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

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Presentation on theme: "Stroke Recovery Etiology and Pathology Deficits Lesion Effects Demographics Stroke Treatment Map of Essential Concepts DM McKeough © 2008 Cerebrovascular."— Presentation transcript:

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

3 Exit Concept Map Concept MapStrokeStroke Demographics Demographics Demographics Etiology and Pathology Etiology and Pathology Etiology and Pathology Etiology and Pathology Lesion Effects Lesion Effects Lesion Effects Lesion Effects Deficits Deficits Deficits Recovery Recovery Recovery Treatment Treatment Treatment Cerebrovascular System Cerebrovascular System Cerebrovascular System Cerebrovascular System Demographics Demographics Demographics Etiology and Pathology Etiology and Pathology Etiology and Pathology Etiology and Pathology Lesion Effects Lesion Effects Lesion Effects Lesion Effects Deficits Deficits Deficits Recovery Recovery Recovery Treatment Treatment Treatment Cerebrovascular System Cerebrovascular System Cerebrovascular System Cerebrovascular System Last Viewed Last Viewed Stroke

4 Exit Concept Map Concept MapDemographicsDemographics Brain Metabolism Brain Metabolism Brain Metabolism Brain Metabolism Oxygen Demands Oxygen Demands Oxygen Demands Oxygen Demands Hemiplegia Hemiplegia Hemiplegia Epidemiology Epidemiology Epidemiology Economic Costs Economic Costs Economic Costs Economic Costs Brain Metabolism Brain Metabolism Brain Metabolism Brain Metabolism Oxygen Demands Oxygen Demands Oxygen Demands Oxygen Demands Hemiplegia Hemiplegia Hemiplegia Epidemiology Epidemiology Epidemiology Economic Costs Economic Costs Economic Costs Economic Costs Last Viewed Last Viewed Demographics

5 Exit Concept Map Concept Map Brain Metabolism Brains sole source of energy is aerobic or oxidative metabolism Brains sole source of energy is aerobic or oxidative metabolism Therefore, the brain requires a constant supply of O 2 and glucose, 24/ 7/ 365 Therefore, the brain requires a constant supply of O 2 and glucose, 24/ 7/ 365 Brains sole source of energy is aerobic or oxidative metabolism Brains sole source of energy is aerobic or oxidative metabolism Therefore, the brain requires a constant supply of O 2 and glucose, 24/ 7/ 365 Therefore, the brain requires a constant supply of O 2 and glucose, 24/ 7/ 365 Last Viewed Last Viewed Demographics Exit Concept Map Concept Map

6 Exit Concept Map Concept Map Oxygen Demands At approximately 3 pounds, the brain accounts for roughly 2% of body mass At approximately 3 pounds, the brain accounts for roughly 2% of body mass Consumes 17% of cardiac output Consumes 17% of cardiac output Responsible for 20% of oxygen consumption at rest Responsible for 20% of oxygen consumption at rest At approximately 3 pounds, the brain accounts for roughly 2% of body mass At approximately 3 pounds, the brain accounts for roughly 2% of body mass Consumes 17% of cardiac output Consumes 17% of cardiac output Responsible for 20% of oxygen consumption at rest Responsible for 20% of oxygen consumption at rest Last Viewed Last Viewed Demographics

7 Exit Concept Map Concept MapHemiplegiaHemiplegia The hallmark of stroke is hemiplegia The hallmark of stroke is hemiplegia Hemiparesis + Hemiparesis + Hemisensory impairment Hemisensory impairment The great vulnerability of the brain to ischemic damage is due to its dependence on aerobic metabolism The great vulnerability of the brain to ischemic damage is due to its dependence on aerobic metabolism The hallmark of stroke is hemiplegia The hallmark of stroke is hemiplegia Hemiparesis + Hemiparesis + Hemisensory impairment Hemisensory impairment The great vulnerability of the brain to ischemic damage is due to its dependence on aerobic metabolism The great vulnerability of the brain to ischemic damage is due to its dependence on aerobic metabolism Last Viewed Last Viewed Demographics

8 Exit Concept Map Concept Map Epidemiology1/12 Stroke is the third leading cause of death and the most common cause of disability in the US (American Heart Association 2005) Stroke is the third leading cause of death and the most common cause of disability in the US (American Heart Association 2005) Last Viewed Last Viewed Demographics

9 Exit Concept Map Concept Map Epidemiology2/12 Incidence Each year about 700,000 people experience a new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacks) (American Heart Association 2005) Each year about 700,000 people experience a new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacks) (American Heart Association 2005) Every 45 seconds someone in the US has a stroke (280 strokes during todays class) Every 45 seconds someone in the US has a stroke (280 strokes during todays class)Incidence Each year about 700,000 people experience a new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacks) (American Heart Association 2005) Each year about 700,000 people experience a new or recurrent stroke. (500,000 are first attacks, and 200,000 are recurrent attacks) (American Heart Association 2005) Every 45 seconds someone in the US has a stroke (280 strokes during todays class) Every 45 seconds someone in the US has a stroke (280 strokes during todays class) Last Viewed Last Viewed Demographics

10 Exit Concept Map Concept Map Epidemiology3/12 Gender Distribution Men > Women x 1.25 Men > Women x 1.25 Ethnic Distribution African-Americans > Whites x 2 African-Americans > Whites x 2 Hispanic Hispanic Native Americans Native Americans Native Alaskans Native Alaskans Whites (American Heart Association 2005) Whites (American Heart Association 2005) Gender Distribution Men > Women x 1.25 Men > Women x 1.25 Ethnic Distribution African-Americans > Whites x 2 African-Americans > Whites x 2 Hispanic Hispanic Native Americans Native Americans Native Alaskans Native Alaskans Whites (American Heart Association 2005) Whites (American Heart Association 2005) Last Viewed Last Viewed Demographics

11 Exit Concept Map Concept Map Epidemiology4/12 Stroke is a condition of the elderly Stroke is a condition of the elderly Incidence increases steadily with age (risk doubles every decade after age 65) Incidence increases steadily with age (risk doubles every decade after age 65) 28% of strokes occur in individuals < 65 years of age 28% 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 elderly Stroke is a condition of the elderly Incidence increases steadily with age (risk doubles every decade after age 65) Incidence increases steadily with age (risk doubles every decade after age 65) 28% of strokes occur in individuals < 65 years of age 28% 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) Last Viewed Last Viewed Demographics

12 Exit Concept Map Concept Map Epidemiology5/12 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. From 1993 to 2003 the death rate from stroke declined 18.5 percent, and the actual number of stroke deaths declined 0.7 percent. Mortality Last Viewed Last Viewed Demographics

13 Exit Concept Map Concept Map Epidemiology6/12 Mortality 22% of men and 25% of women die within first year 22% of men and 25% of women die within first year 2001 stroke killed 163,538 people 2001 stroke killed 163,538 people Every 3.3 minutes someone in US dies of stroke (64 deaths during todays class) 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) ~ 50% of stroke survivors die within 8 years (Males > Females) Death due to MI Death due to MIMortality 22% of men and 25% of women die within first year 22% of men and 25% of women die within first year 2001 stroke killed 163,538 people 2001 stroke killed 163,538 people Every 3.3 minutes someone in US dies of stroke (64 deaths during todays class) 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) ~ 50% of stroke survivors die within 8 years (Males > Females) Death due to MI Death due to MI Last Viewed Last Viewed Demographics

14 Exit Concept Map Concept Map Geographic Distribution Death rate due to stroke per 100,000 in 2001 Epidemiology7/12 Last Viewed Last Viewed Demographics

15 Exit Concept Map Concept Map Epidemiology8/12 Mortality by type of stroke Hemorrhagic38% Hemorrhagic38% Ischemic12% (American Heart Association 2005) Ischemic12% (American Heart Association 2005) Survival rates dramatically decreased by age and co-morbidity Survival rates dramatically decreased by age and co-morbidity Hypertension Hypertension Heart disease Heart disease Diabetes (Post-Stroke Rehabilitation Guideline Panel 1995) Diabetes (Post-Stroke Rehabilitation Guideline Panel 1995) Mortality by type of stroke Hemorrhagic38% Hemorrhagic38% Ischemic12% (American Heart Association 2005) Ischemic12% (American Heart Association 2005) Survival rates dramatically decreased by age and co-morbidity Survival rates dramatically decreased by age and co-morbidity Hypertension Hypertension Heart disease Heart disease Diabetes (Post-Stroke Rehabilitation Guideline Panel 1995) Diabetes (Post-Stroke Rehabilitation Guideline Panel 1995) Last Viewed Last Viewed Demographics

16 Exit Concept Map Concept Map Epidemiology9/12 Recurrence 14% per year, highest in first year 14% per year, highest in first year Risk of stroke increases 10 times after first stroke Risk of stroke increases 10 times after first stroke Recurring strokes produce larger lesions (cumulative effects), greater cortical involvement, greater impairment, higher mortality Recurring strokes produce larger lesions (cumulative effects), greater cortical involvement, greater impairment, higher mortality Outcome and pattern of recovery is similar to first-time stroke Outcome and pattern of recovery is similar to first-time stroke Should receive similar rehab treatment as first-time stroke Should receive similar rehab treatment as first-time strokeRecurrence 14% per year, highest in first year 14% per year, highest in first year Risk of stroke increases 10 times after first stroke Risk of stroke increases 10 times after first stroke Recurring strokes produce larger lesions (cumulative effects), greater cortical involvement, greater impairment, higher mortality Recurring strokes produce larger lesions (cumulative effects), greater cortical involvement, greater impairment, higher mortality Outcome and pattern of recovery is similar to first-time stroke Outcome and pattern of recovery is similar to first-time stroke Should receive similar rehab treatment as first-time stroke Should receive similar rehab treatment as first-time stroke Last Viewed Last Viewed Demographics

17 Exit Concept Map Concept Map Epidemiology10/12 Prevalence About 5,500,000 stroke survivors are alive today About 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 femalesPrevalence About 5,500,000 stroke survivors are alive today About 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 Last Viewed Last Viewed Demographics

18 Exit Concept Map Concept Map Epidemiology11/12 The following activity limitations were observed at six months post-stroke: 50 % had some one-sided paralysis 50 % had some one-sided paralysis 35 % had depression 35 % had depression 30 % were unable to walk without some assistance 30 % were unable to walk without some assistance 26 % were dependent in activities of daily living (grooming, eating, bathing, etc) 26 % were dependent in activities of daily living (grooming, eating, bathing, etc) 26 % were institutionalized in a nursing home 26 % were institutionalized in a nursing home 19 % had aphasia (trouble speaking or understanding the speech of others) 19 % had aphasia (trouble speaking or understanding the speech of others) (Framingham Heart Study 2005) (Framingham Heart Study 2005) The following activity limitations were observed at six months post-stroke: 50 % had some one-sided paralysis 50 % had some one-sided paralysis 35 % had depression 35 % had depression 30 % were unable to walk without some assistance 30 % were unable to walk without some assistance 26 % were dependent in activities of daily living (grooming, eating, bathing, etc) 26 % were dependent in activities of daily living (grooming, eating, bathing, etc) 26 % were institutionalized in a nursing home 26 % were institutionalized in a nursing home 19 % had aphasia (trouble speaking or understanding the speech of others) 19 % had aphasia (trouble speaking or understanding the speech of others) (Framingham Heart Study 2005) (Framingham Heart Study 2005) Last Viewed Last Viewed Demographics

19 Exit Concept Map Concept Map Disability Due to Stroke Stroke is leading cause of chronic disability (Wolfe 2000) Stroke is leading cause of chronic disability (Wolfe 2000) ~70% never return to work ~70% never return to work Stroke is leading cause of inpatient rehab (Granger & Hamilton 1994) Stroke is leading cause of inpatient rehab (Granger & Hamilton 1994) 33% require (A) with ADL at one year post (Murray & Lopez 1996) 33% require (A) with ADL at one year post (Murray & Lopez 1996) 26% of stroke survivors are in SNF (American Heart Association 2005) 26% of stroke survivors are in SNF (American Heart Association 2005) >50% hospitalized with stroke do not require rehab >50% hospitalized with stroke do not require rehab Epidemiology12/12 Last Viewed Last Viewed Demographics

20 Exit Concept Map Concept Map Economic 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 $100,000 Thromboembolic stroke $100,000 Hemorrhagic stroke: Hemorrhagic stroke: Subarachnoid $228,000 Subarachnoid $228,000 Intracerebral $124,000 Intracerebral $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 $100,000 Thromboembolic stroke $100,000 Hemorrhagic stroke: Hemorrhagic stroke: Subarachnoid $228,000 Subarachnoid $228,000 Intracerebral $124,000 Intracerebral $124,000 Last Viewed Last Viewed Demographics

21 Exit Concept Map Concept Map Etiology and Pathology Etiology Etiology Etiology Common Occlusion Sites Common Occlusion Sites Common Occlusion Sites Common Occlusion Sites Risk Factors Risk Factors Risk Factors Risk Factors Stroke Prevention Stroke Prevention Stroke Prevention Stroke Prevention Predictors of Stroke Predictors of Stroke Predictors of Stroke Predictors of Stroke Warning Signs Warning Signs Warning Signs Warning Signs Predictors of Good Outcome Predictors of Good Outcome Predictors of Good Outcome Predictors of Good Outcome Predictors of Bad Outcome Predictors of Bad Outcome Predictors of Bad Outcome Predictors of Bad Outcome Nagi Model Nagi Model Nagi Model Nagi Model Pathophysiology Pathophysiology Pathophysiology Etiology Etiology Etiology Common Occlusion Sites Common Occlusion Sites Common Occlusion Sites Common Occlusion Sites Risk Factors Risk Factors Risk Factors Risk Factors Stroke Prevention Stroke Prevention Stroke Prevention Stroke Prevention Predictors of Stroke Predictors of Stroke Predictors of Stroke Predictors of Stroke Warning Signs Warning Signs Warning Signs Warning Signs Predictors of Good Outcome Predictors of Good Outcome Predictors of Good Outcome Predictors of Good Outcome Predictors of Bad Outcome Predictors of Bad Outcome Predictors of Bad Outcome Predictors of Bad Outcome Nagi Model Nagi Model Nagi Model Nagi Model Pathophysiology Pathophysiology Pathophysiology Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

22 Exit Concept Map Concept Map 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. 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. Ischemic 80% Hemorrhagic 20% Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

23 Exit Concept Map Concept Map 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 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

24 Exit Concept Map Concept Map Risk Factors1/3 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 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 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

25 Exit Concept Map Concept Map Risk Factors2/3 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 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

26 Exit Concept Map Concept Map Genetic Risk Factors for Stroke3/3 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. Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

27 Exit Concept Map Concept Map Stroke Prevention1/2 Exercise reduces the risk of stroke Intense exercise27% Intense exercise27% Intense exercise: jogging 15 to 20 minutes a day on most days Moderate exercise20% Moderate exercise: brisk walks of 30 minutes a day on most days Exercise reduces the risk of stroke Intense exercise27% Intense exercise27% Intense exercise: jogging 15 to 20 minutes a day on most days Moderate exercise20% Moderate exercise: brisk walks of 30 minutes a day on most days J Stroke: Oct 2003 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

28 Exit Concept Map Concept Map Stroke Prevention2/2 Prevention Prevention Clot Buster (Tissue Plasminogen Activator, TPA,) Clot Buster (Tissue Plasminogen Activator, TPA,) Recent research Recent research Tissue grafting Tissue grafting Genetic engineering Genetic engineering Prevention Prevention Clot Buster (Tissue Plasminogen Activator, TPA,) Clot Buster (Tissue Plasminogen Activator, TPA,) Recent research Recent research Tissue grafting Tissue grafting Genetic engineering Genetic engineering Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

29 Exit Concept Map Concept Map Predictors of Stroke Previous stroke Previous stroke Transient ischemic attacks: 35% of thrombotic strokes were preceded by TIA Transient ischemic attacks: 35% of thrombotic strokes were preceded by TIA Previous stroke Previous stroke Transient ischemic attacks: 35% of thrombotic strokes were preceded by TIA Transient ischemic attacks: 35% of thrombotic strokes were preceded by TIA Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

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

31 Exit Concept Map Concept Map Predictors of Good Outcome The higher the socioeconomic status, the better the outcome The higher the socioeconomic status, the better the outcome The higher the education, the better the outcome The higher the education, the better the outcome The more active the premorbid lifestyle, 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 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 Only sensory or only motor impairments (the smaller the lesion), the better the outcome Never loosing consciousness Never loosing consciousness Little comorbidity Little comorbidity The higher the socioeconomic status, the better the outcome The higher the socioeconomic status, the better the outcome The higher the education, the better the outcome The higher the education, the better the outcome The more active the premorbid lifestyle, 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 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 Only sensory or only motor impairments (the smaller the lesion), the better the outcome Never loosing consciousness Never loosing consciousness Little comorbidity Little comorbidity Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

32 Exit Concept Map Concept Map Severe initial functional deficits Severe initial functional deficits Dense sensory or motor impairments Dense sensory or motor impairments Hemianopsia Hemianopsia Severe visuospatial deficits (hemineglect or hemiinattention) Severe visuospatial deficits (hemineglect or hemiinattention) Severe aphasia Severe aphasia Major depression Major depression Lack of return of hand function within 96 hours Lack of return of hand function within 96 hours Altered level of consciousness Altered level of consciousness Severe initial functional deficits Severe initial functional deficits Dense sensory or motor impairments Dense sensory or motor impairments Hemianopsia Hemianopsia Severe visuospatial deficits (hemineglect or hemiinattention) Severe visuospatial deficits (hemineglect or hemiinattention) Severe aphasia Severe aphasia Major depression Major depression Lack of return of hand function within 96 hours Lack of return of hand function within 96 hours Altered level of consciousness Altered level of consciousness Predictors of Bad Outcome1/2 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

33 Exit Concept Map Concept Map Significant comorbidity (medical/surgical instability) Significant comorbidity (medical/surgical instability) Disability prior to stroke Disability prior to stroke Previous stroke (effects are cumulative) Previous stroke (effects are cumulative) Loss of sitting balance Loss of sitting balance Severe cognitive deficits (difficulty following instructions) Severe cognitive deficits (difficulty following instructions) Persistent urinary incontinence Persistent urinary incontinence Older age Older 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 stroke Disability prior to stroke Previous stroke (effects are cumulative) Previous stroke (effects are cumulative) Loss of sitting balance Loss of sitting balance Severe cognitive deficits (difficulty following instructions) Severe cognitive deficits (difficulty following instructions) Persistent urinary incontinence Persistent urinary incontinence Older age Older age (R) CVAs tend to have worse outcomes than (L) CVAs (R) CVAs tend to have worse outcomes than (L) CVAs Predictors of Bad Outcome2/2 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

34 Exit Concept Map Concept Map Nagi Model of Disability Due to Stroke PathologyPathology Impairment Functional Limitation 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 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

35 Exit Concept Map Concept Map Pathophysiology1/10 Transient ischemic attack (TIA) Transient ischemic attack (TIA) Caused by reversible ischemia (usually due to vasospasm). Caused by reversible ischemia (usually due to vasospasm). Results in temporary functional impairment with no residual deficits. Results in temporary functional impairment with no 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 reversible ischemia (usually due to vasospasm). Caused by reversible ischemia (usually due to vasospasm). Results in temporary functional impairment with no residual deficits. Results in temporary functional impairment with no residual deficits. ~35% of TIAs evolve into stroke within 1-3 years ~35% of TIAs evolve into stroke within 1-3 years Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

36 Exit Concept Map Concept Map Pathophysiology2/10 Stroke Stroke Caused by irreversible ischemia Caused by irreversible ischemia Results in a circumscribed area of infarction ( primary damage ) and Results in a circumscribed area of infarction ( primary damage ) and Perimeter of increased pressure due to inflammation ( secondary damage ) Perimeter of increased pressure due to inflammation ( secondary damage ) The most damaging results of vascular occlusion are produced by secondary damage The most damaging results of vascular occlusion are produced by secondary damage Stroke Stroke Caused by irreversible ischemia Caused by irreversible ischemia Results in a circumscribed area of infarction ( primary damage ) and Results in a circumscribed area of infarction ( primary damage ) and Perimeter of increased pressure due to inflammation ( secondary damage ) Perimeter of increased pressure due to inflammation ( secondary damage ) The most damaging results of vascular occlusion are produced by secondary damage The most damaging results of vascular occlusion are produced by secondary damage Primary damage Secondary damage Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

37 Exit Concept Map Concept Map This intermediate infarct of the frontal lobe shows liquefactive necrosis with formation of cystic spaces as resolution begins. Phagocytosis Following Stroke3/10 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

38 Exit Concept Map Concept Map 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 Stroke4/10 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

39 Exit Concept Map Concept Map This is an intermediate to remote infarct in the distribution of the middle cerebral artery. Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology MCA Stroke5/10

40 Exit Concept Map Concept Map 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 Stroke6/10 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

41 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. Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology 7/10 Exit Concept Map Concept Map

42 Exit Concept Map Concept Map 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 Infarction8/10 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

43 Exit Concept Map Concept Map 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 Aneurysms9/10 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

44 Exit Concept Map Concept Map 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 Aneurysms10/10 Last Viewed Last Viewed Etiology and Pathology Etiology and Pathology

45 Exit Concept Map Concept Map Lesion Effects Domains Affected by Stroke Domains Affected by Stroke Domains Affected by Stroke Domains Affected by Stroke Hemispheric Effects Hemispheric Effects Hemispheric Effects Hemispheric Effects Symptoms by Lesion Location Symptoms by Lesion Location Symptoms by Lesion Location Symptoms by Lesion Location Ideational Apraxia Ideational Apraxia Ideational Apraxia Ideational Apraxia Motor Apraxia Motor Apraxia Motor Apraxia Motor Apraxia Domains Affected by Stroke Domains Affected by Stroke Domains Affected by Stroke Domains Affected by Stroke Hemispheric Effects Hemispheric Effects Hemispheric Effects Hemispheric Effects Symptoms by Lesion Location Symptoms by Lesion Location Symptoms by Lesion Location Symptoms by Lesion Location Ideational Apraxia Ideational Apraxia Ideational Apraxia Ideational Apraxia Motor Apraxia Motor Apraxia Motor Apraxia Motor Apraxia Last Viewed Last Viewed Lesion Effects Lesion Effects

46 Exit Concept Map Concept Map Domains Affected by Stroke Motor Motor Sensory Sensory Vision Vision Language Language Cognition Cognition Affect Affect Motor Motor Sensory Sensory Vision Vision Language Language Cognition Cognition Affect Affect Last Viewed Last Viewed Lesion Effects Lesion Effects

47 Exit Concept Map Concept Map Hemispheric Effects Hemispheric Specialization Hemispheric Specialization Hemispheric Specialization Hemispheric Specialization Dominant Hemisphere Dominant Hemisphere Dominant Hemisphere Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Nondominant Hemisphere Stroke in the Nondominant Hemisphere Stroke in the Nondominant Hemisphere Stroke in the Nondominant Hemisphere Hemispheric Specialization Hemispheric Specialization Hemispheric Specialization Hemispheric Specialization Dominant Hemisphere Dominant Hemisphere Dominant Hemisphere Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Dominant Hemisphere Stroke in the Nondominant Hemisphere Stroke in the Nondominant Hemisphere Stroke in the Nondominant Hemisphere Stroke in the Nondominant Hemisphere Last Viewed Last Viewed Lesion Effects Lesion Effects

48 Exit Concept Map Concept Map Hemispheric Specialization Left Hemisphere Intellectual Rational Verbal Analytical Right Hemisphere Perceptive Holistic Spatial Emotional Nonverbal Last Viewed Last Viewed Hemispheric Effects Hemispheric Effects

49 Exit Concept Map Concept Map Dominant Hemisphere Dominant = hemisphere with language (Broca, Wernicke) Dominant = hemisphere with language (Broca, Wernicke) Left hemisphere is the dominant hemisphere in the vast majority of the population (95%) Left hemisphere is the dominant hemisphere in the vast majority of the population (95%) Dominant = hemisphere with language (Broca, Wernicke) Dominant = hemisphere with language (Broca, Wernicke) Left hemisphere is the dominant hemisphere in the vast majority of the population (95%) Left hemisphere is the dominant hemisphere in the vast majority of the population (95%) Last Viewed Last Viewed Hemispheric Effects Hemispheric Effects

50 Exit Concept Map Concept Map 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 apraxiaMotor ideational –Difficulty initiating and sequencing tasks –Delays in information processing –Compulsive behavior with easy frustration –Extreme distractibility Last Viewed Last Viewed Hemispheric Effects Hemispheric Effects

51 Exit Concept Map Concept Map Stroke in the Nondominant Hemisphere Characterized by: Characterized by: Left hemiparesis Left hemiparesis Left sensory loss Left sensory loss Disturbance of spatial orientation * Disturbance of spatial orientation * Left unilateral neglect (in some cases) * Left unilateral neglect (in some cases) * Impairment of hand eye coordination, figure- ground discrimination, form constancy Impairment of hand eye coordination, figure- ground discrimination, form constancy Characterized by: Characterized by: Left hemiparesis Left hemiparesis Left sensory loss Left sensory loss Disturbance of spatial orientation * Disturbance of spatial orientation * Left unilateral neglect (in some cases) * Left unilateral neglect (in some cases) * Impairment of hand eye coordination, figure- ground discrimination, form constancy Impairment of hand eye coordination, figure- ground discrimination, form constancy Dressing and constructional apraxia Dressing and constructional apraxia Poor judgment * Poor judgment * Unrealistic expectations * Unrealistic expectations * Denial of disability * Denial of disability * * Contributes to poor outcome Last Viewed Last Viewed Hemispheric Effects Hemispheric Effects

52 Exit Concept Map Concept Map 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 Cerebellar Ataxia Ipsilateral dysmetria Dysdiadochokinesia Intention tremor Brainstem Gait impairment Diplopia Focal weakness Consciousness and attention impairment Cerebellopontine angle Hearing impairment Ataxia Tinnitus Dizziness Facial palsy Temporal lobe Auditory and perceptual impairment Memory and learning impairment Aphasia (Wernicke) Last Viewed Last Viewed Lesion Effects Lesion Effects

53 Exit Concept Map Concept Map Ideational Apraxia Unable to perform a task either automatically or on command, although individual movements can be made correctly 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 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 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 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 Due to lesion of the parietal lobe in the dominant hemisphere or the corpus callosum Unable to perform a task either automatically or on command, although individual movements can be made correctly 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 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 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 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 Due to lesion of the parietal lobe in the dominant hemisphere or the corpus callosum Dominant Hemisphere Last Viewed Last Viewed Lesion Effects Lesion Effects

54 Exit Concept Map Concept Map Kinetic (Motor) Apraxia Inability to perform fine learned movements in the absence of weakness or sensory loss Inability to perform fine learned movements in the absence of weakness or sensory loss Due to bilateral lesion (disease) of the frontal lobes Due to bilateral lesion (disease) of the frontal lobes Inability to perform fine learned movements in the absence of weakness or sensory loss Inability to perform fine learned movements in the absence of weakness or sensory loss Due to bilateral lesion (disease) of the frontal lobes Due to bilateral lesion (disease) of the frontal lobes Last Viewed Last Viewed Lesion Effects Lesion Effects

55 Exit Concept Map Concept MapDeficitsDeficits Common Deficits Common Deficits Common Deficits Common Deficits Anatomic Substrate of Deficits Anatomic Substrate of Deficits Anatomic Substrate of Deficits Anatomic Substrate of Deficits Common Deficits Common Deficits Common Deficits Common Deficits Anatomic Substrate of Deficits Anatomic Substrate of Deficits Anatomic Substrate of Deficits Anatomic Substrate of Deficits Last Viewed Last Viewed Deficits

56 Exit Concept Map Concept Map Common Deficits Following Stroke DEFICITACUTE (%)CHRONIC (%) Hemiparesis 8848 Incoordination 8661 Dysarthria 5716 Sensory impairment 5324 Aphasia 3618 Memory impairment 3631 Bladder incontinence 299 Dysphagia 134 Last Viewed Last Viewed Deficits

57 Exit Concept Map Concept Map Anatomic Substrate of Deficits DEFICITNEUROANATOMIC SUBSTRATE HemiparesisLesion of cortical motor centers (UMN) IncoordinationLesion of cortical motor centers (dorsolateral and ventromedial systems) DysarthriaLesion of corticobulbar tract (input to CNs) Sensory impairmentLesion of somatosensory cortex AphasiaLesion of language centers (Broca, Wernicke) Memory impairmentLesion of temporal lobe (hippocampus) Bladder incontinenceLesion of autonomic input to sacral region of spinal cord (hypothalamus) DysphagiaLesion of corticobulbar tract (B input to CN X) Last Viewed Last Viewed Deficits

58 Exit Concept Map Concept MapRecoveryRecovery Natural History of Recovery Natural History of Recovery Natural History of Recovery Natural History of Recovery Recovery With Intervention Recovery With Intervention Recovery With Intervention Recovery With Intervention Pattern of Recovery Pattern of Recovery Pattern of Recovery Pattern of Recovery Theories of Recovery Theories of Recovery Theories of Recovery Theories of Recovery Natural History of Recovery Natural History of Recovery Natural History of Recovery Natural History of Recovery Recovery With Intervention Recovery With Intervention Recovery With Intervention Recovery With Intervention Pattern of Recovery Pattern of Recovery Pattern of Recovery Pattern of Recovery Theories of Recovery Theories of Recovery Theories of Recovery Theories of Recovery Last Viewed Last Viewed Recovery

59 Exit Concept Map Concept Map 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 Function * Using conventional rehabilitation approaches (Post-Stroke Rehabilitation Guideline Panel 1995) Last Viewed Last Viewed Recovery

60 Exit Concept Map Concept Map Recovery With Intervention Evidence-based Practice Data now show that natural history of recovery can be changed by the right type of intervention 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 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 Conventional rehabilitation techniques do not change the natural history of recovery Evidence-based Practice Data now show that natural history of recovery can be changed by the right type of intervention 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 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 Conventional rehabilitation techniques do not change the natural history of recovery Last Viewed Last Viewed Recovery

61 Exit Concept Map Concept Map Pattern of Recovery Initially: hypotonia/ flaccidity Initially: hypotonia/ flaccidity Due to the interruption of UMN input to LMN Due to the interruption of UMN input to LMN Days to weeks later: hypertonia/ spasticity Days 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 and Decreased threshold in alpha LMN and Denervation supersensitivity Denervation supersensitivity Initially: hypotonia/ flaccidity Initially: hypotonia/ flaccidity Due to the interruption of UMN input to LMN Due to the interruption of UMN input to LMN Days to weeks later: hypertonia/ spasticity Days 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 and Decreased threshold in alpha LMN and Denervation supersensitivity Denervation supersensitivity Last Viewed Last Viewed Recovery

62 Exit Concept Map Concept Map Theories of the Recovery of Function 1. Resolution of cerebral edema (diaschisis) Resolution of cerebral edema (diaschisis) 2. Reactive synaptogenesis (Collateral sprouting - CNS) Reactive synaptogenesis (Collateral sprouting - CNS) 3. Changes in cortical maps Changes in cortical maps 4. Use of alternate pathways Use of alternate pathways 5. Regenerative synaptogenesis (Wallerian re-generation - PNS) Regenerative synaptogenesis (Wallerian re-generation - PNS) Regenerative synaptogenesis Last Viewed Last Viewed Recovery

63 Exit Concept Map Concept Map Cellular Response to Injury 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 Viewed Last Viewed Theories of Recovery Theories of Recovery

64 Exit Concept Map Concept Map Reactive Synaptogenesis CNS response to injury CNS response to injury No re-establishing functional connections with target cells occurs, any recovery of function occurs via collateral sprouting from intact neurons &/or reorganization (intact systems assume the lost function, neuroplasticity ) No re-establishing functional connections with target cells occurs, any recovery of function occurs via collateral sprouting from intact neurons &/or reorganization (intact systems assume the lost function, neuroplasticity ) CNS response to injury CNS response to injury No re-establishing functional connections with target cells occurs, any recovery of function occurs via collateral sprouting from intact neurons &/or reorganization (intact systems assume the lost function, neuroplasticity ) No re-establishing functional connections with target cells occurs, any recovery of function occurs via collateral sprouting from intact neurons &/or reorganization (intact systems assume the lost function, neuroplasticity ) collateral sprouting +/or reorganizationneuroplasticity collateral sprouting +/or reorganization = neuroplasticity Theories of Recovery Theories of Recovery Last Viewed Last Viewed

65 Exit Concept Map Concept Map Cortical Reorganization 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 Theories of Recovery Theories of Recovery Last Viewed Last Viewed

66 Exit Concept Map Concept Map Cortical Reorganization Taub et al 1998 Use-Dependent Cortical Reorganization After Brain Injury Mechanisms of effectiveness of Constraint-Induced Movement Therapy (CIMT) Theories of Recovery Theories of Recovery Last Viewed Last Viewed

67 Exit Concept Map Concept Map Alternate Pathways What mechanisms underlie the recovery of function? What mechanisms underlie the recovery of function? –Ipsilateral motor tracts take over Theories of Recovery Theories of Recovery Last Viewed Last Viewed

68 Exit Concept Map Concept Map 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 Theories of Recovery Theories of Recovery Last Viewed Last Viewed

69 Exit Concept Map Concept Map Stroke Treatment Referral Patterns Referral Patterns Referral Patterns Referral Patterns Treatment Efficacy Treatment Efficacy Treatment Efficacy Treatment Efficacy Unaffected" Upper Extremity Unaffected" Upper Extremity Unaffected" Upper Extremity Unaffected" Upper Extremity Stroke Treatment Stroke Treatment Stroke Treatment Stroke Treatment Recovery of Locomotion Recovery of Locomotion Recovery of Locomotion Recovery of Locomotion Life Probability Tables Life Probability Tables Life Probability Tables Life Probability Tables Referral Patterns Referral Patterns Referral Patterns Referral Patterns Treatment Efficacy Treatment Efficacy Treatment Efficacy Treatment Efficacy Unaffected" Upper Extremity Unaffected" Upper Extremity Unaffected" Upper Extremity Unaffected" Upper Extremity Stroke Treatment Stroke Treatment Stroke Treatment Stroke Treatment Recovery of Locomotion Recovery of Locomotion Recovery of Locomotion Recovery of Locomotion Life Probability Tables Life Probability Tables Life Probability Tables Life Probability Tables Stroke Treatment Stroke Treatment Last Viewed Last Viewed

70 Exit Concept Map Concept Map Possible Routes Through Medical System Stroke Hospital LOS: 5-7 days IP Rehab 3 hrs/day LOS: 3-4 wks Subacute Rehab 1.5 hrs/day LOS: 5-6 wks SNF Usually permanent Rehab bed Home w H H LOS: ~2 wks Home w H H LOS: ~2 wks Home w H H LOS: ~2 wks Home w H H LOS: ~2 wks 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 Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks Home w OP LOS: ~2-4 wks Stroke Treatment Stroke Treatment Last Viewed Last Viewed

71 Exit Concept Map Concept Map Treatment Efficacy Conventional therapy produces only a modest, temporary improvement in function ( The Lancet Vol 359 No 9302, January 19, 2002) 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. Taub et al., Stroke 2000; 31: 1210) PT treatment effects are achieved through a neuroplastic reorganization of motor control centers (Treatment-Induced Cortical Reorganization After Stroke in Humans. Taub et al., Stroke 2000; 31: 1210) Conventional therapy produces only a modest, temporary improvement in function ( The Lancet Vol 359 No 9302, January 19, 2002) 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. Taub et al., Stroke 2000; 31: 1210) PT treatment effects are achieved through a neuroplastic reorganization of motor control centers (Treatment-Induced Cortical Reorganization After Stroke in Humans. Taub et al., Stroke 2000; 31: 1210) Stroke Treatment Stroke Treatment Last Viewed Last Viewed

72 Exit Concept Map Concept Map Unaffected" Upper Extremity Following stroke, the unaffected UE showed decreases in: Following stroke, the unaffected UE showed decreases in: functional independence due to decreased fine manual dexterity functional independence due to decreased fine manual dexterity activity level due to decreases in kinesthesia and gross dexterity activity level due to decreases in kinesthesia and gross dexterity There is no such thing as an unaffected extremity There is no such thing as an unaffected extremity Following stroke, the unaffected UE showed decreases in: Following stroke, the unaffected UE showed decreases in: functional independence due to decreased fine manual dexterity functional independence due to decreased fine manual dexterity activity level due to decreases in kinesthesia and gross dexterity activity level due to decreases in kinesthesia and gross dexterity There is no such thing as an unaffected extremity There is no such thing as an unaffected extremity Stroke Treatment Stroke Treatment Last Viewed Last Viewed

73 Exit Concept Map Concept Map Stroke Treatment1/2 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 Treatment Stroke Treatment Last Viewed Last Viewed

74 Exit Concept Map Concept Map Stroke Treatment2/2 Acute phase Acute phase MD: thrombolytic agents or acute anticoagulation drugs (TPA) may be successful in reversing primary impairments 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) PT: improve functional ability and prevent secondary impairments (deconditioning, pneumonia, UTI, pressure sores, DVT) Acute phase Acute phase MD: thrombolytic agents or acute anticoagulation drugs (TPA) may be successful in reversing primary impairments 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) PT: improve functional ability and prevent secondary impairments (deconditioning, pneumonia, UTI, pressure sores, DVT) Stroke Treatment Stroke Treatment Last Viewed Last Viewed

75 Exit Concept Map Concept Map Recovery of Locomotion1/5 Locomotor ability is an important factor in determining the degree of physical disability after stroke. (Perry and Mulroy, Stroke. 1995;76) Locomotor ability is an important factor in determining the degree of physical disability after stroke. (Perry and Mulroy, Stroke. 1995;76) > 63% of all stroke survivors have some walking disability > 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 is best predictor of functional ambulation status (Perry and Mulroy, Stroke. 1995;76) Gait velocity of m/s (1-1.8 mph) is required to cross a street during a red light (Podsiodlo 91) Gait velocity of m/s (1-1.8 mph) is required to cross a street during a red light (Podsiodlo 91) Locomotor ability is an important factor in determining the degree of physical disability after stroke. (Perry and Mulroy, Stroke. 1995;76) Locomotor ability is an important factor in determining the degree of physical disability after stroke. (Perry and Mulroy, Stroke. 1995;76) > 63% of all stroke survivors have some walking disability > 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 is best predictor of functional ambulation status (Perry and Mulroy, Stroke. 1995;76) Gait velocity of m/s (1-1.8 mph) is required to cross a street during a red light (Podsiodlo 91) Gait velocity of m/s (1-1.8 mph) is required to cross a street during a red light (Podsiodlo 91) Stroke Treatment Stroke Treatment Last Viewed Last Viewed

76 Exit Concept Map Concept Map Recovery of Locomotion2/5 Gait velocity of 0.8 m/s (1.8 mph) is required for unlimited community ambulation (Podsiodlo 91) 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 from m/s (0.5-1 mph) Gait velocity post-stroke (3 weeks-2 years): ranges from m/s (0.5-1 mph) Recovery of gait speed may continue for up to 2 years after stroke Recovery 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) Recovery of locomotion is best correlated with function of distal muscles (TA, TS) (David Winter) Gait velocity of 0.8 m/s (1.8 mph) is required for unlimited community ambulation (Podsiodlo 91) 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 from m/s (0.5-1 mph) Gait velocity post-stroke (3 weeks-2 years): ranges from m/s (0.5-1 mph) Recovery of gait speed may continue for up to 2 years after stroke Recovery 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) Recovery of locomotion is best correlated with function of distal muscles (TA, TS) (David Winter) Stroke Treatment Stroke Treatment Last Viewed Last Viewed

77 Exit Concept Map Concept Map Recovery of Locomotion3/5 Acutely: Acutely: 51% are non-ambulatory 51% are non-ambulatory 12% ambulate with an assistive device 12% ambulate with an assistive device 37% are (I) 37% are (I) (Copenhagen Stroke Study, Arch Phys Med Rehabil, 1995) Acutely: Acutely: 51% are non-ambulatory 51% are non-ambulatory 12% ambulate with an assistive device 12% ambulate with an assistive device 37% are (I) 37% are (I) (Copenhagen Stroke Study, Arch Phys Med Rehabil, 1995) Stroke Treatment Stroke Treatment Last Viewed Last Viewed

78 Exit Concept Map Concept Map Recovery of Locomotion4/5 Chronically Chronically >66% will regain independence in walking >66% will regain independence in walking Best level of walking function occurs within 11 weeks Best level of walking function occurs within 11 weeks Probability of regaining walking (I) and time to (I) is related to initial severity : Probability of regaining walking (I) and time to (I) is related to initial severity : >78% with no leg paresis >78% with no leg paresis 66% with mild leg paresis 66% with mild leg paresis 28% with moderate leg paresis 28% with moderate leg paresis 21% with severe leg paresis 21% with severe leg paresis 6% with complete leg paralysis 6% 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 weeks Best level of walking function occurs within 11 weeks Probability of regaining walking (I) and time to (I) is related to initial severity : Probability of regaining walking (I) and time to (I) is related to initial severity : >78% with no leg paresis >78% with no leg paresis 66% with mild leg paresis 66% with mild leg paresis 28% with moderate leg paresis 28% with moderate leg paresis 21% with severe leg paresis 21% with severe leg paresis 6% with complete leg paralysis 6% with complete leg paralysis Stroke Treatment Stroke Treatment Last Viewed Last Viewed

79 Exit Concept Map Concept Map Recovery of Locomotion5/5 Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Ambulatory After Stroke: Results of the STEPS RCT Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Ambulatory After Stroke: Results of the STEPS RCT Phase II RCT to determine effects of combined task-specific and LE strength training to improve walking after stroke Phase II RCT to determine effects of combined task-specific and LE strength training to improve walking after stroke Subjects: 80 adults 4 mo – 5 yrs post stroke Subjects: 80 adults 4 mo – 5 yrs post stroke Method: BWSTT, CYCLE, LE-EX, UE-EX Method: BWSTT, CYCLE, LE-EX, UE-EX BWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EX BWSTT/ 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; pre- and post intervention and 6 mo post DV: Self-selected walking speed, fast walking speed, 6MWT; pre- and post intervention and 6 mo post Results: Results: BWSTT more effective than cycling in improving walking speed and maintaining gains at 6 mo. 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: ) LE strength training, alternate days, produced no added benefit (Sullivan et al, (Phys Ther 2007;87: ) Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Ambulatory After Stroke: Results of the STEPS RCT Effects of Task-Specific Locomotor and Strength Training in Adults Who Were Ambulatory After Stroke: Results of the STEPS RCT Phase II RCT to determine effects of combined task-specific and LE strength training to improve walking after stroke Phase II RCT to determine effects of combined task-specific and LE strength training to improve walking after stroke Subjects: 80 adults 4 mo – 5 yrs post stroke Subjects: 80 adults 4 mo – 5 yrs post stroke Method: BWSTT, CYCLE, LE-EX, UE-EX Method: BWSTT, CYCLE, LE-EX, UE-EX BWSTT/ UE-EX, CYCLE / UE-EX, BWSTT/CYCLE, BWSTT/ LE-EX BWSTT/ 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; pre- and post intervention and 6 mo post DV: Self-selected walking speed, fast walking speed, 6MWT; pre- and post intervention and 6 mo post Results: Results: BWSTT more effective than cycling in improving walking speed and maintaining gains at 6 mo. 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: ) LE strength training, alternate days, produced no added benefit (Sullivan et al, (Phys Ther 2007;87: ) Stroke Treatment Stroke Treatment Last Viewed Last Viewed

80 Life-table Probability of Walking After Stroke 150 feet With Assistance1/4 Stroke Treatment Stroke Treatment Last Viewed Last Viewed Exit Concept Map Concept Map

81 Life-table Probability of Walking After Stroke 150 ft. Without Assistance2/4 Stroke Treatment Stroke Treatment Last Viewed Last Viewed Exit Concept Map Concept Map

82 Life-table Probability of Reaching a Barthel Index Score 95. ( I) After Stroke3/4 Stroke Treatment Stroke Treatment Last Viewed Last Viewed Exit Concept Map Concept Map

83 Life-table Probability of Reaching Barthel Index Score > 60 ( Min asst) After Stroke4/4 Stroke Treatment Stroke Treatment Last Viewed Last Viewed Exit Concept Map Concept Map

84 Exit Concept Map Concept Map The Cerebrovascular System Oxygen demands Oxygen demands Oxygen demands Oxygen demands Metabolism Metabolism Metabolism Cerebrovascular disease Cerebrovascular disease Cerebrovascular disease Cerebrovascular disease Blood supply to the brain Blood supply to the brain Blood supply to the brain Blood supply to the brain Carotid system Carotid system Carotid system Carotid system Vertebrobasilar system Vertebrobasilar system Vertebrobasilar system Vertebrobasilar system Circle of Willis Circle of Willis Circle of Willis Circle of Willis Perfusion Territories Perfusion Territories Perfusion Territories Perfusion Territories Cerebellar arteries Cerebellar arteries Cerebellar arteries Cerebellar arteries Venous Drainage Venous Drainage Venous Drainage Venous Drainage Blood supply to spinal cord Blood supply to spinal cord Blood supply to spinal cord Blood supply to spinal cord Patient cases Patient cases Patient cases Patient cases Last Viewed Last Viewed Posture & Balance Posture & Balance

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

86 Exit Concept Map Concept MapMetabolismMetabolism Brains sole source of energy is aerobic or oxidative metabolism. Brains sole source of energy is aerobic or oxidative metabolism. Therefore, the brain requires a constant supply of O 2 and glucose, 24 hours a day. Therefore, the brain requires a constant supply of O 2 and glucose, 24 hours a day. Brains sole source of energy is aerobic or oxidative metabolism. Brains sole source of energy is aerobic or oxidative metabolism. Therefore, the brain requires a constant supply of O 2 and glucose, 24 hours a day. Therefore, the brain requires a constant supply of O 2 and glucose, 24 hours a day. Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

87 Exit Concept Map Concept Map 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. 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. Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

88 Exit Concept Map Concept Map Blood Supply to the Brain1/4 Approximately 1,000 ml/min delivered via two systems. Approximately 1,000 ml/min delivered via two systems. Anterior ( Carotid ) system: Anterior ( Carotid ) system: 70% of supply (35% from each internal carotid artery) 70% of supply (35% from each internal carotid artery) Supplies the superior 2/3 of the brain Supplies the superior 2/3 of the brain Posterior ( Vertebrobasilar ) system: Posterior ( Vertebrobasilar ) system: 30% of supply 30% of supply Supplies the inferior 1/3 of the brain and brainstem Supplies the inferior 1/3 of the brain and brainstem Approximately 1,000 ml/min delivered via two systems. Approximately 1,000 ml/min delivered via two systems. Anterior ( Carotid ) system: Anterior ( Carotid ) system: 70% of supply (35% from each internal carotid artery) 70% of supply (35% from each internal carotid artery) Supplies the superior 2/3 of the brain Supplies the superior 2/3 of the brain Posterior ( Vertebrobasilar ) system: Posterior ( Vertebrobasilar ) system: 30% of supply 30% of supply Supplies the inferior 1/3 of the brain and brainstem Supplies the inferior 1/3 of the brain and brainstem Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

89 Exit Concept Map Concept Map Blood Supply to the Brain2/4 Carotid Perfusion Territory (Superior 2/3) A.A. Verterbo- Basilar Perfusion Territory (Inferior 1/3) Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

90 Anterior system ( Carotid ) 70% of supply (35% from each internal carotid artery) 70% of supply (35% from each internal carotid artery) Supplies the superior 2/3 of the brain Supplies the superior 2/3 of the brain Anterior system ( Carotid ) 70% of supply (35% from each internal carotid artery) 70% of supply (35% from each internal carotid artery) Supplies the superior 2/3 of the brain Supplies the superior 2/3 of the brain Click to animate Carotid System Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System3/4

91 VertebrobasilarSystem Click to animate Posterior system ( Vertebrobasilar ) 30% of supply 30% of supply Supplies the inferior 1/3 of the brain and brainstem Supplies the inferior 1/3 of the brain and brainstem Posterior system ( Vertebrobasilar ) 30% of supply 30% of supply Supplies the inferior 1/3 of the brain and brainstem Supplies the inferior 1/3 of the brain and brainstem Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System4/4

92 Exit Concept Map Concept Map Click to Animate Carotid System1/13 Anterior cerebral artery Middle cerebral artery Anterior communicating artery Internal carotid artery Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

93 Blood Supply to the Brain Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System2/13 Exit Concept Map Concept Map

94 Blood Supply to the Brain3/13 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

95 Exit Concept Map Concept Map Carotid System4/13 Bilateral system, each hemisphere has its own carotid artery. Bilateral system, each hemisphere has its own carotid artery. Supplies the superior two thirds of the brain. Supplies the superior two thirds of the brain. Derived from: aorta, common carotid, internal carotid, carotid foramen (adjacent to optic chiasm) Derived from: aorta, common carotid, internal carotid, carotid foramen (adjacent to optic chiasm) Anterior cerebral artery (ACA) Anterior cerebral artery (ACA) Middle cerebral artery (MCA) Middle cerebral artery (MCA) Bilateral system, each hemisphere has its own carotid artery. Bilateral system, each hemisphere has its own carotid artery. Supplies the superior two thirds of the brain. Supplies the superior two thirds of the brain. Derived from: aorta, common carotid, internal carotid, carotid foramen (adjacent to optic chiasm) Derived from: aorta, common carotid, internal carotid, carotid foramen (adjacent to optic chiasm) Anterior cerebral artery (ACA) Anterior cerebral artery (ACA) Middle cerebral artery (MCA) Middle cerebral artery (MCA) Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

96 Carotid System5/13 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

97 Carotid System6/13 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

98 Carotid System7/13 Lateral fissure Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

99 Exit Concept Map Concept Map Anterior Cerebral Artery8/13 ADAM Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

100 Exit Concept Map Concept Map Middle Cerebral Artery9/13 ADAM Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

101 Exit Concept Map Concept Map Carotid System10/13 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

102 Exit Concept Map Concept Map Middle Cerebral Artery11/13 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

103 Exit Concept Map Concept Map Carotid System12/13 Perfusion territory by artery Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

104 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Carotid Perfusion With Homunculus 13/13 Exit Concept Map Concept Map

105 Exit Concept Map Concept Map Vertebrobasilar System1/9 Supplies the inferior one third of the brain; inferior surface of the temporal and occipital lobes and brainstem. 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 Derived from: subclavian, vertebral, foramen magnum, anterior spinal, posterior inferior cerebellar, basilar, anterior inferior cerebellar, internal auditory, superior cerebellar, posterior cerebral artery Supplies the inferior one third of the brain; inferior surface of the temporal and occipital lobes and brainstem. 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 Derived from: subclavian, vertebral, foramen magnum, anterior spinal, posterior inferior cerebellar, basilar, anterior inferior cerebellar, internal auditory, superior cerebellar, posterior cerebral artery Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

106 Exit Concept Map Concept Map Vertebrobasilar System2/9 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

107 Exit Concept Map Concept Map Vertebrobasilar System3/9 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

108 Exit Concept Map Concept Map Vertebrobasilar System4/9 ADAM Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

109 Exit Concept Map Concept Map Vertebrobasilar System5/9 ADAM Vertebral a. Basilar a. Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

110 Vertebrobasilar System6/9 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

111 Posterior Cerebral Artery7/9 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

112 Posterior Cerebral Artery8/9 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

113 Exit Concept Map Concept Map Posterior Cerebral Artery9/9 Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

114 CircleOfWillis Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System Exit Concept Map Concept Map

115 Exit Concept Map Concept Map Perfusion Territories Watershed Territory Primary Artery Territory Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

116 Exit Concept Map Concept Map 3 Cerebellar Arteries Pons Medulla Superior cerebellar a Anterior inferior cerebellar a Posterior inferior cerebellar a Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

117 Exit Concept Map Concept Map Venous Drainage1/2 Superior sagittal sinus Inferior sagittal sinus Straight sinus Transverse sinus Sigmoid sinus Jugular vein Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

118 Exit Concept Map Concept Map Venous Drainage2/2 Superior sagittal sinus Inferior sagittal sinus Straight sinus Transverse sinus Sigmoid sinus Jugular vein Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

119 Blood Supply to the Spinal Cord Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System1/2 Exit Concept Map Concept Map

120 Exit Concept Map Concept Map Spinal Arteries2/2 Anterior Posterior Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

121 Exit Concept Map Concept Map Patient Cases Occlusion of the anterior spinal artery Occlusion of the anterior spinal artery Occlusion of the anterior spinal artery Occlusion of the anterior spinal artery Sudden Inability to Speak Sudden Inability to Speak Sudden Inability to Speak Sudden Inability to Speak Left Leg Weakness Left Leg Weakness Left Leg Weakness Left Leg Weakness Sudden-onset Worst Headache of Life Sudden-onset Worst Headache of Life Sudden-onset Worst Headache of Life Sudden-onset Worst Headache of Life Decreased Vision in One Eye Decreased Vision in One Eye Decreased Vision in One Eye Decreased Vision in One Eye Left Neglect Left Neglect Left Neglect Left Neglect Occlusion of the anterior spinal artery Occlusion of the anterior spinal artery Occlusion of the anterior spinal artery Occlusion of the anterior spinal artery Sudden Inability to Speak Sudden Inability to Speak Sudden Inability to Speak Sudden Inability to Speak Left Leg Weakness Left Leg Weakness Left Leg Weakness Left Leg Weakness Sudden-onset Worst Headache of Life Sudden-onset Worst Headache of Life Sudden-onset Worst Headache of Life Sudden-onset Worst Headache of Life Decreased Vision in One Eye Decreased Vision in One Eye Decreased Vision in One Eye Decreased Vision in One Eye Left Neglect Left Neglect Left Neglect Left Neglect Last Viewed Last Viewed Cerebrovascular System Cerebrovascular System

122 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. Click for explanation Occlusion of the anterior spinal artery (anterior cord syndrome) in the cervical region would produce what impairments? Last Viewed Last Viewed Patient Cases Patient Cases 1/2 Exit Concept Map Concept Map

123 UMN DRG UMN DRG R L Anterior cord lesion Lateral corticospinal tract lesion Ipsilateral upper motor neurons signs Contralateral loss of pain and temperature sense Lateral spinothalamic tract lesion Anterior Cord Syndrome 2/2 Common causes include anterior spinal artery infarct, trauma, and MS. Click to animate Last Viewed Last Viewed Patient Cases Patient Cases Exit Concept Map Concept Map

124 Exit Concept Map Concept Map Minicase Sudden Inability to Speak 1/5 While standing in the check-out line at the store, 55 year- old 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. Last Viewed Last Viewed Patient Cases Patient Cases

125 Exit Concept Map Concept Map Minicase Sudden Inability to Speak2/5 Her past medical history was notable for overweight, hypertension and type II diabetes. Her past medical history was notable for overweight, hypertension and type II diabetes. Examination revealed loss of the nasal-labial fold on the left and weakness in the left cheek and jaw. Examination revealed loss of the nasal-labial fold on 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 within normal limits. All other movement, sensation, and reflexes were 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, hypertension and type II diabetes. Her past medical history was notable for overweight, hypertension and type II diabetes. Examination revealed loss of the nasal-labial fold on the left and weakness in the left cheek and jaw. Examination revealed loss of the nasal-labial fold on 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 within normal limits. All other movement, sensation, and reflexes were within normal limits. Where is the lesion causing these symptoms? Where is the lesion causing these symptoms? Last Viewed Last Viewed Patient Cases Patient Cases

126 Exit Concept Map Concept Map Minicase Follow-Up Sudden Inability to Speak3/5 As confirmed by CT image, this woman was having a stroke. 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. 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. As confirmed by CT image, this woman was having a stroke. 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. 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. Last Viewed Last Viewed Patient Cases Patient Cases

127 Exit Concept Map Concept Map Productive (Brocas) Aphasia4/5 Produced by a lesion of the inferior frontal gyrus of the dominant hemisphere. Produced by a lesion of the inferior frontal gyrus of the dominant hemisphere. Play recording Play recording Play recording Play recording Produced by a lesion of the inferior frontal gyrus of the dominant hemisphere. Produced by a lesion of the inferior frontal gyrus of the dominant hemisphere. Play recording Play recording Play recording Play recording Last Viewed Last Viewed Patient Cases Patient Cases

128 Exit Concept Map Concept Map Minicase Follow-Up Sudden Inability to Speak5/5 The key signs and symptoms in this case are: Suddenly unable to speak Suddenly unable to speak Consciousness, attention, voluntary movement, and the ability to understand speech were all unaffected 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 the left cheek and jaw Loss of the nasal-labial fold on the left and weakness in the left cheek and jaw Her jaw-jerk reflex was hyperactive Her jaw-jerk reflex was hyperactive The key signs and symptoms in this case are: Suddenly unable to speak Suddenly unable to speak Consciousness, attention, voluntary movement, and the ability to understand speech were all unaffected 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 the left cheek and jaw Loss of the nasal-labial fold on the left and weakness in the left cheek and jaw Her jaw-jerk reflex was hyperactive Her jaw-jerk reflex was hyperactive Last Viewed Last Viewed Patient Cases Patient Cases

129 Exit Concept Map Concept Map Minicase Left Leg Weakness1/5 On attempting to stand after finishing breakfast, a 67-year-old woman fell to the ground, hitting the table 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. Last Viewed Last Viewed Patient Cases Patient Cases

130 Exit Concept Map Concept Map Minicase Left Leg Weakness2/5 Her past history was notable for obesity, hypertension, peripheral vascular disease, and smoking one pack per day for 52 years. 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. 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. 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. 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. Voluntary movement, reflexes, and sensation were intact in all other regions of the body. Where is the lesion causing these symptoms? Where is the lesion causing these symptoms? Her past history was notable for obesity, hypertension, peripheral vascular disease, and smoking one pack per day for 52 years. 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. 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. 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. 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. Voluntary movement, reflexes, and sensation were intact in all other regions of the body. Where is the lesion causing these symptoms? Where is the lesion causing these symptoms? Last Viewed Last Viewed Patient Cases Patient Cases

131 Exit Concept Map Concept Map Minicase Follow-Up Left Leg Weakness3/5 A head CT scan was done and the results suggested a probable right anterior cerebral artery infarct. A head CT scan was done and the results suggested a probable right anterior cerebral artery infarct. Follow-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 Follow-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 A head CT scan was done and the results suggested a probable right anterior cerebral artery infarct. A head CT scan was done and the results suggested a probable right anterior cerebral artery infarct. Follow-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 Follow-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 Last Viewed Last Viewed Patient Cases Patient Cases

132 Exit Concept Map Concept Map Minicase Follow-Up Left Leg Weakness4/5 Last Viewed Last Viewed Patient Cases Patient Cases

133 Exit Concept Map Concept Map Minicase Follow-Up Left Leg Weakness5/5 The key signs and symptoms in this case are: Unable to support her body weight on her left leg 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 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 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 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 Voluntary movement, reflexes, and sensation were intact in all other regions of the body The key signs and symptoms in this case are: Unable to support her body weight on her left leg 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 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 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 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 Voluntary movement, reflexes, and sensation were intact in all other regions of the body Last Viewed Last Viewed Patient Cases Patient Cases

134 Exit Concept Map Concept Map Minicase Sudden-onset Worst Headache of Life1/7 A 68-year-old man suddenly developed the worst of my 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. Last Viewed Last Viewed Patient Cases Patient Cases

135 Exit Concept Map Concept Map Minicase Sudden-onset Worst Headache of Life2/7 History was positive for severe diffuse atherosclerosis, including coronary disease and peripheral vascular disease requiring multiple bypass surgeries. 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. He was obese and smoked two packs a day for 43 years. Examination was unremarkable except for mild nuchal rigidity. Examination was unremarkable except for mild nuchal rigidity. History was positive for severe diffuse atherosclerosis, including coronary disease and peripheral vascular disease requiring multiple bypass surgeries. 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. He was obese and smoked two packs a day for 43 years. Examination was unremarkable except for mild nuchal rigidity. Examination was unremarkable except for mild nuchal rigidity. Last Viewed Last Viewed Patient Cases Patient Cases

136 Exit Concept Map Concept Map Minicase Follow-Up Sudden-onset Worst Headache of Life3/7 Nuchal rigidity is often a sign of meningeal irritation caused by inflammation, infection, or hemorrhage in the subarachnoid space. Nuchal rigidity is often a sign of meningeal irritation caused by inflammation, infection, or hemorrhage in the subarachnoid space. Last Viewed Last Viewed Patient Cases Patient Cases

137 Exit Concept Map Concept Map Minicase Follow-Up Sudden-onset Worst Headache of Life4/7 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. 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. Next he was taken for an angiogram which clearly revealed an aneurysm arising from the region of the anterior communicating artery. 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. 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. Next he was taken for an angiogram which clearly revealed an aneurysm arising from the region of the anterior communicating artery. Last Viewed Last Viewed Patient Cases Patient Cases

138 Exit Concept Map Concept Map 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 Aneurysm5/7 Last Viewed Last Viewed Patient Cases Patient Cases

139 Exit Concept Map Concept Map 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 Aneurysm6/7 Last Viewed Last Viewed Patient Cases Patient Cases

140 Exit Concept Map Concept Map Minicase Follow-Up Sudden-onset Worst Headache of Life7/7 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 few minutes was all over the head and down the neck 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 Examination was unremarkable except for mild nuchal rigidity 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 few minutes was all over the head and down the neck 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 Examination was unremarkable except for mild nuchal rigidity Last Viewed Last Viewed Patient Cases Patient Cases

141 Exit Concept Map Concept Map Minicase Decreased Vision in One Eye1/8 A 63-year-old woman went to an ophthalmologist complaining of episodes of decreased vision in her right eye over the past several weeks. A 63-year-old woman went to an ophthalmologist complaining of episodes of decreased vision in her right eye over the past several weeks. Last Viewed Last Viewed Patient Cases Patient Cases

142 Exit Concept Map Concept Map Minicase Decreased Vision in One Eye2/8 Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease. Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease. About 5-6 weeks ago the patient began having episodes of sudden blurry wavy appearance of her vision. About 5-6 weeks ago the patient began having episodes 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. She believed this was mostly in the right eye but never tried looking with only one eye at a time. Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease. Her medical history was notable for type II diabetes, hypercholesterolemia, and coronary artery disease. About 5-6 weeks ago the patient began having episodes of sudden blurry wavy appearance of her vision. About 5-6 weeks ago the patient began having episodes 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. She believed this was mostly in the right eye but never tried looking with only one eye at a time. Last Viewed Last Viewed Patient Cases Patient Cases

143 Exit Concept Map Concept Map Minicase Decreased Vision in One Eye3/8 Episodes would last for minutes, resolved with no visual impairment, repeated 3-4 times per week, and were never accompanied by pain. Episodes would last for minutes, resolved with no visual impairment, repeated 3-4 times per week, and were never accompanied by pain. Previously she was able to recognize faces during the episodes but was unable to read. 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. The current episode, that began two days ago, has resulted in persistent decreased vision on the right. Episodes would last for minutes, resolved with no visual impairment, repeated 3-4 times per week, and were never accompanied by pain. Episodes would last for minutes, resolved with no visual impairment, repeated 3-4 times per week, and were never accompanied by pain. Previously she was able to recognize faces during the episodes but was unable to read. 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. The current episode, that began two days ago, has resulted in persistent decreased vision on the right. Last Viewed Last Viewed Patient Cases Patient Cases

144 Exit Concept Map Concept Map Minicase Decreased Vision in One Eye4/8 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. Where is the lesion causing these symptoms? Where is the lesion causing these symptoms? 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. Where is the lesion causing these symptoms? Where is the lesion causing these symptoms? Last Viewed Last Viewed Patient Cases Patient Cases

145 Exit Concept Map Concept Map Minicase Follow-Up Decreased Vision in One Eye5/8 The transient episodes of minutes of decreased right-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is suggestive of TIAs preceding a cerebral infarct. The transient episodes of minutes of decreased right-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is suggestive 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. 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. The patients age and past medical history raise the suspicion of cerebrovascular disease of the cause. The transient episodes of minutes of decreased right-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is suggestive of TIAs preceding a cerebral infarct. The transient episodes of minutes of decreased right-sided vision occurring over several weeks, followed by a sudden-onset persistent deficit is suggestive 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. 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. The patients age and past medical history raise the suspicion of cerebrovascular disease of the cause. Last Viewed Last Viewed Patient Cases Patient Cases

146 Exit Concept Map Concept Map Minicase Follow-Up Decreased Vision in One Eye6/8 The patient was sent to the hospital where an initial CT scan suggested a left posterior cerebral artery infarct, and a follow-up MRI confirmed the presence of a left PCS infarct involving the left primary visual cortex. The patient was sent to the hospital where an initial CT scan suggested a left posterior cerebral artery infarct, and a follow-up MRI 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. 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. She was treated with long-term oral anticoagulation. Her right hemianopia did not improve, but over time she learned to adapt to her visual deficit. Her right hemianopia did not improve, but over time she learned to adapt to her visual deficit. The patient was sent to the hospital where an initial CT scan suggested a left posterior cerebral artery infarct, and a follow-up MRI confirmed the presence of a left PCS infarct involving the left primary visual cortex. The patient was sent to the hospital where an initial CT scan suggested a left posterior cerebral artery infarct, and a follow-up MRI 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. 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. She was treated with long-term oral anticoagulation. Her right hemianopia did not improve, but over time she learned to adapt to her visual deficit. Her right hemianopia did not improve, but over time she learned to adapt to her visual deficit. Last Viewed Last Viewed Patient Cases Patient Cases

147 Exit Concept Map Concept Map Minicase Follow-Up Decreased Vision in One Eye7/8 MRI axial T2 weighted image of left posterior cerebral artery (PCA) infarction Last Viewed Last Viewed Patient Cases Patient Cases

148 Exit Concept Map Concept Map Minicase Follow-Up Decreased Vision in One Eye8/8 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 Episodes of sudden blurry/ wavy appearance of her vision in her right eye over the past several weeks Right homonymous hemianopia Right homonymous hemianopia 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 Episodes of sudden blurry/ wavy appearance of her vision in her right eye over the past several weeks Right homonymous hemianopia Right homonymous hemianopia Last Viewed Last Viewed Patient Cases Patient Cases

149 Exit Concept Map Concept Map Minicase Left Neglect1/5 A 61-year-old right-handed man was witnessed slumping to the floor in the grocery store. A 61-year-old right-handed man was witnessed slumping to the floor in the grocery store. Last Viewed Last Viewed Patient Cases Patient Cases

150 Exit Concept Map Concept Map Minicase Left Neglect2/5 On examination in the hospital he denied anything was wrong but said, They called an ambulance because they said I had a stroke. 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 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. 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 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. When shown his left hand and asked what it was, he replied Someones hand. On examination in the hospital he denied anything was wrong but said, They called an ambulance because they said I had a stroke. 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 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. 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 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. When shown his left hand and asked what it was, he replied Someones hand. Last Viewed Last Viewed Patient Cases Patient Cases

151 Exit Concept Map Concept Map Minicase Left Neglect3/5 When asked whos hand it was he replied, The doctors. When asked whos hand it was he replied, The doctors. He had a marked right gaze preference. He had a marked right gaze preference. He had marked weakness in the lower portion of the left face. 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. 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? What lesion is causing this mans symptoms? When asked whos hand it was he replied, The doctors. When asked whos hand it was he replied, The doctors. He had a marked right gaze preference. He had a marked right gaze preference. He had marked weakness in the lower portion of the left face. 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. 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? What lesion is causing this mans symptoms? Last Viewed Last Viewed Patient Cases Patient Cases

152 Exit Concept Map Concept Map Minicase Follow-Up Left Neglect4/5 The patient exhibits several forms of neglect. The patient exhibits several forms of neglect. In addition to anosognosia, he has left sensory neglect, to visual and tactile stimuli, as well as left motor 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. 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. 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. The patient exhibits several forms of neglect. 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. 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. 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. 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. Last Viewed Last Viewed Patient Cases Patient Cases

153 Exit Concept Map Concept Map Minicase Follow-Up Left Neglect5/5 The key signs and symptoms in this case are: Anosognosia Anosognosia Left face, arm and leg plegia with positive Babinskis sign Left face, arm and leg plegia with positive Babinskis sign No blink to threat on the left No blink to threat on the left No voluntary gaze to the left past midline No voluntary gaze to the left past midline No response to pinprick on the left No response to pinprick on the left The key signs and symptoms in this case are: Anosognosia Anosognosia Left face, arm and leg plegia with positive Babinskis sign Left face, arm and leg plegia with positive Babinskis sign No blink to threat on the left No blink to threat on the left No voluntary gaze to the left past midline No voluntary gaze to the left past midline No response to pinprick on the left No response to pinprick on the left Last Viewed Last Viewed Patient Cases Patient Cases Exit Concept Map Concept Map

154 The End © DM McKeough 2008 Last Viewed Last Viewed Concept Map Concept Map Patient Cases Patient Cases


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