Stroke Txt B

Question 1

What’s the most common cause of Stroke

Answer 1

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.

Question 2

What are the causes of Stroke?

Answer 2

1. 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.

Question 3

What’s the path physiology of stroke
Both TIA & Acute stroke

Answer 3

2. 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.
3. 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.
4. 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.
5. 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.
6. 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.

Question 4

• 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.

Question 5

What are the Key Factors Influencing the Outcome of a stroke?

Answer 5

.

1. 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.
2. 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.
3. 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.
4. 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.

Question 6

• 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.

Question 7

What are the Radiological Features of Cerebral Infarction:

How does infarction progress and it’s long term implications

Answer 7

• 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.

Question 8

What’s ICH?

Answer 8

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.

Question 9

What are the risk factors/ causes of ICH

Answer 9

• 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
• 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.

Question 10

What are the path physiology of ICH

Answer 10

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.

Question 11

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.

Question 12

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.

Question 13

What are the common miss diagnosis

Answer 13

• 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),
  • Speech disturbance (slurred or garbled speech).
    These signs are often used in stroke awareness campaigns (such as FAST: Face, Arms, Speech, Time).

Question 14

• 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.

Answer 15

• 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).
• 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).

Question 16

1. 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.
2. 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.
3. 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.

Question 17

What are the Stroke Classifications Based on Symptom Duration and Evolution:

Answer 17

Several terms are used to describe the different types of strokes based on how long symptoms last and how the symptoms evolve:

1. 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.
2. 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.
3. 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).
4. 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.

Question 18

How do you differentiate TIA from stroke?

Answer 18

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.

Question 19

What are the reasons investigations are done in stroke

Answer 19

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.

Question 20

What are the initial investigation you will like to do?

Answer 20

@ 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:

Question 21

What are the Causes and Investigations for Acute Stroke in Young Patients

Answer 21

1. Cerebral Infarction (Ischemic Stroke)
   
   • 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.
   • Premature atherosclerosis: Early development of plaque in arteries.
     
     • Investigation: Serum lipids to check cholesterol levels.
   • 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.
   • Reversible cerebral vasoconstriction syndromes: Temporary narrowing of blood vessels in the brain.
     
     • Investigation: MRI and CTA.
2. 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.
3. Antiphospholipid antibody syndrome: An autoimmune disorder where antibodies increase the risk of clots.
   
   • Investigation: Anticardiolipin antibodies and lupus anticoagulant tests.
4. Systemic Lupus Erythematosus (SLE): An autoimmune disorder that can lead to clotting.
   
   • Investigation: ANA (Antinuclear Antibody test).
5. Vasculitis: Inflammation of blood vessels, leading to stroke.
   
   • Investigation: ESR (Erythrocyte Sedimentation Rate), CRP (C-reactive protein), and ANCA (Anti-Neutrophil Cytoplasmic Antibodies).
6. 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.
7. 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.
8. Fabry’s Disease: A genetic disorder that affects blood vessels.
   
   • Investigation: Measure alpha-galactosidase levels.
9. Sickle Cell Disease: Red blood cell disorder that can lead to stroke due to abnormal clotting.
   
   • Investigation: Sickle cell studies.
10. Neurovascular Syphilis: Infection with syphilis that affects the blood vessels of the brain.
    
    • Investigation: Syphilis serology.

Question 22

What are the Causes and Investigations for Primary Intracerebral Hemorrhage

Answer 22

1. Arteriovenous Malformation (AVM): Abnormal connection between arteries and veins.
   
   • Investigation: MRI or MRA (Magnetic Resonance Angiography) to visualize the blood vessels.
2. Drug misuse: Certain substances, like amphetamines and cocaine, can cause hemorrhage.
   
   • Investigation: Drug screening.
3. Coagulopathy: A condition where blood doesn’t clot properly, leading to bleeding.
   
   • Investigation:
     
     • PT (Prothrombin Time) and APTT (Activated Partial Thromboplastin Time).
     • Platelet count.

Question 23

What are the Causes and Investigations for Subarachnoid Hemorrhage (SAH)

Answer 23

1. Saccular (‘berry’) aneurysm: A bulge in a blood vessel that can rupture.
   
   • Investigation: MRI/MRA to locate the aneurysm.
2. Arteriovenous malformation (AVM): As in intracerebral hemorrhage.
   
   • Investigation: MRI/MRA.
3. 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.

Question 24

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.

1. 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.
2. 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.
   • 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).
3. 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.

Question 25

Approximately 50% of ischemic strokes are due to atherosclerotic thromboembolism originating from major extracranial vessels (such as the carotid arteries). Imaging the vascular system can help identify the cause of the stroke and guide management.

1. Duplex Ultrasound:
   
   • A non-invasive method to assess blood flow and detect carotid artery disease.
   • However, the presence or absence of a carotid bruit (abnormal sound over the artery) is not always a reliable indicator of carotid stenosis.
2. MRA (Magnetic Resonance Angiography) and CTA:
   
   • These imaging techniques are used to non-invasively visualize extracranial and intracranial arteries and assess the extent of stenosis (narrowing) or occlusion.
   • Intra-arterial contrast radiography is rarely used but can be performed in specialized situations.
3. Carotid Endarterectomy:
   
   • If significant stenosis is detected in the carotid arteries, endarterectomy (surgical removal of the plaque) may be considered to prevent future strokes.

Question 26

About 20% of ischemic strokes result from cardioembolic events. The common cardiac causes include:
- Atrial fibrillation (AF).
- Prosthetic heart valves.
- Valvular abnormalities.
- Recent myocardial infarction (heart attack).

Cardiac sources of emboli may be detected by:
1. ECG (Electrocardiogram): Can detect arrhythmias, such as atrial fibrillation, which are common causes of embolic strokes.
2. Transthoracic Echocardiography (TTE): A non-invasive ultrasound of the heart to detect structural abnormalities, including valve issues or clots.
3. Transoesophageal Echocardiography (TOE): A more detailed and sensitive test to look for:
- Endocarditis (infection of heart valves).
- Atrial myxoma (a rare heart tumor).
- Intracardiac thrombi (clots in the heart chambers).
- Patent foramen ovale (a small opening between the heart chambers that can allow clots to pass to the brain).

Identifying the cardiac source of embolism is critical, as it can guide specific treatments, such as anticoagulation, to prevent future embolic events.

Question 27

The management of stroke focuses on four primary goals:
1. Identifying the cause of the stroke to guide treatment.
2. Minimizing brain damage by preventing further ischemia or hemorrhage.
3. Preventing complications, disability, and handicap through supportive care and rehabilitation.
4. Reducing the risk of recurrent strokes and other vascular events, particularly in cases of transient ischemic attack (TIA) where brain damage has not yet occurred.

Effective stroke care begins with rapid admission to a specialized stroke unit. These units are equipped with a multidisciplinary team (physicians, nurses, physiotherapists, occupational therapists, etc.) that provides coordinated care. Research has shown that this approach significantly reduces both mortality and long-term disability.

• Stroke Unit Outcomes: For every 1000 patients managed in a stroke unit, 50 additional patients avoid death or permanent disability compared to those treated in general wards.
• Rehabilitation: Rehabilitation planning should begin alongside acute medical care to ensure timely intervention. Early rehabilitation helps reduce long-term disability and aids recovery.

1. Dysphagia: Swallowing problems (dysphagia) are common in stroke patients and should be assessed early. A simple bedside swallowing test can determine whether the patient can safely take food and medications orally, or if alternative feeding (e.g., nasogastric tube or IV fluids) is needed.
2. Hyperacute Stroke Units (HASUs): Many hospitals now have HASUs to provide patients with immediate access to specialized interventions. These units focus on rapid evaluation and treatment, ensuring patients receive appropriate medical care as soon as possible.

Patients often experience neurological deterioration within the first hours or days following a stroke. This deterioration can occur due to several factors:
- Extension of the infarcted area (the region of dead brain tissue).
- Hemorrhagic transformation (when an ischemic stroke turns into a hemorrhage).
- Brain edema (swelling), which increases intracranial pressure and can cause a mass effect (compression of brain structures).

It is crucial to differentiate patients whose condition is worsening due to stroke-related factors from those with reversible complications, such as:
- Hypoxia (low oxygen levels).
- Sepsis (a severe infection).
- Epileptic seizures.
- Metabolic disturbances (e.g., abnormal blood sugar or electrolyte levels).

By identifying and treating these reversible issues early, outcomes can be improved.

Question 28

How do you manage Specific Stroke-Related Complications:
Cerebellar hematomas
Large Hematomas or Infarctions with Significant Swelling

Answer 28

1. Cerebellar Hematomas/Infarcts: These can cause obstructive hydrocephalus (blockage of cerebrospinal fluid flow), leading to a dangerous buildup of pressure. For these patients:
   
   • Ventricular drainage (inserting a tube to relieve pressure).
   • Decompressive surgery (removing part of the skull to allow the brain to swell without being compressed).
2. Large Hematomas or Infarctions with Significant Swelling:
   
   • Mannitol (a diuretic to reduce brain swelling) or other anti-edema agents may be used to manage brain swelling.
   • Mechanical ventilation might be needed in cases of severe brain edema.
   • Surgical decompression can be considered to reduce intracranial pressure in patients with massive strokes or hemorrhages in the brain.

Question 29

How do you manage a Patient with Acute Stroke

Answer 29

• Assessment: Perform a bedside swallowing assessment to determine if the patient is at risk of aspiration.
• Intervention: If swallowing is unsafe or aspiration is occurring, keep the patient nil by mouth to prevent aspiration pneumonia.

• Assessment: Monitor the patient’s respiratory rate and oxygen saturation.
• Intervention: Administer supplemental oxygen if oxygen saturation is below 95% to ensure adequate oxygenation.

• Assessment: Check peripheral perfusion, pulse, and blood pressure.
• Intervention: Address abnormalities by:
  
  • Administering fluids if signs of dehydration are present.
  • Using anti-arrhythmic medications if needed.
  • Providing inotropic drugs to support heart function if necessary.

• Assessment: Evaluate for signs of dehydration.
• Intervention: Provide fluids either parenterally (intravenously) or through a nasogastric tube if the patient cannot take fluids orally.

• Assessment: Evaluate nutritional status and determine if supplements are required.
• Intervention:
  
  • If dysphagia (difficulty swallowing) persists for more than 48 hours, initiate feeding via a nasogastric tube to ensure adequate nutrition.

• Assessment: Determine if the patient can swallow medications.
• Intervention: For dysphagic patients, consider alternative routes (e.g., intravenous or intramuscular) for essential medications.

• Assessment: Monitor blood pressure regularly.
• Intervention: Avoid abrupt lowering of blood pressure unless there is evidence of hypertensive encephalopathy, aortic dissection, or heart/renal failure. Blood pressure often normalizes within days. Gradual management helps maintain cerebral perfusion.

• Assessment: Measure blood glucose levels.
• Intervention: Treat hyperglycemia (blood glucose levels ≥ 11.1 mmol/L or 200 mg/dL) using insulin infusion or glucose/potassium/insulin (GKI) therapy. Closely monitor to prevent hypoglycemia.

• Assessment: Check for fever (pyrexia) and identify any underlying causes.
• Intervention: Use antipyretics to control fever, as elevated brain temperature can exacerbate brain damage and increase infarct volume.

• Assessment: Evaluate risk of skin breakdown.
• Intervention:
  
  • Treat any infections promptly.
  • Ensure proper nutrition to support skin health.
  • Use a pressure-relieving mattress to reduce pressure ulcers.
  • Regularly turn immobile patients to prevent pressure sores.

• Assessment: Check for constipation and urinary retention.
• Intervention:
  
  • Treat constipation and urinary retention appropriately.
  • Avoid urinary catheterization unless absolutely necessary to prevent urinary retention or pressure area issues.

• Assessment: Evaluate the patient’s mobility and risk of complications from immobility.
• Intervention: Avoid prolonged bed rest. Encourage and facilitate early mobilization to improve recovery and prevent complications related to immobility.

Effective management of an acute stroke patient involves ensuring airway protection, maintaining optimal breathing and circulation, and addressing hydration, nutrition, and medication needs. Regular monitoring and intervention for blood pressure, blood glucose, temperature, pressure areas, and incontinence are critical. Early and appropriate mobilization, alongside supportive care in a specialized stroke unit, significantly improves outcomes and aids in recovery.

Question 30

Reperfusion therapy aims to restore blood flow to the affected brain region, minimizing brain damage and improving recovery outcomes. This can be achieved through thrombolysis or thrombectomy.

• Mechanism: Recombinant tissue plasminogen activator (rt-PA) dissolves blood clots obstructing cerebral blood vessels.
• Timing: For maximum benefit, rt-PA should be administered within 4.5 hours of symptom onset. The sooner it is given, the greater the likelihood of improving patient outcomes.
• Risks: The primary risk associated with rt-PA is the increased chance of hemorrhagic transformation of the cerebral infarct, which can be potentially fatal.
• Contraindications: Key contraindications include:
  
  • Recent or active bleeding
  • Current anticoagulant therapy
  • Significant delay in treatment
• Benefit vs. Risk: Despite the risk of hemorrhage, for carefully selected patients, the benefits of improved outcomes outweigh the risks when rt-PA is administered promptly.

• Mechanism: Mechanical thrombectomy involves physically removing a blood clot from a large-vessel occlusion using specialized devices.
• Indications: It is particularly effective in patients with a large-vessel occlusion and can significantly improve the chances of avoiding disability.
• Timing: Like thrombolysis, thrombectomy should be performed as soon as possible after symptom onset for optimal results.

• Administration: Aspirin (300 mg daily) should be started as soon as possible after an ischemic stroke, unless rt-PA has been administered. In such cases, aspirin should be withheld for at least 24 hours.
• Effectiveness: Aspirin reduces the risk of early recurrence of stroke and has a small but clinically significant effect on long-term outcomes. It can be given orally or via rectal suppository or nasogastric tube if the patient is dysphagic (has difficulty swallowing).

• Historical Use: Heparin was once commonly used to manage acute ischemic stroke.
• Risks: It reduces the risk of early ischemic recurrence and venous thromboembolism but increases the risk of both intracranial and extracranial hemorrhage.
• Current Practice: Routine use of heparin is no longer recommended due to its lack of benefit in improving long-term outcomes and its associated bleeding risks.
• Selective Use: Heparin may be considered in certain scenarios, such as in patients with recent myocardial infarction, arterial dissection, or progressing strokes, but intracranial hemorrhage must be ruled out through brain imaging before starting anticoagulation.

Reperfusion therapies such as thrombolysis and thrombectomy are crucial in acute ischemic stroke management, with timely intervention being key to improving outcomes. While rt-PA can enhance recovery if administered early, it carries a risk of hemorrhage. Aspirin remains a standard post-stroke treatment unless contraindicated. Heparin is no longer routinely used due to its associated bleeding risks and lack of long-term benefit.

Question 31

Coagulation Abnormalities

In cases of intracerebral hemorrhage, it’s crucial to address any coagulation abnormalities promptly to minimize the risk of hematoma expansion. This is especially relevant for patients on anticoagulant therapy like warfarin. The main steps include:

• Reversal of Anticoagulants: For patients on warfarin, the reversal of anticoagulation is essential. This often involves the administration of vitamin K and prothrombin complex concentrates or fresh frozen plasma to rapidly restore normal clotting.
• Clotting Factors: There is no significant evidence supporting the use of clotting factors unless there is a specific clotting defect.

Management of Risk Factors

Managing risk factors is critical to prevent recurrent strokes. Key strategies include:

• Antiplatelet Therapy: Long-term use of antiplatelet drugs (e.g., aspirin) is recommended for secondary stroke prevention. The number needed to treat (NNT) to prevent one recurrent stroke is 100.
• Statins: These medications help lower cholesterol and reduce stroke recurrence. The NNT for statins is 60.
• Oral Anticoagulants: For patients with atrial fibrillation, oral anticoagulants such as warfarin or newer direct oral anticoagulants (DOACs) like dabigatran, rivaroxaban, or apixaban are used. Warfarin requires monitoring with an international normalized ratio (INR) of 2-3. DOACs offer a better safety profile but at a higher cost. The NNT for preventing a stroke in atrial fibrillation with anticoagulants is 15.
• Blood Pressure Management: Reducing blood pressure helps lower the risk of recurrent strokes, even in those with normal blood pressures. The NNT for blood pressure reduction is 50.

Carotid Endarterectomy and Angioplasty

For patients with significant carotid artery stenosis (≥50%) and a history of ischemic stroke or TIA, surgical intervention may be beneficial:

• Carotid Endarterectomy: This procedure removes the plaque from the carotid artery. It is particularly effective in patients with severe stenosis (70-99%) and when performed within a few weeks after a stroke or TIA. The NNT for this surgery is 15, though it carries a 5% risk of stroke.
• Carotid Angioplasty and Stenting: While feasible, these methods have not proven to be as effective as endarterectomy for most patients.
• Asymptomatic Carotid Stenosis: Endarterectomy for asymptomatic stenosis can reduce stroke risk but the benefit is modest and does not justify routine use.

Unusual Causes of Stroke

A small percentage of strokes are due to less common causes, such as:

• Arterial Dissection: This can occur in the carotid or vertebral arteries and often follows minor trauma or presents with neck pain. Diagnosis is typically confirmed with angiography (MRA or CTA). Treatment may involve antiplatelet drugs or anticoagulation.
• Reversible Vasoconstriction Syndromes: These require careful management of blood pressure and overall physiological control.

Effective stroke management involves addressing coagulation abnormalities, controlling risk factors, and considering surgical options when necessary. Prompt and appropriate intervention can significantly impact outcomes and reduce the risk of recurrence.

Question 32

Overview
Subarachnoid hemorrhage (SAH) is a less frequent but serious form of stroke, affecting around 6 in 100,000 people annually. It is more common in women and typically occurs before the age of 65. The immediate mortality rate for aneurysmal SAH is high, approximately 30%, with survivors facing a significant risk of rebleeding, particularly in the first 4 weeks (around 40%). After the initial period, the annual recurrence rate drops to 3%.

Question 33

What are the common causes of sub arachnoid hemorrhage? And it’s location

Answer 33

Causes of SAH
About 85% of SAH cases are due to the rupture of saccular (berry) aneurysms, which arise at the bifurcations of cerebral arteries. These aneurysms frequently occur near the Circle of Willis, a circular arterial structure at the base of the brain. Common sites for aneurysms include:
- Anterior communicating artery (30%)
- Posterior communicating artery (25%)
- Middle cerebral artery (20%)

• Peri- Mesencephalic hemorrhage
• Aterovenous Malformation
• Vertebral artery dissection

Question 34

What are the Increased risk factors for aneurysmal SAH include:

Answer 34

• Family history: First-degree relatives of patients with saccular aneurysms are at a higher risk.
• Associated conditions:
  
  • Polycystic kidney disease: A genetic disorder affecting the kidneys.
  • Congenital connective tissue defects: Conditions like Ehlers-Danlos syndrome, which affect the strength and flexibility of connective tissues.

Question 35

Non-aneurysmal SAH
Approximately 10% of SAH cases are non-aneurysmal in nature, often referred to as peri-mesencephalic hemorrhages. These hemorrhages have a distinct appearance on CT scans and are associated with a benign outcome, meaning lower mortality and recurrence rates compared to aneurysmal SAH.

Other Causes
Around 5% of SAHs are due to:
- Arteriovenous malformations (AVMs): Abnormal tangles of blood vessels connecting arteries and veins.
- Vertebral artery dissection: A tear in the inner lining of the vertebral artery, which supplies blood to the brain.

Subarachnoid hemorrhage is a life-threatening condition, with the majority of cases caused by aneurysmal rupture. Early identification and management of risk factors are crucial, especially in high-risk populations like those with a family history of aneurysms or underlying genetic conditions.

Question 36

hemorrhage involving an aneurysm in the posterior communicating artery, causes pressure on the ____ Nerve and causing what deficit?

Answer 36

oculomotor nerve (cranial nerve III), which can lead to eye movement problems or drooping eyelids.

Question 37

What are the clinical features of SAH

Answer 37

Subarachnoid hemorrhage typically presents with a sudden onset of a severe “thunderclap” headache, often described as the worst headache of the patient’s life. This headache is usually occipital (at the back of the head) and can last for hours or even days. Other key symptoms include:
- Vomiting: This often accompanies the headache and reflects the increased intracranial pressure.
- Raised blood pressure: SAH can cause a sudden spike in blood pressure due to the stress and neurological impact.
- Neck stiffness or pain: This occurs because of irritation of the meninges (the membranes covering the brain) due to the presence of blood in the subarachnoid space. The stiffness usually takes some time to develop.
- Physical exertion triggers: The hemorrhage may occur during activities like straining, sexual excitement, or other exertions.
- Loss of consciousness: SAH can cause sudden unconsciousness. Therefore, if a patient is found comatose with no clear cause, SAH should be considered.

Due to the severe and distinctive nature of the headache, approximately 1 in 8 patients presenting with a sudden severe headache has SAH. For this reason, anyone presenting with these symptoms should be thoroughly investigated to rule out SAH.

On examination, patients are often:
- Distressed and irritable: Due to the severity of the headache and other symptoms.
- Photophobic: Sensitivity to light is common.
- Neck stiffness: A classic sign of meningism, due to the irritation of the meninges by the blood in the subarachnoid space.

Other possible signs include:
- Focal neurological deficits: Hemiparesis (weakness on one side of the body) or aphasia (difficulty speaking) may occur, especially if there is an associated intracerebral hemorrhage.
- Third nerve palsy: Rare but can occur if the hemorrhage involves an aneurysm in the posterior communicating artery, causing pressure on the oculomotor nerve (cranial nerve III), which can lead to eye movement problems or drooping eyelids.
- Subhyaloid hemorrhage: Fundoscopic examination (looking at the back of the eye) may reveal blood accumulation, indicative of bleeding into the subarachnoid space around the optic nerve.

Question 38

What are the investigations you will like to do in a pt. Suspected of having SAH

Answer 38

To confirm a diagnosis of SAH, the following investigations are essential:

1. CT Brain Scan:
   
   • A CT scan is usually the first-line investigation and can detect blood in the subarachnoid space. However, in some cases, small amounts of blood might not be visible, leading to false negatives.
2. Lumbar Puncture:
   
   • If the CT scan is negative but clinical suspicion remains, a lumbar puncture should be performed, ideally 12 hours after symptom onset. This allows for the detection of xanthochromia—the yellow discoloration of cerebrospinal fluid (CSF), indicating the presence of broken-down blood products.
3. Cerebral Angiography:
   
   • If either the CT scan or lumbar puncture confirms SAH, cerebral angiography is necessary to identify the source of the bleeding, typically an aneurysm. This helps guide treatment to prevent recurrent hemorrhage, which is a major concern in SAH patients.

Question 39

How do you manage SAH?

Answer 39

1. Nimodipine:
   
   • Purpose: Nimodipine is a calcium channel blocker used to prevent delayed cerebral ischemia, which can occur due to vasospasm (narrowing of cerebral arteries) after a SAH.
   • Dosage: Typically given intravenously (IV) for 5–14 days at a dose of 30–60 mg, followed by oral administration of 360 mg daily for an additional 7 days. This reduces the risk of ischemic complications after the initial hemorrhage.
2. Aneurysm Treatment:
   
   • Endovascular Coiling: This is a minimally invasive procedure where platinum coils are inserted into the aneurysm via a catheter. The coils promote clotting, sealing off the aneurysm to reduce the risk of rebleeding.
     
     • Advantages: Coiling is preferred over surgery as it is associated with fewer perioperative complications and better outcomes, making it the first-line treatment in most cases.
   • Surgical Clipping: In this procedure, a clip is placed across the neck of the aneurysm to stop blood flow into it. This is usually considered if coiling is not feasible due to the aneurysm’s location or other factors.
3. Arteriovenous Malformation (AVM) Management:
   
   • AVMs are abnormal connections between arteries and veins that can also cause hemorrhage. Treatment options include:
     
     • Surgical Removal: Complete resection of the AVM.
     • Ligation of Feeding Vessels: Tying off the blood vessels supplying or draining the AVM to reduce the risk of bleeding.
     • Embolization: Injection of materials to block the abnormal blood flow through the AVM.
4. Managing Complications:
   
   • Obstructive Hydrocephalus: This condition occurs when blood in the subarachnoid space blocks the normal drainage of cerebrospinal fluid (CSF), leading to increased intracranial pressure. Management may involve placing a shunt to drain the excess fluid.
   • Delayed Cerebral Ischemia: This is caused by vasospasm, which narrows the arteries and reduces blood flow. Vasodilator drugs (to widen the blood vessels) may be used to treat this complication.
   • Hyponatremia: A common electrolyte imbalance in SAH, often related to a condition called cerebral salt wasting. It is usually managed by fluid restriction.
   • Systemic Complications: Due to immobility after SAH, patients are at risk for complications such as chest infections and venous thromboembolism. Preventative measures include mobilizing the patient as soon as possible, as well as antibiotics for infections and anticoagulants to prevent blood clots (if safe to use).

These treatments aim to address the immediate dangers of SAH, prevent rebleeding, and manage the various complications that arise during recovery.