Neurology Practice Questions

Q: Avoiding response is due to which of the following brain lesions?

Contralateral parietal lobe lesions. **Explanation:** The **avoiding response** (or avoiding reaction) is a clinical sign characterized by an involuntary withdrawal or movement away from a tactile stimulus. It is considered a **release phenomenon** resulting from damage to the parietal lobe. **1. Why Option D is Correct:** The parietal lobe is responsible for processing sensory information and spatial awareness. When a lesion occurs in the **parietal lobe**, the normal "approach" or "grasp" tendencies (mediated by the frontal lobe) become unopposed. This results in the affected limb moving away from stimuli or the hand assuming a posture of extension and abduction when touched [2]. Because the motor and sensory pathways decussate, a lesion in one hemisphere manifests as an avoiding response in the **contralateral** (opposite) side of the body [1]. **2. Why Other Options are Incorrect:** * **Options A & B (Frontal Lobe):** Frontal lobe lesions typically produce the opposite effect—the **Grasp Reflex** [2]. In frontal lobe damage, the "avoiding" influence of the parietal lobe is lost, leading to an involuntary "approach" or grasping of objects. * **Option C (Ipsilateral):** Neurological deficits involving the cerebral hemispheres (like the parietal or frontal lobes) almost always manifest on the contralateral side of the body due to the crossing of the corticospinal and sensory tracts [1]. **Clinical Pearls for NEET-PG:** * **Frontal Lobe Lesion:** Leads to "Grasp Reflex" (Involuntary approach) [2]. * **Parietal Lobe Lesion:** Leads to "Avoiding Response" (Involuntary withdrawal). * **Magnetic Gait:** Often associated with frontal lobe/normal pressure hydrocephalus. * **Astereognosis & Hemispatial Neglect:** Classic signs of a parietal lobe lesion (specifically the non-dominant hemisphere for neglect) [3].

Q: A 25-year-old female at 16 weeks of gestation presents with excess vomiting, apathy, ataxia, nystagmus, and ophthalmoplegia. What is the most likely diagnosis?

Wernicke's encephalopathy. ### Explanation **Correct Answer: A. Wernicke’s encephalopathy** **1. Why it is correct:** The patient presents with the classic clinical triad of **Wernicke’s encephalopathy (WE)**: **Ophthalmoplegia** (including nystagmus), **Ataxia**, and **Confusion/Apathy**. In the context of pregnancy, WE is a rare but life-threatening complication of severe **Hyperemesis Gravidarum (HG)**. Prolonged vomiting leads to a critical deficiency of **Vitamin B1 (Thiamine)**. Thiamine is a co-factor for glucose metabolism; when depleted, it causes neuronal cell death, particularly in the mammillary bodies and dorsomedial thalamus. **2. Why the other options are incorrect:** * **B. Hyperemesis gravidarum:** While HG is the *underlying cause* of the thiamine deficiency, it refers specifically to the severe nausea and vomiting. Once neurological symptoms (ataxia, nystagmus) appear, the diagnosis progresses to WE. * **C. Chorea gravidarum:** This is a movement disorder characterized by involuntary, jerky, purposeless movements (chorea) during pregnancy, often associated with a history of rheumatic fever or SLE. It does not present with ophthalmoplegia or ataxia. * **D. Korsakoff’s encephalopathy:** This is the chronic, irreversible stage following WE. It is characterized by profound **anterograde amnesia and confabulation**. The acute presentation of eye signs and ataxia points specifically to Wernicke’s. **3. NEET-PG High-Yield Pearls:** * **The Golden Rule:** Always administer **Thiamine BEFORE Glucose** in a patient with HG. Giving IV dextrose first can precipitate or worsen WE by consuming the last remaining thiamine stores during glycolysis. * **Diagnosis:** Primarily clinical, but MRI may show bilateral symmetrical high signal intensities in the mammillary bodies. * **Triad:** Confusion, Ataxia, and Ophthalmoplegia (only present in ~16-38% of cases, making high clinical suspicion vital).

Q: What is the drug of choice for idiopathic intracranial hypertension?

Acetazolamide. **Explanation:** **Idiopathic Intracranial Hypertension (IIH)**, also known as Pseudotumor Cerebri, is characterized by increased intracranial pressure (ICP) without an identifiable cause (like a tumor or obstruction). **Why Acetazolamide is the Drug of Choice:** Acetazolamide is a **Carbonic Anhydrase Inhibitor**. In the CNS, carbonic anhydrase is essential for the production of Cerebrospinal Fluid (CSF) by the choroid plexus. By inhibiting this enzyme, Acetazolamide significantly reduces the rate of CSF secretion, thereby lowering intracranial pressure. It is the first-line medical therapy, often combined with weight loss [1]. **Analysis of Incorrect Options:** * **B. Glycerol & C. Mannitol:** These are **osmotic diuretics**. While they are highly effective for the *acute* management of cerebral edema or life-threatening elevations in ICP (e.g., head injury), they are not suitable for the long-term management of IIH due to the risk of rebound ICP and electrolyte imbalances. * **D. Dexamethasone:** While glucocorticoids reduce ICP in cases of vasogenic edema (associated with brain tumors or abscesses), they are **not recommended** for IIH. In fact, steroid withdrawal can sometimes trigger or worsen IIH. **Clinical Pearls for NEET-PG:** * **Classic Presentation:** Obese female of childbearing age presenting with headache, papilledema, and "whooshing" tinnitus (pulsatile). * **Side Effects of Acetazolamide:** Paresthesia (most common), metabolic acidosis, and hypokalemia [1]. * **Alternative:** If Acetazolamide is not tolerated, **Topiramate** is an alternative as it also has weak carbonic anhydrase inhibitory activity and aids in weight loss. * **Surgical Management:** If medical therapy fails and vision is threatened, Optic Nerve Sheath Fenestration or CSF shunting is performed.

Q: Which condition presents with normal nerve conduction studies but exhibits flaccidity?

Myasthenia gravis. The clinical presentation of **flaccidity** (lower motor neuron type weakness) with **normal nerve conduction studies (NCS)** is a hallmark of disorders affecting the neuromuscular junction (NMJ) or the muscle itself, rather than the peripheral nerves [4]. 1. **Why Myasthenia Gravis (MG) is correct:** MG is an autoimmune disorder caused by antibodies against acetylcholine receptors at the NMJ [2], [3]. Since the pathology is at the synapse and not the nerve axon or myelin, a **standard NCS** (which measures the speed and amplitude of an impulse along a nerve) remains **normal**. To diagnose MG electrophysiologically, one must perform a **Repetitive Nerve Stimulation (RNS)** test, which shows a decremental response. 2. **Why other options are incorrect:** * **Guillain-Barré Syndrome (GBS):** This is a demyelinating polyradiculoneuropathy. NCS will be **abnormal**, typically showing prolonged F-wave latencies, slowed conduction velocities, or conduction blocks. * **Transverse Myelitis:** This is an upper motor neuron (UMN) lesion of the spinal cord. While it can cause "spinal shock" (temporary flaccidity), the NCS remains normal; however, the clinical context involves sensory levels and bladder involvement, which are absent in MG. * **Traumatic Neuritis:** Direct injury to a nerve causes axonal damage or demyelination, leading to **abnormal NCS** findings (reduced CMAP amplitude or slowing) in the distribution of that nerve [1]. **NEET-PG High-Yield Pearls:** * **NCS vs. RNS:** Standard NCS is normal in MG; **Repetitive Nerve Stimulation (RNS)** is the specific test (showing >10% decrement). * **Ice Pack Test:** A simple bedside test for MG; cold improves neuromuscular transmission and reduces ptosis. * **Pure Motor:** MG presents with fluctuating weakness and ptosis/diplopia but **never** involves sensory loss or loss of autonomic function [3].

Q: III nerve palsy associated with contralateral hemiplegia is known as which syndrome?

Weber's syndrome. ### Explanation **Weber’s Syndrome** is a classic brainstem stroke syndrome involving the **ventral (anterior) midbrain**. It occurs due to an occlusion of the paramedian branches of the posterior cerebral artery. 1. **Why Option A is Correct:** The lesion involves two key structures in the midbrain: * **Fascicles of the Oculomotor Nerve (III):** Results in **ipsilateral** III nerve palsy (ptosis, "down and out" eye, and dilated pupil) [1]. * **Cerebral Peduncle (Corticospinal & Corticobulbar tracts):** Results in **contralateral** hemiplegia of the body and lower face. The combination of ipsilateral cranial nerve deficit and contralateral motor deficit is termed "crossed hemiplegia." 2. **Why Other Options are Incorrect:** * **Benedikt’s Syndrome:** Involves the **tegmentum** of the midbrain. It affects the III nerve and the **Red Nucleus**, leading to ipsilateral III nerve palsy combined with contralateral tremors/chorea (extrapyramidal signs), rather than pure hemiplegia. * **Claude’s Syndrome:** A more posterior midbrain lesion affecting the III nerve and the **Superior Cerebellar Peduncle**, resulting in ipsilateral III nerve palsy and contralateral **ataxia**. * **Avellis Syndrome:** A medullary syndrome (not midbrain) involving the Nucleus Ambiguus and Spinothalamic tract, causing paralysis of the soft palate/larynx and contralateral loss of pain/temperature. ### High-Yield Clinical Pearls for NEET-PG: * **Site of Lesion:** Ventral Midbrain. * **Vessel Involved:** Paramedian branches of the Posterior Cerebral Artery (PCA). * **Rule of 4s:** Remember that CN III and IV are in the midbrain. Any syndrome involving CN III must be a midbrain lesion. * **Mnemonic for Midbrain Syndromes:** * **W**eber = **W**heels (Cerebral peduncle/Motor). * **B**enedikt = **B**allistic (Red nucleus/Tremors). * **C**laude = **C**erebellar (Ataxia).

Q: What is a characteristic feature of subcortical dementia?

Memory loss. **Explanation:** Dementia is broadly classified into **cortical** and **subcortical** types based on the primary site of pathology. **Why Memory Loss is correct:** Memory loss is a core feature of all dementias, including subcortical dementia. However, the *nature* of the memory deficit differs. In subcortical dementia (e.g., Parkinson’s disease, Huntington’s disease, Wilson’s disease, or Multi-infarct dementia), the primary issue is **retrieval failure** rather than an inability to encode new information. Patients often benefit from cues or recognition tasks, unlike cortical dementia (e.g., Alzheimer’s), where there is a failure of storage/encoding. Other hallmark features of subcortical dementia include **psychomotor slowing (bradyphrenia)**, executive dysfunction, and personality changes (apathy/depression). **Why the other options are incorrect:** * **B, C, and D (Aphasia, Dyslexia, Tactile Agnosia):** These are considered **"Cortical Signs."** They represent the "4 As" (Amnesia, Aphasia, Apraxia, Agnosia) typically seen in cortical dementias like Alzheimer’s Disease. * **Aphasia:** Language impairment due to cortical damage (Broca’s/Wernicke’s areas). * **Dyslexia:** Difficulty reading, often linked to the parietal-temporal cortex. * **Tactile Agnosia:** Inability to recognize objects by touch, indicating parietal lobe dysfunction. **High-Yield NEET-PG Pearls:** * **Cortical Dementia:** Alzheimer’s, Pick’s Disease. Features: Early aphasia, agnosia, and severe memory storage loss. * **Subcortical Dementia:** Parkinson’s, Huntington’s, Progressive Supranuclear Palsy (PSP). Features: "Forgetfulness" (retrieval issue), slowed thinking, and prominent motor symptoms. * **Key Differentiator:** If a question mentions "aphasia" or "apraxia," think **Cortical**. If it mentions "psychomotor slowing" or "movement disorders," think **Subcortical**.

Q: Hypokalemic periodic paralysis is inherited as an autosomal dominant disorder with incomplete penetrance. It is caused by a mutation in which of the following channels?

Calcium channel. **Explanation:** **Hypokalemic Periodic Paralysis (HOKPP)** is the most common form of periodic paralysis [1]. It is characterized by episodic muscle weakness triggered by factors that lower serum potassium levels, such as high-carbohydrate meals or strenuous exercise [1]. **Why the Correct Answer is Right:** The primary defect in **Type 1 HOKPP** (accounting for ~70% of cases) is a mutation in the **CACNA1S gene**, which encodes the **α1-subunit of the L-type voltage-gated calcium channel** (Dihydropyridine receptor) in skeletal muscle. This mutation results in an aberrant "gating pore current" that leads to muscle membrane depolarization and inexcitability during periods of low extracellular potassium. **Analysis of Incorrect Options:** * **A. Sodium channel:** Mutations in the **SCN4A** gene (Sodium channel) cause **Hyperkalemic** Periodic Paralysis [1]. While a small subset of HOKPP (Type 2) is caused by sodium channel mutations, the classic and most frequent association taught for exams is the calcium channel. * **B. Potassium channel:** Mutations in potassium channels (e.g., KCNJ2) are associated with **Andersen-Tawil Syndrome**, which presents with periodic paralysis, cardiac arrhythmias (long QT), and skeletal abnormalities. * **C. Chloride channel:** Mutations in the **CLCN1** chloride channel cause **Myotonia Congenita** (Thomsen and Becker diseases), characterized by delayed muscle relaxation rather than episodic paralysis [1]. **Clinical Pearls for NEET-PG:** * **Triggers:** High carb intake (insulin shifts K+ intracellularly), rest after exercise, and stress [1]. * **Treatment:** Acute attacks are treated with oral/IV Potassium. Prophylaxis involves **Acetazolamide** (carbonic anhydrase inhibitor) or potassium-sparing diuretics. * **Thyrotoxic Periodic Paralysis:** A common differential in Asian males; it presents identically to HOKPP but is associated with hyperthyroidism.

Q: What is the typical presentation of a Wernicke's aphasia lesion?

Fluent speech with meaningless content. **Explanation:** Wernicke’s aphasia, also known as **Sensory or Receptive Aphasia**, results from a lesion in the posterior part of the superior temporal gyrus (Brodmann area 22) of the dominant hemisphere. **1. Why Option B is Correct:** In Wernicke’s aphasia, the motor ability to produce speech remains intact, but the **comprehension of language** is lost. Patients exhibit "fluent" speech—meaning the rate, rhythm, and articulation are normal—but the content is "meaningless." This is often described as **"word salad"** or jargon aphasia, where the patient uses neologisms (made-up words) and paraphasias (word substitutions) without realizing their speech lacks sense. **2. Why Other Options are Incorrect:** * **Option A:** Fluent speech with meaningful content describes normal, healthy communication. * **Option C:** Non-fluent speech with meaningful content is the hallmark of **Broca’s Aphasia** (Motor Aphasia). These patients struggle to produce words (telegraphic speech) but understand what is being said to them. * **Option D:** Non-fluent speech with meaningless content is characteristic of **Global Aphasia**, where both Broca’s and Wernicke’s areas (and the arcuate fasciculus) are damaged. **Clinical Pearls for NEET-PG:** * **Anatomical Site:** Posterior Superior Temporal Gyrus (supplied by the inferior division of the Middle Cerebral Artery). * **Key Feature:** Patients are typically **unaware** of their deficit (anosognosia), unlike Broca’s patients who are often frustrated. * **Conduction Aphasia:** If the **Arcuate Fasciculus** (the connection between Broca’s and Wernicke’s) is damaged, the patient has fluent speech and good comprehension but **impaired repetition**. * **Memory Trick:** **W**ernicke’s = **W**ord Salad; **B**roca’s = **B**roken speech.

Question 1

Avoiding response is due to which of the following brain lesions?

Accepted Answer

Contralateral parietal lobe lesions

Answer

Ipsilateral frontal lobe lesions

Answer

Contralateral frontal lobe lesions

Answer

Ipsilateral parietal lobe lesions

Question 2

A 25-year-old female at 16 weeks of gestation presents with excess vomiting, apathy, ataxia, nystagmus, and ophthalmoplegia. What is the most likely diagnosis?

Accepted Answer

Wernicke's encephalopathy

Answer

Hyperemesis gravidarum

Answer

Chorea gravidarum

Answer

Korsakoff's encephalopathy

Question 3

What is the drug of choice for idiopathic intracranial hypertension?

Accepted Answer

Acetazolamide

Answer

Glycerol

Answer

Mannitol

Answer

Dexamethasone

Question 4

A man coughed and developed sudden severe headache and fainting. What is the most probable diagnosis?

Accepted Answer

Subarachnoid hemorrhage

Answer

Migraine

Answer

Cluster headache

Answer

Posterior fossa tumor

Question 5

A 75-year-old woman presents with severe pain in the ear, described as if bathed in acid, and associated with emboli. What is the likely location of the lesion?

Accepted Answer

Thalamus

Answer

Pons

Answer

Temporal region

Answer

Occipital region

Question 6

Which condition presents with normal nerve conduction studies but exhibits flaccidity?

Accepted Answer

Myasthenia gravis

Answer

Guillain-Barré syndrome

Answer

Transverse myelitis

Answer

Traumatic neuritis

Question 7

III nerve palsy associated with contralateral hemiplegia is known as which syndrome?

Accepted Answer

Weber's syndrome

Answer

Benedict's syndrome

Answer

Claude's syndrome

Answer

Avellis syndrome

Question 8

What is a characteristic feature of subcortical dementia?

Accepted Answer

Memory loss

Answer

Aphasia

Answer

Dyslexia

Answer

Tactile agnosia

Question 9

Hypokalemic periodic paralysis is inherited as an autosomal dominant disorder with incomplete penetrance. It is caused by a mutation in which of the following channels?

Accepted Answer

Calcium channel

Answer

Sodium channel

Answer

Potassium channel

Answer

Chloride channel

Question 10

What is the typical presentation of a Wernicke's aphasia lesion?

Accepted Answer

Fluent speech with meaningless content

Answer

Fluent speech with meaningful content

Answer

Non-fluent speech with meaningful content

Answer

Non-fluent speech with meaningless content

Neurology — MCQs

Neurology — MCQs

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