Neuropathology — MCQs

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 91: What is the most common intracranial neoplasm?

A. Gliomas
B. Meningioma
C. Metastasis (Correct Answer)
D. Schwannoma

Explanation: **Explanation:** The correct answer is **Metastasis**. In clinical practice, secondary tumors (metastases) are the most common intracranial neoplasms, outnumbering primary brain tumors by a ratio of approximately 10:1 [1]. **Why Metastasis is Correct:** Metastatic spread to the brain occurs in roughly 20–40% of all cancer patients. The most common primary sources are the **Lung** (most common overall), **Breast**, **Melanoma**, **Renal Cell Carcinoma**, and **Colon** [1]. These tumors typically present as multiple, well-circumscribed lesions at the grey-white matter junction, often surrounded by significant vasogenic edema. **Why the other options are incorrect:** * **Gliomas:** While **Glioblastoma Multiforme (GBM)** is the most common *malignant primary* brain tumor in adults, it is less frequent than metastatic disease [1]. * **Meningioma:** This is the most common *benign primary* intracranial tumor [2]. It arises from the arachnoid cap cells and is typically extra-axial [3]. * **Schwannoma:** These are common peripheral nerve sheath tumors (most frequently involving CN VIII at the cerebellopontine angle), but they are significantly less common than metastases or gliomas [3]. **NEET-PG High-Yield Pearls:** * **Most common primary brain tumor (Adults):** Meningioma (Benign); Glioblastoma (Malignant) [2]. * **Most common brain tumor (Children):** Pilocytic Astrocytoma (Benign); Medulloblastoma (Malignant) [2]. * **Location:** Most adult tumors are **supratentorial**, whereas most pediatric tumors are **infratentorial** [2]. * **Metastasis Rule:** If a question asks for the most common "intracranial neoplasm" without specifying "primary," always choose **Metastasis** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1317-1318. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1319-1320. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728.

Question 92: Pick's body in Pick's disease is composed of which protein?

A. Tau protein (Correct Answer)
B. Alpha synuclein
C. Beta synuclein
D. Aβ amyloid

Explanation: **Explanation:** **Pick’s disease**, a specific subtype of Frontotemporal Lobar Degeneration (FTLD-tau), is characterized pathologically by the presence of **Pick bodies**. These are spherical, silver-staining (argyrophilic) cytoplasmic inclusions found primarily in the neurons of the neocortex and hippocampus [1]. 1. **Why Tau protein is correct:** Pick bodies are composed of **3R tau isoforms** (microtubule-associated proteins). In Pick’s disease, tau protein becomes hyperphosphorylated and aggregates into these distinct round inclusions, leading to "knife-edge" atrophy of the frontal and temporal lobes [1]. 2. **Why other options are incorrect:** * **Alpha-synuclein:** This protein aggregates to form **Lewy bodies**, which are the hallmark of Parkinson’s disease and Dementia with Lewy Bodies (DLB). * **Beta-synuclein:** While related to alpha-synuclein, it is not a primary component of diagnostic inclusions in major neurodegenerative diseases. * **Aβ amyloid:** This protein forms **extracellular neuritic (senile) plaques**, a defining feature of Alzheimer’s disease, not Pick’s disease [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Presentation:** Patients typically present with early **behavioral changes**, disinhibition, and language impairment (aphasia) rather than early memory loss. * **Gross Pathology:** Characterized by circumscribed **"Knife-edge" atrophy** of the frontal and temporal lobes, often sparing the posterior two-thirds of the superior temporal gyrus [1]. * **Microscopy:** Look for **Pick bodies** (intracellular, round, argyrophilic tau inclusions) and **Pick cells** (swollen, chromatolytic neurons). * **Staining:** Pick bodies are highlighted by **Silver stains** (e.g., Bielschowsky or Gallyas) and immunohistochemistry for Tau. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1294-1295. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 720-721.

Question 93: Antoni type A and type B cells are characteristic of which of the following tumors?

A. Neurofibroma
B. Neurilemmoma (Correct Answer)
C. Neurofibrosarcoma
D. Traumatic neuroma

Explanation: **Explanation:** The correct answer is **Neurilemmoma**, more commonly known as a **Schwannoma**. These are benign, encapsulated tumors arising from Schwann cells of the peripheral nerve sheath [1]. **1. Why Neurilemmoma is correct:** The hallmark histological feature of a Schwannoma is the presence of two distinct patterns [1]: * **Antoni A:** Hypercellular areas consisting of spindle cells arranged in interlacing fascicles. A key feature here is **Verocay bodies**, which are formed by two rows of palisading nuclei separated by an acellular zone [1]. * **Antoni B:** Hypocellular, myxoid areas with loosely arranged cells and a prominent microcystic background [1]. **2. Why other options are incorrect:** * **Neurofibroma:** Unlike Schwannomas, neurofibromas are not encapsulated and contain a mixture of cell types (Schwann cells, fibroblasts, mast cells) [1, 4]. They exhibit a "shredded carrot" appearance due to collagen bundles but lack the distinct Antoni A/B organization [1]. * **Neurofibrosarcoma (MPNST):** This is a malignant tumor [3]. While it shows spindle cells, it is characterized by high mitotic activity, necrosis, and cellular atypia rather than Antoni patterns [5]. * **Traumatic Neuroma:** This is a non-neoplastic reactive proliferation of axons and Schwann cells following nerve injury, presenting as a disorganized tangle of nerve fibers. **Clinical Pearls for NEET-PG:** * **S-100 Protein:** Schwannomas show strong and diffuse positivity (high-yield IHC marker). * **Acoustic Neuroma:** A Schwannoma of the CN VIII (vestibulocochlear nerve) at the cerebellopontine angle [2]. * **Bilateral Acoustic Neuromas:** Pathognomonic for **Neurofibromatosis Type 2 (NF2)** [2]. * **Encapsulation:** Schwannomas are encapsulated and can be surgically peeled off the nerve, whereas neurofibromas infiltrate the nerve [1, 4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1250. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1248-1249. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1249-1250. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1250-1251.

Question 94: Which is the most common childhood CNS tumor to metastasize outside the brain?

A. Ependymoma
B. Glioblastoma multiforme
C. Choroid plexus tumor
D. Medulloblastoma (Correct Answer)

Explanation: **Explanation:** **Medulloblastoma** is a highly malignant Grade 4 embryonal tumor arising from the cerebellum. It is the most common malignant brain tumor in children [1]. Its propensity for metastasis is a hallmark feature: 1. **Leptomeningeal Spread:** It frequently spreads via the cerebrospinal fluid (CSF) to the spinal cord, often referred to as "drop metastases." [1] 2. **Extracranial Metastasis:** While CNS tumors rarely spread outside the blood-brain barrier, Medulloblastoma is the most common childhood CNS tumor to do so. The most frequent site for systemic spread is the **bone**, followed by lymph nodes and liver. This often occurs via ventriculoperitoneal (VP) shunts or hematogenous routes. **Analysis of Incorrect Options:** * **Ependymoma:** While these can show CSF seeding (especially the posterior fossa subtype), systemic metastasis is extremely rare compared to medulloblastoma. * **Glioblastoma Multiforme (GBM):** This is the most common primary malignant brain tumor in *adults*. While it is highly invasive locally, it rarely metastasizes outside the CNS in children. * **Choroid Plexus Tumor:** These are rare tumors. While Choroid Plexus Carcinomas can seed the subarachnoid space, they do not have the same high incidence of systemic metastasis as medulloblastoma. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Look for **Homer-Wright rosettes** (pseudorosettes) and small round blue cells. * **Location:** Arises from the **vermis** in children (midline) and cerebellar hemispheres in adults. * **Genetics:** WNT pathway mutations carry the best prognosis; SHH and Group 3/4 have poorer outcomes. * **Radiology:** Appears as a hyperdense mass on CT in the fourth ventricle, causing obstructive hydrocephalus. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315.

Question 95: Lewy bodies are found in the substantia nigra neurons in which of the following conditions?

A. Alzheimer disease
B. Parkinson disease (Correct Answer)
C. Huntington disease
D. Pick disease

Explanation: **Explanation:** **Parkinson Disease (Correct Answer):** The hallmark pathological feature of Parkinson disease (PD) is the loss of dopaminergic neurons in the **substantia nigra pars compacta** [2]. The surviving neurons characteristically contain **Lewy bodies** [1]. These are eosinophilic, round, intracytoplasmic inclusions with a dense core and a pale halo [1]. They are primarily composed of abnormally aggregated **alpha-synuclein** protein [2]. **Incorrect Options:** * **Alzheimer Disease:** Characterized by extracellular **amyloid-beta plaques** and intracellular **neurofibrillary tangles** (composed of hyperphosphorylated tau protein), primarily affecting the hippocampus and cerebral cortex [3]. * **Huntington Disease:** An autosomal dominant disorder caused by CAG repeats [3]. It features atrophy of the **caudate nucleus** and putamen (striatum) with intranuclear inclusions of huntingtin protein. * **Pick Disease (Frontotemporal Dementia):** Characterized by "Pick bodies," which are silver-staining, spherical **tau protein** inclusions. Unlike Lewy bodies, these are found in the frontal and temporal lobes, not the substantia nigra. **High-Yield Clinical Pearls for NEET-PG:** * **Lewy Body Composition:** Alpha-synuclein (High-yield for MCQ) [2]. * **Dementia with Lewy Bodies (DLB):** If dementia occurs within one year of motor symptoms, it is DLB. In DLB, Lewy bodies are found in the **cerebral cortex**, whereas in PD, they are primarily in the **subcortical nuclei** [1][4]. * **Stain:** Lewy bodies are best visualized using **immunohistochemistry for alpha-synuclein** [1] or periodic acid-Schiff (PAS) stain. * **Clinical Triad of PD:** Resting tremor ("pill-rolling"), bradykinesia, and rigidity ("cogwheel"). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1297-1298. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1296-1297. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 719-720. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 723-724.

Question 96: All of the following are features of Pick's disease except?

A. Knife blade atrophy
B. Walnut brain
C. Ballooning degeneration
D. Hirano bodies (Correct Answer)

Explanation: **Pick’s Disease** (a subtype of Frontotemporal Dementia) is characterized by progressive atrophy of the frontal and temporal lobes [1]. ### Why "Hirano bodies" is the correct answer: **Hirano bodies** are eosinophilic, rod-like inclusions found primarily in the pyramidal cells of the hippocampus. While they are associated with aging, they are a hallmark histological feature of **Alzheimer’s disease**, not Pick’s disease. ### Explanation of incorrect options: * **Knife-edge/Blade atrophy (Option A):** This is the classic macroscopic description of Pick’s disease. Severe, asymmetric atrophy of the frontal and temporal gyri leads to thinning so pronounced that the gyri resemble the sharp edge of a knife [1]. * **Walnut brain (Option B):** This refers to the gross appearance of the brain in Pick’s disease. Because the atrophy is sharply circumscribed to the frontal and temporal lobes (sparing the parietal and occipital lobes), the brain takes on the shriveled appearance of a walnut shell. * **Ballooning degeneration (Option C):** Also known as **Pick cells**, these are surviving neurons that appear swollen (ballooned) with cleared-out cytoplasm and displaced nuclei, representing a specific pattern of neuronal injury in this condition. ### High-Yield Clinical Pearls for NEET-PG: * **Pick Bodies:** These are the pathognomonic microscopic findings—spherical, silver-staining (Argyrophilic) cytoplasmic inclusions made of **3R Tau protein**. * **Clinical Presentation:** Unlike Alzheimer’s (which starts with memory loss), Pick’s disease presents early with **personality changes**, social disinhibition, and language impairment. * **Sparing:** Note that the posterior two-thirds of the superior temporal gyrus is typically spared [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1294-1296.

Question 97: Kuru plaques are seen in which of the following neurodegenerative disorders?

A. Alzheimer disease
B. Creutzfeldt-Jakob Disease (CJD) (Correct Answer)
C. Parkinson disease (PD)
D. Multiple system atrophy (MSA)

Explanation: **Explanation:** **Kuru plaques** are extracellular aggregates of abnormal prion proteins ($PrP^{sc}$) and are a hallmark histological feature of **Prion diseases** [1]. In the context of the options provided, they are most characteristically associated with **Creutzfeldt-Jakob Disease (CJD)**, particularly the variant CJD (vCJD) and iatrogenic forms [1], [2]. 1. **Why CJD is correct:** Prion diseases involve the conformational change of normal cellular prion protein ($PrP^c$) into a protease-resistant, misfolded form ($PrP^{sc}$). These misfolded proteins aggregate to form "Kuru plaques," which are PAS-positive, Congo red-positive (showing apple-green birefringence), and typically found in the cerebellum [1]. While classic sporadic CJD shows these plaques in only about 10% of cases, they are a defining feature of Kuru and vCJD [1]. 2. **Why other options are incorrect:** * **Alzheimer Disease:** Characterized by **Senile (Neuritic) plaques** (extracellular Amyloid-beta) and **Neurofibrillary tangles** (intracellular hyperphosphorylated Tau) [3]. * **Parkinson Disease:** Defined by **Lewy bodies**, which are intracellular inclusions of alpha-synuclein found in the substantia nigra. * **Multiple System Atrophy (MSA):** A "synucleinopathy" characterized by **Papp-Lantos bodies** (Glial Cytoplasmic Inclusions) in oligodendrocytes. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of CJD:** Rapidly progressive dementia, myoclonus (startle-induced), and periodic sharp wave complexes on EEG [2]. * **Histology Triad:** Spongiform encephalopathy (vacuolation of neuropil), neuronal loss, and gliosis [1]. * **Protein 14-3-3:** A key CSF biomarker for CJD diagnosis. * **Pulvinar Sign:** High intensity in the posterior thalamus on MRI, highly suggestive of variant CJD. **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] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 712-713. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1294.

Question 98: Which part of the brain is most resistant to hypoxia?

A. Cerebral cortex
B. Basal ganglia
C. Thalamus
D. Structures in the brainstem (Correct Answer)

Explanation: **Explanation:** The susceptibility of brain tissue to hypoxia is determined by the metabolic rate and the density of excitatory neurotransmitter receptors (like NMDA receptors). The brain exhibits **selective vulnerability**, where different regions react differently to decreased oxygen levels. **1. Why the Brainstem is the Correct Answer:** The **brainstem structures** (including the medulla, pons, and midbrain) are the **most resistant** to hypoxic-ischemic injury. This is an evolutionary protective mechanism to preserve vital autonomic functions (respiration and cardiac control) during periods of stress. These areas have a lower metabolic demand compared to the higher centers of the brain. **2. Why the Other Options are Incorrect:** * **Cerebral Cortex (Option A):** Highly sensitive, particularly the pyramidal cells in layers III, V, and VI. Damage here leads to laminar necrosis. * **Basal Ganglia (Option B):** Very sensitive to hypoxia and specific toxins (like Carbon Monoxide). The **striatum** (caudate and putamen) is a frequent site of injury. * **Thalamus (Option C):** Also highly metabolic and susceptible, though generally less so than the hippocampus or specific cortical layers. **High-Yield Clinical Pearls for NEET-PG:** * **Most Sensitive Cell Type:** Neurons are the cells most vulnerable to hypoxia, becoming irreversibly damaged after 5-7 minutes [1]. * **Most Sensitive Specific Neuron:** **Purkinje cells of the Cerebellum**, followed by **Pyramidal cells of the Hippocampus (CA1 area/Sommer sector)**. * **Watershed Areas:** The regions between the territories of major cerebral arteries (e.g., between MCA and ACA) are the first to suffer during systemic hypotension. * **Red Neurons:** The earliest microscopic sign of irreversible hypoxic injury (seen 12–24 hours post-insult), characterized by eosinophilic cytoplasm and pyknotic nuclei. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 704-705.

Question 99: Duret's haemorrhage is typically seen in which part of the brain?

A. Retina
B. Ventricles
C. Midbrain and pons (Correct Answer)
D. None of the above

Explanation: **Explanation:** **Duret hemorrhages** are small, linear or flame-shaped hemorrhages occurring in the midline of the **midbrain and upper pons** [1]. **Pathophysiology:** These hemorrhages are a secondary complication of **transtentorial (uncal) herniation** [1]. When a space-occupying lesion (like a hematoma or tumor) causes the brain to displace downward, it stretches and tears the perforating branches of the **basilar artery** and/or the draining veins [1]. This mechanical shearing leads to focal ischemia and hemorrhagic infarction within the brainstem parenchyma. **Analysis of Options:** * **Option C (Midbrain and pons):** This is the correct anatomical site. The displacement of the brainstem downward through the tentorial notch specifically stresses the vessels supplying these regions [1]. * **Option A (Retina):** Retinal hemorrhages are associated with conditions like hypertension, diabetes, or Terson syndrome (subarachnoid hemorrhage), but are not termed Duret hemorrhages. * **Option B (Ventricles):** Bleeding into the ventricles is termed intraventricular hemorrhage (IVH), commonly seen in germinal matrix hemorrhages in neonates or as an extension of intraparenchymal bleeds in adults. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Sign:** Duret hemorrhages usually signify a fatal progression of increased intracranial pressure; they often present clinically with a rapid decline in consciousness and fixed/dilated pupils. * **Association:** Always link Duret hemorrhage with **Uncal Herniation** and the **Basilar Artery** [1]. * **Morphology:** On a CT scan or autopsy, they appear as "flame-shaped" streaks in the midline of the brainstem (tegmentum) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1257-1258.

Question 100: In Alzheimer's disease, what is plaque primarily composed of?

A. Tau protein
B. Beta amyloid (Correct Answer)
C. Huntington
D. Alpha synuclein

Explanation: **Explanation:** Alzheimer’s Disease (AD) is characterized by the accumulation of two specific protein aggregates: extracellular **Neuritic (Senile) Plaques** and intracellular **Neurofibrillary Tangles (NFTs)** [1]. **Why Beta-amyloid is correct:** Neuritic plaques are primarily composed of **Aβ (Beta-amyloid) peptides** [1]. These are derived from the abnormal cleavage of the Amyloid Precursor Protein (APP) by **β-secretase** and **γ-secretase** [2]. The resulting Aβ peptides (especially Aβ42) are prone to aggregation, forming the core of the extracellular plaques that disrupt synaptic signaling and trigger neuroinflammation [2]. **Analysis of Incorrect Options:** * **A. Tau protein:** While Tau is central to AD, it forms **Neurofibrillary Tangles (NFTs)**, which are *intracellular* inclusions [3]. Tau is a microtubule-associated protein that becomes hyperphosphorylated in AD. * **C. Huntington:** This protein is associated with **Huntington’s Disease**, caused by a CAG trinucleotide repeat expansion on Chromosome 4 [1]. * **D. Alpha-synuclein:** This is the primary component of **Lewy Bodies**, which are the hallmark of Parkinson’s Disease and Lewy Body Dementia [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Mutations in **APP** (Chr 21), **Presenilin 1** (Chr 14), and **Presenilin 2** (Chr 1) lead to early-onset familial AD [2]. * **Risk Factor:** The **ApoE4** allele increases the risk and decreases the age of onset, while **ApoE2** is protective. * **Down Syndrome:** Patients have an increased risk of early AD because the APP gene is located on Chromosome 21 [2]. * **Staining:** Amyloid plaques show **Apple-green birefringence** under polarized light when stained with **Congo Red**. Silver stains (Bielschowsky) are also used to visualize plaques and tangles [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 719-720. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1290-1292. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1294.

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Cellular Pathology of the Nervous System

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Cerebrovascular Diseases

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Trauma to the Central Nervous System

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Infections of the Nervous System

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Demyelinating Diseases

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Neurodegenerative Diseases

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CNS Tumors

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Peripheral Nerve Disorders

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Neuromuscular Junction Diseases

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Congenital and Developmental Disorders

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