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STROKE

ARLYN M. VALENCIA , M.D. Associate Professor, UNSOM Diplomate , American Board Of Psychiatry & Neurology. STROKE. LEARNING OBJECTIVES. To be able to define stroke, discuss its pathophysiology and risk factors To emphasize early evaluation and mana geme nt of stroke patients

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STROKE

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  1. ARLYN M. VALENCIA , M.D. Associate Professor, UNSOM Diplomate, American Board Of Psychiatry & Neurology STROKE

  2. LEARNING OBJECTIVES • To be able to define stroke, discuss its pathophysiology and risk factors • To emphasize early evaluation and management of stroke patients • To discuss the latest stroke treatment strategies • CASE STUDIES: To be able to analyze clinical situations, localize the stroke lesion, determine probable etiology

  3. ”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!” A. Valencia, M.D.

  4. The biology of stroke is such that each moment of ischemia and tissue injury increases the degree of irreversible tissue damage.

  5. CEREBROVASCULAR ACCIDENT OR “BRAIN ATTACK” • Third leading cause of death • 750, 000 cases/year • Leading cause of significant disability • Cost: $40 billion/year

  6. Major Causes of Death in the United Sates, 1995

  7. Annual Economic Costs of Stroke (All Types) In The US

  8. Death Rates for Stroke per 100,000 Population

  9. Types of Stroke • Ischemic, 80% - thrombosis, 50% (small & large-vessel) - embolism, 30% [now believed significantly higher] • Hemorrhagic, 20% - intracerebral (HTN as risk) - subarachnoid (aneurysm)

  10. Stroke vs. TIA • 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) • 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.

  11. Risk Factors for Stroke That Cannot Be Changed • Increased age • Being male • Race (e.g., African-Americans) • Diabetes mellitus • Prior stroke/transient ischemic attacks • Family history of stroke • Asymptomatic carotid bruit

  12. Up to approximately 30% of people who suffer transient attacks (TIAs) will develop a stroke within 5 years.

  13. Relative Incidence of Atherothrombotic Stroke and MI by Age and Gender

  14. Death Rates for Stroke per 100,000 PopulationGroups Defined by Race, Age, and Gender:  1993

  15. Risk Factor For Stroke: Treatable Major • Hypertension • Heart disease, esp. atrial fibrillation • Cigarette smoking • Transient ischemic attacks • Dyslipidemia • Physical inactivity • Obesity Less Well Documented • Excessive alcohol intake / drug abuse • Acute infection*

  16. Alcohol Consumption as a Risk Factor for Stroke • Heavy alcohol consumption may increase risk of stroke by a number of mechanisms. • The reported effects of alcohol consumption on risk of ischemic stroke have been inconsistent. • A differential effect of alcohol consumption on stroke risk in men compared to women has been observed.

  17. Alcohol Consumption as a Risk Factor for Stroke • Light and moderate alcohol use tend to raise levels of high-density-lipoprotein (HDL) -- the "good" lipoprotein. • 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. • There is positive, dose-related effect of alcohol consumption on risk of intracranial hemorrhage, both arachnoid and intracerebral .

  18. Less Well Documented • Geography/climate • Socieconomic factors

  19. The Stroke Belt

  20. Potential Genetic Risk Factors for Stroke • Apolipoprotein E4 • Elevated homocysteine  levels • Factor V mutation

  21. ATHEROSCLEROSIS AND THROMBOSIS Atherosclerosis: decades-long process; progression favored by hypercholesterolemia, HTN, cigarette smoking • Fatty streak: yellowish discoloration on intimal surface of blood • Focal plaques: eccentric thickening at bifurcations; addition of massive extracellular lipids that displaced normal cells and matrix • Complicated fibrous plaques: central acellular area of lipid covered by a cap of smooth muscle cells and collagen

  22. Atherosclerosis and Thrombus Formation:Arterial Wall Injury • Functional alteration of endothelial cell layer • Denuding of endothelium • Superficial intimal injury • Deep intimal & media damage with marked platelet aggregatio and mural thrombosis

  23. Role of Monocytes and T-Lymphocytes in the Transformation to Foam Cells

  24. Oxidation of LDL-Cholesterol

  25. Oxidized LDL-cholesterol Contributes To Atherogenesis In Three Other Ways: It has cytotoxic properties that may promote endothelial injury; It acts as a chemoattractant for circulating monocytes, leading to their increased accumulation with plaques; and Inhibits egress of macrophages from plaques.

  26. Smooth Muscle Cell Migration and Proliferation

  27. Smooth Muscle Cell Migration and Proliferation Along with macrophages, smooth-muscle cells proliferate in the intima during atherogenesis. 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

  28. Role of Platelets • Platelet adhesion may be promoted by type II injury and by toxic products • Platelets release growth factors that stimulate SM migration and proliferation and formation of “fibrointimal lesions” and the outside capsule of “fatty lesions

  29. Plaque Fissuring and Formation of Platelet Thrombus 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)

  30. Potential Outcomes of Plaque Fissuring 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.

  31. Thrombus Formation I -- Platelet Activation 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

  32. Thrombus Formation II -- Platelet Activation and Blood Flow

  33. Thrombus Formation III -- Activation of Coagulation Cascade

  34. Evolution of Cerebral Atherothrombosis

  35. Atherothromboticocclusion of larger arteries • Embolism: Artery-to artrey, cardiogenic • Primary small vessel disease (lipohyalinosis)  

  36. Thromboembolism

  37. Cardiogenic Emboli • 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.

  38. Major Blood Vessels Of The Brain

  39. Major Blood Vessels Of The Brain

  40. Control Centers of the Brain

  41. Cellular Injury During IschemiaNeuronal Function: Importance of Oxygen and Glucose • 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.

  42. The duration, severity, and location of focal cerebral ischemia determine the extent of brain function and thus the severity of stroke Cellular Changes As Ischemia Progresses

  43. Cellular Injury During IschemiaInadequate Energy Supply • Lack of glucose and oxygen deplete the cellular energy stores required to maintain electrical potentials and ion gradients. • The membrane that surrounds each affected neuron becomes "leaky," and the cell loses potassium and adenosine triphosphate (ATP), the tissue's medium for energy exchange

  44. THE ISCHEMIC PENUMBRA

  45. Stroke Warning Signs • Sudden weakness, paralysis, or numbness of the face, arm and the leg on one or both sides of the body • Loss of speech, or difficulty speaking or understanding speech • Dimness or loss of vision, particularly in only one eye • Unexplained dizziness (especially when associated with other neurologic symptoms), unsteadiness, or sudden falls • Sudden severe headache and/or loss of consciousness

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