Cerebrovascular Disorders PDF

2 Cerebrovascular Disorders Distinguish between transient ischemic attacks and cerebral infarctions Dis9nguishing Between Transient Ischemic A>acks (TIAs) and Cerebral Infarc9ons: 1. Defini9on and Dura9on: o TIA: Temporary reduc/on in blood flow to the brain, spinal cord, or re/na,...

2 Cerebrovascular Disorders Distinguish between transient ischemic attacks and cerebral infarctions Dis9nguishing Between Transient Ischemic A>acks (TIAs) and Cerebral Infarc9ons: 1. Defini9on and Dura9on: o TIA: Temporary reduc/on in blood flow to the brain, spinal cord, or re/na, causing reversible neurological dysfunc/on. Symptoms resolve within 24 hours without causing permanent damage. o Cerebral Infarc9on (Stroke): Sustained decrease in blood flow to the brain leading to irreversible damage and long-las/ng or permanent neurological deficits. 2. Presence of Neuronal Death: o TIA: No signs of neuronal death are present. o Cerebral Infarc9on: Neuronal death occurs due to prolonged ischemia. 3. Symptoms and Recovery: o TIA: Symptoms may include temporary weakness, vision problems, or speech difficul/es but fully resolve without interven/on. o Cerebral Infarc9on: Symptoms persist and vary depending on the affected brain region, such as hemiparesis, aphasia, visual disturbances, and dizziness. 4. Risk Factors: Both condi/ons share common risk factors, including hypertension, diabetes, smoking, and atrial fibrilla/on. However, TIAs are oLen considered a warning sign, with a high risk (20%) of developing a full cerebral infarc/on within three months. 5. Pathophysiology: o TIA: Temporary blockage or reduc/on of blood flow, oLen due to small emboli or vascular spasms that resolve spontaneously. o Cerebral Infarc9on: Can result from thrombosis (blockage of a brain artery), embolism (clot traveling from elsewhere), or hemorrhage leading to sustained ischemia. 6. Imaging: o TIA: No permanent damage is detected on imaging. o Cerebral Infarc9on: Imaging (CT or MRI) typically shows brain /ssue damage. 7. Treatment and Management: o TIA: Immediate treatment focuses on preven/ng future strokes using an/platelets, an/coagulants, or vascular interven/ons. o Cerebral Infarc9on: Requires acute interven/on, such as thromboly/cs (tPA) or endovascular therapy, along with rehabilita/on to address deficits. Explain the pathophysiology of ischemic strokes, including thrombo9c strokes, embolic strokes and lacunar strokes. Pathophysiology of Ischemic Strokes, Including Thrombo9c, Embolic, and Lacunar Strokes Overview of Ischemic Stroke Pathophysiology: Ischemic strokes occur when there is a sustained reduc/on in blood flow to the brain, resul/ng in the death of neurons and glial cells. The key feature of an ischemic stroke is the forma/on of an ischemic core, where blood flow is en/rely blocked, leading to rapid cell death. Surrounding this core is the penumbra, an area of par/al blood flow reduc/on, where neurons are at risk but can recover if blood flow is restored promptly. 1. Thrombo9c Stroke: A thrombo/c stroke occurs when a thrombus (blood clot) forms in one of the intracranial arteries or larger arteries supplying the brain. The most common cause is an atherosclero/c plaque that ruptures, ini/a/ng thrombus forma/on. Por/ons of the thrombus can break off and occlude more distal parts of the cerebral vasculature. The slow progression of blockage leads to ischemia and infarc/on. 2. Embolic Stroke: Embolic strokes are caused by emboli that travel from a distant site, oLen from the heart (due to atrial fibrilla/on) or large arteries (such as the aorta or caro/d arteries). These emboli lodge in cerebral arteries, usually smaller ones, causing sudden blockage of blood flow. Unlike thrombo/c strokes, embolic strokes oLen result in more sudden and severe symptoms. Embolic strokes are also commonly followed by secondary strokes due to the persistence of the embolic source. 3. Lacunar Stroke: Lacunar strokes occur due to the occlusion of small penetra/ng arteries that supply deeper brain structures such as the basal ganglia, thalamus, or brainstem. The cause is oLen associated with chronic hypertension, leading to the forma/on of small vessel disease. The resul/ng infarcts are small and located deep within the brain (hence the term “lacunar”). While lacunar strokes generally have a be_er prognosis, they can cause significant deficits depending on the affected area. Pathophysiological Process (Ischemic Cascade): When blood flow is reduced, the ischemic cascade begins: 1. Excitotoxicity: Due to a lack of oxygen and ATP, neurons depolarize, allowing calcium to accumulate intracellularly, causing cell death. 2. Oxida9ve Stress: Reac/ve oxygen species (ROS) are generated, damaging cellular components such as proteins, DNA, and membranes, leading to further necrosis. 3. Inflamma9on: The dying cells release signals that recruit immune cells and ac/vate glial cells, which produce cytokines and ROS, exacerba/ng /ssue damage and increasing blood-brain barrier permeability. Understanding these mechanisms is crucial for targeted therapies, including thromboly/cs (e.g., /ssue plasminogen ac/vator) and emerging treatments like endovascular thrombectomy for larger vessel occlusions. Compare and contrast the pathophysiology of ischemic and hemorrhagic strokes. The pathophysiology of ischemic and hemorrhagic strokes differs significantly, primarily based on the mechanisms of injury, the type of blood flow disrup/on, and their respec/ve cellular consequences. Ischemic Stroke Pathophysiology Ischemic strokes occur due to the occlusion of a cerebral blood vessel, leading to reduced or blocked blood flow and oxygen supply to brain /ssue. Common causes include thrombosis, embolism, or global hypoperfusion (e.g., from shock). The two significant regions of damage are: Ischemic core: Area where blood flow is completely stopped, leading to rapid neuronal death within minutes. Penumbra: Surrounding /ssue with reduced blood flow (60-80% reduc/on). Neurons here can survive for hours, making /mely interven/on cri/cal for recovery. Key pathological processes include: 1. Excitotoxicity: Loss of energy produc/on leads to membrane depolariza/on, excessive glutamate release, and calcium influx, which triggers neuronal damage. 2. Oxida9ve stress: Ischemia promotes reac/ve oxygen species (ROS) produc/on, damaging cellular components (lipids, proteins, DNA). 3. Inflamma9on: Neuronal death triggers an immune response involving microglia and cytokines, exacerba/ng damage and disrup/ng the blood-brain barrier (BBB). The ischemic cascade results in irreversible necrosis and neuronal damage if /mely reperfusion is not achieved. Hemorrhagic Stroke Pathophysiology Hemorrhagic strokes result from the rupture of a blood vessel within the brain (intracerebral) or subarachnoid space. Causes oLen include hypertension, aneurysms, or trauma9c brain injury. The rupture leads to: Pooling of blood, increasing intracranial pressure. Compression of surrounding brain 9ssue, disrup/ng normal perfusion and leading to ischemia in adjacent areas. Key pathological features include: 1. Mechanical pressure and edema: The accumula/on of blood compresses neurons and vasculature, leading to ischemic damage in adjacent /ssue. 2. Toxic effects of blood breakdown: Hemoglobin and iron released from red blood cells are toxic to neurons, causing oxida/ve stress and apoptosis. 3. Secondary ischemia: The compression oLen disrupts blood flow, triggering ischemic cascades similar to those seen in ischemic strokes. 4. Inflammatory response: Immune cells and cytokines infiltrate the site, promo/ng further damage and disrup/on of the BBB. Comparison and Contrast Aspect Ischemic Stroke Hemorrhagic Stroke Primary Blood vessel blockage (thrombus, Blood vessel rupture and bleeding Mechanism embolus) Reduced oxygen and nutrient Mechanical compression and toxic Ini9al Damage delivery blood effects Aspect Ischemic Stroke Hemorrhagic Stroke Pathological Ischemic cascade: excitotoxicity, Mechanical pressure, ischemia, toxic Processes oxida/ve stress, inflamma/on blood products, inflamma/on Secondary Progressive cell death from ongoing Secondary ischemia, edema, and Damage ischemia oxida/ve stress Occurs due to mechanical rupture and BBB Disrup9on Occurs via inflammatory processes inflamma/on Onset of OLen gradual (e.g., embolic stroke OLen sudden, with severe headache or Symptoms may be sudden) unconsciousness Be_er if treated promptly with Variable, oLen worse due to increased Prognosis reperfusion (e.g., tPA) intracranial pressure In summary, ischemic strokes primarily result from vascular occlusion and oxygen depriva/on, while hemorrhagic strokes result from vessel rupture and mechanical damage due to blood pooling. Both share inflammatory responses but differ in their ini/al triggers and primary pathological damage. Describe the clinical manifesta9ons of ischemic and hemorrhagic strokes. Clinical Manifesta9ons of Ischemic and Hemorrhagic Strokes: Ischemic Stroke Clinical Manifesta9ons: Caused by occlusion or significant reduc/on in cerebral blood flow due to a thrombus or embolus. Core symptoms: Hemiparesis, hemisensory loss, visual disturbances, and aphasia (if dominant hemisphere is affected). Progression: Develops over minutes to hours, poten/ally causing permanent damage without /mely interven/on. Neurological impairments depend on the affected brain region: o Contralateral weakness or paralysis (oLen one side of the body). o Language deficits (aphasia) if the middle cerebral artery or dominant hemisphere is involved. o Visual field deficits, dizziness, and coordina/on issues. o Cogni/ve and behavioral changes (depending on affected regions). Early detec/on and treatment can help prevent progression of ischemic damage. Pathophysiology: The ischemic core is the region where blood flow is completely halted, leading to rapid cell death within minutes. The surrounding area, known as the penumbra, can recover if reperfused promptly. The ischemic cascade includes excitotoxicity (sustained calcium influx), oxida/ve stress, and inflammatory responses, all contribu/ng to further neuronal damage. Hemorrhagic Stroke Clinical Manifesta9ons:  Caused by the rupture of a cerebral blood vessel, leading to bleeding into the brain parenchyma or subarachnoid space. Key symptoms: Sudden severe headache ("thunderclap" headache), nausea, vomi/ng, and altered consciousness. Other symptoms: o Rapid onset of neurological deficits. o Hemiparesis, aphasia, or loss of vision (similar to ischemic strokes). o Signs of increased intracranial pressure (ICP) such as papilledema, seizures, or reduced consciousness. o Nuchal rigidity and photophobia (especially in subarachnoid hemorrhages). Pathophysiology: The rupture of blood vessels causes blood pooling, leading to compression of surrounding brain /ssue and increased intracranial pressure. The ischemic cascade is also ini/ated in surrounding regions due to disrupted blood flow. Released hemoglobin from damaged red blood cells can be toxic to neurons, exacerba/ng long-term injury.