Neuropathology — MCQs

A 41-year-old woman presents with a 4-month history of diminished hearing. Physical examination reveals decreased hearing in the left ear, and the Weber tuning fork test lateralizes to the right ear. A head MRI shows a sharply circumscribed, 4-cm mass adjacent to the left pons extending toward the left inferior cerebellar hemisphere, with a smaller 1-cm lesion in a similar location on the right. Family screening identifies a similarly affected 38-year-old sibling. An inherited mutation involving which of the following genes is most likely to be present in this patient?

Q60Easy

Senile plaques in Alzheimer's disease are rich in which component?

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 51: Which area of the brain is relatively resistant to neurofibrillary tangles in Alzheimer's disease?

A. Visual association area
B. Entorhinal cortex
C. Lateral geniculate body (Correct Answer)
D. Cuneal gyrus (Area VI)/temporal lobe

Explanation: Explanation: In Alzheimer’s Disease (AD), the accumulation of **Neurofibrillary Tangles (NFTs)**—composed of hyperphosphorylated tau protein—follows a predictable hierarchical pattern of spread, typically described by the **Braak stages**. **Why the Lateral Geniculate Body is correct:** The pathology of AD characteristically involves the limbic system and association cortices while **sparing primary sensory and motor nuclei** until the very terminal stages. The **Lateral Geniculate Body (LGB)** is a primary sensory relay nucleus of the thalamus for the visual pathway. Like the primary motor cortex and primary sensory zones, the LGB is remarkably resistant to the formation of NFTs, even when surrounding association areas are heavily involved. **Analysis of Incorrect Options:** * **Entorhinal Cortex (B):** This is the **earliest** site of NFT involvement (Braak Stage I & II). It serves as the gateway to the hippocampus; damage here explains early memory deficits. * **Visual Association Area (A):** These areas (e.g., Brodmann areas 18 and 19) are involved in the intermediate to late stages of AD (Braak Stage V-VI) as the pathology spreads from the limbic system to the neocortex. * **Cuneal Gyrus/Temporal Lobe (D):** The temporal lobe is a major hub for AD pathology [1]. While the primary visual cortex (Area 17/V1) in the cuneal gyrus is relatively late to be involved, it is still more susceptible than the subcortical relay nuclei like the LGB. **High-Yield Pearls for NEET-PG:** * **Sequence of NFT spread:** Entorhinal cortex → Hippocampus → Association Neocortex → Primary Neocortex. * **Amyloid vs. Tau:** Amyloid plaques (extracellular) determine the *diagnosis*, but Neurofibrillary Tangles (intracellular) correlate best with the *severity of dementia* [1]. * **Hirano Bodies:** Eosinophilic, rod-like inclusions (actin) found in the hippocampus of AD patients. * **Granulovacuolar Degeneration:** Small clear vacuoles in hippocampal neurons, another hallmark of AD. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1295.

Question 52: What is the most common primary site of origin for leptomeningeal carcinomatosis?

A. Breast (Correct Answer)
B. Thyroid
C. Bone
D. Liver

Explanation: **Explanation:** **Leptomeningeal Carcinomatosis (LC)**, also known as neoplastic meningitis, occurs when malignant cells infiltrate the subarachnoid space and spread via the cerebrospinal fluid (CSF). **Why Breast is Correct:** Breast carcinoma is the **most common primary solid tumor** to cause leptomeningeal spread, accounting for approximately 30–40% of cases. The high incidence is attributed to the biological tendency of breast cancer cells (particularly lobular and HER2-positive subtypes) to seed the CSF via hematogenous spread or direct extension from parenchymal brain metastases [1]. **Analysis of Incorrect Options:** * **B. Thyroid:** While thyroid cancer can metastasize to the brain parenchyma (especially follicular variant), it rarely presents with primary leptomeningeal involvement. * **C. Bone:** Primary bone tumors (like Osteosarcoma) rarely metastasize to the meninges. While cancers like prostate or breast spread *to* bone, bone itself is not a common *origin* for LC. * **D. Liver:** Hepatocellular carcinoma (HCC) typically metastasizes to the lungs and bone; CNS involvement is rare and usually presents as focal parenchymal masses rather than diffuse leptomeningeal seeding. **High-Yield Clinical Pearls for NEET-PG:** * **Top 3 Primary Sources:** 1. Breast Cancer (Most common), 2. Lung Cancer (Small Cell > Non-Small Cell), 3. Melanoma [1]. * **Gold Standard Diagnosis:** CSF Cytology (shows malignant cells, elevated protein, and low glucose). * **Radiological Sign:** "Sugar coating" or linear enhancement of the sulci and cranial nerves on Gadolinium-enhanced MRI (Zuckerguss appearance). * **Common Presentation:** Multifocal neurological deficits (e.g., cranial nerve palsies combined with radiculopathy). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1317-1318.

Question 53: What is the commonest intramedullary spinal tumor?

A. Metastases
B. Neurofibroma
C. Ependymoma (Correct Answer)
D. None of the above

Explanation: ### Explanation **Correct Option: C. Ependymoma** In the adult population, **Ependymoma** is the most common primary intramedullary spinal cord tumor (accounting for approximately 60% of cases). These tumors typically arise from the ependymal cells lining the central canal [1]. They are most frequently found in the **cervical region**. A specific subtype, the *Myxopapillary ependymoma*, is the most common tumor of the **filum terminale** and conus medullaris [1]. **Analysis of Incorrect Options:** * **A. Metastases:** While metastases are the most common cause of spinal malignancy overall, they are typically **extradural** (involving the vertebral bodies). Intramedullary metastases are rare, accounting for only about 1–2% of spinal cord tumors. * **B. Neurofibroma:** These are **extramedullary-intradural** tumors. They arise from the nerve roots rather than the spinal cord parenchyma itself. Along with Schwannomas, they are the most common tumors in the intradural-extramedullary compartment. * **D. None of the above:** Incorrect, as Ependymoma is the established primary intramedullary tumor. **NEET-PG High-Yield Pearls:** * **Pediatric Variation:** In children, **Astrocytomas** are the most common intramedullary tumors (whereas Ependymomas lead in adults). * **Radiology Sign:** Ependymomas are often well-circumscribed and may show the **"Cap sign"** (a rim of hemosiderin at the poles of the tumor) on MRI due to chronic hemorrhage. * **Association:** Spinal ependymomas are strongly associated with **Neurofibromatosis Type 2 (NF2)**. * **Surgical Note:** Unlike astrocytomas, ependymomas usually have a distinct cleavage plane, making surgical resection more feasible. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1312-1313.

Question 54: Which of the following cells is associated with ependymal cells rather than microglial cells?

A. Blepharoplasts (Correct Answer)
B. Rod cells
C. Gitter cells
D. Reservoir for HIV

Explanation: **Explanation:** **1. Why Blepharoplasts are the correct answer:** Blepharoplasts (also known as basal bodies) are microtubule-organizing centers located at the base of cilia. Since **ependymal cells** are ciliated epithelial cells that line the ventricular system of the brain and the central canal of the spinal cord, they contain these structures. In histopathology, the presence of blepharoplasts (demonstrated by PTAH stain) is a classic diagnostic hallmark for **Ependymomas** [1], helping to differentiate them from other glial tumors. **2. Analysis of Incorrect Options (Microglial associations):** * **Rod cells:** These are activated microglia with elongated nuclei [2]. they are typically seen in chronic inflammatory conditions like neurosyphilis (General Paresis of the Insane) and viral encephalitis. * **Gitter cells:** These are "compound granular corpuscles" or "gitterzellen." They represent enlarged, phagocytic microglia (macrophages) laden with lipids, commonly found at sites of liquefactive necrosis (e.g., old cerebral infarcts). * **Reservoir for HIV:** Microglia are the primary targets and reservoirs for HIV in the Central Nervous System. They express CD4 and CCR5 receptors, leading to the formation of **Microglial nodules** [2] and multinucleated giant cells in HIV-associated encephalopathy. **Clinical Pearls for NEET-PG:** * **Ependymoma:** Most common in the 4th ventricle in children and the spinal cord in adults. Look for **Perivascular pseudorosettes** [1] (more common) and True ependymal rosettes. * **Microglia Origin:** Unlike other glial cells (ectodermal), microglia are derived from the **mesoderm** (yolk sac macrophages). * **Stain for Blepharoplasts:** Phosphotungstic Acid Hematoxylin (**PTAH**) stain. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1312-1313. [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 55: What is the protein deposited in Alzheimer's disease?

A. Tau protein (Correct Answer)
B. Alpha synuclein protein
C. Huntington protein
D. Protein 14.3.3.

Explanation: **Explanation:** Alzheimer’s Disease (AD) is characterized by the accumulation of two hallmark proteins: **Amyloid-beta (Aβ)** and **Tau protein** [1]. While Aβ forms extracellular neuritic plaques, the **Tau protein** is responsible for forming **intracellular Neurofibrillary Tangles (NFTs)** [1]. In AD, Tau undergoes hyperphosphorylation, causing it to detach from microtubules and aggregate [2]. This leads to microtubule instability and neuronal death. **Analysis of Options:** * **A. Tau protein (Correct):** As mentioned, hyperphosphorylated Tau forms the diagnostic neurofibrillary tangles in Alzheimer’s [2]. * **B. Alpha-synuclein:** This protein is the primary component of **Lewy bodies**, which are the hallmark of Parkinson’s Disease and Lewy Body Dementia [4]. * **C. Huntingtin protein:** This is an abnormal protein produced due to CAG trinucleotide repeats on chromosome 4, leading to **Huntington’s Disease** [3]. * **D. Protein 14-3-3:** This is a marker of rapid neuronal destruction found in the cerebrospinal fluid (CSF) of patients with **Creutzfeldt-Jakob Disease (CJD)**; it is not a primary deposit but a diagnostic marker. **High-Yield Clinical Pearls for NEET-PG:** * **Genetics:** Early-onset AD is associated with mutations in **APP** (Chr 21), **Presenilin 1** (Chr 14), and **Presenilin 2** (Chr 1). Late-onset is linked to **ApoE4**. * **Morphology:** Grossly, there is symmetrical cortical atrophy (narrowed gyri, widened sulci) and **hydrocephalus ex vacuo** [2]. * **Hirano Bodies:** Eosinophilic, actin-rich inclusions found in the hippocampus of AD patients. * **Staining:** Silver stains (e.g., Bielschowsky) and Congo Red (for amyloid angiopathy) are used to visualize deposits. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1293. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1294-1295. [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] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1296-1297.

Question 56: Neurologic abnormalities have been noted in about one-third of patients with AIDS. Which of the following is NOT seen in HIV involvement of the central nervous system?

A. Perivascular giant cell
B. Vacuolar degeneration of the posterior column
C. Microglial nodule formation
D. Inclusion bodies (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Inclusion bodies**. This question tests the distinction between primary HIV-induced neuropathology and secondary opportunistic infections common in AIDS. **Why Inclusion Bodies are NOT seen in HIV:** HIV is a lentivirus that does not produce characteristic intracellular inclusion bodies [1]. Inclusion bodies are hallmark features of other viral infections seen in AIDS patients, such as **Cowdry Type A** inclusions in Herpes Simplex Virus (HSV) [2] or **"Owl’s eye"** intranuclear inclusions in Cytomegalovirus (CMV). HIV primarily affects the CNS by infecting macrophages and microglia, leading to indirect neuronal damage rather than direct viral replication within neurons [1]. **Analysis of Incorrect Options:** * **A. Perivascular giant cells:** These are the **pathognomonic** histological feature of HIV Encephalitis [1]. They are formed by the fusion of HIV-infected macrophages/microglia. * **B. Vacuolar degeneration of the posterior column:** Also known as **HIV Vacuolar Myelopathy**, this involves the spinal cord (specifically the posterior and lateral columns). It histologically resembles Subacute Combined Degeneration (Vitamin B12 deficiency). * **C. Microglial nodule formation:** This is a common, though non-specific, inflammatory response in HIV Encephalitis where clusters of microglia surround small areas of necrosis [2]. **Clinical Pearls for NEET-PG:** * **HIV Encephalitis (HIVE):** Characterized by the triad of microglial nodules, multinucleated giant cells, and perivascular inflammation [1]. * **Primary CNS Lymphoma:** A common differential in AIDS; it is almost always associated with **EBV** [1]. * **Progressive Multifocal Leukoencephalopathy (PML):** Caused by the **JC virus**, it shows demyelination and "ground-glass" viral inclusions in oligodendrocytes [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 711-712. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1278. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1280-1281.

Question 57: What is the most common tumor in the lateral hemisphere of the brain?

A. Astrocytoma (Correct Answer)
B. Meningioma
C. Ependymoma
D. Medulloblastoma

Explanation: **Explanation:** The correct answer is **Astrocytoma**. **1. Why Astrocytoma is correct:** Astrocytomas are the most common primary intra-axial tumors of the central nervous system [1]. In adults, the cerebral hemispheres (lateral hemispheres) are the most frequent site of involvement [1]. These tumors arise from astrocytes and range from low-grade (Pilocytic) to high-grade (Glioblastoma Multiforme). Glioblastoma (WHO Grade 4) is the most common malignant primary brain tumor in adults and characteristically involves the subcortical white matter of the cerebral hemispheres [2]. **2. Why the other options are incorrect:** * **Meningioma:** While these are the most common overall primary intracranial tumors, they are **extra-axial** (arising from the arachnoid cap cells of the meninges), not tumors "in" the brain parenchyma itself. * **Ependymoma:** These typically arise from the lining of the ventricular system. In children, they are most common in the **fourth ventricle** (infratentorial), while in adults, they are more frequently found in the spinal cord. * **Medulloblastoma:** This is a highly malignant embryonal tumor (WHO Grade 4) that occurs almost exclusively in the **cerebellum** (posterior fossa), primarily in children [1]. **3. NEET-PG High-Yield Pearls:** * **Most common primary brain tumor (Overall):** Meningioma (Extra-axial). * **Most common primary malignant brain tumor (Adults):** Glioblastoma Multiforme (Astrocytoma Grade 4). * **Most common brain tumor (Overall):** Metastasis (usually multiple, at the grey-white junction) [3]. * **Most common site for childhood tumors:** Infratentorial (Cerebellum/Brainstem). * **Most common site for adult tumors:** Supratentorial (Cerebral hemispheres). * **Molecular Marker:** IDH mutation status is now the most critical prognostic factor for classifying astrocytomas. **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. 1310-1311. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1317-1318.

Question 58: Which of the following is typically seen in Alzheimer disease?

A. Neurofibrillary tangles
B. Neuritic plaques (Correct Answer)
C. Pick's protein
D. Amyloid angiopathy

Explanation: **Explanation:** Alzheimer Disease (AD) is the most common cause of dementia in the elderly, characterized by the accumulation of specific protein aggregates [1]. While multiple pathological features exist, **Neuritic (Senile) Plaques** are considered a hallmark diagnostic feature. **1. Why Neuritic Plaques are the correct answer:** Neuritic plaques are extracellular deposits consisting of a central core of **Amyloid-beta (Aβ)** protein surrounded by dystrophic neurites (degenerated axonal or dendritic processes), reactive astrocytes, and microglia [2]. In the context of NEET-PG, these are the classic extracellular lesions used to stage the severity of AD (Braak staging). **2. Analysis of Incorrect Options:** * **Neurofibrillary Tangles (NFTs):** These are intracellular bundles of hyperphosphorylated **Tau protein**. While they are a key feature of AD, they are also found in other neurodegenerative diseases (tauopathies) [1]. * **Pick’s Protein (Pick Bodies):** These are round, silver-staining cytoplasmic inclusions of Tau protein characteristic of **Frontotemporal Dementia (Pick’s Disease)**, not Alzheimer’s [3]. * **Amyloid Angiopathy:** This refers to Aβ deposition in the walls of cerebral blood vessels. While frequently associated with AD (found in approx. 80-90% of cases), it is a vascular complication rather than the primary diagnostic parenchymal lesion [1]. **Clinical Pearls for NEET-PG:** * **Genetics:** Early-onset AD is linked to mutations in **APP** (Chr 21), **Presenilin 1** (Chr 14), and **Presenilin 2** (Chr 1). Late-onset is associated with the **ApoE4** allele. * **Hirano Bodies:** Eosinophilic, actin-rich inclusions found in the hippocampus of AD patients. * **Gross Pathology:** Symmetrical cortical atrophy, compensatory ventricular enlargement (**Hydrocephalus ex-vacuo**), and widening of sulci with narrowing of gyri [3]. * **Biochemical Change:** Significant decrease in **Acetylcholine** levels due to loss of neurons in the Nucleus Basalis of Meynert [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1294. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 721-722. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1294-1295.

Question 59: A 41-year-old woman presents with a 4-month history of diminished hearing. Physical examination reveals decreased hearing in the left ear, and the Weber tuning fork test lateralizes to the right ear. A head MRI shows a sharply circumscribed, 4-cm mass adjacent to the left pons extending toward the left inferior cerebellar hemisphere, with a smaller 1-cm lesion in a similar location on the right. Family screening identifies a similarly affected 38-year-old sibling. An inherited mutation involving which of the following genes is most likely to be present in this patient?

A. NF2 (Correct Answer)
B. TP53
C. PTCH
D. TSC1

Explanation: ### Explanation **Correct Option: A. NF2** The clinical presentation describes a classic case of **Neurofibromatosis Type 2 (NF2)**. The patient has **bilateral vestibular schwannomas** (acoustic neuromas), indicated by the MRI findings of masses at the cerebellopontine angle (CPA) and the clinical finding of sensorineural hearing loss [1]. The presence of bilateral vestibular schwannomas is pathognomonic for NF2 [1], [2]. This is an autosomal dominant condition caused by a mutation in the **NF2 gene** located on **chromosome 22q12**, which encodes the protein **Merlin** (also known as Schwannomin). Merlin acts as a tumor suppressor by regulating cell-to-cell adhesion and cytoskeleton dynamics. **Incorrect Options:** * **B. TP53:** Mutations in this gene (chromosome 17p) lead to **Li-Fraumeni Syndrome**, characterized by a predisposition to sarcomas, breast cancer, leukemia, and adrenal cortical carcinomas, rather than bilateral schwannomas. * **C. PTCH:** Mutations in the *Patched* gene (chromosome 9q) are associated with **Gorlin Syndrome** (Nevoid Basal Cell Carcinoma Syndrome), which presents with multiple basal cell carcinomas, odontogenic keratocysts, and medulloblastomas. * **D. TSC1:** Mutations in *TSC1* (Hamartin) or *TSC2* (Tuberin) cause **Tuberous Sclerosis**, characterized by cortical tubers, subependymal giant cell astrocytomas (SEGA), facial angiofibromas, and renal angiomyolipomas [3]. **Clinical Pearls for NEET-PG:** * **NF2 Mnemonic:** "22" — Gene on chromosome **22**, affects **2** ears (bilateral schwannomas), and **2** eyes (juvenile posterior subcapsular lenticular opacities). * **Associated Tumors in NF2:** Remember the mnemonic **MISME**: **M**ultiple **I**ntracranial **S**chwannomas, **M**eningiomas, and **E**pendymomas (especially of the spinal cord) [1]. * **Histology of Schwannoma:** Look for **Antoni A** (dense cellularity with Verocay bodies) and **Antoni B** (loose, myxoid areas) patterns. S100 positivity is a key IHC marker. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 727-728. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1248-1249. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1318-1319.

Question 60: Senile plaques in Alzheimer's disease are rich in which component?

A. Amyloid (Correct Answer)
B. Tau protein
C. Apolipoprotein E
D. Neuroglia

Explanation: **Explanation:** Alzheimer’s Disease (AD) is characterized by two hallmark pathological findings: **Neuritic (Senile) plaques** and **Neurofibrillary tangles (NFTs)** [1]. **1. Why Amyloid is correct:** Senile plaques are extracellular deposits found in the neuropil. The core of these plaques is primarily composed of **Amyloid-beta (Aβ) peptide**, which is derived from the abnormal cleavage of Amyloid Precursor Protein (APP) by β-secretase and γ-secretase [1], [2]. These Aβ fibrils aggregate into insoluble sheets, forming the "rich" central core of the plaque [1]. **2. Why other options are incorrect:** * **Tau protein:** This is the primary component of **Neurofibrillary Tangles (NFTs)**, which are *intracellular* inclusions [1]. While tau is central to AD pathogenesis, it is not the main constituent of senile plaques. * **Apolipoprotein E (ApoE):** While the ε4 allele of ApoE is a major genetic risk factor for sporadic AD and can be found associated with plaques, it is a minor component compared to the bulk of Aβ. * **Neuroglia:** Reactive astrocytes and microglia are often found at the *periphery* of senile plaques as part of the inflammatory response, but they do not form the plaque's structural core. **High-Yield Clinical Pearls for NEET-PG:** * **Staining:** Amyloid in plaques is best visualized using **Congo Red** (showing apple-green birefringence under polarized light) or **Silver stains** (Bielschowsky) [1]. * **Location:** Senile plaques appear first in the hippocampus and amygdala before involving the neocortex. * **Genetics:** Mutations in **APP (Chr 21)**, **Presenilin 1 (Chr 14)**, and **Presenilin 2 (Chr 1)** lead to early-onset familial AD by increasing Aβ production [2]. * **Hirano Bodies:** Another AD finding; these are actin-rich, eosinophilic rod-like inclusions in hippocampal pyramidal cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1294. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1290-1292.

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