Internal Medicine - Cerebrovascular Diseases

INTERNAL MEDICINE:
Cerebrovascular
Diseases

nianderthalNOTES

INTRODUCTION
-include the following most common devastating
disorders:
1. Ischemic Stroke
2. Hemorrhagic Stroke
3. Cerebrovascular anomalies
-Intracranial aneurysms
-Arteriovenous malformations (AVMs)

-most cerebrovascular diseases manifest by the
abrupt onset of a focal neurologic deficit

STROKE
-DEFINITION: abrupt onset of a neurologic
deficit that is attributable to a focal vascular
cause
-laboratory studies and brain imaging are used
to support the diagnosis
-clinical manifestations are highly variable
because of the complex anatomy of the brain
and its vasculature

STROKE
-OTHER TERMS:
-Cerebral ischemia – caused by reduction in blood flow
that lasts longer than several seconds
-Cerebral infarction – if the cessation of flow lasts for
more than a few minutes, death of brain tissue results
-Transient ischemic attack (TIA) – when blood flow is
quickly restored, brain tissue can recover fully and the
patient’s symptoms are only transient
-Ischemic Penumbra: tissue surrounding the core region
of infarction that is ischemic but reversibly
dysfunctional; imaged by using perfusion-diffusion
imaging with MRI or CT

STROKE
-a generalized reduction in cerebral blood flow due to systemic
hypotension usually produces SYNCOPE
-Global hypoxia-ischemia: widespread brain injury due to
infarction in the border zones between the major cerebral
artery distributions if low cerebral blood flow persists for a
longer duration
-Hypoxic-ischemic encephalopathy: the constellation of cognitive
sequelae that ensues
-Focal ischemia: usually caused by thrombosis of the cerebral
vessels or by an emboli from a proximal arterial source or the
heart
-Intracranial hemorrhage: bleeding directly into or around the
brain; produces symptoms by:
a.) mass effect of neural structures
b.) toxic effect of blood itself
c.) increasing intracranial pressure

APPROACH TO THE PATIENT
-patients with acute stroke often do not seek
medical assistance on their own because:
1. they are rarely in pain
2. they may lose appreciation that something is
wrong (ANOSOGNOSIA)
*sudden onset of any of the following:
-unilateral loss of sensory/motor
function
-changes in vision, gait, speech or
comprehension
-sudden severe headache

-Neurologic symptoms may mimic stroke
SYMPTOM THAT MIMICS STROKE GUIDES TO DIAGNOSIS
-Seizure -history that indicates prior convulsive
activity excludes seizure
-Intracranial tumor -present with acute neurologic symptoms
due to hemorrhage, seizure or
hydrocephalus
-Migraine -sensory disturbance is often prominent,
sensory/motor deficits tend to migrate
slowly across limbs over minutes rather
than seconds as with stroke
-Metabolic encephalopathy -produce fluctuating mental status without
focal neurologic finding

-Once a clinical diagnosis of stroke is made, a brain
imaging study is necessary to determine if the
cause of stroke is ischemia or hemorrhage
-CT IMAGING of the brain is the STANDARD
MODALITY to detect the presence or absence of
intracranial hemorrhage
-Medical management to reduce the risk of
complications becomes the next priority, then
plans for secondary prevention

OVERVIEW OF DIFFERENCES
ISCHEMIC STROKE HEMORRHAGIC STROKE
-85% of stroke cases -15% of stroke cases
-administration of -BP lowering primarily
recombinant tissue considered
plasminogen activator (rTPA) -usually caused by aneurysmal
or endovascular mechanical subarachnoid hemorrhage
thrombectomy may be (SAH) and hypertensive
beneficial in restoring cerebral intracranial hemorrhage
perfusion

ISCHEMIC STROKE
PATHOPHYSIOLOGY:
MAJOR MECHANISMS THAT UNDERLIE ISCHEMIC
STROKE:
1. Occlusion of an intracranial vessel by an embolus
that arises at a distant site – often affects large
intracranial vessels
2. In situ thrombosis of an intracranial vessel –
typically affecting the small penetrating arteries
that arise from the major intracranial arteries
3. Hypoperfusion caused by flow-limiting stenosis of
a major extracranial or intracranial vessel

ISCHEMIC STROKE
PATHOPHYSIOLOGY:
1st: acute occlusion of an intracranial vessel causes
reduction in blood flow to the brain region it
supplies
-magnitude of flow reduction is a function of
collateral blood flow and is dependent on:
1. individual vascular anatomy
2. site of occlusion
3. systemic blood pressure

ISCHEMIC STROKE
PATHOPHYSIOLOGY:
2nd: decrease in cerebral blood flow to zero causes
death of brain tissue within 4-10 minutes
-infarction within an hour: <16-18ml/100g
tissue per minute
-ischemia without infarction (unless
prolonged for hours or days): <20ml/100g tissue
per minute

ISCHEMIC STROKE
PATHOPHYSIOLOGY:
3rd: -if with restored blood flow: patient
experiences TRANSIENT ISCHEMIC ATTACK
-if no change in flow: infarction of ischemic
penumbra
*hence, saving the ischemic penumbra is the goal
of REVASCULARIZATION THERAPIES

ISCHEMIC STROKE
PATHWAYS OF FOCAL CEREBRAL INFARCTION:
1. Necrotic pathway
-with rapid cellular cytoskeletal breakdown due
principally to energy failure of the cell

2. Apoptotic pathway
-cells are programmed to die

ISCHEMIC STROKE
1. NECROTIC PATHWAY:
-Ischemia produces necrosis by starving neurons of
glucose and oxygen
-Mitochondria then fails to produce ATP
-NO ATP means cessation of membrane ion pump
function causing neuronal depolarization which
leads to:
a. increase in intracellular Calcium
b. glutamate release from pre-synaptic terminals
-produces neurotoxicity
*free radicals are produced by membrane lipid
degradation and mitochondrial dysfunction

ISCHEMIC STROKE
2. APOPTOTIC PATHWAY:
-Lesser degrees of ischemia within the ischemic
penumbra favor apoptotic cellular death
causing cells to die days to weeks later

*fever and hyperglycemia worsens brain injury
during ischemia, both must be suppressed as
much as possible

ISCHEMIC STROKE
TREATMENT OF ACUTE ISCHEMIC STROKE:
-After the clinical diagnosis of stroke is made, an orderly process
of evaluation and treatment should follow
-FIRST GOAL: PREVENT OR REVERSE BRAIN INJURY
-attend to the patient’s airway, breathing and circulation
(ABCs)
-treat hypoglycemia or hyperglycemia
-perform a non-contrast head CT scan
*differentiates ischemic and hemorrhagic stroke since NO
reliable clinical finding conclusively separate the two

HEMORRHAGIC ISCHEMIA
-more depressed level of consciousness -deficit is maximal at onset, or remits
-higher initial blood pressure
-worsening of symptoms after onset

ISCHEMIC STROKE
CATEGORIES OF TREATMENT:
-designed to reverse or lessen the amount of
tissue infarction and improve clinical outcome
1. Medical Support
2. IV Thrombolysis
3. Endovascular Techniques
4. Antithrombotic Treatment
5. Neuroprotection
6. Stroke Centers and Rehabilitation

ISCHEMIC STROKE
1. MEDICAL SUPPORT
-IMMEDIATE GOAL: optimize cerebral perfusion in the
surrounding ischemic penumbra
-attention is also directed toward preventing the common
complications of bedridden patients:
-infections
-deep venous thrombosis (DVT)
-blood pressure is lowered in:
-malignant hypertension
-concomitant myocardial ischemia
-BP >185/110 mmHg and thrombolytic therapy is
anticipated
*B1-adrenergic blocker such as ESMOLOL can be a first
step to decrease cardiac work and maintain BP

ISCHEMIC STROKE
1. MEDICAL SUPPORT
-Fever should be treated with antipyretics and surface
cooling
-Serum glucose should be monitored and kept at less than
110mg/dl using an insulin infusion if necessary
-Cerebral edema is treated in 5-10% of patients with water
restriction and IV mannitol to reduce serum osmolarity
 watch out for HYPOVOLEMIA as this may contribute to
hypotension and worsening infarction
*cerebral edema causes obtundation or brain herniation
*peaks on 2nd or 3rd day but can cause mass effect for 10
days

ISCHEMIC STROKE
1. MEDICAL SUPPORT
MEDICAL SUPPORT:
-Hemicraniectomy: craniotomy with temporary removal of
part of the skull; markedly reduces mortality
-Things that should alert physician:
-Cerebellar infarction may mimic labyrinthitis because of
prominent vertigo and vomiting
-Head or neck pain mimics cerebellar stroke from
vertebral artery dissection
-increasing ICP may lead to brainstem compression and
cause respiratory arrest
*prophylactic suboccipital decompression of large
cerebral infarcts before brainstem compression

ISCHEMIC STROKE
2. IV THROMBOLYSIS
rtPA:
-causes an increased incidence of symptomatic
intracerebral hemorrhage
-treatment of IV rtPA within 3 hours of the onset of
ischemic stroke improved clinical outcome
*efficacy likely extended to 4.5 hours if not 6 hours
-time of stroke onset: the time the patient’s symptoms
began or the time the patient was last seen as
normal. Patients who awaken with a stroke have
the onset defined as the time they went to bed

ISCHEMIC STROKE
2. IV THROMBOLYSIS
rtPA:
INDICATIONS CONTRAINDICATIONS
-Clinical diagnosis of STROKE -sustained BP > 185/110 mmHg despite Rx
-onset of symptoms to time of drug -Platelets LESS THAN 100,000; Hematocrit
administration is LESS THAN 3 HOURS LESS THAN 25%; Glucose LESS THAN 50 or
GREATER THAN 400 mg/dl
-CT scan show no hemorrhage or edema of Use of Heparin within 48 HOURS and
GREATER THAN 1/3 of the MCA territory prolonged PTT or elevated INR ; GI bleeding
preceding 21 DAYS
-Age > 18 years old -rapidly improving , minor stroke symptoms
-consent by patient or surrogate -prior stroke or head injury within 3
MONTHS; recent myocardial infarction
-Major surgery in preceding 14 days
-Coma or stupor

ISCHEMIC STROKE
2. IV THROMBOLYSIS
rtPA:
-administer through IV access with TWO PERIPHERAL
LINES (avoid arterial or central line placement
-0.9 mg/kg IV (maximum 90 mg) IV as 10% of total
dose by bolus, followed by remainder of total dose
over 1 hour
-frequent BP monitoring
-no other antithrombotic treatment in 24 hours
-for decline in neurologic status or uncontrolled BP 
STOP INFUSION, give CRYOPRECIPITATE and reimage
brain emergently
-avoid urethral catheterization for > 2 HOURS

ISCHEMIC STROKE
3. ENDOVASCULAR TECHNIQUES
-Vessels that involve a large clot volume and often fail
to open with IV rtPA alone:
-middle cerebral artery (MCA)
-internal carotid artery
-basilar artery
-Endovascular mechanical thrombectomy:
-adjunctive treatment of acute stroke in patients
who are ineligible for, or have contraindications to
thrombolytics, or those who have failed to have
vascular recanalization with IV thrombolytics

ISCHEMIC STROKE
3. ENDOVASCULAR TECHNIQUES
-MERCI: novel endovascular thrombectomy device
restores patency of the occluded vessel within 8
hours of ischemic stroke symptoms; with
successful recanalization at 90 days

ISCHEMIC STROKE
4. ANTITHROMBOTIC TREATMENT
PLATELET INHIBITION:
-ASPIRIN: the ONLY antiplatelet agent that has been
proven effective for the acute treatment of ischemic
stroke
-the use of aspirin within 48 hours of stroke onset
reduced both stroke recurrence risk and mortality
minimally
-ABCIXIMAB: a glycoprotein IIb/IIIa receptor inhibitor
was found to cause excess intracranial hemorrhage
and should be avoided in acute stroke
-CLOPIDOGREL: still being tested to prevent stroke
following TIA and minor ischemic stroke

ISCHEMIC STROKE
4. ANTITHROMBOTIC TREATMENT
ANTICOAGULATION:
-low molecular weight Heparin: failed to show any
benefit over aspirin, and increased bleeding rates

ISCHEMIC STROKE
5. NEUROPROTECTION
-the concept of providing a treatment that
prolongs the brain’s tolerance to ischemia
-includes:
a. use of drugs that block excitatory amino acid
pathways – protects neurons and glia in animals
b. hypothermia – neuroprotective in patients
with cardiac arrest

ISCHEMIC STROKE
6. STROKE CENTERS AND REHABILITATION
-patient care in comprehensive stroke units
followed by rehabilitation services improves
neurologic outcomes and reduces mortality
-proper rehabilitation of the stroke patient includes
early physical, occupational and speech therapy
-GOAL OF REHABILITATION: return the patient
home and to maximize recovery by providing a
safe, progressive regimen suited to the individual
patient

ISCHEMIC STROKE
6. STROKE CENTERS AND REHABILITATION
-RESTRAINT THERAPY: immobilizing the unaffected
side has shown to improve hemiparesis following
stroke

ISCHEMIC STROKE
ETIOLOGY:
-Although the initial management of acute
ischemic stroke often does not depend on the
etiology, establishing a cause is essential in
reducing the risk of recurrence
-Focus on: a.) atrial fibrillation and b.) carotid
atherosclerosis

ISCHEMIC STROKE
CLINICAL EXAMINATION:
FOCUS FINDINGS

-Peripheral and cervical -carotid auscultation for bruits,
vascular system BP, pressure comparison
between arms
-Heart -dysrhythmias, murmurs

-Extremities -peripheral emboli

-Retina -effects of hypertension and
cholesterol emboli
(Hollenhorst plaques)

ISCHEMIC STROKE:
Cardioembolic Stroke
EXAM/LABORATORIES/IMAGING:
-a complete neurologic examination is performed to localized
the site of stroke
-an imaging study of the brain is required for patients being
considered for thrombolysis
-an ECG may demonstrate arrhythmias or reveal MI
-Other tests include:
-CXR -ESR
-urinalysis -serum electrolytes
-CBC -Creatinine/BUN
-blood sugar -PT/PTT
-serum lipid profile -serologic test for syphilis

ISCHEMIC STROKE:
-responsible for 20% of all ischemic strokes
-stroke caused by heart disease is PRIMARILY DUE TO
EMBOLISM of thrombotic material forming on the atrial or
ventricular wall of the left heart valves
-TIA: if the thrombus fragment or lyse quickly
-Characteristics:
-sudden onset
-maximum neurologic deficit at once
-petechial hemorrhage can occur within the ischemic
territory
-Emboli from the HEART most often LODGE IN THE MCA,
posterior cerebral artery or one of their branches,
infrequently, the anterior cerebral artery is involved

ISCHEMIC STROKE:
-Most significant causes:
1. non-rheumatic (non-valvular) atrial fibrillation
-MOST COMMON cause of cerebral embolism
-stroke risk can be calculated using CHADS2
score
CHADS2 score:
CHADS2 RECOMMENDATION POINTS CONDITION
SCORE
1 > 75 years old
0 Aspirin or no
1 Hypertension
antithrombotic
1 Congestive heart failure
1 Aspirin or VKA
1 Diabetes
Greater than VKA
2 Stroke or TIA
(>) 1

ISCHEMIC STROKE:
-Most significant causes:
2. Myocardial Infarction
-especially when transmural and involves
anteroapical ventricular wall
-risk is reduced by anticoagulation
3. prosthetic valves
4. rheumatic heart disease
-increased incidence with prominent mitral
stenosis or atrial fibrillation
5. ischemic cardiomyopathy

ISCHEMIC STROKE:
-paradoxical embolization occurs when venous
thrombi migrate to arterial circulation, usually via
a PATENT FORAMEN OVALE or ATRIAL SEPTAL
DEFECT; detected through bubble-contrast ECG
-Bacterial endocarditis can cause valvular
vegatations that can give rise to septic emboli
*Mycotic aneurysms caused by septic emboli
give rise to SAH or intracerebral hemorrhage

ISCHEMIC STROKE:
Artery-Artery Embolic Stroke
-thrombus formation on atherosclerotic plaques may
embolize to intracranial arteries producing an artery-to-
artery embolic stroke
-Unlike the myocardial vessels, artery-to-artery embolism,
RATHER THAN local thrombosis, is the DOMINANT
VASCULAR MECHANISM causing brain ischemia.
-embolic sources are diseased vessels in the:
-aortic arch
-common carotid arteries
-internal carotid arteries
-basilar arteries
-vertebral arteries
-carotid bifurcation – MOST COMMON SOURCE

ISCHEMIC STROKE:
-Carotid Atherosclerosis:
-atheroscerois within the carotid artery occurs
most frequently with the common carotid
bifurcation and proximal internal carotid artery
-Risk factors:
-male -smoking
-older age -hypertension
-diabetes -hypercholesterolemia
-produces 10% of ischemic stroke

ISCHEMIC STROKE:
-Carotid Atherosclerosis:
-Classification is based on:
1. whether stenosis is symptomatic or
asymptomatic
-symptomatic – patient has experienced
a stroke within the vascular
distribution of the artery
- associated with greater risk
of subsequent stroke
2. degree of stenosis

ISCHEMIC STROKE:
Artery-to-Artery Embolic Stroke
-Other causes of Artery-to-Artery embolic stroke:
1. Intracranial atherosclerosis
-produces stroke through an embolic
mechanism or by in situ thrombosis
-common in Asian and African-Americans

ISCHEMIC STROKE:
Artery-to-Artery Embolic Stroke
-Other causes of Artery-to-Artery embolic stroke:
2. Dissection
-common source in the young: internal carotid, vertebral
arteries or vessels beyond the circle of Willis
-characteristic: painful, precedes stroke by hours or days
-causes: -connective tissue disorders (such as Ehlers-
Danlos type IV, Marfan’s disease, cystic medial necrosis and
fibromuscular dysplasia), trauma (usually on carotid and
vertebral arteries)
-most dissections heal spontaneously, and stroke or TIA
beyond 2 weeks are uncommon
-treatment: anticoagulants  antiplatelets
EXTRACRANIAL dissection INTRACRANIAL dissection
-do not cause hemorrhage because of -may produce SAH because vessels are
tough adventitia of vessels thin and may form pseudoaneurysms

ISCHEMIC STROKE:
Small-Vessel Stroke
-lacunar infarction: infarction following atherothrombotic or
lipohyalinotic occlusion a small artery (30-300 micrometer) in the
brain
-account for 20% of all strokes

PATHOPHYSIOLOGY:
-arteries that give rise to 30-300 micrometer branches that
penetrate the cerebrum or brainstem:
-MCA
-circle of Willis
-anterior and posterior communicating
-basilar
vertebral

ISCHEMIC STROKE:
Small-Vessel Stroke
PATHOPHYSIOLOGY:
-small branches can occlude either by:
1. atherothrombotic disease at its origin
-thrombosis cause small infarcts called lacunes
-infarct size: 3mm to 2cm
2. development of lipohyalinotic thickening

-Principal risk factors:
-age
-hypertension

ISCHEMIC STROKE:
Small-Vessel Stroke
CLINICAL MANIFESTATIONS:
-Lacunar Syndromes:
1. Pure motor hemiparesis
-infarct location: posterior limb of the internal
capsule or basis pontis
-involves mostly the arms, face, legs
2. Pure sensory stroke
-infarct location: ventral thalamus
3. Ataxic hemiparesis
-infarct location: ventral pons or internal capsule
4. Dysarthria and clumsy hand
-infarct location: ventral pons or genu of internal
capsule

ISCHEMIC STROKE:
Small-Vessel Stroke
CLINICAL MANIFESTATIONS:
-transient symptoms may occur several times a day
and last only a few minutes
-a large-vessel source may manifest initially as a
lacunar syndrome

SECONDARY PREVENTION:
-risk factor modification especially BP reduction

STROKE: LESS COMMON CAUSES
1. Hypercoagulable disorders
2. Venous sinus thrombosis
3. Sickle cell anemia
4. Fibromuscular dysplasia
5. Temporal giant cell arteritis
6. Necrotizing (granulomatous) arteritis
7. Primary Central Nervous System Vasculitis
8. Drugs: amphetamines, cocaine
9. Moyamoya Disease
10. Reversible posterior leukoencephalopathy
11. Leukoaraiosis / periventricular white matter disease
12. CADASIL (cerebral autosomal dominant arteriopathy with
subcortical infarcts and leukoencephalopathy)

LESS COMMON CAUSES OF STROKE:
Hypercoagulable disorders
-primarily cause INCREASED RISK of VENOUS
THROMBOSIS and therefore may cause VENOUS
SINUS THROMBOSIS
-Protein S deficiency & Homocysteinemia: may cause
arterial thromboses
-SLE with Libmann-Sacks endocarditis: can cause
embolic stroke
-requires long term anticoagulation to prevent
further stroke

Venous sinus thrombosis
-affected location: lateral or sagittal sinus or small
cortical vessels
-occurs as a complication of:
-oral contraceptive use
-pregnancy and the post-partum period
-inflammatory bowel disease
-intracranial infections (meningitis)
-dehydration
-thrombophilia

Venous sinus thrombosis
-manifestations:
-headache
-focal neurologic symptoms
-paraparesis and seizures
-CT is normal unless presence of hemorrhage
-signs of increased ICP/coma in greater degrees
-Venous thrombosis is readily visualized by MR or CT
venography
-treatment: IV heparin regardless of intracranial hemorrhage
-Vitamin K antagonists – if without hypercoagulability
*anticoagulation is continued indefinitely if
thrombophilia is diagnosed

Sickle cell anemia (SS Disease)
-common cause of stroke in children
-predicted by high velocity of blood flow within
MCAs using transcranial Doppler ultrasonography
-Treatment: aggressive exchange transfusion

Fibromuscular dysplasia
-affects the cervical arteries
*carotid/vertebral arteries show multiple rings of
segmental narrowing alternating with dilatation
-OCCLUSION is usually INCOMPLETE
-more common in women
-often asymptomatic but may be associated with
audible bruit, TIA or stroke
-may involve renal arteries and cause hypertension
-Treatment: anticoagulation or antiplatelet

Temporal giant cell arteritis
-common in elderly with the temporal arteries
undergoing subacute granulomatous inflammation
with giant cells
-blindness: due to occlusion of posterior ciliary
arteries; prevented with GLUCOCORTiCOIDS
-rarely causes stroke because the internal carotid
artery is not inflamed
-Takayasu’s arteritis: idiopathic giant cell arteritis
involving great vessels arising from the aortic arch;
may cause carotid or vertebral thrombosis

Necrotizing (granulomatous) arteritis
-occurs alone or in association with generalized
polyarteritis nodosa or granulomatosis with
polyangiitis (Wgener’s)
-involves the distal small branches (<2mm diameter)
of the main intracranial arteries
-produces small ischemic effects on the brain, optic
nerve and spinal cord
-CSF: pleocytosis, increased protein level

Primary Central Nervous System Vasculitis
-rare
-affects small or medium-sized vessels
-without apparent systemic vasculitis
-can follow the post-partum period and are self-
limited
-differential diagnosis includes inflammatory and
non-inflammatory causes

Drugs – amphetamines, cocaine
-cause stroke by acute hypertension or drug induced
vasculopathy
-Phenylpropanolamine, cocaine, methamphetamine:
linked with intracranial hemorrhage

Moyamoya Disease
-occlusive disease involving large intracranial arteries
especially:
-distal internal carotid
-stem of MCA and ACA
-lenticulostriate arteries develop rich collateral circulation
around the occlusive lesion, which gives the “puff of smoke”
impression
-common in Asian chilren or young adults but appears the
same in adults with atherosclerosis associated with diabetes
-Treatment: anticoagulation is risky
-surgical bypass of extracranial carotid arteries to the dura or
MCAs may prevent stroke and hemorrhage

Reversible posterior leukoencephalopathy
-can occur in head injury, seizure, migraine,
sympathomimetic drug use, eclampsia and
postpartum period
-may involve widespread cerebral segmental
vasoconstriction and edema
-manifestation: headache, fluctuating neurologic
symptoms especially visual
-ischemia reverses completely

Leukoaraiosis / periventricular white matter disease
-result of multiple small-vessel infarcts within the
subcortical white matter
-CT/MRI: areas of white matter injury surrounding
the ventricles within the corona radiata; lacunar
infarction are also seen
-caused by chronic hypertension leading to
lipohyalanosis of small penetrating arteries within
the white matter
-may lead to SUBCORTICAL DEMENTIA SYNDROME –
which may be prevented/delayed with
antihypertensive medications

CADASIL (cerebral autosomal dominant arteriopathy
with subcortical infarcts and leukoencephalopathy)
-an inherited disorder that presents as:
-small-vessel stroke
-progressive dementia
-extensive white matter changes seen in MRI
-manifestation: migraine with aura, transient motor
or sensory deficits
-onset is usually on the 4th or 5th decade of life
-caused by mutation in Notch-3

Other monogenic ischemic stroke syndrome

- CARASIL (cerebral autosomal recessive
arteriopathy with subcortical infarcts and
leukoencephalopathy)
- Hereditary endotheliopathy, retinopathy,
nephropathy, and stroke (HERNS)
- Fabry’s disease

TRANSIENT ISCHEMIC ATTACK
-episodes of stroke symptoms that last only briefly
-standard definition of duration is <24 hours, but
most TIAs last <1 hour
-has similar causes as ischemic stroke; may herald
stroke
-may arise from an emboli to the brain or an in situ
thrombosis
-newer definitions of TIA categorize those with new
infarct as having ischemic stroke rather than TIA
regardless of symptom duration

TRANSIENT ISCHEMIC ATTACK
-Amaurosis fugax: transient monocular blindness, occurs from
emboli to the central retinal artery of one eye
-indicates carotid stenosis or local opthalmic artery disease
-risk of stroke after TIA is 10-15% in the first 3 months with most
events occuring in the first 2 days
-risk is estimated using ABCD2 method
-improvement characteristic of TIA is contraindication to
thrombolysis CLINICAL FACTOR SCORE
A: AGE: greater than/equal to 60 years 1
B: BLOOD PRESSURE: SBP >140 mmhg or DBP >90 mmHg 1
C: CLINICAL SYMPTOMS
-Unilateral weakness 2
-Speech disturbance without weakness 1
D1: DURATION
- greater than 60 minutes 2
-10 to 59 minutes 1
D2: DIABETES (oral medications or insulin) 1

TREATMENT: Primary and Secondary
Prevention of Stroke and TIA
GENERAL PRINCIPLES:
-identification and control of modifiable risk factors
is the best strategy to reduce the burden of stroke

ATHEROSCLEROSIS RISK FACTORS:
1. Older age
2. Family history of thrombotic stroke
3. Hypertension
-most significant risk factor
-Rx: use of thiazide diuretics, ACE-inhibitors
4. Tobacco smoking – discouraged
5. Abnormal blood cholesterol (high LDL, low HDL)
-Rx: statin drugs
6. Prior stroke or TIA – greater risk
7. Cardiac conditions – atrial fibrillation, MI
8. Oral contraceptives and hormone replacement therapy
9. Hypercoagulable states
10. Diabetes
-Rx: pioglitazone – agonist of peroxisome proliferator-activated
receptor gamma

ANTIPLATELET AGENTS:
-inhibits the formation of intraarterial platelet aggregates
-most commonly used:
1. Aspirin – acetylates platelate cyclooxygenase, which
irreversibly inhibits the formation in platelets of thromboxane
A2, a platelet aggregating and vasoconstricting prostaglandin
-paradoxically inhibits formation of prostacyclin, an
antiaggregating and vasodilating prostaglandin
-50-325 mg/day of aspirin for stroke prevention

2. Clopidogrel – block ADP receptor on platelets and thus prevent
the cascade resulting in activation of glycoprotein IIB/IIIa that
leads to fibrinogen binding to the platelet and consequent
platelet activation
-rarely causes TTP, but does not cause neutropenia

ANTIPLATELET AGENTS:
3. Dipyridamole (extended-release) – an antiplatelet agent that
inhibits the uptake of adenosine by a variety of cells,
including those of the vascular endothelium 
accumulated adenosine is an inhibitor of aggregation
-potentiates effects of prostacyclin and nitrous oxide

4. Ticlopidine – rarely used, alternative to Clopidogrel
-same action as Clopidogrel
-more effective than aspirin but causes more side
effects such as diarrhea, neutropenia, thrombotic
thrombocytopenic purpura (TTP)

ANTICOAGULATION THERAPY AND EMBOLIC STROKE:
-anticoagulation is safe for patients with chronic nonrheumatic
atrial fibrillation and prevent cerebral embolism
-the decision to use anticoagulation for primary prevention is
based primarily on risk factors
*history of TIA or stroke favors anticoagulation
-anticoagulation also reduces the risk of embolism in acute MI
-3-month course of anticoagulation when there is:
-Q wave infarction
-substantial left ventricular dysfunction
-congestive heart failure
-mural thrombosis
-atrial fibrillation (VKA if atrial fibrillation persists)

ANTICOAGULATION THERAPY AND
NONCARDIOGENIC STROKE:
-warfarin has no benefit over aspirin
-no support for long-term use of VKAs for preventing
atherothrombotic stroke for either intracranial or
extracranial cerebrovascular disease

TREATMENT: Carotid Atherosclerosis
-can be removed surgically (endarterectomy) or
mitigated with endovascular stenting with or
without balloon angioplasty
-Surgical:
- Endarterectomy is most beneficial when
performed within 2 weeks of symtpom onset,
benefit is more pronounced in patients >75 years
old, and benefit men more than women
-Endovascular Therapy:
-endovascular stenting with balloon angioplasty
used to open stenotic carotid arteries

STROKE SYNDROMES
DIVISION OF STROKE SYNDROMES:
1. LARGE-vessel stroke within the ANTERIOR
circulation

2. LARGE-vessel stroke within the POSTERIOR
circulation

3. SMALL-vessel of either vascular bed

STROKE SYNDROMES
CEREBRAL HEMISPHERE, LATERAL ASPECT:
STRUCTURES INVOLVED SIGNS AND SYMPTOMS
-Somatic motor area for -paralysis of the contralateral face, arm and leg
face and arm -sensory impairment over the same are (pinprick, cotton
-Fibers descending from the touch, vibration, position, 2-point discrimination,
leg area to enter the corona stereognosis, tactile localization, barognosis,
radiata and corresponding cutaneographia)
somatic sensory sytem
-Motor speech area of the -Motor aphasia
DOMINANT hemisphere
-Central, suprasylvian -Central aphasia -word deafness -sensory
speech area agraphia
-Parietooccipital cortex of -anomia -jargon speech
the dominant hemisphere GERSTMANN SYNDROME:
-acalculia -alexia
-finger agnosia -right-left confusion
-Central speech area -Conduction aphasia

STROKE SYNDROMES
CEREBRAL HEMISPHERE, LATERAL ASPECT:
-non-dominant parietal lobe -Apractagnosia of the dominant hemisphere
(corresponds to speech area -inaccurate localization on the half field
in dominant hemisphere) -distortion of visual coordinates
-agnosia for the left half of external space
-visual illusions -upside-down reading
-anosognosia -unilateral neglect
-hemiasomatognosia -dressing apraxia
-constructional apraxia -inability to judge distance
-Optic radiation deep to -homonymous hemianopia
second temporal -homonymous inferior quadrantonopia
convolution
-Frontal contraversive eye -paralysis of the conjugate gaze to the opposite side
field
-Projecting fibers

STROKE SYNDROMES
CEREBRAL HEMISPHERE, MEDIAL ASPECT:
-Motor leg area -Paralysis of the opposite foot and leg
-Arm area of cortex -A lesser degree of paresis of opposite arm
-fibers descending to corona
radiata
-Sensory area for foot and -Cortical sensory loss over toes, foot, and leg
leg
-Sensorimotor area in -Urinary incontinence
paracentral lobule
-Medial surface of the -Contralateral grasp reflex
posterior frontal lobe; likely -sucking reflex
supplemental motor area - gegenhalten (paratonic rigidity)

STROKE SYNDROMES
CEREBRAL HEMISPHERE, MEDIAL ASPECT:
-Uncertain localization— -Abulia (akinetic mutism)
probably cingulate gyrus -reflex distraction to sights and sounds
and medial inferior portion -intermittent interruption
of frontal, parietal, and -slowness -lack of spontaneity
temporal lobes -delay -whispering
-Frontal cortex near leg -Impairment of gait and stance (gait apraxia)
motor area
-Corpus callosum -Dyspraxia of left limbs
-tactile aphasia in left limbs

STROKE SYNDROMES
LEVEL OF MEDULLA:
SYNDROME VESSEL(S) SIDE OF INNER SIGNS AND SYMPTOMS
OCCLUDED LESION STRUCTURES
INVOLVED
-Medial -vertebral artery - -same -Ipsilateral twelfth -Paralysis with atrophy of
medullary branch of nerve one-half half the tongue
syndrome vertebral or lower
basilar artery
-opposite -Contralateral -Paralysis of arm and leg,
pyramidal tract sparing face
and medial -impaired tactile and
lemniscus proprioceptive sense over
one-half the body
-Lateral -vertebral artery -same -Descending tract -Pain, numbness, impaired
medullary -posterior inferior -nucleus fifth sensation over one-half the
syndrome cerebellar artery nerve face
-superior, middle,
or inferior lateral
medullary arteries

STROKE SYNDROMES
LEVEL OF MEDULLA:
INVOLVED
-Lateral -vertebral artery -same -Uncertain— -Ataxia of limbs, falling to
medullary -posterior inferior restiform body, side of lesion
syndrome cerebellar artery cerebellar
-superior, middle, hemisphere,
or inferior lateral cerebellar fibers,
medullary arteries spinocerebellar
tract
-same -Vestibular nucleus -Nystagmus
-diplopia
-oscillopsia
-vertigo
-nausea
-vomiting
-same -Nucleus and -Loss of taste
tractus solitarius

STROKE SYNDROMES
LEVEL OF MEDULLA:
INVOLVED
-Lateral -vertebral artery -same -Descending Horner's syndrome:
medullary -posterior inferior sympathetic tract -Miosis
syndrome cerebellar artery -Ptosis
-superior, middle, -Decreased sweating
or inferior lateral
medullary arteries
-same -Issuing fibers -Dysphagia
ninth and tenth -hoarseness
nerves -paralysis of palate
-paralysis of vocal cord
-diminished gag reflex
-same -Cuneate -Numbness of ipsilateral
-gracile nuclei arm, trunk, or leg

STROKE SYNDROMES
LEVEL OF MEDULLA:
INVOLVED
-Lateral -vertebral artery -same -Genuflected -Weakness of lower face
medullary -posterior inferior upper motor
syndrome cerebellar artery neuron fibers to
-superior, middle, ipsilateral facial
or inferior lateral nucleus
medullary arteries
-opposite -Spinothalamic -Impaired pain and thermal
tract sense over half the body,
sometimes face
-Total -vertebral artery -Combination of medial and
unilateral lateral syndromes
medullary
syndrome

STROKE SYNDROMES
LEVEL OF MEDULLA:
INVOLVED
-Lateral -vertebral artery -Combination of lateral
pontomedul medullary and lateral
lary inferior pontine syndrome
syndrome
-Basilar -basilar artery -Bilateral long tract -Bilateral long tract signs
artery -arteries arising in -cerebellar and (sensory and motor;
syndrome the posterior peripheral cranial cerebellar and peripheral
cerebral artery nerves cranial nerve abnormalities)
distribution
-Corticobulbar and -Paralysis or weakness of all
corticospinal tracts extremities, plus all bulbar
bilaterally musculature

STROKE SYNDROMES
LEVEL OF THE INFERIOR PONS:
INVOLVED
-Medial -paramedian -same -Center for -Paralysis of conjugate gaze
inferior branch of basilar conjugate lateral to side of lesion
pontine artery gaze (preservation of
syndrome convergence)
-Vestibular nucleus -Nystagmus
-Likely middle -Ataxia of limbs and gait
cerebellar
peduncle
-Abducens nerve -Diplopia on lateral gaze
-opposite -Corticobulbar and -Paralysis of face, arm, and
corticospinal tract leg
in lower pons

STROKE SYNDROMES
INVOLVED
-Medial -paramedian -opposite -Medial lemniscus -Impaired tactile and
inferior branch of basilar proprioceptive sense over
pontine artery one-half of the body
syndrome
-Lateral -anterior inferior -same -Vestibular nerve -Horizontal and vertical
inferior cerebellar artery or nucleus nystagmus
pontine -vertigo
syndrome -nausea
-vomiting
-oscillopsia
-Seventh nerve -Facial paralysis
-Center for -Paralysis of conjugate gaze
conjugate lateral to side of lesion
gaze

STROKE SYNDROMES
INVOLVED
-Lateral -anterior inferior -same -Auditory nerve or -Deafness
inferior cerebellar artery cochlear nucleus -tinnitus
pontine
syndrome
-Middle cerebellar -Ataxia
peduncle and
cerebellar
hemisphere
-Descending tract -Impaired sensation over
and nucleus fifth face
nerve
tract sense over one-half the
body (may include face)

STROKE SYNDROMES
LEVEL OF THE MIDPONS:
INVOLVED
-Medial -paramedian -same -Pontine nuclei -Ataxia of limbs and gait
midpontine branch of (more prominent in bilateral
syndrome midbasilar artery involvement)
-Medial lemniscus -Variable impaired touch
and proprioception when
lesion extends posteriorly
-Lateral -short -same -Middle cerebellar -Ataxia of limbs
midpontine circumferential peduncle
syndrome artery
Motor fibers or -Paralysis of muscles of
nucleus of fifth mastication
nerve

STROKE SYNDROMES
LEVEL OF THE MIDPONS:
INVOLVED
-Lateral -short -same -Sensory fibers or -Impaired sensation over
midpontine circumferential nucleus of fifth side of face
syndrome artery nerve
tract sense on limbs and trunk

STROKE SYNDROMES
LEVEL OF THE SUPERIOR PONS:
INVOLVED
-Medial -paramedian -same -Superior and/or -Cerebellar ataxia
superior branches of upper middle cerebellar (probably)
pontine basilar artery peduncle
syndrome
-Medial -Internuclear
longitudinal ophthalmoplegia
fasciculus
-Localization -Myoclonic syndrome,
uncertain—central palate, pharynx, vocal
tegmental bundle, cords, respiratory
dentate projection, apparatus, face, oculomotor
inferior olivary apparatus, etc
nucleus

STROKE SYNDROMES
INVOLVED
-Medial -paramedian -opposite -Corticobulbar and -Paralysis of face, arm, and
superior branches of upper corticospinal tract leg
pontine basilar artery
syndrome
-Medial lemniscus -Rarely touch, vibration, and
position are affected
-Lateral -superior -same -Middle and -Ataxia of limbs and gait,
superior cerebellar artery superior cerebellar falling to side of lesion
pontine peduncles,
syndrome superior surface of
cerebellum,
dentate nucleus
-Vestibular nucleus -Dizziness
-nausea, vomiting
-horizontal nystagmus

STROKE SYNDROMES
INVOLVED
-Lateral -superior -same -Pontine -Paresis of conjugate gaze
superior cerebellar artery contralateral gaze (ipsilateral)
pontine
syndrome
-Uncertain -Skew deviation
-Descending Horner's syndrome:
sympathetic fibers -Miosis
-Ptosis
-Decreased sweating over
face
-Dentate nucleus -Tremor
-superior
cerebellar
peduncle

STROKE SYNDROMES
INVOLVED
-Lateral -superior -opposite -Spinothalamic -Impaired pain and thermal
superior cerebellar artery tract sense on face, limbs, and
pontine trunk
syndrome
-Medial lemniscus -Impaired touch, vibration,
(lateral portion) and position sense, more in
leg than arm (there is a
tendency to incongruity of
pain and touch deficits)

STROKE SYNDROMES
LEVEL OF THE MIDBRAIN:
INVOLVED
-Medial -paramedian -same -Third nerve fibers -Eye "down and out"
midbrain branches of upper secondary to unopposed
syndrome basilar arteries action of fourth and sixth
-proximal cranial nerves
posterior cerebral -with dilated and
arteries unresponsive pupil
descending in crus
cerebri

STROKE SYNDROMES
LEVEL OF THE MIDBRAIN:
INVOLVED
-Lateral -small penetrating -same -Third nerve fibers -Eye "down and out"
midbrain arteries arising -third nerve secondary to unopposed
syndrome from posterior nucleus action of fourth and sixth
cerebral artery cranial nerves
-with dilated and
unresponsive pupil
-opposite -Red nucleus -Hemiataxia, hyperkinesias,
-dentatorubro- tremor
thalamic pathway

STROKE WITHIN
THE ANTERIOR CIRCULATION
-The internal carotid artery and its branches
comprise the ANTERIOR CIRCULATION of the
BRAIN
-causes of occlusion:
-intrinsic disease of the vessel
-emboli from proximal source
-occlusion of each major intracranial vessel has
distinct clinical manifestations

STROKE WITHIN
OCCLUSION of the MIDDLE CEREBRAL ARTERY:
-occlusion of the proximal MCA or one of its major branches
is MOST OFTEN due to an embolus RATHER THAN
intracranial atherothrombosis
-collateral formation via leptomeningeal vessels prevents
MCA stenosis from becoming symptomatic
-cortical branches of the MCA supply the lateral surface of
the hemisphere except for:
1. the frontal pole and a strip along the superomedial
border of the frontal and parietal lobes supplied by the
ACA
2. the lower temporal and occipital pole convolutions
supplied by the PCA

STROKE WITHIN
-proximal MCA (M1 segment) gives rise to lenticulostriate
arteries (penetrating branches) that supply the following:
-putamen
-outer globus pallidus
-posterior limb of the internal capsule
-adjacent corona radiata
-most of the caudate nucleus
-MCA divides into superior and inferior divisions (M2
branches) in the sylvian fissure:
-inferior – supply inferior parietal & temporal complex
-superior – supply frontal & superior parietal complex

STROKE WITHIN
-occlusion of the entire MCA at its origin, with limited distal
collaterals lead to the following clinical findings:
-contralateral hemiplegia
-hemianesthesia
-homonymous hemianopia
-1-2 day gaze preference to the ipsilateral side
-dysarthria (due to facial weakness)
DOMINANT HEMISPHERE NONDOMINANT HEMISPHERE
INVOLVEMENT INVOLVEMENT
-Global aphasia -anosognosia
-constructional apraxia
-neglect

STROKE WITHIN
COMPLETE SYNDROME PARTIAL SYNDROME
-most often occlusion of MCA stem -presence of cortical collateral blood
flow
-emboli that causes incomplete
occlusion
-occlusion of distal MCA branches or
fragment and move distally

STROKE WITHIN
LOCATION OF OCCLUSION SYMPTOMS
-single branch -hand or hand and arm weakness (brachial syndrome)
-facial weakness with Broca’s aphasia with or without
arm weakness (opercular syndrome)
-proximal superior division and -sensory disturbance
infarcted frontal and parietal -motor weakness
cortices -Broca’s aphasia
-inferior division supplying -Wernicke’s aphasia without weakness
posterior part (temporal cortex) of -Jargon speech and inability to comprehend written
the dominant hemisphere and spoken language
-contralateral homonymous superior quadrantanopia
inferior division of the -hemineglect
nondominant hemisphere -spatial agnosia without weakness

STROKE WITHIN
-lenticulostriate vessel (stroke -pure motor stroke or sensory-motor stroke
within the internal capsule) contralateral to the lesion
-ischemia in the genu of the -1st: facial weakness arm weakness  leg weakness
internal capsule (moving -contralateral hand: ataxia, dysarthria
posteriorly)
-lacunar infarction in globus -few clinical symptoms
pallidus and putamen -parkinsonism
-hemiballismus

STROKE WITHIN
OCCLUSION of the ANTERIOR CEREBRAL ARTERY:
-ACA is divided into 2 segments:
1. precommunal (A1) circle of Willis or stem –
-connects the internal carotid to the anterior
communicating artery
-gives rise to deep penetrating branches that supply the:
-anterior limb of the internal capsule
-amygdala
-anterior perforate substance
-anterior hypothalamus
-inferior part of the head of the caudate nucleus
2. postcommunal (A2) –
-distal to the anterior communicating artery

STROKE WITHIN
OCCLUSION of the ANTERIOR CEREBRAL ARTERY:
-occlusion of the ACA is usually well tolerated due to
collateral flow through the anterior communicating
and through the MCA and PCA
-single A2 segment -contralateral symptoms
-A2 segments from a single -may affect both hemispheres and thus result to:
anterior cerebral stem -profound abulia –delay verbal and motor response
(contralateral A1 segment atresia) -bilateral pyramidal signs with paraparesis and
quadriparesis
-urinary incontinence

STROKE WITHIN
OCCLUSION of the ANTERIOR CHOROIDAL ARTERY:
-anterior choroidal artery arises from the internal carotid
artery and supplies the posterior limb of the internal
capsule and the white matter posterolateral to it, through
which GENICOLOCALCARINE fibers pass
-collateral: penetrating vessels of the proximal MCA,
posterior communicating artery, posterior choroidal
arteries
*presence of collateral cause minimal deficits
-anterior choroidal strokes are often caused by IN SITU
thrombosis, and iatrogenic occlusion during surgical
clipping of aneurysms arising from the internal carotid
artery

STROKE WITHIN
OCCLUSION of the ANTERIOR CHOROIDAL
ARTERY:
-anterior choroidal artery -COMPLETE syndrome consists:
-contralateral hemiplegia
-hemianesthesia (hypesthesia)
-homonymous hemianopia

STROKE WITHIN
OCCLUSION of the INTERNAL CAROTID ARTERY:
-clinical picture depends on cause of ischemia:
-thrombus
-embolism
-low flow
-the cortex supplied by the MCA territory is affected
MOST OFTEN
-may go unnoticed with a COMPETENT circle of Willis
-in stenotic lesions, a high-pitched carotid bruit fading
into DIASTOLE is heard  becomes fainter and
disappears when occlusion is imminent

STROKE WITHIN
OCCLUSION of the INTERNAL CAROTID ARTERY:
-propagation into the MCA -symptoms of proximal MCA
-may have massive infarction of deep white matter
and cortical surface
-origins of ACA and MCA at the top -abulia
of carotid artery -stupor with hemiplegia
-hemianesthesia
-aphasia
-anosognosia
-fetal posterior cerebral artery -symptoms referable to its peripheral territory
(PCA arises from the internal
carotid artery)
-opthalmic artery -recurrent transient monocular blindness (amaurosis
fugax)

STROKE WITHIN
OCCLUSION of the COMMON CAROTID ARTERY:
-Signs and symptoms the same with internal
carotid occlusion
-Jaw claudication: low flow in external carotid
branches
-Bilateral common carotid artery occlusion:
Takayasu’s arteritis

STROKE WITHIN
THE POSTERIOR CIRCULATION
-the POSTERIOR CIRCULATION is composed of:
-paired vertebral arteries  join to form 
-basilar artery  divides 
-paired posterior cerebral arteries
*these arteries give rise to circumferential and deep
penetrating branches that supply the:
-cerebellum
-brainstem
-diencephalon
-hippocampus
-medial temporal and occipital lobes
*occlusion of each vessel produces its own distinctive
symptom

STROKE WITHIN
OCCLUSION of the POSTERIOR CEREBRAL ARTERY:
-origin of the PCA:
75% - from bifurcation of the basilar artery
20% - one from the ipsilateral internal carotid
artery via the posterior communicating artery
5% - both from the respective ipsilateral internal
carotid arteries

STROKE WITHIN
-PCA syndromes:
-usually result from atheroma formation or emboli that lodge at
the top of the basilar artery
-may also be due to vertebral artery dissection or fibromuscular
dysplasia
-2 clinical syndromes are COMMONLY observed with PCA occlusion:
1. P1 syndrome
-midbrain, subthalamic, thalamic signs
-due to disease of the proximal P1 segment or its penetrating
branches
2. P2 syndrome
-cortical temporal and occipital lobe signs
-due to occlusion of the P2 segment distal to the junction of
the PCA with the posterior communicating artery

STROKE WITHIN
P1 SYNDROMES

-Ipsilateral subthalamus and medial thalamus -CLAUDE’S SYNDROME: third nerve palsy with
-Ipsilateral cerebral peduncle and midbrain contralateral ataxia
-WEBER’S SYNDROME: third nerve palsy with
contralateral hemiplegia
-red nucleus -ataxia
-dentatorubrothalamic tract
-cerebral peduncle -hemiplegia
-subthalamic nucleus -hemiballismus

-artery of Percheron -paresis of upward gaze
-drowsiness
-abulia
-extensive infarction in the midbrain and -coma -bilateral pyramidal signs
subthalamus with bilateral PCA occlusion -unreactive pupils -decerebrate rigidity

STROKE WITHIN
P1 SYNDROMES

-penetrating branches o f thalamic and -less extensive thalamic and thalamocapsular
thalamogeniculate arteries lacunar syndromes
Thalamic Dejerine-Roussy syndrome:
-consists of:
-contralateral hemisensory loss 
-agonizing, searing, burning pain in the affected area
-persistent and responds poorly to analgesics
-anticonvulsants (carbamazepine or gabapentin) or tricyclic
antidepressants show benefits

STROKE WITHIN
P2 SYNDROMES
LOCATION OF OCCLUSION/INFARCTION SYMPTOMS

-distal PCA (infarction of medial temporal and -contralateral homonymous hemianopia WITH
occipital lobes) macula sparing
*occasionally, only the upper quadrant of
visual field is involved
-calcarine cortex -patient is aware of visual defects

dominant hemisphere: -acute disturbance in memory but clears
-medial temporal lobe
-hippocampus
dominant hemisphere: -alexia WITHOUT agraphia
-splenium of the corpus callosum *amnestic aphasia may occur even without
callosal involvement
-PCA -peduncular hallucinosis: visual hallucinations of
brightly colored scenes and objects

STROKE WITHIN
P2 SYNDROMES

-bilateral infarction in the distal PCA -cortical blindness (blindness with preserved
PLR)
-ANTON’S SYNDROME: unaware/deny blindness
-infarction secondary to low flow in the -BALINT’S SYNDROME: disorder of orderly visual
“watershed” between distal PCA and MCA scanning of the environment
territories -palinopsia: persistence of visual image for
*as occurs after cardiac arrest several minutes
-asimultanagnosia: inability to synthesize whole
image
-top of the basilar artery -central or peripheral territory symptoms
-HALLMARK: sudden onset of bilateral signs –
-ptosis -pupillary asymmetry
-somnolence -lack of reaction to light

STROKE WITHIN
OCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR
ARTERIES:
-The vertebral artery arises from the INNOMINATE artery on
the RIGHT and the SUBCLAVIAN artery on the LEFT
SEGMENT COURSE
V1 -from origin to entrance of 5th/6th transverse vertebral foramen
V2 -traverses the vertebral foramina from C6 to C2
V3 -passes through the vertebral foramen and circles around the arch of
the atlas to pierce the dura at the foramen magnum

V4 -courses upward to join the other vertebral artery to form the basilar
artery
-ONLY V4 gives rise to branches that SUPPLY THE BRAINSTEM and
CEREBELLUM

STROKE WITHIN
OCCLUSION of the VERTEBRAL and POSTERIOR CEREBELLAR ARTERIES:
-Atherothrombotic lesions have a predilection for V1 and V4 segments
of the vertebral artery
-V1 may produce posterior circulation emboli but collateral flow
from contralateral vertebral artery, ascending cervical, thyrocervical
or occipital arteries prevent low flow TIAs or stroke
-but when one vertebral artery is atretic, collateral flow may be
insufficient
-low flow TIAs consist of:
-syncope
-vertigo
-alternating hemiplegia

STROKE WITHIN
ARTERIES:
-Atherothrombotic lesions have a predilection for V1 and V4
segments of the vertebral artery
-V4 can promote thrombus formation as:
-embolism
-basilar artery thrombosis – with propagation
-if the SUBCLAVIAN ARTERY is occluded proximal to the origin of
the vertebral artery there is reversal in the direction of blood
flow in the ipsilateral vertebral artery
*exercise of the ipsilateral arm may increase demand on
vertebral flow, producing posterior circulation TIAs /
“SUBCLAVIAN STEAL”

STROKE WITHIN
ARTERIES:
-V2 and V3 are subject to:
-dissection
-fibromuscular dysplasia
-encroachment by osteophytic spurs within the
vertebral foramina

STROKE WITHIN
ARTERIES:
-The posterior inferior cerebellar artery (PICA):
-PROXIMAL segment supplies the LATERAL MEDULLA
-DISTAL branches supply the INFERIOR surface of the
cerebellum

-stenosis proximal to the origin of the PICA can threaten both
the lateral medulla and the inferior surface of the
cerebellum

STROKE WITHIN
ARTERIES:

-V4 segment (ischemia of lateral medulla) -vertigo
-numbness of ipsilateral face; contralateral limbs
-diplopia
-hoarseness
-dysarthria
-dysphagia
-ipsilateral Horner’s syndrome (lateral medullary
/ Wallenberg’s syndrome)
-medullary penetrating branches -partial syndromes
-PICA
-infarction of the pyramid -rarely, medial medullary syndrome
-contralateral hemiparesis of the arm and leg,
sparing the face

STROKE WITHIN
ARTERIES:

-medial lemniscus -contralateral loss of joint position sense
-emerging hypoglossal nerves -ipsilateral tongue weakness
-cerebellar infarction with edema -sudden respiratory arrest (due to raised ICP in
the posterior fossa)
-before arrest ensues, the following are absent
or present briefly:
-drowsiness -Babinski signs
-dysarthria -bifacial weakness

-Gait unsteadiness, headache, dizziness, nausea and vomiting may
be the only early symptoms and signs and should arouse
suspicion of impending complication, which may require
neurosurgical decompression, often with an excellent outcome

STROKE WITHIN
OCCLUSION of the BASILAR ARTERY:
-the basilar artery supply the base of the pons and the superior
cerebellum; they fall into 3 GROUPS:
1. Paramedian
-7-10 in number
-supply a wedge of pons on either side of the midline
2. Short circumferential
-5-7 in number
-supply the lateral 2/3 of the pons and middle and
superior cerebellar peduncles
3. Bilateral long circumferential
-2 in number
-course around the pons to supply superior and
anterior inferior cerebellum

STROKE WITHIN
-atheromatous lesions occur anywhere the basilar trunk but
are MOST FREQUENT in the PROXIMAL BASILAR and DISTAL
VERTEBRAL segments
-clinical picture depends on the availability of retrograde
collateral flow from the posterior communicating arteries
-emboli from the heart or proximal vertebral or basilar
segments are MORE COMMONLY responsible for “top of
the basilar” syndromes
-COMPLETE BASILAR OCCLUSION: constellation of bilateral
long tract signs (sensory and motor) with signs of cranial
nerve and cerebellar dysfunction

STROKE WITHIN
- “LOCKED-IN” state of preserved consciousness with
quadriplegia and cranial nerve signs suggest COMPLETE
PONTINE and LOWER MIDBRAIN infarction
-TIAs in the proximal basilar distribution may produce vertigo,
other symptoms include diplopia, dysarthria, facial or
circumoral numbness and hemisensory symptoms
-symptoms of BASILAR BRANCH affect ONE side of the
brainste; symptoms of BASILAR ARTERY affect BOTH sides
-TIAs are short lived (5-30 minutes) but repititive
-Rx: heparin to prevent clot propagation

STROKE WITHIN

-basilar artery with infarction -bilateral brainstem signs:
-gaze paresis/internuclear opthalmoplegia
-ipsilateral hemiparesis
-unequivocal signs of bilateral pontine disease

-branch of basilar artery -unilateral symptoms:
-signs involving motor, sensory and cranial
nerves
-superior cerebellar artery -severe ipsilateral cerebellar ataxia
-nausea and vomiting
-dysarthria
-contralateral loss of pain and temperature
sensation over the extremities, body and face
Rarely:
-partial deafness -Horner’s syndrome
-ataxic tremor of ipsilateral upper limb
-palatal myoclonus

STROKE WITHIN

-anterior inferior cerebellar artery ipsilateral :
-deafness, facial weakness, vertigo, nausea and
vomiting, nystagmus, tinnitus, cerebellar ataxia,
Horner’s syndrome, paresis of conjugate lateral
gaze
contralateral:
-loss of pain and temperature sensation
*an occlusion close to the origin may cause
CORTICOSPINAL TRACT SIGNS
-one of the short circumferential branches of the -affects the lateral 2/3 of the pons and middle or
basilar artery superior cerebellar peduncle
-one of the paramedian branches -affects a wedge-shaped area on either side of
the medial pons

IMAGING STUDIES: CT SCANS
-identify or exclude hemorrhage as the cause of
stroke and they identify extraparenchymal
hemorrhages, neoplasms, abscesses, and other
conditions masking as stroke
-CT OBTAINED in the FIRST SEVERAL HOURS after
an infarction generally SHOW NO ABNORMALITY
-Infarct may not be seen reliably for 24-48 hours
-CT may fail to show small ischemic stroke in the
posterior fossa because of bone artifact, also on
the cortical surface

IMAGING STUDIES: CT SCANS
-contrast enhanced CT allow visualization of venous
structures
-CT angiography readily:
- identifies carotid disease and intracranial vascular
occlusions
-area of brain infarct, ischemic penumbra after IV
bolus of contrast
-sensitive in detecting SAH
-NON-CONTRAST HEAD CT IS THE IMAGING
MODALITY OF CHOICE IN PATIENTS WITH ACUTE
STROKE

IMAGING STUDIES: MRI
-reliably documents the extent and location of infarction in
ALL AREAS of the brain, including the posterior fossa and
cortical surface
-LESS SENSITIVE than CT in DETECTING ACUTE BLOOD
-diffusion-weighted imaging and fluid-attenuated inversion
recovery (FLAIR) is MORE SENSITIVE for EARLY BRAIN
INFARCTION than MR sequences or CT
-MR perfusion studies use IV GADOLINIUM contrast
-MR angiography is highly sensitive for stenosis of
extracranial internal carotid arteries and large intracranial
vessels
-MRI with fat saturation visualize extra or intracranial arterial
dissection

IMAGING STUDIES: MRI
-compared to CT, MRI is:
-less sensitive for acute blood products
-more expensive
-time consuming
-less readily available
-limited with Claustrophobia
-MRI is more useful outside the acute period by:
-more clearly defining the extent of tissue injury
-discriminating new from old regions of brain
infarction

IMAGING STUDIES:
CEREBRAL ANGIOGRAPHY
-conventional X-RAY cerebral angiography is the GOLD
STANDARD for:
-identifying and quantifying atherosclerotic stenoses of
the cerebral arteries
-characterizing other pathologies
-coupled with endovascular techniques for cerebral
revascularization
-risks of cerebral angiography:
-arterial damage
-groin hemorrhage
-embolic stroke
-renal failure from contrast nephropathy
*reserved when less invasive means are inadequate

IMAGING STUDIES:
ULTRASOUND TECHNIQUES
-Transcranial Doppler (TCD)
-can detect stenontic lesions in large intracranial
arteries because such lesions increase systolic
flow velocity
-can assist thrombolysis and improve large artery
recanalization following rTPA administration

IMAGING STUDIES:
PERFUSION TECHNIQUES
-both xenon techniques (xenon-CT) and PET can
quantify cerebral blood flow
-generally used for research BUT can be useful for
determining the significance of arterial stenosis
and planning for revascularization surgery
-CT perfusion increases the sensitivity of detecting
ischemia and can measure ischemic penumbra

INTRACRANIAL HEMORRHAGE
INTRODUCTION:
-Hemorrhages are classified by their location and
underlying vascular pathology.
-Types:
-Subdural and epidural hemorrhage – usually
caused by trauma
-Subarachnoid hemorrhages – produced by
trauma and rupture of intracranial aneurysms
-Intraparenchymal and Intraventricular
hemorrhages

DIAGNOSIS:
-Intracranial hemorrhage is often discovered on
non-contrast CT imaging of the brain during the
acute evaluation of stroke
*CT imaging is preferred method for acute stroke
evaluation over MRI since it is more sensitive on
acute blood

EMERGENCY MANAGEMENT:
-Airway – reduction in the level of consciousness is common
and progressive
-Initial BP is maintained until CT scan results are reviewed
*BP can be safely lowered using nicardipine , labetalol or
esmolol (non-vasodilating IV drugs)
-Mean arterial pressure is maintained <130mmHg, unless an
increase in ICP is suspected
-Stuporous or comatose patients generally are treated
presumptively for elevated ICP with:
-tracheal intubation -mannitol administration
-hyperventilation -elevation of the head of bed

INTRAPARENCHYMAL HEMORRHAGE
-MOST COMMON TYPE OF INTRACRANIAL HEMORRHAGE
-particularly high in Asians and Blacks
-Major causes:
1. hypertension
2. trauma
3. cerebral amyloid angiopathy
-Risk factors:
-advanced age
-heavy alcohol consumption
-cocaine and methamphetamine use (most important
cause in the young)

HYPERTENSIVE
PATHOPHYSIOLOGY:
-usually results from spontaneous rupture of a small
penetrating artery deep in the brain
-can also be due to hemorrhagic disorders, neoplasms,
vascular malformations
*suspected in non-hypertensives and in uncommon sites
-Most Common Sites:
-basal ganglia especially the putamen
-thalamus
-cerebellum
-pons

HYPERTENSIVE
PATHOPHYSIOLOGY:
-hemorrhage may lead herniation and death
-most develop over 30-90 minutes compared
hemorrhage caused by anticoagulant therapy
that evolve for 24-48 hours

Internal Medicine - Cerebrovascular Diseases

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