Neurology Practice Questions

Q: What is a contraindication for thrombolytic therapy (PA) in ischemic stroke?

Comatose patient. **Explanation:** Thrombolytic therapy with recombinant tissue plasminogen activator (rtPA) is the gold standard for acute ischemic stroke [1], but it carries a significant risk of hemorrhagic transformation. Therefore, strict adherence to inclusion and exclusion criteria is mandatory. **Why "Comatose patient" is the correct answer:** A comatose state (depressed level of consciousness) is considered a relative contraindication or a reason for extreme caution. In the context of a suspected stroke, coma often suggests a very large hemispheric infarction, a brainstem stroke, or a non-ischemic cause (such as metabolic encephalopathy or post-ictal state). Large-volume infarcts have a significantly higher risk of symptomatic intracranial hemorrhage (sICH) following thrombolysis, and the clinical benefit in a comatose patient is often negligible compared to the risks. **Analysis of Incorrect Options:** * **A. Clinical diagnosis of stroke:** This is a prerequisite (inclusion criterion). Thrombolysis is initiated based on a clinical diagnosis supported by a CT scan to rule out hemorrhage [1]. * **B. Systolic BP < 180 mm Hg:** This is actually a requirement for therapy. To safely administer rtPA, BP must be maintained below **185/110 mm Hg**. * **C. Onset 185/110, it must be lowered (e.g., using Labetalol or Nicardipine) before starting rtPA. * **Golden Hour:** The benefit of rtPA is time-dependent; "Time is Brain." * **Exclusion Lab Value:** Platelet count 1.7.

Q: All of the following cause subcortical dementia, EXCEPT?

Alzheimer's disease. ### Explanation Dementia is broadly classified into **Cortical** and **Subcortical** types based on the primary site of pathology and the clinical presentation. **1. Why Alzheimer’s Disease is the Correct Answer:** Alzheimer’s disease is the prototypical **Cortical Dementia**. The pathology primarily involves the cerebral cortex (specifically the hippocampus and temporoparietal lobes). Clinically, it is characterized by "The 4 A's": **Amnesia** (memory loss), **Aphasia** (language impairment), **Apraxia** (motor task failure), and **Agnosia** (failure to recognize objects). In cortical dementia, motor functions usually remain intact until the very late stages. **2. Analysis of Incorrect Options (Subcortical Dementias):** Subcortical dementias involve structures like the basal ganglia, thalamus, and brainstem. They are characterized by "psychomotor slowing," personality changes, and early motor symptoms. * **Parkinsonism:** Dementia occurs due to Lewy body deposition in subcortical nuclei; it features prominent bradyphrenia (slowed thinking) and motor tremors. * **HIV Encephalopathy (AIDS Dementia Complex):** Primarily affects the subcortical white matter and basal ganglia, leading to cognitive slowing and motor deficits. * **Progressive Supranuclear Palsy (PSP):** A "Parkinson-plus" syndrome involving subcortical degeneration; it presents with vertical gaze palsy and subcortical cognitive decline. **Clinical Pearls for NEET-PG:** * **Cortical Dementia:** Memory + Language + Perception (e.g., Alzheimer’s, Pick’s disease). * **Subcortical Dementia:** Memory + Movement + Mood (e.g., Huntington’s, Wilson’s, PSP, Parkinson’s). * **Key Distinguisher:** Aphasia and Agnosia are **absent** in subcortical dementia but **present** in cortical dementia. * **Multi-infarct dementia** can be both cortical and subcortical depending on the site of the stroke.

Q: What is the first-line treatment for generalized onset tonic-clonic seizures?

Lamotrigine. **Explanation:** The management of Generalized Tonic-Clonic Seizures (GTCS) has evolved, with a shift toward broad-spectrum Antiepileptic Drugs (AEDs) that offer better tolerability and fewer drug interactions. **Why Lamotrigine is Correct:** **Lamotrigine** is currently considered a first-line treatment for generalized onset tonic-clonic seizures. It acts by blocking voltage-gated sodium channels and inhibiting the release of glutamate. It is preferred due to its broad-spectrum efficacy and favorable side-effect profile compared to older agents. Notably, it is also a first-line choice in pregnancy (though doses may need adjustment). While **Valproate** was historically the "gold standard," Lamotrigine and Levetiracetam are now preferred first-line options, especially in females of childbearing age due to Valproate’s teratogenicity. **Analysis of Incorrect Options:** * **Phenytoin:** While effective for GTCS, it is no longer first-line due to its non-linear (zero-order) kinetics, narrow therapeutic index, and significant long-term side effects (gingival hyperplasia, hirsutism, osteomalacia). * **Levetiracetam:** This is also a first-line broad-spectrum AED. However, in many standardized clinical guidelines and recent NEET-PG patterns, Lamotrigine is frequently highlighted as the preferred initial monotherapy for generalized seizures. * **Ethosuximide:** This is the drug of choice for **Absence Seizures** only. It is ineffective against GTCS as it specifically targets T-type calcium channels in the thalamus. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC) for GTCS:** Valproate (Most effective, but avoid in pregnancy); Lamotrigine/Levetiracetam (Preferred alternatives). * **DOC for Absence Seizures:** Ethosuximide (Valproate if GTCS is also present). * **DOC for Myoclonic Seizures:** Valproate. * **Stevens-Johnson Syndrome (SJS):** A serious risk with Lamotrigine; always start with a low dose and titrate slowly.

Q: A patient is able to recognise a person by name but not by face. The lesion in this case is in which lobe of the brain?

Temporal lobe. ### Explanation The clinical scenario describes **Prosopagnosia** (face blindness), which is the inability to recognize familiar faces despite intact vision and the ability to recognize individuals by other cues, such as their voice or name [1]. **1. Why the Temporal Lobe is Correct:** Face recognition is a complex cognitive process localized to the **Fusiform Gyrus** (specifically the Fusiform Face Area), which is located on the basal surface of the **temporal and occipital lobes** [3]. In clinical neurology and standard medical examinations, prosopagnosia is most strongly associated with lesions in the **inferior temporal lobe** (often bilateral or right-sided) [1]. This area is part of the "ventral stream" (the "What" pathway) of visual processing, which identifies objects and faces. **2. Why Other Options are Incorrect:** * **Frontal Lobe:** Primarily involved in executive function, motor control (Broca’s area), and personality. Lesions here lead to motor aphasia or behavioral changes, not recognition deficits. * **Occipital Lobe:** While the primary visual cortex is here, a pure occipital lesion would cause visual field defects (like hemianopia) or cortical blindness, rather than a specific deficit in facial recognition [3]. * **Post Parietal Region:** This area is part of the "dorsal stream" (the "Where" pathway), involved in spatial awareness and motion. Lesions here lead to neglect syndromes, optic ataxia, or Balint’s syndrome. **3. High-Yield Clinical Pearls for NEET-PG:** * **Prosopagnosia:** Associated with the **Fusiform Gyrus** [1]. * **Agnosia:** Failure of recognition not due to sensory deficit [2]. * **Visual Agnosia:** Inability to name an object by sight (Temporal lobe) [2]. * **Astereognosis:** Inability to recognize objects by touch (Parietal lobe) [2]. * **Anosognosia:** Denial of illness (Right parietal lobe).

Q: A 60-year-old man presents to the emergency department with a generalized tonic-clonic seizure. He has no prior history of similar episodes or any other medical illnesses. Lorazepam 2 mg was administered, resulting in the cessation of seizure activity. Which of the following is the least likely cause of seizure in this patient?

Genetic disorder. ### Explanation The correct answer is **D. Genetic disorder**. **Why Genetic Disorder is the least likely:** Genetic (idiopathic) epilepsies typically manifest in childhood, adolescence, or early adulthood (usually before age 25). It is highly improbable for a primary genetic epilepsy to present for the first time at age 60 [1]. In an elderly patient with a "new-onset" seizure, the focus must always be on identifying **acquired** structural, metabolic, or toxic causes. **Analysis of Incorrect Options:** * **A. Alcohol withdrawal:** This is a common cause of new-onset seizures in adults. Withdrawal seizures typically occur 6–48 hours after the last drink and often present as generalized tonic-clonic seizures. * **B. Hyperglycemia:** Metabolic derangements (hypoglycemia, hyperglycemia, hyponatremia, or uremia) are frequent triggers for provoked seizures in the elderly. Non-ketotic hyperglycemia is a particularly well-known cause of focal or generalized seizures. * **C. Brain tumor:** In patients over the age of 50, structural brain lesions are a leading cause of new-onset seizures. Primary brain tumors (like glioblastoma) or metastatic disease (from lung or breast) must be ruled out via neuroimaging (MRI). **Clinical Pearls for NEET-PG:** * **Most common cause of seizures in elderly:** Stroke (Cerebrovascular disease) is the #1 cause, followed by neurodegenerative diseases (Alzheimer’s) and tumors. * **First-line management:** For status epilepticus or acute seizures, IV Lorazepam (0.1 mg/kg) is the benzodiazepine of choice. * **Work-up:** Any adult with a first-time seizure requires a CT/MRI to rule out structural lesions and blood work to rule out metabolic disturbances [1].

Q: A nurse is assessing the motor function of an unconscious male client. Which of the following would the nurse plan to use to test the client's peripheral response to pain?

Nail bed pressure. **Explanation:** In the assessment of an unconscious patient, distinguishing between **central** and **peripheral** painful stimuli is crucial for evaluating neurological integrity and the Glasgow Coma Scale (GCS) motor component. **1. Why Nail Bed Pressure is Correct:** To test a **peripheral response**, the stimulus must be applied to a limb. Applying pressure to the nail bed (using a pen or similar object) triggers a spinal reflex or a purposeful withdrawal/localization response. This helps determine if the patient can perceive pain in the extremities and whether the motor pathway from the brain to the peripheral nerves is intact. **2. Analysis of Incorrect Options:** * **A. Sternal Rub:** This is a **central stimulus**. It involves firm pressure on the sternum and is used to assess the brain's overall arousal level rather than peripheral nerve function. * **C. Pressure on the Orbital Rim:** This involves applying pressure to the supraorbital notch. It is a **central stimulus** used to elicit a response from the cranial nerves and the brainstem. * **D. Squeezing the Sternocleidomastoid (Trapezius Squeeze):** Squeezing the trapezius muscle or the sternocleidomastoid is considered a **central stimulus** because it targets the proximal midline structures. **NEET-PG High-Yield Pearls:** * **Central Stimulus:** Used to elicit the "Best Motor Response" in GCS (e.g., Trapezius squeeze, Supraorbital pressure, Sternal rub). * **Peripheral Stimulus:** Used specifically to check for localized nerve injury or spinal cord integrity (e.g., Nail bed pressure). * **Clinical Caution:** Avoid repeated sternal rubs as they can cause bruising and tissue damage. Supraorbital pressure is contraindicated in patients with suspected frontal skull fractures. * **GCS Motor Scoring:** Localization (M5) requires the patient to move a limb toward a central stimulus, whereas Withdrawal (M4) is a flexion response to a peripheral stimulus.

Q: Tumefactive lesions are seen most commonly in which disease?

Multiple sclerosis. ### Explanation **Correct Answer: B. Multiple Sclerosis** **Tumefactive Demyelinating Lesions (TDLs)** are a rare variant of demyelinating disease characterized by large, tumor-like brain lesions. These lesions are typically defined as being **>2 cm in diameter**, often associated with perilesional edema and mass effect. While they can mimic high-grade gliomas or brain abscesses on imaging, they are most commonly associated with **Multiple Sclerosis (MS)** [1]. On MRI, TDLs often show a characteristic **"open-ring" enhancement**, where the incomplete portion of the ring faces the gray matter of the cortex [1]. This is a high-yield diagnostic sign for demyelination over malignancy. **Why other options are incorrect:** * **A. Reiter’s Disease (Reactive Arthritis):** This is a seronegative spondyloarthropathy characterized by the triad of urethritis, conjunctivitis, and arthritis. It does not involve the central nervous system (CNS) white matter. * **C. Paget Disease:** This is a localized disorder of bone remodeling resulting in thickened, structurally weak bone. While it can cause neurological complications via nerve compression (e.g., deafness or spinal stenosis), it does not produce intraparenchymal brain lesions. * **D. Marfan Syndrome:** This is a connective tissue disorder caused by *FBN1* gene mutations. It primarily affects the skeletal, ocular, and cardiovascular systems (e.g., aortic dissection), not the CNS parenchyma. **NEET-PG High-Yield Pearls:** * **Imaging Hallmark:** Open-ring enhancement (suggests an active inflammatory front) [1]. * **Histology:** Creutzfeldt cells (astrocytes with fragmented nuclear material) are often seen in TDLs. * **Management:** Unlike tumors, TDLs usually show a dramatic response to high-dose intravenous corticosteroids. * **Differential:** Marburg variant of MS is a fulminant, monophasic form of demyelination that can also present with large, aggressive lesions.

Q: Which of the following causes distal myopathy?

Myotonic dystrophy. In clinical neurology, most primary muscle diseases (myopathies) present with **proximal** muscle weakness (e.g., difficulty climbing stairs or combing hair). However, a specific subset of conditions presents with **distal** weakness (difficulty with hand grip or foot drop). **Why Myotonic Dystrophy is Correct:** **Myotonic Dystrophy (Type 1)** is the most common adult-onset muscular dystrophy. Unlike Duchenne or Becker, it characteristically involves the **distal muscles** (hands and feet), along with the face, neck (sternocleidomastoids), and ptosis. The underlying pathology involves a CTG repeat expansion in the DMPK gene, leading to "myotonia" (delayed muscle relaxation). **Analysis of Incorrect Options:** * **Duchenne (DMD) and Becker (BMD) Muscular Dystrophy:** These are X-linked recessive disorders caused by dystrophin mutations [1]. They classically present with **proximal** weakness, starting in the pelvic girdle (Gower’s sign) and progressing to the shoulder girdle. * **Polymyositis:** This is an inflammatory myopathy. The hallmark clinical feature is subacute, symmetrical **proximal** muscle weakness. Distal involvement is rare and usually occurs only in very advanced stages. **NEET-PG High-Yield Pearls:** * **Distal Myopathy Differential:** Myotonic Dystrophy, Inclusion Body Myositis (IBM - involves finger flexors), Miyoshi Myopathy, and Welander Myopathy. * **Myotonic Dystrophy Clinical Triad:** Distal weakness + Myotonia (grip/percussion) + Multi-system involvement (Frontal balding, Cataracts, Heart block, and Gonadal atrophy). * **Genetic Pattern:** Myotonic Dystrophy Type 1 shows **Anticipation** (worsening severity in successive generations due to triplet repeat expansion).

Q: The site of lesion in unilateral past pointing nystagmus is?

Cerebellar hemisphere. ### Explanation The correct answer is **D. Cerebellar hemisphere.** **1. Understanding the Mechanism** Past pointing (dysmetria) and nystagmus are classic signs of cerebellar dysfunction. When a lesion occurs in the **cerebellar hemisphere**, it disrupts the coordination of voluntary movements on the **ipsilateral** (same) side. * **Past pointing:** In cerebellar lesions, the patient overshoots the target because the cerebellum fails to provide the necessary "braking" signal to the muscles. * **Nystagmus:** Cerebellar nystagmus is typically coarse, gaze-evoked, and increases in intensity when looking toward the side of the lesion. The combination of unilateral past pointing and nystagmus strongly localizes the pathology to the cerebellar hemisphere rather than the vestibular apparatus. **2. Analysis of Incorrect Options** * **Options A & B (Posterior/Superior Semicircular Canals):** Lesions in the semicircular canals (like BPPV) cause positional vertigo and specific patterns of nystagmus (e.g., geotropic or torsional). While vestibular lesions cause past pointing, it is usually compensatory and occurs in the direction of the slow component of nystagmus, unlike the primary motor incoordination seen in cerebellar lesions. * **Option C (Flocculonodular Lobe):** This is the "vestibulocerebellum." Lesions here primarily cause **truncal ataxia** and equilibrium imbalances (drunken gait) rather than unilateral limb signs like past pointing. **3. Clinical Pearls for NEET-PG** * **Rule of Sides:** Cerebellar lesions produce **ipsilateral** symptoms (Ataxia, Hypotonia, Past pointing, Intention tremor). * **Vestibular vs. Cerebellar Nystagmus:** Vestibular nystagmus is suppressed by visual fixation; cerebellar nystagmus is **not** suppressed and may even be enhanced. * **Finger-Nose Test:** This is the standard clinical bedside test to elicit past pointing in suspected cerebellar hemisphere lesions.

Question 1

What is a contraindication for thrombolytic therapy (PA) in ischemic stroke?

Accepted Answer

Comatose patient

Answer

Clinical diagnosis of stroke

Answer

Systolic blood pressure < 180 mm of Hg

Answer

Onset of symptoms < 4.5 hours

Question 2

All of the following cause subcortical dementia, EXCEPT?

Accepted Answer

Alzheimer's disease

Answer

Parkinsonism

Answer

HIV encephalopathy

Answer

Progressive Supranuclear palsy

Question 3

What is the first-line treatment for generalized onset tonic-clonic seizures?

Accepted Answer

Lamotrigine

Answer

Phenytoin

Answer

Levetiracetam

Answer

Ethosuximide

Question 4

A patient is able to recognise a person by name but not by face. The lesion in this case is in which lobe of the brain?

Accepted Answer

Temporal lobe

Answer

Frontal lobe

Answer

Occipital lobe

Answer

Post parietal region

Question 5

A 60-year-old man presents to the emergency department with a generalized tonic-clonic seizure. He has no prior history of similar episodes or any other medical illnesses. Lorazepam 2 mg was administered, resulting in the cessation of seizure activity. Which of the following is the least likely cause of seizure in this patient?

Accepted Answer

Genetic disorder

Answer

Alcohol withdrawal

Answer

Hyperglycemia

Answer

Brain tumor

Question 6

A nurse is assessing the motor function of an unconscious male client. Which of the following would the nurse plan to use to test the client's peripheral response to pain?

Accepted Answer

Nail bed pressure

Answer

Sternal rub

Answer

Pressure on the orbital rim

Answer

Squeezing of the sternocleidomastoid muscle

Question 7

Tumefactive lesions are seen most commonly in which disease?

Accepted Answer

Multiple sclerosis

Answer

Reiter's disease

Answer

Paget disease

Answer

Marfan syndrome

Question 8

Which of the following causes distal myopathy?

Accepted Answer

Myotonic dystrophy

Answer

Duchenne Muscular Dystrophy

Answer

Becker Muscular Dystrophy

Answer

Polymyositis

Question 9

The site of lesion in unilateral past pointing nystagmus is?

Accepted Answer

Cerebellar hemisphere

Answer

Posterior semicircular canal

Answer

Superior semicircular canal

Answer

Flocculonodular lobe

Question 10

A patient presents with the following neurological findings: loss of pain and temperature sensation over the left side of the face, loss of pain and temperature sensation in the right arm and leg, and normal tactile and vibratory sensations on the face, body, and extremities. Where is the lesion located?

Accepted Answer

Dorsolateral medulla

Answer

Mesencephalon at the level of the inferior colliculus

Answer

Spinal cord at the cervical enlargement

Answer

Posterior limb of the internal capsule

Neurology — MCQs

Neurology — MCQs

On this page

Practice by Chapter

Want unlimited practice?