[NEUROLOGY] ISCHEMIC STROKE

ISCHEMIC STROKE
Maria Grace Ang-De Guzman, MD

DEFINITION OF TERMS
 Stroke  Sudden focal neurologic syndrome due to
cerebrovascular disease
 Cerebrovascular disease designates any abnormality of the
brain resulting from a pathologic process of the blood
vessels
 Pathologic Processes:
 Occlusion of the lumen by embolus or thrombus
 Rupture of a vessel
 Stroke Deaths > MI Deaths
 An altered permeability of the vessel wall
 Increased viscosity of other change in the quality of the
blood flowing through the cerebral vessels TYPES OF STROKE
 Infarct  Blockage of an artery
 We don’t use the term “Cerebrovascular Accident
(CVA)” anymore  Since it is not an “accident,” we now
call it “Cerebrovascular Disease (CVD)”
 Temporal Profile (Clinical Course): Acute, sudden, focal
neurologic deficit arising from pathologic process of the
blood vessels  Vascular in nature

STROKE: WHO DEFINITION

 “A rapidly developing clinical signs of focal (or global)
disturbance of cerebral function lasting >24 hours (unless
interrupted by surgery or death) with no apparent cause
other than of vascular origin.”
 Stroke is a brain attack, is an emergency, is treatable and is
preventable
INCIDENCE OF STROKE
 One of the leading causes of death and disability throughout
the world
 Affects 20M people in the world every year
 Kills 5M people annually
 Is the #2 killer worldwide
 Frequently the predominant vascular disease in any given
region in Asia
 Is the #1 killer in Asia
 WHO estimates 2.7 M stroke deaths in Asia in 2000
 Infarct/Ischemic Stroke  Due to the UNDERLYING
PATHOPHYSIOLOGY
 Could be:
 Thrombotic/Atherosclerotic – Inherent to the
occlusion
 Embolic – From somewhere else (Big arteries such
as carotids)  Dislodged thrombus  Emboli
 Cardiac  Cardio-embolic or Thrombo-embolic
 Shape: Follows the distribution
 Vascular territory of each artery is triangular in
shape

 Temporal Profile: Abrupt, acute, occurring 24 hours

or more

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 [NEUROLOGY] ISCHEMIC STROKE

THROMBOTIC EMBOLIC 2. Perinatal and Postnatal, circulatory disorders resulting in:

 Saltatory in fashion  Deficit is maximum at
(stepwise/ladder) the onset
 Example: 65 year old  Example: 55 year old
man, upon waking up, female, upon waking
noted difficulty in up, noted total
lifting the left arm, paralysis of the right
limping of the left leg, side (0/5)
and drooping of the
left nasolabial fold. In  Usually cardio-embolic
the afternoon, noted  Atrial Fibrillation
further weakening of  History of Rheumatic
the left side. Upon Heart Disease,
arrival at the ER, Valvular Heart
almost 0/5
Disease, Congenital
 Blood flow is slowly
Heart Disease
occluded
 Irregularities in the
cardiac rate
a. Cardiorespiratory failure and generalized ischemia – état
marbre
b. Periventricular infarcts
c. Matrix hemorrhages and ischemic foci in premature
infants
d. Hemorrhagic disease of the newborn
3. Infancy and Childhood: Vascular diseases associated with:
a. Ischemic infarction
b. Congenital heart disease and paradoxical embolism
c. Moyamoya
d. Bacterial endocarditis, rheumatic fever, lupus
erythematosus
e. Sickle cell anemia
f. Mitochondrial disorders (MELAs)
g. Homocystinuria and Fabry’s angiokeratosis

 Hemorrhagic  Rupture of an artery 4. Adolescence and Early Adult Life: Vascular occlusion or
hemorrhage with:
a. Pregnancy and Puerperium
b. Estrogen-related stroke
c. Migraine
d. Vascular malformations
e. Premature atherosclerosis
f. Arteritis
g. Valvular heart disease
 Hemorrhagic Stroke  Based on the LOCATION
h. Sickle cell anemia
 INTRACEREBRAL HEMORRHAGE  In the brain
i. Antiphospholipid arteriopathy, plasma C-protein
matter?
deficiency and other coagulopathies
 SUBARACHNOID HEMORRHAGE  within the
j. Moyamoya, Takayasu disease
subarachnoid space
k. Arterial dissections
l. Amyloid angiopathy
STROKE TYPES IN ASIA
Cerebral Intracranial Hemorrhage 5. Middle Age
Country a. Atherosclerotic thrombosis and embolism
Infarction (%) ICH (%) SAH (%)
China NDA NDA NDA b. Cardiogenic embolism
Hong Kong 70 30 - c. Primary (hypertensive) cerebral heemorrhage
India 70-80 18-20 - d. Ruptured saccular aneurysm
Indonesia 67 26 1 e. Dissecting aneurysm
Malaysia 61 33 3 f. Fibromuscular dysplasia
Philippines 71 19 10
Singapore 70 27 - 6. Late Adult Life
Korea 48 31 18
a. Atherosclerotic thrombotic occlusive disease
Taiwan 61 33 4
b. Embolic occlusive disease
Thailand 70-80 18-20 -
c. Lacunar state
Japan 72 17 8
d. Brain hemorrhage (multiple causes)
e. Multi-infarct dementia
CEREBROVASCULAR DISEASES CHARACTERISTIC OF EACH
f. Binswanger disease
AGE PERIOD
1. Prenatal circulatory diseases leading to:
RISK FACTORS
a. Porencephaly
b. Hydrancephaly  Could be classified into: Modifiable or Non-modifiable
c. Hypoxic-ischemic damage
d. Unilateral cerebral infarction  Behavior or trait that increases your risk of stroke

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 [NEUROLOGY] ISCHEMIC STROKE

 The most important of these are hypertension, heart
disease, Atrial Fibrillation, Diabetes Mellitus, cigarette
smoking & hyperlipidemia
 Hypertension  Long-standing, poorly-controlled
 Heart Disease  Coronary Artery Disease, previous
attack
 Heavy Alcohol Drinking
 Others:
 Systemic diseases associated with a hypercoagulable
state
 Use of birth control pills
 Hypercoaguable State  Hematologic problem or
exogenous problem
 OCPs  Make the blood hypercoaguable
 Neoplasms, Malignancies
 Embolic Strokes:
 Structural cardiac disease and arrhythmias, particularly
Atrial Fibrillation (↑’s incidence of stroke about 6x; and by
18x if there is also rheumatic valvular disease), bacterial
and nonbacterial (marantic) endocarditis and right-to-left
shunts between the cardiac chambers or in the lung
 Documented the importance of long-duration cigarette
smoking in the development of carotid atherosclerosis
 Low potassium intake and reduced serum levels of
potassium intake and reduced serum levels of potassium,
have been associated with an increased stroke rate in
several studies
NON-MODIFIABLE RISK FACTORS
 Genetically determined, cannot be changed
 Relative risk
 Age – Doubles per decade after age 55
 Gender – Males > Females
 Previous Stroke – 10x
 Race – Ethnicity – Black > White
 Heredity
 Importance of long-duration cigarette smoking in the
development of carotid atherosclerosis has been
documented
 Nicotine and CO decrease oxygen in the brain and
damages blood vessels
 If you quit smoking, your stroke risk goes down
significantly from 2 years onwards (Kawachi et al, 1993)
 Diabetes Mellitus
 Increases stroke risk by 1.5-3x
 Macrovascular  Cerebral arteries, Coronary arteries
 Microvascular  Arteries going to the foot  Prone
to diabetic foot
 Heart Disease
 Atrial fibrillation and other forms of heart disease causes
blood clot to form in the heart
 AF increases stroke risk by up to 18x
 Hypercholesterolemia
 Causes formation of plaques in the blood vessels
 Increases stroke risk by 2x
 Heavy Alcohol Intake
 Increases stroke risk by up to 4x
 Hemorrhagic strokes  Dose-dependent risk
 Cerebral infarction  Biphasic effect (protective if
moderate up to 2 drinks BUT increase risk if excessive)
 Obesity
 Physical Inactivity/Sedentary Lifestyle
 Increases chance of being overweight
 Increases stroke risk by 1.3x
 Cardiovascular disease by 1.5-2.4x
 Stress and Anger
 High intensity stress risk of fatal stroke: 1.5-1.9x
 Expressed anger risk of stroke: 2x
 Trigger hemodynamic, vasoconstrictive and hemostatic
forces leading to atherosclerosis
 Sympathetic arousal and neuroendocrine activation
 Heavy Snoring
 Heavy snoring is usually associated with obesity

MODIFIABLE RISK FACTORS  Medical Conditions

 Hypertension  Result from Unhealthy Lifestyle
 Blood pressure >140/90 is high
 Increased stroke risk by 3-5 ISCHEMIC STROKE SUBTYPES AND DISTRIBUTION
 Most important risk factor (NINDS Stroke Data Bank)
 Associated with arterial disease and ICH  Atherosclerotic Infarction (20%)
 ~70% present among stroke patients
 The higher the BP, the higher the risk  Also called Thrombotic Infarction

 Charcot Bouchard Aneurysm  Acquired  Lacunar Infarction (25%)

microaneurysms secondary to long standing  Small strokes secondary to lipohyalinosis
hypertension
 1 to less than 2 cm diameter
 Cigarette Smoking  Cardioembolic Infarction (20%)
 Any amount of smoking increases stroke risk by 2.5x

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 Cryptogenic Infarction (30%)
 Cause of infarct most often undetermined  Non-
thrombotic, non-lacunar, non-embolic
 Patent Foramen Ovale (Congenital Heart Disease)
 Kuya Kim Atienza
 Infarction of Other Undetermined Cause (5%)
PATHOPHYSIOLOGY
 Ischemic Stroke
 Deficit is based on the territory of the artery
- Carotid System  3H: Homonymous Hemianopsia,
Hemiplegia, Hemisensory
- Vertebro-basilar  Cranial Nerve Deficit
- Pontine  Quadriplegia
- Posterior  Cranial Nerves, Cerebellar, Occipital
TWO PROCESSES:
1. Loss in the supply of oxygen and glucose secondary to
vascular occlusion
2. An array of changes in cellular metabolism consequent to
the collapse of energy-producing processes, ultimately with
disintegration of cell membranes
Note: The effects of ischemia whether functional and
reversible or structural and irreversible, depend on its degree
and duration
 Stroke  Irreversible
 TIA  Not a stroke but warning that a stroke may
happen
 Focal/global deficit
 Vascular in origin
 Less than 24 hours (But actually, attack usually lasts
from a few minutes)
 Reversible
 CT scan and MRI unremarkable
 Reduction of cerebral blood flow below 10-12ml/100g
brain/min leads to infarction
 Critical levels of hypoperfusion that abolishes function that
leads to tissue damage: CBF 12-23 ml/100g brain/min
 To easily remember: 1-2-3  Critical Level of
Hypoperfusion is 12-23ml/100g brain/min
 Ischemic Penumbra  Region of marginal perfusion
 Penumbra  Area surrounding the necrotic tissue
 Goal: Save ischemic penumbra  Minimize deficit
 Increase in K+ levels (efflux from depolarized cells)
 Depleted ATP
 Reduction in creatine phosphate
[NEUROLOGY] ISCHEMIC STROKE
 Ischemic Necrosis: CBF 6-8ml/100g/min
 Release of excitatory NT (glutamate, aspartate)
 Increase in intracellular calcium levels
 Increase in extracellular K+
 Depletion in ATP
 Reduction in creatine phosphate
 Cellular acidosis
 Activation of free fatty acids
 Accumulation of PG’s leukotrienes, and free radicals
 Pale Infarction  Issue are devoid of blood
 Necrotic infarct
 Red, Hemorrhagic Infarction  Due to extravasation of
blood vessels from small vessels in the infarcted tissue (due
usually to cerebral embolism)
 Transformation secondary to Embolic Stroke
 EMBOLIC INFARCT/STROKE WITH HEMORRHAGIC
CONVERSION/TRANSFORMATION
 Dislodged thrombus  Ischemic Stroke  After
some time, dislodge embolus  (+) Reperfusion 
Petechial hemorrhage/accumulation of big
hemorrhage
VASCULAR FACTORS
 Center of an Ischemic Stroke  ZONE OF INFARCTION
 Necrotic tissue swells rapidly, mainly because of
excessive intracellular and intercellular water content.
 Anoxia also causes necrosis and swelling of cerebral
tissue (although in a different distribution), oxygen
lack must be a factor common to both infarction and
anoxic encephalopathy.
 The effects of ischemia, whether functional and
reversible or structural and irreversible, depend on its
degree and duration.
 The margins of the infarct are hyperemic, being
nourished by meningeal collaterals, and here there is
only minimal or no parenchymal damage.
VASCULAR ANATOMY
 CEREBRAL BLOOD SUPPLY
ANTERIOR CIRCULATION POSTERIOR CIRCULATION
 Carotid system  Vertebrobasilar system
 Supplies 80% of the brain  Supplies 20% of the brain
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 [NEUROLOGY] ISCHEMIC STROKE

INTERNAL CAROTID SYSTEM  CT SCANNING

 INTERNAL CAROTID SYSTEM  Computed Axial Tomography (CAT) Scan

 4 Segments:  (-) CT scan but will neurologic signs and symptoms 
1. Cervical Treat at ischemic stroke
2. Petrous  Imaging of choice for acute ischemic stroke
3. Cavernous
4. Supraclenoid  Demonstrates and accurately localizes even small
- Branches: hemorrhages, hemorrhagic infarcts, subarachnoid blood,
 Anterior Cerebral clots in and around aneurysms, regions of infarct necrosis
 Middle Cerebral and AVM’s

 Anterior portion of the brain involving the frontal, temporal,

and parietal lobes, is supplied by the carotid arteries (CA)
 CA arises from the innominate artery on the right and aortic
arch on the left. At level of upper neck CA branches into
internal and external.
 The internal carotid artery terminates into the middle (MCA)
and anterior (ACA) cerebral arteries.
 MCA perfuses the cortex, parietal lobe, temporal lobe,
internal capsule, and portions of the basal ganglia
 ACA forms the anterior portion of the circle of Willis and
 MRI
supplies portions of the frontal lobe
 Imaging of choice for acute ischemic stroke 
VERTEBROBASILLAR SYSTEM Particularly DWI
 VERTEBROVASCULAR  Demonstrates lesion also seen on CT scanning reveals flow
SYSTEM voids in vessels, hemosiderin and iron pigment, and the
 2 Vertebral Arteries alterations resulting from ischemic necrosis and gliosis
 1 Basilar Arteries  Particularly advantageous in demonstrating small lacunar
 2 Posterior Cerebral lesions deep in the hemispheres and abnormalities in the
Arteries brainstem ( a region obscured by adjacent bone in CT
 Superior Cerebellar scans)
 Anterior Inferior  Diffusion-Weighted Technique (DWI)  Allows early
Cerebellar detection of an infarctive lesion within minutes of the
 Posterior Cerebellar stroke

 Perfuses the posterior part of the brain including the

occipital lobe, cerebellum, and brainstem
 Vertebral arteries arise from the subclavian arteries and give
off branches supplying the medulla and portions of the
cerebellum
 Basilar artery is formed by the junction of the two vertebral  DOPPLER ULTRASOUND STUDIES
arteries and gives off a variety of penetrating arteries  Demonstrate atheromatous
supplying the brainstem and portions of the basal ganglia plaques and stenoses of large
before dividing into the posterior cerebral arteries vessels, particularly of the carotid
but also the vertebrobasilar arteries
DIAGNOSTIC PROCEDURES
NEUROIMAGING STUDIES  TRANSCRANIAL DOPPLER
 Continue to enhance the clinical study of stroke patients;  Occlusion or spasm of the main
they allow the demonstration of both the cerebra lesion and vessel can be seen using
the affected blood vessels ultrasound

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 [NEUROLOGY] ISCHEMIC STROKE

 ARTERIOGRAPHY  Anti-Thrombotics
 Accurately demonstrates  Anti-Hypertensives
stenosis and occlusions of  IV fluids, Bed rest
the larger vessels, as well as  Close monitoring
aneurysms, vascular  Surgery, clipping of aneurysm
malformations, and other
vessel diseases such as SPECIFIC MANAGEMENT – TREATMENT OPTIONS
arteritis and vasospasm  Stroke Unit Admission
 Conventional dye-injection  Anti-Thrombotic Agents:
angiography has been supplanted by magnetic resonance  Anti-Platelets (ASA, Clopidogrel, Cilostazol, etc)
angiography (MRA) and venography (MRV) for the  Anticoagulants (Heparin, Warfarin, LMWH)
visualization of large intracranial arteries and veins
 These have the advantage of safety but do not yet give  Used for valvular heart diseases
refined images of the smaller vessels and are not as
accurate as angiography in measuring the severity of  Thrombolytic Therapy (r-TPA)
stenosis of a vessel  Not as frequently used than anti-platelet and anti-
 Spiral CT angiography now offer images of better coagulants
resolution, comparable to conventional arteriograms  Aided by MRI or CT Scan

OTHER PROCEDURES  Neuroprotectants

 LUMBAR PUNCTURE
 Indicates whether blood has entered the subarachnoid
space (from aneurysm, vascular malformation,
hypertensive hemorrhage, and some instances of
hemorrhagic infarction)
 The cerebrospinal fluid (CSF) is clear in cases of “pale”
infarction from thrombosis and embolism
 Avoidance of hypotension by computing the MAP
 Avoid hypoxemia by mechanical ventilation
 Avoid hypo or hyperglycemia by Capillary Blood
Glucose monitoring (CBG)
 Avoid hypo or hypernatremia to prevent seizures
 Avoid hyperthermia by giving cooling mattresses

 High suspicion for subarachnoid hemorrhage but (-)
CT scan  Since the blood spills in the subarachnoid
space, you can still get results doing lumbar puncture
 Grossly bloody or Xanthocromic
 Infarct secondary to infection (Neurosyphillis)  CSF
test for Treponema
 Hemicraniectomy (surgery) – last option
 Subjected to criteria
 Contraindicated for lacunar strokes and large MCA
strokes
 Large strokes  those that are within 48 hours

 ELECTROENCEPHALOGRAM (EEG) NEUROPROTECTION

 Has lost favor in stroke diagnosis but is probably  Avoid the following:
underutilized as a readily available means of detecting  Hypotension (treat only if MAP > 130mmHg)
cortical infarction in the wake of ischemia of a regin of one  Hypoxemia
hemisphere  Hyperglycemia
 It allows a distinction to be made between occlusion of a  Hyponatremia
small and large vessel, because focal EEG abnormalities  Fever
are sparse or absent with a deep lacunar stroke
 The EEG is most useful soon after stroke, when the only DECOMPRESSIVE HEMICRANIECTOMY
available alternative is the CT scan, which often does not  Large MCA Infarction Syndrome:
visualize the infarct until several days have passed  Clinical:
- Changes in sensorium
 Some patients with cortical infarcts develop post- - Dense hemiparesis/plegia
stroke seizures 2 years around the stroke  EEG to - Hemisensory loss
test if it really is seizure or just spasticity - Aphasia – if dominant
- Hemianopsia
- Neglect
MANAGEMENT OF STROKE - Gaze preference
 Medical  CT Scan:
 Thrombolysis - Dense MCA sign

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 [NEUROLOGY] ISCHEMIC STROKE

- Hypodensity ≥ 1/3 MCA territory  Generally, Dominant Hemisphere Infarcts:

- Effacement of sulci  The right side of the body is controlled by the left side
of the cerebral hemisphere  Contralateral
 Dense MCA sign (yellow arrow) due to thrombosed
 If the manifestation involves sensory deficits but not
MCA
language and cognition, probably there is no cortical
 Other feature seen:
involvement during stroke but more of a small lesion
 Edematous
or a lacunar stroke.
 Absence of the sylvian fissure
 Flattening or effacement of the sulci
 TRANSIENT ISCHEMIC ATTACKS
 Such cases must undergo hemicraniectomy
 “Mini-strokes”
immediately
 A warning stroke due to transient blockage of the
vessels
 Malignant MCA Infarction  Symptoms occur rapidly and iast relatively a short
 As above + the following developing within 38 hours period
 Occurs in 10-13% of large MCA infarction
 Hemispheric MCA or MCA + ACA territory ischemic stroke  Anterior TIA
with massive cerebral edema - TIA that occurs on the Anterior circulation
 Clinical: - Manifested by the 3HS.
- Progressive sensorial change  Posterior TIA or Vertebrobasilar TIA
- Head turning - Manifested more of CN palsies
 CT Scan:
- Hypodensity ≥ 2/3 of MCA territory The occurrence of carotid TIA, is a predictor of stroke,
- Evidence of brain edema cerebral infarct and MI.
- Contralateral shift
- Midbrain compression Amarosis Fugams
- Transient monocular blindness
- Ipsilateral involvement of the ophthalmic artery
 Asymptomatic Carotid Stenosis
 70% decrease of blood flow
 No signs of transient ischemic attack SAMPLE CASES
 Symptomatic Carotid Stenosis CASE 1:
 More than 7%  70 year old male
 With signs of transient ischemic attack  Sudden onset right side hemiplegia, hemianesthesia/
sensory
 Palpation of the Carotid Artery
 Eyes deviated to left (preferential gaze to left)
 Compare carotid pulse with the examiner’s pulse
by palpation.  Difficulty with speech/language
 Use the bell of the diaphragm when no carotid
pulse palpated. DO NOT PALPATE
SIMULTANEOUSLY as it may cause embolization of
the thrombus.

STROKE SYNDROMES
DOMINANT HEMISPHERE NONDOMINANT HEMISPHERE
Majority of right handed
and most left-handed
patients have dominance
Less predictable syndrome
for speech and language MCA STROKE
located in the left  Contralateral hemiplegia and hemianesthesia: Arm and face
hemisphere
> leg
Left hemispheres Attention defects:
 Deviation of the head and eyes toward side of infarct “gaze
infarction is characterized Extinction and neglect
preference”
by Aphasia (both motor –
Broca’s and sensory –
Behavioral changes:  Global aphasia (in dominant hemisphere)
Wernicke’s) and Apraxia
acute confusion and delirium  Hemianopsia, hemineglect

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 [NEUROLOGY] ISCHEMIC STROKE

 MCA STROKE  LEFT MIDDLE CEREBRAL ARTERY
 3H:
 Hemiplegia  Right sided weakness
 Hemisensory  Right sided numbness
 Homonymous Hemianopsia  Preferential gaze to
the left
CASE 2:
 68 year old female
 Woke up with weakness in right leg
 Slight right side weakness leg > arm
 Family states she has “impaired judgment and insight”
 “Seems like a baby: sucking and grasping”
 Cranial nerve deficits and involvement of cerebellum and
neurosensory tracts
 Diplopia, dysphagia, dysarthria, dizziness, vertigo, ataxia
 Pain and temperature deficits in the face occur on opposite
side of the body
 WALLENBERG SYNDROME  Lateral Medullary
Syndrome
 Medulla  Supplied by vertebral arteries
 Lateral Part of Medulla  PICA
 Cranial Nerve Deficits  Diplopia, Dysphagia,
Dysarthria
CASE 4:
 55 year old male
 Diabetic, hypertensive for 15 years
 Sudden onset of being unable to move left side of the body
 Able to talk  Language and speech intact
 Sensation intact

LACUNAR INFARCTION
 Lesion of small penetrating branch
arteries in to BG, thalamus, pons,
internal capsule
 “Pure strokes”
ACA STROKE  Motor, sensory, ataxic
hemiparesis
 Weakness of the leg
 Usually result in hemiparesis of
 +/- proximal muscle weakness in the upper extremities
face, arm and leg
 Affect frontal lobe: impaired judgment and insight, change
 Lack of impairment of consciousness, aphasia, or visual
in affect
disturbances
 Presence of primitive grasp and suck reflexes
 More common in blacks and history of HTN, DM
 Language impairment (common finding)
 60% of patients with lacunar infarctions will be independent
at 1 year following stroke
 Here, the location of the lesion is on the leg. Based on
anatomy and knowledge on the homunculus, the lower
 Pure Motor + Intact Language  LACUNAR INFARCTION
extremities are in the territory of ACA.
 Pure Motor: Basal Ganglia
 Primitive reflexes are usually inhibited by the frontal
 Pure Sensory: Thalamus
lobe, when there is ischemia, these reflexes becomes
 Diameter: 1-2 cm
uninhibited and reappear.
 Pathophysiology: Lipohyalinosis/Fibrinoid deposits 
 ACA Territory  Supplies the basal and medial aspects
NOT ATHEROSCLEROSIS
of the cerebral hemispheres and extends to the
 Clues:
anterior 2/3 of parietal love.
 (-) Aphasia
 (-) Homonymous Hemianopsia
CASE 3:  Awake/Alert
 77 year old male
 Sudden onset of dizziness
CASE 5:
 Double vision
 85 year old female
 On examination, has pain and temperature deficit on half
 In ICU, post-repair of ruptured abdominal aortic artery
of face and on opposite side of body
aneurysm
 GCS 15
VERTEBROBASILAR SYSTEM
 Heterogeneous syndromes and presentations

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 [NEUROLOGY] ISCHEMIC STROKE

 Complaining of difficulty moving her leg and that it feels

numb

WATERSHED INFARCTION
 Occurs in vulnerable
areas supplied by distal
distribution cerebral
arteries during periods
of hypotension
 Infarction between the
ACA and MCA presents
with hemiparesis and
hemianesthesia,
predominantly in the leg
 Dominant hemisphere infarctions: decrease in verbal ability
with preserved comprehension
 Infarction involving the posterior watershed area presents
with homonymous hemianopia +/- hypoesthesia in the face
and legs

 Watershed Territories: CORTICO-MENINGEAL

ANATOSMOSIS

THANK YOU PABEBE GIRLS PRECIOUS ANGELIQUE AND

NICOLLETE PAULA <3 :*

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