Neuropathology — MCQs

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 371: Which of the following statements is true regarding HSV encephalitis?

A. Hemorrhagic lesions are seen (Correct Answer)
B. Caused by HSV-1
C. Eosinophilic inclusion bodies are seen
D. Caused by Varicella zoster virus

Explanation: ***Hemorrhagic lesions are seen*** - **Hemorrhagic necrosis** of the **temporal lobes** is the pathognomonic feature of HSV encephalitis [3] - The hemorrhagic nature helps differentiate it from other viral encephalitides - Classically affects the **medial temporal lobes** and **inferior frontal lobes** bilaterally [2] - MRI shows hemorrhagic changes with mass effect in these regions *Caused by HSV-1* - While **HSV-1** causes >90% of HSV encephalitis cases in adults and children, this statement is technically correct - However, **hemorrhagic lesions** are the more distinctive pathological feature being tested - HSV-1 is the causative agent, but the hemorrhagic pathology is the key diagnostic finding *Eosinophilic inclusion bodies are seen* - **Cowdry type A intranuclear inclusion bodies** are indeed seen in HSV encephalitis [1] - These are **eosinophilic** with a clear halo around them - While true, this is a microscopic finding, whereas hemorrhagic lesions are the macroscopic hallmark *Caused by Varicella zoster virus* - VZV causes **varicella** (chickenpox) and **herpes zoster** (shingles) [2] - VZV can cause encephalitis but with different clinical and pathological features - HSV encephalitis is specifically caused by **herpes simplex virus**, not varicella zoster virus **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 365-366. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1278-1279. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1278.

Question 372: Which of the following best describes a type of injury that occurs after the initial head trauma?

A. Primary injury (damage at the time of trauma).
B. Delayed complications (e.g., ischemia, edema).
C. Initial trauma (primary impact).
D. Secondary injury (complications after initial trauma). (Correct Answer)

Explanation: ***Secondary injury (complications after initial trauma)*** - **Secondary injury** describes the physiological events and processes that occur minutes to days after the initial impact, such as **ischemia**, **edema**, and inflammation [1]. - These events exacerbate the damage initiated by the primary injury and can lead to worsened neurological outcomes. *Delayed complications (e.g., ischemia, edema).* - While **ischemia** and **edema** are examples of delayed complications, the term "delayed complications" is less precise than "secondary injury" in describing the broad range of pathophysiological processes. - **Secondary injury** encompasses the various cellular and molecular cascades that follow the initial trauma [1]. *Primary injury (damage at the time of trauma).* - **Primary injury** refers to the direct damage that occurs at the exact moment of impact, such as **contusions**, **lacerations**, and **axonal shearing** [2]. - This type of injury is irreversible and cannot be prevented after the trauma has occurred. *Initial trauma (primary impact).* - **Initial trauma** or **primary impact** refers to the immediate mechanical forces applied to the head. - This phrase describes the event itself rather than the resulting biological injury. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 701-702. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1262-1264.

Question 373: Neuritic plaques are associated with which of the following diseases?

A. Alzheimer's disease (Correct Answer)
B. Multiple sclerosis
C. Stroke
D. Parkinson's disease

Explanation: ***Alzheimer's disease*** - **Neuritic plaques**, composed primarily of **beta-amyloid protein**, are a hallmark neuropathological feature of Alzheimer's disease [1], [2]. - These plaques accumulate extracellularly in the brain, contributing to synaptic dysfunction and neuronal loss [2]. *Multiple sclerosis* - Multiple sclerosis is characterized by **demyelination** within the central nervous system, forming plaques or lesions. - These plaques are distinct from the neuritic plaques of Alzheimer's and are primarily composed of inflammatory cells and demyelinated axons. *Stroke* - A stroke is an acute event resulting from **ischemia** (lack of blood flow) or **hemorrhage** in the brain. - The brain changes in stroke are related to tissue death due to vascular compromise, not the accumulation of protein aggregates like neuritic plaques. *Parkinson's disease* - Parkinson's disease is characterized by **Lewy bodies** (alpha-synuclein aggregates) in dopaminergic neurons [3]. - While also a neurodegenerative disease, Parkinson's does not feature neuritic plaques as a primary pathological finding. **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. 1292-1294. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 719-720.

Question 374: All of the following are true statements about glioblastoma, except which of the following?

A. Pseudo-palisading necrosis
B. Microvascular proliferation
C. WHO grade IV tumour
D. Perineuronal satellitosis (Correct Answer)

Explanation: ***Perineuronal satellitosis*** - This is an observed phenomenon in glioblastoma, but it is not a defining feature of the tumor itself. - It reflects a specific response of **neuronal cells** to nearby glioma cells, rather than a characteristic of glioblastoma. *WHO grade IV tumour* - Glioblastoma is classified as a **WHO grade IV tumor**, indicating its aggressive nature and poor prognosis [1]. - This classification is based on **molecular and histological features** typical of high-grade astrocytomas. *Pseudo-palisading necrosis* - This feature describes the arrangement of tumor cells around necrotic areas, which is a common characteristic of glioblastoma [1]. - It reflects the aggressive behavior and high **cellular density** in areas of necrosis. *Microvascular proliferation* - This refers to the formation of numerous small blood vessels and is a hallmark of glioblastoma's **vascularity and aggressiveness** [1]. - Such proliferation is crucial for providing oxygen and nutrients to the tumor, contributing to its growth. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1308-1311.

Question 375: The most common calcifying brain tumor in a child is:

A. Craniopharyngioma (Correct Answer)
B. Glioma
C. Medulloblastoma
D. Meningioma

Explanation: ***Craniopharyngioma*** - This tumor is known for its **cystic and solid components** and a high propensity for **calcification**, making it the most common calcifying brain tumor in children. - It arises from **Rathke's pouch remnants**, typically located in the **suprasellar region**, which often leads to **endocrine dysfunction** and visual disturbances. *Medulloblastoma* - While it is a common pediatric brain tumor [1], primarily located in the **cerebellum** [1], [2], it is less commonly associated with significant calcification. - It is a highly malignant tumor originating from **neuroectodermal cells** and is known for its propensity to **disseminate** via CSF pathways [2]. *Glioma* - This is a broad category of tumors arising from **glial cells**, and while some types can calcify (e.g., oligodendroglioma), calcification is not a defining or most common feature across all pediatric gliomas. - The most common pediatric gliomas, such as **pilocytic astrocytomas**, are typically cystic [1] with a mural nodule and often do not show extensive calcification. *Meningioma* - These tumors arise from the **meninges** [3] and are more prevalent in adults, with pediatric cases being relatively rare. - While meningiomas can calcify, especially psammomatous types, they are not the most common calcifying brain tumor in the pediatric population compared to craniopharyngiomas. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 725-726. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1319-1320.

Question 376: 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 377: In which location is spinal muscular atrophy primarily observed?

A. Anterior horn (Correct Answer)
B. Peripheral nerve
C. Neuromuscular junction
D. Dorsal root ganglion

Explanation: ***Anterior horn*** - **Spinal muscular atrophy (SMA)** is a genetic disorder caused by mutations in the **SMN1 gene** leading to degeneration of **alpha motor neurons** in the **anterior horn** of the spinal cord [1]. - This results in progressive **muscle weakness and atrophy** due to loss of motor neuron innervation to skeletal muscles [2]. - The pathology is specifically localized to the **anterior horn cells**, making this the primary site of disease [1]. *Peripheral nerve* - Peripheral neuropathies involve primary pathology of **axons or myelin sheaths** in peripheral nerves outside the CNS [1]. - While peripheral nerve function is compromised in SMA due to absent innervation, the **primary lesion is at the motor neuron cell body** in the anterior horn, not the peripheral nerve itself [2]. *Neuromuscular junction* - Disorders like **myasthenia gravis** affect signal transmission at the neuromuscular junction, causing fluctuating weakness. - In SMA, the defect is **upstream** at the motor neuron level, not at the junction where nerve meets muscle [2]. *Dorsal root ganglion* - The **dorsal root ganglion** contains **sensory neuron cell bodies**, not motor neurons. - Sensory function is typically **preserved in SMA**, distinguishing it from mixed sensorimotor disorders. - Diseases affecting dorsal root ganglia (e.g., sensory neuronopathies) present with sensory loss, not pure motor weakness. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 730-731. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1247-1248.

Question 378: 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.

Question 379: Which type of necrosis is seen in the brain?

A. Coagulative
B. Liquefactive (Correct Answer)
C. Fat
D. Fibrinoid

Explanation: ***Liquefactive*** - Liquefactive necrosis is characterized by the transformation of tissue into a **liquid viscous mass**, commonly seen in the brain after **ischemic injury**. - Often associated with brain **infarcts** or **abscess formation**, where cell death results in the accumulation of **neutrophils and pus**. [1] *Fibrinoid* - Fibrinoid necrosis is typically associated with **immune-mediated vascular damage**, not commonly seen in the brain. - This type of necrosis occurs in conditions like **polyarteritis nodosa** or **lupus**, where **fibrin-like protein** deposits are found in vessel walls. *Coagulative* - Coagulative necrosis usually occurs in **myocardial infarction** and is characterized by the preservation of cell outlines due to **denaturation of proteins**. - It is not typical in brain tissue, which undergoes liquefactive necrosis in cases of cell death. *Fat* - Fat necrosis is primarily associated with **enzymatic destruction of adipose tissue**, often related to pancreatic damage or trauma. - It is not relevant to brain necrosis, which does not characteristically present with fat necrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269.

Question 380: Which of the following statements about primary CNS lymphoma is true?

A. It has an association with EBV.
B. Reticulin staining is performed.
C. It is an indolent disease with a good prognosis.
D. It is primarily a B-cell type. (Correct Answer)

Explanation: ***abc*** - Primary CNS lymphoma is predominantly a **B-cell malignancy** [1], which supports the correct representation of statement (b). - It has a significant **association with Epstein-Barr virus (EBV)**, particularly in immunocompromised individuals [1], making (c) accurate as well. *bcd* - Though (b) and (c) are correct, statement (d) is false; **primary CNS lymphoma** is typically an **aggressive disease** with a poor prognosis [1]. - Hence, the inclusion of (d) makes this option incorrect. *ab* - While (b) is true regarding its classification as a B-cell tumor, statement (a) is misleading; **reticulin staining** is not a standard diagnostic tool for this condition. - Only having two correct statements makes this option incomplete. *acd* - Statement (a) is incorrect as **reticulin staining** is not used for this lymphoma, making the option false overall. - Additionally, (d) misrepresents the disease as primary CNS lymphoma is rather **aggressive**, not indolent. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1315-1316.

Practice by Chapter

Cellular Pathology of the Nervous System

Practice Questions

Cerebrovascular Diseases

Practice Questions

Trauma to the Central Nervous System

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Infections of the Nervous System

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Demyelinating Diseases

Practice Questions

Neurodegenerative Diseases

Practice Questions

CNS Tumors

Practice Questions

Peripheral Nerve Disorders

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Neuromuscular Junction Diseases

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Congenital and Developmental Disorders

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