Neuropathology — MCQs

Neuropathology Indian Medical PG Practice Questions and MCQs

Question 221: A 68-year-old obese woman (BMI = 34 kg/m2) suffers a stroke and expires. Histologic examination of the brain at autopsy reveals extensive arteriolar lipohyalinosis and numerous Charcot-Bouchard aneurysms. Which of the following best accounts for the pathogenesis of these autopsy findings?

A. Atherosclerosis
B. Autoimmunity
C. Diabetes
D. Hypertension (Correct Answer)

Explanation: **Explanation:** The correct answer is **Hypertension**. This case describes the classic pathological hallmarks of chronic hypertensive cerebrovascular disease [2]. **1. Why Hypertension is Correct:** Chronic hypertension is the primary driver of **arteriolar lipohyalinosis** (also known as hyaline arteriolosclerosis) [4]. High pressure causes leakage of plasma proteins into the vessel wall and increased collagen deposition, leading to thickening and weakening of the small penetrating arteries (e.g., lenticulostriate arteries). This weakening results in the formation of **Charcot-Bouchard aneurysms** [1]. These are microscopic pseudoaneurysms (usually <300 µm) that typically occur in the basal ganglia, thalamus, and pons [5]. Their rupture is the most common cause of **intracerebral hemorrhage** [2]. **2. Why Incorrect Options are Wrong:** * **A. Atherosclerosis:** While hypertension accelerates atherosclerosis, atherosclerosis typically affects **large, elastic arteries** (like the carotid or Circle of Willis) and leads to thrombotic strokes or Berry aneurysms (at bifurcations), not lipohyalinosis of small penetrating vessels [3]. * **B. Autoimmunity:** Vasculitis (e.g., PAN) can cause aneurysms, but they are inflammatory in nature and do not present with lipohyalinosis [1]. * **C. Diabetes:** Diabetes causes microangiopathy and accelerates atherosclerosis, but it is not the primary cause of Charcot-Bouchard aneurysms; hypertension is the specific hemodynamic trigger for these lesions. **Clinical Pearls for NEET-PG:** * **Charcot-Bouchard vs. Berry Aneurysm:** Charcot-Bouchard occurs in **small vessels** (basal ganglia) due to **hypertension** and causes **intracerebral hemorrhage** [1]. Berry aneurysms occur in the **Circle of Willis** due to **congenital wall defects** and cause **subarachnoid hemorrhage** [2]. * **Lacunar Infarcts:** Lipohyalinosis can also lead to small, cavitary infarcts known as lacunae. * **Most common site for hypertensive bleed:** Putamen (Basal Ganglia) [5]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 273-274. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 705-706. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 704-705. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 498-499. [5] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1270-1272.

Question 222: A 5-year-old child presents with a posterior fossa mass. A biopsy of the mass reveals rosettes. What is the most likely histological feature observed?

A. Homer Wright rosette (Correct Answer)
B. Perivascular pseudorosette
C. Flexner-Wintersteiner rosette
D. None of the above

Explanation: **Explanation:** The clinical presentation of a **posterior fossa mass** in a 5-year-old child is highly suggestive of **Medulloblastoma**, the most common malignant brain tumor of childhood. Histologically, Medulloblastoma is a "Small Round Blue Cell Tumor" characterized by the presence of **Homer Wright rosettes** [1]. **1. Why Homer Wright Rosettes are correct:** Homer Wright rosettes consist of tumor cells arranged in a circle around a central **fibrillar (neuropil) core**, without a central lumen or blood vessel [1]. These are "true" rosettes indicating neuroectodermal differentiation and are a hallmark of Medulloblastoma and Neuroblastoma. **2. Analysis of Incorrect Options:** * **Perivascular Pseudorosettes:** These consist of tumor cells arranged around a **central blood vessel** [2]. While common in the posterior fossa, they are the characteristic hallmark of **Ependymomas**, not Medulloblastomas [2]. * **Flexner-Wintersteiner Rosettes:** These feature a **central lumen** (containing cytoplasmic extensions). They are highly specific for **Retinoblastoma** and are rarely seen in CNS tumors. **Clinical Pearls for NEET-PG:** * **Medulloblastoma Location:** Always arises in the **cerebellum** (vermis in children, hemispheres in adults). * **Drop Metastasis:** Medulloblastoma has a high propensity to spread via CSF to the spinal cord [3]. * **Genetics:** WNT subtype has the best prognosis; Group 3 (MYC amplification) has the worst. * **Classic Imaging:** A midline mass in the 4th ventricle causing obstructive hydrocephalus. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 484-485. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1312-1313. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1314-1315.

Question 223: Which of the following is NOT a characteristic feature of cerebral malaria?

A. Perivascular demyelination
B. Durck granuloma
C. Proliferated glial cells arranged radially
D. Lesion is not related to the parasite (Correct Answer)

Explanation: **Cerebral Malaria** is a severe neurological complication of *Plasmodium falciparum* infection, characterized by the sequestration of parasitized Red Blood Cells (RBCs) in the cerebral microvasculature. ### **Explanation of the Correct Option** **D. Lesion is not related to the parasite:** This statement is **incorrect** (making it the right answer for a "NOT" question). The hallmark of cerebral malaria pathogenesis is the **cytoadherence** of infected RBCs to the vascular endothelium (via PfEMP-1 protein). This leads to microvascular obstruction, hypoxia, and local inflammatory responses. Therefore, the lesions are directly and fundamentally related to the presence of the parasite. ### **Analysis of Incorrect Options** * **A. Perivascular demyelination:** In severe cases, the inflammatory response and vascular leakage lead to focal areas of demyelination around the affected small vessels. * **B. Durck Granuloma:** This is the **pathognomonic** histological feature of cerebral malaria. It consists of a central area of necrosis (often a small vessel) surrounded by microglial proliferation [1]. * **C. Proliferated glial cells arranged radially:** This describes the microscopic appearance of the **Durck granuloma**. Microglial cells and astrocytes proliferate and organize radially around the focus of necrotic brain tissue [1]. ### **NEET-PG High-Yield Pearls** * **Pathogenesis:** Sequestration of RBCs in capillaries and post-capillary venules. * **Key Histology:** **Durck Granulomas** (microglial nodules) and **petechial hemorrhages** in the white matter (Ring hemorrhages) [1]. * **Clinical Presentation:** Sudden onset of high fever, seizures, and symmetrical encephalopathy (coma). * **Diagnosis:** Presence of *P. falciparum* on peripheral smear + Coma (GCS <11) + Exclusion of other causes. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1255-1256.

Question 224: Marchiafava-Bignami disease is characterized by which of the following?

A. Callosal atrophy (Correct Answer)
B. Cerebellar atrophy
C. Brainstem atrophy
D. Cerebral peduncular atrophy

Explanation: **Explanation:** **Marchiafava-Bignami Disease (MBD)** is a rare, progressive neurological disorder characterized by symmetric **demyelination and necrosis of the corpus callosum**. 1. **Why Callosal Atrophy is Correct:** The primary pathology in MBD involves the destruction of the central layers of the corpus callosum (the "sandwich sign" on MRI). Chronic cases lead to significant thinning and **callosal atrophy**. It is classically associated with chronic alcoholism, particularly the consumption of inexpensive red wine, though it is now understood to be linked more broadly to malnutrition and alcohol-induced metabolic derangements. 2. **Why Other Options are Incorrect:** * **Cerebellar Atrophy:** This is a hallmark of chronic alcohol abuse (specifically affecting the anterior vermis), but it is not the defining feature of MBD. * **Brainstem Atrophy:** Typically seen in neurodegenerative conditions like Progressive Supranuclear Palsy (PSP) or Multiple System Atrophy (MSA-P). * **Cerebral Peduncular Atrophy:** Usually occurs secondary to Wallerian degeneration following a massive cortical stroke (infarction of the internal capsule). **High-Yield Clinical Pearls for NEET-PG:** * **Classic Triad:** Dementia, gait instability, and dysarthria in a chronic alcoholic. * **Imaging Gold Standard:** MRI shows T2/FLAIR hyperintensities in the corpus callosum (acute) or thinning/atrophy (chronic). * **Differential Diagnosis:** Must be distinguished from **Wernicke Encephalopathy** (affects mammillary bodies/thalamus) and **Central Pontine Myelinolysis** (affects the pons). * **Key Pathological Feature:** Symmetrical demyelination of the body of the corpus callosum, often sparing the dorsal and ventral edges.

Question 225: Which of the following is NOT a feature of Alzheimer's disease?

A. Narrowing of ventricles (Correct Answer)
B. Hirano bodies
C. Amyloid deposits
D. Neuritic plaques

Explanation: **Explanation:** Alzheimer’s Disease (AD) is characterized by progressive cortical atrophy, primarily affecting the hippocampus and the frontal, temporal, and parietal lobes [1]. **Why "Narrowing of ventricles" is the correct answer:** In Alzheimer’s disease, the significant loss of neurons and synapses leads to **brain atrophy**. As the brain parenchyma shrinks (atrophy), the fluid-filled spaces within the brain undergo **compensatory enlargement** to fill the void [1]. This phenomenon is known as **Hydrocephalus ex-vacuo**. Therefore, AD is characterized by **widening (dilation)** of the ventricles, not narrowing. **Analysis of incorrect options:** * **Hirano bodies:** These are eosinophilic, rod-like inclusions found primarily in the pyramidal cells of the hippocampus. They are composed of actin and are a classic microscopic feature of AD. * **Amyloid deposits:** AD involves the deposition of **Amyloid-beta (Aβ) peptides** [1]. These are derived from the Amyloid Precursor Protein (APP) and form the core of senile plaques and deposit in vessel walls (Cerebral Amyloid Angiopathy). * **Neuritic plaques:** Also known as senile plaques, these are extracellular lesions consisting of a central core of Aβ amyloid surrounded by dystrophic neurites, microglia, and astrocytes [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Gross features:** Symmetrical cortical atrophy, narrowed gyri, and widened sulci [1]. * **Neurofibrillary Tangles (NFTs):** Intracellular bundles of filaments containing **hyperphosphorylated Tau protein** [2]. The density of NFTs correlates better with the severity of dementia than plaques [1]. * **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 [1]. * **Silver stains:** Used to visualize plaques and tangles (e.g., Bielschowsky or Modified Bielschowsky stain). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 719-722. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1292-1293.

Question 226: Which of the following is NOT a cellular event in the sequence of an ischemic brain infarct?

A. Intense neuronal eosinophilia
B. Influx of polymorphonuclear neutrophils (PMNs)
C. Proliferation of astrocytes
D. Ingress of macrophages and apoptosis (Correct Answer)

Explanation: The sequence of events following an ischemic brain infarct follows a predictable chronological pattern of necrosis and repair. [1] **Explanation of the Correct Answer:** **Option D (Ingress of macrophages and apoptosis)** is the correct answer because it is factually inaccurate in the context of the sequence. While **macrophages** do enter the area (typically after 48–72 hours) to clear debris, the primary mode of cell death in a major ischemic infarct is **liquefactive necrosis**, not apoptosis. [1] Apoptosis is a programmed, energy-dependent process, whereas ischemia leads to a catastrophic loss of ATP, resulting in cell swelling and necrotic rupture. **Analysis of Incorrect Options:** * **A. Intense neuronal eosinophilia:** This is the earliest histological sign (12–24 hours), known as **"Red Neurons."** It occurs due to pyknosis of the nucleus and loss of cytoplasmic RNA. [1] * **B. Influx of PMNs:** Neutrophils are the first inflammatory cells to arrive, peaking between 24–48 hours post-infarct. [1] * **C. Proliferation of astrocytes:** Known as **Reactive Gliosis**, this begins around 1 week. Astrocytes enlarge and multiply to form a "glial scar" around the liquefactive cavity. [2] **NEET-PG High-Yield Pearls:** 1. **Timeline of Infarct:** * 12–24 hrs: Red Neurons. * 24–72 hrs: Neutrophilic infiltrate. * 3–7 days: Macrophage (Microglia) infiltration; cells appear foamy (**Gitter cells**). * 2–3 weeks: Liquefactive necrosis and Gliosis. [1] 2. **Type of Necrosis:** Brain ischemia uniquely results in **liquefactive necrosis** (unlike coagulative necrosis in the heart/kidney). [1] 3. **The Glial Scar:** Unlike peripheral tissues that heal with collagen (fibrosis), the CNS heals via **astrocytic proliferation**. [2] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1268-1269. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.

Question 227: Duret Hemorrhages are seen in which organ?

A. Lung
B. Brain (Correct Answer)
C. Kidney
D. Heart

Explanation: **Explanation:** **Duret hemorrhages** are small, linear or flame-shaped hemorrhages occurring in the **midbrain and pons** [1]. They are a classic manifestation of severe intracranial pathology, specifically resulting from **transtentorial (uncal) herniation** [1]. **Why the Brain is Correct:** When intracranial pressure (ICP) rises significantly (due to a tumor, hematoma, or edema), the brain tissue is displaced downward through the tentorial notch. This mechanical shift causes the stretching and tearing of the **perforating branches of the basilar artery** and/or the draining veins [1]. The resulting ischemia and rupture lead to focal hemorrhages in the brainstem (midbrain and pons), which are often fatal as they affect vital cardiac and respiratory centers. **Why Other Options are Incorrect:** * **Lung:** Hemorrhages here are typically associated with pulmonary embolism (infarction), trauma, or Goodpasture syndrome, but are never referred to as Duret hemorrhages. * **Kidney:** Renal hemorrhages or infarcts are usually due to emboli or vasculitis. * **Heart:** Myocardial hemorrhages are generally associated with reperfusion injury or trauma. **High-Yield Clinical Pearls for NEET-PG:** * **Location:** Specifically the midline of the **midbrain and upper pons** [1]. * **Mechanism:** Secondary to **descending transtentorial herniation** [1]. * **Clinical Significance:** Usually indicates a terminal event or a very poor prognosis. * **Differential:** Do not confuse with **Kernohan’s notch**, which is a groove in the cerebral peduncle caused by compression against the tentorium, leading to ipsilateral hemiparesis (a false localizing sign). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1257-1258.

Question 228: What is the commonest type of intracranial tumor in adults?

A. Astrocytoma (Correct Answer)
B. Medulloblastoma
C. Neurofibroma
D. Secondaries

Explanation: **Explanation:** The classification of intracranial tumors depends significantly on whether the origin is primary or secondary and the age group of the patient. **1. Why Astrocytoma is correct:** Among **primary** intracranial tumors in adults, **Gliomas** are the most frequent, and **Astrocytomas** (ranging from low-grade to Glioblastoma Multiforme) constitute the largest subgroup of gliomas [1]. While some textbooks debate the incidence of Meningiomas versus Glioblastomas, in the context of NEET-PG and standard pathology references (like Robbins), Astrocytomas are considered the most common primary CNS malignancy in adults [2]. **2. Analysis of Incorrect Options:** * **Medulloblastoma:** This is a highly malignant primitive neuroectodermal tumor (PNET). It is the most common malignant brain tumor in **children**, typically arising in the cerebellum, but is rare in adults [1], [4]. * **Neurofibroma:** These are peripheral nerve sheath tumors. While they can occur in the context of Neurofibromatosis, they are not primary intracranial tumors (unlike Schwannomas, which can affect the CN VIII) [4]. * **Secondaries (Metastasis):** While metastatic deposits are technically the most common intracranial tumors overall in adults (often outnumbering primary tumors) [3], the question typically refers to **primary** tumors unless "metastasis" is the intended high-yield answer for "most common overall." In most standard medical examinations, if "Astrocytoma" is the marked key, the focus is on primary neuroepithelial tumors. **High-Yield Clinical Pearls for NEET-PG:** * **Most common primary brain tumor (Adults):** Glioblastoma Multiforme (a Grade IV Astrocytoma) [4]. * **Most common benign intracranial tumor (Adults):** Meningioma [4]. * **Most common source of brain secondaries:** Lung cancer > Breast cancer > Melanoma [3]. * **Most common infratentorial tumor (Children):** Cerebellar Astrocytoma (specifically Pilocytic Astrocytoma) [1], [4]. * **Rosenthal Fibers:** Characteristic histological finding in Pilocytic Astrocytoma. **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. 1308-1311. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1317-1318. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Central Nervous System, pp. 1319-1320.

Question 229: What is the characteristic histopathological finding of Hirano bodies?

A. Rabies
B. Alzheimer's disease (Correct Answer)
C. Pick's disease
D. Viral encephalitis

Explanation: **Explanation:** **Hirano bodies** are eosinophilic, rod-like or cucumber-shaped intracellular inclusions found primarily within the pyramidal neurons of the **hippocampus**. Ultrastructurally, they consist of paracrystalline arrays of actin and actin-associated proteins. * **Why Alzheimer’s Disease (AD) is correct:** While Hirano bodies can be seen in normal aging, they are significantly more numerous in neurodegenerative conditions, most characteristically **Alzheimer’s disease** [1]. They represent a breakdown in the cytoskeleton and are considered one of the microscopic hallmarks of AD, alongside neurofibrillary tangles (tau protein) and neuritic plaques (amyloid-beta) [1]. **Analysis of Incorrect Options:** * **A. Rabies:** Characterized by **Negri bodies**, which are eosinophilic, round-to-oval cytoplasmic inclusions found typically in Purkinje cells of the cerebellum and pyramidal cells of the hippocampus. * **C. Pick’s Disease:** Characterized by **Pick bodies**, which are round, silver-staining (argyrophilic) cytoplasmic inclusions made of 3R tau protein [2]. * **D. Viral Encephalitis:** Often presents with **Cowdry Type A** inclusions (e.g., Herpes Simplex Virus) or microglial nodules, rather than actin-rich Hirano bodies. **High-Yield Clinical Pearls for NEET-PG:** * **Hirano bodies = Actin** (High-yield biochemical component). * **Location:** Hippocampus (Sommer’s sector/CA1). * **Alzheimer’s Histology Triad:** Neuritic (Senile) plaques, Neurofibrillary tangles, and Granulovacuolar degeneration/Hirano bodies [1]. * **Silver Stains:** Used for plaques and tangles, but Hirano bodies are easily seen on routine **H&E stain**. **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. 1294-1295.

Question 230: What is the most common nerve in the neck from which schwannoma arises?

A. Trigeminal nerve
B. Accessory nerve
C. Hypoglossal nerve
D. Vestibular portion of the acoustic nerve (Correct Answer)

Explanation: **Explanation:** **1. Why the Correct Answer is Right:** Schwannomas are benign, encapsulated tumors arising from Schwann cells of the cranial or peripheral nerves. The **vestibular portion of the 8th cranial nerve (Vestibular nerve)** is the most common site for intracranial and head/neck schwannomas [1]. When located at the cerebellopontine (CP) angle, they are often referred to as "Acoustic Neuromas," though they histologically originate from the vestibular branch [1]. These tumors typically arise at the **Obersteiner-Redlich zone**, which is the transition point between central (oligodendrocyte) and peripheral (Schwann cell) myelin [2]. **2. Why the Other Options are Wrong:** * **Trigeminal Nerve (A):** The 5th cranial nerve is the second most common site for intracranial schwannomas, but it is significantly less frequent than the vestibular nerve. * **Accessory (B) and Hypoglossal (C) Nerves:** While schwannomas can arise from any nerve covered by Schwann cells, the lower cranial nerves (IX, X, XI, XII) are rare primary sites. In the neck, vagal schwannomas are more common than those of the accessory or hypoglossal nerves, but none surpass the vestibular nerve in frequency. **3. NEET-PG High-Yield Pearls:** * **Histology:** Look for **Antoni A** (hypercellular, Verocay bodies) and **Antoni B** (hypocellular, myxoid) patterns [3]. * **Immunohistochemistry:** Schwannomas are characteristically **S-100 positive** (strong and diffuse). * **Genetics:** Bilateral vestibular schwannomas are pathognomonic for **Neurofibromatosis Type 2 (NF2)**, associated with a mutation on chromosome 22 [1], [2]. * **Clinical Sign:** The earliest symptom is usually sensorineural hearing loss or tinnitus due to compression of the adjacent cochlear branch. **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. Peripheral Nerves and Skeletal Muscles, p. 1250.

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Cellular Pathology of the Nervous System

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Cerebrovascular Diseases

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Trauma to the Central Nervous System

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Infections of the Nervous System

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Demyelinating Diseases

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Neurodegenerative Diseases

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CNS Tumors

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Peripheral Nerve Disorders

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Neuromuscular Junction Diseases

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Congenital and Developmental Disorders

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