Neuropathology — MCQs

A patient presents with severe headaches, develops convulsions, and dies. Autopsy reveals the brain has a "Swiss cheese" appearance due to numerous small cysts containing milky fluid. Microscopic examination shows a scolex with hooklets within one of these cysts. What is the causative agent for this disease?

Q48Easy

Neurofibrillary tangles, senile plaques, and amyloid angiopathy are associated with which of the following causes of dementia?

Q49Medium

Which of the following statements is not true about Glioblastoma?

Q50Medium

All of the following are true of watershed infarcts except?

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 41: What is the pathological change observed in the brain in cerebral malaria?

A. Cerebral edema
B. Microvascular occlusion (Correct Answer)
C. Increased intracranial pressure
D. Space occupying lesion

Explanation: **Explanation:** The hallmark pathological feature of cerebral malaria (caused by *Plasmodium falciparum*) is **microvascular occlusion**. This occurs due to a process called **sequestration**. Infected erythrocytes express *P. falciparum* erythrocyte membrane protein 1 (PfEMP-1), which binds to endothelial receptors like **ICAM-1** and **CD36**. This leads to cytoadherence, "rosetting" (binding to uninfected RBCs), and "clumping" (binding to platelets), effectively clogging the cerebral capillaries and venules. This mechanical obstruction leads to hypoxia, breakdown of the blood-brain barrier, and the formation of **Durck’s granulomas** (perivascular microglial nodules surrounding a small focus of necrosis). **Analysis of Options:** * **Option B (Correct):** As explained, the sequestration of parasitized RBCs in the microvasculature is the primary pathological event leading to the clinical manifestations of cerebral malaria [1]. * **Option A & C (Incorrect):** While cerebral edema and increased intracranial pressure (ICP) are often *consequences* of the microvascular obstruction and inflammatory response, they are secondary physiological changes rather than the primary pathological mechanism defining the disease. * **Option D (Incorrect):** Cerebral malaria is a diffuse encephalopathy. It does not present as a localized space-occupying lesion (like a tuberculoma or abscess). **High-Yield Pearls for NEET-PG:** * **Durck’s Granulomas:** The pathognomonic microscopic finding in cerebral malaria. * **PfEMP-1:** The key protein responsible for cytoadherence. * **Malaria Pigment:** Hemozoin (iron-containing pigment) is often seen within the sequestered RBCs and Kupffer cells. * **Clinical Definition:** Coma (Glasgow Coma Scale <11) in the presence of *P. falciparum* parasitemia, after excluding other causes of encephalopathy [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1274-1275.

Question 42: Inclusions in oligodendrocytes are a characteristic feature of which condition?

A. Creutzfeldt-Jakob disease
B. Chronic inflammatory demyelinating polyneuropathy (CIDP)
C. Herpes simplex virus (HSV) encephalitis
D. Progressive multifocal leukoencephalopathy (PML) (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Progressive multifocal leukoencephalopathy (PML)** PML is a demyelinating disease caused by the reactivation of the **JC virus** (a polyomavirus) in immunocompromised patients (e.g., HIV/AIDS, transplant recipients) [1]. The virus selectively infects **oligodendrocytes**, the myelin-producing cells of the CNS, as their nuclei may harbor viral inclusions [4]. Histologically, this leads to the pathognomonic finding of **ground-glass viral inclusions** within the enlarged nuclei of oligodendrocytes [1]. Additionally, "bizarre" reactive astrocytes are often seen. **Analysis of Incorrect Options:** * **A. Creutzfeldt-Jakob disease:** This is a prion disease characterized by **spongiform encephalopathy** (vacuolation of the neuropil and neurons) [2]. It does not feature viral inclusions [3]. * **B. CIDP:** This is a chronic autoimmune-mediated demyelinating disease of the **Peripheral Nervous System (PNS)**. It involves Schwann cells, not oligodendrocytes, and is characterized by "onion bulb" formations due to repetitive demyelination and remyelination. * **C. HSV Encephalitis:** While HSV produces inclusions, they are typically **Cowdry Type A** intranuclear inclusions found in **neurons** and glia, primarily localized to the temporal lobes. **NEET-PG High-Yield Pearls:** * **JC Virus:** "John Cunningham" virus; targets oligodendrocytes leading to demyelination [1]. * **Imaging:** PML presents as non-enhancing, multifocal white matter lesions on MRI (T2/FLAIR hyperintensity) without mass effect. * **Subacute Sclerosing Panencephalitis (SSPE):** Caused by the Measles virus; features inclusions in *both* neurons (Cowdry A) and oligodendrocytes (Wuerth-Grünthal). * **Negri Bodies:** Eosinophilic cytoplasmic inclusions in pyramidal neurons of the hippocampus and Purkinje cells of the cerebellum (Pathognomonic for **Rabies**). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1280-1281. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1284-1286. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 712-713. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256.

Question 43: Porencephaly is due to what cause?

A. Dandy-Walker syndrome
B. Cerebral infarction (Correct Answer)
C. Fetal alcohol syndrome
D. All of the above

Explanation: **Explanation:** **Porencephaly** refers to the presence of smooth-walled, fluid-filled cysts or cavities within the cerebral hemispheres that typically communicate with the ventricular system or the subarachnoid space. **1. Why Cerebral Infarction is correct:** The primary underlying mechanism of porencephaly is an **ischemic insult** or **cerebral infarction** occurring during late fetal life or the early neonatal period [1]. Unlike adults, where infarction leads to a glial scar, the immature fetal brain undergoes **liquefactive necrosis** without significant gliosis [2]. This leads to the dissolution of brain tissue and the formation of a permanent cystic cavity (a process often termed "encephalomalacia") [2]. **2. Why other options are incorrect:** * **Dandy-Walker Syndrome:** This is a congenital malformation of the cerebellum characterized by agenesis of the cerebellar vermis, cystic dilation of the fourth ventricle, and an enlarged posterior fossa. It does not typically cause parenchymal porencephalic cysts [1]. * **Fetal Alcohol Syndrome (FAS):** FAS is associated with microcephaly, holoprosencephaly, and neuronal migration defects (like heterotopias), but it is not a primary cause of porencephaly. **3. NEET-PG High-Yield Pearls:** * **Schizencephaly vs. Porencephaly:** Schizencephaly is a developmental cleft (lined by gray matter) due to migration failure, whereas Porencephaly is an acquired destructive lesion (lined by white matter/gliosis) due to vascular insult [2]. * **Hydranencephaly:** This is the most extreme form of porencephaly where the cerebral hemispheres are almost entirely replaced by a CSF-filled sac, usually due to bilateral occlusion of the internal carotid arteries. * **Genetic Link:** Mutations in the **COL4A1** gene are a known hereditary cause of small vessel fragility leading to porencephaly. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1260-1261. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 706-707.

Question 44: Which receptor on the neuronal membrane is implicated in the development of glioma?

A. CD-117
B. CD-133 (Correct Answer)
C. CD-33
D. CD-45

Explanation: **Explanation:** The correct answer is **CD-133**. **Why CD-133 is correct:** CD-133 (also known as Prominin-1) is a pentaspan transmembrane glycoprotein that serves as a hallmark marker for **Cancer Stem Cells (CSCs)** in various tumors, most notably **Gliomas**. In the context of neuro-oncology, CD-133+ cells within a tumor mass are considered "brain tumor-initiating cells." These cells possess the capacity for self-renewal and multilineage differentiation, contributing to the initiation, progression, and high rate of recurrence in high-grade gliomas like Glioblastoma Multiforme (GBM). **Analysis of Incorrect Options:** * **CD-117 (c-KIT):** This is a tyrosine kinase receptor primarily associated with Gastrointestinal Stromal Tumors (GIST), Mastocytosis, and Seminomas. * **CD-33:** This is a myeloid-specific marker. It is highly expressed on the surface of blast cells in **Acute Myeloid Leukemia (AML)** and is the target for the drug Gemtuzumab ozogamicin [1]. * **CD-45:** Known as the **Leukocyte Common Antigen (LCA)**, it is expressed on all hematopoietic cells (except mature RBCs). It is used in IHC to differentiate lymphomas from carcinomas or sarcomas. **High-Yield Clinical Pearls for NEET-PG:** * **GFAP (Glial Fibrillary Acidic Protein):** The most common IHC marker used to identify tumors of glial origin (Astrocytomas, Ependymomas) [2]. * **IDH-1 Mutation:** A critical prognostic marker in the WHO classification of CNS tumors; IDH-mutant gliomas generally have a better prognosis than IDH-wildtype [2]. * **1p/19q Co-deletion:** The molecular signature for **Oligodendroglioma** [2]. * **Ki-67:** A proliferation index marker; higher values correlate with higher tumor grade and aggressiveness. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 312-313. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1308-1312.

Question 45: All of the following are congenital myopathies EXCEPT:

A. Nemaline myopathy
B. Central core disease
C. Centronuclear myopathy
D. Mitochondrial myopathy (Correct Answer)

Explanation: **Explanation:** The distinction between **Congenital Myopathies** and other muscle disorders is a high-yield topic in NEET-PG. Congenital myopathies are a specific group of genetic muscle disorders characterized by **structural abnormalities** within the muscle fibers, typically presenting at birth with hypotonia ("floppy infant syndrome") and static or slowly progressive weakness [1]. **Why Mitochondrial Myopathy is the correct answer:** While mitochondrial myopathies are genetic, they are classified as **Metabolic Myopathies**, not congenital myopathies. They are caused by mutations in mitochondrial DNA (mtDNA) or nuclear DNA encoding mitochondrial proteins [1]. Their hallmark is impaired oxidative phosphorylation, leading to multi-system involvement (e.g., Kearns-Sayre syndrome, MELAS). **Analysis of Incorrect Options:** * **Nemaline Myopathy:** The most common congenital myopathy. It is characterized by the presence of **"Nemaline rods"** (thread-like structures) composed of ̑-actinin, visible on Gomori trichrome stain. * **Central Core Disease:** Characterized by pale, well-demarcated "cores" in Type 1 fibers that lack oxidative enzyme activity. It is strongly associated with mutations in the **RYR1 gene** and carries a high risk of **Malignant Hyperthermia**. * **Centronuclear Myopathy:** Defined by the presence of nuclei located in the center of the muscle fiber (resembling fetal myotubes) rather than the periphery. The most severe form is the X-linked **Myotubular Myopathy**. **NEET-PG High-Yield Pearls:** * **Stain of Choice:** Gomori Trichrome is essential for identifying rods (Nemaline) and ragged red fibers (Mitochondrial). * **Mitochondrial Hallmark:** "Ragged Red Fibers" on biopsy and "Parking lot" inclusions on Electron Microscopy. * **Clinical Clue:** If a question mentions a child with hypotonia and a family history of anesthesia complications, think **Central Core Disease** [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1247-1248.

Question 46: Which of the following is the characteristic pathological feature of Parkinson's disease?

A. Lewy bodies (Correct Answer)
B. Babes nodule
C. Neurofibrillary tangle
D. Negri bodies

Explanation: **Explanation:** **Parkinson’s Disease (PD)** is a chronic neurodegenerative disorder characterized by the loss of dopaminergic neurons in the **substantia nigra pars compacta** [3]. 1. **Why Lewy Bodies are correct:** The hallmark pathological feature of PD is the presence of **Lewy bodies** [1]. These are eosinophilic, round, intracytoplasmic inclusions found within the surviving neurons [2]. Their primary component is **alpha-synuclein**, a protein that undergoes misfolding and aggregation [1]. On microscopy, they often show a dense core with a pale peripheral halo. 2. **Why other options are incorrect:** * **Babes nodules:** These are clusters of microglia (microglial nodules) found in the brain of patients with **Rabies**. * **Neurofibrillary tangles (NFTs):** These are intracellular aggregates of hyperphosphorylated **tau protein**, characteristic of **Alzheimer’s disease** [4]. * **Negri bodies:** These are eosinophilic, sharply outlined cytoplasmic inclusions found specifically in the pyramidal cells of the hippocampus and Purkinje cells of the cerebellum in **Rabies**. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Lewy bodies in PD are primarily found in the **substantia nigra** [1]. If Lewy bodies are found extensively in the **cerebral cortex** early in the disease, the diagnosis is **Lewy Body Dementia (LBD)** [2]. * **Clinical Triad:** Resting tremor ("pill-rolling"), bradykinesia, and "cogwheel" rigidity. * **Stain:** Alpha-synuclein immunohistochemistry is the most sensitive method to identify Lewy bodies [2]. * **Depigmentation:** Macroscopically, there is a visible loss of pigment (melanin) in the substantia nigra and locus coeruleus [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1296-1297. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1297-1298. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 723-724. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 719-720.

Question 47: A patient presents with severe headaches, develops convulsions, and dies. Autopsy reveals the brain has a "Swiss cheese" appearance due to numerous small cysts containing milky fluid. Microscopic examination shows a scolex with hooklets within one of these cysts. What is the causative agent for this disease?

A. Taenia saginata
B. Taenia solium (Correct Answer)
C. Diphyllobothrium latum
D. Echinococcus granulosa

Explanation: **Explanation:** The clinical presentation and autopsy findings are characteristic of **Neurocysticercosis (NCC)**, the most common parasitic infection of the central nervous system worldwide. **1. Why Taenia solium is correct:** Neurocysticercosis is caused by the ingestion of **eggs** of *Taenia solium* (pork tapeworm) through contaminated food or water (fecal-oral route) [2]. Once ingested, the oncospheres hatch, penetrate the intestinal wall, and hematogenously disseminate to the brain [1]. Here, they form **Cysticercus cellulosae**. The "Swiss cheese" appearance refers to the presence of multiple small, fluid-filled cysts within the brain parenchyma. The pathognomonic microscopic finding is the presence of a **scolex with four suckers and a rostellum of hooklets** within the cyst. **2. Why the other options are incorrect:** * **Taenia saginata:** Known as the beef tapeworm. Humans are definitive hosts, but *T. saginata* does **not** cause cysticercosis in humans because the eggs are not infectious to man. * **Diphyllobothrium latum:** The fish tapeworm. It primarily causes Vitamin B12 deficiency (megaloblastic anemia) and does not form parenchymal brain cysts. * **Echinococcus granulosus:** Causes **Hydatid disease** [2]. While it can affect the brain, it typically forms a **single, large, unilocular cyst** (often with daughter cysts) rather than the multiple small "Swiss cheese" cysts seen in NCC. **Clinical Pearls for NEET-PG:** * **Most common presentation:** New-onset seizures/convulsions in an adult. * **Imaging (CT/MRI):** Shows stages—Vesicular (viable scolex, "hole-with-dot" appearance), Colloidal (ring enhancement), and Calcified (granuloma). * **Treatment:** Albendazole or Praziquantel (administered with corticosteroids to reduce inflammation from dying larvae). * **Key Distinction:** Ingesting **larvae** (undercooked pork) causes intestinal Taeniasis; ingesting **eggs** causes Cysticercosis [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1274-1275. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 403-404.

Question 48: Neurofibrillary tangles, senile plaques, and amyloid angiopathy are associated with which of the following causes of dementia?

A. Creutzfeldt-Jakob disease
B. Vascular dementia
C. Niemann-Pick disease
D. Alzheimer's disease (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Alzheimer's disease** Alzheimer’s disease (AD) is the most common cause of dementia in the elderly [1]. The diagnosis is characterized by three hallmark histopathological features: 1. **Neurofibrillary Tangles (NFTs):** Intracellular inclusions made of hyperphosphorylated **tau protein** [1], [2]. 2. **Senile (Neuritic) Plaques:** Extracellular deposits consisting of a central core of **Amyloid-beta (Aβ)** protein surrounded by dystrophic neurites [1], [2]. 3. **Amyloid Angiopathy:** Deposition of Aβ protein within the walls of cerebral blood vessels, increasing the risk of lobar hemorrhage [2]. --- ### Why the other options are incorrect: * **A. Creutzfeldt-Jakob disease:** This is a prion disease characterized by **spongiform encephalopathy** (vacuolation of neurons and gray matter) and the presence of PrPSc protein, not amyloid plaques or tangles. * **B. Vascular dementia:** This results from multiple cortical or subcortical infarcts (**multi-infarct dementia**) [1]. The pathology shows areas of necrosis, gliosis, and atherosclerosis rather than proteinaceous tangles. * **C. Niemann-Pick disease:** This is a lysosomal storage disorder. Type C can present with dementia, but the pathology involves the accumulation of **sphingomyelin** and cholesterol within cells, leading to "foam cells." --- ### 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 associated with the **ApoE4** allele. * **Hirano Bodies:** Eosinophilic, rod-like inclusions (actin) often 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. * **Down Syndrome:** Patients with Trisomy 21 develop AD-like pathology early (by age 40) because the APP gene is located on chromosome 21. **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.

Question 49: Which of the following statements is not true about Glioblastoma?

A. Also known as Butterfly tumor
B. Frontal lobe of the brain is a common location
C. It belongs to WHO grade 3 Astrocytoma (Correct Answer)
D. Serpentine necrosis and glomeruloid bodies are characteristic features

Explanation: **Explanation:** **1. Why Option C is the Correct (False) Statement:** Glioblastoma (GBM) is classified as a **WHO Grade 4** tumor, not Grade 3. It is the most aggressive and common primary malignant brain tumor in adults. According to the updated WHO classification, Grade 3 astrocytomas are termed "Anaplastic Astrocytomas." The hallmark that upgrades an astrocytoma to Grade 4 (GBM) is the presence of **necrosis** and/or **microvascular proliferation** [1]. **2. Analysis of Other Options:** * **Option A (Butterfly Tumor):** GBM frequently crosses the midline via the **corpus callosum**, involving both cerebral hemispheres. On imaging, this symmetrical spread resembles the wings of a butterfly, hence the name "Butterfly Glioma." * **Option B (Frontal Lobe):** While GBM can occur anywhere in the CNS, the **frontal and temporal lobes** are the most common supratentorial locations. * **Option D (Characteristic Features):** Histopathology of GBM is classic for **Serpentine (palisading) necrosis**, where areas of dead tissue are surrounded by crowded tumor cells, and **Glomeruloid bodies**, which are tufts of multilayered, proliferating endothelial cells resembling renal glomeruli [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Molecular Marker:** IDH-wildtype status is now a defining feature of primary Glioblastoma in the latest WHO classification. * **Age Group:** Most common in the 5th to 7th decades of life [2]. * **Genetic Associations:** Often associated with **EGFR amplification** and PTEN mutations [2]. * **Prognosis:** Poor, despite aggressive surgery, radiotherapy, and chemotherapy (Temozolomide) [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1310-1311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1308-1310.

Question 50: All of the following are true of watershed infarcts except?

A. Seen at the junction of major cerebral arteries
B. Seen in subcortical white matter (Correct Answer)
C. Cerebral vasospasm may cause it
D. Associated with hypoxic-ischemic encephalopathy

Explanation: **Explanation:** **Watershed (Border Zone) Infarcts** occur at the most distal reaches of the arterial blood supply, where the territories of two major cerebral arteries meet [1]. These areas are most vulnerable to reductions in perfusion pressure. **1. Why Option B is the Correct Answer (The False Statement):** Watershed infarcts primarily affect the **cerebral cortex**, specifically the wedge-shaped areas at the junctions of major arteries. While deep watershed zones exist (near the basal ganglia), the classic "watershed" description refers to the **cortical border zones**. Subcortical white matter is more typically associated with lacunar infarcts (due to small vessel disease) rather than classic global hypotensive watershed events [2]. **2. Analysis of Other Options:** * **Option A:** This is a defining feature. The most common site is the border between the **Anterior Cerebral Artery (ACA) and Middle Cerebral Artery (MCA)**. * **Option C:** Any condition that severely reduces blood flow can trigger these infarcts. While systemic hypotension (e.g., cardiac arrest) is the most common cause, severe **cerebral vasospasm** (often post-subarachnoid hemorrhage) can reduce distal perfusion enough to cause watershed ischemia [1]. * **Option D:** Watershed infarcts are a localized manifestation of **Hypoxic-Ischemic Encephalopathy (HIE)**. In HIE, global hypoperfusion leads to damage in the most metabolically active or hemodynamically vulnerable areas. **High-Yield Clinical Pearls for NEET-PG:** * **"Man-in-a-barrel" Syndrome:** A classic clinical presentation of ACA-MCA watershed infarcts, characterized by proximal arm and leg weakness with sparing of the face and distal extremities. * **Most Vulnerable Cells:** Purkinje cells of the cerebellum and Pyramidal cells of the Hippocampus (Sommer sector/CA1) are the first to die during global ischemia [1]. * **Morphology:** On gross examination, these appear as wedge-shaped areas of necrosis at the distal-most points of arterial territories. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 150-151. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1269-1270.

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