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About This Presentation
neuro
Slide Content
Cerebrovascular Cerebrovascular
DiseasesDiseases
Alina Valdes, M.D.
DiseasesDiseases
Alina Valdes, M.D.
Stroke - Background
•Symptoms begin abruptlySymptoms begin abruptly
–Inadequate blood flow
•Ischemic stroke
–Focal – thrombotic or embolic occlusion
of major artery
–Global – inadequate cerebral perfusion
–Hemorrhage
•Parenchymal – into brain tissue
•Subarachnoid – surrounding
subarachnoid space
•Approximately 80% are Approximately 80% are
ischemic in originischemic in origin
•Symptoms begin abruptlySymptoms begin abruptly
–Inadequate blood flow
•Ischemic stroke
–Focal – thrombotic or embolic occlusion
of major artery
–Global – inadequate cerebral perfusion
–Hemorrhage
•Parenchymal – into brain tissue
•Subarachnoid – surrounding
subarachnoid space
•Approximately 80% are Approximately 80% are
ischemic in originischemic in origin
•Third leading medical cause of Third leading medical cause of
death and second most frequent death and second most frequent
cause of morbidity in developed cause of morbidity in developed
countriescountries
•Rates similar among men and Rates similar among men and
womenwomen
•Incidence and rate of mortality Incidence and rate of mortality
higher in blacks than whiteshigher in blacks than whites
•Since 1990, incidence in U.S. has Since 1990, incidence in U.S. has
declined about 1.5%, probably as declined about 1.5%, probably as
result of improvements in general result of improvements in general
public health and decline of public health and decline of
cardiovascular deaths and better cardiovascular deaths and better
control of risk factorscontrol of risk factors
death and second most frequent death and second most frequent
cause of morbidity in developed cause of morbidity in developed
countriescountries
•Rates similar among men and Rates similar among men and
womenwomen
•Incidence and rate of mortality Incidence and rate of mortality
higher in blacks than whiteshigher in blacks than whites
•Since 1990, incidence in U.S. has Since 1990, incidence in U.S. has
declined about 1.5%, probably as declined about 1.5%, probably as
result of improvements in general result of improvements in general
public health and decline of public health and decline of
cardiovascular deaths and better cardiovascular deaths and better
control of risk factorscontrol of risk factors
Risk Factors for Ischemic
Strokes
•DiabetesDiabetes
•HypertensionHypertension
•SmokingSmoking
•Family history of premature vascular Family history of premature vascular
diseasedisease
•HyperlipidemiaHyperlipidemia
•Atrial fibrillationAtrial fibrillation
•History of transient ischemic attack History of transient ischemic attack (TIA)
•History of recent myocardial infarctionHistory of recent myocardial infarction
•History of congestive heart failure History of congestive heart failure (LV
ejection fraction < 25%)
•Drugs Drugs (sympathomimetics, oral contraceptive
pill, cocaine)
Strokes
•DiabetesDiabetes
•HypertensionHypertension
•SmokingSmoking
•Family history of premature vascular Family history of premature vascular
diseasedisease
•HyperlipidemiaHyperlipidemia
•Atrial fibrillationAtrial fibrillation
•History of transient ischemic attack History of transient ischemic attack (TIA)
•History of recent myocardial infarctionHistory of recent myocardial infarction
•History of congestive heart failure History of congestive heart failure (LV
ejection fraction < 25%)
•Drugs Drugs (sympathomimetics, oral contraceptive
pill, cocaine)
Cerebral Circulation
•Anterior CirculationAnterior Circulation
–Common carotid arteryCommon carotid artery bifurcates
into:
•External
•Internal
–Enters skull through carotid canal and
passes through cavernous sinus
–Gives off ophthalmic, anterior
choroidal, and posterior communicating
arteries
•Anterior CirculationAnterior Circulation
–Common carotid arteryCommon carotid artery bifurcates
into:
•External
•Internal
–Enters skull through carotid canal and
passes through cavernous sinus
–Gives off ophthalmic, anterior
choroidal, and posterior communicating
arteries
–Bifurcates into anterior
cerebral artery and middle
cerebral artery
»Anterior cerebral artery
supplies medial surfaces of
cerebral hemispheres
»Middle cerebral artery
supplies lateral surface,
basal ganglia, and
subcortical white matter
cerebral artery and middle
cerebral artery
»Anterior cerebral artery
supplies medial surfaces of
cerebral hemispheres
»Middle cerebral artery
supplies lateral surface,
basal ganglia, and
subcortical white matter
•Posterior CirculationPosterior Circulation
–Vertebral arteriesVertebral arteries go up within transverse
processes of cervical vertebrae
•Intracranial vertebral artery gives off:
–Anterior spinal artery
–Posterior inferior cerebellar artery
–Both Vertebral arteries then join to form:
•Basilar artery at pontomedullary
junction
–Supplies cerebellum via anterior
inferior cerebellar artery and superior
cerebellar artery
–Bifurcates into posterior cerebral
arteries at level of pontomesencephalic
junction
–Vertebral arteriesVertebral arteries go up within transverse
processes of cervical vertebrae
•Intracranial vertebral artery gives off:
–Anterior spinal artery
–Posterior inferior cerebellar artery
–Both Vertebral arteries then join to form:
•Basilar artery at pontomedullary
junction
–Supplies cerebellum via anterior
inferior cerebellar artery and superior
cerebellar artery
–Bifurcates into posterior cerebral
arteries at level of pontomesencephalic
junction
•Circle of WillisCircle of Willis
–Formed at base of brain by:
•Union of both anterior cerebral arteries
via the anterior communicating artery and
•Union of the middle cerebral artery with
the posterior cerebral artery via the
posterior communicating artery
–Allows communication between both
anterior circulations as well as between
posterior and anterior circulations on each
side
–Congenital anomalies frequent so may have
reduction of collateral blood supply if
adjacent vessel becomes occluded
–Formed at base of brain by:
•Union of both anterior cerebral arteries
via the anterior communicating artery and
•Union of the middle cerebral artery with
the posterior cerebral artery via the
posterior communicating artery
–Allows communication between both
anterior circulations as well as between
posterior and anterior circulations on each
side
–Congenital anomalies frequent so may have
reduction of collateral blood supply if
adjacent vessel becomes occluded
Physiology
•Brain has few energy storesBrain has few energy stores
•Relies on extensive and reliable cerebral Relies on extensive and reliable cerebral
blood flowblood flow
•Autoregulation: Autoregulation: maintains cerebral blood
flow at constant level despite wide variation in
cerebral perfusion pressure
•Cerebral blood flow remains relatively Cerebral blood flow remains relatively
constant when mean arterial pressure constant when mean arterial pressure
between 50 and 150 mm Hgbetween 50 and 150 mm Hg
•In chronic systemic hypertension, upper In chronic systemic hypertension, upper
and lower levels of autoregulation raised, and lower levels of autoregulation raised,
so have higher tolerance of hypertension so have higher tolerance of hypertension
but less to effects of hypotensionbut less to effects of hypotension
•Brain has few energy storesBrain has few energy stores
•Relies on extensive and reliable cerebral Relies on extensive and reliable cerebral
blood flowblood flow
•Autoregulation: Autoregulation: maintains cerebral blood
flow at constant level despite wide variation in
cerebral perfusion pressure
•Cerebral blood flow remains relatively Cerebral blood flow remains relatively
constant when mean arterial pressure constant when mean arterial pressure
between 50 and 150 mm Hgbetween 50 and 150 mm Hg
•In chronic systemic hypertension, upper In chronic systemic hypertension, upper
and lower levels of autoregulation raised, and lower levels of autoregulation raised,
so have higher tolerance of hypertension so have higher tolerance of hypertension
but less to effects of hypotensionbut less to effects of hypotension
Ischemic Stroke
•May result from:May result from:
–Thrombotic or embolic occlusion of major
vessel causing decreased blood blow to
supplied area
–Decreased systemic perfusion
•If ischemia prolonged, results in If ischemia prolonged, results in
infarction infarction (necrosis)
–“pale” infarct – anemic
–“hemorrhagic” infarct – in areas of
endothelial necrosis
•May result from:May result from:
–Thrombotic or embolic occlusion of major
vessel causing decreased blood blow to
supplied area
–Decreased systemic perfusion
•If ischemia prolonged, results in If ischemia prolonged, results in
infarction infarction (necrosis)
–“pale” infarct – anemic
–“hemorrhagic” infarct – in areas of
endothelial necrosis
•Ischemic penumbraIschemic penumbra
–Transition zone between normal and
infarcted central core
–Moderately ischemic tissue
–Target area for salvage
•Global cerebral ischemiaGlobal cerebral ischemia
–Usually results from cardiac arrest or
ventricular fibrillation
–Susceptible populations of neurons:
•Hippocampus
•Cerebellar Purkinje cells
•Deeper layers of cerebral cortex
(causing laminar necrosis)
–Transition zone between normal and
infarcted central core
–Moderately ischemic tissue
–Target area for salvage
•Global cerebral ischemiaGlobal cerebral ischemia
–Usually results from cardiac arrest or
ventricular fibrillation
–Susceptible populations of neurons:
•Hippocampus
•Cerebellar Purkinje cells
•Deeper layers of cerebral cortex
(causing laminar necrosis)
•Pure hypoxiaPure hypoxia
–Causes cerebral dysfunction
•Lethargy and confusion
–Rarely causes irreversible brain injury
•Hypoglycemia – exacerbates
–May be reversible if blood flow
restored within 15 minutes
–Causes cerebral dysfunction
•Lethargy and confusion
–Rarely causes irreversible brain injury
•Hypoglycemia – exacerbates
–May be reversible if blood flow
restored within 15 minutes
•Cerebral edemaCerebral edema
–Cytotoxic – intracellular
•Develops rapidly in ischemic neurons as
ion pumps fail
–Vasogenic – interstitial
•Occurs as damage to endothelial cells
disrupts blood-brain barrier and allows
macromolecules to enter interstitial space
–Can cause transtentorial herniation
and death due to increase brain fluid
content (as much as 10%) in 3 to 5
days
–Cytotoxic – intracellular
•Develops rapidly in ischemic neurons as
ion pumps fail
–Vasogenic – interstitial
•Occurs as damage to endothelial cells
disrupts blood-brain barrier and allows
macromolecules to enter interstitial space
–Can cause transtentorial herniation
and death due to increase brain fluid
content (as much as 10%) in 3 to 5
days
Causes of Acute Cerebral
Ischemia
•FocalFocal
–Mural abnormalities
•Atherosclerosis – approximately 2/3 of
strokes
–Embolization of plaque to distal vessels
(artery-to-artery)
–In situ thrombosis
•Vasculitis
•Vasospasm (migraine, subarachnoid
hemorrhage)
•Compression (by tumor, aneurysm)
•Fibromuscular dysplasia/Moyamoya
•Dissection (spontaneous, traumatic)
Ischemia
•FocalFocal
–Mural abnormalities
•Atherosclerosis – approximately 2/3 of
strokes
–Embolization of plaque to distal vessels
(artery-to-artery)
–In situ thrombosis
•Vasculitis
•Vasospasm (migraine, subarachnoid
hemorrhage)
•Compression (by tumor, aneurysm)
•Fibromuscular dysplasia/Moyamoya
•Dissection (spontaneous, traumatic)
–Embolism
•Cardiogenic (atrial fibrillation,
mural thrombus, myxoma, valvular
vegetations) – majority of remaining
1/3
•Artery-to-artery
•Fat
•Air
•Paradoxical (emboli of venous origin
passing through a patent foramen
ovale)
•Cardiogenic (atrial fibrillation,
mural thrombus, myxoma, valvular
vegetations) – majority of remaining
1/3
•Artery-to-artery
•Fat
•Air
•Paradoxical (emboli of venous origin
passing through a patent foramen
ovale)
–Hematologic
•Hypercoagulable state
•Sickle cell disease
•Homocystinuria
•Antiphospholipid antibodies (lupus
anticoagulant, anticardiolipin
antibodies)
•Protein C or protein S deficiency
•Hypercoagulable state
•Sickle cell disease
•Homocystinuria
•Antiphospholipid antibodies (lupus
anticoagulant, anticardiolipin
antibodies)
•Protein C or protein S deficiency
•GlobalGlobal
–Hypoperfusion
•Cardiac arrest
•Ventricular fibrillation
–Hypoperfusion
•Cardiac arrest
•Ventricular fibrillation
Transient Ischemic Attack
(TIA)
•Transient neurologic deficit due Transient neurologic deficit due
to reduced blood flowto reduced blood flow
•Lasting less than 24 hours – Lasting less than 24 hours –
most resolve within 1 hourmost resolve within 1 hour
•Full functional recoveryFull functional recovery
(TIA)
•Transient neurologic deficit due Transient neurologic deficit due
to reduced blood flowto reduced blood flow
•Lasting less than 24 hours – Lasting less than 24 hours –
most resolve within 1 hourmost resolve within 1 hour
•Full functional recoveryFull functional recovery
Stroke - Classes
•Completed strokeCompleted stroke
–Infarction has happened
–Usually have maximal clinical deficit at time
of symptoms
–Variable recovery over time
•Stroke in evolutionStroke in evolution
–Symptom progression
–Propagation of thrombus or worsening
cerebral edema or hemorrhage into
infarcted area
–Coexistent medical conditions may
adversely affect outcome
•Completed strokeCompleted stroke
–Infarction has happened
–Usually have maximal clinical deficit at time
of symptoms
–Variable recovery over time
•Stroke in evolutionStroke in evolution
–Symptom progression
–Propagation of thrombus or worsening
cerebral edema or hemorrhage into
infarcted area
–Coexistent medical conditions may
adversely affect outcome
•Lacunar strokeLacunar stroke
–Small, deep infarction involving penetrating
branch of large cerebral artery
–Usually associated with chronic
hypertension
–In normotensive patients, probably result of
microatheroma of penetrating arteries,
especially of basal ganglia, thalamus, and
white matter of internal capsule and pons
•RINDRIND
–Neuro deficit > 24 hours but reverses
within 3 weeks
–Small, deep infarction involving penetrating
branch of large cerebral artery
–Usually associated with chronic
hypertension
–In normotensive patients, probably result of
microatheroma of penetrating arteries,
especially of basal ganglia, thalamus, and
white matter of internal capsule and pons
•RINDRIND
–Neuro deficit > 24 hours but reverses
within 3 weeks
Clinical Presentations of
Acute Stroke
•Alteration in ConsciousnessAlteration in Consciousness
–Stupor or Coma
–Confusion or agitation/memory loss
–Seizures
–Delirium
•HeadacheHeadache
–Intense or unusually severe
–Associated with decreased level of
consciousness/neurological deficit
–Unusual/severe neck or facial pain
Acute Stroke
•Alteration in ConsciousnessAlteration in Consciousness
–Stupor or Coma
–Confusion or agitation/memory loss
–Seizures
–Delirium
•HeadacheHeadache
–Intense or unusually severe
–Associated with decreased level of
consciousness/neurological deficit
–Unusual/severe neck or facial pain
•Aphasia Aphasia (incoherent speech or difficulty
understanding speech)
•Facial weakness or asymmetryFacial weakness or asymmetry
–Paralysis of facial muscles (e.g., when
patients speaks or smiles)
–May be on same side (ipsilateral) or
opposite side contralateral to limb paralysis
•Incoordination, weakness, Incoordination, weakness,
paralysis, or sensory loss of one or paralysis, or sensory loss of one or
more limbs more limbs (usually one half of the
body and in particular the hand)
understanding speech)
•Facial weakness or asymmetryFacial weakness or asymmetry
–Paralysis of facial muscles (e.g., when
patients speaks or smiles)
–May be on same side (ipsilateral) or
opposite side contralateral to limb paralysis
•Incoordination, weakness, Incoordination, weakness,
paralysis, or sensory loss of one or paralysis, or sensory loss of one or
more limbs more limbs (usually one half of the
body and in particular the hand)
•Ataxia Ataxia (poor balance, clumsiness, or
difficulty walking)
•Visual lossVisual loss
–Monocular or binocular
–May be partial loss of the field
•Intensive vertigo, double vision, Intensive vertigo, double vision,
unilateral hearing loss, nausea, unilateral hearing loss, nausea,
vomiting, photophobia, or vomiting, photophobia, or
phonophobiaphonophobia
difficulty walking)
•Visual lossVisual loss
–Monocular or binocular
–May be partial loss of the field
•Intensive vertigo, double vision, Intensive vertigo, double vision,
unilateral hearing loss, nausea, unilateral hearing loss, nausea,
vomiting, photophobia, or vomiting, photophobia, or
phonophobiaphonophobia
Left (Dominant)
Hemisphere Stroke:
Common Pattern
•AphasiaAphasia
•Right hemiparesisRight hemiparesis
•Right-sided sensory lossRight-sided sensory loss
•Right visual field defectRight visual field defect
•Poor right conjugate gazePoor right conjugate gaze
•DysarthriaDysarthria
•Difficulty reading, writing, or Difficulty reading, writing, or
calculatingcalculating
Hemisphere Stroke:
Common Pattern
•AphasiaAphasia
•Right hemiparesisRight hemiparesis
•Right-sided sensory lossRight-sided sensory loss
•Right visual field defectRight visual field defect
•Poor right conjugate gazePoor right conjugate gaze
•DysarthriaDysarthria
•Difficulty reading, writing, or Difficulty reading, writing, or
calculatingcalculating
Right (Non-dominant)
Hemisphere Stroke:
Common Pattern
•Neglect of left visual fieldNeglect of left visual field
•Extinction of left-sided stimuliExtinction of left-sided stimuli
•Left hemiparesisLeft hemiparesis
•Left-sided sensory lossLeft-sided sensory loss
•Left visual field defectLeft visual field defect
•Poor left conjugate gazePoor left conjugate gaze
•DysarthriaDysarthria
•Spatial disorientationSpatial disorientation
Hemisphere Stroke:
Common Pattern
•Neglect of left visual fieldNeglect of left visual field
•Extinction of left-sided stimuliExtinction of left-sided stimuli
•Left hemiparesisLeft hemiparesis
•Left-sided sensory lossLeft-sided sensory loss
•Left visual field defectLeft visual field defect
•Poor left conjugate gazePoor left conjugate gaze
•DysarthriaDysarthria
•Spatial disorientationSpatial disorientation
Brain Stem / Cerebellum /
Posterior Hemisphere Stroke:
Common Pattern
•Motor or sensory loss in all four limbsMotor or sensory loss in all four limbs
•Crossed signsCrossed signs
•Limb or gait ataxiaLimb or gait ataxia
•DysarthriaDysarthria
•Dysconjugate gazeDysconjugate gaze
•NystagmusNystagmus
•AmnesiaAmnesia
•Bilateral visual field defectsBilateral visual field defects
Posterior Hemisphere Stroke:
Common Pattern
•Motor or sensory loss in all four limbsMotor or sensory loss in all four limbs
•Crossed signsCrossed signs
•Limb or gait ataxiaLimb or gait ataxia
•DysarthriaDysarthria
•Dysconjugate gazeDysconjugate gaze
•NystagmusNystagmus
•AmnesiaAmnesia
•Bilateral visual field defectsBilateral visual field defects
Small Subcortical Small Subcortical
Hemisphere or Brain Stem Hemisphere or Brain Stem
Stroke: Common PatternStroke: Common Pattern
•Pure MotorPure Motor
–Weakness of face and limbs on one side of the body
without abnormalities of higher brain function,
sensation, or vision
•Pure SensoryPure Sensory
–Decreased sensation of face and limbs on one side
of the body without abnormalities of higher brain
function, motor function, or vision
Hemisphere or Brain Stem Hemisphere or Brain Stem
Stroke: Common PatternStroke: Common Pattern
•Pure MotorPure Motor
–Weakness of face and limbs on one side of the body
without abnormalities of higher brain function,
sensation, or vision
•Pure SensoryPure Sensory
–Decreased sensation of face and limbs on one side
of the body without abnormalities of higher brain
function, motor function, or vision
Differential Diagnosis of Differential Diagnosis of
StrokeStroke
•Ischemic stroke/ Hemorrhagic strokeIschemic stroke/ Hemorrhagic stroke
•TIATIA
•RINDRIND
•Craniocerebral / cervical traumaCraniocerebral / cervical trauma
•Meningitis/encephalitisMeningitis/encephalitis
•Intracranial massIntracranial mass
–Tumor
–Subdural hematoma
•Seizure with persistent neurological signsSeizure with persistent neurological signs
–Vs. Todd’s paralysis – transient hemiparesis
StrokeStroke
•Ischemic stroke/ Hemorrhagic strokeIschemic stroke/ Hemorrhagic stroke
•TIATIA
•RINDRIND
•Craniocerebral / cervical traumaCraniocerebral / cervical trauma
•Meningitis/encephalitisMeningitis/encephalitis
•Intracranial massIntracranial mass
–Tumor
–Subdural hematoma
•Seizure with persistent neurological signsSeizure with persistent neurological signs
–Vs. Todd’s paralysis – transient hemiparesis
•Migraine with persistent Migraine with persistent
neurological signsneurological signs
–Vs. hemiplegic migraine – weakness
contralateral to side of headache
•MetabolicMetabolic
–Hyperglycemia (nonketotic
hyperosmolar coma)
–Hypoglycemia
–Post-cardiac arrest ischemia
–Drug/narcotic overdose
neurological signsneurological signs
–Vs. hemiplegic migraine – weakness
contralateral to side of headache
•MetabolicMetabolic
–Hyperglycemia (nonketotic
hyperosmolar coma)
–Hypoglycemia
–Post-cardiac arrest ischemia
–Drug/narcotic overdose
Tests for the Emergent Tests for the Emergent
Evaluation of the Patient Evaluation of the Patient
With Acute Ischemic StrokeWith Acute Ischemic Stroke
•CT of the brain without contrastCT of the brain without contrast
–Only 5% of acute ischemic strokes readily
visible in first 24 hours
•ElectrocardiogramElectrocardiogram
•Chest x-rayChest x-ray
Evaluation of the Patient Evaluation of the Patient
With Acute Ischemic StrokeWith Acute Ischemic Stroke
•CT of the brain without contrastCT of the brain without contrast
–Only 5% of acute ischemic strokes readily
visible in first 24 hours
•ElectrocardiogramElectrocardiogram
•Chest x-rayChest x-ray
•Hematologic studiesHematologic studies (complete blood
count, platelet count, prothrombin time,
partial thromboplastin time)
•Lipid profileLipid profile
•Sed rateSed rate
•Serum electrolytesSerum electrolytes
•Blood glucoseBlood glucose
•Renal and hepatic chemical analysesRenal and hepatic chemical analyses
•National Institutes of Health Scale National Institutes of Health Scale
(NIHSS) score score
count, platelet count, prothrombin time,
partial thromboplastin time)
•Lipid profileLipid profile
•Sed rateSed rate
•Serum electrolytesSerum electrolytes
•Blood glucoseBlood glucose
•Renal and hepatic chemical analysesRenal and hepatic chemical analyses
•National Institutes of Health Scale National Institutes of Health Scale
(NIHSS) score score
The NIH Stroke ScaleThe NIH Stroke Scale
•Administer stroke scale items in the order
listed. Record performance in each category
after each subscale exam. Do not go back and
change scores. Follow directions provided for
each exam technique. Scores should reflect
what the patient does, not what the clinician
thinks the patient can do. The clinician should
record answers while administering the exam
and work quickly. Except where indicated, the
patient should not be coached (i.e., repeated
requests to patient to make a special effort).
•Administer stroke scale items in the order
listed. Record performance in each category
after each subscale exam. Do not go back and
change scores. Follow directions provided for
each exam technique. Scores should reflect
what the patient does, not what the clinician
thinks the patient can do. The clinician should
record answers while administering the exam
and work quickly. Except where indicated, the
patient should not be coached (i.e., repeated
requests to patient to make a special effort).
IF ANY ITEM IS LEFT UNTESTED, A DETAILED EXPLANATION MUST BE CLEARLY IF ANY ITEM IS LEFT UNTESTED, A DETAILED EXPLANATION MUST BE CLEARLY
WRITTEN ON THE FORM. ALL UNTESTED ITEMS WILL BE REVIEWED BY THE WRITTEN ON THE FORM. ALL UNTESTED ITEMS WILL BE REVIEWED BY THE
MEDICAL MONITOR, AND DISCUSSED WITH THE EXAMINER BY TELEPHONE.MEDICAL MONITOR, AND DISCUSSED WITH THE EXAMINER BY TELEPHONE.
Instructions
Scale Definition Score
1a. Level of Consciousness: The investigator
must choose a response, even if a full
evaluation is prevented by such obstacles as
an endotracheal tube, language barrier,
orotracheal trauma/bandages. A 3 is scored
only if the patient makes no movement (other
than reflexive posturing) in response to
noxious stimulation.
•0 = Alert; keenly responsive.
•1 = Not alert, but arousable by
minor stimulation to obey, answer,
or respond.
•2 = Not alert, requires repeated
stimulation to attend, or is obtunded
and requires strong or painful
stimulation to make movements
(not stereotyped).
•3 = Responds only with reflex
motor or autonomic effects or totally
unresponsive, flaccid, areflexic.
____
WRITTEN ON THE FORM. ALL UNTESTED ITEMS WILL BE REVIEWED BY THE WRITTEN ON THE FORM. ALL UNTESTED ITEMS WILL BE REVIEWED BY THE
MEDICAL MONITOR, AND DISCUSSED WITH THE EXAMINER BY TELEPHONE.MEDICAL MONITOR, AND DISCUSSED WITH THE EXAMINER BY TELEPHONE.
Instructions
Scale Definition Score
1a. Level of Consciousness: The investigator
must choose a response, even if a full
evaluation is prevented by such obstacles as
an endotracheal tube, language barrier,
orotracheal trauma/bandages. A 3 is scored
only if the patient makes no movement (other
than reflexive posturing) in response to
noxious stimulation.
•0 = Alert; keenly responsive.
•1 = Not alert, but arousable by
minor stimulation to obey, answer,
or respond.
•2 = Not alert, requires repeated
stimulation to attend, or is obtunded
and requires strong or painful
stimulation to make movements
(not stereotyped).
•3 = Responds only with reflex
motor or autonomic effects or totally
unresponsive, flaccid, areflexic.
____
1b. LOC Questions: The patient is asked the
month and his/her age. The answer must be
correct - there is no partial credit for being close.
Aphasic and stuporous patients who do not
comprehend the questions will score 2. Patients
unable to speak because of endotracheal
intubation, orotracheal trauma, severe dysarthria
from any cause, language barrier or any other
problem not secondary to aphasia are given a 1.
It is important that only the initial answer be
graded and that the examiner not "help" the
patient with verbal or non-verbal cues.
• 0 = Answers both questions
correctly.
•1 = Answers one question
correctly.
•
•2 = Answers neither question
correctly.
____
1c. LOC Commands: The patient is asked to open
and close the eyes and then to grip and release
the non-paretic hand. Substitute another one step
command if the hands cannot be used. Credit is
given if an unequivocal attempt is made but not
completed due to weakness. If the patient does
not respond to command, the task should be
demonstrated to them (pantomime) and score
the result (i.e., follows none, one or two
commands). Patients with trauma, amputation, or
other physical impediments should be given
suitable one-step commands. Only the first
attempt is scored.
•0 = Performs both tasks
correctly
•
•1 = Performs one task correctly
•
•2 = Performs neither task
correctly
____
month and his/her age. The answer must be
correct - there is no partial credit for being close.
Aphasic and stuporous patients who do not
comprehend the questions will score 2. Patients
unable to speak because of endotracheal
intubation, orotracheal trauma, severe dysarthria
from any cause, language barrier or any other
problem not secondary to aphasia are given a 1.
It is important that only the initial answer be
graded and that the examiner not "help" the
patient with verbal or non-verbal cues.
• 0 = Answers both questions
correctly.
•1 = Answers one question
correctly.
•
•2 = Answers neither question
correctly.
____
1c. LOC Commands: The patient is asked to open
and close the eyes and then to grip and release
the non-paretic hand. Substitute another one step
command if the hands cannot be used. Credit is
given if an unequivocal attempt is made but not
completed due to weakness. If the patient does
not respond to command, the task should be
demonstrated to them (pantomime) and score
the result (i.e., follows none, one or two
commands). Patients with trauma, amputation, or
other physical impediments should be given
suitable one-step commands. Only the first
attempt is scored.
•0 = Performs both tasks
correctly
•
•1 = Performs one task correctly
•
•2 = Performs neither task
correctly
____
2. Best Gaze: Only horizontal eye movements will
be tested. Voluntary or reflexive (oculocephalic)
eye movements will be scored but caloric testing
is not done. If the patient has a conjugate
deviation of the eyes that can be overcome by
voluntary or reflexive activity, the score will be 1.
If a patient has an isolated peripheral nerve
paresis (CN III, IV or VI) score a 1. Gaze is
testable in all aphasic patients. Patients with
ocular trauma, bandages, pre-existing blindness
or other disorder of visual acuity or fields should
be tested with reflexive movements and a choice
made by the investigator. Establishing eye contact
and then moving about the patient from side to
side will occasionally clarify the presence of a
partial gaze palsy.
•0 = Normal
•
•1 = Partial gaze palsy. This
score is given when gaze is
abnormal in one or both eyes,
but where forced deviation or
total gaze paresis are not
present.
•
•2 = Forced deviation, or total
gaze paresis not overcome by
the oculocephalic maneuver.
____
be tested. Voluntary or reflexive (oculocephalic)
eye movements will be scored but caloric testing
is not done. If the patient has a conjugate
deviation of the eyes that can be overcome by
voluntary or reflexive activity, the score will be 1.
If a patient has an isolated peripheral nerve
paresis (CN III, IV or VI) score a 1. Gaze is
testable in all aphasic patients. Patients with
ocular trauma, bandages, pre-existing blindness
or other disorder of visual acuity or fields should
be tested with reflexive movements and a choice
made by the investigator. Establishing eye contact
and then moving about the patient from side to
side will occasionally clarify the presence of a
partial gaze palsy.
•0 = Normal
•
•1 = Partial gaze palsy. This
score is given when gaze is
abnormal in one or both eyes,
but where forced deviation or
total gaze paresis are not
present.
•
•2 = Forced deviation, or total
gaze paresis not overcome by
the oculocephalic maneuver.
____
3. Visual: Visual fields (upper and lower
quadrants) are tested by confrontation, using
finger counting or visual threat as appropriate.
Patient must be encouraged, but if they look at
the side of the moving fingers appropriately,
this can be scored as normal. If there is
unilateral blindness or enucleation, visual fields
in the remaining eye are scored. Score 1 only if
a clear-cut asymmetry, including
quadrantanopia is found. If patient is blind from
any cause score 3. Double simultaneous
stimulation is performed at this point. If there is
extinction patient receives a 1 and the results
are used to answer question 11.
•0 = No visual loss
•
•1 = Partial hemianopia
•
•2 = Complete hemianopia
•
•3 = Bilateral hemianopia (blind
including cortical blindness)
____
4. Facial Palsy: Ask, or use pantomime to
encourage the patient to show teeth or raise
eyebrows and close eyes. Score symmetry of
grimace in response to noxious stimuli in the
poorly responsive or non-comprehending
patient. If facial trauma/bandages, orotracheal
tube, tape or other physical barrier obscures the
face, these should be removed to the extent
possible.
•0 = Normal symmetrical
movement
•1 = Minor paralysis (flattened
nasolabial fold, asymmetry on
smiling)
•2 = Partial paralysis (total or near
total paralysis of lower face)
•3 = Complete paralysis of one or
both sides (absence of facial
movement in the upper and lower
face)
____
quadrants) are tested by confrontation, using
finger counting or visual threat as appropriate.
Patient must be encouraged, but if they look at
the side of the moving fingers appropriately,
this can be scored as normal. If there is
unilateral blindness or enucleation, visual fields
in the remaining eye are scored. Score 1 only if
a clear-cut asymmetry, including
quadrantanopia is found. If patient is blind from
any cause score 3. Double simultaneous
stimulation is performed at this point. If there is
extinction patient receives a 1 and the results
are used to answer question 11.
•0 = No visual loss
•
•1 = Partial hemianopia
•
•2 = Complete hemianopia
•
•3 = Bilateral hemianopia (blind
including cortical blindness)
____
4. Facial Palsy: Ask, or use pantomime to
encourage the patient to show teeth or raise
eyebrows and close eyes. Score symmetry of
grimace in response to noxious stimuli in the
poorly responsive or non-comprehending
patient. If facial trauma/bandages, orotracheal
tube, tape or other physical barrier obscures the
face, these should be removed to the extent
possible.
•0 = Normal symmetrical
movement
•1 = Minor paralysis (flattened
nasolabial fold, asymmetry on
smiling)
•2 = Partial paralysis (total or near
total paralysis of lower face)
•3 = Complete paralysis of one or
both sides (absence of facial
movement in the upper and lower
face)
____
5 & 6. Motor Arm and Leg: The limb is placed
in the appropriate position: extend the arms
(palms down) 90 degrees (if sitting) or 45
degrees (if supine) and the leg 30 degrees
(always tested supine). Drift is scored if the
arm falls before 10 seconds or the leg before 5
seconds. The aphasic patient is encouraged
using urgency in the voice and pantomime but
not noxious stimulation. Each limb is tested in
turn, beginning with the non-paretic arm. Only
in the case of amputation or joint fusion at the
shoulder or hip may the score be "9" and the
examiner must clearly write the explanation for
scoring as a "9".
•0 = No drift, limb holds 90 (or 45)
degrees for full 10 seconds.
•1 = Drift, Limb holds 90 (or 45) degrees,
but drifts down before full 10 seconds;
does not hit bed or other support.
•2 = Some effort against gravity, limb
cannot get to or maintain (if cued) 90 (or
45) degrees, drifts down to bed, but has
some effort against gravity.
•3 = No effort against gravity, limb falls.
•4 = No movement
9 = Amputation, joint fusion explain:
______________________
•5a. Left Arm
•5b. Right Arm
____
____
•0 = No drift, leg holds 30 degrees
position for full 5 seconds.
•1 = Drift, leg falls by the end of the 5
second period but does not hit bed.
•2 = Some effort against gravity; leg falls
to bed by 5 seconds, but has some effort
against gravity.
•3 = No effort against gravity, leg falls to
bed immediately.
•4 = No movement
•9 = Amputation, joint fusion
explain:_________________
•6a. Left Leg
•6b. Right Leg
____
____
in the appropriate position: extend the arms
(palms down) 90 degrees (if sitting) or 45
degrees (if supine) and the leg 30 degrees
(always tested supine). Drift is scored if the
arm falls before 10 seconds or the leg before 5
seconds. The aphasic patient is encouraged
using urgency in the voice and pantomime but
not noxious stimulation. Each limb is tested in
turn, beginning with the non-paretic arm. Only
in the case of amputation or joint fusion at the
shoulder or hip may the score be "9" and the
examiner must clearly write the explanation for
scoring as a "9".
•0 = No drift, limb holds 90 (or 45)
degrees for full 10 seconds.
•1 = Drift, Limb holds 90 (or 45) degrees,
but drifts down before full 10 seconds;
does not hit bed or other support.
•2 = Some effort against gravity, limb
cannot get to or maintain (if cued) 90 (or
45) degrees, drifts down to bed, but has
some effort against gravity.
•3 = No effort against gravity, limb falls.
•4 = No movement
9 = Amputation, joint fusion explain:
______________________
•5a. Left Arm
•5b. Right Arm
____
____
•0 = No drift, leg holds 30 degrees
position for full 5 seconds.
•1 = Drift, leg falls by the end of the 5
second period but does not hit bed.
•2 = Some effort against gravity; leg falls
to bed by 5 seconds, but has some effort
against gravity.
•3 = No effort against gravity, leg falls to
bed immediately.
•4 = No movement
•9 = Amputation, joint fusion
explain:_________________
•6a. Left Leg
•6b. Right Leg
____
____
7. Limb Ataxia: This item is aimed at finding evidence
of a unilateral cerebellar lesion. Test with eyes open. In
case of visual defect, insure testing is done in intact
visual field. The finger-nose-finger and heel-shin tests
are performed on both sides, and ataxia is scored only
if present out of proportion to weakness. Ataxia is
absent in the patient who cannot understand or is
paralyzed. Only in the case of amputation or joint
fusion may the item be scored "9", and the examiner
must clearly write the explanation for not scoring. In
case of blindness test by touching nose from extended
arm position.
•0 = Absent
•1 = Present in one limb
•2 = Present in two limbs
If present, is ataxia in
Right arm 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
Left arm 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
Right leg 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
Left leg 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
____
____
____
____
of a unilateral cerebellar lesion. Test with eyes open. In
case of visual defect, insure testing is done in intact
visual field. The finger-nose-finger and heel-shin tests
are performed on both sides, and ataxia is scored only
if present out of proportion to weakness. Ataxia is
absent in the patient who cannot understand or is
paralyzed. Only in the case of amputation or joint
fusion may the item be scored "9", and the examiner
must clearly write the explanation for not scoring. In
case of blindness test by touching nose from extended
arm position.
•0 = Absent
•1 = Present in one limb
•2 = Present in two limbs
If present, is ataxia in
Right arm 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
Left arm 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
Right leg 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
Left leg 1 = Yes 2 = No
9 = amputation or joint
fusion, explain
___________________
____
____
____
____
8. Sensory: Sensation or grimace to pin prick
when tested, or withdrawal from noxious
stimulus in the obtunded or aphasic patient.
Only sensory loss attributed to stroke is scored
as abnormal and the examiner should test as
many body areas [arms (not hands), legs,
trunk, face] as needed to accurately check for
hemisensory loss. A score of 2, "severe or
total," should only be given when a severe or
total loss of sensation can be clearly
demonstrated. Stuporous and aphasic patients
will therefore probably score 1 or 0. The patient
with brain stem stroke who has bilateral loss of
sensation is scored 2. If the patient does not
respond and is quadriplegic score 2. Patients in
coma (item 1a=3) are arbitrarily given a 2 on
this item.
•0 = Normal; no sensory loss.
•
•1 = Mild to moderate sensory
loss; patient feels pinprick is less
sharp or is dull on the affected
side; or there is a loss of superficial
pain with pinprick but patient is
aware he/she is being touched.
•
•2 = Severe to total sensory loss;
patient is not aware of being
touched in the face, arm, and leg.
____
when tested, or withdrawal from noxious
stimulus in the obtunded or aphasic patient.
Only sensory loss attributed to stroke is scored
as abnormal and the examiner should test as
many body areas [arms (not hands), legs,
trunk, face] as needed to accurately check for
hemisensory loss. A score of 2, "severe or
total," should only be given when a severe or
total loss of sensation can be clearly
demonstrated. Stuporous and aphasic patients
will therefore probably score 1 or 0. The patient
with brain stem stroke who has bilateral loss of
sensation is scored 2. If the patient does not
respond and is quadriplegic score 2. Patients in
coma (item 1a=3) are arbitrarily given a 2 on
this item.
•0 = Normal; no sensory loss.
•
•1 = Mild to moderate sensory
loss; patient feels pinprick is less
sharp or is dull on the affected
side; or there is a loss of superficial
pain with pinprick but patient is
aware he/she is being touched.
•
•2 = Severe to total sensory loss;
patient is not aware of being
touched in the face, arm, and leg.
____
9. Best Language: A great deal of
information about comprehension will be
obtained during the preceding sections of
the examination. The patient is asked to
describe what is happening in the attached
picture, to name the items on the attached
naming sheet, and to read from the
attached list of sentences. Comprehension is
judged from responses here as well as to all
of the commands in the preceding general
neurological exam. If visual loss interferes
with the tests, ask the patient to identify
objects placed in the hand, repeat, and
produce speech. The intubated patient
should be asked to write. The patient in
coma (question 1a=3) will arbitrarily score 3
on this item. The examiner must choose a
score in the patient with stupor or limited
cooperation but a score of 3 should be used
only if the patient is mute and follows no
one step commands .
•0 = No aphasia, normal
•
•1 = Mild to moderate aphasia; some
obvious loss of fluency or facility of
comprehension, without significant
limitation on ideas expressed or form
of expression. Reduction of speech
and/or comprehension, however,
makes conversation about provided
material difficult or impossible. For
example in conversation about
provided materials examiner can
identify picture or naming card from
patient's response.
•
•2 = Severe aphasia; all
communication is through fragmentary
expression; great need for inference,
questioning, and guessing by the
listener. Range of information that can
be exchanged is limited; listener
carries burden of communication.
Examiner cannot identify materials
provided from patient response.
•
•3 = Mute, global aphasia; no usable
speech or auditory comprehension.
____
information about comprehension will be
obtained during the preceding sections of
the examination. The patient is asked to
describe what is happening in the attached
picture, to name the items on the attached
naming sheet, and to read from the
attached list of sentences. Comprehension is
judged from responses here as well as to all
of the commands in the preceding general
neurological exam. If visual loss interferes
with the tests, ask the patient to identify
objects placed in the hand, repeat, and
produce speech. The intubated patient
should be asked to write. The patient in
coma (question 1a=3) will arbitrarily score 3
on this item. The examiner must choose a
score in the patient with stupor or limited
cooperation but a score of 3 should be used
only if the patient is mute and follows no
one step commands .
•0 = No aphasia, normal
•
•1 = Mild to moderate aphasia; some
obvious loss of fluency or facility of
comprehension, without significant
limitation on ideas expressed or form
of expression. Reduction of speech
and/or comprehension, however,
makes conversation about provided
material difficult or impossible. For
example in conversation about
provided materials examiner can
identify picture or naming card from
patient's response.
•
•2 = Severe aphasia; all
communication is through fragmentary
expression; great need for inference,
questioning, and guessing by the
listener. Range of information that can
be exchanged is limited; listener
carries burden of communication.
Examiner cannot identify materials
provided from patient response.
•
•3 = Mute, global aphasia; no usable
speech or auditory comprehension.
____
10. Dysarthria: If patient is thought to be normal
an adequate sample of speech must be obtained
by asking patient to read or repeat words from the
attached list. If the patient has severe aphasia, the
clarity of articulation of spontaneous speech can be
rated. Only if the patient is intubated or has other
physical barrier to producing speech, may the item
be scored "9", and the examiner must clearly write
an explanation for not scoring. Do not tell the
patient why he/she is being tested.
•0 = Normal
•1 = Mild to moderate; patient
slurs at least some words and,
at worst, can be understood with
some difficulty.
•2 = Severe; patient's speech is
so slurred as to be unintelligible
in the absence of or out of
proportion to any dysphasia, or
is mute/anarthric.
•9 = Intubated or other physical
barrier,
explain____________________
____
11. Extinction and Inattention (formerly Neglect):
Sufficient information to identify neglect may be
obtained during the prior testing. If the patient has
a severe visual loss preventing visual double
simultaneous stimulation, and the cutaneous
stimuli are normal, the score is normal. If the
patient has aphasia but does appear to attend to
both sides, the score is normal. The presence of
visual spatial neglect or anosagnosia may also be
taken as evidence of abnormality. Since the
abnormality is scored only if present, the item is
never untestable.
•0 = No abnormality.
•
•1 = Visual, tactile, auditory,
spatial, or personal inattention or
extinction to bilateral
simultaneous stimulation in one
of the sensory modalities.
•
•2 = Profound hemi-inattention
or hemi-inattention to more than
one modality. Does not
recognize own hand or orients to
only one side of space.
____
an adequate sample of speech must be obtained
by asking patient to read or repeat words from the
attached list. If the patient has severe aphasia, the
clarity of articulation of spontaneous speech can be
rated. Only if the patient is intubated or has other
physical barrier to producing speech, may the item
be scored "9", and the examiner must clearly write
an explanation for not scoring. Do not tell the
patient why he/she is being tested.
•0 = Normal
•1 = Mild to moderate; patient
slurs at least some words and,
at worst, can be understood with
some difficulty.
•2 = Severe; patient's speech is
so slurred as to be unintelligible
in the absence of or out of
proportion to any dysphasia, or
is mute/anarthric.
•9 = Intubated or other physical
barrier,
explain____________________
____
11. Extinction and Inattention (formerly Neglect):
Sufficient information to identify neglect may be
obtained during the prior testing. If the patient has
a severe visual loss preventing visual double
simultaneous stimulation, and the cutaneous
stimuli are normal, the score is normal. If the
patient has aphasia but does appear to attend to
both sides, the score is normal. The presence of
visual spatial neglect or anosagnosia may also be
taken as evidence of abnormality. Since the
abnormality is scored only if present, the item is
never untestable.
•0 = No abnormality.
•
•1 = Visual, tactile, auditory,
spatial, or personal inattention or
extinction to bilateral
simultaneous stimulation in one
of the sensory modalities.
•
•2 = Profound hemi-inattention
or hemi-inattention to more than
one modality. Does not
recognize own hand or orients to
only one side of space.
____
Additional item, not a part of the NIH Stroke
Scale score.
A. Distal Motor Function: The patient's hand is
held up at the forearm by the examiner and
patient is asked to extend his/her fingers as
much as possible. If the patient can't or doesn't
extend the fingers the examiner places the
fingers in full extension and observes for any
flexion movement for 5 seconds. The patient's
first attempts only are graded. Repetition of the
instructions or of the testing is prohibited.
•0 = Normal (No flexion after 5
seconds)
•
•1 = At least some extension after
5 seconds, but not fully extended.
Any movement of the fingers which
is not command is not scored.
•
•2 = No voluntary extension after 5
seconds. Movements of the fingers
at another time are not scored.
a. Left Arm
b. Right Arm
____
____
Scale score.
A. Distal Motor Function: The patient's hand is
held up at the forearm by the examiner and
patient is asked to extend his/her fingers as
much as possible. If the patient can't or doesn't
extend the fingers the examiner places the
fingers in full extension and observes for any
flexion movement for 5 seconds. The patient's
first attempts only are graded. Repetition of the
instructions or of the testing is prohibited.
•0 = Normal (No flexion after 5
seconds)
•
•1 = At least some extension after
5 seconds, but not fully extended.
Any movement of the fingers which
is not command is not scored.
•
•2 = No voluntary extension after 5
seconds. Movements of the fingers
at another time are not scored.
a. Left Arm
b. Right Arm
____
____
Primary Stroke PreventionPrimary Stroke Prevention
•Reduction of risk factorsReduction of risk factors
–Treat hypertension
–Stop smoking
–Treat diabetes
–Treat hyperlipidemia
•Reduction of risk factorsReduction of risk factors
–Treat hypertension
–Stop smoking
–Treat diabetes
–Treat hyperlipidemia
•Atrial fibrillationAtrial fibrillation
–Increases yearly risk of stroke 17-fold in
setting of valvular heart disease
–Anticoagulation with warfarin to INR of 2 to
3
–Treat with aspirin, 325 mg/day if
nonvalvular or no other risk factors
–Long-term anticoagulation if prosthetic
heart valve
–No warfarin if bacterial endocarditis due to
risk of cerebral hemorrhage from septic
embolization
–Increases yearly risk of stroke 17-fold in
setting of valvular heart disease
–Anticoagulation with warfarin to INR of 2 to
3
–Treat with aspirin, 325 mg/day if
nonvalvular or no other risk factors
–Long-term anticoagulation if prosthetic
heart valve
–No warfarin if bacterial endocarditis due to
risk of cerebral hemorrhage from septic
embolization
•Transient ischemic attackTransient ischemic attack
–Significant risk factor for recurrent stroke, with
average 5% risk per year
–Prophylactic antiplatelet therapy shown to prevent
secondary effects
•Aspirin
•Ticlopidine – Ticlid: thrombotic stroke reduction
•Clopidogrel – Plavix: reduce events associated
with atherosclerosis that include strokes, MI,
PVD
–Treat with warfarin if significant risk for cardiogenic
thromboembolism
–Hospital admission for new-onset and recurrent
TIA’s unless confident in diagnosis of etiology
–Angiography – treat medically or surgically
–Significant risk factor for recurrent stroke, with
average 5% risk per year
–Prophylactic antiplatelet therapy shown to prevent
secondary effects
•Aspirin
•Ticlopidine – Ticlid: thrombotic stroke reduction
•Clopidogrel – Plavix: reduce events associated
with atherosclerosis that include strokes, MI,
PVD
–Treat with warfarin if significant risk for cardiogenic
thromboembolism
–Hospital admission for new-onset and recurrent
TIA’s unless confident in diagnosis of etiology
–Angiography – treat medically or surgically
•Carotid stenosisCarotid stenosis
–Asymptomatic bruit or extracranial stenosis less
than 60%
•Treat with antiplatelet drugs
–Extracranial stenosis more than 70% (with or
without symptoms)
•Carotid endarterectomy
–Moderate asymptomatic stenosis (60%-70%)
•Medical versus surgical therapy
•Aortic arch thrombiAortic arch thrombi
–Detectable with transesophageal echocardiography
–Potential sources of emboli, especially if > 4 mm
in thickness
–Thick plaque independent predictor of recurrent
stroke
–Thrombectomy option for refractory disease
–Asymptomatic bruit or extracranial stenosis less
than 60%
•Treat with antiplatelet drugs
–Extracranial stenosis more than 70% (with or
without symptoms)
•Carotid endarterectomy
–Moderate asymptomatic stenosis (60%-70%)
•Medical versus surgical therapy
•Aortic arch thrombiAortic arch thrombi
–Detectable with transesophageal echocardiography
–Potential sources of emboli, especially if > 4 mm
in thickness
–Thick plaque independent predictor of recurrent
stroke
–Thrombectomy option for refractory disease
Management of Acute Management of Acute
StrokeStroke
•General measuresGeneral measures
–Reduce risk of complications from
immobility
•Pneumonia
•DVT
•UTI
–Physical, occupational, and speech therapy
–Evaluation of swallowing
–Treatment of HTN and DM
–Correction of dehydration
–Prevention and treatment of fever
–Poststroke depression
StrokeStroke
•General measuresGeneral measures
–Reduce risk of complications from
immobility
•Pneumonia
•DVT
•UTI
–Physical, occupational, and speech therapy
–Evaluation of swallowing
–Treatment of HTN and DM
–Correction of dehydration
–Prevention and treatment of fever
–Poststroke depression
•Use of anticoagulantsUse of anticoagulants
–Antiplatelet therapy remains treatment of choice to
prevent recurrent thromboembolism in majority of
patients
–Anticoagulation may be appropriate
•Atrial fibrillation
•Recent MI
•Suspected propagation of thrombus or stroke in
evolution
–Cranial CT needed to rule out intracerebral or
subarachnoid hemorrhage
–Baseline PT, PTT, platelet count, tests for
hypercoagulable states
–History of active peptic ulceration or uncontrolled
hypertension
–Antiplatelet therapy remains treatment of choice to
prevent recurrent thromboembolism in majority of
patients
–Anticoagulation may be appropriate
•Atrial fibrillation
•Recent MI
•Suspected propagation of thrombus or stroke in
evolution
–Cranial CT needed to rule out intracerebral or
subarachnoid hemorrhage
–Baseline PT, PTT, platelet count, tests for
hypercoagulable states
–History of active peptic ulceration or uncontrolled
hypertension
•Thrombolysis – t-PAThrombolysis – t-PA
–Guidelines for treatment:
•Present within 3 hours of onset of clearly
defined stroke – frequency of
symptomatic hemorrhage most likely
increases after this time
•CT scan shows no evidence of
intracranial hemorrhage
–No anticoagulants or antiplatelet
agents given for 24 hours
–Avoid BP values > defined above
–Guidelines for treatment:
•Present within 3 hours of onset of clearly
defined stroke – frequency of
symptomatic hemorrhage most likely
increases after this time
•CT scan shows no evidence of
intracranial hemorrhage
–No anticoagulants or antiplatelet
agents given for 24 hours
–Avoid BP values > defined above
–Guidelines not to treat:
•Previous stroke or serious head trauma in
preceding 3 months
•History of intracranial hemorrhage
•Repeated systolic BP’s > 185 mm Hg or
diastolic BP’s > 110 mm Hg
•Requires aggressive treatment to reduce
BP to specified limits
•Taking anticoagulants or propensity to
hemorrhage
•Recent invasive surgical procedure
•Rapidly improving neurological deficit or
minor symptoms
•Previous stroke or serious head trauma in
preceding 3 months
•History of intracranial hemorrhage
•Repeated systolic BP’s > 185 mm Hg or
diastolic BP’s > 110 mm Hg
•Requires aggressive treatment to reduce
BP to specified limits
•Taking anticoagulants or propensity to
hemorrhage
•Recent invasive surgical procedure
•Rapidly improving neurological deficit or
minor symptoms
–Statistically significant improvement in stroke scale
scores at 24 hours
–At 3 months following stroke, proportion of patients
with minimal or no disability was higher in treated
patients
–No significant differences in mortality between
treated and untreated
–No increase in number of patients given t-PA and
left with severe disability
–Treated patients more likely to sustain
symptomatic intracerebral hemorrhage within first
36 hours
•Tended to have severe neurologic deficits and
cerebral edema on CT
–Rate of asymptomatic intracerebral hemorrhage
similar among treated (8%) and control (6%)
scores at 24 hours
–At 3 months following stroke, proportion of patients
with minimal or no disability was higher in treated
patients
–No significant differences in mortality between
treated and untreated
–No increase in number of patients given t-PA and
left with severe disability
–Treated patients more likely to sustain
symptomatic intracerebral hemorrhage within first
36 hours
•Tended to have severe neurologic deficits and
cerebral edema on CT
–Rate of asymptomatic intracerebral hemorrhage
similar among treated (8%) and control (6%)
•Cerebral edemaCerebral edema
–Large hemispheric infarctions can
cause brain shift and transtentorial
herniation
–Intubation and hyperventilation
produce transient cerebral
vasoconstriction and may reduce
intracranial pressure
–Mannitol reduces volume surrounding
unaffected brain but also transient
–Corticosteroids no benefit in cytotoxic
edema
–Large hemispheric infarctions can
cause brain shift and transtentorial
herniation
–Intubation and hyperventilation
produce transient cerebral
vasoconstriction and may reduce
intracranial pressure
–Mannitol reduces volume surrounding
unaffected brain but also transient
–Corticosteroids no benefit in cytotoxic
edema
•Hypertensive encephalopathyHypertensive encephalopathy
–Diffuse cerebral effects of HTN not caused
by infarction or hemorrhage
–Potentially reversible with control of BP
–Headache, visual blurring, confusion, and
drowsiness
–May have seizures
–BP usually very high (250/150)
–Papilledema and retinal hemorrhages
usually seen on fundoscopy
–CT and MRI show diffuse cerebral edema,
especially in occipital lobes
–Medical emergency
–Prompt but controlled lowering of BP
avoiding hypotension
–Diffuse cerebral effects of HTN not caused
by infarction or hemorrhage
–Potentially reversible with control of BP
–Headache, visual blurring, confusion, and
drowsiness
–May have seizures
–BP usually very high (250/150)
–Papilledema and retinal hemorrhages
usually seen on fundoscopy
–CT and MRI show diffuse cerebral edema,
especially in occipital lobes
–Medical emergency
–Prompt but controlled lowering of BP
avoiding hypotension
Extensive right-sided Extensive right-sided
cerebral infarctioncerebral infarction (left
side of picture)
demonstrated by
unenhanced CT scan,
performed 4 days after the
onset of stroke. There is
no evidence of
hemorrhage. High-quality
CT scanners allow
diagnosis of cerebral
infarction within 6-8 hours
of onset.
cerebral infarctioncerebral infarction (left
side of picture)
demonstrated by
unenhanced CT scan,
performed 4 days after the
onset of stroke. There is
no evidence of
hemorrhage. High-quality
CT scanners allow
diagnosis of cerebral
infarction within 6-8 hours
of onset.
Cerebral embolismCerebral embolism in a
patient following cardiac
surgery, demonstrated by
unenhanced CT scan. The
open arrowhead points to
a high-density embolus
within the distal right
internal carotid artery;
the filled arrowhead
points to a similar
embolus in the right
middle cerebral artery.
There is extensive
hypodensity in the right
middle cerebral artery
distribution, reflecting an
extensive area of
infarction.
patient following cardiac
surgery, demonstrated by
unenhanced CT scan. The
open arrowhead points to
a high-density embolus
within the distal right
internal carotid artery;
the filled arrowhead
points to a similar
embolus in the right
middle cerebral artery.
There is extensive
hypodensity in the right
middle cerebral artery
distribution, reflecting an
extensive area of
infarction.
Right-sided facial palsy Right-sided facial palsy
resulting from stroke.resulting from stroke. The
patient also had right
hemiplegia and complete
aphasia. The signs are those
of upper motor neuron
lesion. The limbs are at first
flaccid and areflexic, but
after a variable period the
reflexes recover and become
exaggerated, and an
extensor plantar response
appears. Weakness in the
face and elsewhere may
recover gradually over a
variable period of time.
resulting from stroke.resulting from stroke. The
patient also had right
hemiplegia and complete
aphasia. The signs are those
of upper motor neuron
lesion. The limbs are at first
flaccid and areflexic, but
after a variable period the
reflexes recover and become
exaggerated, and an
extensor plantar response
appears. Weakness in the
face and elsewhere may
recover gradually over a
variable period of time.
Loss of postural stability Loss of postural stability
is common following is common following
stroke.stroke. When the non-
dominant hemisphere is
involved, walking apraxia
and loss of postural control
are usually apparent. The
patient is unable to sit
upright and tends to fall
sideways. Appropriate
support with pillows or
cushions should be
provided.
is common following is common following
stroke.stroke. When the non-
dominant hemisphere is
involved, walking apraxia
and loss of postural control
are usually apparent. The
patient is unable to sit
upright and tends to fall
sideways. Appropriate
support with pillows or
cushions should be
provided.
Intracerebral HemorrhageIntracerebral Hemorrhage
•Diffuse – subarachnoid hemorrhageDiffuse – subarachnoid hemorrhage
•Focal – intraparenchymalFocal – intraparenchymal
•Accounts for 20% of all strokesAccounts for 20% of all strokes
•Acute rise in intracranial pressure Acute rise in intracranial pressure
from arterial rupture frequently from arterial rupture frequently
results in LOC at outsetresults in LOC at outset
•Some patients die from herniationSome patients die from herniation
•Diffuse – subarachnoid hemorrhageDiffuse – subarachnoid hemorrhage
•Focal – intraparenchymalFocal – intraparenchymal
•Accounts for 20% of all strokesAccounts for 20% of all strokes
•Acute rise in intracranial pressure Acute rise in intracranial pressure
from arterial rupture frequently from arterial rupture frequently
results in LOC at outsetresults in LOC at outset
•Some patients die from herniationSome patients die from herniation
Causes of Spontaneous Causes of Spontaneous
Intracerebral Hemorrhage Intracerebral Hemorrhage
(ICH)(ICH)
•Intraparenchymal hemorrhageIntraparenchymal hemorrhage
–Trauma
–Hypertension
–Amyloid (congophilic) angiopathy
–Arteriovenous malformation
–Bleeding diathesis (anticoagulants, thrombolytics)
–Drugs (amphetamines, cocaine)
•Subarachnoid hemorrhageSubarachnoid hemorrhage
–Congenital saccular aneurysm (85%)
–Unknown (15%)
Intracerebral Hemorrhage Intracerebral Hemorrhage
(ICH)(ICH)
•Intraparenchymal hemorrhageIntraparenchymal hemorrhage
–Trauma
–Hypertension
–Amyloid (congophilic) angiopathy
–Arteriovenous malformation
–Bleeding diathesis (anticoagulants, thrombolytics)
–Drugs (amphetamines, cocaine)
•Subarachnoid hemorrhageSubarachnoid hemorrhage
–Congenital saccular aneurysm (85%)
–Unknown (15%)
Hypertensive intracerebral hemorrhage
•Often occurs at same sites affected by lacunar
infarctions
•Charcot-Bouchard aneurysms: microaneurysms
identified pathologically in some cases
•Commonest sites:
–Putamen – 40%
–Thalamus – 12%
–Lobar white matter – 15% to 20%
–Caudate – 8%
–Pons – 8%
–Cerebellum – 8%
•CT readily identifies
•Severity of headache generally correlates with
size
•Often occurs at same sites affected by lacunar
infarctions
•Charcot-Bouchard aneurysms: microaneurysms
identified pathologically in some cases
•Commonest sites:
–Putamen – 40%
–Thalamus – 12%
–Lobar white matter – 15% to 20%
–Caudate – 8%
–Pons – 8%
–Cerebellum – 8%
•CT readily identifies
•Severity of headache generally correlates with
size
•Decreased level of alertness caused by:
–Mass effect
–Increased intracranial pressure
–Direct involvement of brain stem reticular
activating system
•Seizures more frequent during acute
phase than in ischemic stroke
•Both basal ganglia and thalamic
hemorrhages may rupture into adjacent
ventricle and cause secondary
hydrocephalus
•Cerebellar hemorrhage may cause
obstructive hydrocephalus from
compression of fourth ventricle
–Mass effect
–Increased intracranial pressure
–Direct involvement of brain stem reticular
activating system
•Seizures more frequent during acute
phase than in ischemic stroke
•Both basal ganglia and thalamic
hemorrhages may rupture into adjacent
ventricle and cause secondary
hydrocephalus
•Cerebellar hemorrhage may cause
obstructive hydrocephalus from
compression of fourth ventricle
•With hematoma, level of
consciousness often worsens
first 24 to 48 hours after initial
symptoms due to edema around
lesion
•Herniation if edema causes
enough brain shift
–Direct pressure on vital brain
stem structures
–Infarction of adjacent blood
vessels due to compression
consciousness often worsens
first 24 to 48 hours after initial
symptoms due to edema around
lesion
•Herniation if edema causes
enough brain shift
–Direct pressure on vital brain
stem structures
–Infarction of adjacent blood
vessels due to compression
Lobar hemorrhage
•Occur in peripheral distribution of
cerebral white matter
•More benign prognosis since usually
smaller than hypertensive bleeds
•Young persons:
–Arteriovenous malformations
–Ingestion of sympathomimetic drugs
•Elderly persons:
–Congophilic amyloid angiopathy –
signs develop insidiously as in
anticoagulant-associated hemorrhage
•Occur in peripheral distribution of
cerebral white matter
•More benign prognosis since usually
smaller than hypertensive bleeds
•Young persons:
–Arteriovenous malformations
–Ingestion of sympathomimetic drugs
•Elderly persons:
–Congophilic amyloid angiopathy –
signs develop insidiously as in
anticoagulant-associated hemorrhage
Diagnosis, Management, Diagnosis, Management,
and Prognosis of ICHand Prognosis of ICH
•CT diagnostic test of choiceCT diagnostic test of choice
–hyperintense area with mass effect and
later hypointense surrounding edema
•MRI less sensitive in early stagesMRI less sensitive in early stages
•Management depends on size and Management depends on size and
locationlocation
–In acute phase, mass effect far greater than
in large cerebral infarction, so greater risk
of herniation and death
–In chronic phase, prognosis for surviving
patients much better than with ischemic
stroke
and Prognosis of ICHand Prognosis of ICH
•CT diagnostic test of choiceCT diagnostic test of choice
–hyperintense area with mass effect and
later hypointense surrounding edema
•MRI less sensitive in early stagesMRI less sensitive in early stages
•Management depends on size and Management depends on size and
locationlocation
–In acute phase, mass effect far greater than
in large cerebral infarction, so greater risk
of herniation and death
–In chronic phase, prognosis for surviving
patients much better than with ischemic
stroke
•Therapy directed at reducing mass Therapy directed at reducing mass
effecteffect
–Medical: controlled hyperventilation or
mannitol
–Surgical: rare
•Saved for cerebellar hemorrhages where
at risk for acute obstructive
hydrocephalus by compression of fourth
ventricle or direct pressure on caudal
brain stem
effecteffect
–Medical: controlled hyperventilation or
mannitol
–Surgical: rare
•Saved for cerebellar hemorrhages where
at risk for acute obstructive
hydrocephalus by compression of fourth
ventricle or direct pressure on caudal
brain stem
Hemorrhagic cerebral Hemorrhagic cerebral
infarctioninfarction demonstrated
by unenhanced CT scan one
day after the onset of
stroke. Note the high-
density hemorrhage within
the low density of the
edematous, infarcted region
in the right hemisphere.
Hemorrhage is evident from
its onset on CT scanning.
infarctioninfarction demonstrated
by unenhanced CT scan one
day after the onset of
stroke. Note the high-
density hemorrhage within
the low density of the
edematous, infarcted region
in the right hemisphere.
Hemorrhage is evident from
its onset on CT scanning.
Intracranial AneurysmsIntracranial Aneurysms
•Three forms:Three forms:
–Fusiform
•Represent ectatic dilatations of large arteries,
usually basilar or intracranial carotid
•Rarely rupture but may compress adjacent
brain tissue or cranial nerves and cause local
neurologic dysfunction
•Rarely surgically accessible
–Mycotic
•Occur with bacterial endocardits from septic
emboli
•Often multiple
•Located distally in arterial tree
•Accessible to surgical repair if not respond to
antibiotics
•Three forms:Three forms:
–Fusiform
•Represent ectatic dilatations of large arteries,
usually basilar or intracranial carotid
•Rarely rupture but may compress adjacent
brain tissue or cranial nerves and cause local
neurologic dysfunction
•Rarely surgically accessible
–Mycotic
•Occur with bacterial endocardits from septic
emboli
•Often multiple
•Located distally in arterial tree
•Accessible to surgical repair if not respond to
antibiotics
–Saccular
•Form at arterial bifurcations
•80% located in anterior circulation
•Congenital defect in artery with gradual
deterioration from hemodynamic stress
•Higher incidence in patients with polycystic
kidney disease and Marfan’s syndrome
•Present in approximately 6% of population
•Multiple in 25% of cases
•Annual incidence of rupture only 10 per
100,000
•If rupture, 33% die before reach hospital;
another 20% die in hospital
•Only 30% recover without significant disability
•Form at arterial bifurcations
•80% located in anterior circulation
•Congenital defect in artery with gradual
deterioration from hemodynamic stress
•Higher incidence in patients with polycystic
kidney disease and Marfan’s syndrome
•Present in approximately 6% of population
•Multiple in 25% of cases
•Annual incidence of rupture only 10 per
100,000
•If rupture, 33% die before reach hospital;
another 20% die in hospital
•Only 30% recover without significant disability
Right cavernous Right cavernous
carotid aneurysmcarotid aneurysm
(arrowed), shown on
coronal MRI. The signal
void at the periphery of
the aneurysm represents
flowing blood, while the
intensity in the central
portion may represent
either a clot or slowly
flowing blood. MRI may
demonstrate aneurysms
clearly, but is much less
successful than CT at
demonstrating the
presence or absence of
blood in the subarachnoid
space.
carotid aneurysmcarotid aneurysm
(arrowed), shown on
coronal MRI. The signal
void at the periphery of
the aneurysm represents
flowing blood, while the
intensity in the central
portion may represent
either a clot or slowly
flowing blood. MRI may
demonstrate aneurysms
clearly, but is much less
successful than CT at
demonstrating the
presence or absence of
blood in the subarachnoid
space.
Berry aneurysm Berry aneurysm
on the anterior on the anterior
communicating communicating
artery (a).artery (a). The
angiogram also
shows that the
anterior cerebral
artery (b) is in
spasm.
on the anterior on the anterior
communicating communicating
artery (a).artery (a). The
angiogram also
shows that the
anterior cerebral
artery (b) is in
spasm.
Subarachnoid HemorrhageSubarachnoid Hemorrhage
•Aneurysms can rupture any time but Aneurysms can rupture any time but
more common during strenuous activitymore common during strenuous activity
•Most common manifestation is headacheMost common manifestation is headache
–“worst headache of my life”
•Neck pain and rigidityNeck pain and rigidity
•Loss of consciousness and vomiting Loss of consciousness and vomiting
commoncommon
•Seen on CT in 95% of cases – location Seen on CT in 95% of cases – location
may suggest site of rupturemay suggest site of rupture
•Normal CT not rule out so do lumbar Normal CT not rule out so do lumbar
puncturepuncture – xanthochromia (develops after 6
hours)
•Aneurysms can rupture any time but Aneurysms can rupture any time but
more common during strenuous activitymore common during strenuous activity
•Most common manifestation is headacheMost common manifestation is headache
–“worst headache of my life”
•Neck pain and rigidityNeck pain and rigidity
•Loss of consciousness and vomiting Loss of consciousness and vomiting
commoncommon
•Seen on CT in 95% of cases – location Seen on CT in 95% of cases – location
may suggest site of rupturemay suggest site of rupture
•Normal CT not rule out so do lumbar Normal CT not rule out so do lumbar
puncturepuncture – xanthochromia (develops after 6
hours)
•Contrast CT or MRI can show aneurysms Contrast CT or MRI can show aneurysms
> 5 mm as well as arteriovenous > 5 mm as well as arteriovenous
malformationsmalformations
•Gold standard – cerebral angiographyGold standard – cerebral angiography
–Intracranial aneurysms
–Performed when considering surgery
•ComplicationsComplications
–Hypertension (systemic and intracranial)
–Vasospasm – peak timing is between 5 and
9 days after bleed and may cause change in
neuro status
–Hemorrhage (rebleeding)
–Hydrocephalus
–Hyponatremia (SIADH; cerebral salt
wasting)
> 5 mm as well as arteriovenous > 5 mm as well as arteriovenous
malformationsmalformations
•Gold standard – cerebral angiographyGold standard – cerebral angiography
–Intracranial aneurysms
–Performed when considering surgery
•ComplicationsComplications
–Hypertension (systemic and intracranial)
–Vasospasm – peak timing is between 5 and
9 days after bleed and may cause change in
neuro status
–Hemorrhage (rebleeding)
–Hydrocephalus
–Hyponatremia (SIADH; cerebral salt
wasting)
Hunt and Hess Classification of Hunt and Hess Classification of
Subarachnoid HemorrhageSubarachnoid Hemorrhage
•Classification SymptomsClassification Symptoms
–Grade I
•Asymptomatic of minimal headache and slight nuchal
rigidity.
–Grade II
•Moderate to severe headache, nuchal rigidity, no
neurological deficit other than cranial nerve palsy.
–Grade III
•Drowsiness, confusion, or mild focal deficit.
–Grade IV
•Stupor, moderate to severe hemiparesis, possible
early decerebrate ridigity and vegetative
disturbance.
–Grade V
•Deep coma, decerebrate ridigity, moribund appearance.
Subarachnoid HemorrhageSubarachnoid Hemorrhage
•Classification SymptomsClassification Symptoms
–Grade I
•Asymptomatic of minimal headache and slight nuchal
rigidity.
–Grade II
•Moderate to severe headache, nuchal rigidity, no
neurological deficit other than cranial nerve palsy.
–Grade III
•Drowsiness, confusion, or mild focal deficit.
–Grade IV
•Stupor, moderate to severe hemiparesis, possible
early decerebrate ridigity and vegetative
disturbance.
–Grade V
•Deep coma, decerebrate ridigity, moribund appearance.
Subarachnoid hemorrhage from an anterior communicating Subarachnoid hemorrhage from an anterior communicating
artery aneurysm.artery aneurysm. This uncontrasted CT scan shows areas of
increased density representing blood in the interhemispheric fissure
(arrows) and the septum pellucidum (arrowheads). A lesser amount
of blood is present in the sylvan fissures and the perimesencephalic
cistern.
artery aneurysm.artery aneurysm. This uncontrasted CT scan shows areas of
increased density representing blood in the interhemispheric fissure
(arrows) and the septum pellucidum (arrowheads). A lesser amount
of blood is present in the sylvan fissures and the perimesencephalic
cistern.
Vascular MalformationsVascular Malformations
•Venous angiomasVenous angiomas
–Most common
–Tend to lie close to brain surface
•Capillary telangiectasesCapillary telangiectases
–Composed of capillaries
–Typically located within brain stem
•Cavernous angiomasCavernous angiomas
–Composed of dilated sinusoidal channels
–Readily seen on CT
–Rarely bleed
•Venous angiomasVenous angiomas
–Most common
–Tend to lie close to brain surface
•Capillary telangiectasesCapillary telangiectases
–Composed of capillaries
–Typically located within brain stem
•Cavernous angiomasCavernous angiomas
–Composed of dilated sinusoidal channels
–Readily seen on CT
–Rarely bleed
•Arteriovenous malformationsArteriovenous malformations
–Composed of tangles of arteries connected directly
to veins
–May produce headache, seizures, or hemorrhage
–Account for 1% of all strokes
–Initial bleed before fourth decade – 7% rebleed in
first year after
–Hemorrhage into brain parenchyma, subarachnoid
space, or intraventricular space
–In older patients (> 55 years), treated
conservatively
–In younger patients, mostly treated with surgical
removal but also by irradiation with embolization
of artery
–Composed of tangles of arteries connected directly
to veins
–May produce headache, seizures, or hemorrhage
–Account for 1% of all strokes
–Initial bleed before fourth decade – 7% rebleed in
first year after
–Hemorrhage into brain parenchyma, subarachnoid
space, or intraventricular space
–In older patients (> 55 years), treated
conservatively
–In younger patients, mostly treated with surgical
removal but also by irradiation with embolization
of artery
Left parietal Left parietal
arteriovenous arteriovenous
malformation,malformation, shown
in an anteroposterior
view of an internal
carotid angiogram.
Bleeding from AVM is
usually less severe than
that from aneurysms,
but their size may lead
to other symptoms
including epilepsy.
arteriovenous arteriovenous
malformation,malformation, shown
in an anteroposterior
view of an internal
carotid angiogram.
Bleeding from AVM is
usually less severe than
that from aneurysms,
but their size may lead
to other symptoms
including epilepsy.
Glasgow Outcome Scale Glasgow Outcome Scale
(GOS)(GOS)
•1) Good recoveryGood recovery - patient can lead a
full and independent life with or without
minimal neurological deficit.
•2) Moderately disabledModerately disabled - patient has
neurological or intellectual impairment
but is independent.
•3) Severely disabledSeverely disabled - Patient
conscious but totally dependent on
others to get through daily activities.
•4) Vegetative survivalVegetative survival
•5) DeadDead
(GOS)(GOS)
•1) Good recoveryGood recovery - patient can lead a
full and independent life with or without
minimal neurological deficit.
•2) Moderately disabledModerately disabled - patient has
neurological or intellectual impairment
but is independent.
•3) Severely disabledSeverely disabled - Patient
conscious but totally dependent on
others to get through daily activities.
•4) Vegetative survivalVegetative survival
•5) DeadDead
Infarction in CT Imaging of Infarction in CT Imaging of
the Brain in Acute Strokethe Brain in Acute Stroke
•Infarction:Infarction: focal hypodense area, in
cortical, subcortical, or deep gray or
white matter, following vascular
territory, or watershed distribution.
Early subtle findings include obscuration
of gray/white matter contrast and
effacement of sulci, or "insular ribbon."
the Brain in Acute Strokethe Brain in Acute Stroke
•Infarction:Infarction: focal hypodense area, in
cortical, subcortical, or deep gray or
white matter, following vascular
territory, or watershed distribution.
Early subtle findings include obscuration
of gray/white matter contrast and
effacement of sulci, or "insular ribbon."
•Hemorrhage:Hemorrhage: hyperdense image in
white or deep gray matter, with or
without involvement of cortical surface
(40 to 90 HU). Petechial refers to
scattered hyperdense points, coalescing
to form irregularly hyperdense areas
with hypodense interruptions.
Hematoma refers to a solid,
homogeneously hyperdense image.
white or deep gray matter, with or
without involvement of cortical surface
(40 to 90 HU). Petechial refers to
scattered hyperdense points, coalescing
to form irregularly hyperdense areas
with hypodense interruptions.
Hematoma refers to a solid,
homogeneously hyperdense image.
•Hyperdense image in major Hyperdense image in major
intracranial artery:intracranial artery: suggestive of
vascular embolic material.
•Calcification:Calcification: hyperdense image within
or attached to vessel wall (>120 HU).
•Incidental:Incidental: silent infarct, subdural
collection, tumor, giant aneurysm,
arteriovenous malformation.
intracranial artery:intracranial artery: suggestive of
vascular embolic material.
•Calcification:Calcification: hyperdense image within
or attached to vessel wall (>120 HU).
•Incidental:Incidental: silent infarct, subdural
collection, tumor, giant aneurysm,
arteriovenous malformation.
Infarction in MRI of the Infarction in MRI of the
Brain in Acute StrokeBrain in Acute Stroke
•Acute:Acute: Subtle low signal (hypointense) on T1,
often difficult to see at this stage, and high
signal (hyperintense) on spin density and/or
T2-weighted and proton density-weighted
images starting 8 h after onset; should follow
vascular distribution. Mass effect maximal at 24
h, sometimes starting 2 h after onset, even in
the absence of parenchymal signal changes. No
parenchymal enhancement with paramagnetic
contrast agent. Territorial intravascular
paramagnetic contrast enhancement of "slow-
flow" arteries in hyperacute infarcts; at 48 h,
parenchymal and meningeal enhancement can
be expected.
Brain in Acute StrokeBrain in Acute Stroke
•Acute:Acute: Subtle low signal (hypointense) on T1,
often difficult to see at this stage, and high
signal (hyperintense) on spin density and/or
T2-weighted and proton density-weighted
images starting 8 h after onset; should follow
vascular distribution. Mass effect maximal at 24
h, sometimes starting 2 h after onset, even in
the absence of parenchymal signal changes. No
parenchymal enhancement with paramagnetic
contrast agent. Territorial intravascular
paramagnetic contrast enhancement of "slow-
flow" arteries in hyperacute infarcts; at 48 h,
parenchymal and meningeal enhancement can
be expected.
•Subacute (1 wk or older):Subacute (1 wk or older): Low signal
on T1, high signal on T2-weighted
images. Follows vascular distribution.
Revascularization and blood-brain
barrier breakdown may cause
parenchymal enhancement with
contrast agents.
•Old (several weeks to years):Old (several weeks to years): Low
signal on T1, high signal on T2. Mass
effect disappears after 1 mo. Loss of
tissue with large infarcts. Parenchymal
enhancement fades after several
months.
on T1, high signal on T2-weighted
images. Follows vascular distribution.
Revascularization and blood-brain
barrier breakdown may cause
parenchymal enhancement with
contrast agents.
•Old (several weeks to years):Old (several weeks to years): Low
signal on T1, high signal on T2. Mass
effect disappears after 1 mo. Loss of
tissue with large infarcts. Parenchymal
enhancement fades after several
months.
Hemorrhage in MRI of the Hemorrhage in MRI of the
BrainBrain
•HyperacuteHyperacute
–Hours old, mainly oxyhemoglobin with
surrounding edema
–T1 Weighted: Hypointense
–T2 Weighted: Hyperintense
•AcuteAcute
–Days old, mainly deoxyhemoglobin with
surrounding edema
–T1 Weighted: Hypointense
–T2 Weighted: Hypointense, surrounded by
hyperintense margin
BrainBrain
•HyperacuteHyperacute
–Hours old, mainly oxyhemoglobin with
surrounding edema
–T1 Weighted: Hypointense
–T2 Weighted: Hyperintense
•AcuteAcute
–Days old, mainly deoxyhemoglobin with
surrounding edema
–T1 Weighted: Hypointense
–T2 Weighted: Hypointense, surrounded by
hyperintense margin
•SubacuteSubacute
–Weeks old, mainly methemoglobin
–T1 Weighted: Hyperintense
–T2 Weighted: Hypointense, early subacute
with predominantly intracellular
methemoglobin. Hyperintense, late
subacute with predominantly extracellular
methemoglobin
•ChronicChronic
–Years old, hemosiderin slit or hemosiderin
margin surrounding fluid cavity
–T1 Weighted: Hypointense
–T2 Weighted: Hypointense slit, or
hypointense margin surrounding
hyperintense fluid cavity
–Weeks old, mainly methemoglobin
–T1 Weighted: Hyperintense
–T2 Weighted: Hypointense, early subacute
with predominantly intracellular
methemoglobin. Hyperintense, late
subacute with predominantly extracellular
methemoglobin
•ChronicChronic
–Years old, hemosiderin slit or hemosiderin
margin surrounding fluid cavity
–T1 Weighted: Hypointense
–T2 Weighted: Hypointense slit, or
hypointense margin surrounding
hyperintense fluid cavity
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