Stroke Txt B Flashcards
What’s the most common cause of Stroke
Most cases are caused by thromboembolic disease, where a blood clot forms (thrombosis) or travels from another part of the body (embolism) and blocks an artery.
What are the causes of Stroke?
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Causes:
- Atherosclerosis: This is the buildup of plaque in the arteries. When this occurs in major extracranial arteries, such as the carotid artery or the aortic arch, it increases the risk of cerebral infarction. These vessels supply blood to the brain, and blockage due to plaque can reduce or stop blood flow, leading to infarction.
- Embolism from the Heart: Around 20% of cerebral infarctions are due to emboli (blood clots or debris) that travel from the heart and block cerebral arteries.
- Thrombosis in Small Vessels: Another 20% are caused by in situ thrombosis, where clots form directly inside small perforating vessels in the brain, such as the lenticulostriate arteries. These cause lacunar infarctions, which are small, localized strokes.
- Rare Causes: Around 5% of cases stem from conditions like vasculitis (inflammation of blood vessels), endocarditis (infection of the heart valves), or cerebral venous disease.
What’s the path physiology of stroke
Both TIA & Acute stroke
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Progression:
- A cerebral infarction does not occur immediately after a vessel is blocked. It may take several hours for the damage to complete, even though the patient’s symptoms may be severe right after the blockage.
- Collateral circulation: When a cerebral artery is blocked, blood flow from neighboring arteries through anastomotic channels can sometimes compensate and prevent the infarction. These channels may restore enough blood flow to avoid severe damage.
- If these compensatory mechanisms fail, ischemia (lack of oxygen) starts, and if blood flow is not restored, the ischemia can lead to an infarction.
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Ischemia and Neuronal Damage:
- Different thresholds of blood flow affect neurons in different ways. As blood flow decreases, neurons begin to fail. Initially, there is loss of electrical activity, leading to neurological deficits (such as weakness or speech difficulties).
- At this stage, neurons are still alive, and if blood flow is restored, these deficits may resolve. This temporary issue is called a Transient Ischemic Attack (TIA).
- If the blood flow continues to decline, irreversible damage begins, leading to cell death.
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Pathophysiology of Neuronal Death:
- Hypoxia (lack of oxygen) causes cells to produce less ATP (the energy currency of the cell), which is essential for maintaining cellular functions like membrane pumps.
- Without ATP, sodium and water flood into the cells, causing cytotoxic edema (swelling of the brain cells), while excessive glutamate release leads to further cellular damage by allowing calcium and sodium to enter neurons.
- Calcium influx triggers destructive enzymes within neurons, further promoting cell death.
- Inflammatory mediators released by brain cells such as microglia and astrocytes exacerbate the injury, ultimately killing all cells in the area.
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Anaerobic Metabolism:
- When oxygen is low, cells rely on anaerobic metabolism, which produces lactic acid. This buildup of acid lowers the tissue pH, further damaging brain cells.
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Neuroprotection:
- There have been efforts to develop neuroprotective drugs that could slow down or prevent the irreversible damage from occurring. However, these have not yet proven effective in clinical trials.
- Cerebral infarction is commonly due to thromboembolic disease, either from atherosclerosis or clots from the heart.
- Small vessel thrombosis can lead to lacunar infarctions.
- The brain has mechanisms to compensate for reduced blood flow, but if they fail, irreversible ischemia and cell death occur.
- Neuronal death involves multiple mechanisms, including energy failure, glutamate release, calcium influx, and inflammation.
- Neuroprotective therapies have not been successful so far, though research continues.
This explanation should provide a clearer understanding of cerebral infarction, its causes, and the process leading to brain tissue death.
What are the Key Factors Influencing the Outcome of a stroke?
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- Circulatory Homeostasis: If the brain’s compensatory mechanisms, such as collateral circulation from other arteries, are effective, they may prevent or limit damage to brain tissue. However, if these fail, ischemia will progress to infarction.
- Metabolic Demand: Areas of the brain with high metabolic needs (such as those involved in active processes like thinking or movement) are more susceptible to damage during ischemia. They require more oxygen and glucose, and if these are not supplied, the tissue will die more quickly.
- Severity and Duration of Blood Flow Reduction: A prolonged or severe reduction in blood flow increases the likelihood of permanent brain damage. Shorter or less severe blockages may lead to temporary dysfunction or transient ischemic attacks (TIAs), where blood flow is restored before permanent damage occurs.
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Temperature and Glucose Levels:
- High brain temperature, such as in cases of fever, increases the likelihood of a larger infarction for a given reduction in blood flow. Heat makes the brain more vulnerable to ischemic injury.
- High blood glucose levels (e.g., in diabetic patients) can also exacerbate brain damage, leading to larger infarct volumes. This is partly due to glucose’s role in generating lactic acid under anaerobic conditions, which worsens cellular injury.
- After a cerebral infarction, there is a risk of haemorrhagic transformation, where blood leaks into the infarcted brain tissue. This occurs when blood flow is restored to the infarcted area, especially in patients who have received antithrombotic (blood-thinning) or thrombolytic (clot-dissolving) drugs, which make the blood more prone to bleeding.
- Larger infarcts have a higher risk of this transformation due to the greater degree of damage and vulnerability of the blood vessels in the infarcted region.
What are the Radiological Features of Cerebral Infarction:
How does infarction progress and it’s long term implications
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Imaging studies (such as CT or MRI scans) show a cerebral infarction as a lesion that consists of both dead and swollen, but potentially recoverable, brain tissue.
- Dead brain tissue undergoes autolysis (self-destruction), a process in which the brain cells begin to break down.
- Ischaemic penumbra refers to the area surrounding the infarct that is still salvageable if blood flow is restored in time. This is an important concept because treatment efforts focus on saving this at-risk tissue.
- Initially, the infarcted area swells and reaches its maximum size a few days after the stroke onset. This swelling may cause a mass effect, where the swollen tissue puts pressure on nearby brain structures, potentially worsening symptoms.
- In severe cases, the swelling may be so significant that it requires decompressive craniectomy, a surgical procedure where part of the skull is removed to relieve pressure and prevent further brain damage.
- After a few weeks, the swelling subsides, and the infarcted area is replaced by a fluid-filled cavity. This sharply defined cavity is the permanent result of the tissue death, leaving a space where brain tissue once was.
In summary, the final outcome of a cerebral infarction depends on various factors such as the brain’s compensatory abilities, the duration and severity of the blood flow reduction, and the patient’s physiological state (e.g., temperature and glucose levels). Imaging can reveal the extent of damage, and in some cases, interventions like decompressive surgery may be needed to manage complications like swelling.
What’s ICH?
Intracerebral haemorrhage (ICH) accounts for about 10% of acute stroke cases, though it is more prevalent in low-income countries. This condition occurs when a blood vessel within the brain ruptures, leading to bleeding into the brain tissue (parenchyma). While it can occur spontaneously, it may also arise in a patient with subarachnoid haemorrhage (SAH), where the bleeding extends from the subarachnoid space into the brain tissue itself.
What are the risk factors/ causes of ICH
- Hypertension (high blood pressure), which weakens blood vessels over time
- Cerebral amyloid angiopathy (a condition where amyloid deposits in blood vessels make them more prone to rupture)
- Use of anticoagulants or blood-thinning medications
- Brain tumors
- Arteriovenous malformations (AVMs) or aneurysms
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Head trauma
Other factors, such as heavy alcohol consumption, drug use (especially stimulants like cocaine), and certain blood disorders, can also contribute to the risk of ICH.
Here’s an explanation of the causes of intracerebral haemorrhage (ICH) and the associated risk factors, organized by the underlying disease and contributing factors:
- Age: As people get older, blood vessels lose elasticity and become more prone to rupture, increasing the risk of ICH.
- Hypertension (High Blood Pressure): Chronically high blood pressure is the most significant risk factor for ICH. It weakens the walls of blood vessels over time, leading to rupture.
- High Cholesterol: Elevated cholesterol contributes to the formation of plaques in the blood vessels, which can make them more fragile and prone to damage.
- Amyloid Angiopathy: This condition involves the accumulation of amyloid protein in the walls of blood vessels, particularly in the elderly, which weakens the vessels and increases the risk of spontaneous bleeding.
- Familial (Rare): Some rare hereditary conditions can predispose individuals to small-vessel disease, increasing the likelihood of ICH.
- Anticoagulant Therapy: Medications such as warfarin, used to thin the blood, can increase the risk of bleeding if the dosage is not carefully managed or if there is an injury to the blood vessels.
- Blood Dyscrasia: This refers to abnormal blood conditions, such as low platelet counts or clotting disorders, which can impair the blood’s ability to form clots and increase the likelihood of bleeding.
- Thrombolytic Therapy: Drugs used to dissolve clots in patients with ischemic stroke or heart attacks can sometimes cause excessive bleeding, leading to ICH.
- Arteriovenous Malformation (AVM): An AVM is a tangle of abnormal blood vessels that bypass the normal capillary system, putting significant pressure on vessel walls and increasing the risk of rupture.
- Cavernous Haemangioma: This is a benign vascular lesion made up of clusters of dilated blood vessels. While generally asymptomatic, it can occasionally rupture and cause ICH.
- Alcohol: Chronic alcohol use can lead to hypertension, liver dysfunction (affecting clotting factors), and brain vessel fragility, all of which increase the risk of ICH.
- Amphetamines: Stimulant drugs like amphetamines increase blood pressure and heart rate, putting significant stress on blood vessels and potentially leading to rupture.
- Cocaine: Cocaine is a powerful vasoconstrictor that causes sudden increases in blood pressure, which can rupture weak blood vessels, leading to ICH.
In summary, ICH can result from various underlying conditions that affect the integrity of blood vessels, impair blood clotting, or create vascular anomalies. Age, hypertension, and substance misuse are among the most prominent risk factors associated with these causes.
What are the path physiology of ICH
When a blood vessel ruptures within the brain, explosive entry of blood into the brain parenchyma occurs, which immediately disrupts the function of that area. Neurons in the affected region are damaged, and the white-matter fiber tracts that transmit signals across the brain are torn apart. The initial damage is compounded by the fact that the haemorrhage can expand in size over the first few minutes or hours, worsening the neurological damage.
- Cerebral oedema (swelling) often surrounds the site of the haemorrhage, further increasing pressure inside the skull. This combination of swelling and haematoma (blood clot) acts like a mass lesion, compressing adjacent brain structures.
- If the bleeding and oedema are significant, the increased pressure can cause a shift of intracranial contents. This can lead to transtentorial coning (herniation), where part of the brain is forced through openings in the skull, such as the tentorial notch, which is often fatal. This rapid shift can cause brainstem compression, leading to a shutdown of vital functions like breathing and heart rate, resulting in rapid death if not treated immediately.
In patients who survive the acute phase, the haematoma (the collection of blood within the brain tissue) is gradually reabsorbed over time. However, the damage to the brain tissue leaves a haemosiderin-lined slit. Haemosiderin is a breakdown product of blood that is deposited in the tissue as the haematoma is reabsorbed, leaving a permanent scar or cavity in the brain.
Distinguishing between a primary intracerebral haemorrhage (where bleeding occurs spontaneously) and a secondary haemorrhage into an area of brain infarction (stroke caused by a clot) can be difficult, both clinically and on imaging studies. Both types can appear similar in terms of symptoms and radiological findings (e.g., on CT or MRI scans), especially if the haemorrhage is large. In either case, the damage can be extensive, and the prognosis depends on the size and location of the bleed, as well as the speed and effectiveness of medical intervention.
In summary, intracerebral haemorrhage is a devastating condition caused by the rupture of a blood vessel within the brain. The bleeding causes immediate damage to neurons and white matter, and if left unchecked, it can expand and lead to dangerous complications like brain herniation. The extent of recovery depends on the size of the haemorrhage, the presence of cerebral oedema, and how quickly medical intervention is provided.
clinical features of both acute stroke and transient ischaemic attack (TIA):
Both acute stroke and TIA share a common feature: they are characterized by rapid-onset, focal deficits in brain function. The difference lies in the duration of symptoms:
- TIA: Symptoms are transient, meaning they resolve within a short period (typically within 24 hours), without causing permanent brain damage.
- Stroke: Symptoms are persistent and lead to long-term damage unless treated promptly.
- Sudden Onset: Symptoms appear quickly, usually over the course of minutes. This distinguishes stroke and TIA from conditions with gradual onset.
- Focal Deficit: The symptoms affect specific areas of brain function, depending on the location of the affected blood vessel. This results in localized problems like weakness in a particular limb or difficulty speaking.
- Negative Symptoms: The hallmark of stroke and TIA is the sudden loss of function, such as weakness or numbness. There are no positive features like abnormal movements (such as seizures or spasms). The focus is on what’s lost, not additional symptoms.
- If the history fits with a rapid-onset, focal neurological deficit, the probability that the event is vascular (stroke or TIA) is very high, with less than 5% chance that it is due to something else.
- If symptoms appear over hours or days, other causes must be considered, as this would be unusual for a stroke or TIA.
What are the common miss diagnosis
- Symptoms like delirium, memory disturbance, and balance problems are often mistaken for stroke, but these are more likely to be caused by conditions that mimic stroke (e.g., infections, metabolic disorders, or tumors).
- Transient symptoms like syncope (fainting), amnesia, delirium, and dizziness do not typically indicate a TIA, because these are not caused by focal brain dysfunction.
- Public health campaigns emphasize recognizing common stroke symptoms like:
- Facial weakness (drooping on one side of the face),
- Arm weakness (inability to lift one or both arms),
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Speech disturbance (slurred or garbled speech).
These signs are often used in stroke awareness campaigns (such as FAST: Face, Arms, Speech, Time).
- The location and size of the brain lesion dictate the clinical presentation and are important in guiding treatment decisions. For example, if a stroke occurs due to blockage of the carotid artery, the patient may be a candidate for carotid endarterectomy, a surgical procedure to remove the blockage.
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Cerebral Hemisphere: Unilateral (one-sided) symptoms, such as:
- Motor deficit (weakness on one side of the body),
- Aphasia (inability to speak or understand language) if the left hemisphere is involved,
- Neglect (lack of awareness of one side of the body) if the right hemisphere is involved,
- Visual field defect (loss of vision in part of the visual field).
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Brainstem or Cerebellum:
- Symptoms may include ataxia (uncoordinated movement),
- Diplopia (double vision),
- Vertigo (feeling of spinning),
- Bilateral weakness (weakness on both sides of the body).
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Reduced Consciousness:
- A reduced level of consciousness often suggests that the stroke or lesion is large, particularly in the cerebral hemisphere.
- However, reduced consciousness can also result from damage to the brainstem, which is crucial for controlling vital functions like breathing and heart rate.
- Complications such as obstructive hydrocephalus (when fluid buildup increases pressure in the brain), hypoxia (lack of oxygen), or severe systemic infection (like sepsis) can also cause decreased consciousness.
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Headache and Vomiting:
- The combination of a severe headache and vomiting at the time of stroke onset points to intracerebral hemorrhage (bleeding within the brain). This is because the sudden increase in pressure from the bleeding can cause these symptoms.
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General Examination:
- A thorough physical exam can help uncover the cause of the stroke and reveal any complications or other underlying conditions (comorbidities) the patient may have. For example, hypertension is a common risk factor for both ischemic and hemorrhagic stroke.
What are the Stroke Classifications Based on Symptom Duration and Evolution:
Several terms are used to describe the different types of strokes based on how long symptoms last and how the symptoms evolve:
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Transient Ischaemic Attack (TIA):
- A TIA is a mini-stroke, where symptoms resolve within 24 hours.
- While the 24-hour cut-off is arbitrary, the important point is that TIAs do not cause permanent brain damage.
- A TIA generally indicates that there’s no large cerebral infarction or hemorrhage.
- A specific type of TIA called amaurosis fugax occurs when there is a temporary loss of vision in one eye, usually due to a blockage in the retinal artery.
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Stroke:
- A stroke occurs when symptoms last more than 24 hours. This longer duration increases the likelihood of permanent brain damage.
- Minor Stroke: Sometimes, a stroke is described as minor if the symptoms last longer than 24 hours but do not result in major disability.
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Progressing Stroke (Stroke in Evolution):
- This term refers to a stroke where the neurological deficits worsen after the initial presentation. This progression can be due to several factors:
- Increasing volume of infarction (the area of dead brain tissue grows),
- Hemorrhagic transformation (bleeding into the infarcted area),
- Increasing cerebral edema (brain swelling).
- This term refers to a stroke where the neurological deficits worsen after the initial presentation. This progression can be due to several factors:
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Completed Stroke:
- A completed stroke is one where the focal neurological deficit (such as weakness or speech problems) persists but is not worsening. The damage is done, and the symptoms are stable.
How do you differentiate TIA from stroke?
When a patient presents with neurological symptoms, it’s often hard to determine whether it’s a TIA or a stroke unless the symptoms have already resolved:
- Stroke: The patient has persisting symptoms, indicating possible permanent damage.
- TIA: The patient’s symptoms have resolved, indicating temporary disruption of blood flow without permanent injury.
In both cases, prompt diagnosis and treatment are crucial to prevent further damage or recurrence. Early interventions, such as thrombolytic therapy or procedures like carotid endarterectomy, can significantly improve outcomes.
What are the reasons investigations are done in stroke
The purpose of investigating a patient with an acute stroke is to:
- Confirm that the lesion is vascular in origin.
- Differentiate between an infarction (blockage of blood flow) and hemorrhage (bleeding).
- Identify the underlying vascular disease and associated risk factors.
What are the initial investigation you will like to do?
@ Bedside I will check the glucose level why?
The initial approach for most stroke patients involves:
1. Blood tests to assess for common vascular risk factors like:
- High cholesterol or lipid levels.
- Blood clotting abnormalities.
2. ECG (Electrocardiogram) to check for any heart conditions, especially arrhythmias like atrial fibrillation, which can cause blood clots.
3. Brain imaging: This is crucial to determine whether the stroke is due to an infarct (ischemic stroke) or hemorrhage. The most common imaging methods include:
- CT scan (Computed Tomography): A quick imaging technique to detect hemorrhage.
- MRI (Magnetic Resonance Imaging): Provides a more detailed image and is better at detecting ischemic strokes, especially in smaller areas of the brain.
In cases where the stroke cause isn’t clear, or when the patient is young (younger people are less likely to have strokes due to atherosclerosis), additional tests are often needed to explore rarer causes. Below are the conditions and associated investigations:
What are the Causes and Investigations for Acute Stroke in Young Patients
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Cerebral Infarction (Ischemic Stroke)
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Cardiac embolism: Blood clots formed in the heart can travel to the brain.
- Investigation: Echocardiography, particularly transoesophageal echocardiography (TOE), which provides a detailed view of the heart.
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Premature atherosclerosis: Early development of plaque in arteries.
- Investigation: Serum lipids to check cholesterol levels.
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Arterial dissection: Tear in the artery wall, often seen in younger patients.
- Investigation: MRI (Magnetic Resonance Imaging) and CTA (Computed Tomography Angiography) to visualize arteries.
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Reversible cerebral vasoconstriction syndromes: Temporary narrowing of blood vessels in the brain.
- Investigation: MRI and CTA.
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Cardiac embolism: Blood clots formed in the heart can travel to the brain.
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Thrombophilia: A tendency to form abnormal blood clots due to blood disorders.
- Investigations:
- Protein C, Protein S, and Antithrombin III levels.
- Factor V Leiden and prothrombin gene mutation.
- Homocystinuria: Urine tests for amino acids and methionine loading test.
- Investigations:
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Antiphospholipid antibody syndrome: An autoimmune disorder where antibodies increase the risk of clots.
- Investigation: Anticardiolipin antibodies and lupus anticoagulant tests.
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Systemic Lupus Erythematosus (SLE): An autoimmune disorder that can lead to clotting.
- Investigation: ANA (Antinuclear Antibody test).
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Vasculitis: Inflammation of blood vessels, leading to stroke.
- Investigation: ESR (Erythrocyte Sedimentation Rate), CRP (C-reactive protein), and ANCA (Anti-Neutrophil Cytoplasmic Antibodies).
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CADASIL and CARASIL: Rare genetic conditions affecting small blood vessels in the brain.
- Investigations:
- MRI brain for characteristic changes.
- Genetic analysis and sometimes skin biopsy.
- Investigations:
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Mitochondrial Cytopathy: Mitochondrial diseases affecting energy production can lead to strokes.
- Investigations:
- Serum lactate levels.
- White cell mitochondrial DNA analysis.
- Muscle biopsy and mitochondrial molecular genetics.
- Investigations:
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Fabry’s Disease: A genetic disorder that affects blood vessels.
- Investigation: Measure alpha-galactosidase levels.
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Sickle Cell Disease: Red blood cell disorder that can lead to stroke due to abnormal clotting.
- Investigation: Sickle cell studies.
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Neurovascular Syphilis: Infection with syphilis that affects the blood vessels of the brain.
- Investigation: Syphilis serology.
What are the Causes and Investigations for Primary Intracerebral Hemorrhage
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Arteriovenous Malformation (AVM): Abnormal connection between arteries and veins.
- Investigation: MRI or MRA (Magnetic Resonance Angiography) to visualize the blood vessels.
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Drug misuse: Certain substances, like amphetamines and cocaine, can cause hemorrhage.
- Investigation: Drug screening.
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Coagulopathy: A condition where blood doesn’t clot properly, leading to bleeding.
- Investigation:
- PT (Prothrombin Time) and APTT (Activated Partial Thromboplastin Time).
- Platelet count.
- Investigation:
What are the Causes and Investigations for Subarachnoid Hemorrhage (SAH)
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Saccular (‘berry’) aneurysm: A bulge in a blood vessel that can rupture.
- Investigation: MRI/MRA to locate the aneurysm.
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Arteriovenous malformation (AVM): As in intracerebral hemorrhage.
- Investigation: MRI/MRA.
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Vertebral dissection: A tear in the vertebral artery.
- Investigation: MRI/MRA.
These investigations help pinpoint the exact cause of a stroke and guide further management and prevention strategies, especially in younger patients where traditional risk factors like atherosclerosis may not be the primary cause.
Neuroimaging plays a critical role in the diagnosis and management of acute stroke. The main objectives of imaging are to:
1. Confirm the vascular origin of the lesion.
2. Distinguish between hemorrhagic (bleeding) and ischemic (blockage) strokes.
3. Identify other potential brain abnormalities, like tumors or hematomas, that may mimic stroke symptoms.
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CT Scan (Computed Tomography):
- Widely available and is the most practical initial brain imaging method in stroke patients.
- Immediate role: A CT scan can quickly identify hemorrhages within minutes of stroke onset, which is critical for deciding treatment (see Fig. 26.9).
- Limitations: In ischemic strokes, especially in the early stages, changes might be absent or subtle on a CT scan. It may take time for infarction signs to appear (see Fig. 26.13), and small infarcts might not be visible at all.
- When to use: For some patients, a CT scan within 24 hours is sufficient, but in certain urgent cases, an immediate CT scan is essential to guide therapy (Box 26.7).
- Advanced use: CT perfusion scanning can assess abnormal blood flow in the brain by injecting contrast dye, which is especially helpful in ischemic stroke management.
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MRI (Magnetic Resonance Imaging):
- Diffusion-weighted imaging (DWI) on MRI detects ischemia earlier than CT.
- MRI is more sensitive than CT in diagnosing strokes that affect the brainstem and cerebellum.
- It can reliably differentiate between hemorrhagic and ischemic strokes, even if the stroke occurred several weeks earlier.
- Longer scan times and less availability than CT limit MRI use in emergency settings.
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Utility: MRI can reveal more specific details about the cause of the stroke, such as:
- Lacunar infarcts (indicating small-vessel disease).
- Peripheral infarcts (suggesting embolism from an extracranial source).
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CTA (CT Angiography):
- CTA is increasingly used to visualize vessel occlusion and can help determine if the patient is suitable for clot retrieval procedures.
- It can also provide information on the presence of vascular malformations, aneurysms, or amyloid angiopathy in hemorrhagic strokes.