Neurology Practice Questions

Q: A 76-year-old woman is brought to the emergency department due to sudden loss of right-sided motor function in her face, arm, and leg. She has a past medical history of hypertension, hypercholesterolemia, and a previous transient ischemic attack. She was recently placed on Coumadin for new-onset atrial fibrillation. A computed tomography (CT) scan was performed. Which of the following neurologic structures is most commonly involved in this patient's injury?

Putamen. **Explanation:** The patient presents with a classic **hypertensive intracerebral hemorrhage (ICH)**. In an elderly patient with hypertension and anticoagulation (Coumadin) use, sudden focal neurological deficits are highly suggestive of a hemorrhagic stroke [1]. **1. Why Putamen is Correct:** The **putamen** is the most common site for spontaneous hypertensive intracerebral hemorrhage (involved in ~35-50% of cases). These hemorrhages typically occur due to the rupture of **Charcot-Bouchard aneurysms** in the small, deep penetrating branches of the middle cerebral artery (specifically the **lenticulostriate arteries**) [1]. Because the putamen lies adjacent to the internal capsule, large bleeds often compress or extend into the capsule, resulting in the contralateral hemiparesis (face, arm, and leg) seen in this patient [1]. **2. Why Other Options are Incorrect:** * **Internal Capsule:** While frequently involved via extension or compression from a putaminal bleed, it is less commonly the *primary* site of origin compared to the putamen. * **Thalamus:** This is the second most common site for hypertensive ICH. Thalamic bleeds typically present with prominent **sensory loss** rather than pure motor deficits and may involve upward gaze palsy. * **Corpus Callosum:** This is an extremely rare site for hypertensive hemorrhage; it is more commonly associated with high-grade gliomas (butterfly glioma) or trauma (diffuse axonal injury). **Clinical Pearls for NEET-PG:** * **Order of Frequency for Hypertensive ICH:** Putamen (Most common) > Thalamus > Pons > Cerebellum. * **Charcot-Bouchard Aneurysms:** Small microaneurysms in basal ganglia vessels; distinct from Berry aneurysms (which cause Subarachnoid Hemorrhage). * **CT Scan:** The gold standard for differentiating ischemic from hemorrhagic stroke in the acute setting (hemorrhage appears hyperdense/white) [1].

Q: Small fiber neuropathy is typically seen in which of the following conditions?

HIV. Small Fiber Neuropathy (SFN) involves selective damage to the small-diameter myelinated (Aδ) and unmyelinated (C) nerve fibers [1]. These fibers mediate pain, temperature sensation, and autonomic functions [2]. 1. Why HIV is the Correct Answer: HIV-associated distal sensory polyneuropathy (DSPN) is the most common neurological complication of HIV. It primarily manifests as a Small Fiber Neuropathy. The virus and its proteins (like gp120) cause indirect neurotoxicity via macrophage activation and cytokine release, leading to "dying-back" axonal degeneration. Patients typically present with "burning feet" syndrome, hyperalgesia, and allodynia, often with preserved reflexes and motor strength initially. 2. Why the Other Options are Incorrect: * Vitamin B12 Deficiency: Characteristically causes Subacute Combined Degeneration (SCD) of the spinal cord. It involves large fibers (posterior columns), leading to loss of vibration and position sense, and the pyramidal tracts. * Acute Intermittent Porphyria (AIP): This typically presents as a motor-predominant neuropathy. It mimics Guillain-Barré Syndrome (GBS) with proximal muscle weakness and autonomic instability, rather than a primary small fiber sensory loss. * Cisplatin Toxicity: This chemotherapeutic agent is notorious for causing a large fiber sensory neuronopathy (ganglionopathy) by damaging the dorsal root ganglia. It results in significant sensory ataxia and loss of proprioception. Clinical Pearls for NEET-PG: * Common causes of SFN: Diabetes Mellitus (most common overall), HIV, Amyloidosis, Sarcoidosis, and Tangier disease [1][2]. * Diagnosis: The "Gold Standard" for diagnosing SFN is Skin Biopsy to measure Intraepidermal Nerve Fiber Density (IENFD). * Nerve Conduction Studies (NCS): In pure SFN, NCS results are typically normal because they only measure large-diameter fiber conduction [2].

Q: 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?

Zidovudine + Lamivudine + Indinavir for 4 weeks. **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].

Q: Thrombosis of which of the following cerebral vessels most commonly leads to hemiplegia?

Middle cerebral artery. The **Middle Cerebral Artery (MCA)** is the most common site for cerebral thrombosis and embolism [1]. It is the largest branch of the internal carotid artery and supplies the majority of the lateral surface of the hemisphere, including the **precentral gyrus (motor cortex)** and the **internal capsule**. 1. **Why MCA is correct:** The MCA supplies the motor areas responsible for the face, arm, and trunk. Furthermore, its deep branches (Lenticulostriate arteries) supply the posterior limb of the internal capsule, where motor fibers for the entire contralateral half of the body are densely packed. Therefore, an MCA stroke typically results in **contralateral hemiplegia** (usually affecting the face and arm more than the leg). 2. **Why other options are incorrect:** * **Anterior Cerebral Artery (ACA):** Supplies the medial surface of the brain. A stroke here causes motor deficits primarily in the **contralateral lower limb** (leg and foot), rather than total hemiplegia. * **Posterior Cerebral Artery (PCA):** Primarily supplies the occipital lobe and midbrain. Clinical presentation usually involves **visual field defects** (homonymous hemianopia) rather than primary motor loss. * **Lateral Cerebral Artery:** This is not a standard anatomical term in neuroanatomy; it is likely a distractor for the MCA. **High-Yield Facts for NEET-PG:** * **Charcot’s Artery of Cerebral Hemorrhage:** The largest of the lenticulostriate branches of the MCA; it is the most common site for hypertensive hemorrhage. * **MCA Stroke Triad:** Contralateral hemiplegia, contralateral hemisensory loss, and Aphasia (if the dominant hemisphere is involved). * **ACA Stroke:** Characterized by urinary incontinence and "leg > arm" motor deficit.

Q: Carpal tunnel syndrome is caused by all of the following conditions EXCEPT:

Addison's disease. **Explanation:** Carpal Tunnel Syndrome (CTS) is a clinical condition resulting from the compression of the **median nerve** as it passes through the carpal tunnel, beneath the flexor retinaculum. Any condition that increases the volume of the tunnel contents or decreases the size of the tunnel can lead to CTS. **Why Addison’s Disease is the correct answer:** Addison’s disease (primary adrenocortical insufficiency) is characterized by a deficiency of cortisol and aldosterone [2]. It typically leads to weight loss and dehydration, which does not cause fluid retention or space-occupying lesions in the carpal tunnel. In contrast, **Cushing’s syndrome** (excess cortisol) and **Acromegaly** are endocrine causes of CTS due to soft tissue hypertrophy [1]. **Analysis of other options:** * **Rheumatoid Arthritis:** This is a common cause due to **synovitis** (inflammation of the synovial sheaths of the flexor tendons), which increases pressure within the tunnel [1]. * **Hypothyroidism:** Myxedematous tissue and **glycosaminoglycan deposition** in the connective tissues lead to increased pressure on the median nerve. * **Diabetes Mellitus:** Chronic hyperglycemia leads to the glycosylation of collagen and microvascular changes, making the nerve more susceptible to compression and ischemia. **High-Yield Clinical Pearls for NEET-PG:** * **Most common nerve compressed:** Median nerve. * **Sensory loss:** Affects the lateral 3.5 digits (spares the thenar eminence due to the superficial palmar cutaneous branch arising proximal to the tunnel). * **Motor loss:** Weakness and atrophy of **LOAF** muscles (Lateral two Lumbricals, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis). * **Clinical Tests:** Phalen’s test (most sensitive) and Tinel’s sign. * **Other common associations:** Pregnancy (fluid retention), Amyloidosis, and Chronic Renal Failure (hemodialysis-associated).

Q: Involvement of the pyramidal tract leads to all of the following except?

Fasciculation. This question tests the fundamental distinction between **Upper Motor Neuron (UMN)** and **Lower Motor Neuron (LMN)** lesions. [1] ### Why Fasciculation is the Correct Answer The **pyramidal tract** (Corticospinal tract) is the primary UMN pathway. [2] **Fasciculations** (visible muscle twitches) are a hallmark of **LMN lesions**, such as those affecting the anterior horn cells or peripheral nerves. [1] They occur due to the spontaneous depolarization of denervated motor units. In a pure pyramidal tract (UMN) lesion, the motor unit remains intact, so fasciculations are absent. ### Explanation of Incorrect Options (UMN Features) The other options are classic features of a pyramidal tract lesion: * **Spasticity (A):** UMN lesions lead to a loss of inhibitory control over the spinal cord, resulting in "clasp-knife" hypertonia. [3] * **Hyper-reflexia (B):** The loss of descending inhibition leads to an exaggerated muscle stretch reflex (increased deep tendon reflexes). [3] * **Positive Babinski Sign (D):** This is the pathognomonic sign of pyramidal tract damage, where the great toe dorsiflexes and other toes fan out in response to plantar stimulation. ### High-Yield Clinical Pearls for NEET-PG | Feature | UMN Lesion (Pyramidal) | LMN Lesion | | :--- | :--- | :--- | | **Muscle Tone** | Spastic (Hypertonia) [3] | Flaccid (Hypotonia) [1] | | **Reflexes** | Hyper-reflexia [3] | Hypo-reflexia/Areflexia | | **Atrophy** | Minimal (Disuse only) | Marked and Early [1] | | **Fasciculations** | Absent | **Present** [1] | | **Plantar Response** | Extensor (Babinski +) | Flexor (Normal) | **Note:** In the acute phase of a UMN lesion (e.g., acute stroke), "Spinal Shock" may occur, temporarily presenting with LMN-like features (flaccidity and areflexia) before spasticity develops.

Q: A 65-year-old diabetic woman develops weakness on the left side of the face, right arm, and right leg. She also has diplopia on left lateral gaze. What is the site of the lesion?

Left pons. ### Explanation This clinical presentation describes a **crossed hemiplegia** (ipsilateral cranial nerve palsy with contralateral motor weakness), which is the hallmark of a **brainstem lesion** [1]. **1. Why Left Pons is correct:** * **Ipsilateral Facial Weakness:** The patient has left-sided facial weakness. The facial nerve (CN VII) nucleus and fibers are located in the **pons**. In the brainstem, cranial nerve deficits occur on the same side as the lesion. * **Diplopia on Left Gaze:** This indicates a left **Abducens (CN VI) nerve** palsy [2]. The CN VI nucleus is also located in the pons. * **Contralateral Hemiparesis:** The right-sided weakness of the arm and leg is due to the involvement of the **Corticospinal tract** before it decussates in the medulla [1]. A lesion in the left pons affects the descending fibers, causing weakness on the right side of the body. * **Clinical Correlation:** This specific constellation (CN VI/VII palsy + contralateral hemiplegia) is known as **Millard-Gubler Syndrome**. **2. Why other options are incorrect:** * **Right Pons:** A lesion here would cause right-sided facial weakness and left-sided body weakness. * **Midbrain (Right/Left):** Midbrain lesions typically involve the **Oculomotor nerve (CN III)**, leading to ptosis and a "down and out" eye, rather than facial weakness or lateral gaze palsy. **3. High-Yield Pearls for NEET-PG:** * **Rule of 4s:** CN V, VI, VII, and VIII are associated with the **Pons**. * **Crossed Hemiplegia = Brainstem:** Always look for the side of the cranial nerve deficit to localize the side of the lesion [1]. * **Foville Syndrome:** Similar to Millard-Gubler but includes conjugate gaze palsy toward the side of the lesion (due to PPRF involvement). * **Diabetes:** A major risk factor for lacunar infarcts in the small perforating branches of the basilar artery supplying the pons.

Q: Which of the following is not a feature of a lateral cerebellar lesion?

Resting tremor. The cerebellum is responsible for the coordination, precision, and timing of voluntary movements. It acts as a "comparator," correcting errors during active movement. ### **Explanation of the Correct Answer** **A. Resting tremor:** This is the correct answer because resting tremors are a hallmark of **Basal Ganglia** lesions (specifically Parkinson’s disease), not cerebellar lesions. In contrast, cerebellar lesions result in **Intention tremors**, which appear or worsen during the execution of a purposeful movement and disappear at rest. ### **Analysis of Incorrect Options** * **B. Dysarthria:** Cerebellar lesions often cause "scanning speech" or "staccato speech," where words are broken into individual syllables with irregular emphasis. This is a form of motor speech disorder (dysarthria) due to poor coordination of the muscles of phonation. * **C. Nystagmus:** The cerebellum (specifically the vestibulocerebellum) coordinates eye movements. Damage leads to nystagmus, typically characterized by a fast component toward the side of the lesion. * **D. Loss of coordination:** This is the definition of **Ataxia**. Lateral cerebellar lesions affect the cerebrocerebellum, leading to decomposition of movement, dysmetria (past-pointing), and dysdiadochokinesia (inability to perform rapid alternating movements). ### **NEET-PG High-Yield Pearls** * **DANISH Mnemonic:** To remember cerebellar signs: **D**ysdiadochokinesia/Dysmetria, **A**taxia, **N**ystagmus, **I**ntention tremor, **S**lurred (scanning) speech, **H**ypotonia. * **Ipsilateral Rule:** Cerebellar lesions always manifest clinical signs on the **same side** as the lesion (ipsilateral) because the pathways decussate twice ("double-crossing"). * **Midline vs. Lateral:** Midline (vermis) lesions cause truncal ataxia and gait instability, while lateral (hemisphere) lesions cause limb ataxia and kinetic tremors.

Q: A 63-year-old man presents to the emergency department with transient symptoms of vertigo, slurred speech, diplopia, and paresthesia. He is symptom-free now, and clinical examination is entirely normal. His past medical history is significant for osteoarthritis, hypertension, and dyslipidemia. Which of the following is the most likely cause for his symptoms?

Posterior circulation transient ischemic attack (TIA). **Explanation:** The patient’s presentation is classic for a **Transient Ischemic Attack (TIA)** involving the **posterior (vertebrobasilar) circulation**. A TIA is defined as a transient episode of neurological dysfunction caused by focal brain, spinal cord, or retinal ischemia, without acute infarction [1]. 1. **Why Option A is correct:** The "4 Ds"—**D**izziness (vertigo), **D**iplopia, **D**ysarthria (slurred speech), and **D**ysphagia—along with sensory changes (paresthesia), are hallmark signs of brainstem or cerebellar ischemia [2]. The fact that the patient is now symptom-free with a normal clinical exam fits the definition of a TIA [1]. His risk factors (hypertension, dyslipidemia, age) further support an atherosclerotic etiology [3]. 2. **Why the other options are incorrect:** * **Anterior communicating artery aneurysm:** These typically present with features of subarachnoid hemorrhage (sudden "thunderclap" headache) or visual field defects due to compression, rather than transient brainstem symptoms. * **Hypertensive encephalopathy:** This presents with severe hypertension (usually Grade IV retinopathy), headache, confusion, and seizures. It does not typically cause focal, transient brainstem deficits that resolve completely. * **Pseudobulbar palsy:** This is a chronic clinical syndrome characterized by emotional lability, dysarthria, and dysphagia due to bilateral upper motor neuron lesions [2]. It is not transient or episodic. **NEET-PG High-Yield Pearls:** * **ABCD2 Score:** Used to predict the risk of stroke after a TIA (Age, Blood pressure, Clinical features, Duration, Diabetes). * **Posterior Circulation:** Supplies the "5 Cs"—Cerebellum, Cranial nerve nuclei, Colliculi, Conjugate gaze center, and Cortex (Occipital). * **Imaging:** Diffusion-weighted MRI is the gold standard to rule out an actual infarct (Stroke) in patients with TIA symptoms.

Question 1

A 76-year-old woman is brought to the emergency department due to sudden loss of right-sided motor function in her face, arm, and leg. She has a past medical history of hypertension, hypercholesterolemia, and a previous transient ischemic attack. She was recently placed on Coumadin for new-onset atrial fibrillation. A computed tomography (CT) scan was performed. Which of the following neurologic structures is most commonly involved in this patient's injury?

Accepted Answer

Putamen

Answer

Corpus callosum

Answer

Internal capsule

Answer

Thalamus

Question 2

Small fiber neuropathy is typically seen in which of the following conditions?

Accepted Answer

HIV

Answer

Vitamin B12 deficiency

Answer

Acute intermittent porphyria (AIP)

Answer

Cisplatin toxicity

Question 3

A patient presents with a right homonymous hemianopia, saccadic pursuit movements, and defective optokinetic nystagmus. Where is the lesion most likely located?

Accepted Answer

Parietal lobe

Answer

Frontal lobe

Answer

Occipital lobe

Answer

Temporal lobe

Question 4

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?

Accepted Answer

Zidovudine + Lamivudine + Indinavir for 4 weeks

Answer

Zidovudine + Lamivudine for 4 weeks

Answer

Zidovudine + Lamivudine + Nevirapine for 4 weeks

Answer

Zidovudine + Stavudine + Nevirapine for 4 weeks

Question 5

Thrombosis of which of the following cerebral vessels most commonly leads to hemiplegia?

Accepted Answer

Middle cerebral artery

Answer

Anterior cerebral artery

Answer

Posterior cerebral artery

Answer

Lateral cerebral artery

Question 6

Carpal tunnel syndrome is caused by all of the following conditions EXCEPT:

Accepted Answer

Addison's disease

Answer

Rheumatoid arthritis

Answer

Hypothyroidism

Answer

Diabetes mellitus

Question 7

Involvement of the pyramidal tract leads to all of the following except?

Accepted Answer

Fasciculation

Answer

Spasticity

Answer

Hyper-reflexia

Answer

Positive Babinski sign

Question 8

A 65-year-old diabetic woman develops weakness on the left side of the face, right arm, and right leg. She also has diplopia on left lateral gaze. What is the site of the lesion?

Accepted Answer

Left pons

Answer

Right pons

Answer

Right midbrain

Answer

Left midbrain

Question 9

Which of the following is not a feature of a lateral cerebellar lesion?

Accepted Answer

Resting tremor

Answer

Dysarthria

Answer

Nystagmus

Answer

Loss of coordination of movements

Question 10

A 63-year-old man presents to the emergency department with transient symptoms of vertigo, slurred speech, diplopia, and paresthesia. He is symptom-free now, and clinical examination is entirely normal. His past medical history is significant for osteoarthritis, hypertension, and dyslipidemia. Which of the following is the most likely cause for his symptoms?

Accepted Answer

Posterior circulation transient ischemic attack (TIA)

Answer

Anterior communicating artery aneurysm

Answer

Hypertensive encephalopathy

Answer

Pseudobulbar palsy

Neurology — MCQs

Neurology — MCQs

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