Neurology Practice Questions

Q: Which cranial nerve is involved in Weber syndrome?

III. **Explanation:** **Weber Syndrome** (Superior Alternating Hemiplegia) is a midbrain stroke syndrome typically caused by an occlusion of the paramedian branches of the **posterior cerebral artery**. **1. Why Option B is Correct:** The lesion involves the **ventral (anterior) midbrain**. This area contains the **oculomotor nerve (CN III) fascicles** [1] and the **cerebral peduncle** (containing the corticospinal and corticobulbar tracts). Damage to the CN III fibers results in an **ipsilateral** (same side) third nerve palsy, characterized by ptosis, a "down and out" eye, and a dilated pupil [1]. **2. Why Incorrect Options are Wrong:** * **Option A (CN II):** The optic nerve is part of the diencephalon and is not located in the midbrain. Lesions here cause visual field defects, not brainstem syndromes. * **Option C (CN IV):** The trochlear nerve nuclei are in the lower midbrain, but the nerve exits posteriorly. It is involved in syndromes affecting the dorsal midbrain (e.g., Parinaud syndrome), not the ventral aspect. * **Option D (CN V):** The trigeminal nerve nuclei span the brainstem, but the nerve exits at the level of the **pons**. Lesions here would suggest Millard-Gubler or Foville syndrome. **3. Clinical Pearls for NEET-PG:** * **The "Alternating" Rule:** Brainstem syndromes are "alternating" because they present with **ipsilateral** cranial nerve deficits and **contralateral** hemiplegia (due to damage to the corticospinal tract before it decussates in the medulla). * **Weber vs. Benedikt:** Both involve CN III. However, Weber involves the cerebral peduncle (hemiparesis), while **Benedikt syndrome** involves the red nucleus/substantia nigra (resulting in tremors/ataxia). * **Classic Presentation:** Ipsilateral CN III palsy [1] + Contralateral spastic paralysis.

Q: A 20-year-old man suffered a significant closed head injury after a diving accident, resulting in minor memory impairment but a full recovery. A few months later, he experiences a witnessed loss of consciousness with some arm and leg twitching. Following the event, he is disoriented for 2 hours before returning to his baseline. There was no incontinence or tongue biting, and his examination is normal. Which of the following is the most likely diagnosis?

Generalized seizure. **Explanation:** The patient presents with a classic case of **Post-traumatic Epilepsy (PTE)**. The key to the diagnosis lies in the **Post-ictal state** (disorientation for 2 hours), which is the most reliable clinical feature distinguishing a seizure from syncope [2]. **1. Why Generalized Seizure is correct:** The history of a significant closed head injury (diving accident) creates a cortical scar that acts as an epileptogenic focus. The witnessed loss of consciousness followed by motor activity (twitching) and a prolonged period of post-event confusion (2 hours) strongly points toward a seizure [1]. While the seizure may have started focally (given the trauma) [3], the immediate loss of consciousness and bilateral motor involvement categorize it as a generalized event (or a focal seizure with bilateral tonic-clonic evolution). **2. Why other options are incorrect:** * **Syncope & Cardiac Arrhythmia:** Recovery in syncope is almost instantaneous [2]. A post-ictal state lasting 2 hours is incompatible with syncope, where the brain resumes normal function as soon as perfusion is restored. * **Focal Seizure:** While the etiology is focal (trauma), a "focal seizure" (without impairment of awareness) would not involve a loss of consciousness or a prolonged post-ictal state [3]. **NEET-PG Clinical Pearls:** * **Post-ictal Confusion:** The "Gold Standard" clinical differentiator. Syncope = 5–30 minutes (or hours) [2]. * **Tongue Biting:** If present, lateral tongue biting is highly specific for generalized tonic-clonic seizures [1]. * **Post-traumatic Epilepsy:** Risk is highest in the first year following severe head trauma (depressed skull fracture, intracranial hemorrhage, or prolonged loss of consciousness). * **Todd’s Paralysis:** Focal neurological deficit (e.g., hemiparesis) following a seizure, lasting minutes to 24 hours, indicating a focal onset.

Q: CT scan of the head should be performed before lumbar puncture in all of the following conditions except?

Hypertension. The primary concern before performing a lumbar puncture (LP) is the risk of **brain herniation** due to a sudden pressure gradient change. A CT scan is indicated prior to LP only when there is clinical suspicion of increased intracranial pressure (ICP) or a space-occupying lesion (SOL). **Explanation of the Correct Answer:** * **A. Hypertension:** Chronic or essential hypertension is not a contraindication to LP. While a hypertensive emergency can cause encephalopathy, hypertension itself does not imply a risk of herniation unless accompanied by focal neurological deficits or papilledema. Therefore, a CT is not routinely required for hypertensive patients before an LP. **Explanation of Incorrect Options:** * **B. Immunocompromised state:** Patients with HIV/AIDS or those on immunosuppressants are at high risk for CNS infections (e.g., Toxoplasmosis, Cryptococcoma) or lymphomas, which act as SOLs. A CT is mandatory to rule out mass effect. * **C. Kernohan-Woltman sign:** This is a "false localizing sign" where a mass (like a subdural hematoma) causes the contralateral cerebral peduncle to be compressed against the tentorial edge, resulting in ipsilateral hemiparesis. It signifies advanced mass effect and impending herniation, making a pre-LP CT vital. * **D. Low GCS score:** A depressed level of consciousness (GCS 60, Immunocompromised state, History of CNS disease (stroke, mass), Recent seizure (within 1 week), Papilledema, Focal neurological deficits, and Abnormal level of consciousness. * **Kernohan’s Notch:** Remember it causes **ipsilateral** hemiparesis (paradoxical sign). * **Treatment:** If LP is delayed for CT in suspected meningitis, **always start empirical antibiotics first.**

Q: Which of the following statements is false regarding Multiple Sclerosis (MS)?

The pathological hallmark is axonal degeneration.. **Explanation:** **1. Why Option C is the correct (False) statement:** The pathological hallmark of Multiple Sclerosis (MS) is **demyelination**, not axonal degeneration [1]. MS is primarily an immune-mediated inflammatory disease where the myelin sheath surrounding the axons in the Central Nervous System (CNS) is destroyed by T-cells and B-cells [1]. While axonal loss/degeneration does occur (and is the major cause of permanent disability), it is a **secondary** process or a later consequence of the primary demyelinating insult. **2. Analysis of other options:** * **Option A:** This is a true statement. MS shows a strong female predilection (approx. 3:1 ratio) and typically presents in young adults (peak age 20–40 years) [1]. * **Option B:** These are well-established environmental risk factors. Low Vitamin D levels, cigarette smoking, and Epstein-Barr Virus (EBV) infection are high-yield risk factors associated with MS. * **Option C:** This is true. The **HLA-DRB1*15:01** allele is the strongest genetic risk factor identified, contributing significantly to the disease's heritability. **3. High-Yield Clinical Pearls for NEET-PG:** * **Lhermitte’s Sign:** An electric shock-like sensation radiating down the spine upon neck flexion (indicates cervical cord involvement). * **Uhthoff’s Phenomenon:** Worsening of neurological symptoms (especially vision) with increased body temperature. * **McDonald Criteria:** Used for diagnosis; requires "dissemination in time and space" [1]. * **CSF Findings:** Presence of **Oligoclonal bands** (IgG) not found in the serum [1]. * **MRI:** The gold standard investigation; look for **Dawson’s fingers** (periventricular demyelinating plaques) [1]. * **Treatment:** Acute relapses are managed with **IV Methylprednisolone**; Disease-Modifying Therapies (DMTs) like Interferon-beta or Ocrelizumab are used for long-term management [1].

Q: A man presents with aphasia, characterized by an inability to name objects and poor repetition, while comprehension, fluency, and articulation remain unaffected. What is the likely diagnosis?

Conduction aphasia. The clinical presentation described is a classic case of **Conduction Aphasia**. The hallmark of this condition is a **disproportionate impairment in repetition** despite preserved fluency and comprehension. **1. Why Conduction Aphasia is correct:** Conduction aphasia results from a lesion in the **arcuate fasciculus**, the white matter tract that connects Wernicke’s area (comprehension) to Broca’s area (production) [1]. Because both areas are intact, the patient can understand speech and produce fluent sentences. However, because the "bridge" between them is damaged, they cannot relay information from the sensory to the motor area, leading to poor repetition and word-finding difficulties (anomia) [1]. **2. Analysis of Incorrect Options:** * **Anomic Aphasia:** While it involves difficulty naming objects, repetition is typically **preserved**. It is the mildest form of aphasia. * **Transcortical Sensory Aphasia:** Similar to Wernicke’s (poor comprehension), but **repetition is remarkably preserved**. It occurs due to lesions in the watershed areas surrounding Wernicke’s area. * **Broca’s Aphasia:** Characterized by non-fluent, "telegraphic" speech and impaired articulation [1]. Comprehension is preserved, but repetition is impaired. **3. NEET-PG High-Yield Pearls:** * **The Repetition Test:** This is the most critical step in differentiating standard aphasias from "Transcortical" aphasias. In all Transcortical aphasias, repetition is **intact**. * **Arcuate Fasciculus:** Classically associated with conduction aphasia; located in the parietal operculum [1]. * **Paraphasic Errors:** Patients with conduction aphasia often make phonemic errors (e.g., saying "pork" instead of "fork") and will repeatedly try to correct themselves.

Q: Epilepsia partialis continua is present in which of the following conditions?

Rasmussen's encephalitis. **Explanation:** **Epilepsia Partialis Continua (EPC)** is a rare form of focal status epilepticus characterized by continuous, rhythmic, and repetitive muscle jerks (myoclonus) involving a specific body part (usually a hand or face). It remains localized to the site of origin but can persist for hours, days, or even years. [1] **1. Why Rasmussen’s Encephalitis is correct:** Rasmussen’s Encephalitis (RE) is the classic and most common cause of EPC in children. It is a progressive, chronic inflammatory disease (likely autoimmune) affecting one cerebral hemisphere. The localized cortical inflammation leads to intractable focal seizures, of which EPC is a hallmark feature. Over time, it results in progressive hemiparesis and cognitive decline. **2. Why the other options are incorrect:** * **Japanese Encephalitis (JE):** While JE is a common cause of viral encephalitis in India, it typically presents with generalized seizures, movement disorders (parkinsonism due to thalamic involvement), and altered sensorium, rather than the localized, continuous focal jerking of EPC. * **Tuberculosis Meningitis (TBM):** TBM primarily involves the basal meninges. While it can cause seizures due to infarcts or hydrocephalus, EPC is not a characteristic or defining feature of this condition. **Clinical Pearls for NEET-PG:** * **Definition:** EPC is defined as focal motor seizures occurring at least every few seconds for a minimum of one hour. * **Site of Pathology:** The "pacemaker" for EPC is located in the **Motor Cortex (Brodmann area 4)**. * **Other Causes:** In adults, EPC is often caused by focal cortical lesions like tumors, strokes, or metabolic derangements (e.g., Non-ketotic Hyperglycemic Coma). [1] * **Treatment of RE:** Often requires hemispherectomy in refractory cases to stop the progression of the disease.

Q: All of the following manifestations may be associated with lacunar infarcts, except:

Quadriplegia. **Explanation:** Lacunar infarcts are small (0.2 to 15 mm in diameter) subcortical strokes resulting from the occlusion of small penetrating branches of the cerebral arteries (e.g., lenticulostriate, thalamoperforating arteries). They are typically caused by **lipohyalinosis** or microatheroma secondary to chronic hypertension or diabetes. **Why Quadriplegia is the Correct Answer:** Quadriplegia (paralysis of all four limbs) implies a massive, bilateral involvement of the motor pathways, usually localized to the cervical spinal cord or the brainstem (e.g., a large basilar artery occlusion). Lacunar infarcts, by definition, are focal and small. While a lacunar stroke in the internal capsule can cause dense hemiplegia (one side), it cannot anatomically involve enough territory to cause simultaneous quadriplegia. **Analysis of Incorrect Options:** * **Pure Motor Loss:** The most common lacunar syndrome. It occurs due to an infarct in the **posterior limb of the internal capsule** or the basis pontis. * **Pure Sensory Loss:** Occurs due to a lacunar infarct in the **ventral posterolateral (VPL) nucleus of the thalamus** [1]. * **Ataxia:** Seen in **Ataxic Hemiparesis**, a classic lacunar syndrome where weakness and ataxia occur on the same side, typically due to lesions in the internal capsule or pons. **NEET-PG High-Yield Pearls:** 1. **Five Classic Lacunar Syndromes:** 1) Pure Motor Hemiparesis, 2) Pure Sensory Stroke, 3) Ataxic Hemiparesis, 4) Clumsy Hand-Dysarthria Syndrome, and 5) Mixed Sensorimotor Stroke. 2. **Key Risk Factor:** Hypertension is the single most important risk factor [2]. 3. **Imaging:** MRI (DWI) is more sensitive than CT for detecting these small lesions. 4. **Absence of "Cortical Signs":** Lacunar infarcts **never** present with aphasia, agnosia, neglect, or visual field defects, as the cerebral cortex is spared.

Q: Eaton Lambert syndrome is associated with which of the following?

Anti P/Q antibody. **Lambert-Eaton Myasthenic Syndrome (LEMS)** is a paraneoplastic autoimmune disorder of the neuromuscular junction, most commonly associated with **Small Cell Lung Cancer (SCLC)** [1]. ### Explanation of Options: * **A. Anti P/Q antibody (Correct):** LEMS is caused by autoantibodies directed against **presynaptic P/Q-type voltage-gated calcium channels (VGCC)** [1]. These antibodies block the influx of calcium into the nerve terminal, preventing the release of acetylcholine into the synaptic cleft, which leads to muscle weakness [1]. * **B. Anti-Hu antibody:** These are typically associated with **Paraneoplastic Encephalomyelitis** or sensory neuronopathy, also seen in Small Cell Lung Cancer, but not LEMS [2]. * **C. Anti-Jo-1 antibody:** This is a classic marker for **Dermatomyositis/Polymyositis**, specifically associated with "Antisynthetase Syndrome" (interstitial lung disease, Raynaud's, and mechanic's hands). * **D. Large cell carcinoma:** LEMS is strongly associated with **Small Cell Lung Cancer (SCLC)** (approx. 50-60% of cases), not large cell carcinoma [1]. ### High-Yield Clinical Pearls for NEET-PG: * **Clinical Triad:** Proximal muscle weakness (starts in lower limbs), autonomic dysfunction (dry mouth, erectile dysfunction), and depressed deep tendon reflexes. * **The "Lambert Sign":** Unlike Myasthenia Gravis, strength and reflexes in LEMS **improve with repeated muscle contraction** (post-exercise facilitation). * **Electrophysiology (NCS/EMG):** Shows a **"Decrement-Increment"** pattern. There is a low baseline compound muscle action potential (CMAP) that shows a **significant increment (>100%)** following high-frequency repetitive nerve stimulation or brief exercise. * **Treatment:** The first-line symptomatic treatment is **Amifampridine (3,4-diaminopyridine)**, which prolongs the depolarization of the presynaptic membrane [1].

Question 1

Which cranial nerve is involved in Weber syndrome?

Accepted Answer

III

Answer

II

Answer

IV

Answer

V

Question 2

A 20-year-old man suffered a significant closed head injury after a diving accident, resulting in minor memory impairment but a full recovery. A few months later, he experiences a witnessed loss of consciousness with some arm and leg twitching. Following the event, he is disoriented for 2 hours before returning to his baseline. There was no incontinence or tongue biting, and his examination is normal. Which of the following is the most likely diagnosis?

Accepted Answer

Generalized seizure

Answer

Syncope

Answer

Focal seizure

Answer

Cardiac arrhythmia

Question 3

Which of the following best describes a patient with a classical migraine?

Accepted Answer

A pulsating unilateral headache worsened with the movements of the head

Answer

A unilateral headache with unilateral visual loss and muscle aches

Answer

A left retro-orbital headache with rhinorrhea and red eye

Answer

A visual deficit that persists after cessation of a unilateral headache

Question 4

CT scan of the head should be performed before lumbar puncture in all of the following conditions except?

Accepted Answer

Hypertension

Answer

Immunocompromised state

Answer

Kernohan-Woltman sign

Answer

Low GCS score

Question 5

Which of the following statements is false regarding Multiple Sclerosis (MS)?

Accepted Answer

The pathological hallmark is axonal degeneration.

Answer

It is more common in women, with an age of onset typically between 20-40 years.

Answer

Risk factors include vitamin D deficiency and cigarette smoking.

Answer

HLA DRB1 in MHC class II is associated with approximately 10% of disease risk.

Question 6

A man presents with aphasia, characterized by an inability to name objects and poor repetition, while comprehension, fluency, and articulation remain unaffected. What is the likely diagnosis?

Accepted Answer

Conduction aphasia

Answer

Anomic aphasia

Answer

Transcortical sensory aphasia

Answer

Broca's aphasia

Question 7

Epilepsia partialis continua is present in which of the following conditions?

Accepted Answer

Rasmussen's encephalitis

Answer

Japanese encephalitis

Answer

Tuberculosis meningitis

Answer

None of the above

Question 8

Reversible dementia is a feature of which of the following conditions?

Accepted Answer

Hypothyroidism

Answer

Alzheimer's disease

Answer

Pick's disease

Answer

Multi-infarct dementia

Question 9

All of the following manifestations may be associated with lacunar infarcts, except:

Accepted Answer

Quadriplegia

Answer

Pure motor loss

Answer

Pure sensory loss

Answer

Ataxia

Question 10

Eaton Lambert syndrome is associated with which of the following?

Accepted Answer

Anti P/Q antibody

Answer

Anti HU antibody

Answer

Anti Jo 1 antibody

Answer

Large cell carcinoma

Neurology — MCQs

Neurology — MCQs

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