You are on page 1of 86

STROKE

ARLYN M. VALENCIA , M.D.


Associate Professor, UNSOM
Diplomate, American Board Of Psychiatry &
Neurology
LEARNING OBJECTIVES

To be able to define stroke, discuss its


pathophysiology and risk factors
To emphasize early evaluation and management
of stroke patients
To discuss the latest stroke treatment strategies

CASE STUDIES: To be able to analyze clinical


situations, localize the stroke lesion, determine
probable etiology
THE BRAIN IS A VERY UNIQUE, HIGH-MAINTENANCE END- ORGAN. IT IS VERY
DEPENDENT ON MOMENT-TO-MOMENT SUPPLY OF GLUCOSE AND OXYGEN TO
SUSTAIN ITS HIGH-POWERED ACTIVITIES. IT IS VERY SENSITIVE TO THE
SYSTEMIC STATE. ANY SEVERE MEDICAL INSULT, THEREBY, HAS
TREMENDOUS IMPACT ON THE BRAIN METABOLISM. ANY MEDICAL
EMERGENCY IS A NEUROLOGIC EMERGENCY!

A. Valencia, M.D.
The biology of stroke
is such that each
moment of ischemia
and tissue injury
increases the degree
of irreversible tissue
damage.
CEREBROVASCULAR ACCIDENT OR BRAIN ATTACK

Third leading cause of death


750, 000 cases/year
Leading cause of significant disability
Cost: $40 billion/year
Major Causes of Death in the United Sates, 1995
Annual Economic Costs of Stroke (All Types) In The US
Death Rates for Stroke per 100,000 Population
Types of Stroke
Ischemic, 80%
- thrombosis, 50% (small
& large-vessel)
- embolism, 30% [now
believed significantly
higher]
Hemorrhagic, 20%
- intracerebral (HTN as
risk)
- subarachnoid
(aneurysm)
Stroke vs. TIA
Transient ischemic attack (TIA): A clinical
syndrome characterized by an acute loss of focal
brain or monocular function with symptoms lasting
less than 24 hrs and which is thought to be due to
inadequate cerebral or ocular blood supply, without
ischemic changes in Diffusion Weighted Imaging
(DWI)

Stroke: Clinical syndrome characterized by an acute


loss of focal brain or monocular function with
symptoms lasting greater than 24 hrs and which is
thought to be due to inadequate cerebral or ocular
blood supply.
Risk Factors for Stroke That Cannot Be Changed

Increased age
Being male
Race (e.g., African-Americans)
Diabetes mellitus
Prior stroke/transient ischemic attacks
Family history of stroke
Asymptomatic carotid bruit
Up to approximately 30% of people who suffer
transient attacks (TIAs) will develop a stroke within 5
years.
Relative Incidence of Atherothrombotic
Stroke and MI by Age and Gender
Death Rates for Stroke per 100,000 Population
Groups Defined by Race, Age, and Gender: 1993
Risk Factor For Stroke: Treatable
Major
Hypertension
Heart disease, esp. atrial fibrillation
Cigarette smoking
Transient ischemic attacks
Dyslipidemia
Physical inactivity
Obesity

Less Well Documented


Excessive alcohol intake / drug abuse
Acute infection*
Alcohol Consumption as a Risk Factor for Stroke

Heavy alcohol consumption may increase risk


of stroke by a number of mechanisms.
The reported effects of alcohol consumption
on risk of ischemic stroke have been
inconsistent.
A differential effect of alcohol consumption
on stroke risk in men compared to women
has been observed.
Alcohol Consumption as a Risk Factor for Stroke

Light and moderate alcohol use tend to raise


levels of high-density-lipoprotein (HDL) -- the
"good" lipoprotein.
Heavy drinking or binge drinking, is related to an
increased incidence of stroke as a cause of death
Light or moderate alcohol consumption, is
related to a reduced risk of coronary heart
disease.
There is positive, dose-related effect of alcohol
consumption on risk of intracranial hemorrhage,
both arachnoid and intracerebral .
Less Well Documented

Geography/climate
Socieconomic factors
The Stroke Belt
Potential Genetic Risk Factors for Stroke

Apolipoprotein E4

Elevated homocysteine levels

Factor V mutation
ATHEROSCLEROSIS AND THROMBOSIS

Atherosclerosis: decades-long process; progression


favored by hypercholesterolemia, HTN, cigarette smoking
Fatty streak: yellowish discoloration on intimal surface of
blood
Focal plaques: eccentric thickening at bifurcations;
addition of massive extracellular lipids that displaced
normal cells and matrix
Complicated fibrous plaques: central acellular area of
lipid covered by a cap of smooth muscle cells and collagen
Atherosclerosis and Thrombus Formation:
Arterial Wall Injury

Functional alteration of
endothelial cell layer

Denuding of endothelium
Superficial intimal injury

Deep intimal & media


damage with marked
platelet aggregatio and
mural thrombosis
Role of Monocytes and T-Lymphocytes in
the Transformation to Foam Cells
Oxidation of LDL-Cholesterol
Oxidized LDL-cholesterol Contributes To
Atherogenesis In Three Other Ways:

It has cytotoxic properties that may promote


endothelial injury;
It acts as a chemoattractant for circulating
monocytes, leading to their increased
accumulation with plaques; and
Inhibits egress of macrophages from plaques.
Smooth Muscle Cell Migration and Proliferation
Smooth Muscle Cell Migration and
Proliferation

Along with macrophages, smooth-


muscle cells proliferate in the
intima during atherogenesis.

Smooth muscle cell layer makes up


a substantial bulk of the
atherosclerotic lesion, which may
rise several millimeters above the
surface of the surrounding intima
Role of Platelets

Platelet adhesion may be


promoted by type II injury
and by toxic products
Platelets release growth
factors that stimulate SM
migration and proliferation
and formation of
fibrointimal lesions and
the outside capsule of
fatty lesions
Plaque Fissuring and Formation of Platelet Thrombus

The vulnerability of such a


structure to fissuring
appears to be related to
circumferential stress on
the plaque cap in systole,
as well as infiltration of the
cap tissue with foam cells
(with reduction of total
collagen content and a
concomitant fall in tensile
strength)
Potential Outcomes of Plaque Fissuring
Acute episodes of
transient ischemia and
ischemic stroke (as well
as myocardial
infarction, unstable
angina, as sudden
death) may be
precipitated by
thrombosis on
atherosclerotic
plaques.
Thrombus Formation I -- Platelet Activation

On contact with collagen, platelets


become activated, with platelet
adhesion, secretion of platelet
contents, and platelet aggregation at
the site of injury. The activated
platelet surface is an essential
catalytic surface for several
coagulation reactions that generate
thrombin, a key factor in the
coagulation sequence
Thrombus Formation II -- Platelet
Activation and Blood Flow
Thrombus Formation III -- Activation of Coagulation Cascade
Evolution of Cerebral Atherothrombosis
Atherothrombotic occlusion of
larger arteries

Embolism: Artery-to artrey,


cardiogenic

Primary small vessel disease


(lipohyalinosis)
Thromboembolism
Cardiogenic Emboli

Cardiogenic emboli
lodge in the middle
cerebral artery or its
branches in 80% of
cases, in the posterior
cerebral artery or its
branches 10% of the
time, and in the vertebral
artery or its branches in
the remaining 10% of
cases.
Major Blood Vessels Of The Brain
Major Blood Vessels Of The Brain
Control Centers of the Brain
Cellular Injury During Ischemia
Neuronal Function: Importance of Oxygen and Glucose

The transient change in


voltage induced by the
action potential is
determined by the
concentration of ions on
either side of the cell
membrane. Maintaining
these ionic gradients is an
energy-consuming process
that requires a constant
supply of glucose and
oxygen to the neuron.

Cellular Changes As Ischemia Progresses

The duration, severity, and location of focal cerebral ischemia


determine the extent of brain function and thus the severity of
stroke
Cellular Injury During Ischemia
Inadequate Energy Supply Lack of glucose and
oxygen deplete the
cellular energy stores
required to maintain
electrical potentials and
ion gradients.

The membrane that


surrounds each affected
neuron becomes "leaky,"
and the cell loses
potassium and
adenosine triphosphate
(ATP), the tissue's
medium for energy
exchange
THE ISCHEMIC PENUMBRA
Stroke Warning Signs

Sudden weakness, paralysis, or numbness of the face, arm


and the leg on one or both sides of the body

Loss of speech, or difficulty speaking or understanding


speech

Dimness or loss of vision, particularly in only one eye

Unexplained dizziness (especially when associated with


other neurologic symptoms), unsteadiness, or sudden falls

Sudden severe headache and/or loss of consciousness


Left & Right Hemispheric
Stroke: Common Patterns
Middle Cerebral Artery (MCA): supplies the
lateral surface of hemisphere except for:
1. frontal lobe
2. strip along superomedial border of
frontal lobe
3. lowest temporal convolutions
Most frequently affected in embolic &
thrombotic stroke
Left and Right Hemisphere Stroke: Common Patterns

Left (Dominant) Hemisphere Right (Non-dominant)


Stroke: Common Pattern Hemisphere Stroke: Common
Pattern

Aphasia Neglect of left visual field


Right hemiparesis Extinction of left-sided
stimuli
Right-sided sensory loss
Left hemiparesis
Right visual field defect
Left-sided sensory loss
Poor right conjugate gaze
Left visual field defect
Dysarthria Poor left conjugate gaze
Difficulty reading, writing, Dysarthria
or calculating Spatial disorientation
Posterior Circulation (Vertebrobasilar
Territory) Stroke

Ataxia, gait abnormalities


Diplopia, oscillopsia, nystagmus,
dysconjugate eye movements
Nausea & vomiting (center is in area post-
rema)
Crossed hemiparesis, hemisensory deficits
Headache more common
Differential Diagnosis of Stroke

Craniocerebral / cervical trauma


Meningitis/encephalitis
Intracranial mass
Tumor
Subdural hematoma
Seizure with persistent neurological signs
Migraine with persistent neurological signs
Metabolic
Hyperglycemia
Hypoglycemia
Post-cardiac arrest ischemia
Drug/narcotic overdose
AHA Stroke Council Recommended Assessment of a
Person with Suspected Stroke

EMS should be instructed in the rapid recognition,


evaluation, treatment and transport
Baseline assessment within minutes, CT scan ASAP; use
National Institutes of Health Stroke Scale (NIHSS)
AHA Stroke Council Recommended Assessment of a
Person with Suspected Stroke

EMS should be instructed in the rapid recognition,


evaluation, treatment and transport
Baseline assessment within minutes, CT scan ASAP; use
National Institutes of Health Stroke Scale (NIHSS)

Immediate evaluation of the following:


1. Airway
2. Vital signs
3. General medical assessment (including
evidence of injury, cardiovascular
abnormalities)
4. Neurological assessment (frequent)
EVALUATION AND WORK-UP

History and PE
Computed Tomography (CT) scan of the
head
12-lead EKG, chest X-ray
Complete blood count, PT, PTT
Chemistries (sodium, phosphate, glucose
abnormalities may mimic stroke)
Urine and serum toxicology (drugs and
alcohol)
Under special circumstances, the following
tests may be required:

Cervical spine x-ray


Arterial blood gas
Lumbar puncture
Electroencephalogram (EEG)
Other Neuroimaging Techniques
& Ancillary Tests

Magnetic Resonance Imaging (MRI)


Diffusion Weighted Imaging (DWI),
Magnetic Resonance Angiography
(MRA)
Ultrasound (Carotid Duplex,
Transcranial Doppler, 2-D echo)
Conventional Angiography
Single Photon Emission Computed
Tomography (SPECT)
Positron Emission Tomography
Computed Tomography
Carotid Duplex
Transcranial Doppler
Cerebral Angiography
Functional abnormality
demonstrated with
PET exceeds that seen
with structural imaging
techniques such as X-
ray, CT, or MRI and is
more representative
depiction of the
underlying functional
state of the brain.
SPECT and Xenon Contrast CT
EMERGENT SUPPORTIVE CARE OF ACUTE STROKE PATIENT

Maintenance of adequate tissue oxygenation:


protecting the airway, O2 inhalation
Maintaining optimal blood pressure
(autoregulation faulty or lost in stroke
patients)
STROKE MANAGEMENT
EMERGENT SUPPORTIVE CARE OF ACUTE STROKE PATIENT

Management of blood glucose abnormalities


(hyperglycemia associated with poorer
prognosis)
Management of fever and infections
(ischemia worsened by hyperthermia,
improved by hypothermia
IV TPA (< 3hours)
IA fibrinolysis (< 6 hours)
IA MERCI retriever < 8 hours
Endovascular temperature control
Acute Stroke Treatment

Intravenous recombinant tissue plasminogen


activator (TPA): within 3 hours of stroke
symptom onset
Intraarterial TPA: within 6 hours; MCA territory
stroke by angiography
The Merci Retrieval System
Hypothermia For Acute Stroke:
Intravascular Cooling
Physiologic Effects Of Various
Levels Of Hypothermia
Known Factors That Cause Stroke Progression

Hypotension
Hyperglycemia
Hyperthermia
Infection
Cerebral hypoperfusion
Brain Edema
TREATMENT OF BRAIN SWELLING
Cerebral perfusion pressure =MAP-ICP

Fluid Restriction (1200 ml /day/m2)


Controlled hyperventilation: 25 mm Hg
Mannitol, 0.25 mg/kg IV over 20 minutes; repeat
PRN, serum osmolality maintained in the range
of 300-320mOsm/l
Barbiturate coma, with ICP monitoring
(subarachnoid bolt, IV catheter or Camino
catheter): maintain CPP greater than 50 mmHg;
pentobarbital serum level of 2-4 mg/dl
Surgery (wait 2 weeks)
Management of Cerebral Edema, Increased
Intracranial Pressure and Hydrocephalus
Brain edema peaks at 3-5 days
Treatment includes:
1. hyperventilation (lower PCO2)
2. osmotic diuretics
3. drainage of CSF (ventriculostomy)
4. surgery (lobectomy)
Neuroprotective Agents

Several trials going on


So far, trial on one free-radical scavenger
showed positive results
Phase II trials have proven beneficial; Phase III
(human efficacy trials) non-benefial to
negative
Common measures may neuroprotect
Stroke Prevention

Anticoagulants (Heparin, Warfarin)


Antiplatelets (aspirin, clopidogrel
dipyridamole/ASA combination,
ticlopidine)
Statin
ARB (-sartan), or ACE inhibitor + HCTZ
Carotid endarterectomy if indicated
Carotid or intracranial stent.
Risk factor control!!!
Concept of Stroke Teams &
Stroke Units
Time is brain
Stroke awareness
Common mistakes may
lead to fatal
consequences
Boutique stroke
neurology: Patients
will receive best care;
length of stay
shortened
THANK YOU!

You might also like