the posterior fossa.
Patients with vasospasm.
Cases in which the aneurysm lacks a defined surgical neck
(although these are also difficult to "coil")
Patients with multiple aneurysms in different arterial territories if
the surgical risk is high
37. • Stent placed in case of larger
neck for the stabilization
of the coil.
38. • Step 5: Check the coils
• Step : Remove the
catether
39. Evaluation after open /endovascular
surgery
MRI – MRI
compatible clips
Fatal cerebral
hemorrhage if
incompatible
CTA superior to MRI
DSA Catheter
Angiography superior