Cerebrovascular Diseases — MCQs
What is the most common cause of subarachnoid hemorrhage?
Thrombosis of which cerebral vessels leads to hemiplegia?
Which of the following is NOT considered a risk factor for atherosclerosis?
Which vessel is most likely damaged in an extradural (epidural) hemorrhage?
Identify the condition in the image below?
Which of the following is not a prominent risk factor for stroke?
An elderly man has become progressively unable to live independently over the past several years, requiring assistance with daily activities. He has no motor or sensory deficits on physical examination, but is unable to give the current date or state his location. At autopsy, a large superficial left parietal lobe hemorrhage is found, along with numerous neocortical neuritic plaques and neurofibrillary tangles in the brain. Which mechanism is most likely responsible for his disease?
Loss of striatal fibres in caudate nucleus is associated with?
What is the histological appearance of the brain in Creutzfeldt-Jakob disease?
All of the following are causes of vasogenic-type cerebral edema except which of the following?
Cerebrovascular Diseases Indian Medical PG Practice Questions and MCQs
Question 1: What is the most common cause of subarachnoid hemorrhage?
- A. Rupture of berry aneurysm (Correct Answer)
- B. Non-aneurysmal hemorrhage
- C. Arteriovenous malformation
- D. Vertebral artery dissection
Explanation: ***Rupture of berry aneurysm*** - **Rupture of a berry (saccular) aneurysm** is responsible for approximately 85% of all non-traumatic subarachnoid hemorrhages [1]. - These aneurysms are typically located at the **bifurcations of cerebral arteries** within the Circle of Willis. *Arteriovenous malformation* - **Arteriovenous malformations (AVMs)** are abnormal connections between arteries and veins, bypassing the capillary system. - While AVMs can cause subarachnoid hemorrhage, they are a less common cause compared to ruptured berry aneurysms. *Vertebral artery dissection* - **Vertebral artery dissection** involves a tear in the inner lining of the vertebral artery, often leading to stroke or other posterior circulation symptoms. - Subarachnoid hemorrhage from vertebral artery dissection is rare and typically associated with an intramural hematoma extending into the subarachnous space. *Non-aneurysmal hemorrhage* - **Non-aneurysmal subarachnoid hemorrhage** (also known as perimesencephalic subarachnoid hemorrhage) accounts for a small percentage of cases, with no identifiable aneurysm on angiography [1]. - The bleeding is usually confined to the perimesencephalic cisterns and generally has a better prognosis than aneurysmal hemorrhage.
Question 2: Thrombosis of which cerebral vessels leads to hemiplegia?
- A. Anterior cerebral
- B. Middle cerebral (Correct Answer)
- C. Posterior cerebral
- D. Not applicable
Explanation: Everything below the bolded header ***Middle cerebral*** relates to the vessel responsible for hemiplegia. ***Middle cerebral*** - Thrombosis of the **middle cerebral artery (MCA)** commonly leads to contralateral **hemiplegia** (weakness on one side of the body), particularly affecting the face and arm more than the leg [1]. - The MCA supplies blood to the primary motor cortex areas responsible for **volitional movement** of these body parts [1]. *Anterior cerebral* - Thrombosis of the **anterior cerebral artery (ACA)** typically causes contralateral weakness, but it predominantly affects the **leg** more than the arm or face [1]. - The ACA supplies the motor cortex areas controlling the **lower limbs** [1]. *Posterior cerebral* - Thrombosis of the **posterior cerebral artery (PCA)** primarily causes **visual field defects** (e.g., contralateral homonymous hemianopsia) due to involvement of the occipital lobe [1]. - While it can cause other neurological deficits, **hemiplegia** is not its most common or prominent presentation [1]. *Not applicable* - This option is incorrect because specific cerebral vessel thrombosis clearly leads to distinct neurological deficits, including **hemiplegia**, depending on the affected artery and its vascular territory [1].
Question 3: Which of the following is NOT considered a risk factor for atherosclerosis?
- A. Smoking
- B. Low LDL cholesterol (Correct Answer)
- C. Hypercholesterolemia
- D. Hypertension
Explanation: ***Low LDL cholesterol*** - **Low levels of low-density lipoprotein (LDL) cholesterol** are protective against atherosclerosis [3]. - LDL cholesterol is often referred to as "bad" cholesterol because high levels contribute to the **buildup of fatty plaques in arteries**. *Smoking* - **Smoking** is a major independent risk factor for atherosclerosis, damaging the **endothelium** and promoting plaque formation. - It increases **oxidative stress** and reduces **nitric oxide bioavailability**, leading to vasoconstriction and inflammation [2]. *Hypercholesterolemia* - **Hypercholesterolemia**, particularly high levels of **LDL cholesterol**, is a primary risk factor as it contributes to the deposition of cholesterol in arterial walls [3]. - This leads to the formation of **atheromatous plaques** which narrow arteries and impede blood flow [1]. *Hypertension* - **Hypertension (high blood pressure)** damages the arterial walls, making them more susceptible to the accumulation of plaque [1]. - The constant high pressure creates **shear stress**, compromising the integrity of the **endothelial lining**.
Question 4: Which vessel is most likely damaged in an extradural (epidural) hemorrhage?
- A. Basilar artery
- B. Vertebral artery
- C. Middle meningeal artery (Correct Answer)
- D. Anterior cerebral artery
Explanation: Middle meningeal artery - An extradural (epidural) hemorrhage often results from head trauma, especially to the temporal region, which can cause a fracture across the course of the middle meningeal artery [1]. - This artery runs in a groove on the inner surface of the temporal bone, making it vulnerable to laceration during trauma [1]. Basilar artery - The basilar artery is located at the base of the brainstem and is a common site for strokes, but not typically involved in an extradural hemorrhage. - Damage to the basilar artery usually leads to subarachnoid hemorrhage or ischemic stroke, not an epidural hematoma. Vertebral artery - The vertebral arteries ascend through the cervical vertebrae and join to form the basilar artery, supplying the posterior circulation of the brain. - Damage to these arteries is typically associated with neck trauma or dissection, leading to subarachnoid hemorrhage or ischemia, not an epidural hemorrhage. Anterior cerebral artery - The anterior cerebral artery supplies the frontal lobes and medial aspects of the cerebral hemispheres. - While it can be involved in subarachnoid or intracranial hemorrhages from aneurysm rupture or trauma, it is not the typical source of an epidural hematoma.
Question 5: Identify the condition in the image below?
- A. Lacunar infarct (Correct Answer)
- B. Embolic infarct
- C. Thrombotic infarct
- D. Intracerebral hemorrhage
Explanation: ***Lacunar infarct*** - The image displays a small, well-demarcated **hypodensity** (darker area) in the basal ganglia region, characteristic of a lacunar infarct. - Lacunar infarcts are typically caused by **occlusion of small perforating arteries** and result in small, deep infarcts, often appearing as precise, round or ovoid lesions on CT. *Embolic infarct* - Embolic infarcts tend to be **larger**, wedge-shaped, and often extend to the cortical surface, unlike the deep, small lesion seen. - They are commonly associated with a **cardiac source** or large artery atherosclerosis leading to distal embolization. *Thrombotic infarct* - Thrombotic infarcts are usually **larger** areas of infarction due to occlusion of a major artery, often preceded by symptoms like TIAs. - While they also appear hypodense, they are typically **more extensive** and less precisely defined than a lacunar infarct in the early stages. *Intracerebral hemorrhage* - Intracerebral hemorrhage would appear as a **hyperdense** (bright white) area on a non-contrast CT scan due to the presence of acute blood. - The image clearly shows a **hypodense lesion**, ruling out acute hemorrhage.
Question 6: Which of the following is not a prominent risk factor for stroke?
- A. Smoking
- B. Moderate alcohol consumption (Correct Answer)
- C. Elevated cholesterol
- D. High blood pressure
Explanation: ***Moderate alcohol consumption*** - While excessive alcohol intake is a risk factor for stroke, **moderate alcohol consumption** (e.g., one drink per day for women, two for men) has not been consistently shown to be a prominent risk factor; some studies even suggest a potential protective effect, though this remains controversial. - The impact of moderate alcohol on stroke risk is complex and often confounded by other lifestyle factors, making it less direct and prominent compared to other listed risk factors. *Smoking* - **Smoking** is a major modifiable risk factor for stroke, significantly increasing the risk of both ischemic and hemorrhagic stroke [2]. - It damages **blood vessels**, promotes **atherosclerosis**, and increases **blood clotting**, all of which contribute to stroke. *Elevated cholesterol* - **High cholesterol levels**, particularly high low-density lipoprotein (LDL) cholesterol, contribute to the development of **atherosclerosis**, which can narrow and harden arteries in the brain and neck [3]. - This narrowing significantly increases the risk of **ischemic stroke** by forming plaques that can rupture or lead to clot formation [1]. *High blood pressure* - **High blood pressure (hypertension)** is the single most important modifiable risk factor for stroke, increasing the risk of both ischemic and hemorrhagic strokes [2]. - It directly damages **blood vessel walls**, leading to **atherosclerosis** and making vessels more prone to **rupture** (hemorrhagic stroke) or obstruction (ischemic stroke).
Question 7: An elderly man has become progressively unable to live independently over the past several years, requiring assistance with daily activities. He has no motor or sensory deficits on physical examination, but is unable to give the current date or state his location. At autopsy, a large superficial left parietal lobe hemorrhage is found, along with numerous neocortical neuritic plaques and neurofibrillary tangles in the brain. Which mechanism is most likely responsible for his disease?
- A. Conformational change in the prion protein (PrP)
- B. Dopamine deficiency
- C. Expansion of polyglutamine repeats
- D. Aggregation of Aβ peptide (Correct Answer)
Explanation: ***Aggregation of Ab peptide*** - The presence of **neocortical neuritic plaques** containing **Aβ (Amyloid beta) peptides** is indicative of Alzheimer's disease, where peptide aggregation is a crucial mechanism [1,2]. - This aggregation leads to **neurodegeneration** and associated symptoms, aligning with the patient's cognitive decline and sudden coma [2]. *Dopamine deficiency* - Primarily associated with **Parkinson's disease**, which typically presents with **motor deficits** such as tremors and rigidity, unlike this patient's purely cognitive symptoms. - Dopamine deficiency does not explain the findings of **neurosenile plaques** and **tangles** in the context of an 86-year-old male. *Conformational change in the prion protein (PrP)* - This mechanism relates primarily to **prion diseases** like Creutzfeldt-Jakob disease, characterized by rapid neurological decline and distinctive histopathological findings. - There is no evidence of **prion-like degeneration** or **spongiform changes** noted in this patient's brain autopsy findings. *Expansion of polyglutamine repeats* - This is primarily associated with **Huntington's disease**, marked by **chorea and cognitive decline**, rooted in basal ganglia dysfunction, which is not applicable here. - The findings in this patient relate more to **Alzheimer's disease** pathology than polyglutamine expansion disorders. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 721-722. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1290-1294.
Question 8: Loss of striatal fibres in caudate nucleus is associated with?
- A. Hemiballismus
- B. Huntington's disease (Correct Answer)
- C. Charcot-Marie-Tooth disease
- D. Parkinson's disease
Explanation: ***Huntington's disease*** - This neurodegenerative disorder is pathologically characterized by **atrophy of the striatum**, particularly the **caudate nucleus** [1]. - The loss of striatal neurons, especially medium spiny neurons, leads to the characteristic **chorea** and cognitive decline [1]. *Hemiballismus* - Characterized by **unilateral, violent, flinging movements** of the limbs. - It is typically caused by a lesion in the **subthalamic nucleus**, not the caudate nucleus. *Charcot-Marie-Tooth disease* - A group of inherited disorders that affect the **peripheral nerves**, leading to muscle weakness and sensory loss. - This condition does not involve the degeneration of the striatal fibers in the caudate nucleus. *Parkinson's disease* - Primarily caused by the degeneration of **dopaminergic neurons** in the **substantia nigra pars compacta**. - While it affects the basal ganglia circuitry, its primary pathology is not the loss of striatal fibers in the caudate nucleus but rather a **dopamine deficiency**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1299-1300.
Question 9: What is the histological appearance of the brain in Creutzfeldt-Jakob disease?
- A. Neuronophagia
- B. Micro abscess
- C. Demyelination
- D. Spongiform changes (Correct Answer)
Explanation: ***Spongiform changes*** - The hallmark histological feature of **Creutzfeldt-Jakob disease (CJD)** is **spongiform degeneration**, characterized by vacuolation of neuronal cell bodies [1]. - It results in a **spongy appearance** of the affected brain regions, particularly in the **cerebral cortex** and **basal ganglia** [1]. *Neuronophagia (can occur in various contexts, not specific to CJD)* - Neuronophagia refers to the phagocytic activity involving **dying neurons**, which can occur in various conditions but is not a defining feature of CJD [2]. - It indicates the presence of **inflammation** or a response to neuronal injury rather than specific changes seen in CJD. *Demyelination (associated with multiple sclerosis)* - Demyelination is primarily associated with conditions like **multiple sclerosis** and is characterized by loss of **myelin sheaths** around neurons. - This is not related to CJD, which involves **prion protein accumulation** and subsequent neuronal degeneration. *Micro abscess (indicative of bacterial infections)* - Micro abscesses indicate localized collections of **pus** typically seen in **bacterial infections**, which is incongruent with the pathophysiology of CJD. - In CJD, there are no signs of **inflammation** or **neutrophilic infiltration** associated with abscess formation [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1284-1286. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256.
Question 10: All of the following are causes of vasogenic-type cerebral edema except which of the following?
- A. Tumors
- B. Cerebral hemorrhage
- C. Infections
- D. Hydrocephalus (Correct Answer)
Explanation: ***Hydrocephalus*** - Hydrocephalus causes interstitial edema, not vasogenic edema, due to increased **intraventricular pressure** leading to CSF extravasation into the periventricular white matter. - This is characterized by fluid accumulation in the ventricles due to impaired **CSF flow or absorption**, rather than blood-brain barrier disruption [3]. *Tumors* - **Brain tumors** are a common cause of vasogenic edema because they disrupt the **blood-brain barrier (BBB)**, allowing plasma proteins and fluid to leak into the extracellular space [4]. - The abnormal vasculature associated with tumors is often fenestrated, contributing to increased vascular permeability and **extracellular fluid accumulation**. *Cerebral hemorrhage* - Hemorrhage causes vasogenic edema by disrupting the **blood-brain barrier**, allowing blood components and fluid to leak into the surrounding brain tissue [1]. - The breakdown products of blood, such as **thrombin** and **hemoglobin**, can also directly damage endothelial cells and increase vascular permeability. *Infections* - Infections like **abscesses** or **meningitis** lead to vasogenic edema through inflammation, which increases the permeability of the **blood-brain barrier** [2]. - Inflammatory mediators and **bacterial toxins** can damage endothelial cells, allowing fluid and proteins to extravasate into the extracellular space. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 703-704. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1275-1276. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1256-1257. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 699-700.
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