Neuropathology — MCQs

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 201: What is the most common location for diffuse axonal injuries?

A. Brain stem
B. Corpus callosum
C. Anterior one-third of the spinal cord
D. Junction of grey and white matter (Correct Answer)

Explanation: **Explanation:** **Diffuse Axonal Injury (DAI)** is a form of traumatic brain injury caused by high-velocity acceleration-deceleration or rotational forces [1]. These forces create a "shearing" effect on axons. **Why the Grey-White Matter Junction is the most common site:** The primary mechanism behind DAI is the difference in **density and rigidity** between the grey matter (neuronal cell bodies) and white matter (axonal tracts). When the brain undergoes rapid rotation, these two layers move at different speeds. The interface—the **grey-white matter junction**—experiences the maximum shear stress, leading to the stretching and tearing of axons. **Analysis of Incorrect Options:** * **Corpus Callosum (Option B):** This is the **second most common** site. It is typically involved in more severe trauma (Grade II DAI) compared to the grey-white junction (Grade I). * **Brain Stem (Option A):** This is the **third most common** site, specifically the dorsolateral aspect of the midbrain and superior cerebellar peduncles. Involvement indicates the most severe form of injury (Grade III DAI). * **Anterior one-third of the spinal cord (Option C):** This is irrelevant to DAI; it is the territory supplied by the anterior spinal artery and is associated with Anterior Cord Syndrome. **High-Yield Clinical Pearls for NEET-PG:** * **Imaging:** CT is often normal (clinicoradiological dissociation). **MRI (especially Susceptibility Weighted Imaging - SWI)** is the gold standard, showing "petechial hemorrhages." * **Histopathology:** Characterized by **"Axonal Swellings" or "Retraction Bulbs."** [1] * **Staining:** Silver stains or Immunohistochemistry for **Beta-Amyloid Precursor Protein (B-APP)** or **Ubiquitin** are used to identify damaged axons early (within 2–4 hours). * **Clinical Presentation:** A patient who is comatose immediately after trauma without a visible mass lesion on CT. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1261-1264.

Question 202: What is the secondary structure of prion proteins in prion diseases like Creutzfeldt-Jakob disease (CJD)?

A. Beta sheets (Correct Answer)
B. Beta bend
C. Beta turn
D. Alpha helix

Explanation: **Explanation:** Prion diseases, such as Creutzfeldt-Jakob disease (CJD), are caused by the conformational change of a normal cellular protein ($PrP^C$) into an abnormal, infectious isoform ($PrP^{Sc}$) [1]. 1. **Why Beta sheets are correct:** The fundamental pathogenesis of prion disease involves a post-translational modification where the **alpha-helical** content of the normal protein is converted into **beta-pleated sheets** [1]. This structural shift makes the protein ($PrP^{Sc}$) resistant to proteolysis (protease-resistant), insoluble, and capable of inducing similar conformational changes in neighboring normal proteins, leading to neurotoxic aggregation [1]. 2. **Why the other options are incorrect:** * **Alpha helix:** This is the predominant secondary structure of the **normal** prion protein ($PrP^C$) [1]. In the disease state, these helices are replaced by beta sheets. * **Beta bend and Beta turn:** These are specific types of secondary structures that involve a change in direction of the polypeptide chain (usually involving 4 amino acids). While they exist in many proteins, they are not the defining structural hallmark of the pathogenic prion transition. **High-Yield Clinical Pearls for NEET-PG:** * **Histology:** Characterized by **spongiform encephalopathy** (vacuolation of neurons and neuropil) without inflammatory infiltrate. * **Diagnosis:** Detection of **14-3-3 protein** in CSF is a sensitive marker for CJD. * **Genetics:** Most cases are sporadic, but familial forms are linked to mutations in the **PRNP gene** on chromosome 20 [1]. * **Staining:** Prion aggregates can be visualized with Congo Red (showing apple-green birefringence) as they behave like amyloid, though they are distinct from classic Alzheimer’s amyloid. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1284.

Question 203: A 35-year-old man with Down syndrome dies of acute lymphoblastic leukemia. Gross examination of the patient's brain at autopsy shows mild microcephaly and underdevelopment of the superior temporal gyri. Histologic examination would most likely show which of the following neuropathologic changes?

A. AA amyloidosis
B. Lewy bodies
C. Negri bodies
D. Neurofibrillary tangles (Correct Answer)

Explanation: **Explanation:** The correct answer is **Neurofibrillary tangles (D)**. **Why it is correct:** Patients with **Down Syndrome (Trisomy 21)** have an extra copy of the **Amyloid Precursor Protein (APP) gene**, which is located on chromosome 21 [1]. This leads to the overproduction of beta-amyloid, resulting in the premature development of **Alzheimer-like neuropathology** [1], [2]. By age 35–40, virtually all individuals with Down syndrome exhibit the classic hallmarks of Alzheimer’s disease: **Neurofibrillary tangles** (composed of hyperphosphorylated tau protein) and **Senile (Neuritic) plaques** (composed of amyloid-beta) [1], [2]. Gross findings like microcephaly and underdeveloped superior temporal gyri are also characteristic of the Down syndrome phenotype [1]. **Why incorrect options are wrong:** * **A. AA amyloidosis:** This is systemic amyloidosis associated with chronic inflammatory conditions (e.g., Rheumatoid Arthritis). It does not typically involve the brain parenchyma. * **B. Lewy bodies:** These are alpha-synuclein inclusions found in Parkinson’s disease and Lewy Body Dementia, not specifically associated with the early-onset pathology of Down syndrome. * **C. Negri bodies:** These are eosinophilic cytoplasmic inclusions found in Purkinje cells and hippocampal neurons, pathognomonic for **Rabies**. **High-Yield NEET-PG Pearls:** * **Gene Link:** APP gene is on Chromosome 21; hence, Trisomy 21 = early Alzheimer’s [2]. * **Histology:** Neurofibrillary tangles are **intracellular** (Tau), while Senile plaques are **extracellular** (Aβ) [1], [2]. * **Malignancy Link:** Down syndrome patients have a 10–20x increased risk of leukemia (**ALL** after age 5, **AMKL/M7** before age 5). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 720-721. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1290-1292.

Question 204: Mutations in the merlin protein are associated with which of the following tumors?

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

Explanation: **Explanation:** The **merlin protein** (also known as schwannomin) is a tumor suppressor protein encoded by the ***NF2* gene** located on chromosome **22q12**. It plays a critical role in regulating cell-to-cell adhesion and contact inhibition. **Why Meningioma is correct:** Loss of the *NF2* gene is the most common genetic alteration in **Meningiomas** [1]. Mutations or deletions of *NF2* (and subsequent loss of merlin) are found in approximately 50–60% of sporadic meningiomas and nearly 100% of meningiomas associated with Neurofibromatosis Type 2 [1], [2]. Merlin deficiency leads to uncontrolled proliferation of arachnoidal cells. **Why other options are incorrect:** * **Astrocytoma:** These are primarily associated with mutations in *IDH1/2*, *TP53*, and *ATRX* (for diffuse astrocytomas) or *BRAF* (for pilocytic astrocytomas). * **Medulloblastoma:** These are linked to the WNT or SHH signaling pathways, or mutations in *MYC* and *PTCH1* [3]. * **Oligodendroglioma:** The hallmark genetic signature is the **co-deletion of 1p and 19q**, along with *IDH* mutations. **High-Yield Clinical Pearls for NEET-PG:** * **NF2 Association:** Mutations in the *NF2* gene lead to the "MISME" syndrome: **M**ultiple **I**ntracranial **S**chwannomas (classically bilateral acoustic neuroma), **M**eningiomas, and **E**pendymomas [2]. * **Psammoma Bodies:** These are characteristic concentric calcifications often seen in the meningothelial and transitional subtypes of meningiomas [1], [2]. * **Chromosome 22:** Remember "22" for *NF2* (Neurofibromatosis type **2** on chromosome **22**). This is a frequent target for questions regarding tumor suppressor genes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1316-1317. [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. Neoplasia, pp. 306-307.

Question 205: A 40-year-old lady is diagnosed to have a frontal lobe brain tumor. The lesion is characterized by focal necrosis surrounded by ring-like enhancement. What is the most likely diagnosis?

A. Glioblastoma multiforme (Correct Answer)
B. Oligodendroglioma
C. Ependymoma
D. Astrocytoma

Explanation: **Explanation:** The clinical presentation and imaging findings are classic for **Glioblastoma Multiforme (GBM)**, the most common and most aggressive primary malignant brain tumor in adults [1]. **Why Glioblastoma Multiforme (GBM) is correct:** The hallmark of GBM on neuroimaging is a **"ring-enhancing lesion."** This occurs because the tumor grows so rapidly that it outstrips its blood supply, leading to a central area of **focal necrosis** [1]. The surrounding "ring" represents the viable, highly vascularized tumor periphery where the blood-brain barrier is disrupted, allowing contrast leakage [2]. Histologically, this corresponds to "pseudopalisading necrosis" and microvascular proliferation [1]. **Why the other options are incorrect:** * **Oligodendroglioma:** Typically presents as a calcified mass in the frontal lobe. On imaging, it lacks the aggressive ring enhancement and is histologically characterized by a "fried-egg" appearance and "chicken-wire" vasculature. * **Ependymoma:** More common in children (fourth ventricle) or the spinal cord in adults. It is characterized by perivascular pseudorosettes and is not typically associated with large areas of central necrosis in the frontal lobe. * **Astrocytoma (Low-grade):** While GBM is technically a Grade IV Astrocytoma, lower-grade astrocytomas (Grade II/III) usually present as non-enhancing or diffusely infiltrating lesions without central necrosis. **High-Yield Pearls for NEET-PG:** * **Butterfly Glioma:** GBM can cross the corpus callosum, involving both hemispheres. * **Molecular Marker:** IDH-mutation status is now the primary prognostic factor (IDH-wildtype has a worse prognosis) [3]. * **GFAP Positive:** Like all astrocytic tumors, GBM is positive for Glial Fibrillary Acidic Protein. * **Differential for Ring-Enhancing Lesions (Mnemonic: MAGIC DR):** Metastasis, Abscess, Glioblastoma, Infarct, Contusion, Demyelination, Radiation necrosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, p. 1310. [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. 1308-1310.

Question 206: Glioblastoma multiforme may occur in the following locations, except:

A. Cerebrum of adult
B. Brain stem of child
C. Spinal cord of adult
D. Adrenal medulla of child (Correct Answer)

Explanation: **Explanation:** The correct answer is **D. Adrenal medulla of child**. **Glioblastoma (GBM)** is a Grade 4 astrocytoma, which is a primary tumor of the central nervous system (CNS) arising from glial cells (astrocytes) [1]. The adrenal medulla, however, is derived from **neural crest cells** and is part of the peripheral nervous system. In children, the most common tumor arising from the adrenal medulla is **Neuroblastoma**, not Glioblastoma. **Analysis of Options:** * **A. Cerebrum of adult:** This is the most common site for GBM [2]. It typically presents as a large, necrotic mass in the cerebral hemispheres, often crossing the corpus callosum (Butterfly Glioma) [1]. * **B. Brain stem of child:** While GBM is primarily an adult tumor, high-grade gliomas (including Diffuse Intrinsic Pontine Gliomas or DIPG) occur in the brainstem of children and are histologically similar to GBM [2]. * **C. Spinal cord of adult:** Although rare compared to intracranial sites, GBM can occur anywhere in the CNS axis, including the spinal cord. **NEET-PG High-Yield Pearls:** 1. **Hallmark Histology:** Look for **pseudopalisading necrosis** and **microvascular (glomeruloid) proliferation** [1]. 2. **Molecular Marker:** **IDH-mutation status** is now critical for classification (WHO 2021). Most GBMs are IDH-wildtype [1]. 3. **Radiology:** Classically presents as a **ring-enhancing lesion** on MRI due to central necrosis [1]. 4. **GFAP Positivity:** As a glial tumor, GBM is strongly positive for Glial Fibrillary Acidic Protein (GFAP). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1308-1311. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 725-726.

Question 207: Medulloblastoma associated Turcot syndrome is characterized by mutation in which of the following genes?

A. KRAS
B. TP53
C. APC (Correct Answer)
D. PTEN

Explanation: **Explanation:** **Turcot Syndrome** is a rare genetic disorder characterized by the association of primary central nervous system (CNS) tumors with familial adenomatous polyposis (FAP) or hereditary non-polyposis colorectal cancer (HNPCC) [1]. It is categorized into two distinct types based on the genetic mutation and the type of brain tumor: 1. **Turcot Syndrome Type 2 (The APC Mutation):** This is the correct answer. It is associated with mutations in the **APC (Adenomatous Polyposis Coli)** gene (5q21). Clinically, it presents as **Medulloblastoma** (specifically the WNT-subtype) and extensive colonic polyposis [3]. 2. **Turcot Syndrome Type 1:** This is associated with mutations in DNA mismatch repair genes (like **MLH1** or **PMS2**). Clinically, it presents as **Glioblastoma Multiforme (GBM)** and fewer colonic polyps [1]. **Analysis of Incorrect Options:** * **A. KRAS:** Primarily involved in the MAP-kinase pathway; mutations are common in pancreatic, lung, and colorectal cancers, but not the defining feature of Turcot syndrome. * **B. TP53:** Mutations are seen in **Li-Fraumeni Syndrome**, which involves various tumors (sarcomas, breast cancer, brain tumors), but not specifically the Medulloblastoma-Polyposis constellation. * **D. PTEN:** Mutations are associated with **Cowden Syndrome**, characterized by dysplastic gangliocytoma of the cerebellum (Lhermitte-Duclos disease) and hamartomatous polyps. **High-Yield Clinical Pearls for NEET-PG:** * **Medulloblastoma** is the most common malignant brain tumor in children, typically arising in the **cerebellum** (vermis) [2], [3]. * **Homer-Wright Rosettes** are a classic histological finding in Medulloblastoma. * **WNT-subtype Medulloblastoma** (associated with APC) carries the **best prognosis** among all molecular subgroups [3]. * **Mnemonic:** **"A-P-C"** = **A**denomatous **P**olyposis + **C**erebellar tumor (Medulloblastoma). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 817. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 306-307. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315.

Question 208: An 8-month-old boy exhibits severe motor, sensory, and cognitive impairments. Brain biopsy shows a disease of white matter characterized by the accumulation of "globoid cells." Biochemical studies reveal an absence of galactocerebroside b-galactosidase activity. What is the appropriate diagnosis?

A. Alexander disease
B. Hurler disease
C. Krabbe disease (Correct Answer)
D. Metachromatic leukodystrophy

Explanation: The clinical presentation and biochemical findings point directly to **Krabbe disease** (Globoid Cell Leukodystrophy), an autosomal recessive lysosomal storage disorder [1]. **1. Why Krabbe Disease is Correct:** The deficiency of the enzyme **galactocerebroside $\beta$-galactosidase** (galactosylceramidase) leads to the accumulation of **galactosylsphingosine (psychosine)**, which is toxic to oligodendrocytes and Schwann cells. This results in widespread demyelination. The pathognomonic histological feature is the presence of **"Globoid cells"**—large, multinucleated macrophages filled with undigested galactocerebroside—found in the white matter [1]. **2. Why Other Options are Incorrect:** * **Alexander disease:** A leukodystrophy caused by mutations in the *GFAP* gene. It is characterized histologically by **Rosenthal fibers** (eosinophilic inclusions in astrocytes), not globoid cells. * **Hurler disease:** A Mucopolysaccharidosis (MPS I) caused by $\alpha$-L-iduronidase deficiency [2]. It presents with coarse facial features, hepatosplenomegaly, and corneal clouding, rather than isolated white matter destruction [2]. * **Metachromatic leukodystrophy (MLD):** Caused by **Arylsulfatase A** deficiency. While it involves demyelination, it is characterized by the accumulation of sulfatides that stain brown/purple with toluidine blue (metachromasia), not globoid cells [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Enzyme Defect:** Galactocerebroside $\beta$-galactosidase. * **Hallmark:** Globoid cells (multinucleated macrophages) [1]. * **Clinical Triad:** Irritability, developmental delay, and progressive motor deterioration (stiffness/spasticity). * **Inheritance:** Autosomal Recessive. * **Key Distinction:** Unlike many other storage diseases, Krabbe disease does **not** typically present with organomegaly. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1304-1305. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 163-164.

Question 209: Which of the following cancers metastasize to the brain the least?

A. Hypernephroma
B. Breast carcinoma
C. Choriocarcinoma
D. Prostatic carcinoma (Correct Answer)

Explanation: **Explanation:** Brain metastases are significantly more common than primary intracranial tumors [2]. The frequency of metastasis depends on the primary tumor's hematogenous spread potential and its affinity for neural tissue. **Why Prostatic Carcinoma is the Correct Answer:** Prostate cancer is notorious for its predilection for **bone**, specifically the axial skeleton (vertebrae), via the **Batson venous plexus** [3]. While it frequently involves the skull or the dura (pachymeningeal metastasis), it **rarely involves the brain parenchyma** itself [2]. Among the options provided, it has the lowest incidence of intraparenchymal brain metastasis. **Analysis of Incorrect Options:** * **Hypernephroma (Renal Cell Carcinoma):** RCC is a highly vascular tumor with a strong tendency for hematogenous spread. It is one of the classic "big five" primaries that metastasize to the brain, often presenting as solitary, hemorrhagic lesions [2]. * **Breast Carcinoma:** This is the **second most common** cause of brain metastasis overall (after Lung Cancer) [2]. It frequently spreads to the posterior fossa and can present as multiple lesions or leptomeningeal carcinomatosis. * **Choriocarcinoma:** This germ cell tumor is characterized by early and aggressive hematogenous spread. It has a very high affinity for the brain [2], and these metastases are classically **hemorrhagic** due to the tumor's trophoblastic nature. **NEET-PG High-Yield Pearls:** 1. **Most common source of brain metastasis:** Lung Cancer (specifically Small Cell and Adenocarcinoma) [1], [2]. 2. **Most common source in children:** Neuroblastoma. 3. **"Hemorrhagic" Brain Metastases:** Remember the mnemonic **"CHUMP"** – **C**horiocarcinoma, **H**ypernephroma (RCC), **U**pper GI (Melanoma), **M**elanoma, and **P**ancreas/Thyroid. 4. **Location:** Most metastases occur at the **grey-white matter junction**, where tapering blood vessels trap tumor emboli. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lung, pp. 724-725. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1317-1318. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 993-994.

Question 210: Group atrophy of muscle fibers denotes:

A. Enlarged motor units with all muscle fibers disproportionately reduced
B. Enlarged motor units with all muscle fibers reduced to the same size (Correct Answer)
C. Reduced motor units with all muscle fibers reduced to the same size
D. Reduced motor units with all muscle fibers disproportionately reduced

Explanation: ### Explanation **Concept: Denervation and Reinnervation** Group atrophy is the hallmark of **neurogenic muscle disease** (e.g., Amyotrophic Lateral Sclerosis or Spinal Muscular Atrophy) [1]. 1. **Denervation:** When a motor neuron dies, the muscle fibers it supplied lose their trophic support and shrink (atrophy) [3]. 2. **Reinnervation:** Neighboring healthy axons "sprout" to rescue these orphaned fibers [3]. This process incorporates the fibers into a new, **enlarged motor unit** [1]. 3. **Group Atrophy:** If this surviving "giant" motor neuron subsequently dies, all the fibers it rescued—which are now numerous and clustered together—undergo simultaneous atrophy [2]. Because they lose their nerve supply at the same time, they shrink uniformly, resulting in **enlarged motor units with all muscle fibers reduced to the same size.** **Analysis of Incorrect Options:** * **Option A & D:** These are incorrect because "disproportionate reduction" implies varied stages of atrophy. In group atrophy, the fibers are affected synchronously, leading to a uniform, small, angular appearance [3]. * **Option C:** This is incorrect because the motor unit is not reduced; it is pathologically enlarged due to the compensatory reinnervation (axonal sprouting) that occurred before the final failure [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Fiber Type Grouping:** This is the precursor to group atrophy. Normal muscle has a "checkerboard" pattern of Type 1 and Type 2 fibers [3]. Reinnervation causes fibers of the same type to cluster together [1]. * **Target Fibers:** Seen in the early stages of denervation (cytoskeletal reorganization). * **Angulated Fibers:** Individual atrophied fibers in neurogenic switching typically appear angulated rather than round [3]. * **Contrast with Myopathic Change:** Myopathies (like Duchenne) show fiber size **variability** (hypertrophy + atrophy), central nuclei, and endomysial fibrosis, rather than grouped atrophy [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1239-1240. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 730-731. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1240.

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Cellular Pathology 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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