Stroke pathophysiology detailed version. pptx

Pathophysiology of stroke

1. Stroke Dr. Jesmitha J M PhD Scholar

2. Definition A stroke (cerebrovascular accident/CVA) is a sudden loss of neurological function due to interruption of blood flow to a part of the brain , resulting in tissue ischemia and neuronal injury . There are two main types : Ischemic stroke (~85%) – due to arterial occlusion (thrombosis or embolism) Hemorrhagic stroke (~15%) – due to rupture of a blood vessel causing bleeding into brain tissue or subarachnoid space

3. Ischemic Stroke An ischemic stroke is a sudden loss of blood flow to a region of the brain due to arterial obstruction , resulting in neuronal injury and neurological deficits lasting >24 hours (or leading to death ). If symptoms resolve within 24 hours → it’s called a Transient Ischemic Attack (TIA ) . Cerebral Blood Flow Basics Brain receives ~15% of cardiac output and consumes ~20% of body’s oxygen. Normal cerebral blood flow (CBF): 50–60 mL/100 g/min. When CBF <20 mL/100 g/min → electrical failure , and <10 mL/100 g/min → irreversible cell death (infarction).

4. Classification of Ischemic stroke Type Mechanism / Cause Thrombotic Atherosclerotic plaque rupture → local clot Embolic Embolus from heart or artery lodges in brain Lacunar Small vessel occlusion (deep penetrating arteries) Hypoperfusion Global low flow (e.g., cardiac arrest, shock)

5. Clinical presentation of stroke

6. Other Signs and symptoms Headache Nausea Vomiting Dizziness Seizures Numbness Painful stiff neck

7. Risk Factors Modifiable Non-Modifiable Hypertension Age (risk doubles each decade after 55) Diabetes mellitus Male sex Dyslipidemia (↑LDL, ↓HDL) Family history of stroke or TIA Smoking Prior stroke or TIA cardiac diseases (MI, valvular disease) Genetic thrombophilia Obesity, physical inactivity Race (higher in African & South Asian populations) Alcohol abuse Carotid artery disease Oral Contraceptives Sickle cell disease

8. Pathophysiology A. Vascular Occlusion Most ischemic strokes occur due to thrombosis or embolism . Thrombotic stroke: local clot forms on atherosclerotic plaque Embolic stroke: clot travels and lodges in cerebral vessels. B. Reduced Cerebral Perfusion Blood flow falls below 18–20 mL/100 g/min → neurons can’t generate ATP. Energy failure → Na⁺/K⁺-ATPase pump stops → cell depolarization .

9. C. Ionic Imbalance and Excitotoxicity Massive release of glutamate Glutamate overstimulates receptors → influx of Ca²⁺ and Na⁺ into neurons. Ca²⁺ activates destructive enzymes (proteases, lipases, endonucleases). Result → neuronal Ischemia, swelling and death.

10. D. Free Radical Formation and Inflammation Ischemic neurons generate reactive oxygen species (ROS) . Microglia and endothelial cells release IL-1, TNF- α, IL-6 , worsening injury. Blood–brain barrier (BBB) becomes leaky → vasogenic edema . E. Formation of core and penumbra Ischemic core: <10 mL/100 g/min flow → irreversible neuronal necrosis within minutes. Ischemic penumbra: 20–30 mL/100 g/min → functionally silent but potentially salvageable with early reperfusion (e.g., thrombolysis).

11. Ischemic Core Definition: The central zone of the infarct where blood flow is severely reduced (<10 mL/100 g/min) . Effect: Neurons suffer irreversible damage within minutes (usually 5–10 minutes). ATP depletion stops sodium-potassium pump → sodium and water enter cells → cytotoxic edema → cell lysis . Outcome: Permanent neuronal necrosis (dead tissue). Therapeutic implication: Cannot be salvaged , even with reperfusion. Ischemic Penumbra Definition: The surrounding zone of tissue around the core, where blood flow is moderately reduced (20–30 mL/100 g/min) . Effect: Neurons are functionally silent (cannot fire signals) due to low energy supply, But the cell membranes remain intact — the tissue is still alive but at risk . Outcome: If blood flow is restored quickly (e.g., via thrombolysis or mechanical thrombectomy ), the penumbra can recover . Therapeutic implication: This is the target of acute stroke therapy — “Save the penumbra.”

12. Every minute of untreated ischemic stroke → loss of ~2 million neurons .

13. Haemorrhagic Stroke A hemorrhagic stroke occurs when a cerebral blood vessel ruptures , leading to bleeding into brain tissue ( intracerebral hemorrhage - ICH) or into the subarachnoid space (subarachnoid hemorrhage - SAH ) . This bleeding increases intracranial pressure (ICP) , compresses nearby brain tissue, and leads to secondary ischemia and neuronal death .

14. Type Location Clinical Clue Intracerebral Hemorrhage (ICH) Inside brain parenchyma Sudden focal deficits + headache Subarachnoid Hemorrhage (SAH) Between arachnoid and pia mater "Thunderclap" headache — worst ever Intraventricular Hemorrhage Blood enters ventricles Acute raised ICP, coma Subdural/Epidural Hemorrhage Due to trauma Crescent/biconvex bleed on CT

15. Risk Factors ✔ Modifiable Chronic hypertension (most common) Anticoagulant/antiplatelet use (warfarin) Smoking & alcohol abuse Head trauma Illicit drug use (cocaine, amphetamines → ↑ BP) ✔ Non-Modifiable Age (>55 years) Male sex Asian or African descent Genetic disorders (Polycystic kidney disease, Marfan , Ehlers- Danlos )

16. Signs and Symptoms Intracerebral Hemorrhage (ICH) Sudden severe headache Focal neurological deficits (hemiplegia, speech issues) Vomiting Rapidly deteriorating consciousness Subarachnoid Hemorrhage (SAH) “Thunderclap headache” – worst of life Neck stiffness (meningeal irritation) Photophobia, vomiting Loss of consciousness or sudden collapse Kernig’s / Brudzinski’s sign positive

17. Pathophysiology

18. Diagnosis CT Brain MRI CBC , coagulation profile BP Carotid Doppler

19. Complications of Stroke 1. Neurological Complications Recurrent stroke: Patients who have had one stroke are at higher risk of another. Seizures: More common after hemorrhagic stroke or cortical involvement. Cognitive impairment / dementia: Especially with multiple strokes or involvement of large brain areas. Movement disorders: Parkinsonism, tremors, or ataxia can develop in some cases. Sensory deficits: Persistent numbness, tingling, or pain (central post-stroke pain).

20. Complications of Stroke 2. Motor Complications Hemiplegia / hemiparesis: Weakness or paralysis on one side of the body. Spasticity / contractures: Muscle stiffness and shortening of tendons over time. Balance and coordination problems: Increased risk of falls. Shoulder subluxation: Partial dislocation due to weakness in shoulder muscles.

21. Complications of Stroke 3. Speech and Swallowing Complications Aphasia: Difficulty with speaking, understanding, reading, or writing (depends on lesion location). Dysarthria: Slurred or slow speech due to weakened muscles. Dysphagia: Difficulty swallowing, increasing the risk of aspiration pneumonia. 4 . Cognitive and Psychological Complications Memory deficits: Short-term memory often affected. Attention and executive function issues: Difficulty planning, organizing, or multitasking. Depression and anxiety: Very common; may affect recovery. Emotional lability / pseudobulbar affect: Sudden episodes of laughing or crying without cause.

22. Complications of Stroke 5. Cardiovascular and Autonomic Complications Blood pressure fluctuations: Especially in acute stroke phase. Arrhythmias: Stroke patients can develop irregular heart rhythms. Deep vein thrombosis (DVT) / pulmonary embolism: Due to immobility. Orthostatic hypotension: Especially in prolonged bed rest. 6. Other Systemic Complications Pressure sores / ulcers: From immobility, especially in bedridden patients. Urinary retention / incontinence: Can lead to infections. Constipation: Due to immobility or medications. Infections: Pneumonia (often aspiration-related) and urinary tract infections are common.