Neurosurgery (Vascular) – Dr.
Orata Reference:
ISCHEMIC DISEASE
 85% of acute cerebrovascular events secondary
to ischemic stroke
 Symptoms of acute ischemic stroke vary based
on the functions of the neural tissues supplied
by the occluded vessel, and the presence or
absence of collateral circulation.
o The circle of Willis provides extensive
collateral circulation, as it connects the
right and left carotid arteries to each
other and posterior circulation to each
of the vertebrobasilar system.
 Neurologic deficit from occlusive disease may be
temporary or permanent
o Transient ischemic attack (temporary)
 A patient with sudden-onset
focal neurologic deficit that
resolves within 24 hours.
THROMBOTIC DISEASE
 The most common area of thrombosis is the
carotid artery in the cervical area of the neck.
o Can be asymptomatic.
 Intracranial arterial occlusion by local thrombus
formation may occur, but it is rare compared to
embolic occlusion.
MANAGEMENT
 No neurologic deficit requires no treatment
 Carotid endarterectomy
o A patient with new neurologic deficit
o A confirmed complete carotid occlusion
STROKE
ANTERIOR CEREBRAL ARTERY STROKE
 ACA supplies the medial frontal and parietal
lobes, including the motor strip, as it courses
into the interhemispheric fissure
 ACA stroke results in contralateral leg weakness.
MIDDLE CEREBRAL ARTERY STROKE
 MCA supplies the lateral frontal and parietal
lobes and the temporal lobe
 MCA stroke results in contralateral face and arm
weakness.
POSTERIOR CEREBRAL ARTERY STROKE
 Supplies the occipital lobe
 Stroke results in contralateral homonymous
hemianopsia
PPT and Recordings (Nov. 2020)
POSTERIOR INFERIOR CEREBELLAR ARTERY STROKE
 Supplies the lateral medulla and the inferior half
of the cerebellar hemispheres
 lateral medullary or Wallenberg’s syndrome
o Results in nausea, vomiting, nystagmus,
dysphagia, ipsilateral Horner’s
syndrome, and ipsilateral limb ataxia
DIAGNOSTIC
 Head CT must be performed immediately to
differentiate ischemic from hemorrhagic stroke
o Acute hematoma – bright
o Acute ischemic stroke – normal CT
 Request MRI (more sensitive
in screening ischemic stroke)
MANAGEMENT
TWO GOALS:
 Reopen the
occluded vessel
 Maintain blood flow to ischemic “penumbra”
tissues bordering the vascular territory
MEDICAL
 Reopening the vessel (recombinant tPA)
o Permissive hypertension allows for
maximal cerebral perfusion
o It will lyse the occlusion
o Optimal mean arterial pressure goal is
between 100 to 140 mmHg
o Window period: 3 hours
SURGICAL
 Decompressive hemicraniectomy (MCA stoke)
or suboccipital craniectomy (posterior fossa
stroke)
o Significant swelling from an MCA or
cerebellar strokes may cause herniation
and brainstem injury.
o >3 hours or tPA is not applicable
HEMORRHAGIC DISEASES
 15% of acute cerebrovascular events
 Hypertension and amyloid angiopathy account
for most intraparenchymal hemorrhages
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  Causes local neuronal injury and dysfunction TREATMENT
and also may cause global dysfunction due to  Evacuation of hematoma
mass effect if sufficiently large  Small thalamic hematoma, ventriculostomy
o Cause immediate concussive-like o To relieve the hydrocephalus
neuronal dysfunction by exposure of o To drain hematoma
the brain to intra-arterial pressure
pulsations CEREBRAL ANEURYSM
o Cause delayed ischemia from cerebral  Focal dilatation of the vessel wall and is most
arterial vasospasm often a balloon like outpouching, but may also
 Typically occurs within the basal ganglia or be saccular (have a neck and a dome) fusiform
cerebellum (uniform dilatation).
 Occur at branch points of major vessels (e.g.,
MANIFESTATIONS internal carotid artery bifurcation), or at the
 Lethargy or obtundation origin of smaller vessels (e.g., posterior
o Results from brain shift and herniation communicating artery or ophthalmic artery)
secondary to mass effect from the  85% of aneurysms  anterior circulation
hematoma in deep structures  SAH patients are also at risk for cerebral
 Hemorrhagic strokes tend to present with a vasospasm
relatively gradual decline in neurologic function o Cerebral arteries constrict
as the hematoma expands. pathologically and can cause ischemia
% LOCATION SYMPTOMS or stroke from 4 to 21 days after SAH.
1-6 Brainstem Often Devastating  Mortality rate of 50% in the first month
(Excluding Pons)  Approximately 1/3 of survivors return to pre-
10 Cerebellum Lethargy or coma SAH function, and the remaining 2/3 have mild
secondary to severe disability
to brainstem/ or  Most require rehabilitation after hospitalization.
hydrocephalus
10-15 Pons Hemiparesis; may be
devastating
10-20 Cerebral White Depends on location
Matter (Lobar) (weakness, numbness,
partial loss of visual
field)
15 Thalamus Contralateral
hemisensory loss
50 Basal ganglia Contralateral
(MC) (putamen, Globus hemiparesis
pallidus), internal
capsule

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 MANIFESTATIONS  Small AVMs present with hemorrhage more
 SAH results in a sudden, severe “thunderclap” often than large AVMs, which tend to present
headache with seizures
 Classically describe “the worst headache of my
life.”
 Presenting neurologic symptoms may range
from mild headache to coma to sudden death.
 Common location PCA, MCA, Basilar, PICA
aneurysm

DIAGNOSIS
 CT is rapid, noninvasive, and approximately 95%
sensitive
o In patients with suspicious symptoms
but negative head CT, a lumbar
puncture (LP) should be performed.
o An LP with xanthochromia and high red
blood cell counts (usually 100,000/mL)
 Confirm findings:
o 4 vessels angiogram – Invasive; gold
standard. Both therapeutic and
diagnostic.
o CT/MR angiogram - noninvasive
TREATMENT
 EARLY ANEURYSMAL OCCLUSION
o Placement of a titanium clip across the
aneurysm neck
o “coil” the aneurysm via an
endovascular approach.
 CEREBRAL VASOSPASM
o Maintenance of optimal perfusion with
hypertension and mild hypervolemia
o Analgesics or NSAIDs – headache
o Nimodipine
 CLIPPING – GOLD STANDARD
 COILING
TREATMENT
 Definitive therapy for the AVM usually is
delayed 3 to 4 weeks to allow the brain to
recover from acute injury
o Less risk of devastating early rebleeding
from AVMs, and vasospasm is much
less common.
 Three therapeutic modalities for AVM:
o Microsurgical excision – complete
excision of the aneurysm. Indicated in
small and easily accessible AVMs.
o Interventional radiology or
endovascular embolization – deeply
seated located AVMs
o Stereotactic radiosurgery/ gamma knife
– size is <3cm. Deeply seated located
AVMs

ARTERIOVENOUS MALFORMATIONS
 Dilated arteries and veins without an
intervening capillary bed
 Nidus of the AVM contains a tangled mass of
vessels but no neural tissue
 AVMs hemorrhage at an average rate of 2% to
4% a year

MANIFESTATIONS
 Asymptomatic
 May present with Subarachnoid Hemorrhage
 Intraparenchymal hemorrhage (esp. lobar), or You only live once so think...
seizures

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