Neurology — MCQs

Neurology Indian Medical PG Practice Questions and MCQs

Question 11: What is the chance of vertical transmission of Hepatitis B?

A. 25-30% (Correct Answer)
B. 40%
C. 60%
D. 90-95%

Explanation: **Explanation:** The risk of vertical transmission (mother-to-child) of Hepatitis B Virus (HBV) is primarily determined by the mother's serological status, specifically the presence of the **HBeAg (Hepatitis B e-antigen)**, which signifies high viral replication. 1. **Why 25-30% is correct:** In a general population of HBV-infected pregnant women (including both HBeAg-positive and HBeAg-negative mothers), the overall risk of vertical transmission without immunoprophylaxis is approximately **25-30%**. Most of these transmissions occur during the peripartum period (delivery) due to contact with maternal blood and vaginal secretions [1]. 2. **Analysis of Incorrect Options:** * **Option B (40%) & C (60%):** These figures do not correspond to standard epidemiological benchmarks for HBV transmission. * **Option D (90-95%):** This is a high-yield distractor. While 90-95% is not the *overall* transmission rate, it represents the risk of transmission if the mother is **both HBsAg and HBeAg positive**. Additionally, 90% is the risk that a neonate infected at birth will develop **chronic** Hepatitis B [1]. **Clinical Pearls for NEET-PG:** * **Timing:** Most vertical transmission occurs during **delivery** (birth canal). Transplacental (in-utero) transmission is rare (<5%). * **Prevention:** Administration of the **HBV vaccine and HBIG (Hepatitis B Immunoglobulin)** to the newborn within 12 hours of birth reduces the transmission risk by >90%. * **Antiviral Therapy:** If maternal HBV DNA is >200,000 IU/mL, Tenofovir is recommended starting at 28–32 weeks gestation to further reduce transmission risk. * **Breastfeeding:** Is **not** contraindicated in HBV-positive mothers, provided the infant receives the recommended immunoprophylaxis.

Question 12: What is the most common opportunistic fungal infection in patients with HIV?

A. Histoplasmosis
B. Candidiasis (Correct Answer)
C. Cryptosporidium
D. Cryptococcus

Explanation: **Explanation:** The correct answer is **Candidiasis**. In the context of HIV/AIDS, fungal infections are significant markers of disease progression. **Oropharyngeal Candidiasis (Thrush)** is recognized as the most common opportunistic fungal infection overall in HIV patients [1]. It typically occurs when the CD4 count falls below 200–500 cells/mm³. While it is not an AIDS-defining illness itself, its presence is a strong clinical predictor of progression to AIDS. Esophageal candidiasis, however, is considered an AIDS-defining condition [1]. **Analysis of Incorrect Options:** * **Histoplasmosis:** This is a regional fungal infection (endemic in certain river valleys). While it is a common opportunistic infection in specific geographic areas, it is not the most common globally or generally compared to Candida. * **Cryptosporidium:** This is a **protozoan** parasite, not a fungus. It causes chronic watery diarrhea in AIDS patients (CD4 <100 cells/mm³). * **Cryptococcus:** *Cryptococcus neoformans* is the most common cause of opportunistic **fungal meningitis** in HIV patients [1], but it is less frequent than mucosal Candidiasis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common opportunistic infection (overall):** *Pneumocystis jirovecii* (formerly a fungus, now classified as a yeast-like fungus; however, in many traditional classifications, Candidiasis remains the most frequent fungal manifestation). * **Most common fungal meningitis:** Cryptococcosis (diagnosed via India Ink preparation or CrAg lateral flow assay) [1]. * **CD4 Thresholds:** * Thrush: <500 cells/mm³ * Pneumocystis: <200 cells/mm³ * Cryptococcus/Histoplasmosis: <100 cells/mm³ * CMV/MAC: <50 cells/mm³

Question 13: Hecht's pneumonia is typically seen in:

A. Measles (Correct Answer)
B. Malaria
C. RSV
D. Pneumococcus

Explanation: **Explanation:** **Hecht’s Pneumonia**, also known as **Giant Cell Interstitial Pneumonia**, is a severe and often fatal complication of the **Measles virus (Rubeola)** [1]. It typically occurs in immunocompromised individuals (e.g., those with leukemia, HIV, or severe malnutrition) who are unable to mount an effective T-cell response [1]. 1. **Why Measles is Correct:** The Measles virus causes the fusion of infected epithelial cells, leading to the formation of characteristic **multinucleated giant cells** (Warthin-Finkeldey cells) containing eosinophilic intranuclear and intracytoplasmic inclusion bodies. In Hecht’s pneumonia, these giant cells infiltrate the alveolar spaces [1]. Notably, this condition can occur without the classic measles rash (exanthem) in immunocompromised patients [1]. 2. **Why Other Options are Incorrect:** * **Malaria:** Primarily causes Pulmonary Edema or ARDS due to capillary leakage and red cell sequestration, not giant cell pneumonia. * **RSV:** While a common cause of bronchiolitis and pneumonia in infants, it is characterized by syncytia formation but is not associated with the specific "Hecht’s" eponymous giant cell pathology. * **Pneumococcus:** Causes classic lobar pneumonia characterized by intra-alveolar neutrophilic exudate (Red/Grey hepatization), not interstitial giant cell changes. **High-Yield Clinical Pearls for NEET-PG:** * **Warthin-Finkeldey Cells:** Pathognomonic multinucleated giant cells found in lymphoid tissue and lungs in Measles. * **Koplik Spots:** Small white spots on the buccal mucosa; the hallmark pre-eruptive sign of Measles [1]. * **Vitamin A:** Supplementation is recommended for all children with acute measles to reduce morbidity and mortality. * **SSPE:** A late neurological complication of measles occurring years after the initial infection [1].

Question 14: A resident doctor sustained a needle stick injury while sampling blood of a patient who is HIV positive. A decision is taken to offer him post-exposure prophylaxis. Which one of the following would be the best recommendation?

A. Zidovudine + Lamivudine for 4 weeks
B. Zidovudine + Lamivudine + Nevirapine for 4 weeks
C. Zidovudine + Lamivudine + Indinavir for 4 weeks (Correct Answer)
D. Zidovudine + Stavudine + Nevirapine for 4 weeks

Explanation: **Explanation:** The management of needle stick injuries in healthcare workers involves assessing the risk of transmission and initiating **Post-Exposure Prophylaxis (PEP)** [1]. According to the standard guidelines (NACO/CDC) applicable to this scenario, the goal is to use a multi-drug regimen to prevent viral replication. **Why Option C is Correct:** In high-risk exposures (such as a needle stick from a known HIV-positive patient), an **expanded regimen** is preferred over a basic regimen [2]. This typically consists of **two Nucleoside Reverse Transcriptase Inhibitors (NRTIs)**—Zidovudine and Lamivudine—combined with a **Protease Inhibitor (PI)** like Indinavir (or Lopinavir/Ritonavir in more recent guidelines) [2]. The duration of PEP is strictly **4 weeks (28 days)**. **Analysis of Incorrect Options:** * **Option A:** This is a "basic regimen." While used for low-risk exposures, a needle stick from a known positive patient warrants the addition of a third drug for maximum efficacy [2]. * **Option B:** Nevirapine is contraindicated in PEP because of the risk of severe hepatotoxicity and Stevens-Johnson Syndrome in HIV-negative individuals receiving it for prophylaxis. * **Option D:** Combining Zidovudine and Stavudine is pharmacologically irrational as they compete for the same phosphorylation pathway (antagonistic effect). **NEET-PG High-Yield Pearls:** * **Timing:** PEP should ideally be started within **2 hours**, but can be initiated up to **72 hours** post-exposure. It is generally not recommended after 72 hours. * **Current Preferred Regimen (Updated):** While Indinavir was the classic choice, modern guidelines now prefer **Tenofovir + Lamivudine + Dolutegravir** due to better tolerability. * **Testing Schedule:** Baseline testing [1] is followed by repeat HIV testing at 6 weeks, 12 weeks, and 6 months [1].

Question 15: A subject was brought to the Casualty with a history of RTA and head injury. On examination, he was conscious. When the doctor asked questions about the incident, his answers were irrelevant to the questions, but his speech was fluent. What could be the possible site of injury?

A. Brain stem
B. Inferior frontal gyrus
C. Superior temporal gyrus (Correct Answer)
D. Pre-central gyrus

Explanation: ***Correct Answer: Superior temporal gyrus*** - The patient exhibits **fluent aphasia** (fluent speech) with severely **impaired comprehension** (irrelevant answers), which is the hallmark of **Wernicke's aphasia** [1]. - **Wernicke's area**, responsible for language comprehension, is located in the posterior aspect of the dominant hemisphere's **superior temporal gyrus** [1]. *Incorrect: Pre-central gyrus* - This area houses the primary **motor cortex**; damage typically results in contralateral **hemiparesis** or paralysis, not selective language comprehension deficits [1]. - Although cortical damage can cause speech articulation issues (**dysarthria**), it does not account for the specific fluent aphasia with catastrophic loss of understanding described. *Incorrect: Inferior frontal gyrus* - The dominant inferior frontal gyrus contains **Broca's area**, damage to which results in **non-fluent aphasia** (impaired speech production) with preserved comprehension [1]. - This presentation (fluent speech, poor comprehension) is diametrically opposite to the expected profile of **Broca's aphasia** [1]. *Incorrect: Brain stem* - Injury here often causes severe alterations in **consciousness**, cranial nerve palsies, or **dysarthria** due to involvement of motor pathways. - The brain stem is not primarily involved in complex, higher-order language functions like comprehension; pure Wernicke's aphasia is a **cortical syndrome** [1].

Question 16: A patient presents with contralateral face, arm, and leg weakness. NCCT shows intracerebral hemorrhage (ICH). What is the most likely location of the CNS bleed?

A. Pons
B. Midbrain
C. Basal ganglia (Correct Answer)
D. Medulla

Explanation: ***Basal ganglia*** - The **basal ganglia**, particularly the **putamen**, is the most common site for hypertensive intracerebral hemorrhage, which aligns perfectly with the deep parenchymal bleed seen on the provided NCCT scan. - A lesion in this location classically damages the adjacent **internal capsule**, where motor fibers for the face, arm, and leg are tightly packed, resulting in **contralateral hemiparesis**. *Midbrain* - A midbrain hemorrhage would present with distinct cranial nerve deficits, most notably **oculomotor nerve (CN III) palsy**, causing a "down and out" eye position, ptosis, and a dilated pupil. - Other characteristic signs include altered consciousness and **vertical gaze palsy** (Parinaud syndrome), which are absent in this patient's pure motor presentation. *Pons* - Pontine hemorrhages have a catastrophic presentation, typically causing a rapid descent into **coma**, **quadriplegia**, and classic **pinpoint pupils** due to disruption of descending sympathetic pathways. - The patient's presentation of contralateral hemiparesis without coma or pupillary changes is inconsistent with a pontine bleed. *Medulla* - Medullary hemorrhages are rare and cause specific brainstem syndromes like **Wallenberg syndrome**, characterized by vertigo, nystagmus, dysphagia, and ipsilateral facial numbness. - These syndromes involve complex crossed sensory and motor deficits, not the uniform contralateral motor weakness described in the question.

Question 17: What is the probable diagnosis for a patient who exhibits miosis, anhidrosis, mild ptosis, and a persistent small pupil even in low light conditions?

A. Horner syndrome (Correct Answer)
B. Argyll Robertson pupil
C. Marcus Gunn pupil
D. Adie's tonic pupil

Explanation: No changes were made to the text as none of the provided references reached the relevance threshold of 7/10 for the specific topic of Horner syndrome diagnosis and its differentials. The provided references largely discussed coagulation (mislabeled chapters), neurological signs of intracranial pressure, or general pupillary reflexes without specific diagnostic criteria for Horner syndrome or its differentiating features like anhidrosis.

Question 18: A 30-year-old male presents with deep-seated retro-orbital pain from cluster headache. What is the best management?

A. Oxygen (Correct Answer)
B. Verapamil
C. Lithium
D. Topiramate

Explanation: ***Oxygen*** - **High-flow oxygen** (100% at 7-15 L/min) is the safest and most effective **first-line abortive treatment** for an acute cluster headache attack [1] - It works rapidly to cause **vasoconstriction** and often terminates the severe retro-orbital pain within **15 to 20 minutes** - This is the preferred treatment for acute attacks due to its rapid onset and excellent safety profile *Verapamil* - Verapamil is a calcium channel blocker and is considered the **first-line prophylactic agent** for both episodic and chronic cluster headache, not acute treatment [1] - Its mechanism of action requires time, rendering it ineffective for terminating an ongoing acute pain episode - Used to prevent future attacks, not to abort current ones *Lithium* - Lithium is a prophylactic treatment reserved mainly for patients with **chronic cluster headache** or those who do not respond to Verapamil [1] - It has a slow onset of action and is not used to manage the acute pain of a cluster attack - Requires therapeutic monitoring due to narrow therapeutic window [1] *Topiramate* - Topiramate is an established prophylactic treatment primarily for **migraine**, and occasionally used as a second-line prophylactic agent for cluster headache - As a prophylactic medication, it plays **no role** in the acute termination or abortive management of a cluster headache episode

Question 19: A patient presents with symmetrical leg weakness and areflexia. He had developed diarrhoea 2 weeks ago. He was diagnosed as having GBS. What is the cause?

A. Cord inflammation
B. Demyelination of the spinal cord
C. Demyelination of A, B-fibers (Correct Answer)
D. Demyelination of B-fibers

Explanation: ***Demyelination of A, B-fibers***- GBS is an acute **demyelinating polyneuropathy** primarily affecting the myelin sheath of peripheral nerves and nerve roots (PNS involvement) [1].- Demyelination of large myelinated **A-fibers** (motor and sensory) explains the severe **symmetrical weakness** and **areflexia** [1]; demyelination of **B-fibers** contributes to common **autonomic dysfunction**.*Demyelination of B-fibers*- B-fibers are primarily **preganglionic autonomic fibers**; their demyelination causes autonomic instability (e.g., blood pressure fluctuation) but does not account for the profound motor weakness and areflexia that define GBS [2].- The cardinal features of GBS (weakness and areflexia) result from damage to the larger **A-fibers** (motor nerves) [1]. *Demyelination of the spinal cord*- GBS is a disease of the **Peripheral Nervous System (PNS)**, affecting nerve roots and peripheral nerves [2].- Demyelination confined to the spinal cord is characteristic of **Central Nervous System (CNS)** demyelinating diseases, such as **Transverse Myelitis** or **Multiple Sclerosis** [3]. *Cord inflammation*- **Spinal cord inflammation** or myelitis is a CNS process and typically results in upper motor neuron signs (spasticity, brisk reflexes) or distinct sensory levels, which are not seen in GBS.- GBS involves inflammation and attack on the **peripheral nerve myelin** or axons, specifically in the nerve roots and distal peripheral nerves [1].

Question 20: A 35-year-old female with progressive limb weakness for the past 1 year. On examination, muscle fasciculations and hypertonia are noted, and the sensory system is intact. What is the diagnosis?

A. Multifocal motor neuropathy
B. Becker muscular dystrophy
C. Spinal muscular atrophy
D. ALS (Correct Answer)

Explanation: ***Correct: ALS (Amyotrophic Lateral Sclerosis)*** - This patient presents with the classic triad of ALS: **progressive limb weakness, fasciculations (LMN sign), and hypertonia/spasticity (UMN sign)** [1] - The combination of **both upper and lower motor neuron signs** is pathognomonic for ALS [1] - **Sensory sparing** is characteristic - ALS affects motor neurons only [1] - Age and progressive course over 1 year fits the typical presentation - El Escorial criteria require UMN + LMN signs in multiple regions *Incorrect: Multifocal motor neuropathy* - This is a **pure lower motor neuron disorder** with conduction block - Would present with fasciculations and weakness but **NO hypertonia** (no UMN involvement) [1] - Treatable with immunotherapy, making it an important differential to exclude [1] *Incorrect: Becker muscular dystrophy* - This is a **primary muscle disease**, not a motor neuron disorder - **No fasciculations** would be present (fasciculations indicate motor neuron pathology) [2] - Predominantly affects males (X-linked), presents with proximal weakness and calf pseudohypertrophy - Elevated CK levels would be expected *Incorrect: Spinal muscular atrophy* - This is a **pure lower motor neuron disorder** due to anterior horn cell degeneration - Would NOT present with **hypertonia or UMN signs** - Typically presents in childhood/early life with symmetric proximal weakness - Associated with SMN1 gene mutations

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Cerebrovascular Diseases

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Seizure Disorders and Epilepsy

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Headache Disorders

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Movement Disorders

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Demyelinating Diseases

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Neurodegenerative Disorders

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Neuromuscular Junction Disorders

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Peripheral Neuropathies

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CNS Infections

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Neuro-oncology

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Neurology — MCQs

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