STROKE<br />ARLYN M. VALENCIA , M.D.<br />Associate Professor, UNSOM<br />Diplomate, American Board Of Psychiatry & Neurol...
LEARNING OBJECTIVES<br />To be able to define stroke, discuss its pathophysiology and risk factors<br />To emphasize early...
”THE BRAIN IS A VERY UNIQUE, HIGH-MAINTENANCE END- ORGAN. IT IS VERY DEPENDENT ON MOMENT-TO-MOMENT SUPPLY OF GLUCOSE AND O...
     The   biology of    stroke <br />     is such that each moment of ischemia and tissue injury increases   the    degre...
CEREBROVASCULAR ACCIDENT OR “BRAIN ATTACK”<br />Third leading cause of death<br />750, 000 cases/year<br />Leading cause o...
Major Causes of Death in the United Sates, 1995<br />
Annual Economic Costs of Stroke (All Types) In The US<br />  <br />
Death Rates for Stroke per 100,000 Population<br />
Types of Stroke<br />Ischemic, 80%<br />     - thrombosis, 50% (small & large-vessel)<br />     - embolism, 30% [now belie...
Stroke vs. TIA<br />Transient ischemic attack (TIA): A clinical syndrome characterized by an acute loss of focal brain or ...
Risk Factors for Stroke That Cannot Be Changed<br />Increased age <br />Being male <br />Race (e.g., African-Americans) <b...
Up to approximately 30% of people who suffer transient attacks (TIAs) will develop a stroke within 5 years.<br />
Relative Incidence of Atherothrombotic Stroke and MI by Age and Gender<br />
Death Rates for Stroke per 100,000 PopulationGroups Defined by Race, Age, and Gender:  1993<br />
Risk Factor For Stroke: Treatable<br />Major <br />Hypertension <br />Heart disease, esp. atrial fibrillation <br />Cigare...
Alcohol Consumption as a Risk Factor for Stroke<br />Heavy alcohol consumption may increase risk of stroke by a number of ...
Alcohol Consumption as a Risk Factor for Stroke<br />Light and moderate alcohol use tend to raise levels of high-density-l...
Less Well Documented<br />Geography/climate <br />Socieconomic factors <br />
The Stroke Belt<br />
Potential Genetic Risk Factors for Stroke<br />Apolipoprotein E4<br />Elevated homocysteine  levels<br />Factor V mutation...
ATHEROSCLEROSIS AND THROMBOSIS<br />Atherosclerosis: decades-long process; progression favored by hypercholesterolemia, HT...
Focal plaques: eccentric thickening at bifurcations; addition of massive extracellular lipids that displaced normal cells ...
Complicated fibrous plaques: central acellular area of lipid covered by a cap of smooth muscle cells and collagen</li></li...
Role of Monocytes and T-Lymphocytes in the Transformation to Foam Cells<br />
Oxidation of LDL-Cholesterol<br />
Oxidized LDL-cholesterol   Contributes To Atherogenesis In Three Other Ways:<br />It has cytotoxic properties that may pro...
Smooth Muscle Cell Migration and Proliferation<br />
Smooth Muscle Cell Migration and Proliferation<br />Along with macrophages, smooth-muscle cells proliferate in the intima ...
Role of Platelets<br />   <br />Platelet adhesion may be promoted by type II injury and by  toxic products<br />Platelets ...
Plaque Fissuring and Formation of Platelet Thrombus<br />The vulnerability of such a structure to fissuring appears to be ...
Potential Outcomes of Plaque Fissuring<br />Acute episodes of transient ischemia and ischemic stroke (as well as myocardia...
Thrombus Formation I -- Platelet Activation<br />On contact with collagen, platelets become activated, with platelet adhes...
Thrombus Formation II -- Platelet Activation and Blood Flow<br />
Thrombus Formation III -- Activation of Coagulation Cascade<br />
Evolution of Cerebral Atherothrombosis<br />
Atherothromboticocclusion of larger arteries<br />Embolism: Artery-to artrey, cardiogenic<br />Primary small vessel diseas...
Thromboembolism<br />
Cardiogenic Emboli<br />Cardiogenic emboli lodge in the middle cerebral artery or its branches in 80% of cases, in the pos...
Major Blood Vessels Of The Brain<br />
Major Blood Vessels Of The Brain<br />
Control Centers of the Brain<br />
Cellular Injury During IschemiaNeuronal Function: Importance of Oxygen and Glucose<br />The transient change in voltage in...
Cellular Changes As Ischemia Progresses<br />The duration, severity, and location of focal cerebral ischemia determine the...
Cellular Injury During IschemiaInadequate Energy Supply<br />Lack of glucose and oxygen deplete the cellular energy stores...
THE ISCHEMIC PENUMBRA<br />
Stroke Warning Signs<br />Sudden weakness, paralysis, or numbness of the face, arm and the leg on one or both sides of the...
Left & Right HemisphericStroke: Common Patterns<br />Middle Cerebral Artery (MCA): supplies the lateral surface of hemisph...
Left and Right Hemisphere Stroke: Common Patterns  <br />Left (Dominant) Hemisphere Stroke: Common Pattern<br />Right (Non...
Posterior Circulation (Vertebrobasilar Territory) Stroke<br />Ataxia, gait abnormalities<br />Diplopia, oscillopsia, nysta...
Differential Diagnosis of Stroke<br />Craniocerebral / cervical trauma<br />Meningitis/encephalitis<br />Intracranial mass...
AHA Stroke Council Recommended Assessment of a Person with Suspected Stroke<br />EMS should be instructed in the rapid rec...
AHA Stroke Council Recommended Assessment of a Person with Suspected Stroke<br />EMS should be instructed in the rapid rec...
EVALUATION AND WORK-UP<br />History and PE<br />Computed Tomography (CT) scan of the head<br />12-lead EKG, chest X-ray<br...
Under special circumstances, the following tests may be required:<br />Cervical spine x-ray<br />Arterial blood gas<br />L...
Other Neuroimaging Techniques & Ancillary Tests  <br />Magnetic Resonance Imaging (MRI)<br />Diffusion Weighted Imaging (D...
Computed Tomography<br />
Carotid Duplex<br />
Transcranial Doppler<br />
Cerebral Angiography<br />
Functional abnormality demonstrated with PET exceeds that seen with structural imaging techniques such as X-ray, CT, or MR...
SPECT and Xenon Contrast CT<br />
EMERGENT SUPPORTIVE CARE OF ACUTE STROKE PATIENT<br />Maintenance of adequate tissue oxygenation: protecting the airway, O...
STROKE MANAGEMENT<br />
EMERGENT SUPPORTIVE CARE OF ACUTE STROKE PATIENT<br />Management of blood glucose abnormalities (hyperglycemia associated ...
ACUTE SROKE CARE 2007: <br />Therapies with <br />FDA Approval or <br />Positive Trials For Ischemic Stroke<br />IV TPA (&...
Acute Stroke Treatment<br />Intravenous recombinant tissue plasminogen activator (TPA): within 3 hours of stroke symptom o...
The Merci Retrieval System<br />
Hypothermia For Acute Stroke:Intravascular Cooling<br />
Physiologic Effects Of Various Levels Of Hypothermia<br />
Known Factors That Cause Stroke Progression<br />Hypotension<br />Hyperglycemia<br />Hyperthermia<br />Infection<br />Cere...
Brain Edema<br />
TREATMENT OF BRAIN SWELLING<br />Cerebral perfusion pressure =MAP-ICP<br />Fluid Restriction (1200 ml /day/m2)<br />Contro...
Management of Cerebral Edema, Increased Intracranial Pressure and Hydrocephalus<br />Brain edema peaks at 3-5 days<br />Tr...
Neuroprotective Agents<br />Several trials going on<br />So far, trial on one free-radical scavenger showed positive resul...
Stroke Prevention<br />Anticoagulants (Heparin, Warfarin)<br />Antiplatelets (aspirin, clopidogreldipyridamole/ASA combina...
Concept of Stroke Teams &Stroke Units<br />“Time is brain”<br />Stroke awareness <br />Common mistakes may lead to fatal c...
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STROKE LECTURE By Arlyn M. Valencia, M.D. Associate Professo University Of Nevada School Of Medicine, Diplomate American Board Of Psychiatry & Neurology

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STROKE LECTURE By Arlyn M. Valencia, M.D. Associate Professo University Of Nevada School Of Medicine, Diplomate American Board Of Psychiatry & Neurology

  1. 1. STROKE<br />ARLYN M. VALENCIA , M.D.<br />Associate Professor, UNSOM<br />Diplomate, American Board Of Psychiatry & Neurology<br />
  2. 2.
  3. 3. LEARNING OBJECTIVES<br />To be able to define stroke, discuss its pathophysiology and risk factors<br />To emphasize early evaluation and management of stroke patients <br />To discuss the latest stroke treatment strategies<br />CASE STUDIES: To be able to analyze clinical situations, localize the stroke lesion, determine probable etiology<br />
  4. 4. ”THE BRAIN IS A VERY UNIQUE, HIGH-MAINTENANCE END- ORGAN. IT IS VERY DEPENDENT ON MOMENT-TO-MOMENT SUPPLY OF GLUCOSE AND OXYGEN TO SUSTAIN ITS HIGH-POWERED ACTIVITIES. IT IS VERY SENSITIVE TO THE SYSTEMIC STATE. ANY SEVERE MEDICAL INSULT, THEREBY, HAS TREMENDOUS IMPACT ON THE BRAIN METABOLISM. ANY MEDICAL EMERGENCY IS A NEUROLOGIC EMERGENCY!”<br />A. Valencia, M.D.<br />
  5. 5. The biology of stroke <br /> is such that each moment of ischemia and tissue injury increases the degree<br /> of irreversible tissue<br /> damage.<br />
  6. 6. CEREBROVASCULAR ACCIDENT OR “BRAIN ATTACK”<br />Third leading cause of death<br />750, 000 cases/year<br />Leading cause of significant disability<br />Cost: $40 billion/year<br />
  7. 7. Major Causes of Death in the United Sates, 1995<br />
  8. 8. Annual Economic Costs of Stroke (All Types) In The US<br />  <br />
  9. 9. Death Rates for Stroke per 100,000 Population<br />
  10. 10. Types of Stroke<br />Ischemic, 80%<br /> - thrombosis, 50% (small & large-vessel)<br /> - embolism, 30% [now believed significantly higher]<br />Hemorrhagic, 20%<br /> - intracerebral (HTN as risk)<br /> - subarachnoid (aneurysm)<br />
  11. 11. Stroke vs. TIA<br />Transient ischemic attack (TIA): A clinical syndrome characterized by an acute loss of focal brain or monocular function with symptoms lasting less than 24 hrs and which is thought to be due to inadequate cerebral or ocular blood supply, without ischemic changes in Diffusion Weighted Imaging (DWI)<br />Stroke: Clinical syndrome characterized by an acute loss of focal brain or monocular function with symptoms lasting greater than 24 hrs and which is thought to be due to inadequate cerebral or ocular blood supply.<br />
  12. 12. Risk Factors for Stroke That Cannot Be Changed<br />Increased age <br />Being male <br />Race (e.g., African-Americans) <br />Diabetes mellitus <br />Prior stroke/transient ischemic attacks <br />Family history of stroke <br />Asymptomatic carotid bruit<br />
  13. 13. Up to approximately 30% of people who suffer transient attacks (TIAs) will develop a stroke within 5 years.<br />
  14. 14. Relative Incidence of Atherothrombotic Stroke and MI by Age and Gender<br />
  15. 15.
  16. 16. Death Rates for Stroke per 100,000 PopulationGroups Defined by Race, Age, and Gender:  1993<br />
  17. 17. Risk Factor For Stroke: Treatable<br />Major <br />Hypertension <br />Heart disease, esp. atrial fibrillation <br />Cigarette smoking <br />Transient ischemic attacks<br />Dyslipidemia<br />Physical inactivity<br />Obesity   <br />Less Well Documented<br />Excessive alcohol intake / drug abuse <br />Acute infection* <br />
  18. 18. Alcohol Consumption as a Risk Factor for Stroke<br />Heavy alcohol consumption may increase risk of stroke by a number of mechanisms. <br />The reported effects of alcohol consumption on risk of ischemic stroke have been inconsistent. <br />A differential effect of alcohol consumption on stroke risk in men compared to women has been observed.<br />
  19. 19. Alcohol Consumption as a Risk Factor for Stroke<br />Light and moderate alcohol use tend to raise levels of high-density-lipoprotein (HDL) -- the &quot;good&quot; lipoprotein.<br />Heavy drinking or binge drinking, is related to an increased incidence of stroke as a cause of death Light or moderate alcohol consumption, is related to a reduced risk of coronary heart disease.<br />There is positive, dose-related effect of alcohol consumption on risk of intracranial hemorrhage, both arachnoid and intracerebral .<br />
  20. 20. Less Well Documented<br />Geography/climate <br />Socieconomic factors <br />
  21. 21. The Stroke Belt<br />
  22. 22. Potential Genetic Risk Factors for Stroke<br />Apolipoprotein E4<br />Elevated homocysteine  levels<br />Factor V mutation<br />
  23. 23. ATHEROSCLEROSIS AND THROMBOSIS<br />Atherosclerosis: decades-long process; progression favored by hypercholesterolemia, HTN, cigarette smoking<br /><ul><li>Fatty streak: yellowish discoloration on intimal surface of blood
  24. 24. Focal plaques: eccentric thickening at bifurcations; addition of massive extracellular lipids that displaced normal cells and matrix
  25. 25. Complicated fibrous plaques: central acellular area of lipid covered by a cap of smooth muscle cells and collagen</li></li></ul><li>Atherosclerosis and Thrombus Formation:Arterial Wall Injury<br />Functional alteration of endothelial cell layer<br />Denuding of endothelium<br />Superficial intimal injury<br />Deep intimal & media damage with marked platelet aggregatio and mural thrombosis<br />
  26. 26. Role of Monocytes and T-Lymphocytes in the Transformation to Foam Cells<br />
  27. 27. Oxidation of LDL-Cholesterol<br />
  28. 28. Oxidized LDL-cholesterol Contributes To Atherogenesis In Three Other Ways:<br />It has cytotoxic properties that may promote endothelial injury;<br />It acts as a chemoattractant for circulating monocytes, leading to their increased accumulation with plaques; and <br />Inhibits egress of macrophages from plaques.<br />
  29. 29. Smooth Muscle Cell Migration and Proliferation<br />
  30. 30. Smooth Muscle Cell Migration and Proliferation<br />Along with macrophages, smooth-muscle cells proliferate in the intima during atherogenesis.<br />Smooth muscle cell layer makes up a substantial bulk of the atherosclerotic lesion, which may rise several millimeters above the surface of the surrounding intima<br />
  31. 31. Role of Platelets<br />   <br />Platelet adhesion may be promoted by type II injury and by toxic products<br />Platelets release growth factors that stimulate SM migration and proliferation and formation of “fibrointimal lesions” and the outside capsule of “fatty lesions<br />
  32. 32. Plaque Fissuring and Formation of Platelet Thrombus<br />The vulnerability of such a structure to fissuring appears to be related to circumferential stress on the plaque cap in systole, as well as infiltration of the cap tissue with foam cells (with reduction of total collagen content and a concomitant fall in tensile strength)<br />
  33. 33. Potential Outcomes of Plaque Fissuring<br />Acute episodes of transient ischemia and ischemic stroke (as well as myocardial infarction, unstable angina, as sudden death) may be precipitated by thrombosis on atherosclerotic plaques.<br />
  34. 34. Thrombus Formation I -- Platelet Activation<br />On contact with collagen, platelets become activated, with platelet adhesion, secretion of platelet contents, and platelet aggregation at the site of injury.  The activated platelet surface is an essential catalytic surface for several coagulation reactions that generate thrombin, a key factor in the coagulation sequence <br />
  35. 35. Thrombus Formation II -- Platelet Activation and Blood Flow<br />
  36. 36. Thrombus Formation III -- Activation of Coagulation Cascade<br />
  37. 37.
  38. 38. Evolution of Cerebral Atherothrombosis<br />
  39. 39. Atherothromboticocclusion of larger arteries<br />Embolism: Artery-to artrey, cardiogenic<br />Primary small vessel disease (lipohyalinosis)  <br />
  40. 40. Thromboembolism<br />
  41. 41. Cardiogenic Emboli<br />Cardiogenic emboli lodge in the middle cerebral artery or its branches in 80% of cases, in the posterior cerebral artery or its branches 10% of the time, and in the vertebral artery or its branches in the remaining 10% of cases.<br />
  42. 42. Major Blood Vessels Of The Brain<br />
  43. 43. Major Blood Vessels Of The Brain<br />
  44. 44. Control Centers of the Brain<br />
  45. 45.
  46. 46. Cellular Injury During IschemiaNeuronal Function: Importance of Oxygen and Glucose<br />The transient change in voltage induced by the action potential is determined by the concentration of ions on either side of the cell membrane.  Maintaining these ionic gradients is an energy-consuming process that requires a constant supply of glucose and oxygen to the neuron.<br />  <br />
  47. 47. Cellular Changes As Ischemia Progresses<br />The duration, severity, and location of focal cerebral ischemia determine the extent of brain function and thus the severity of stroke<br />
  48. 48. Cellular Injury During IschemiaInadequate Energy Supply<br />Lack of glucose and oxygen deplete the cellular energy stores required to maintain electrical potentials and ion gradients.<br />The membrane that surrounds each affected neuron becomes &quot;leaky,&quot; and the cell loses potassium and adenosine triphosphate (ATP), the tissue&apos;s medium for energy exchange<br />
  49. 49. THE ISCHEMIC PENUMBRA<br />
  50. 50.
  51. 51. Stroke Warning Signs<br />Sudden weakness, paralysis, or numbness of the face, arm and the leg on one or both sides of the body<br />Loss of speech, or difficulty speaking or understanding speech<br />Dimness or loss of vision, particularly in only one eye<br />Unexplained dizziness (especially when associated with other neurologic symptoms), unsteadiness, or sudden falls<br />Sudden severe headache and/or loss of consciousness<br />
  52. 52. Left & Right HemisphericStroke: Common Patterns<br />Middle Cerebral Artery (MCA): supplies the lateral surface of hemisphere except for:<br /> 1. frontal lobe<br /> 2. strip along superomedial border of frontal lobe<br /> 3. lowest temporal convolutions<br />Most frequently affected in embolic & thrombotic stroke<br />
  53. 53. Left and Right Hemisphere Stroke: Common Patterns  <br />Left (Dominant) Hemisphere Stroke: Common Pattern<br />Right (Non-dominant) Hemisphere Stroke: Common Pattern <br />Aphasia <br />Right hemiparesis<br />Right-sided sensory loss <br />Right visual field defect <br />Poor right conjugate gaze <br />Dysarthria<br />Difficulty reading, writing, or calculating <br />Neglect of left visual field <br />Extinction of left-sided stimuli <br />Left hemiparesis<br />Left-sided sensory loss <br />Left visual field defect <br />Poor left conjugate gaze <br />Dysarthria<br />Spatial disorientation <br />
  54. 54. Posterior Circulation (Vertebrobasilar Territory) Stroke<br />Ataxia, gait abnormalities<br />Diplopia, oscillopsia, nystagmus, dysconjugate eye movements<br />Nausea & vomiting (center is in area post-rema)<br />Crossed hemiparesis, hemisensory deficits<br />Headache more common<br />
  55. 55.
  56. 56. Differential Diagnosis of Stroke<br />Craniocerebral / cervical trauma<br />Meningitis/encephalitis<br />Intracranial mass<br />Tumor <br />Subdural hematoma <br />Seizure with persistent neurological signs<br />Migraine with persistent neurological signs<br />Metabolic<br />Hyperglycemia <br />Hypoglycemia <br />Post-cardiac arrest ischemia <br />Drug/narcotic overdose <br />  <br />
  57. 57. AHA Stroke Council Recommended Assessment of a Person with Suspected Stroke<br />EMS should be instructed in the rapid recognition, evaluation, treatment and transport <br />Baseline assessment within minutes, CT scan ASAP; use National Institutes of Health Stroke Scale (NIHSS)<br />
  58. 58. AHA Stroke Council Recommended Assessment of a Person with Suspected Stroke<br />EMS should be instructed in the rapid recognition, evaluation, treatment and transport <br />Baseline assessment within minutes, CT scan ASAP; use National Institutes of Health Stroke Scale (NIHSS)<br />Immediate evaluation of the following:<br /> 1. Airway <br /> 2. Vital signs<br /> 3. General medical assessment (including<br /> evidence of injury, cardiovascular <br /> abnormalities)<br /> 4. Neurological assessment (frequent) <br />
  59. 59. EVALUATION AND WORK-UP<br />History and PE<br />Computed Tomography (CT) scan of the head<br />12-lead EKG, chest X-ray<br />Complete blood count, PT, PTT<br />Chemistries (sodium, phosphate, glucose abnormalities may mimic stroke)<br />Urine and serum toxicology (drugs and alcohol) <br />
  60. 60. Under special circumstances, the following tests may be required:<br />Cervical spine x-ray<br />Arterial blood gas<br />Lumbar puncture<br />Electroencephalogram (EEG) <br />
  61. 61. Other Neuroimaging Techniques & Ancillary Tests <br />Magnetic Resonance Imaging (MRI)<br />Diffusion Weighted Imaging (DWI),<br /> Magnetic Resonance Angiography (MRA)<br />Ultrasound (Carotid Duplex, Transcranial Doppler, 2-D echo)<br /> Conventional Angiography<br />Single Photon Emission Computed Tomography (SPECT) <br />Positron Emission Tomography<br />
  62. 62.
  63. 63. Computed Tomography<br />
  64. 64.
  65. 65. Carotid Duplex<br />
  66. 66. Transcranial Doppler<br />
  67. 67. Cerebral Angiography<br />
  68. 68. Functional abnormality demonstrated with PET exceeds that seen with structural imaging techniques such as X-ray, CT, or MRI and is more representative depiction of the underlying functional state of the brain.<br />
  69. 69. SPECT and Xenon Contrast CT<br />
  70. 70. EMERGENT SUPPORTIVE CARE OF ACUTE STROKE PATIENT<br />Maintenance of adequate tissue oxygenation: protecting the airway, O2 inhalation<br />Maintaining optimal blood pressure (autoregulation faulty or lost in stroke patients)<br />
  71. 71. STROKE MANAGEMENT<br />
  72. 72. EMERGENT SUPPORTIVE CARE OF ACUTE STROKE PATIENT<br />Management of blood glucose abnormalities (hyperglycemia associated with poorer prognosis)<br />Management of fever and infections (ischemia worsened by hyperthermia, improved by hypothermia<br />
  73. 73. ACUTE SROKE CARE 2007: <br />Therapies with <br />FDA Approval or <br />Positive Trials For Ischemic Stroke<br />IV TPA (&lt; 3hours)<br /> IA fibrinolysis (&lt; 6 hours)<br /> IA MERCI retriever &lt; 8 hours<br /> Endovascular temperature control<br />
  74. 74.
  75. 75.
  76. 76. Acute Stroke Treatment<br />Intravenous recombinant tissue plasminogen activator (TPA): within 3 hours of stroke symptom onset<br />Intraarterial TPA: within 6 hours; MCA territory stroke by angiography<br />
  77. 77. The Merci Retrieval System<br />
  78. 78. Hypothermia For Acute Stroke:Intravascular Cooling<br />
  79. 79. Physiologic Effects Of Various Levels Of Hypothermia<br />
  80. 80. Known Factors That Cause Stroke Progression<br />Hypotension<br />Hyperglycemia<br />Hyperthermia<br />Infection<br />Cerebral hypoperfusion<br />
  81. 81. Brain Edema<br />
  82. 82. TREATMENT OF BRAIN SWELLING<br />Cerebral perfusion pressure =MAP-ICP<br />Fluid Restriction (1200 ml /day/m2)<br />Controlled hyperventilation: 25 mm Hg<br />Mannitol, 0.25 mg/kg IV over 20 minutes; repeat PRN, serum osmolality maintained in the range of 300-320mOsm/l<br />Barbiturate coma, with ICP monitoring (subarachnoid bolt, IV catheter or Camino catheter): maintain CPP greater than 50 mmHg; pentobarbital serum level of 2-4 mg/dl<br />Surgery (wait 2 weeks)<br />
  83. 83. Management of Cerebral Edema, Increased Intracranial Pressure and Hydrocephalus<br />Brain edema peaks at 3-5 days<br />Treatment includes:<br /> 1. hyperventilation (lower PCO2)<br /> 2. osmotic diuretics<br /> 3. drainage of CSF (ventriculostomy)<br /> 4. surgery (lobectomy)<br />
  84. 84. Neuroprotective Agents<br />Several trials going on<br />So far, trial on one free-radical scavenger showed positive results<br />Phase II trials have proven beneficial; Phase III (human efficacy trials) non-benefial to negative<br />Common measures may “neuroprotect”<br />
  85. 85. Stroke Prevention<br />Anticoagulants (Heparin, Warfarin)<br />Antiplatelets (aspirin, clopidogreldipyridamole/ASA combination, ticlopidine)<br />Statin<br />ARB (-sartan), or ACE inhibitor + HCTZ<br />Carotid endarterectomy if indicated<br />Carotid or intracranial stent.<br />Risk factor control!!!<br />
  86. 86. Concept of Stroke Teams &Stroke Units<br />“Time is brain”<br />Stroke awareness <br />Common mistakes may lead to fatal consequences<br />“Boutique stroke neurology”: Patients will receive best care; length of stay shortened<br />
  87. 87. THANK YOU!<br />

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