NEUROLOGY II

LE2: CEREBROVASCULAR DISEASES

Ida Ingrid Rocha-Tulagan, MD

STROKE RISK FACTORS

▪ Sudden onset of focal neurologic deficit due to Non-modifiable
an underlying vascular pathology 1. Age: Increased incidence after age 55
2. Sex: Yes? When and where? Char. Male >
Two major types: Female
1. Ischemic stroke – due to occlusion of a cerebral 3. Race (African Americans 2x > whites > Asians)
blood vessel and causes cerebral infarction 4. Fam Hx
2. Hemorrhagic – results from a rupture of a blood Modifiable
vessel or an abnormal vascular structure directly HTN, TIA, VHD DM, Smoking
into and around the brain AFib, CAD Hyperlipidemia
Carotid Stenosis Alcohol abuse
TRANSIENT ISCHEMIC ATTACK Hypercoaguable states Drugs (Cocaine)
▪ Brief reversible episode of ischemic brain  RBC, hct, fibrinogen Migraine, OSA
disturbance without evidence of cerebral Protein C and S Patent foramen ovale
infarction deficiency Sickle cell anemia,
▪ Transient spells of hemiparesis, aphasia, Cancer
numbness, dysarthria, diplopia, ataxia,
monocular blindness or combinations thereof Differentials
▪ Can reflect involvement of any cerebral artery
Seizures Transient global
▪ 20% of infarcts that follow TIAs occur within a
Systemic infection amnesia
month after first attack; 50% within a year
Brain tumor Dementia
▪ May precede or accompany the development of
Toxic-Metabolic Demyelinating disease
stroke, or can occur by themselves
Positional Vertigo Cervical spine fracture
Cardiac Myasthenia gravis
Differential Diagnosis:
Syncope Parkinsonism
▪ Seizures Trauma Hypertensive
▪ Migraine Subdural hematoma encephalopathy
▪ Syncope Herpes encephalitis Conversion disorder
▪ Transient Global Amnesia
TYPES OF STROKE
Consider stroke if they experience… THROMBOTIC
▪ Sudden numbness or weakness in the face, arm, ▪ Perfusion failure distal to site of severe stenosis
or leg especially on one side of the face or body or occlusion of major vessels
▪ Sudden confusion, trouble speaking or ▪ Involvement of large intracranial (basilar, carotid)
understanding / Extracranial (carotid, vertebral) arteries
▪ Sudden trouble seeing in one or both eyes ▪ ~50% preceded by one or more transient
▪ Sudden trouble walking, dizziness, loss of balance ischemic attacks
or coordination ▪ May be a single episode evolving in a few
▪ Sudden severe headache with no known cause minutes/hours, or may have intermittent
progression
▪ May have embolism from extracranial arteries
affected by stenosis or ulcer.
▪ Characteristically occurs during sleep
Atherothrombosis mechanisms

▪ STROKE is the second leading cause of

morbidity with a prevalence of about 0.9%. (next
to heartbreak. #1 cardiovascular dse)
▪ Ischemic stroke comprises 70% while
hemorrhagic stroke comprises 30%.

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 NEUROLOGY II
LE2: CEREBROVASCULAR DISEASES
Ida Ingrid Rocha-Tulagan, MD

▪ Occlusive plaque or thrombus occupies lumen of ▪ Strong correlation with hypertension (up to 81%);
a major intracerebral/extracranial vessel, also associated with micro-atheroma,
stopping blood flow to areas of brain supplied microembolism or rarely arteritis
▪ Atherosclerotic occlusion of extracranial ICA ▪ Onset may be abrupt or gradual
causing infarction in the WATERSHED AREAS ▪ Absence of higher cortical function involvement
(between territories of the major branches of ICA) (aphasia, apraxia, hemineglect, hemianopia).
▪ Emboli may form over a plaque in a proximal ▪ Often pure motor or pure sensory syndromes
vessel (proximal ICA) and cause stroke in one of
the distal territories of that vessel Other pathologies leading to ischemic brain
damage
Common sites of atheromatous plaque formation ▪ Arterial dissection
1. ICA at origin from common carotid artery ▪ Thrombosis of cerebral veins and dural sinuses
2. Cervical part of vertebral arteries and at junction ▪ Vasculitis
to form basilar artery ▪ Vessel thrombosis due to hypercoagulable
3. Stem or at main bifurcation of mcas conditions
4. Proximal PCAS ▪ Vasospasm
5. Proximal ACAS ▪ Fat/tumor embolism

▪ Atherosclerosis tends to chiefly affect the large- Pathophysiology of Cerebral Infarction

caliber blood vessels
▪ Loss of oxygen supply and glucose due to
▪ Most significant stenoses/occlusions occur in the
vascular occlusion
carotid bifurcations and proximal portions of
− Changes in cellular metabolism
the ICAs, vertebral arteries are likely to develop
− Collapse in energy-producing processes
lesions at the sites of origin from the subclavian
− Disintegration of cell structures and
arteries
membranes (necrosis)
EMBOLIC
The Ischemic Penumbra
▪ Develops most rapidly among all types of
ischemic stroke
▪ Neurologic deficit is immediate
▪ Seizures may occur at onset of stroke
▪ Cortical signs more frequent
▪ May cause severe neurologic deficits that are
temporary; symptoms resolve as the embolus
fragments.

Sources of emboli
▪ Mural thrombi, cardiac arrhythmia (atrial
fibrillation) ▪ In the area of the ischemia, there is a CENTRAL
▪ Recent myocardial infarction CORE with marked reduction in Cerebral Blood
▪ Intra-arterial, from occluded/stenotic carotid or Flow and an ISCHEMIC PENUMBRA
vertebral artery surrounding the core with a marginal blood flow.
▪ Atheromatous plaques in ascending aorta ▪ Ischemic penumbra is the tissue which is
▪ Systemic venous system, via septal defects (i.e., functionally impaired and is at risk of infarction
Patent Foramen Ovale) and has the potential to be salvaged by
▪ Valvular disease (endocarditis; prosthetic heart reperfusion.
valves; mitral stenosis)
▪ Cerebral arteriography STROKE SYNDROMES
▪ Tumors (cardiac myxoma and fibroelastoma) ▪ Anterior Circulation: ICA, MCA, ACA, Anterior
▪ Undetermined in 20-30% chroidal art.
▪ Post Circulation: PCA, BA, PICA, VA
LACUNAR INFARCTION
▪ Lacunes = small infarcts (< 15 mm) seen in the Internal Carotid Artery
putamen, pons, thalamus, caudate, and internal ▪ Clinical manifestations most variable
capsule. ▪ In continuity with the vessels of the circle of Willis
▪ Occlusion of small arteries or deep penetrating and of the orbit
branches of large vessels ▪ Occlusion may be silent (30-40%)
▪ TIAs are cardinal signs of stenosis
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 NEUROLOGY II
LE2: CEREBROVASCULAR DISEASES
Ida Ingrid Rocha-Tulagan, MD
▪ Transient monocular blindness (amaurosis
fugax) precedes stroke in 10-25% of patients
▪ Hypoperfusion → watershed infarcts
▪ Zone of maximal ischemia lies between the two
vascular territories (cortical wathershed)
▪ Cortical border zone infarctions
Infarctions of
the cortex and adjacent subcortical white matter
located at the border zone of ACA/MCA and
MCA/PCA
▪ Internal border zone infarctions
Infarctions of
the deep white matter of the centrum semiovale
and corona radiata at the border zone between
lenticulostriate perforators and the deep
penetrating cortical branches of the MCA or at the
border zone of deep white matter branches of the
MCA and the ACA.
Middle Cerebral Artery
▪ The cortical branches of the MCA supply the
lateral surface of the hemisphere
▪ In the sylvian fissure, the MCA divides into the
superior and inferior divisions (M2 branches)
– Inferior division supplies: Inferior parietal and
temporal cortex
– Superior division supplies: Frontal and
superior parietal cortex
▪ MCA Occlusion occurs at stem or at one of the
two divisions of the artery in the sylvian sulcus.
CLASS 2021 P atricia Abigail Felipe
The proximal MCA (M1 segment) supplies the
following:
▪ Putamen
▪ Outer globus pallidus
▪ Posterior limb of the internal capsule
▪ Corona radiata
▪ Most of the caudate nucleus
Complete Middle Cerebral Artery Occlusion
▪ When MCA is occluded at its
origin (main trunk):
– contralateral hemiplegia,
hemianesthesia,
homonymous hemianopia,
gaze preference to the
ipsilateral side
– Dysarthria due to facial weakness
– global aphasia
– anosognosia, constructional apraxia, and neglect
Middle Cerebral Artery: Partial Syndromes
Superior Division (Rolandic and prerolandic
areas):
▪ Sensory and motor deficits on contralateral face
and arm > leg
▪ Head and eyes deviated toward side of infarct.
▪ Left-side lesion (dominant hemisphere)—global
aphasia initially, then turns into Broca’s aphasia
(motor speech disorder).
▪ Right side lesion (nondominant hemisphere)—
deficits on spatial perception, hemineglect,
constructional apraxia, dressing apraxia.
▪ Transient loss of consciousness is uncommon
Inferior Division (lateral temporal and inferior
parietal lobes)
▪ Lesion on either side → superior quadrantanopia
or homonymous hemianopsia
▪ Left side lesion →Wernicke’s aphasia
▪ Right side lesion → left visual neglect
▪ Brachial syndrome: embolic occlusion of a
single branch include hand, or arm and hand,
weakness alone
▪ Frontal Opercular Syndrome: facial weakness
with nonfluent (Broca) aphasia, with or without
arm weakness
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 NEUROLOGY II
LE2: CEREBROVASCULAR DISEASES
Ida Ingrid Rocha-Tulagan, MD
Anterior Cerebral Artery
▪ Precommunal Circle of Willis (A1) Connects ICA
to the ACA
▪ Postcommunal segment (A2)
▪ Occlusion of the proximal ACA is usually well
tolerated because of collateral flow through the
anterior communicating artery and collaterals
through the MCA and PCA
▪ Pericallosal artery (A3)
▪ Main terminal branch of the ACA
▪ ACA Supplies the anterior limb of the internal
capsule, the anterior perforate substance,
amygdala, anterior hypothalamus, and the
inferior part of the head of the caudate nucleus
Anterior Cerebral Artery
▪ Paralysis of opposite foot
and leg (Motor leg area)
▪ Mild weakness or no
involvement of opposite arm
▪ Cortical sensory loss over
toes, foot, and leg (Sensory
area for foot and leg)
▪ Urinary incontinence (Sensorimotor area in
paracentral lobule) with contralateral grasp reflex
▪ Gait apraxia: Frontal cortex near leg motor area
▪ Occlusion of both ACAs → aphasia, paraplegia,
incontinence, and frontal lobe/personality
dysfunction
▪ Dyspraxia of left limbs, tactile aphasia in left
limbs: Corpus callosum
▪ Abulia (akinetic mutism), slowness, lack of
spontaneity, whispering, reflex distraction to
sights and sounds: Probable involvement of
cingulate gyrus and medial inferior portion of
frontal, parietal, and temporal lobes
Anterior Choroidal Artery
▪ Direct branch of ICA
▪ Supplies posterior limb of
internal capsule and part of
hippocampus
▪ Lacunar syndrome: pure
motor stroke or sensorimotor stroke
contralateral to the lesion
CLASS 2021 P atricia Abigail Felipe
The Vertebrobasilar System
▪ supply the brain stem (medulla, pons, and
midbrain), cerebellum, occipital lobes, posterior
temporal lobes, and thalamus (not visible in this
view).
▪ consists of the extracranial and intracranial
vertebral arteries, which unite to form the basilar
artery, which runs midline along the ventral
surface of the brain stem, feeding it with small,
deep perforators until it merges with the circle of
Willis to give off the posterior cerebral arteries.
SSx
– Vertigo
– Nystagmus
– Ipsilateral cranial nerve dysfunction
– Motor function abnormalities (often bilateral)
– Presence of crossed signs: motor/sensory
deficit on ipsilateral face and opposite side of
body; with ataxia, dysphagia, dysarthria
– Absence of cortical signs such as aphasia or
cognitive deficits
Posterior Cerebral Artery
▪ Proximal
segment: supplies
substantia nigra,
red nucleus,
mammillary body,
oculomotor nerve,
trochlear nerve,
thalamus,
cerebral
peduncle, hippocampus
▪ Distal segment - Laterobasal aspects of the
temporal and occipital lobe
▪ Provides major supply to midbrain and
inferomedial parts of temporal & occipital lobes →
occlusion produces a great variety of clinical
effects
Posterior Cerebral Artery Occlusion
▪ Visual field cuts (cortical blindness when
bilateral)
▪ May have prosopagnosia (cannot read faces)
▪ Alexia (cannot read)
▪ Transcortical sensory aphasia (loss of power
to comprehend written or spoken words; patient
can repeat)
Syndromes of the Vertebrobasilar System
Benedikt Syndrome
▪ Obstruction of interpeduncular branches of
basilar or posterior cerebral artery or both.
▪ Ipsilateral III nerve paralysis with mydriasis,
contralateral hypesthesia (medial lemniscus),
contralateral hyperkinesia (ataxia, tremor,
chorea, athetosis) due to damage to red nucleus
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 NEUROLOGY II
LE2: CEREBROVASCULAR DISEASES
Ida Ingrid Rocha-Tulagan, MD

Syndromes of the Paramedian Area ▪ “Locked-in syndrome”

(Medial Brainstem) – tetraparesis with patients only able to move
▪ Paramedian area contains: eyes vertically or blink
– Motor nuclei of CNs – patient remains fully conscious secondary to
– Cortico-spinal tract sparing of the reticular activating system
– Medial lemniscus – caused by bilateral lesions of the ventral pons
– Cortico-bulbar tract (basilar artery occlusion)
– Signs/symptoms: ▪ Occlusion of the superior cerebellar artery
– contralateral hemiparalysis – Ipsilateral cerebellar ataxia, nausea and
– ipsilateral CN paralysis vomiting, dysarthria, contralateral loss of pain
and temp sensation
▪ Occlusion of the anterior inferior cerebellar
artery
– Ipsilateral deafness, facial weakness, vertigo,
nausea and vomiting, nystagmus, tinnitus and
contralateral loss of pain and temperature
sensation
▪ Emboli, if they get through the vertebral arteries,
usually lodge in one of the posterior cerebral
arteries or at the upper bifurcation of the basilar
artery.
▪ May cause internuclear ophthalmoplegia,
Lateral Medullary (Wallenberg) Syndrome conjugate horizontal gaze palsy, ocular bobbing.
Ptosis, nystagmus common but variable. May
From occlusion of:
see palatal myoclonus, coma.
1. vertebral arteries (~80%)
2. posterior inferior cerebellar artery (PICA)
Basilar Artery Syndrome
3. superior lateral medullary artery
4. middle lateral medullary artery
5. inferior lateral medullary artery

Lacunar Infarction Syndromes

Basilar Artery Occlusion

Occlusion may arise in several ways:
1. atherosclerotic plaque in the basilar artery itself
(usually lower third)
2. occlusion of both vertebral arteries
3. occlusion of one vertebral artery when it is the only
one of adequate size
▪ Atheromatous lesions are most frequent in the
proximal basilar (lower 3rd) and the distal
vertebral segments
▪ Complete basilar occlusion:
– a constellation of bilateral long tract signs
(sensory and motor) with signs of cranial
nerve and cerebellar dysfunction

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 NEUROLOGY II
LE2: CEREBROVASCULAR DISEASES
Ida Ingrid Rocha-Tulagan, MD

HEMORRHAGIC STROKES ▪ PE: signs of meningeal irritation, decreased

consciousness, CN III or IV palsy, may or may not
have focal deficits
▪ Mortality 25% during first 24 hours
▪ Risk of rebleeding within one month 30%; 2.2%
per year during first decade

Intracranial Arterial Aneurysms

▪ Localized dilatation of the arterial lumen due to a

Hypertensive Intracerebral Hemorrhage
▪ Sudden onset of headache, and/or loss of
consciousness
▪ Vomiting at onset in 22%–44%
▪ Seizures occur in 10% of cases (first few days
after onset)
▪ Sites: putamen, thalamus, pons, cerebellum;
some from white matter
▪ Frequently extends to ventricular subarachnoid
space
▪ Preceded by formation of “false” aneurysms
(microaneurysms) of Charcot & Bouchard =
arterial wall dilations secondary to hypertension
defect in the media and internal elastic
lamina, causing a ballooning of the intima
▪ Sizes vary from 1 to >10mm
▪ Produce symptoms by exerting pressure on
adjacent structures but more often present with
rupture and bleeding into the subarachnoid
space or into the brain parenchyma
▪ Most common cause- devt anomaly: others
occasionally from atherosclerosis or infected
emboli from the heart (endocarditis causing
mycotic aneurysms)
Arteriovenous Malformations

▪ Consists of a tangle of dilated vessels that form

an abnormal communication between the
arterial and venous systems: an AV fistula
▪ Composed of coiled mass of arteries and veins
with displacement rather than invasion of normal
brain tissue
▪ Congenital lesions originating early in fetal life
▪ Ok good night, sleep na u =)

Subarachnoid Hemorrhage
Clinical diagnosis:
▪ worst headache in 80% of
patients
▪ May be associated with
vomiting, stiff neck, loss
of consciousness or
focal neurologic deficits,
seizures in 20%

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CLASS 2021 P atricia Abigail Felipe