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Pathophysiology of Stroke Sid M. Shah, MD Assistant Residency Director Assistant Clinical Professor Department of Emergency Medicine Michigan State University.

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Presentation on theme: "Pathophysiology of Stroke Sid M. Shah, MD Assistant Residency Director Assistant Clinical Professor Department of Emergency Medicine Michigan State University."— Presentation transcript:

1 Pathophysiology of Stroke Sid M. Shah, MD Assistant Residency Director Assistant Clinical Professor Department of Emergency Medicine Michigan State University East Lansing, MI

2 Sid Shah, MD Pathogenesis of Stroke: Ischemia & Hemorrhage Ischemia: lack of circulating blood deprives the neurons of oxygen and nourishment Hemorrhage: Extravascular release of blood causes damage by cutting off connecting pathways, resulting in local or generalized pressure injury

3 Sid Shah, MD Acute Ischemic Injury The occlusion of a large vessel (such as MCA) is rarely complete and cerebral blood flow (CBF) depends on the degree of obstruction, and collateral circulation Many factors influence progression and extent of ischemic injury

4 Sid Shah, MD Conditions influencing progression and extent of ischemic injury Rate & duration of the ischemic event Collateral circulation in the involved area of the brain Systemic circulation & arterial blood pressure Coagulation abnormalities Temperature Glucose

5 Sid Shah, MD Pathophysiology at Macro Tissue Level Cerebral Blood Flow (CBF) –Ischemic Thresholds Ischemic Penumbra and Window of Opportunity

6 Sid Shah, MD CBF & Ischemic Thresholds Normal CBF  cc/100 g/minute –Varies in different regions of the brain CBF 20-30cc/100g/min  Loss of electrical activity CBF 10 cc/100g/min  Neuronal death

7 Sid Shah, MD Ischemic Penumbra & Window Of Opportunity Ischemic zone that surrounds a central core of infarction with CBF of 25% to 50% of normal and loss of auto regulation Viability of brain tissue is preserved if perfusion is restored within a critical time period (2 to 4 hours?)

8 Sid Shah, MD Microcellular Mechanisms of Neuronal Injury Development of microcirculatory disturbances –Formation of micro thrombi –Accumulation of noxious metabolites –Interaction of endothelial cells with PMN leukocytes & platelets –PMNs trigger neuronal necrosis

9 Sid Shah, MD Microcellular Mechanisms of Neuronal Injury: Excitotoxicity Ischemia depletes neuronal energy stores causing energy dependent membrane ion pumps to fail This results in increased extracellular glutamate concentration Release of excitotoxic Glutamate & Aspartate open up calcium channels resulting in influx of calcium, sodium and chloride and out flux of potassium causing irreversible neuronal damage

10 Sid Shah, MD Timing of Neuronal Death Coagulation necrosis Apoptosis

11 Sid Shah, MD Coagulation Necrosis A process of cell death that evolves over 6 hours to 12 hours Necrotic death is attributed to effects of physical, chemical and osmotic damage to the plasma membrane Morphology of dying cells is distinct from that of cells dying from apoptosis

12 Sid Shah, MD Apoptosis “Programmed cell death” triggered by ischemia, evolves over 2 hours Ischemia activates latent “suicide” proteins that triggers an autolytic process mediated by DNA cleavage

13 Sid Shah, MD Major Categories of Ischemic Stroke Thrombosis Embolism Global-Ischemic or Hypotensive Stroke

14 Sid Shah, MD Thrombotic Stroke Atherosclerosis: the commonest pathology of vascular obstruction leading to thrombosis Other pathological causes: –Fibro muscular dysplasia –Arteritis (Giant Cell & Takayasu) –Dissection of vessel wall and hemorrhage into atheromatous plaque –Hypercoaguability

15 Sid Shah, MD Embolic Stroke Two most common sources of emboli: –Left sided cardiac chambers –Artery to artery stroke: as in detachment of a thrombus from ICA at the site of a plaque Many embolic strokes become “hemorrhagic” Generally “smaller” strokes than thrombotic strokes

16 Sid Shah, MD Embolism

17 Ischemic Stroke Due To Hemodynamic Crisis: “Hypotensive Stroke” Any event causing abrupt drop in blood pressure results in critical compromise of CBF (cerebral blood flow) and hence cerebral perfusion. Sites affected by critically low CBF are located at the end of an arterial territory. Hence the term “watershed or boundary zone infarct.”

18 Sid Shah, MD Watershed Infarcts Resulting From Hemodynamic Crisis (Hypotensive Stroke)

19 Sid Shah, MD Selective Vulnerability of Neurons to Global Ischemia Hippocampus: pyramidal cell layer Cerebral cortex: Purkinje cell layer Cerebellar cortex  The increased vulnerability of these neurons is due to the abundance of neurotransmitter glutamate in these neurons

20 Sid Shah, MD Complications Of Restoration of Blood Flow: Hemorrhage and Edema Arterial occlusion causes ischemia to capillaries, arterioles and vascular walls in addition to the deleterious effects on neurons Hemorrhage (red infarcts) result when the fragile “ischemic” or “injured” vessels rupture after sudden restoration of blood flow Vasogenic edema can also occur following a massive stroke or sudden restoration of blood flow to an ischemic area

21 Sid Shah, MD

22 Factors Associated With Red Infarcts (Hemorrhagic Transformation) Size of the infarct - bigger infarcts have a higher chance of becoming hemorrhagic Richness of collateral circulation Use of anti-coagulants Treatment with thrombolytic agents


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