StrokeConceptMap 2

Etiology and Pathology
Lesion Effects
Demographics Deficits
Stroke
Map of Essential Concepts
Recovery Stroke Treatment
DM McKeough
Cerebrovascular System
2008
Stroke

Demographics Etiology and Pathology Lesion Effects Deficits Recovery Treatment Cerebrovascular System
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Demographics

Brain Metabolism Oxygen Demands Hemiplegia Epidemiology Economic Costs
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Brain Metabolism

Brains sole source of energy is aerobic or oxidative metabolism Therefore, the brain requires a constant supply of O2 and glucose, 24/ 7/ 365
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Demographics
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Oxygen Demands

At approximately 3 pounds, the brain accounts for roughly 2% of body mass Consumes 17% of cardiac output Responsible for 20% of oxygen consumption at rest
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Hemiplegia

The hallmark of stroke is hemiplegia

Hemiparesis + Hemisensory impairment
The great vulnerability of the brain to ischemic damage is due to its dependence on aerobic metabolism
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Epidemiology

(American Heart Association 2005)
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Stroke is the third leading cause of death and the most common cause of disability in the US
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Epidemiology
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Incidence Each year about 700,000 people experience a new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacks) attacks)
Every 45 seconds someone in the US has a stroke (280 strokes during todays class)
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Demographics
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Epidemiology
Gender Distribution Men > Women x 1.25 Ethnic Distribution African-Americans > Whites x 2 African Hispanic Native Americans Native Alaskans Whites
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Epidemiology

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Stroke is a condition of the elderly Incidence increases steadily with age (risk doubles every decade after age 65) 28% of strokes occur in individuals < 65 years of age
(Copenhagen Stroke Study, Arch Phys Med Rehabil, 1995)
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Demographics
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Epidemiology
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Mortality From 1993 to 2003 the death rate from stroke declined 18.5 percent, and the actual number of stroke deaths declined 0.7 percent.
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Epidemiology
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Mortality 22% of men and 25% of women die within first year

2001 stroke killed 163,538 people Every 3.3 minutes someone in US dies of stroke (64
deaths during todays class)
~ 50% of stroke survivors die within 8 years (Males > Females)

Death due to MI
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Epidemiology
Geographic Distribution
Death rate due to stroke per 100,000 in 2001
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Epidemiology
Mortality by type of stroke Hemorrhagic 38% Ischemic 12% (American Heart Association 2005)

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

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Epidemiology
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Recurrence 14% per year, highest in first year Risk of stroke increases 10 times after first stroke Recurring strokes produce larger lesions (cumulative effects), greater cortical involvement, greater impairment, higher mortality Outcome and pattern of recovery is similar to first-time firststroke Should receive similar rehab treatment as first-time firststroke
Epidemiology
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Prevalence About 5,500,000 stroke survivors are alive today 2,400,000 are males and 3,000,000 are females
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Epidemiology

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The following activity limitations were observed at six months post-stroke: post50 % had some one-sided paralysis one35 % had depression 30 % were unable to walk without some assistance 26 % were dependent in activities of daily living (grooming, eating, bathing, etc) 26 % were institutionalized in a nursing home 19 % had aphasia (trouble speaking or understanding the speech of others)
(Framingham Heart Study 2005)

Epidemiology
Disability Due to Stroke

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Stroke is leading cause of chronic disability (Wolfe 2000) ~70% never return to work Stroke is leading cause of inpatient rehab (Granger & Hamilton 1994) 33% require (A) with ADL at one year post (Murray & Lopez 1996) 26% of stroke survivors are in SNF
>50% hospitalized with stroke do not require rehab

Economic Costs

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

Thromboembolic stroke Hemorrhagic stroke: Subarachnoid Intracerebral
$100,000 $228,000 $124,000
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Etiology Common Occlusion Sites Risk Factors Stroke Prevention Predictors of Stroke Warning Signs Predictors of Good Outcome Predictors of Bad Outcome Nagi Model Pathophysiology
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Etiology of Stroke

Stroke is a neurologic deficit of sudden onset due to interruption of the blood supply to the brain resulting in infarction and permanent CNS damage.
Hemorrhagic 20%
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Ischemic 80%
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Common 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
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Risk Factors
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
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Less Well Documented (perhaps partly modifiable)

Geography/climate Socioeconomic factors
Source: American Stroke Association. Heart and Stroke Facts. 1996.
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Risk Factors

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Modifiable Risk Factor

Major

Hypertension Heart disease, especially atrial fibrillation Cigarette smoking Transient ischemic attacks Increased serum cholesterol / lipids Physical inactivity Obesity Excessive alcohol intake / drug abuse Acute infection* * Not listed in the ASA publication
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Secondary

Less Well Documented

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Genetic Risk Factors for Stroke 3/3

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.
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Stroke Prevention
Exercise reduces the risk of stroke
Intense exercise 27%
Intense exercise: jogging 15 to 20 minutes a day on most days
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Moderate exercise
20%
Moderate exercise: brisk walks of 30 minutes a day on most days

J Stroke: Oct 2003
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Stroke Prevention

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Prevention

Clot Buster (Tissue Plasminogen Activator, TPA,)
Recent research

Tissue grafting Genetic engineering
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Predictors of Stroke

Previous stroke Transient ischemic attacks: 35% of thrombotic strokes were preceded by TIA
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Warning Signs

Characterized by sudden onset focal neurological deficit Warning signs: Call for medical assistance Sudden numbness or weakness of the face, arm or leg, especially on one side of the body Sudden confusion, trouble speaking or understanding Sudden trouble seeing in one or both eyes Sudden trouble walking, dizziness, loss of balance or coordination Sudden, severe headache with no known cause (American Stroke Association 2000)
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Predictors of Good Outcome

The higher the socioeconomic status, the better the outcome The higher the education, the better the outcome The more active the premorbid lifestyle, the better the outcome All things being equal, the younger the age, the better the outcome Only sensory or only motor impairments (the smaller the lesion), the better the outcome Never loosing consciousness Little comorbidity
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Predictors of Bad Outcome 1/2

Severe initial functional deficits Dense sensory or motor impairments Hemianopsia Severe visuospatial deficits (hemineglect or hemiinattention) Severe aphasia Major depression Lack of return of hand function within 96 hours Altered level of consciousness
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Predictors of Bad Outcome 2/2

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

Pathology
Ischemia produces CNS lesion (neuronal death) Impairment
Functional
Limitation Impairments limit ability to perform B/I ADL
Disability
CNS lesion produces hemiplegia & spasticity
ADL limitations prevent ability to perform expected social role
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Pathophysiology

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Transient ischemic attack (TIA)

Caused by reversible ischemia (usually due to vasospasm). Results in temporary functional impairment with no residual deficits. ~35% of TIAs evolve into stroke within 1-3 years 1-
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Pathophysiology

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Stroke
Caused by irreversible ischemia Results in a circumscribed area of infarction (primary damage) (primary damage) and Perimeter of increased pressure due to inflammation (secondary (secondary damage) damage) The most damaging results of vascular occlusion are produced by secondary damage

Primary damage Secondary damage
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Phagocytosis Following Stroke 3/10
This intermediate infarct of the frontal lobe shows liquefactive necrosis with formation of cystic spaces as resolution begins.
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Phagocytosis Following Stroke
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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.
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MCA Stroke
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This is an intermediate to remote infarct in the distribution of the middle cerebral artery.
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MCA Stroke
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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.
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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.
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Watershed Infarction
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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. Last Viewed
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Berry Aneurysms
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.
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Berry Aneurysms
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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.
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Lesion Effects

Domains Affected by Stroke Hemispheric Effects Symptoms by Lesion Location Ideational Apraxia Motor Apraxia
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Domains Affected by Stroke

Motor Sensory Vision Language Cognition Affect
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Hemispheric Effects

Hemispheric Specialization Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Nondominant Hemisphere
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Hemispheric Specialization
Left Hemisphere Intellectual Rational Verbal Analytical Right Hemisphere Perceptive Holistic Spatial Emotional Nonverbal
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Dominant Hemisphere

Dominant = hemisphere with language (Broca, Wernicke) Left hemisphere is the dominant hemisphere in the vast majority of the population (95%)
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Stroke in the 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
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Stroke in the Nondominant Hemisphere

Characterized by:

Left hemiparesis Left sensory loss Disturbance of spatial orientation * Left unilateral neglect (in some cases) * Impairment of hand eye coordination, figurefigureground discrimination, form constancy
Hemispheric Effects
Dressing and constructional apraxia Poor judgment * Unrealistic expectations * Denial of disability * * Contributes to poor outcome
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Symptoms by Lesion Location

Frontal Movement impairment Personality changes Cognitive impairment Delayed initiation Aphasia (Broca) Parietal Somatosensory impairment Spatial relations impairment Homonymous visual deficits Agnosia Language comprehension impairment Occipital Homonymous hemianopsia Eye movement impairment
Temporal lobe Auditory and perceptual impairment Memory and learning impairment Aphasia (Wernicke)
Cerebellopontine angle Brainstem Hearing impairment Gait impairment Ataxia Diplopia Tinnitus Focal weakness Dizziness Consciousness and Lesion Effects Last Viewed Facial palsy attention impairmentConcept Map
Cerebellar Ataxia Ipsilateral dysmetria Dysdiadochokinesia Intention tremor
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Ideational Apraxia

Unable to perform a task either automatically or on command, although individual movements can be made correctly Patient does not understand the concept of the act, cannot retain the idea, or cannot formulate motor patterns required Often unable to describe the process of a task Given toothpaste and brush, will try to apply toothpaste w/o removing cap, or may put tube into mouth
Due to lesion of the parietal lobe in the dominant hemisphere or the corpus callosum
Dominant Hemisphere
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Kinetic (Motor) Apraxia

Inability to perform fine learned movements in the absence of weakness or sensory loss Due to bilateral lesion (disease) of the frontal lobes
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Deficits

Common Deficits Anatomic Substrate of Deficits
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Common Deficits Following Stroke

DEFICIT Hemiparesis Incoordination Dysarthria Sensory impairment Aphasia Memory impairment Bladder incontinence Dysphagia ACUTE (%) 88 86 57 53 36 36 29 13 CHRONIC (%) 48 61 16 24 18 31 9 4
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Anatomic Substrate of Deficits

DEFICIT Hemiparesis Incoordination Dysarthria Sensory impairment Aphasia Memory impairment Bladder incontinence Dysphagia Last Viewed NEUROANATOMIC SUBSTRATE Lesion of cortical motor centers (UMN) Lesion of cortical motor centers (dorsolateral and ventromedial systems) Lesion of corticobulbar tract (input to CNs) Lesion of somatosensory cortex Lesion of language centers (Broca, Wernicke) Lesion of temporal lobe (hippocampus) Lesion of autonomic input to sacral region of spinal cord (hypothalamus) Lesion of corticobulbar tract (B input to CN X) Deficits Concept Map Exit
Recovery

Natural History of Recovery Recovery With Intervention Pattern of Recovery Theories of Recovery
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Recovery
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Natural History of Recovery

120 100 80 Function 60 40 20 0
* Using conventional
rehabilitation approaches
CV A
or bi d
m o
m o 12
19
m o
Pr em
(Post-Stroke Rehabilitation Guideline Panel 1995)
Function
Recovery
Majority of recovery of function occurs in the first 3 months From 3 mo. - 1 yr. recovery may continue at much slower rate
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Recovery With Intervention

EvidenceEvidence-based Practice Data now show that natural history of recovery can be changed by the right type of intervention Constraint induced therapy (CIT) and weight supported treadmill training (WSTT) change the natural history of recovery Conventional rehabilitation techniques do not change the natural history of recovery
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Recovery
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Pattern of Recovery

Initially: hypotonia/ flaccidity

Due to the interruption of UMN input to LMN
Days to weeks later: hypertonia/ spasticity

??? A leading question in stroke recovery Due in part to

Decreased threshold in alpha LMN and Denervation supersensitivity

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Recovery
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Theories of the Recovery of Function

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)
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Regenerative synaptogenesis
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Recovery
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Cellular Response to Injury

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
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Theories of Recovery
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Reactive Synaptogenesis

CNS response to injury No re-establishing functional reconnections with target cells occurs, any recovery of function occurs via collateral sprouting from intact neurons &/or reorganization (intact systems assume the lost function, neuroplasticity) neuroplasticity)
collateral sprouting +/or reorganization = neuroplasticity
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Cortical Reorganization

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 longterm
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Cortical Reorganization
Use-Dependent Cortical Reorganization After Brain Injury
Mechanisms of effectiveness of Constraint-Induced Movement Therapy (CIMT)

Taub et al 1998 Last Viewed Theories of Recovery Concept Map Exit
Alternate Pathways

What mechanisms underlie the recovery of function?

Ipsilateral motor tracts take over
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Regenerative 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
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Stroke Treatment

Referral Patterns Treatment Efficacy Unaffected" Upper Extremity Stroke Treatment Recovery of Locomotion Life Probability Tables
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Possible Routes Through Medical System

IP Rehab 3 hrs/day LOS: 3-4 wks Subacute Rehab 1.5 hrs/day LOS: 5-6 wks Stroke Hospital
LOS: 5-7 days
Home w H H LOS: ~2 wks Home w H H LOS: ~2 wks
Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks
SNF Usually permanent Rehab bed Home w H H LOS: ~2 wks Home w H H Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks
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Stroke Treatment
Treatment Efficacy

Conventional therapy produces only a modest, temporary improvement in function (The Lancet Vol 359
No 9302, January 19, 2002)
PT treatment effects are achieved through a neuroplastic reorganization of motor control centers (Treatment-Induced Cortical Reorganization After Stroke in Humans. (TreatmentTaub et al., Stroke 2000; 31: 1210)
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Unaffected" Upper Extremity

Following stroke, the unaffected UE showed decreases in:

functional independence due to decreased fine manual dexterity activity level due to decreases in kinesthesia and gross dexterity
There is no such thing as an unaffected extremity

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Stroke Treatment

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Prevention

Reduce modifiable risk factors

Vigorous exercise
(J Stroke: Oct 2003)
MD: antiplatlet or anticoagulant therapy
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Stroke Treatment
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Stroke Treatment

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Acute phase

MD: thrombolytic agents or acute anticoagulation drugs (TPA) may be successful in reversing primary impairments PT: improve functional ability and prevent secondary impairments (deconditioning, pneumonia, UTI, pressure sores, DVT)
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Recovery of Locomotion

and Mulroy, Stroke. 1995;76)
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Locomotor ability is an important factor in determining the degree of physical disability after stroke. (Perry > 63% of all stroke survivors have some walking disability Gait velocity is best predictor of functional ambulation status (Perry and Mulroy, Stroke. 1995;76) Gait velocity of 0.5-0.8 m/s (1-1.8 mph) is required to 0.5(1cross a street during a red light (Podsiodlo 91)
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Gait velocity of 0.8 m/s (1.8 mph) is required for unlimited community ambulation (Podsiodlo 91) Gait velocity post-stroke (3 weeks-2 years): ranges postweeksfrom 0.25-0.5 m/s (0.5-1 mph) 0.25(0.5Recovery of gait speed may continue for up to 2 years after stroke Recovery of locomotion is best correlated with function of distal muscles (TA, TS) (David Winter)
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Acutely:

51% are non-ambulatory non12% ambulate with an assistive device 37% are (I)
(Copenhagen Stroke Study, Arch Phys Med Rehabil, 1995)
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Chronically

>66% will regain independence in walking Best level of walking function occurs within 11 weeks Probability of regaining walking (I) and time to (I) is related to initial severity :
>78% with no leg paresis 66% with mild leg paresis 28% with moderate leg paresis 21% with severe leg paresis 6% with complete leg paralysis

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Effects of Task-Specific Locomotor and Strength Training in Adults Who Were TaskAmbulatory After Stroke: Results of the STEPS RCT Phase II RCT to determine effects of combined task-specific and LE taskstrength training to improve walking after stroke Subjects: 80 adults 4 mo 5 yrs post stroke Method: BWSTT, CYCLE, LE-EX, UE-EX LEUE
BWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EX UEUELE-

Dosage: 4/wk x 6wks (24 sessions) DV: Self-selected walking speed, fast walking speed, 6MWT; Selfprepre- and post intervention and 6 mo post Results:

BWSTT more effective than cycling in improving walking speed and maintaining gains at 6 mo. LE strength training, alternate days, produced no added benefit (Sullivan et al, (Phys Ther 2007;87:1580-1602) 2007;87:1580Stroke Treatment Concept Map Exit
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LifeLife-table Probability of Walking After Stroke u 150 feet With Assistance 1/4
120 100 80 60 40 20 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 Weeks After Stroke Probability (%) Motor Only Motor + Sensory Motor + Sensory + Visual
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LifeLife-table Probability of Walking After Stroke u 150 ft. Without Assistance 2/4
100 80 60 40 20 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 Pr o b a b ility (% ) Motor Only Motor + Sensory Motor + Sensory + Visual
Weeks After Stroke
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LifeLife-table Probability of Reaching a Barthel Index Score u 95. (} I) (} After Stroke 3/4
100 Probability (%) 80 60 40 20 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 Weeks After Stroke Motor Only Motor + Sensory Motor + Sensory + Vis ual
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LifeLife-table Probability of Reaching Barthel Index Score > 60 (} Min asst) After Stroke 4/4
120 100 80 60 40 20 0 2 4 6 8 10 12 14 16 18 20 22 24 26 28 30 Weeks After Stroke Probability (%) Motor Only Motor + Sensory Motor + Sensory + Visual
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The Cerebrovascular System

Oxygen demands Metabolism Cerebrovascular disease Blood supply to the brain Carotid system Vertebrobasilar system Circle of Willis Perfusion Territories Cerebellar arteries Venous Drainage Blood supply to spinal cord Patient cases
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Oxygen Demands

The CNS (brain and spinal cord) is the best protected organ in the human body including mechanisms to protect its blood supply At approximately 3 pounds, the brain accounts for about 2% of body mass Consumes 17% of cardiac output Responsible for 20% of oxygen consumption at rest

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Metabolism

Brains sole source of energy is aerobic or oxidative metabolism. Therefore, the brain requires a constant supply of O2 and glucose, 24 hours a day.
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Cerebrovascular Disease

While the blood supply to the brain is highly protected, cerebrovascular disease is the third leading cause of death in American adults and the number one cause of chronic functional disability requiring rehabilitative intervention.
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Blood Supply to the Brain 1/4

Approximately 1,000 ml/min delivered via two systems.

Anterior (Carotid) system: (Carotid)

70% of supply (35% from each internal carotid artery) Supplies the superior 2/3 of the brain
Posterior (Vertebrobasilar) Vertebrobasilar) system:

30% of supply Supplies the inferior 1/3 of the brain and brainstem
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Blood Supply to the Brain 2/4

Carotid Perfusion Territory (Superior 2/3)
VerterboBasilar Perfusion Territory (Inferior 1/3)
A.
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Carotid System
Anterior system (Carotid) (Carotid)

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70% of supply (35% from each internal carotid artery) Supplies the superior 2/3 of the brain
Click to animate
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Vertebrobasilar System
Posterior system Vertebrobasilar) (Vertebrobasilar)
30% of supply Supplies the inferior 1/3 of the brain and brainstem

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Click to animate
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Carotid System
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Anterior cerebral artery Anterior communicating artery Middle cerebral artery
Internal carotid artery
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Blood Supply to the Brain
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Blood Supply to the Brain
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Carotid System

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Bilateral system, each hemisphere has its own carotid artery. Supplies the superior two thirds of the brain. Derived from: aorta, common carotid, internal carotid, carotid foramen (adjacent to optic chiasm) Anterior cerebral artery (ACA) Middle cerebral artery (MCA)
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Carotid System
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Carotid System
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Carotid System
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Lateral fissure
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Anterior Cerebral Artery 8/13
ADAM
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Middle Cerebral Artery
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ADAM
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Carotid System
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Middle Cerebral Artery 11/13
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Carotid System
Perfusion territory by artery
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Carotid Perfusion With Homunculus
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Supplies the inferior one third of the brain; inferior surface of the temporal and occipital lobes and brainstem. Derived from: subclavian, vertebral, foramen magnum, anterior spinal, posterior inferior cerebellar, basilar, anterior inferior cerebellar, internal auditory, superior cerebellar, posterior cerebral artery
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ADAM
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Basilar a.
Vertebral a.
ADAM
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Vertebrobasilar System 6/9
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Posterior Cerebral Artery
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Circle Of Willis
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Perfusion Territories
Watershed Territory
Primary Artery Territory

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3 Cerebellar Arteries
Superior cerebellar a
Pons Anterior inferior cerebellar a
Medulla
Posterior inferior cerebellar a Last Viewed Cerebrovascular System Concept Map Exit
Venous Drainage
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Superior sagittal sinus Inferior sagittal sinus Straight sinus Transverse sinus Sigmoid sinus Jugular vein
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Venous Drainage
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Superior sagittal sinus Inferior sagittal sinus Straight sinus Transverse sinus Sigmoid sinus Jugular vein
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Blood Supply to the Spinal Cord
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Spinal Arteries
Anterior Posterior
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Patient Cases

Occlusion of the anterior spinal artery Sudden Inability to Speak Left Leg Weakness SuddenSudden-onset Worst Headache of Life Decreased Vision in One Eye Left Neglect
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Occlusion of the anterior spinal artery (anterior cord syndrome) in the cervical region would produce what impairments?
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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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Anterior Cord Syndrome

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UMN UMN
DRG DRG
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Common causes include anterior spinal artery infarct, trauma, and MS. Last Viewed Patient Cases
Anterior cord lesion Lateral corticospinal tract lesion

Ipsilateral upper motor neurons signs
Lateral spinothalamic tract lesion

Contralateral loss of pain and temperature sense Concept Map Exit
Minicase
Sudden Inability to Speak 1/5
While standing in the check-out line at the store, 55 yearcheckyearold retired nurse realized she was suddenly unable to speak. Consciousness, attention, voluntary movement, and the ability to understand speech were all unaffected. Incredulous, but believing she knew what is happening to her. She left the store and drove herself directly to the emergency room. In the ER she communicated to doctors what she thought was occurring. With difficulty she uttered two words: stroke and speech.
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Minicase
Sudden Inability to Speak

2/5

Her past medical history was notable for overweight, hypertension and type II diabetes. Examination revealed loss of the nasal-labial fold on nasalthe left and weakness in the left cheek and jaw. Her jaw-jerk reflex was hyperactive. jawAll other movement, sensation, and reflexes were within normal limits. Where is the lesion causing these symptoms?
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Minicase Follow-Up FollowSudden Inability to Speak

3/5
As confirmed by CT image, this woman was having a stroke. The occlusion involved a deep penetrating branch of the middle cerebral artery supplying the inferior frontal gyrus on the left causing weakness in the lower part of the right face and tongue and Brocas aphasia.
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Productive (Brocas) Aphasia 4/5

Produced by a lesion of the inferior frontal gyrus of the dominant hemisphere.
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Minicase Follow-Up FollowSudden Inability to Speak 5/5

The key signs and symptoms in this case are: Suddenly unable to speak Consciousness, attention, voluntary movement, and the ability to understand speech were all unaffected Loss of the nasal-labial fold on the left and weakness in nasalthe left cheek and jaw Her jaw-jerk reflex was hyperactive jaw-
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Minicase Left Leg Weakness
1/5
On attempting to stand after finishing breakfast, a 67-year-old woman fell to the ground, hitting the 67-yeartable on the way down, because she was unable to support her body weight on her left leg. She called for help from her husband who was unable to get her off the floor and called for emergency assistance.
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Minicase Left Leg Weakness

2/5

Her past history was notable for obesity, hypertension, peripheral vascular disease, and smoking one pack per day for 52 years. She had hyperactive deep tendon reflexes in her left knee and ankle, and a positive Babinski sign in her left foot. The left leg was flaccid and she had no voluntary control of movement. She had mild impairment of light touch, pain, and temperature sensation in her left leg. Voluntary movement, reflexes, and sensation were intact in all other regions of the body. Where is the lesion causing these symptoms?
Minicase Follow-Up FollowLeft Leg Weakness

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A head CT scan was done and the results suggested a probable right anterior cerebral artery infarct. FollowFollow-up hear CT scan one month later confirmed the presence of a hypodense area on the anterior medial aspect of the right hemisphere consistent with a right anterior cerebral artery infarct
4/5
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5/5
The key signs and symptoms in this case are: Unable to support her body weight on her left leg Hyperactive deep tendon reflexes in her left knee and ankle, and a positive Babinski sign in her left foot The left leg was flaccid and she had no voluntary control of movement She had mild impairment of light touch, pain, and temperature sensation in her left leg Voluntary movement, reflexes, and sensation were intact in all other regions of the body
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Minicase
SuddenSudden-onset Worst Headache of Life 1/7 A 68-year-old man suddenly developed the worst of 68-yearmy life. On the morning of admission he was sitting watching TV when at 9:00 am he suddenly developed an explosive headache worse than anything he had ever experienced. The headache began in the bifrontal area and over the next few minutes all over the head and down the neck. He denied loss of consciousness, nausea, vomiting or vision changes.
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SuddenSudden-onset Worst Headache of Life

2/7
History was positive for severe diffuse atherosclerosis, including coronary disease and peripheral vascular disease requiring multiple bypass surgeries. He was obese and smoked two packs a day for 43 years. Examination was unremarkable except for mild nuchal rigidity.
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Minicase Follow-Up FollowSuddenSudden-onset Worst Headache of Life

3/7
Nuchal rigidity is often a sign of meningeal irritation caused by inflammation, infection, or hemorrhage in the subarachnoid space.
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Minicase Follow-Up FollowSuddenSudden-onset Worst Headache of Life

4/7
The man underwent emergency head CT which demonstrated regions of hyperdensity in the subarachnoid space consistent with subarachnoid hemorrhage layering in the medial longitudinal fissure, lateral fissure, and around the brainstem. Next he was taken for an angiogram which clearly revealed an aneurysm arising from the region of the anterior communicating artery. artery.
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Berry Aneurysm
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.
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Berry Aneurysm
6/7
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.
Minicase Follow-Up FollowSuddenSudden-onset Worst Headache of Life 7/7 The key signs and symptoms in this case are: Suddenly developed the worst of my life Headache began in the bifrontal area and over the next few minutes was all over the head and down the neck Examination was unremarkable except for mild nuchal rigidity
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Minicase
Decreased Vision in One Eye

1/8
A 63-year-old woman went to an 63-yearophthalmologist complaining of episodes of decreased vision in her right eye over the past several weeks.
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Minicase

2/8
Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease. About 5-6 weeks ago the patient began having 5episodes of sudden blurry wavy appearance of her vision. She believed this was mostly in the right eye but never tried looking with only one eye at a time.
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Minicase Decreased Vision in One Eye

3/8
Episodes would last for 15-20 minutes, resolved with 15no visual impairment, repeated 3-4 times per week, and 3were never accompanied by pain. Previously she was able to recognize faces during the episodes but was unable to read. The current episode, that began two days ago, has resulted in persistent decreased vision on the right.
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Minicase

4/8
Neurologic examination revealed fluent speech. Pupils 3 mm, constricting to 2 mm bilaterally. Normal fundi. Visual acuity 20/30 right and 20/25 left. Visual field testing revealed a right homonymous hemianopia. Extraocular movements intact. Facial sensation intact to light touch and pinprick. Face symmetrical. Normal palate elevation. Normal shoulder shrug. Tongue midline. Where is the lesion causing these symptoms?
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Minicase Follow-Up FollowDecreased Vision in One Eye

5/8
The transient episodes of 15-20 minutes of decreased 15rightright-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is suddensuggestive of TIAs preceding a cerebral infarct. A right homonymous hemianopia can be caused by a lesion in the left hemisphere visual pathway anywhere from the left optic tract to the primary visual cortex. The patients age and past medical history raise the suspicion of cerebrovascular disease of the cause.
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Minicase Follow-Up FollowDecreased Vision in One Eye

6/8

The patient was sent to the hospital where an initial CT scan suggested a left posterior cerebral artery infarct, and a follow-up followMRI confirmed the presence of a left PCS infarct involving the left primary visual cortex. An magnetic resonance angiogram (MRA) revealed several stenoses of the cerebral vessels compatible with diffuse intracranial atherosclerotic disease. She was treated with long-term oral anticoagulation. longHer right hemianopia did not improve, but over time she learned to adapt to her visual deficit.
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Minicase Follow-Up FollowDecreased Vision in One Eye 7/8
MRI axial T2 weighted image of left posterior cerebral artery (PCA) infarction
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Minicase Follow-Up FollowDecreased Vision in One Eye 8/8

The key signs and symptoms in this case are: Episodes of sudden blurry/ wavy appearance of her vision in her right eye over the past several weeks Right homonymous hemianopia
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Minicase Left Neglect

1/5
A 61-year-old right-handed man was witnessed 61-year- rightslumping to the floor in the grocery store.
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2/5

On examination in the hospital he denied anything was wrong but said, They called an ambulance because they said I had a stroke. He was unaware of having any impairment and wanted to go home. He had profound left visual field neglect , no blink to threat on 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 of the page. When shown his left hand and asked what it was, he replied Someones hand.
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3/5
When asked whos hand it was he replied, The doctors. He had a marked right gaze preference. He had marked weakness in the lower portion of the left face. Strength was 0/5 in the left arm and leg, the left plantar response was upgoing, and there was no response to pinprick on the left side. What lesion is causing this mans symptoms?
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Minicase Follow-Up FollowLeft Neglect

4/5
The patient exhibits several forms of neglect. In addition to anosognosia, he has left sensory neglect, to visual and tactile stimuli, as well as left motor neglect. These signs and symptoms are most commonly seen in patients with nondominant (usually right) parietal lobe lesions. Given the sudden onset of the deficits, involvement of the left arm and leg, the presence of sensory and motor deficits, and the patients age, the most likely cause is ischemic infarction of the right internal carotid artery. artery.
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Minicase Follow-Up FollowLeft Neglect
5/5
The key signs and symptoms in this case are: Anosognosia Left face, arm and leg plegia with positive Babinskis sign No blink to threat on the left No voluntary gaze to the left past midline No response to pinprick on the left
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The End
DM McKeough 2008
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StrokeConceptMap 2

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Etiology and Pathology

Brain Metabolism Oxygen Demands Hemiplegia Epidemiology Economic Costs

The hallmark of stroke is hemiplegia

Hemiparesis + Hemisensory impairment

(American Heart Association 2005)

~ 50% of stroke survivors die within 8 years (Males > Females)

Survival rates dramatically decreased by age and co-morbidity co  

Hypertension Heart disease Diabetes (Post(Post-Stroke Rehabilitation Guideline Panel 1995)

>50% hospitalized with stroke do not require rehab

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

Thromboembolic stroke Hemorrhagic stroke:  Subarachnoid  Intracerebral

$100,000 $228,000 $124,000

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Common Occlusion Sites

Etiology and Pathology

 Less Well Documented (perhaps partly modifiable)

Etiology and Pathology

Modifiable Risk Factor

Less Well Documented

Genetic Risk Factors for Stroke 3/3

Etiology and Pathology

Moderate exercise: brisk walks of 30 minutes a day on most days

Etiology and Pathology

Clot Buster (Tissue Plasminogen Activator, TPA,)

Tissue grafting Genetic engineering

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Predictors of Good Outcome

Etiology and Pathology

Predictors of Bad Outcome 1/2

Etiology and Pathology

Predictors of Bad Outcome 2/2

Etiology and Pathology

Nagi Model of Disability Due to Stroke

CNS lesion produces hemiplegia & spasticity

ADL limitations prevent ability to perform expected social role

Etiology and Pathology

Transient ischemic attack (TIA)

Etiology and Pathology

Primary damage Secondary damage

Etiology and Pathology

Phagocytosis Following Stroke 3/10

Etiology and Pathology

Phagocytosis Following Stroke

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Etiology and Pathology

Domains Affected by Stroke

Motor Sensory Vision Language Cognition Affect

Stroke in the Dominant Hemisphere

Stroke in the Nondominant Hemisphere

Symptoms by Lesion Location

Cerebellar Ataxia Ipsilateral dysmetria Dysdiadochokinesia Intention tremor

Kinetic (Motor) Apraxia

Common Deficits Anatomic Substrate of Deficits

Survival rates dramatically decreased by age and co-morbidity co

Thromboembolic stroke Hemorrhagic stroke: Subarachnoid Intracerebral

Less Well Documented (perhaps partly modifiable)