FMGE 2025 — Pathology

Q: What is the earliest time after myocardial infarction when triphenyl tetrazolium chloride (TTC) staining can detect infarcted tissue?

3 hours. ***3 hours***- **TTC (Triphenyl Tetrazolium Chloride)** staining detects viable myocardium by reacting with **lactate dehydrogenase** (LDH) and other mitochondrial dehydrogenases, resulting in a **brick-red color** [1].- Necrotic myocardium loses these enzymes, preventing the color change and leaving the infarcted tissue **pale yellow**; this process usually takes at least **3 hours** post-occlusion to be grossly detectable [1].*1 hour*- The time interval is too short for the complete depletion of **dehydrogenases** from the infarcted cells necessary to prevent the TTC reaction and produce a visually distinct **pale area**.- Reliable gross detection by TTC requires cellular necrosis advanced enough to cause enzyme leakage, which typically requires more time than 1 hour [1].*30 minutes*- At 30 minutes post-MI, myocardial damage is often still in the stage of **reversible injury**, and the cell membranes and internal enzyme systems are still largely intact [2].- This limited timeframe does not allow for sufficient enzyme leakage or inactivation required to produce a clear negative (unstained) reaction with the **tetrazolium salt** [1].*Immediately*- Immediate staining will show uniformly red tissue because sufficient time has not passed for the irreversible cell injury (**necrosis**) and subsequent loss of intrinsic **enzymatic activity**.- Myocardium must undergo several hours of severe ischemia and necrosis before the gross chemical findings detected by **TTC** become apparent [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552. [Practice more Pathology PYQs on OnCourse]

38 Previous Year Questions with Answers & Explanations

Questions

A child diagnosed with von Willebrand disease requires an understanding of the role of von Willebrand factor (vWF). What does von Willebrand factor primarily combine with?

A male presents with a history of vestibular schwannoma and psammoma bodies in the brain. Which of the following is the most likely diagnosis?

What is the earliest time after myocardial infarction when triphenyl tetrazolium chloride (TTC) staining can detect infarcted tissue?

Which of the following is a change seen in irreversible cell injury?

Histopathological examination showed follicular cells with abundant pink eosinophilic cytoplasm WITHOUT nuclear grooves or ground-glass nuclei. This is most characteristic of?

Which of the following is not related to disease progression?

Which gene mutation is most commonly associated with Burkitt's lymphoma?

An elderly man presents with an ulcerative lesion at the inner canthus of his eye with pearly margins. On microscopic examination, it shows a palisading arrangement of cells. Identify the lesion:

A 50 year old female presented with a breast mass that was operated and the microscopic examination in given. What is the diagnosis?

Q10

The CSF findings in bacterial meningitis would include which of the following?

FMGE 2025 - Pathology FMGE Practice Questions and MCQs

Question 1: A child diagnosed with von Willebrand disease requires an understanding of the role of von Willebrand factor (vWF). What does von Willebrand factor primarily combine with?

A. Prothrombin
B. ADP
C. Glycoprotein Ib (Correct Answer)
D. Platelet factor 3

Explanation: ***Glycoprotein Ib***- vWF bridges exposed subendothelial **collagen** to the platelet surface receptor **Glycoprotein Ib (GPIb)**, which is crucial for initiating platelet **adhesion** during primary hemostasis [1], [2].- A deficiency in vWF (von Willebrand disease) or a defect in GPIb (Bernard-Soulier syndrome) impairs this initial binding step [1], [3].*Platelet factor 3*- Platelet factor 3 (PF3) refers to the **phospholipid surface** (cell membrane) of activated platelets, which serves as a necessary platform for the assembly of clotting factors (e.g., the **tenase** and **prothrombinase** complexes) in secondary hemostasis.- Although critical for clotting, PF3 does not represent the primary receptor that vWF binds to on the platelet surface.*ADP*- **Adenosine diphosphate (ADP)** is a chemical mediator released from platelet dense granules that acts to amplify platelet **activation** and promote **aggregation** (by activating P2Y12 and P2Y1 receptors) [1].- ADP is involved after initial adhesion and promotes platelet-platelet interactions (aggregation) via GP IIb/IIIa receptors, not the binding of vWF (adhesion) via GPIb [1], [3].*Prothrombin*- **Prothrombin (Factor II)** is a circulating zymogen that converts to thrombin (Factor IIa) in the common coagulation pathway, leading to the formation of **fibrin** (secondary hemostasis).- While vWF stabilizes **Factor VIII** (another coagulation factor), it does not primarily bind or activate Prothrombin; its main direct platelet interaction is with GPIb [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669.

Question 2: A male presents with a history of vestibular schwannoma and psammoma bodies in the brain. Which of the following is the most likely diagnosis?

A. Oligodendroglioma
B. Pilocytic astrocytoma
C. Meningioma (Correct Answer)
D. GBM (Glioblastoma Multiforme)

Explanation: Correct: Meningioma - The presence of **psammoma bodies** (calcified, laminated, concentric whorls) is a classic histological feature highly characteristic of meningiomas, particularly the meningothelial and transitional subtypes [1], [2]. - The association with a vestibular schwannoma (especially if bilateral) strongly suggests **Neurofibromatosis Type 2 (NF2)**, where patients frequently develop multiple meningiomas alongside bilateral vestibular schwannomas [1]. - This combination of findings makes meningioma the most likely diagnosis. *Incorrect: GBM (Glioblastoma Multiforme)* - This is a highly aggressive, grade IV astrocytoma characterized histologically by pseudopalisading necrosis and microvascular proliferation [3]. - GBM typically occurs in older adults and is not characterized by psammoma bodies or a direct association with vestibular schwannomas observed in NF2 [3], [4]. *Incorrect: Pilocytic astrocytoma* - This is generally a low-grade (Grade I) tumor, prominent in children and young adults, often presenting in the cerebellum [4]. - Histological hallmarks include the presence of Rosenthal fibers (thick, eosinophilic corkscrew fibers) and bipolar cells, distinct from psammoma bodies. *Incorrect: Oligodendroglioma* - Histologically, these tumors are known for calcification and a characteristic 'fried-egg' appearance (round nuclei with clear perinuclear halos) and delicate branching capillaries. - While they can calcify, their characteristic histology does not include psammoma bodies, and they are not typically linked to NF2 or vestibular schwannomas. **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. The Central Nervous System, pp. 1316-1317. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1310. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1319-1320.

Question 3: What is the earliest time after myocardial infarction when triphenyl tetrazolium chloride (TTC) staining can detect infarcted tissue?

A. 3 hours (Correct Answer)
B. 1 hour
C. 30 minutes
D. Immediately

Explanation: ***3 hours***- **TTC (Triphenyl Tetrazolium Chloride)** staining detects viable myocardium by reacting with **lactate dehydrogenase** (LDH) and other mitochondrial dehydrogenases, resulting in a **brick-red color** [1].- Necrotic myocardium loses these enzymes, preventing the color change and leaving the infarcted tissue **pale yellow**; this process usually takes at least **3 hours** post-occlusion to be grossly detectable [1].*1 hour*- The time interval is too short for the complete depletion of **dehydrogenases** from the infarcted cells necessary to prevent the TTC reaction and produce a visually distinct **pale area**.- Reliable gross detection by TTC requires cellular necrosis advanced enough to cause enzyme leakage, which typically requires more time than 1 hour [1].*30 minutes*- At 30 minutes post-MI, myocardial damage is often still in the stage of **reversible injury**, and the cell membranes and internal enzyme systems are still largely intact [2].- This limited timeframe does not allow for sufficient enzyme leakage or inactivation required to produce a clear negative (unstained) reaction with the **tetrazolium salt** [1].*Immediately*- Immediate staining will show uniformly red tissue because sufficient time has not passed for the irreversible cell injury (**necrosis**) and subsequent loss of intrinsic **enzymatic activity**.- Myocardium must undergo several hours of severe ischemia and necrosis before the gross chemical findings detected by **TTC** become apparent [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 552-554. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 552.

Question 4: Which of the following is a change seen in irreversible cell injury?

A. Amorphous density of mitochondria (Correct Answer)
B. Cellular Swelling
C. Bleb formation
D. Clumping of chromatin

Explanation: ***Amorphous density of mitochondria***- This refers to the formation of large, irregular, dense calcium deposits within the mitochondrial matrix, which is a classic morphological feature indicating irreparable damage to the organelle [1].- The presence of these **amorphous densities** signifies severe mitochondrial dysfunction, including the complete loss of inner membrane potential and irreversible failure of **oxidative phosphorylation**, committing the cell to necrosis [2].*Bleb formation*- Small, transient surface blebs are common manifestations of **reversible** cell injury resulting from alterations in the cytoskeleton due to ATP depletion [1].- While uncontrolled blebbing is a feature preceding plasma membrane rupture in necrosis, its simple occurrence is not exclusively tied to irreversible injury, unlike profound mitochondrial changes [4].*Clumping of chromatin*- This initial condensation of nuclear material is characteristic of **reversible** cell injury, often due to decreased ATP causing a decrease in nuclear components and an acidic intracellular environment.- This reversible change must progress to irreversible nuclear hallmarks like **pyknosis** (irreversible condensation) or karyorrhexis/karyolysis to confirm cell death [4].*Cellular Swelling*- **Cellular swelling** (or hydropic change) is the most common manifestation of **reversible** cell injury [4], resulting from the failure of the ATP-dependent **Na+/K+ pump** [3].- This failure leads to the influx and accumulation of intracellular sodium and water, a condition that can be reversed if oxygenation and ATP synthesis are restored [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 53-55. [2] 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. 102-103. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 56-57. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 53.

Question 5: Histopathological examination showed follicular cells with abundant pink eosinophilic cytoplasm WITHOUT nuclear grooves or ground-glass nuclei. This is most characteristic of?

A. Follicular CA (Correct Answer)
B. Papillary CA
C. Medullary CA
D. Anaplastic CA

Explanation: ***Follicular CA (Hürthle cell variant)*** - The description of **follicular cells with abundant pink eosinophilic cytoplasm** is characteristic of the **Hürthle cell variant** (also known as the oncocytic or oxyphil variant) of follicular thyroid carcinoma. - This **eosinophilic appearance** is due to the presence of numerous abnormal **mitochondria** within the cytoplasm of the tumor cells. - The **absence of nuclear features** (grooves, ground-glass nuclei) helps distinguish this from the Hürthle cell variant of papillary carcinoma [2], [3]. - Diagnosis requires evidence of **capsular or vascular invasion** to differentiate from Hürthle cell adenoma [1], [5]. *Papillary CA* - While papillary carcinoma can also have a **Hürthle cell variant**, it would show characteristic **nuclear changes** including **Orphan Annie eye nuclei** (ground-glass chromatin), **nuclear grooves**, and **intranuclear pseudoinclusions** [3], [4]. - The question specifically excludes these nuclear features, making follicular carcinoma more likely. - The classic variant shows papillary architecture with defining nuclear features [3]. *Medullary CA* - This tumor originates from **parafollicular C-cells** (not follicular cells) and is characterized by the presence of **amyloid deposits** (derived from calcitonin) in the stroma [4], [5]. - The tumor cells are usually spindle or polygonal and lack the described eosinophilic follicular cell morphology. - Positive for **calcitonin** and **CEA** on immunohistochemistry. *Anaplastic CA* - Anaplastic carcinoma is highly undifferentiated and consists of bizarre, **highly pleomorphic cells**, including spindle cells and **multinucleated giant cells** [4]. - It is characterized by extensive necrosis, high mitotic activity, and lacks the structural and cellular uniformity of differentiated follicular tumors. - Shows aggressive invasive behavior with poor prognosis [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1100-1101. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, pp. 1099-1100. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Endocrine System, p. 1099. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 429-430. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 428-429.

Question 6: Which of the following is not related to disease progression?

A. Depth
B. Stage of Cancer
C. Duration (Correct Answer)
D. Site

Explanation: ***Duration*** - While a history of a long-standing lesion that changes is important for diagnosis, the absolute duration of its existence is not a primary prognostic factor used in staging skin cancers like melanoma. - Prognosis is determined by objective pathological features like depth and evidence of spread [3], not how long the patient reports having had the lesion. *Depth* - The **vertical depth of invasion** (e.g., **Breslow depth** for melanoma) is the single most important prognostic factor for primary cutaneous tumors [2]. - A greater depth directly correlates with an increased risk of **metastasis** and poorer survival rates, thus being a key measure of disease progression [4]. *Site* - The **病理部位 (anatomical location)** of the primary tumor is a known independent prognostic factor for melanoma. - Tumors located on the head, neck, trunk, hands, or feet often have a worse prognosis than those on the extremities. *Stage of Cancer* - The **stage** of cancer, determined by systems like **TNM** (Tumor, Node, Metastasis), is a comprehensive summary of the disease's extent [1]. - It is the definitive measure of disease progression, integrating primary tumor characteristics, lymph node involvement, and distant metastasis to guide treatment and predict outcome [1]. **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. 236-237. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 650-651. [3] 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. 36-37. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1151-1152.

Question 7: Which gene mutation is most commonly associated with Burkitt's lymphoma?

A. p53
B. Rb
C. p21
D. C-myc (Correct Answer)

Explanation: ***C-myc*** - Burkitt's lymphoma is characterized by the **t(8;14) translocation** in 80% of cases [1] - This translocation juxtaposes the **C-myc oncogene (chromosome 8)** with the **immunoglobulin heavy chain locus (chromosome 14)** [1] - Results in **constitutive overexpression of C-myc**, driving uncontrolled cell proliferation [1] - This is a **pathognomonic molecular feature** of Burkitt's lymphoma [1] - Variants include t(2;8) and t(8;22) involving immunoglobulin light chain loci [1] *p53* - Tumor suppressor gene involved in many cancers - Not the characteristic mutation defining Burkitt's lymphoma - May be involved in disease progression but not the hallmark feature *Rb* - Retinoblastoma gene, another tumor suppressor - Associated with retinoblastoma and osteosarcoma - Not characteristic of Burkitt's lymphoma *p21* - Cyclin-dependent kinase inhibitor (CDKN1A) - Involved in cell cycle regulation - Not the defining genetic alteration in Burkitt's lymphoma **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325.

Question 8: An elderly man presents with an ulcerative lesion at the inner canthus of his eye with pearly margins. On microscopic examination, it shows a palisading arrangement of cells. Identify the lesion:

A. Melanocytic melanoma
B. Basal cell carcinoma (Correct Answer)
C. Keratoacanthoma
D. Squamous cell carcinoma

Explanation: ***Basal cell carcinoma*** - The clinical presentation of an ulcerative lesion with **pearly margins**, especially in a sun-exposed area like the inner canthus, is a classic sign of nodular **basal cell carcinoma (BCC)** [1]. - Histologically, the pathognomonic feature is nests of **basaloid cells** with a **peripheral palisading** arrangement, as described and shown in the image [1], [2]. *Squamous cell carcinoma* - **Squamous cell carcinoma (SCC)** typically presents as a scaly, crusted, or erythematous lesion and usually lacks the characteristic **pearly** borders seen in BCC [2]. - Microscopically, SCC is characterized by invasive nests of atypical keratinocytes, often with the formation of **keratin pearls** and intercellular bridges, not palisading [2]. *Keratoacanthoma* - A **keratoacanthoma** is a rapidly growing, dome-shaped tumor with a central, **keratin-filled crater**, which is a distinct clinical feature not described here [2]. - Histologically, it resembles a well-differentiated SCC and does not show the basaloid cells with peripheral palisading characteristic of BCC [2]. *Melanocytic melanoma* - **Melanoma** is a malignancy of melanocytes, typically presenting as a pigmented lesion following the **ABCDE** criteria (Asymmetry, Border irregularity, Color variation, Diameter >6mm, Evolving). - Histology shows atypical melanocytes, not basaloid cells. The cells may contain melanin pigment and have prominent nucleoli, which differs from the microscopic findings in this case. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Skin, pp. 1158-1160. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Disorders Involving Inflammatory And Haemopoietic Cells, pp. 643-645.

Question 9: A 50 year old female presented with a breast mass that was operated and the microscopic examination in given. What is the diagnosis?

A. Mucinous carcinoma breast (Correct Answer)
B. Medullary carcinoma
C. Lobular carcinoma breast
D. Phyllodes tumour

Explanation: ***Mucinous carcinoma breast*** - The micrograph shows clusters and nests of relatively uniform tumor cells floating in abundant extracellular **mucin**, which is the hallmark of this diagnosis. - This subtype of invasive ductal carcinoma is typically well-differentiated, hormone receptor-positive (**ER/PR positive**), and carries a more favorable prognosis than conventional invasive ductal carcinoma. *Lobular carcinoma breast* - This carcinoma is characterized by small, discohesive tumor cells infiltrating the stroma individually or in a **single-file** or **“Indian file”** pattern, which is not seen here [1]. - A key feature is the loss of **E-cadherin** expression, leading to the discohesive nature of the cells [3]. *Medullary carcinoma* - Histologically, this tumor presents as poorly differentiated cells arranged in solid, **syncytial sheets** with a prominent **lymphoplasmacytic infiltrate** [2]. - The image lacks both the syncytial growth pattern and the dense inflammatory background characteristic of medullary carcinoma [2]. *Phyllodes tumour* - This is a biphasic **fibroepithelial tumor**, characterized by a hypercellular stromal component and an epithelial component arranged in a **leaf-like** (phyllodes) architecture. - The defining feature is the proliferating stroma, whereas the image shows a carcinoma defined by its epithelial cells and extracellular mucin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 454-455. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 455-456. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Breast, pp. 1068-1069.

Question 10: The CSF findings in bacterial meningitis would include which of the following?

A. Elevated WBC count with normal glucose
B. Decreased protein and elevated glucose
C. Normal white blood cell count
D. Elevated protein and decreased glucose (Correct Answer)

Explanation: **Elevated protein and decreased glucose (Correct)** - The inflammation and damage to the **blood-brain barrier** during bacterial infection allow large plasma proteins to leak into the CSF, causing **elevated protein** levels [1]. - Bacteria rapidly metabolize CSF **glucose**, or transport into the CSF is impaired, resulting in characteristically **low (decreased) glucose** levels (typically <40 mg/dL or CSF:blood glucose ratio <0.4) [1]. - This combination (high protein + low glucose + neutrophilic pleocytosis) forms the **classic CSF triad** of bacterial meningitis [1]. *Normal white blood cell count (Incorrect)* - Bacterial meningitis triggers a marked inflammatory response, resulting in severe CSF **pleocytosis** (high WBC count), often exceeding 1000 cells/mm³ [1]. - The primary cell type is usually **neutrophils** (**polymorphonuclear leukocytes**), which rules out a normal WBC count [1]. *Decreased protein and elevated glucose (Incorrect)* - CSF protein is typically **elevated** in bacterial meningitis due to compromised blood-brain barrier integrity, making 'decreased protein' incorrect [1]. - **Elevated glucose** is contrary to the hallmark finding of severe hypoglycemia (low glucose) caused by bacterial consumption and impaired glucose transport [1]. *Elevated WBC count with normal glucose (Incorrect)* - Although CSF **WBC count is elevated** (pleocytosis), a **normal glucose** level is incompatible with established bacterial meningitis, where glucose is characteristically low [1]. - Elevated WBC with normal glucose is more suggestive of conditions like early **viral meningitis** or some non-infectious inflammatory disorders [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 708-709. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1274-1275.