Stroke Recovery Etiology and Pathology Deficits Lesion Effects Demographics Stroke Treatment Map of...

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Etiology and Pathology

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Cerebrovascular System

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StrokeStrokeStrokeStroke DemographicsDemographics Etiology and PathologyEtiology and Pathology Lesion EffectsLesion Effects DeficitsDeficits RecoveryRecovery TreatmentTreatment Cerebrovascular SystemCerebrovascular System

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DemographicsDemographicsDemographicsDemographics Brain MetabolismBrain Metabolism Oxygen DemandsOxygen Demands HemiplegiaHemiplegia EpidemiologyEpidemiology Economic CostsEconomic Costs

Last ViewedLast Viewed DemographicsDemographics


Brain MetabolismBrain MetabolismBrain MetabolismBrain Metabolism Brain’s sole source of energy is aerobic or Brain’s sole source of energy is aerobic or

oxidative metabolismoxidative metabolism

Therefore, the brain requires a constant supply Therefore, the brain requires a constant supply of Oof O22 and glucose, 24/ 7/ 365 and glucose, 24/ 7/ 365

Brain’s sole source of energy is aerobic or Brain’s sole source of energy is aerobic or oxidative metabolismoxidative metabolism

Therefore, the brain requires a constant supply Therefore, the brain requires a constant supply of Oof O22 and glucose, 24/ 7/ 365 and glucose, 24/ 7/ 365

Last ViewedLast Viewed DemographicsDemographics ExitExitConcept MapConcept Map


Oxygen DemandsOxygen DemandsOxygen DemandsOxygen Demands At approximately 3 pounds, the brain accounts At approximately 3 pounds, the brain accounts

for roughly 2% of body massfor roughly 2% of body mass Consumes 17% of cardiac outputConsumes 17% of cardiac output Responsible for 20% of oxygen consumption Responsible for 20% of oxygen consumption

at restat rest

At approximately 3 pounds, the brain accounts At approximately 3 pounds, the brain accounts for roughly 2% of body massfor roughly 2% of body mass

Consumes 17% of cardiac outputConsumes 17% of cardiac output Responsible for 20% of oxygen consumption Responsible for 20% of oxygen consumption

at restat rest



HemiplegiaHemiplegiaHemiplegiaHemiplegia The hallmark of strokeThe hallmark of stroke isis

hemiplegiahemiplegia Hemiparesis + Hemiparesis + Hemisensory impairmentHemisensory impairment

The great vulnerability of the The great vulnerability of the brain to ischemic damage is brain to ischemic damage is due to its dependence on due to its dependence on aerobic metabolismaerobic metabolism



EpidemiologyEpidemiology 1/121/12EpidemiologyEpidemiology 1/121/12 Stroke is the third leading cause of death and Stroke is the third leading cause of death and

the most common cause of disability in the the most common cause of disability in the US US (American Heart Association 2005)(American Heart Association 2005)

Stroke is the third leading cause of death and Stroke is the third leading cause of death and the most common cause of disability in the the most common cause of disability in the US US (American Heart Association 2005)(American Heart Association 2005)



EpidemiologyEpidemiology 2/122/12EpidemiologyEpidemiology 2/122/12IncidenceIncidence Each year about 700,000 people experience a Each year about 700,000 people experience a

new or recurrent stroke. (500,000 are first new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacksattacks, and 200,000 are recurrent attacks) ) (American Heart Association 2005)(American Heart Association 2005)

Every 45 seconds someone in the US has a Every 45 seconds someone in the US has a strokestroke (280 strokes during today’s class)(280 strokes during today’s class)

IncidenceIncidence Each year about 700,000 people experience a Each year about 700,000 people experience a

new or recurrent stroke. (500,000 are first new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacksattacks, and 200,000 are recurrent attacks) ) (American Heart Association 2005)(American Heart Association 2005)

Every 45 seconds someone in the US has a Every 45 seconds someone in the US has a strokestroke (280 strokes during today’s class)(280 strokes during today’s class)



EpidemiologyEpidemiology 3/123/12EpidemiologyEpidemiology 3/123/12Gender DistributionGender Distribution Men > WomenMen > Women xx 1.251.25

Ethnic DistributionEthnic Distribution African-Americans > Whites x 2African-Americans > Whites x 2 HispanicHispanic Native AmericansNative Americans Native AlaskansNative Alaskans WhitesWhites (American Heart Association 2005)(American Heart Association 2005)

Gender DistributionGender Distribution Men > WomenMen > Women xx 1.251.25

Ethnic DistributionEthnic Distribution African-Americans > Whites x 2African-Americans > Whites x 2 HispanicHispanic Native AmericansNative Americans Native AlaskansNative Alaskans WhitesWhites (American Heart Association 2005)(American Heart Association 2005)



EpidemiologyEpidemiology 4/124/12EpidemiologyEpidemiology 4/124/12 Stroke is a condition of the elderlyStroke is a condition of the elderly Incidence increases steadily with age Incidence increases steadily with age

(risk doubles every decade after age 65)(risk doubles every decade after age 65) 28% of strokes occur in individuals < 65 years of age28% of strokes occur in individuals < 65 years of age

(Copenhagen Stroke Study, Arch Phys Med Rehabil, 1995)(Copenhagen Stroke Study, Arch Phys Med Rehabil, 1995)

Stroke is a condition of the elderlyStroke is a condition of the elderly Incidence increases steadily with age Incidence increases steadily with age

(risk doubles every decade after age 65)(risk doubles every decade after age 65) 28% of strokes occur in individuals < 65 years of age28% of strokes occur in individuals < 65 years of age




EpidemiologyEpidemiology 5/125/12EpidemiologyEpidemiology 5/125/12MortalityMortality From 1993 to 2003 the death rate from stroke declined 18.5 From 1993 to 2003 the death rate from stroke declined 18.5

percent, and the actual number of stroke deaths declined 0.7 percent.percent, and the actual number of stroke deaths declined 0.7 percent.

MortalityMortality From 1993 to 2003 the death rate from stroke declined 18.5 From 1993 to 2003 the death rate from stroke declined 18.5

percent, and the actual number of stroke deaths declined 0.7 percent.percent, and the actual number of stroke deaths declined 0.7 percent.



EpidemiologyEpidemiology 6/126/12EpidemiologyEpidemiology 6/126/12

Mortality Mortality 22% of men and 25% of women die within first 22% of men and 25% of women die within first

yearyear 2001 stroke killed 163,538 people2001 stroke killed 163,538 people Every 3.3 minutes someone in US dies of strokeEvery 3.3 minutes someone in US dies of stroke (64 (64

deaths during today’s class)deaths during today’s class)

~ 50% of stroke survivors die within 8 years ~ 50% of stroke survivors die within 8 years (Males > Females)(Males > Females) Death due to MIDeath due to MI

Mortality Mortality 22% of men and 25% of women die within first 22% of men and 25% of women die within first

yearyear 2001 stroke killed 163,538 people2001 stroke killed 163,538 people Every 3.3 minutes someone in US dies of strokeEvery 3.3 minutes someone in US dies of stroke (64 (64

deaths during today’s class)deaths during today’s class)

~ 50% of stroke survivors die within 8 years ~ 50% of stroke survivors die within 8 years (Males > Females)(Males > Females) Death due to MIDeath due to MI



Geographic Geographic DistributionDistribution

Death rate due to stroke per 100,000 in 2001




EpidemiologyEpidemiology 8/12 8/12 EpidemiologyEpidemiology 8/12 8/12

Mortality by type of strokeMortality by type of stroke HemorrhagicHemorrhagic 38%38% IschemicIschemic 12% 12% (American Heart Association 2005)(American Heart Association 2005)

Survival rates dramatically decreased by age and Survival rates dramatically decreased by age and co-morbidityco-morbidity HypertensionHypertension Heart diseaseHeart disease Diabetes Diabetes (Post-Stroke Rehabilitation Guideline Panel 1995)(Post-Stroke Rehabilitation Guideline Panel 1995)

Mortality by type of strokeMortality by type of stroke HemorrhagicHemorrhagic 38%38% IschemicIschemic 12% 12% (American Heart Association 2005)(American Heart Association 2005)

Survival rates dramatically decreased by age and Survival rates dramatically decreased by age and co-morbidityco-morbidity HypertensionHypertension Heart diseaseHeart disease Diabetes Diabetes (Post-Stroke Rehabilitation Guideline Panel 1995)(Post-Stroke Rehabilitation Guideline Panel 1995)



EpidemiologyEpidemiology 9/129/12EpidemiologyEpidemiology 9/129/12RecurrenceRecurrence 14% per year, highest in first year14% per year, highest in first year Risk of stroke increases 10 times after first strokeRisk of stroke increases 10 times after first stroke Recurring strokes produce larger lesions (cumulative Recurring strokes produce larger lesions (cumulative

effects), greater cortical involvement, greater impairment, effects), greater cortical involvement, greater impairment, higher mortalityhigher mortality

Outcome and pattern of recovery is similar to first-time Outcome and pattern of recovery is similar to first-time strokestroke

Should receive similar rehab treatment as first-time strokeShould receive similar rehab treatment as first-time stroke

RecurrenceRecurrence 14% per year, highest in first year14% per year, highest in first year Risk of stroke increases 10 times after first strokeRisk of stroke increases 10 times after first stroke Recurring strokes produce larger lesions (cumulative Recurring strokes produce larger lesions (cumulative

effects), greater cortical involvement, greater impairment, effects), greater cortical involvement, greater impairment, higher mortalityhigher mortality

Outcome and pattern of recovery is similar to first-time Outcome and pattern of recovery is similar to first-time strokestroke

Should receive similar rehab treatment as first-time strokeShould receive similar rehab treatment as first-time stroke




PrevalencePrevalence About 5,500,000 stroke survivors are alive todayAbout 5,500,000 stroke survivors are alive today 2,400,000 are males and 3,000,000 are females 2,400,000 are males and 3,000,000 are females

PrevalencePrevalence About 5,500,000 stroke survivors are alive todayAbout 5,500,000 stroke survivors are alive today 2,400,000 are males and 3,000,000 are females 2,400,000 are males and 3,000,000 are females



EpidemiologyEpidemiology 11/1211/12EpidemiologyEpidemiology 11/1211/12The following activity limitations were observed at The following activity limitations were observed at six months post-stroke:six months post-stroke:

50 % had some one-sided paralysis50 % had some one-sided paralysis 35 % had depression35 % had depression 30 % were unable to walk without some assistance30 % were unable to walk without some assistance 26 % were dependent in activities of daily living26 % were dependent in activities of daily living

(grooming, eating, bathing, etc) (grooming, eating, bathing, etc) 26 % were institutionalized in a nursing home26 % were institutionalized in a nursing home 19 % had aphasia (trouble speaking or understanding19 % had aphasia (trouble speaking or understanding

the speech of others) the speech of others) (Framingham Heart Study (Framingham Heart Study

2005)2005)

The following activity limitations were observed at The following activity limitations were observed at six months post-stroke:six months post-stroke:

50 % had some one-sided paralysis50 % had some one-sided paralysis 35 % had depression35 % had depression 30 % were unable to walk without some assistance30 % were unable to walk without some assistance 26 % were dependent in activities of daily living26 % were dependent in activities of daily living

(grooming, eating, bathing, etc) (grooming, eating, bathing, etc) 26 % were institutionalized in a nursing home26 % were institutionalized in a nursing home 19 % had aphasia (trouble speaking or understanding19 % had aphasia (trouble speaking or understanding

the speech of others) the speech of others) (Framingham Heart Study (Framingham Heart Study

2005)2005)Last ViewedLast Viewed DemographicsDemographics


Disability Due to StrokeDisability Due to Stroke Stroke is leading cause of chronic Stroke is leading cause of chronic

disabilitydisability (Wolfe 2000)(Wolfe 2000)

~70% never return to work~70% never return to work Stroke is leading cause of inpatient Stroke is leading cause of inpatient

rehabrehab (Granger & Hamilton 1994)(Granger & Hamilton 1994)

33% require (A) with ADL at one year 33% require (A) with ADL at one year

postpost (Murray & Lopez 1996)(Murray & Lopez 1996)

26% of stroke survivors are in SNF26% of stroke survivors are in SNF (American Heart Association 2005)(American Heart Association 2005)

>50% hospitalized with stroke do not >50% hospitalized with stroke do not require rehabrequire rehab

EpidemiologyEpidemiology 12/1212/12



Economic CostsEconomic CostsEconomic CostsEconomic Costs Estimated: $56.8 billion per year in the US Estimated: $56.8 billion per year in the US Life time costs:Life time costs:

Thromboembolic stroke Thromboembolic stroke $100,000$100,000 Hemorrhagic stroke:Hemorrhagic stroke:

Subarachnoid Subarachnoid $228,000$228,000 Intracerebral Intracerebral $124,000$124,000

Estimated: $56.8 billion per year in the US Estimated: $56.8 billion per year in the US Life time costs:Life time costs:

Thromboembolic stroke Thromboembolic stroke $100,000$100,000 Hemorrhagic stroke:Hemorrhagic stroke:

Subarachnoid Subarachnoid $228,000$228,000 Intracerebral Intracerebral $124,000$124,000



Etiology and PathologyEtiology and PathologyEtiology and PathologyEtiology and Pathology EtiologyEtiology Common Occlusion SitesCommon Occlusion Sites Risk FactorsRisk Factors Stroke PreventionStroke Prevention Predictors of Stroke Predictors of Stroke Warning SignsWarning Signs Predictors of Good OutcomePredictors of Good Outcome Predictors of Bad OutcomePredictors of Bad Outcome Nagi ModelNagi Model PathophysiologyPathophysiology

Last ViewedLast Viewed Etiology and PathologyEtiology and Pathology


Etiology of StrokeEtiology of StrokeEtiology of StrokeEtiology of Stroke Stroke is a neurologic Stroke is a neurologic

deficit of deficit of sudden onsetsudden onset due to interruption of the due to interruption of the blood supply to the brain blood supply to the brain resulting in infarction resulting in infarction and and permanentpermanent CNS CNS damage.damage.

Stroke is a neurologic Stroke is a neurologic deficit of deficit of sudden onsetsudden onset due to interruption of the due to interruption of the blood supply to the brain blood supply to the brain resulting in infarction resulting in infarction and and permanentpermanent CNS CNS damage.damage.

Ischemic 80%

Hemorrhagic 20%



Common Occlusion SitesCommon Occlusion SitesCommon Occlusion SitesCommon Occlusion Sites

• Occlusion commonly occurs in areas of turbulent blood flow

• Turbulent flow damages intimal lining of vessel

• Repair process initiates platelet deposition and thrombus formation



Risk FactorsRisk Factors 1/31/3Risk FactorsRisk Factors 1/31/3 Non-modifiable Risk Factors

Increased age Being male Race (e.g., African-Americans) Diabetes mellitus Prior stroke/transient ischemic attacks Family history of stroke Asymptomatic carotid bruit

Less Well Documented (perhaps partly modifiable) Geography/climate Socioeconomic factors

Source: American Stroke Association. Heart and Stroke Facts. 1996.

Non-modifiable Risk Factors Increased age Being male Race (e.g., African-Americans) Diabetes mellitus Prior stroke/transient ischemic attacks Family history of stroke Asymptomatic carotid bruit

Less Well Documented (perhaps partly modifiable) Geography/climate Socioeconomic factors

Source: American Stroke Association. Heart and Stroke Facts. 1996.



Risk FactorsRisk Factors 2/32/3Risk FactorsRisk Factors 2/32/3 Modifiable Risk Factor

Major Hypertension Heart disease, especially atrial fibrillation Cigarette smoking Transient ischemic attacks

Secondary Increased serum cholesterol / lipids Physical inactivity Obesity

Less Well Documented Excessive alcohol intake / drug abuse Acute infection*

* Not listed in the ASA publication

Modifiable Risk Factor Major

Hypertension Heart disease, especially atrial fibrillation Cigarette smoking Transient ischemic attacks

Secondary Increased serum cholesterol / lipids Physical inactivity Obesity

Less Well Documented Excessive alcohol intake / drug abuse Acute infection*

* Not listed in the ASA publication



Genetic Risk Factors for StrokeGenetic Risk Factors for Stroke 3/33/3Genetic Risk Factors for StrokeGenetic Risk Factors for Stroke 3/33/3 Apolipoprotein E4 Elevated homocysteine levels Factor V mutation

Apolipoproteins -- important in the transport of lipids in plasma. Apolipoprotein E (Apo E) forms part of all plasma concentration is closely correlated with plasma triglyceride concentrations. The presence of the apolipoprotein protein-E4 allele has also been associated with an increased risk for stroke; however, reports are conflicting.

Apolipoprotein E4 Elevated homocysteine levels Factor V mutation

Apolipoproteins -- important in the transport of lipids in plasma. Apolipoprotein E (Apo E) forms part of all plasma concentration is closely correlated with plasma triglyceride concentrations. The presence of the apolipoprotein protein-E4 allele has also been associated with an increased risk for stroke; however, reports are conflicting.



Stroke PreventionStroke Prevention 1/21/2Stroke PreventionStroke Prevention 1/21/2

Exercise reduces the risk of strokeExercise reduces the risk of stroke

Intense exerciseIntense exercise 27%27%Intense exercise: jogging 15 to 20 Intense exercise: jogging 15 to 20

minutes a day on most daysminutes a day on most days

Moderate exerciseModerate exercise 20%20%Moderate exercise: brisk walks of Moderate exercise: brisk walks of 30 minutes a day on most days30 minutes a day on most days

Exercise reduces the risk of strokeExercise reduces the risk of stroke

Intense exerciseIntense exercise 27%27%Intense exercise: jogging 15 to 20 Intense exercise: jogging 15 to 20

minutes a day on most daysminutes a day on most days

Moderate exerciseModerate exercise 20%20%Moderate exercise: brisk walks of Moderate exercise: brisk walks of 30 minutes a day on most days30 minutes a day on most days

J Stroke: Oct 2003



Stroke PreventionStroke Prevention 2/22/2Stroke PreventionStroke Prevention 2/22/2 PreventionPrevention

““Clot Buster” Clot Buster” (Tissue Plasminogen (Tissue Plasminogen Activator, TPA,)Activator, TPA,)

Recent researchRecent research Tissue graftingTissue grafting Genetic engineeringGenetic engineering

PreventionPrevention ““Clot Buster” Clot Buster”

(Tissue Plasminogen (Tissue Plasminogen Activator, TPA,)Activator, TPA,)

Recent researchRecent research Tissue graftingTissue grafting Genetic engineeringGenetic engineering



Predictors of Stroke Predictors of Stroke Predictors of Stroke Predictors of Stroke

Previous strokePrevious stroke Transient ischemic attacks: 35% of thrombotic Transient ischemic attacks: 35% of thrombotic

strokes were preceded by TIAstrokes were preceded by TIA

Previous strokePrevious stroke Transient ischemic attacks: 35% of thrombotic Transient ischemic attacks: 35% of thrombotic

strokes were preceded by TIAstrokes were preceded by TIA



Warning SignsWarning SignsWarning SignsWarning Signs Characterized by Characterized by suddensudden onsetonset focal focal

neurological deficitneurological deficit Warning signs: Call for medical assistanceWarning signs: Call for medical assistance

Sudden numbness or weakness of the Sudden numbness or weakness of the face, arm or leg, especially on one side face, arm or leg, especially on one side of the body of the body

Sudden confusion, trouble speaking or Sudden confusion, trouble speaking or understanding understanding

Sudden trouble seeing in one or both Sudden trouble seeing in one or both eyes eyes

Sudden trouble walking, dizziness, loss Sudden trouble walking, dizziness, loss of balance or coordination of balance or coordination

Sudden, severe headache with no known Sudden, severe headache with no known cause cause (American Stroke Association 2000)(American Stroke Association 2000)



Predictors of Good Outcome Predictors of Good Outcome Predictors of Good Outcome Predictors of Good Outcome The higher the socioeconomic status, the better the outcomeThe higher the socioeconomic status, the better the outcome The higher the education, the better the outcomeThe higher the education, the better the outcome The more active the premorbid lifestyle, the better the outcomeThe more active the premorbid lifestyle, the better the outcome All things being equal, the younger the age, the better the outcomeAll things being equal, the younger the age, the better the outcome Only sensory or only motor impairments (the smaller the lesion), the Only sensory or only motor impairments (the smaller the lesion), the

better the outcomebetter the outcome Never loosing consciousnessNever loosing consciousness Little comorbidityLittle comorbidity

The higher the socioeconomic status, the better the outcomeThe higher the socioeconomic status, the better the outcome The higher the education, the better the outcomeThe higher the education, the better the outcome The more active the premorbid lifestyle, the better the outcomeThe more active the premorbid lifestyle, the better the outcome All things being equal, the younger the age, the better the outcomeAll things being equal, the younger the age, the better the outcome Only sensory or only motor impairments (the smaller the lesion), the Only sensory or only motor impairments (the smaller the lesion), the

better the outcomebetter the outcome Never loosing consciousnessNever loosing consciousness Little comorbidityLittle comorbidity



Severe initial functional deficitsSevere initial functional deficits Dense sensory or motor impairmentsDense sensory or motor impairments HemianopsiaHemianopsia Severe visuospatial deficits (hemineglect or hemiinattention)Severe visuospatial deficits (hemineglect or hemiinattention) Severe aphasiaSevere aphasia Major depressionMajor depression Lack of return of hand function within 96 hoursLack of return of hand function within 96 hours Altered level of consciousnessAltered level of consciousness

Severe initial functional deficitsSevere initial functional deficits Dense sensory or motor impairmentsDense sensory or motor impairments HemianopsiaHemianopsia Severe visuospatial deficits (hemineglect or hemiinattention)Severe visuospatial deficits (hemineglect or hemiinattention) Severe aphasiaSevere aphasia Major depressionMajor depression Lack of return of hand function within 96 hoursLack of return of hand function within 96 hours Altered level of consciousnessAltered level of consciousness

Predictors of Bad OutcomePredictors of Bad Outcome 1/2 1/2 Predictors of Bad OutcomePredictors of Bad Outcome 1/2 1/2



Significant comorbidity (medical/surgical instability)Significant comorbidity (medical/surgical instability) Disability prior to strokeDisability prior to stroke Previous stroke (effects are cumulative)Previous stroke (effects are cumulative) Loss of sitting balanceLoss of sitting balance Severe cognitive deficits (difficulty following instructions)Severe cognitive deficits (difficulty following instructions) Persistent urinary incontinencePersistent urinary incontinence Older ageOlder age (R) CVAs tend to have worse outcomes than (L) CVAs (R) CVAs tend to have worse outcomes than (L) CVAs

Significant comorbidity (medical/surgical instability)Significant comorbidity (medical/surgical instability) Disability prior to strokeDisability prior to stroke Previous stroke (effects are cumulative)Previous stroke (effects are cumulative) Loss of sitting balanceLoss of sitting balance Severe cognitive deficits (difficulty following instructions)Severe cognitive deficits (difficulty following instructions) Persistent urinary incontinencePersistent urinary incontinence Older ageOlder age (R) CVAs tend to have worse outcomes than (L) CVAs (R) CVAs tend to have worse outcomes than (L) CVAs

Predictors of Bad OutcomePredictors of Bad Outcome 2/22/2Predictors of Bad OutcomePredictors of Bad Outcome 2/22/2



Nagi Model of Disability Nagi Model of Disability Due to StrokeDue to Stroke

Nagi Model of Disability Nagi Model of Disability Due to StrokeDue to Stroke

PathologyPathologyPathologyPathology ImpairmentFunctionalLimitation

Disability

Ischemia produces CNS lesion(neuronal death)

CNS lesion produces hemiplegia & spasticity

Impairments limit ability to perform B/I ADL

ADL limitations prevent ability to perform expected social role



PathophysiologyPathophysiology 1/101/10PathophysiologyPathophysiology 1/101/10

Transient ischemic attack (TIA)Transient ischemic attack (TIA) Caused by Caused by reversiblereversible ischemia (usually due to ischemia (usually due to

vasospasm).vasospasm). Results in temporary functional impairment with Results in temporary functional impairment with

nono residual deficits. residual deficits. ~35% of TIAs evolve into stroke within 1-3 years~35% of TIAs evolve into stroke within 1-3 years

Transient ischemic attack (TIA)Transient ischemic attack (TIA) Caused by Caused by reversiblereversible ischemia (usually due to ischemia (usually due to

vasospasm).vasospasm). Results in temporary functional impairment with Results in temporary functional impairment with

nono residual deficits. residual deficits. ~35% of TIAs evolve into stroke within 1-3 years~35% of TIAs evolve into stroke within 1-3 years



PathophysiologyPathophysiology 2/102/10PathophysiologyPathophysiology 2/102/10 StrokeStroke

Caused by Caused by irreversibleirreversible ischemia ischemia Results in a circumscribed area Results in a circumscribed area

of infarction (of infarction (primary damageprimary damage) ) andand

Perimeter of increased pressure Perimeter of increased pressure due to inflammation (due to inflammation (secondary secondary damagedamage) )

The most damaging results of The most damaging results of vascular occlusion are produced vascular occlusion are produced by by secondarysecondary damage damage

Primary damagePrimary damagePrimary damagePrimary damage

Secondary damageSecondary damageSecondary damageSecondary damage



This intermediate infarct of the frontal lobe shows liquefactive necrosis with formation of cystic spaces as resolution begins.

Phagocytosis Following StrokePhagocytosis Following Stroke 3/103/10



Here is a large remote cerebral infarction. Resolution of the infarction has left a huge cystic space encompassing much of the cerebral hemisphere in this neonate.

Phagocytosis Following StrokePhagocytosis Following Stroke 4/104/10



This is an intermediate to remote infarct in the distribution of the middle cerebral artery.


MCA StrokeMCA Stroke 5/105/10


Here is a cerebral infarct from an arterial embolus, which often leads to a hemorrhagic appearance. There is edema which obscures the structures. The acutely edematous infarcted tissue may produce a mass effect. Note the decrease in size of the ventricle on the left with shift of the midline.

MCA StrokeMCA Stroke 6/106/10


This magnetic resonance imaging (MRI) scan demonstrates subacute infarctions in the right basal ganglia and also near the

gray-white junction in the posterior parietal region.


7/10



The bilaterally symmetric dark discolored areas seen superiorly and just lateral to the midline represent recent infarction in the watershed zone between anterior and middle cerebral arterial circulations. Such watershed infarctions can occur with relative or absolute hypoperfusion of the brain.

Watershed InfarctionWatershed Infarction 8/108/10



The circle of Willis has been dissected, and three berry aneurysms are seen. Multiple aneurysms are seen in about 20-30% of cases of berry aneurysm. Such aneurysms are "congenital" in the sense that the defect in the arterial wall is present from birth, but the actual aneurysm takes years to develop, so that rupture is most likely to occur in young to middle age adults.

Berry AneurysmsBerry Aneurysms 9/109/10



The white arrow on the black card marks the site of a ruptured berry aneurysm in the circle of Willis. This is a major cause for subarachnoid hemorrhage.

Berry AneurysmsBerry Aneurysms 10/1010/10



Lesion EffectsLesion EffectsLesion EffectsLesion Effects Domains Affected by StrokeDomains Affected by Stroke Hemispheric EffectsHemispheric Effects Symptoms by Lesion LocationSymptoms by Lesion Location Ideational ApraxiaIdeational Apraxia Motor ApraxiaMotor Apraxia

Last ViewedLast Viewed Lesion EffectsLesion Effects


Domains Affected by Stroke Domains Affected by Stroke Domains Affected by Stroke Domains Affected by Stroke MotorMotor SensorySensory VisionVision LanguageLanguage CognitionCognition Affect Affect

MotorMotor SensorySensory VisionVision LanguageLanguage CognitionCognition Affect Affect



Hemispheric EffectsHemispheric EffectsHemispheric EffectsHemispheric Effects Hemispheric SpecializationHemispheric Specialization Dominant HemisphereDominant Hemisphere Stroke in the Dominant HemisphereStroke in the Dominant Hemisphere Stroke in the Nondominant HemisphereStroke in the Nondominant Hemisphere



Hemispheric SpecializationHemispheric SpecializationHemispheric SpecializationHemispheric Specialization

Left Hemisphere• Intellectual• Rational• Verbal• Analytical

RightHemisphere• Perceptive• Holistic• Spatial• Emotional• Nonverbal

Last ViewedLast Viewed Hemispheric EffectsHemispheric Effects


Dominant HemisphereDominant HemisphereDominant HemisphereDominant Hemisphere Dominant = hemisphere with language Dominant = hemisphere with language

(Broca, Wernicke)(Broca, Wernicke) Left hemisphere is the dominant hemisphere Left hemisphere is the dominant hemisphere

in the vast majority of the population (95%)in the vast majority of the population (95%)

Dominant = hemisphere with language Dominant = hemisphere with language (Broca, Wernicke)(Broca, Wernicke)

Left hemisphere is the dominant hemisphere Left hemisphere is the dominant hemisphere in the vast majority of the population (95%)in the vast majority of the population (95%)



Stroke in the Stroke in the Dominant Hemisphere Dominant Hemisphere

Stroke in the Stroke in the Dominant Hemisphere Dominant Hemisphere

Characterized by:

– Right hemiparesis

– Right sensory loss (Hemiplegia = hemiparesis + hemisensory impairment)

– Disturbance of language and temporal ordering

– Motor and ideational apraxia

– Difficulty initiating and sequencing tasks

– Delays in information processing

– Compulsive behavior with easy frustration

– Extreme distractibility



Stroke in the Stroke in the Nondominant HemisphereNondominant Hemisphere

Stroke in the Stroke in the Nondominant HemisphereNondominant Hemisphere

Characterized by: Characterized by: Left hemiparesisLeft hemiparesis Left sensory lossLeft sensory loss Disturbance of spatial Disturbance of spatial

orientation *orientation * Left unilateral neglect (in Left unilateral neglect (in

some cases) *some cases) * Impairment of hand eye Impairment of hand eye

coordination, figure-ground coordination, figure-ground discrimination, form discrimination, form constancyconstancy

Characterized by: Characterized by: Left hemiparesisLeft hemiparesis Left sensory lossLeft sensory loss Disturbance of spatial Disturbance of spatial

orientation *orientation * Left unilateral neglect (in Left unilateral neglect (in

some cases) *some cases) * Impairment of hand eye Impairment of hand eye

coordination, figure-ground coordination, figure-ground discrimination, form discrimination, form constancyconstancy

Dressing and Dressing and constructional apraxiaconstructional apraxia

Poor judgment *Poor judgment *

Unrealistic expectations *Unrealistic expectations *

Denial of disability *Denial of disability *

* Contributes to poor outcome



Symptoms by Lesion LocationSymptoms by Lesion LocationSymptoms by Lesion LocationSymptoms by Lesion Location

FrontalMovement impairmentPersonality changesCognitive impairmentDelayed initiationAphasia (Broca)

ParietalSomatosensory impairmentSpatial relations impairmentHomonymous visual deficitsAgnosiaLanguage comprehensionimpairment

OccipitalHomonymous hemianopsiaEye movement impairment

CerebellarAtaxiaIpsilateral dysmetriaDysdiadochokinesiaIntention tremorBrainstem

Gait impairmentDiplopiaFocal weaknessConsciousness and

attention impairment

Cerebellopontine angleHearing impairmentAtaxiaTinnitusDizzinessFacial palsy

Temporal lobeAuditory and perceptual impairmentMemory and learning impairmentAphasia (Wernicke)



Ideational ApraxiaIdeational ApraxiaIdeational ApraxiaIdeational Apraxia Unable to perform a task either automatically or Unable to perform a task either automatically or

on command, although individual movements on command, although individual movements can be made correctlycan be made correctly

Patient does not understand the concept of the Patient does not understand the concept of the act, cannot retain the idea, or cannot formulate act, cannot retain the idea, or cannot formulate motor patterns requiredmotor patterns required

Often unable to describe the process of a task Often unable to describe the process of a task Given toothpaste and brush, will try to apply Given toothpaste and brush, will try to apply

toothpaste w/o removing cap, or may put tube toothpaste w/o removing cap, or may put tube into mouthinto mouth

Due to lesion of the parietal lobe in the Due to lesion of the parietal lobe in the dominant hemisphere or the corpus callosumdominant hemisphere or the corpus callosum

Unable to perform a task either automatically or Unable to perform a task either automatically or on command, although individual movements on command, although individual movements can be made correctlycan be made correctly

Patient does not understand the concept of the Patient does not understand the concept of the act, cannot retain the idea, or cannot formulate act, cannot retain the idea, or cannot formulate motor patterns requiredmotor patterns required

Often unable to describe the process of a task Often unable to describe the process of a task Given toothpaste and brush, will try to apply Given toothpaste and brush, will try to apply

toothpaste w/o removing cap, or may put tube toothpaste w/o removing cap, or may put tube into mouthinto mouth

Due to lesion of the parietal lobe in the Due to lesion of the parietal lobe in the dominant hemisphere or the corpus callosumdominant hemisphere or the corpus callosum

Dominant Hemisphere



Kinetic (Motor) Apraxia Kinetic (Motor) Apraxia Kinetic (Motor) Apraxia Kinetic (Motor) Apraxia Inability to perform fine Inability to perform fine

learned movements in learned movements in the absence of weakness the absence of weakness or sensory lossor sensory loss

Due to bilateral lesion Due to bilateral lesion (disease) of the frontal (disease) of the frontal lobeslobes

Inability to perform fine Inability to perform fine learned movements in learned movements in the absence of weakness the absence of weakness or sensory lossor sensory loss

Due to bilateral lesion Due to bilateral lesion (disease) of the frontal (disease) of the frontal lobeslobes



DeficitsDeficitsDeficitsDeficits Common DeficitsCommon Deficits Anatomic Substrate of DeficitsAnatomic Substrate of Deficits

Last ViewedLast Viewed DeficitsDeficits


Common Deficits Following StrokeCommon Deficits Following StrokeCommon Deficits Following StrokeCommon Deficits Following Stroke

DEFICIT ACUTE (%) CHRONIC (%)

Hemiparesis 88 48

Incoordination 86 61

Dysarthria 57 16

Sensory impairment 53 24

Aphasia 36 18

Memory impairment 36 31

Bladder incontinence 29 9

Dysphagia 13 4



Anatomic Substrate of DeficitsAnatomic Substrate of DeficitsAnatomic Substrate of DeficitsAnatomic Substrate of DeficitsDEFICIT NEUROANATOMIC SUBSTRATE

Hemiparesis Lesion of cortical motor centers (UMN)

Incoordination Lesion of cortical motor centers (dorsolateral and ventromedial systems)

Dysarthria Lesion of corticobulbar tract (input to CNs)

Sensory impairment Lesion of somatosensory cortex

Aphasia Lesion of language centers (Broca, Wernicke)

Memory impairment Lesion of temporal lobe (hippocampus)

Bladder incontinence Lesion of autonomic input to sacral region of spinal cord (hypothalamus)

Dysphagia Lesion of corticobulbar tract (B input to CN X)



RecoveryRecoveryRecoveryRecovery Natural History of RecoveryNatural History of Recovery Recovery With InterventionRecovery With Intervention Pattern of RecoveryPattern of Recovery Theories of RecoveryTheories of Recovery

Last ViewedLast Viewed RecoveryRecovery


Natural History of Recovery Natural History of Recovery Natural History of Recovery Natural History of Recovery

• Majority of recovery of function occurs in the first 3 months• From 3 mo. - 1 yr. recovery may continue at much slower rate

020406080

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Function Recovery

Function

* Using “conventional”rehabilitationapproaches

(Post-Stroke Rehabilitation Guideline Panel 1995)



Recovery With InterventionRecovery With InterventionRecovery With InterventionRecovery With InterventionEvidence-based PracticeEvidence-based Practice Data now show that natural history of recovery can be Data now show that natural history of recovery can be

changed by the changed by the rightright type of intervention type of intervention Constraint induced therapy (CIT) and weight supported Constraint induced therapy (CIT) and weight supported

treadmill training (WSTT) change the natural history of treadmill training (WSTT) change the natural history of recoveryrecovery

““Conventional” rehabilitation techniques Conventional” rehabilitation techniques do notdo not change change the natural history of recoverythe natural history of recovery



Pattern of RecoveryPattern of Recovery Pattern of RecoveryPattern of Recovery Initially: hypotonia/ flaccidityInitially: hypotonia/ flaccidity

Due to the interruption of UMN input to LMNDue to the interruption of UMN input to LMN

Days to weeks later: hypertonia/ spasticityDays to weeks later: hypertonia/ spasticity ??? A leading question in stroke recovery ??? A leading question in stroke recovery Due in part to Due in part to

Decreased threshold in alpha LMN andDecreased threshold in alpha LMN and Denervation supersensitivityDenervation supersensitivity

Initially: hypotonia/ flaccidityInitially: hypotonia/ flaccidity Due to the interruption of UMN input to LMNDue to the interruption of UMN input to LMN

Days to weeks later: hypertonia/ spasticityDays to weeks later: hypertonia/ spasticity ??? A leading question in stroke recovery ??? A leading question in stroke recovery Due in part to Due in part to

Decreased threshold in alpha LMN andDecreased threshold in alpha LMN and Denervation supersensitivityDenervation supersensitivity



Theories of theTheories of theRecovery of FunctionRecovery of Function

Theories of theTheories of theRecovery of FunctionRecovery of Function

1. Resolution of cerebral edema (diaschisis)

2. Reactive synaptogenesis (Collateral sprouting - CNS)

3. Changes in cortical maps

4. Use of alternate pathways

5. Regenerative synaptogenesis (Wallerian re-generation - PNS)

Regenerative synaptogenesis



Cellular Response to InjuryCellular Response to InjuryCellular Response to InjuryCellular Response to Injury What is diaschisis?What is diaschisis? What is diaschisis?What is diaschisis?

– Temporary disruption of function produced by shock or damage to brain tissue (≈ spinal shock of the brain)

– Includes loss of function of brain regions distant from primary site of injury

– Possibly due to decreased blood flow, decreased metabolism or physiological

disruption

Last ViewedLast Viewed Theories of RecoveryTheories of Recovery


Reactive SynaptogenesisReactive SynaptogenesisReactive SynaptogenesisReactive Synaptogenesis CNS response to injuryCNS response to injury

No re-establishing functional No re-establishing functional connections with target cells connections with target cells occurs, any recovery of function occurs, any recovery of function occurs via occurs via collateral sproutingcollateral sprouting from from intact neurons &/or intact neurons &/or reorganizationreorganization (intact systems assume the lost (intact systems assume the lost function, function, neuroplasticityneuroplasticity))

CNS response to injuryCNS response to injury

No re-establishing functional No re-establishing functional connections with target cells connections with target cells occurs, any recovery of function occurs, any recovery of function occurs via occurs via collateral sproutingcollateral sprouting from from intact neurons &/or intact neurons &/or reorganizationreorganization (intact systems assume the lost (intact systems assume the lost function, function, neuroplasticityneuroplasticity))

collateral sprouting +/or reorganizationcollateral sprouting +/or reorganization = neuroplasticityneuroplasticity

Theories of RecoveryTheories of RecoveryLast ViewedLast Viewed


Cortical ReorganizationCortical ReorganizationCortical ReorganizationCortical Reorganization What mechanisms underlie the recovery of function?What mechanisms underlie the recovery of function? What mechanisms underlie the recovery of function?What mechanisms underlie the recovery of function?

– Changes in cortical maps– Following central injuries: (Stroke)

– Intact adjacent areas of the cortex expand into quiet areas (due to unmasking of silent synapses)

– Following peripheral injuries: (Amputation) – Same

– Following injury cortical mapping is responsive to training– Changes are progressive and reversible– Once the task was learned, mapping changes persist long-

term



Cortical ReorganizationCortical ReorganizationCortical ReorganizationCortical Reorganization

Taub et al 1998

Use-Dependent Cortical Reorganization After Brain Injury

Mechanisms of effectiveness of Constraint-Induced Movement Therapy (CIMT)



Alternate PathwaysAlternate PathwaysAlternate PathwaysAlternate Pathways What mechanisms underlie the recovery of function?What mechanisms underlie the recovery of function? What mechanisms underlie the recovery of function?What mechanisms underlie the recovery of function?

– Ipsilateral motor tracts take over



Regenerative SynaptogenesisRegenerative Synaptogenesis PNS Response to Injury

Begins 3-7 days post injury

Wallerian degeneration is the process whereby functional connections with target cells may be re-established following injury

Wallerian re-generation may permit recovery of lost function



Stroke TreatmentStroke TreatmentStroke TreatmentStroke Treatment Referral PatternsReferral Patterns Treatment EfficacyTreatment Efficacy ““Unaffected" Upper ExtremityUnaffected" Upper Extremity Stroke TreatmentStroke Treatment Recovery of LocomotionRecovery of Locomotion Life Probability TablesLife Probability Tables

Stroke TreatmentStroke TreatmentLast ViewedLast Viewed


Possible Routes Possible Routes Through Medical SystemThrough Medical System

Possible Routes Possible Routes Through Medical SystemThrough Medical System

StrokeStroke HospitalLOS: 5-7 days

IP Rehab3 hrs/dayLOS: 3-4 wks

Subacute Rehab1.5 hrs/dayLOS: 5-6 wks

SNF Usually permanent• Rehab bed

Home w H HHome w H H

Home w H HLOS: ~2 wksHome w H HLOS: ~2 wks



Home w OPLOS: ~2-4 wks










Treatment Efficacy Treatment Efficacy Treatment Efficacy Treatment Efficacy

Conventional therapy produces only a modest, Conventional therapy produces only a modest, temporary improvement in function temporary improvement in function ((The LancetThe Lancet Vol 359 Vol 359 No 9302, January 19, 2002)No 9302, January 19, 2002)

PT treatment effects are achieved through a PT treatment effects are achieved through a neuroplastic reorganization of motor control neuroplastic reorganization of motor control centers centers (Treatment-Induced Cortical Reorganization After Stroke in Humans. (Treatment-Induced Cortical Reorganization After Stroke in Humans.

Taub et al., Stroke 2000; 31: 1210)Taub et al., Stroke 2000; 31: 1210)

Conventional therapy produces only a modest, Conventional therapy produces only a modest, temporary improvement in function temporary improvement in function ((The LancetThe Lancet Vol 359 Vol 359 No 9302, January 19, 2002)No 9302, January 19, 2002)

PT treatment effects are achieved through a PT treatment effects are achieved through a neuroplastic reorganization of motor control neuroplastic reorganization of motor control centers centers (Treatment-Induced Cortical Reorganization After Stroke in Humans. (Treatment-Induced Cortical Reorganization After Stroke in Humans.

Taub et al., Stroke 2000; 31: 1210)Taub et al., Stroke 2000; 31: 1210)



““Unaffected" Upper Extremity Unaffected" Upper Extremity ““Unaffected" Upper Extremity Unaffected" Upper Extremity

Following stroke, the unaffected UE showed Following stroke, the unaffected UE showed decreases in:decreases in: functional independence due to decreased fine functional independence due to decreased fine

manual dexteritymanual dexterity activity level due to decreases in kinesthesia and activity level due to decreases in kinesthesia and

gross dexterity gross dexterity

There is no such thing as an “unaffected” There is no such thing as an “unaffected” extremityextremity

Following stroke, the unaffected UE showed Following stroke, the unaffected UE showed decreases in:decreases in: functional independence due to decreased fine functional independence due to decreased fine

manual dexteritymanual dexterity activity level due to decreases in kinesthesia and activity level due to decreases in kinesthesia and

gross dexterity gross dexterity

There is no such thing as an “unaffected” There is no such thing as an “unaffected” extremityextremity



Stroke TreatmentStroke Treatment 1/2 1/2 Stroke TreatmentStroke Treatment 1/2 1/2 Prevention Prevention

Reduce modifiable risk factors Reduce modifiable risk factors Vigorous exercise Vigorous exercise ((J Stroke: Oct 2003)

MD: antiplatlet or anticoagulant therapy MD: antiplatlet or anticoagulant therapy

Prevention Prevention Reduce modifiable risk factors Reduce modifiable risk factors

Vigorous exercise Vigorous exercise ((J Stroke: Oct 2003)

MD: antiplatlet or anticoagulant therapy MD: antiplatlet or anticoagulant therapy



Stroke TreatmentStroke Treatment 2/22/2Stroke TreatmentStroke Treatment 2/22/2 Acute phase Acute phase

MD: thrombolytic agents or acute anticoagulation MD: thrombolytic agents or acute anticoagulation drugs (TPA) may be successful in reversing drugs (TPA) may be successful in reversing primaryprimary impairmentsimpairments

PT: improve functional ability and prevent PT: improve functional ability and prevent secondarysecondary impairments (deconditioning, pneumonia, UTI, impairments (deconditioning, pneumonia, UTI, pressure sores, DVT)pressure sores, DVT)



Recovery of LocomotionRecovery of Locomotion 1/51/5Recovery of LocomotionRecovery of Locomotion 1/51/5 Locomotor ability is an important factor in determining Locomotor ability is an important factor in determining

the degree of physical disability after stroke.the degree of physical disability after stroke. (Perry and (Perry and Mulroy, Stroke. 1995;76)Mulroy, Stroke. 1995;76)

> 63% of all stroke survivors have some walking > 63% of all stroke survivors have some walking disabilitydisability

Gait velocity is best predictor of functional ambulation Gait velocity is best predictor of functional ambulation status status (Perry and Mulroy, Stroke. 1995;76)(Perry and Mulroy, Stroke. 1995;76)

Gait velocity of 0.5-0.8 m/s (1-1.8 mph) is required to Gait velocity of 0.5-0.8 m/s (1-1.8 mph) is required to cross a street during a red light cross a street during a red light (Podsiodlo ’91)(Podsiodlo ’91)

Locomotor ability is an important factor in determining Locomotor ability is an important factor in determining the degree of physical disability after stroke.the degree of physical disability after stroke. (Perry and (Perry and Mulroy, Stroke. 1995;76)Mulroy, Stroke. 1995;76)

> 63% of all stroke survivors have some walking > 63% of all stroke survivors have some walking disabilitydisability

Gait velocity is best predictor of functional ambulation Gait velocity is best predictor of functional ambulation status status (Perry and Mulroy, Stroke. 1995;76)(Perry and Mulroy, Stroke. 1995;76)

Gait velocity of 0.5-0.8 m/s (1-1.8 mph) is required to Gait velocity of 0.5-0.8 m/s (1-1.8 mph) is required to cross a street during a red light cross a street during a red light (Podsiodlo ’91)(Podsiodlo ’91)



Recovery of LocomotionRecovery of Locomotion 2/52/5Recovery of LocomotionRecovery of Locomotion 2/52/5

Gait velocity of 0.8 m/s (1.8 mph) is required for Gait velocity of 0.8 m/s (1.8 mph) is required for unlimited community ambulation unlimited community ambulation (Podsiodlo ’91)(Podsiodlo ’91)

Gait velocity post-stroke (3 weeks-2 years): ranges Gait velocity post-stroke (3 weeks-2 years): ranges from 0.25-0.5 m/s (0.5-1 mph)from 0.25-0.5 m/s (0.5-1 mph)

Recovery of gait speed may continue for up to 2 years Recovery of gait speed may continue for up to 2 years after strokeafter stroke

Recovery of locomotion is best correlated with Recovery of locomotion is best correlated with function of distal muscles (TA, TS) function of distal muscles (TA, TS) (David Winter)(David Winter)

Gait velocity of 0.8 m/s (1.8 mph) is required for Gait velocity of 0.8 m/s (1.8 mph) is required for unlimited community ambulation unlimited community ambulation (Podsiodlo ’91)(Podsiodlo ’91)

Gait velocity post-stroke (3 weeks-2 years): ranges Gait velocity post-stroke (3 weeks-2 years): ranges from 0.25-0.5 m/s (0.5-1 mph)from 0.25-0.5 m/s (0.5-1 mph)

Recovery of gait speed may continue for up to 2 years Recovery of gait speed may continue for up to 2 years after strokeafter stroke

Recovery of locomotion is best correlated with Recovery of locomotion is best correlated with function of distal muscles (TA, TS) function of distal muscles (TA, TS) (David Winter)(David Winter)



Recovery of LocomotionRecovery of Locomotion 3/53/5Recovery of LocomotionRecovery of Locomotion 3/53/5 Acutely:Acutely:

51% are non-ambulatory51% are non-ambulatory 12% ambulate with an assistive device12% ambulate with an assistive device 37% are (I)37% are (I)


Acutely:Acutely: 51% are non-ambulatory51% are non-ambulatory 12% ambulate with an assistive device12% ambulate with an assistive device 37% are (I)37% are (I)




Recovery of LocomotionRecovery of Locomotion 4/54/5Recovery of LocomotionRecovery of Locomotion 4/54/5 Chronically Chronically

>66% will regain independence in walking>66% will regain independence in walking Best level of walking function occurs within 11 weeksBest level of walking function occurs within 11 weeks Probability of regaining walking (I) and time to (I) is Probability of regaining walking (I) and time to (I) is

related to initial severity :related to initial severity : >78% with no leg paresis>78% with no leg paresis 66% with mild leg paresis66% with mild leg paresis 28% with moderate leg paresis28% with moderate leg paresis 21% with severe leg paresis21% with severe leg paresis 6% with complete leg paralysis6% with complete leg paralysis

Chronically Chronically >66% will regain independence in walking>66% will regain independence in walking Best level of walking function occurs within 11 weeksBest level of walking function occurs within 11 weeks Probability of regaining walking (I) and time to (I) is Probability of regaining walking (I) and time to (I) is

related to initial severity :related to initial severity : >78% with no leg paresis>78% with no leg paresis 66% with mild leg paresis66% with mild leg paresis 28% with moderate leg paresis28% with moderate leg paresis 21% with severe leg paresis21% with severe leg paresis 6% with complete leg paralysis6% with complete leg paralysis



Recovery of LocomotionRecovery of Locomotion 5/55/5Recovery of LocomotionRecovery of Locomotion 5/55/5 Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Effects of Task-Specific Locomotor and Strength Training in Adults Who Were

Ambulatory After Stroke: Results of the STEPS RCTAmbulatory After Stroke: Results of the STEPS RCT Phase II RCT to determine effects of combined task-specific and LE Phase II RCT to determine effects of combined task-specific and LE

strength training to improve walking after strokestrength training to improve walking after stroke Subjects: 80 adults 4 mo – 5 yrs post strokeSubjects: 80 adults 4 mo – 5 yrs post stroke Method: BWSTT, CYCLE, LE-EX, UE-EXMethod: BWSTT, CYCLE, LE-EX, UE-EX

BWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EXBWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EX Dosage: 4/wk x 6wks (24 sessions)Dosage: 4/wk x 6wks (24 sessions) DV: Self-selected walking speed, fast walking speed, 6MWT; DV: Self-selected walking speed, fast walking speed, 6MWT;

pre- and post intervention and 6 mo postpre- and post intervention and 6 mo post Results: Results:

BWSTT more effective than cycling in improving walking speed and BWSTT more effective than cycling in improving walking speed and maintaining gains at 6 mo.maintaining gains at 6 mo.

LE strength training, alternate days, produced no added benefitLE strength training, alternate days, produced no added benefit

(Sullivan et al, (Phys Ther 2007;87:1580-1602)(Sullivan et al, (Phys Ther 2007;87:1580-1602)

Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Ambulatory After Stroke: Results of the STEPS RCTAmbulatory After Stroke: Results of the STEPS RCT Phase II RCT to determine effects of combined task-specific and LE Phase II RCT to determine effects of combined task-specific and LE

strength training to improve walking after strokestrength training to improve walking after stroke Subjects: 80 adults 4 mo – 5 yrs post strokeSubjects: 80 adults 4 mo – 5 yrs post stroke Method: BWSTT, CYCLE, LE-EX, UE-EXMethod: BWSTT, CYCLE, LE-EX, UE-EX

BWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EXBWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EX Dosage: 4/wk x 6wks (24 sessions)Dosage: 4/wk x 6wks (24 sessions) DV: Self-selected walking speed, fast walking speed, 6MWT; DV: Self-selected walking speed, fast walking speed, 6MWT;

pre- and post intervention and 6 mo postpre- and post intervention and 6 mo post Results: Results:

BWSTT more effective than cycling in improving walking speed and BWSTT more effective than cycling in improving walking speed and maintaining gains at 6 mo.maintaining gains at 6 mo.

LE strength training, alternate days, produced no added benefitLE strength training, alternate days, produced no added benefit

(Sullivan et al, (Phys Ther 2007;87:1580-1602)(Sullivan et al, (Phys Ther 2007;87:1580-1602)Stroke TreatmentStroke TreatmentLast ViewedLast Viewed

Life-table Probability of Walking After Life-table Probability of Walking After StrokeStroke

150 feet 150 feet WithWith Assistance Assistance 1/4 1/4

Life-table Probability of Walking After Life-table Probability of Walking After StrokeStroke

150 feet 150 feet WithWith Assistance Assistance 1/4 1/4

020

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2 4 6 8 10 12 14 16 18 20 22 24 26 28 30

Weeks After Stroke

Pro

ba

bili

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%)

Motor Only

Motor + Sensory

Motor + Sensory + Visual

Stroke TreatmentStroke TreatmentLast ViewedLast Viewed ExitExitConcept MapConcept Map

Life-table Probability of Walking After Life-table Probability of Walking After Stroke Stroke

150 ft. 150 ft. WithoutWithout Assistance Assistance2/4 2/4

Life-table Probability of Walking After Life-table Probability of Walking After Stroke Stroke

150 ft. 150 ft. WithoutWithout Assistance Assistance2/4 2/4

0

20

40

60

80

100

2 4 6 8 10 12 14 16 18 20 22 24 26 28 30

Weeks After Stroke

Prob

abili

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)

Motor Only

Motor + Sensory



Life-table Probability of Reaching a Life-table Probability of Reaching a Barthel Index Score Barthel Index Score 95. ( 95. ( I) I)

After StrokeAfter Stroke 3/43/4

Life-table Probability of Reaching a Life-table Probability of Reaching a Barthel Index Score Barthel Index Score 95. ( 95. ( I) I)

After StrokeAfter Stroke 3/43/4

0

20

40

60

80

100

2 4 6 8 10 12 14 16 18 20 22 24 26 28 30

Weeks After Stroke

Pro

ba

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Motor + Sensory



Life-table Probability of Reaching Life-table Probability of Reaching Barthel Index Score > 60 Barthel Index Score > 60 (( Min asst) After Stroke Min asst) After Stroke 4/44/4

Life-table Probability of Reaching Life-table Probability of Reaching Barthel Index Score > 60 Barthel Index Score > 60 (( Min asst) After Stroke Min asst) After Stroke 4/44/4

020

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Motor + Sensory




The Cerebrovascular SystemThe Cerebrovascular SystemThe Cerebrovascular SystemThe Cerebrovascular System Oxygen demandsOxygen demands MetabolismMetabolism Cerebrovascular diseaseCerebrovascular disease Blood supply to the brainBlood supply to the brain Carotid systemCarotid system Vertebrobasilar systemVertebrobasilar system Circle of WillisCircle of Willis Perfusion TerritoriesPerfusion Territories Cerebellar arteriesCerebellar arteries Venous DrainageVenous Drainage Blood supply to spinal cordBlood supply to spinal cord Patient casesPatient cases

Last ViewedLast Viewed Posture & BalancePosture & Balance


Oxygen DemandsOxygen DemandsOxygen DemandsOxygen Demands

The CNS (brain and spinal cord) is the best protected The CNS (brain and spinal cord) is the best protected organ in the human body including mechanisms to organ in the human body including mechanisms to protect its blood supplyprotect its blood supply

At approximately 3 pounds, the brain accounts for At approximately 3 pounds, the brain accounts for about 2% of body massabout 2% of body mass

Consumes 17% of cardiac output Consumes 17% of cardiac output

Responsible for 20% of oxygen consumption at restResponsible for 20% of oxygen consumption at rest

The CNS (brain and spinal cord) is the best protected The CNS (brain and spinal cord) is the best protected organ in the human body including mechanisms to organ in the human body including mechanisms to protect its blood supplyprotect its blood supply

At approximately 3 pounds, the brain accounts for At approximately 3 pounds, the brain accounts for about 2% of body massabout 2% of body mass

Consumes 17% of cardiac output Consumes 17% of cardiac output

Responsible for 20% of oxygen consumption at restResponsible for 20% of oxygen consumption at rest

Last ViewedLast Viewed Cerebrovascular SystemCerebrovascular System


MetabolismMetabolismMetabolismMetabolism Brain’s sole source of energy is aerobic or Brain’s sole source of energy is aerobic or

oxidative metabolism.oxidative metabolism.

Therefore, the brain requires a constant supply Therefore, the brain requires a constant supply of Oof O22 and glucose, 24 hours a day. and glucose, 24 hours a day.

Brain’s sole source of energy is aerobic or Brain’s sole source of energy is aerobic or oxidative metabolism.oxidative metabolism.

Therefore, the brain requires a constant supply Therefore, the brain requires a constant supply of Oof O22 and glucose, 24 hours a day. and glucose, 24 hours a day.



Cerebrovascular DiseaseCerebrovascular DiseaseCerebrovascular DiseaseCerebrovascular Disease While the blood supply to the brain is highly While the blood supply to the brain is highly

protected, cerebrovascular disease is the third protected, cerebrovascular disease is the third leading cause of death in American adults and leading cause of death in American adults and the number one cause of chronic functional the number one cause of chronic functional disability requiring rehabilitative intervention.disability requiring rehabilitative intervention.

While the blood supply to the brain is highly While the blood supply to the brain is highly protected, cerebrovascular disease is the third protected, cerebrovascular disease is the third leading cause of death in American adults and leading cause of death in American adults and the number one cause of chronic functional the number one cause of chronic functional disability requiring rehabilitative intervention.disability requiring rehabilitative intervention.



Blood Supply to the BrainBlood Supply to the Brain 1/41/4 Blood Supply to the BrainBlood Supply to the Brain 1/41/4 Approximately 1,000 ml/min Approximately 1,000 ml/min

delivered via two systems.delivered via two systems. Anterior (Anterior (CarotidCarotid) system:) system:

70% of supply (35% from each 70% of supply (35% from each internal carotid artery)internal carotid artery)

Supplies the superior 2/3 of the Supplies the superior 2/3 of the brainbrain

Posterior Posterior ((VertebrobasilarVertebrobasilar)) system:system:

30% of supply30% of supply Supplies the inferior 1/3 of the Supplies the inferior 1/3 of the

brain and brainstembrain and brainstem

Approximately 1,000 ml/min Approximately 1,000 ml/min delivered via two systems.delivered via two systems. Anterior (Anterior (CarotidCarotid) system:) system:

70% of supply (35% from each 70% of supply (35% from each internal carotid artery)internal carotid artery)

Supplies the superior 2/3 of the Supplies the superior 2/3 of the brainbrain

Posterior Posterior ((VertebrobasilarVertebrobasilar)) system:system:

30% of supply30% of supply Supplies the inferior 1/3 of the Supplies the inferior 1/3 of the

brain and brainstembrain and brainstem



Blood Supply to the BrainBlood Supply to the Brain 2/42/4Blood Supply to the BrainBlood Supply to the Brain 2/42/4

CarotidPerfusionTerritory(Superior 2/3)

A.

Verterbo-BasilarPerfusionTerritory(Inferior 1/3)


Anterior system (Anterior system (CarotidCarotid)) 70% of supply (35% from 70% of supply (35% from

each internal carotid artery)each internal carotid artery) Supplies the superior 2/3 of Supplies the superior 2/3 of

the brainthe brain

Anterior system (Anterior system (CarotidCarotid)) 70% of supply (35% from 70% of supply (35% from

each internal carotid artery)each internal carotid artery) Supplies the superior 2/3 of Supplies the superior 2/3 of

the brainthe brain

Click to animateClick to animate

Carotid SystemCarotid System


3/43/4

VertebrobasilarVertebrobasilarSystemSystem

Click to animateClick to animate

Posterior system Posterior system ((VertebrobasilarVertebrobasilar))

30% of supply30% of supply Supplies the inferior 1/3 of Supplies the inferior 1/3 of

the brain and brainstemthe brain and brainstem

Posterior system Posterior system ((VertebrobasilarVertebrobasilar))

30% of supply30% of supply Supplies the inferior 1/3 of Supplies the inferior 1/3 of

the brain and brainstemthe brain and brainstem


4/44/4


Click to Animate

Carotid SystemCarotid System 1/131/13

Anterior cerebral artery

Middle cerebral artery

Anterior communicating artery

Internal carotid artery


Blood SupplyBlood Supply to the Brain to the Brain

Blood SupplyBlood Supply to the Brain to the Brain


2/132/13


Blood Supply to the BrainBlood Supply to the Brain 3/133/13Blood Supply to the BrainBlood Supply to the Brain 3/133/13

Last ViewedLast Viewed Cerebrovascular SystemCerebrovascular System ExitExitConcept MapConcept Map


Carotid SystemCarotid System 4/134/13Carotid SystemCarotid System 4/134/13

Bilateral system, each Bilateral system, each hemisphere has its own carotid hemisphere has its own carotid artery.artery.

Supplies the superior two thirds Supplies the superior two thirds of the brain.of the brain.

Derived from: aorta, common Derived from: aorta, common carotid, internal carotid, carotid carotid, internal carotid, carotid foramen (adjacent to optic foramen (adjacent to optic chiasm)chiasm) Anterior cerebral arteryAnterior cerebral artery (ACA) (ACA) Middle cerebral arteryMiddle cerebral artery (MCA) (MCA)

Bilateral system, each Bilateral system, each hemisphere has its own carotid hemisphere has its own carotid artery.artery.

Supplies the superior two thirds Supplies the superior two thirds of the brain.of the brain.

Derived from: aorta, common Derived from: aorta, common carotid, internal carotid, carotid carotid, internal carotid, carotid foramen (adjacent to optic foramen (adjacent to optic chiasm)chiasm) Anterior cerebral arteryAnterior cerebral artery (ACA) (ACA) Middle cerebral arteryMiddle cerebral artery (MCA) (MCA)



Lateral fissure



Anterior Cerebral ArteryAnterior Cerebral Artery 8/138/13Anterior Cerebral ArteryAnterior Cerebral Artery 8/138/13

ADAM



Middle Cerebral ArteryMiddle Cerebral Artery 9/139/13Middle Cerebral ArteryMiddle Cerebral Artery 9/139/13

ADAM



Middle Cerebral ArteryMiddle Cerebral Artery 11/1311/13Middle Cerebral ArteryMiddle Cerebral Artery 11/1311/13




Perfusion territory by artery



Carotid Carotid PerfusionPerfusion

With With HomunculusHomunculus

13/1313/13



Vertebrobasilar SystemVertebrobasilar System 1/91/9 Vertebrobasilar SystemVertebrobasilar System 1/91/9

Supplies the inferior one third of Supplies the inferior one third of the brain; inferior surface of the the brain; inferior surface of the temporal and occipital lobes and temporal and occipital lobes and brainstem.brainstem.

Derived from: subclavian, Derived from: subclavian, vertebral, foramen magnum, vertebral, foramen magnum, anterior spinal, posterior inferior anterior spinal, posterior inferior cerebellar, basilar, anterior cerebellar, basilar, anterior inferior cerebellar, internal inferior cerebellar, internal auditory, superior cerebellar, auditory, superior cerebellar, posterior cerebral arteryposterior cerebral artery

Supplies the inferior one third of Supplies the inferior one third of the brain; inferior surface of the the brain; inferior surface of the temporal and occipital lobes and temporal and occipital lobes and brainstem.brainstem.

Derived from: subclavian, Derived from: subclavian, vertebral, foramen magnum, vertebral, foramen magnum, anterior spinal, posterior inferior anterior spinal, posterior inferior cerebellar, basilar, anterior cerebellar, basilar, anterior inferior cerebellar, internal inferior cerebellar, internal auditory, superior cerebellar, auditory, superior cerebellar, posterior cerebral arteryposterior cerebral artery



Vertebrobasilar SystemVertebrobasilar System 2/92/9Vertebrobasilar SystemVertebrobasilar System 2/92/9




ADAM




ADAM

Vertebral a.

Basilar a.


Posterior Cerebral ArteryPosterior Cerebral Artery 7/97/9Posterior Cerebral ArteryPosterior Cerebral Artery 7/97/9


Posterior Cerebral ArteryPosterior Cerebral Artery 8/98/9Posterior Cerebral ArteryPosterior Cerebral Artery 8/98/9



Posterior Cerebral ArteryPosterior Cerebral Artery9/99/9Posterior Cerebral ArteryPosterior Cerebral Artery9/99/9


CircleCircleOfOf

WillisWillis



Perfusion TerritoriesPerfusion TerritoriesPerfusion TerritoriesPerfusion TerritoriesWatershed Territory

Primary Artery Territory



3 Cerebellar Arteries3 Cerebellar Arteries3 Cerebellar Arteries3 Cerebellar Arteries

Pons

Medulla

Superior cerebellar a

Anterior inferior cerebellar a

Posterior inferior cerebellar a



Venous DrainageVenous Drainage 1/21/2Venous DrainageVenous Drainage 1/21/2

Superior sagittal sinus

Inferior sagittal sinus

Straight sinus

Transverse sinus

Sigmoid sinus

Jugular vein



Venous DrainageVenous Drainage 2/22/2Venous DrainageVenous Drainage 2/22/2

Superior sagittal sinus

Inferior sagittal sinus

Straight sinus

Transverse sinus

Sigmoid sinus

Jugular vein


BloodBloodSupplySupplyto theto the

Spinal Spinal CordCord

BloodBloodSupplySupplyto theto the

Spinal Spinal CordCord


1/21/2



Spinal ArteriesSpinal Arteries 2/22/2Spinal ArteriesSpinal Arteries 2/22/2Anterior Posterior



Patient CasesPatient CasesPatient CasesPatient Cases Occlusion of the anterior spinal arteryOcclusion of the anterior spinal artery Sudden Inability to SpeakSudden Inability to Speak Left Leg WeaknessLeft Leg Weakness Sudden-onset Worst Headache of LifeSudden-onset Worst Headache of Life Decreased Vision in One EyeDecreased Vision in One Eye Left NeglectLeft Neglect


Click for answer

The anterior spinal artery perfuses the anterior 2/3 of the spinal cord including the ventral horns as well as all tracts in the lateral and anterior columns, bilaterally. Damage to the lateral corticospinal tracts cause upper motor neuron signs, bilaterally, below the lesion level. Damage to lower motor neurons in the ventral horns cause lower motor neuron signs, bilaterally, at the lesion level. Damage to the lateral spinothalamic tracts cause absence of pain and temperature sensation, bilaterally, below the lesion level. Sparing of the dorsal columns leaves light touch, vibration, and position sense intact throughout.

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Occlusion of the anterior spinal artery (anterior cord syndrome) in the cervical region would produce what impairments?

Last ViewedLast Viewed Patient CasesPatient Cases

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UMN

DRG

UMN

DRG

R L

Anterior cord lesion

Lateral corticospinal tract lesionIpsilateral upper motor neurons signs

Contralateral loss of pain and temperature sense

Lateral spinothalamic tract lesion

Anterior Cord Syndrome 2/2Anterior Cord Syndrome 2/2

Common causes include anterior spinal artery infarct, trauma, and MS.

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MinicaseMinicaseSudden Inability to SpeakSudden Inability to Speak 1/51/5

MinicaseMinicaseSudden Inability to SpeakSudden Inability to Speak 1/51/5

While standing in the check-out line at the store, 55 year-While standing in the check-out line at the store, 55 year-old retired nurse realized she was suddenly unable to old retired nurse realized she was suddenly unable to speak. Consciousness, attention, voluntary movement, speak. Consciousness, attention, voluntary movement, and the ability to understand speech were all unaffected. and the ability to understand speech were all unaffected. Incredulous, but believing she knew what is happening to Incredulous, but believing she knew what is happening to her. She left the store and drove herself directly to the her. She left the store and drove herself directly to the emergency room. In the ER she communicated to emergency room. In the ER she communicated to doctors what she thought was occurring. With difficulty doctors what she thought was occurring. With difficulty she uttered two words: “stroke” and “speech”.she uttered two words: “stroke” and “speech”.

While standing in the check-out line at the store, 55 year-While standing in the check-out line at the store, 55 year-old retired nurse realized she was suddenly unable to old retired nurse realized she was suddenly unable to speak. Consciousness, attention, voluntary movement, speak. Consciousness, attention, voluntary movement, and the ability to understand speech were all unaffected. and the ability to understand speech were all unaffected. Incredulous, but believing she knew what is happening to Incredulous, but believing she knew what is happening to her. She left the store and drove herself directly to the her. She left the store and drove herself directly to the emergency room. In the ER she communicated to emergency room. In the ER she communicated to doctors what she thought was occurring. With difficulty doctors what she thought was occurring. With difficulty she uttered two words: “stroke” and “speech”.she uttered two words: “stroke” and “speech”.



MinicaseMinicase Sudden Inability to SpeakSudden Inability to Speak 2/52/5

MinicaseMinicase Sudden Inability to SpeakSudden Inability to Speak 2/52/5

Her past medical history was notable for overweight, Her past medical history was notable for overweight, hypertension and type II diabetes. hypertension and type II diabetes.

Examination revealed loss of the nasal-labial fold on Examination revealed loss of the nasal-labial fold on the left and weakness in the left cheek and jaw. the left and weakness in the left cheek and jaw.

Her jaw-jerk reflex was hyperactive. Her jaw-jerk reflex was hyperactive. All other movement, sensation, and reflexes were All other movement, sensation, and reflexes were

within normal limits. within normal limits.

Where is the lesion causing these symptoms?Where is the lesion causing these symptoms?

Her past medical history was notable for overweight, Her past medical history was notable for overweight, hypertension and type II diabetes. hypertension and type II diabetes.

Examination revealed loss of the nasal-labial fold on Examination revealed loss of the nasal-labial fold on the left and weakness in the left cheek and jaw. the left and weakness in the left cheek and jaw.

Her jaw-jerk reflex was hyperactive. Her jaw-jerk reflex was hyperactive. All other movement, sensation, and reflexes were All other movement, sensation, and reflexes were

within normal limits. within normal limits.




Minicase Follow-UpMinicase Follow-Up Sudden Inability to SpeakSudden Inability to Speak 3/53/5


As confirmed by CT image, this woman was having a As confirmed by CT image, this woman was having a stroke. stroke.

The occlusion involved a deep penetrating branch of The occlusion involved a deep penetrating branch of the the middle cerebral arterymiddle cerebral artery supplying the inferior frontal supplying the inferior frontal gyrus on the gyrus on the leftleft causing weakness in the lower part of causing weakness in the lower part of the right face and tongue and Broca’s aphasia. the right face and tongue and Broca’s aphasia.

As confirmed by CT image, this woman was having a As confirmed by CT image, this woman was having a stroke. stroke.

The occlusion involved a deep penetrating branch of The occlusion involved a deep penetrating branch of the the middle cerebral arterymiddle cerebral artery supplying the inferior frontal supplying the inferior frontal gyrus on the gyrus on the leftleft causing weakness in the lower part of causing weakness in the lower part of the right face and tongue and Broca’s aphasia. the right face and tongue and Broca’s aphasia.



Productive (Broca’s) AphasiaProductive (Broca’s) Aphasia 4/54/5Productive (Broca’s) AphasiaProductive (Broca’s) Aphasia 4/54/5 Produced by a lesion of Produced by a lesion of

the inferior frontal gyrus the inferior frontal gyrus of the dominant of the dominant hemisphere.hemisphere.

Play recordingPlay recording

Produced by a lesion of Produced by a lesion of the inferior frontal gyrus the inferior frontal gyrus of the dominant of the dominant hemisphere.hemisphere.

Play recordingPlay recording





The key signs and symptoms in this case are:The key signs and symptoms in this case are: Suddenly unable to speakSuddenly unable to speak Consciousness, attention, voluntary movement, and Consciousness, attention, voluntary movement, and

the ability to understand speech were all unaffectedthe ability to understand speech were all unaffected Loss of the nasal-labial fold on the left and weakness in Loss of the nasal-labial fold on the left and weakness in

the left cheek and jawthe left cheek and jaw Her jaw-jerk reflex was hyperactiveHer jaw-jerk reflex was hyperactive

The key signs and symptoms in this case are:The key signs and symptoms in this case are: Suddenly unable to speakSuddenly unable to speak Consciousness, attention, voluntary movement, and Consciousness, attention, voluntary movement, and

the ability to understand speech were all unaffectedthe ability to understand speech were all unaffected Loss of the nasal-labial fold on the left and weakness in Loss of the nasal-labial fold on the left and weakness in

the left cheek and jawthe left cheek and jaw Her jaw-jerk reflex was hyperactiveHer jaw-jerk reflex was hyperactive



MinicaseMinicaseLeft Leg WeaknessLeft Leg Weakness 1/51/5


On attempting to stand after finishing breakfast, a On attempting to stand after finishing breakfast, a 67-year-old woman fell to the ground, hitting the 67-year-old woman fell to the ground, hitting the table on the way down, because she was unable table on the way down, because she was unable to support her body weight on her left leg. She to support her body weight on her left leg. She called for help from her husband who was unable called for help from her husband who was unable to get her off the floor and called for emergency to get her off the floor and called for emergency assistance. assistance.

On attempting to stand after finishing breakfast, a On attempting to stand after finishing breakfast, a 67-year-old woman fell to the ground, hitting the 67-year-old woman fell to the ground, hitting the table on the way down, because she was unable table on the way down, because she was unable to support her body weight on her left leg. She to support her body weight on her left leg. She called for help from her husband who was unable called for help from her husband who was unable to get her off the floor and called for emergency to get her off the floor and called for emergency assistance. assistance.





Her past history was notable for obesity, hypertension, Her past history was notable for obesity, hypertension, peripheral vascular disease, and smoking one pack per day for peripheral vascular disease, and smoking one pack per day for 52 years. 52 years.

She had hyperactive deep tendon reflexes in her left knee and She had hyperactive deep tendon reflexes in her left knee and ankle, and a positive Babinski sign in her left foot. ankle, and a positive Babinski sign in her left foot.

The left leg was flaccid and she had no voluntary control of The left leg was flaccid and she had no voluntary control of movement. movement.

She had mild impairment of light touch, pain, and temperature She had mild impairment of light touch, pain, and temperature sensation in her left leg. sensation in her left leg.

Voluntary movement, reflexes, and sensation were intact in all Voluntary movement, reflexes, and sensation were intact in all other regions of the body. other regions of the body.


Her past history was notable for obesity, hypertension, Her past history was notable for obesity, hypertension, peripheral vascular disease, and smoking one pack per day for peripheral vascular disease, and smoking one pack per day for 52 years. 52 years.

She had hyperactive deep tendon reflexes in her left knee and She had hyperactive deep tendon reflexes in her left knee and ankle, and a positive Babinski sign in her left foot. ankle, and a positive Babinski sign in her left foot.

The left leg was flaccid and she had no voluntary control of The left leg was flaccid and she had no voluntary control of movement. movement.

She had mild impairment of light touch, pain, and temperature She had mild impairment of light touch, pain, and temperature sensation in her left leg. sensation in her left leg.

Voluntary movement, reflexes, and sensation were intact in all Voluntary movement, reflexes, and sensation were intact in all other regions of the body. other regions of the body.




Minicase Follow-UpMinicase Follow-Up Left Leg WeaknessLeft Leg Weakness 3/53/5


A head CT scan was done and the results A head CT scan was done and the results suggested a probable rightsuggested a probable right anterior cerebral anterior cerebral artery infarct. artery infarct.

Follow-up hear CT scan one month later Follow-up hear CT scan one month later confirmed the presence of a hypodense area on confirmed the presence of a hypodense area on the anterior medial aspect of the right the anterior medial aspect of the right hemisphere consistent with a hemisphere consistent with a right anterior right anterior cerebral arterycerebral artery infarct infarct

A head CT scan was done and the results A head CT scan was done and the results suggested a probable rightsuggested a probable right anterior cerebral anterior cerebral artery infarct. artery infarct.

Follow-up hear CT scan one month later Follow-up hear CT scan one month later confirmed the presence of a hypodense area on confirmed the presence of a hypodense area on the anterior medial aspect of the right the anterior medial aspect of the right hemisphere consistent with a hemisphere consistent with a right anterior right anterior cerebral arterycerebral artery infarct infarct





The key signs and symptoms in this case are:The key signs and symptoms in this case are: Unable to support her body weight on her left legUnable to support her body weight on her left leg Hyperactive deep tendon reflexes in her left knee and ankle, and Hyperactive deep tendon reflexes in her left knee and ankle, and

a positive Babinski sign in her left foota positive Babinski sign in her left foot The left leg was flaccid and she had no voluntary control of The left leg was flaccid and she had no voluntary control of

movementmovement She had mild impairment of light touch, pain, and temperature She had mild impairment of light touch, pain, and temperature

sensation in her left legsensation in her left leg Voluntary movement, reflexes, and sensation were intact in all Voluntary movement, reflexes, and sensation were intact in all

other regions of the bodyother regions of the body

The key signs and symptoms in this case are:The key signs and symptoms in this case are: Unable to support her body weight on her left legUnable to support her body weight on her left leg Hyperactive deep tendon reflexes in her left knee and ankle, and Hyperactive deep tendon reflexes in her left knee and ankle, and

a positive Babinski sign in her left foota positive Babinski sign in her left foot The left leg was flaccid and she had no voluntary control of The left leg was flaccid and she had no voluntary control of

movementmovement She had mild impairment of light touch, pain, and temperature She had mild impairment of light touch, pain, and temperature

sensation in her left legsensation in her left leg Voluntary movement, reflexes, and sensation were intact in all Voluntary movement, reflexes, and sensation were intact in all

other regions of the bodyother regions of the body



MinicaseMinicaseSudden-onset Worst Headache of LifeSudden-onset Worst Headache of Life 1/71/7


A 68-year-old man suddenly developed “the worst of A 68-year-old man suddenly developed “the worst of my life.” On the morning of admission he was sitting my life.” On the morning of admission he was sitting watching TV when at 9:00 am he suddenly developed watching TV when at 9:00 am he suddenly developed an explosive headache worse than anything he had an explosive headache worse than anything he had ever experienced. The headache began in the bifrontal ever experienced. The headache began in the bifrontal area and over the next few minutes all over the head area and over the next few minutes all over the head and down the neck. He denied loss of consciousness, and down the neck. He denied loss of consciousness, nausea, vomiting or vision changes. nausea, vomiting or vision changes.

A 68-year-old man suddenly developed “the worst of A 68-year-old man suddenly developed “the worst of my life.” On the morning of admission he was sitting my life.” On the morning of admission he was sitting watching TV when at 9:00 am he suddenly developed watching TV when at 9:00 am he suddenly developed an explosive headache worse than anything he had an explosive headache worse than anything he had ever experienced. The headache began in the bifrontal ever experienced. The headache began in the bifrontal area and over the next few minutes all over the head area and over the next few minutes all over the head and down the neck. He denied loss of consciousness, and down the neck. He denied loss of consciousness, nausea, vomiting or vision changes. nausea, vomiting or vision changes.





History was positive for severe diffuse History was positive for severe diffuse atherosclerosis, including coronary disease and atherosclerosis, including coronary disease and peripheral vascular disease requiring multiple peripheral vascular disease requiring multiple bypass surgeries. bypass surgeries.

He was obese and smoked two packs a day for He was obese and smoked two packs a day for 43 years. 43 years.

Examination was unremarkable except for mild Examination was unremarkable except for mild nuchal rigidity. nuchal rigidity.

History was positive for severe diffuse History was positive for severe diffuse atherosclerosis, including coronary disease and atherosclerosis, including coronary disease and peripheral vascular disease requiring multiple peripheral vascular disease requiring multiple bypass surgeries. bypass surgeries.

He was obese and smoked two packs a day for He was obese and smoked two packs a day for 43 years. 43 years.

Examination was unremarkable except for mild Examination was unremarkable except for mild nuchal rigidity. nuchal rigidity.



Minicase Follow-UpMinicase Follow-UpSudden-onset Worst Headache of LifeSudden-onset Worst Headache of Life 3/73/7


Nuchal rigidity is often a sign of meningeal Nuchal rigidity is often a sign of meningeal irritation caused by inflammation, infection, or irritation caused by inflammation, infection, or hemorrhage in the subarachnoid space.hemorrhage in the subarachnoid space.

Nuchal rigidity is often a sign of meningeal Nuchal rigidity is often a sign of meningeal irritation caused by inflammation, infection, or irritation caused by inflammation, infection, or hemorrhage in the subarachnoid space.hemorrhage in the subarachnoid space.





The man underwent emergency head CT which The man underwent emergency head CT which demonstrated regions of hyperdensity in the demonstrated regions of hyperdensity in the subarachnoid space consistent with subarachnoid subarachnoid space consistent with subarachnoid hemorrhage layering in the medial longitudinal hemorrhage layering in the medial longitudinal fissure, lateral fissure, and around the brainstem. fissure, lateral fissure, and around the brainstem.

Next he was taken for an angiogram which clearly Next he was taken for an angiogram which clearly revealed an revealed an aneurysmaneurysm arising from the region of the arising from the region of the anterior communicating arteryanterior communicating artery. .

The man underwent emergency head CT which The man underwent emergency head CT which demonstrated regions of hyperdensity in the demonstrated regions of hyperdensity in the subarachnoid space consistent with subarachnoid subarachnoid space consistent with subarachnoid hemorrhage layering in the medial longitudinal hemorrhage layering in the medial longitudinal fissure, lateral fissure, and around the brainstem. fissure, lateral fissure, and around the brainstem.

Next he was taken for an angiogram which clearly Next he was taken for an angiogram which clearly revealed an revealed an aneurysmaneurysm arising from the region of the arising from the region of the anterior communicating arteryanterior communicating artery. .



The circle of Willis has been dissected, and three berry aneurysms are seen. Multiple aneurysms are seen in about 20-30% of cases of berry aneurysm. Such aneurysms are "congenital" in the sense that the defect in the arterial wall is present from birth, but the actual aneurysm takes years to develop, so that rupture is most likely to occur in young to middle age adults.

Berry AneurysmBerry Aneurysm 5/75/7



The white arrow on the black card marks the site of a ruptured berry aneurysm in the circle of Willis. This is a major cause for subarachnoid hemorrhage.

Berry AneurysmBerry Aneurysm 6/76/7





The key signs and symptoms in this case are:The key signs and symptoms in this case are: Suddenly developed “the worst of my life”Suddenly developed “the worst of my life” Headache began in the bifrontal area and over the next Headache began in the bifrontal area and over the next

few minutes was all over the head and down the neckfew minutes was all over the head and down the neck Examination was unremarkable except for mild nuchal Examination was unremarkable except for mild nuchal

rigidityrigidity

The key signs and symptoms in this case are:The key signs and symptoms in this case are: Suddenly developed “the worst of my life”Suddenly developed “the worst of my life” Headache began in the bifrontal area and over the next Headache began in the bifrontal area and over the next

few minutes was all over the head and down the neckfew minutes was all over the head and down the neck Examination was unremarkable except for mild nuchal Examination was unremarkable except for mild nuchal

rigidityrigidity



MinicaseMinicase Decreased Vision in One EyeDecreased Vision in One Eye 1/81/8


A 63-year-old woman went to an A 63-year-old woman went to an ophthalmologist complaining of episodes of ophthalmologist complaining of episodes of decreased vision in her “right eye” over the decreased vision in her “right eye” over the past several weeks. past several weeks.

A 63-year-old woman went to an A 63-year-old woman went to an ophthalmologist complaining of episodes of ophthalmologist complaining of episodes of decreased vision in her “right eye” over the decreased vision in her “right eye” over the past several weeks. past several weeks.





Her medical history was notable for type II diabetes, Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease.hypercholesterolemia, and coronary artery disease.

About 5-6 weeks ago the patient began having About 5-6 weeks ago the patient began having “episodes of sudden blurry wavy” appearance of her “episodes of sudden blurry wavy” appearance of her vision. vision.

She believed this was mostly in the right eye but never She believed this was mostly in the right eye but never tried looking with only one eye at a time. tried looking with only one eye at a time.

Her medical history was notable for type II diabetes, Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease.hypercholesterolemia, and coronary artery disease.

About 5-6 weeks ago the patient began having About 5-6 weeks ago the patient began having “episodes of sudden blurry wavy” appearance of her “episodes of sudden blurry wavy” appearance of her vision. vision.

She believed this was mostly in the right eye but never She believed this was mostly in the right eye but never tried looking with only one eye at a time. tried looking with only one eye at a time.





Episodes would last for 15-20 minutes, resolved with Episodes would last for 15-20 minutes, resolved with no visual impairment, repeated 3-4 times per week, and no visual impairment, repeated 3-4 times per week, and were never accompanied by pain. were never accompanied by pain.

Previously she was able to recognize faces during the Previously she was able to recognize faces during the episodes but was unable to read. episodes but was unable to read.

The current episode, that began two days ago, has The current episode, that began two days ago, has resulted in persistent decreased vision on the right.resulted in persistent decreased vision on the right.

Episodes would last for 15-20 minutes, resolved with Episodes would last for 15-20 minutes, resolved with no visual impairment, repeated 3-4 times per week, and no visual impairment, repeated 3-4 times per week, and were never accompanied by pain. were never accompanied by pain.

Previously she was able to recognize faces during the Previously she was able to recognize faces during the episodes but was unable to read. episodes but was unable to read.

The current episode, that began two days ago, has The current episode, that began two days ago, has resulted in persistent decreased vision on the right.resulted in persistent decreased vision on the right.





Neurologic examination revealed fluent speech. Neurologic examination revealed fluent speech. Pupils 3 mm, constricting to 2 mm bilaterally. Pupils 3 mm, constricting to 2 mm bilaterally. Normal fundi. Visual acuity 20/30 right and 20/25 left. Normal fundi. Visual acuity 20/30 right and 20/25 left. Visual field testing revealed a right homonymous hemianopia. Visual field testing revealed a right homonymous hemianopia. Extraocular movements intact. Extraocular movements intact. Facial sensation intact to light touch and pinprick. Facial sensation intact to light touch and pinprick. Face symmetrical. Normal palate elevation. Face symmetrical. Normal palate elevation. Normal shoulder shrug. Tongue midline. Normal shoulder shrug. Tongue midline.


Neurologic examination revealed fluent speech. Neurologic examination revealed fluent speech. Pupils 3 mm, constricting to 2 mm bilaterally. Pupils 3 mm, constricting to 2 mm bilaterally. Normal fundi. Visual acuity 20/30 right and 20/25 left. Normal fundi. Visual acuity 20/30 right and 20/25 left. Visual field testing revealed a right homonymous hemianopia. Visual field testing revealed a right homonymous hemianopia. Extraocular movements intact. Extraocular movements intact. Facial sensation intact to light touch and pinprick. Facial sensation intact to light touch and pinprick. Face symmetrical. Normal palate elevation. Face symmetrical. Normal palate elevation. Normal shoulder shrug. Tongue midline. Normal shoulder shrug. Tongue midline.




MinicaseMinicase Follow-UpFollow-UpDecreased Vision in One EyeDecreased Vision in One Eye 5/85/8


The transient episodes of 15-20 minutes of decreased The transient episodes of 15-20 minutes of decreased right-sided vision occurring over several weeks, right-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is followed by a sudden-onset persistent deficit is suggestive of TIAs preceding a cerebral infarct. suggestive of TIAs preceding a cerebral infarct.

A right homonymous hemianopia can be caused by a A right homonymous hemianopia can be caused by a lesion in the left hemisphere visual pathway anywhere lesion in the left hemisphere visual pathway anywhere from the left optic tract to the primary visual cortex. from the left optic tract to the primary visual cortex.

The patient’s age and past medical history raise the The patient’s age and past medical history raise the suspicion of cerebrovascular disease of the cause. suspicion of cerebrovascular disease of the cause.

The transient episodes of 15-20 minutes of decreased The transient episodes of 15-20 minutes of decreased right-sided vision occurring over several weeks, right-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is followed by a sudden-onset persistent deficit is suggestive of TIAs preceding a cerebral infarct. suggestive of TIAs preceding a cerebral infarct.

A right homonymous hemianopia can be caused by a A right homonymous hemianopia can be caused by a lesion in the left hemisphere visual pathway anywhere lesion in the left hemisphere visual pathway anywhere from the left optic tract to the primary visual cortex. from the left optic tract to the primary visual cortex.

The patient’s age and past medical history raise the The patient’s age and past medical history raise the suspicion of cerebrovascular disease of the cause. suspicion of cerebrovascular disease of the cause.





The patient was sent to the hospital where an initial CT scan The patient was sent to the hospital where an initial CT scan suggested a suggested a left posterior cerebral arteryleft posterior cerebral artery infarct, and a follow-up infarct, and a follow-up MRI confirmed the presence of a left PCS infarct involving the MRI confirmed the presence of a left PCS infarct involving the left primary visual cortex. left primary visual cortex.

An magnetic resonance angiogram (MRA) revealed several An magnetic resonance angiogram (MRA) revealed several stenoses of the cerebral vessels compatible with diffuse stenoses of the cerebral vessels compatible with diffuse intracranial atherosclerotic disease. intracranial atherosclerotic disease.

She was treated with long-term oral anticoagulation. She was treated with long-term oral anticoagulation. Her right hemianopia did not improve, but over time she learned Her right hemianopia did not improve, but over time she learned

to adapt to her visual deficit. to adapt to her visual deficit.

The patient was sent to the hospital where an initial CT scan The patient was sent to the hospital where an initial CT scan suggested a suggested a left posterior cerebral arteryleft posterior cerebral artery infarct, and a follow-up infarct, and a follow-up MRI confirmed the presence of a left PCS infarct involving the MRI confirmed the presence of a left PCS infarct involving the left primary visual cortex. left primary visual cortex.

An magnetic resonance angiogram (MRA) revealed several An magnetic resonance angiogram (MRA) revealed several stenoses of the cerebral vessels compatible with diffuse stenoses of the cerebral vessels compatible with diffuse intracranial atherosclerotic disease. intracranial atherosclerotic disease.

She was treated with long-term oral anticoagulation. She was treated with long-term oral anticoagulation. Her right hemianopia did not improve, but over time she learned Her right hemianopia did not improve, but over time she learned

to adapt to her visual deficit. to adapt to her visual deficit.





MRI axial T2 weighted image of left posterior cerebral artery (PCA) infarction





The key signs and symptoms in this case are:The key signs and symptoms in this case are: Episodes of sudden “blurry/ wavy” appearance of her Episodes of sudden “blurry/ wavy” appearance of her

vision in her “right eye” over the past several weeksvision in her “right eye” over the past several weeks Right homonymous hemianopiaRight homonymous hemianopia

The key signs and symptoms in this case are:The key signs and symptoms in this case are: Episodes of sudden “blurry/ wavy” appearance of her Episodes of sudden “blurry/ wavy” appearance of her

vision in her “right eye” over the past several weeksvision in her “right eye” over the past several weeks Right homonymous hemianopiaRight homonymous hemianopia



MinicaseMinicase Left NeglectLeft Neglect 1/51/5


A 61-year-old right-handed man was witnessed A 61-year-old right-handed man was witnessed slumping to the floor in the grocery store. slumping to the floor in the grocery store.

A 61-year-old right-handed man was witnessed A 61-year-old right-handed man was witnessed slumping to the floor in the grocery store. slumping to the floor in the grocery store.





On examination in the hospital he denied anything was wrong On examination in the hospital he denied anything was wrong but said, “They called an ambulance because they said I had a but said, “They called an ambulance because they said I had a stroke.” stroke.”

He was unaware of having any impairment and wanted to go He was unaware of having any impairment and wanted to go home. home.

He had profound left visual field neglect , no blink to threat on He had profound left visual field neglect , no blink to threat on the left, and no voluntary gaze to the left past midline. the left, and no voluntary gaze to the left past midline.

When trying to right, he moved the pen in the air off to the right When trying to right, he moved the pen in the air off to the right of the page. of the page.

When shown his left hand and asked what it was, he replied When shown his left hand and asked what it was, he replied “Someone’s hand.”“Someone’s hand.”

On examination in the hospital he denied anything was wrong On examination in the hospital he denied anything was wrong but said, “They called an ambulance because they said I had a but said, “They called an ambulance because they said I had a stroke.” stroke.”

He was unaware of having any impairment and wanted to go He was unaware of having any impairment and wanted to go home. home.

He had profound left visual field neglect , no blink to threat on He had profound left visual field neglect , no blink to threat on the left, and no voluntary gaze to the left past midline. the left, and no voluntary gaze to the left past midline.

When trying to right, he moved the pen in the air off to the right When trying to right, he moved the pen in the air off to the right of the page. of the page.

When shown his left hand and asked what it was, he replied When shown his left hand and asked what it was, he replied “Someone’s hand.”“Someone’s hand.”





When asked who’s hand it was he replied, “The When asked who’s hand it was he replied, “The doctor’s.” doctor’s.”

He had a marked right gaze preference. He had a marked right gaze preference. He had marked weakness in the lower portion of the He had marked weakness in the lower portion of the

left face. left face. Strength was 0/5 in the left arm and leg, the left plantar Strength was 0/5 in the left arm and leg, the left plantar

response was upgoing, and there was no response to response was upgoing, and there was no response to pinprick on the left side.pinprick on the left side.

What lesion is causing this man’s symptoms? What lesion is causing this man’s symptoms?

When asked who’s hand it was he replied, “The When asked who’s hand it was he replied, “The doctor’s.” doctor’s.”

He had a marked right gaze preference. He had a marked right gaze preference. He had marked weakness in the lower portion of the He had marked weakness in the lower portion of the

left face. left face. Strength was 0/5 in the left arm and leg, the left plantar Strength was 0/5 in the left arm and leg, the left plantar

response was upgoing, and there was no response to response was upgoing, and there was no response to pinprick on the left side.pinprick on the left side.

What lesion is causing this man’s symptoms? What lesion is causing this man’s symptoms?



MinicaseMinicase Follow-UpFollow-UpLeft NeglectLeft Neglect 4/54/5


The patient exhibits several forms of neglect. The patient exhibits several forms of neglect. In addition to anosognosia, he has left sensory neglect, to In addition to anosognosia, he has left sensory neglect, to

visual and tactile stimuli, as well as left motor neglect. visual and tactile stimuli, as well as left motor neglect. These signs and symptoms are most commonly seen in These signs and symptoms are most commonly seen in

patients with nondominant (usually right) parietal lobe lesions. patients with nondominant (usually right) parietal lobe lesions.

Given the sudden onset of the deficits, involvement of the left Given the sudden onset of the deficits, involvement of the left arm and leg, the presence of sensory and motor deficits, and arm and leg, the presence of sensory and motor deficits, and the patient’s age, the most likely cause is ischemic infarction the patient’s age, the most likely cause is ischemic infarction of the of the right internal carotidright internal carotid arteryartery. .

The patient exhibits several forms of neglect. The patient exhibits several forms of neglect. In addition to anosognosia, he has left sensory neglect, to In addition to anosognosia, he has left sensory neglect, to

visual and tactile stimuli, as well as left motor neglect. visual and tactile stimuli, as well as left motor neglect. These signs and symptoms are most commonly seen in These signs and symptoms are most commonly seen in

patients with nondominant (usually right) parietal lobe lesions. patients with nondominant (usually right) parietal lobe lesions.

Given the sudden onset of the deficits, involvement of the left Given the sudden onset of the deficits, involvement of the left arm and leg, the presence of sensory and motor deficits, and arm and leg, the presence of sensory and motor deficits, and the patient’s age, the most likely cause is ischemic infarction the patient’s age, the most likely cause is ischemic infarction of the of the right internal carotidright internal carotid arteryartery. .





The key signs and symptoms in this case are:The key signs and symptoms in this case are: AnosognosiaAnosognosia Left face, arm and leg plegia with positive Babinski’s Left face, arm and leg plegia with positive Babinski’s

signsign No blink to threat on the leftNo blink to threat on the left No voluntary gaze to the left past midlineNo voluntary gaze to the left past midline No response to pinprick on the leftNo response to pinprick on the left

The key signs and symptoms in this case are:The key signs and symptoms in this case are: AnosognosiaAnosognosia Left face, arm and leg plegia with positive Babinski’s Left face, arm and leg plegia with positive Babinski’s

signsign No blink to threat on the leftNo blink to threat on the left No voluntary gaze to the left past midlineNo voluntary gaze to the left past midline No response to pinprick on the leftNo response to pinprick on the left

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