Cerebrovascular Disease

Includes Ischemic Stroke and Hemorrhagic

Stroke
Stroke is the second leading cause of death
worldwide, causing 6.2 million deaths in 2011

CVD Strokes cause ~200,000 deaths each year in the

United States and are a major cause of disability

incidence of cerebrovascular diseases increases

with age
 Cerebral ischemia  caused by a
reduction in blood flow that lasts longer
than several seconds
CVD
Infarction  death of brain tissue; if the
cessation of blood flow lasts for more
than a few minutes
 When blood flow is quickly restored, brain
tissue can recover fully and the patient’s
symptoms are only transient
Transient
Ischemic
Attack all neurologic signs and symptoms resolve
within 24 h without evidence of brain
infarction on brain imaging
 abrupt onset of a neurologic deficit that is
attributable to a focal vascular cause

Stroke/ neurologic signs and symptoms last for >24 h

Cerebrovascul or brain infarction is demonstrated

ar Accident
generalized reduction in cerebral blood flow
due to systemic hypotension produces
syncope
 Focal ischemia or infarction  caused by
thrombosis of the cerebral vessels or by
emboli from a proximal arterial source or the
heart

CVD Intracranial hemorrhage  caused by

bleeding directly into or around the brain and
produces neurologic symptoms from the toxic
effects of blood itself, or by increasing
intracranial pressure
Approach
to Patient
Ischemic stroke
 Pathophysiology

Acute occlusion on an intracranial vessel causing reduction of blood flow

Zero blood flow causes death of brain tissue in 4-10 minuets
<16-18 mL/100g causes infarction in an hour
<20mL/100g cause ischemia without infarction unless prolonged for
several hours to days
TIA transient ischemic attack
Ischemic penumbra - ischemic but reversible dysfunctional tissue
surrounding a core area of infarction
Focal cerebral infarction occur via two distinct pathways
1 necrotic pathway in which cellular cytoskeleton breakdown is
rapid, due principally to energy failure of the cell
2 apoptotic pathway
Fever and hyperglycemia worsens brain injuries in ischemia (
glucose >11.1 mmol/L)
 Treatment

Goal is to prevent or reverse brain injury

Attend to patient’s ABC

Treat hypo and hyperglycemia

No contrast head CT scan to differentiate ischemia from

hemorrhage
 Intravenous thrombolysis

IV rtPA(0.9mg/kg to a 90-mg maximum; 10% as bolus

Endovascular revas ularization

Large vessel occlusion

Middle cerebral artery, intracranial internal carotid artery, and

basilar artery

For patients with contraindications to thrombolitics

Antithrombotic treatments

Platelet inhibitions- aspirin is the only antiplatelet agent with proven

effects to acute ischemic stroke

Anticoagulations - not recommended for atherothrombotic stroke

 Etiology of ischemic stroke

Cardioembolic stroke
20% of all ischemic stroke
Caused by embolism of thrombotic material forming at the atrial or ventricaular or
the left heart valve
Embolic strokes occurs suddenly with maximum neurologic deficit present at
onset
Intracranial internal carotid artery, Middle cerebral artery, and posterior cerebral
artery
Most significant causes of cardioembolic stroke:

Nonrheumatic atrial fibrillation, MI, prosthetic valves, rheumatic

heart disease, ischemic cardiomyopathy

Paradoxical embolization – venous thrombi migrates to the atrial

circulation, usually via a patent foramen ovale, or atrial septal
defect.
Artery to artery embolic stoke
Dominant vasclar mechanism causing large vessel brain ischemia
Embolic source
Aortic arch, common carotid, internal carotid, vertebral, and basilar arteries
Carotid artherosclerosis occurs more commonly along the common carotid
bifurcation, and proximal internal carotid artery
Male, older age, smoker, hypertensive, DM, and hypercolesterolemia
10% of all ischemic stroke
Small – Vessel stroke

Lacunar infarction refers to infarction following

artherothrombotic or lipohyalinotic occlusion

20% of all strokes

Transient Ischemic Attacks
 ▪ TIAs are episodes of stroke symptoms with a duration of
<24 h
▪ Relevant brain infarction on brain imaging  classified
as stroke regardless of the duration of symptoms
TIA
▪ the occluded blood vessel reopens and neurologic
function is restored
 ▪ The risk of stroke after a TIA is ~10–15% in the first 3
months (first 2 days)

TIA ▪ Combination of aspirin and clopidogrel has been

recently reported to prevent stroke following TIA better
than aspirin alone
Risk Assessment
 ▪ Atherosclerosis Risk Factors:
▪ Older age, diabetes mellitus, hypertension, tobacco
smoking, abnormal blood cholesterol (particularly, low
high-density lipoprotein [HDL] and/or elevated low-
Primary and density lipoprotein [LDL])
Secondary
Prevention of ▪ all hypertension should be treated to a target of less than
140–150/90 mmHg
Stroke and TIA ▪ statin drugs reduce the risk of stroke even in patients
without elevated LDL or low HDL
▪ Tobacco smoking should be discouraged
 ▪ Antiplatelet agents

▪ Platelet antiaggregation agents can prevent

Primary and atherothrombotic events, including TIA and stroke, by
inhibiting the formation of intraarterial platelet aggregates
Secondary (form on diseased arteries, induce thrombus formation,
Prevention of and occlude or embolize into the distal circulation)

Stroke and TIA ▪ Most commonly used: Aspirin, clopidogrel, and the
combination of aspirin plus extended-release
dipyridamole
 Primary and ▪ Anticoagulation Therapy
Secondary ▪ anticoagulation with a Vit. K Antagonist reduces the risk by
about 67%
Prevention of ▪ reduces the risk of embolism in acute MI
Stroke and TIA
Intracranial Hemorrhage
 ▪ airway management
▪ BP lowering (SBP to <140 mmHg with initial SBP of150–
220 mmHg)
▪ Patients who have ICP monitors  maintain the
cerebral perfusion pressure (MAP - ICP) above 60
Emergency mmHg

Management ▪ Stuporous or comatose patients with clinical and

imaging signs of herniation  treated presumptively
for elevated ICP
▪ tracheal intubation, administration of osmotic diuretics
such as mannitol or hypertonic saline, and elevation of the
head of the bed while surgical consultation is obtained
Intracerebral Hemorrhage
 ▪ Approx. 10% of all strokes
▪ 35–45% of patients die within the first month
▪ Asians and blacks

Epidemiology
▪ Risk Factors:
▪ Advanced age
▪ heavy alcohol consumption
 ▪ Hypertension
▪ coagulopathy
Etiology ▪ sympathomimetic drugs (cocaine, methamphetamine)
▪ cerebral amyloid angiopathy
Hypertensive Intracerebral
Hemorrhage
Pathophysiology
 ▪ Most hypertensive ICHs initially develop over 30–90 min
▪ Within 48 h, macrophages begin to phagocytize the
hemorrhage at its outer surface
Pathophysiology ▪ After 1–6 months, the hemorrhage is generally resolved
to a slitlike orange cavity lined with glial scar and
hemosiderin-laden macrophages
 ▪ abrupt onset of a focal neurologic deficit
▪ Seizures are uncommon
▪ Worsens over 30–90 min and is associated with a
diminishing level of consciousness and signs of
Clinical increased ICP such as headache and vomiting

Manifestations ▪ putamen  most common site for hypertensive

hemorrhage
▪ adjacent internal capsule is usually damaged
▪ Contralateral hemiparesis  sign
 Clinical
Manifestations
 ▪ Thalamic hemorrhages:
▪ contralateral hemiplegia or hemiparesis from pressure on,
Clinical or dissection into, the adjacent internal capsule

Manifestations ▪ Aphasia/constructional apraxia or mutism

▪ homonymous visual field defect
 ▪ Pontine Hemorrhage
▪ deep coma with quadriplegia often occurs over a few
minutes

Clinical ▪ prominent decerebrate rigidity and “pinpoint” (1 mm)

pupils that react to light
Manifestations ▪ Impaired Oculocephalic Reflex/Maneuver and
Oculovestibular Reflex
▪ Hyperpnea, severe hypertension, and hyperhidrosis
 ▪ Cerebellar Hemorrhage
Clinical ▪ occipital headache, repeated vomiting, and ataxia of gait
Manifestations ▪ Dizziness or vertigo
 ▪ Lobar Hemorrhage
▪ occipital hemorrhage  hemianopia
▪ left temporal hemorrhage  aphasia and delirium
▪ parietal hemorrhage  hemisensory loss
▪ Frontal hemorrhage  arm weakness
Clinical
Manifestations ▪ Large hemorrhages  stupor or coma
▪ focal headaches, vomiting
▪ drowsy
▪ Stiff neck and seizures are uncommon
 ▪ routine blood chemistries and hematologic studies
▪ CT imaging reliably detects acute focal hemorrhages in
Diagnostics the supratentorial space

▪ MRI is not necessary for primary diagnosis

 ▪ noncontrast CT imaging of the brain during the acute
evaluation of stroke
Diagnosis ▪ CT imaging is the preferred method for acute stroke
evaluation
Treatment
 ▪ For cerebellar hemorrhages >3 cm in diameter will
require surgical evacuation
▪ hematomas between 1 and 3 cm require careful
observation for signs of impaired consciousness,
Treatment progressive hydrocephalus, and precipitous respiratory
failure

▪ Cerebral perfusion pressure (MAP minus ICP) above 60

mmHg
 ▪ reducing chronic hypertension
▪ eliminating excessive alcohol use
Prevention ▪ discontinuing use of illicit drugs such as cocaine and
amphetamines