Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 341: GABA transmission is facilitated by which of the following drugs?

A. Vigabatrin (Correct Answer)
B. Carbamazepine
C. Phenytoin
D. Buspirone

Explanation: The correct answer is **Vigabatrin**. GABA (Gamma-Aminobutyric Acid) is the primary inhibitory neurotransmitter in the CNS. Facilitation of GABAergic transmission can occur via direct receptor agonism, positive allosteric modulation, or by increasing the synaptic concentration of GABA. **1. Why Vigabatrin is correct:** Vigabatrin is a structural analogue of GABA that acts as a **selective, irreversible inhibitor of GABA-transaminase (GABA-T)**. GABA-T is the enzyme responsible for the degradation of GABA. By inhibiting this enzyme, Vigabatrin significantly increases the levels of GABA in the synaptic cleft, thereby facilitating inhibitory neurotransmission [2]. **2. Why the other options are incorrect:** * **Carbamazepine & Phenytoin:** These are primarily **Sodium ($Na^+$) channel blockers**. They stabilize the inactivated state of voltage-gated sodium channels, preventing high-frequency repetitive firing of action potentials [1, 3]. They do not have a direct effect on GABA transmission. * **Buspirone:** This is a non-benzodiazepine anxiolytic that acts as a **partial agonist at 5-$HT_{1A}$ receptors**. It does not interact with the GABAergic system, which explains its lack of sedative, hypnotic, or anticonvulsant properties. **High-Yield Clinical Pearls for NEET-PG:** * **Vigabatrin Side Effect:** A classic "must-know" side effect is **permanent bilateral visual field constriction** (concentric peripheral vision loss), requiring regular perimetry monitoring. * **Drug of Choice:** Vigabatrin is the drug of choice for **Infantile Spasms (West Syndrome)** associated with Tuberous Sclerosis. * **Tiagabine:** Another GABA-facilitating drug that works by inhibiting the GABA transporter (**GAT-1**), preventing GABA reuptake [1, 2].

Question 342: Which of the following drugs is used for smoking cessation?

A. Bupropion (Correct Answer)
B. Buspirone
C. Venlafaxine
D. Fluoxetine

Explanation: **Explanation:** **Bupropion (Option A)** is the correct answer. It is an atypical antidepressant that acts as a **Norepinephrine-Dopamine Reuptake Inhibitor (NDRI)**. In the context of smoking cessation, it works by increasing dopamine levels in the nucleus accumbens, which mimics the reward pathway of nicotine and reduces withdrawal symptoms and the urge to smoke. It is FDA-approved for this purpose and is often started 1–2 weeks before the "quit date." **Why the other options are incorrect:** * **Buspirone (Option B):** A selective 5-HT1A partial agonist used primarily as an **anxiolytic** for Generalized Anxiety Disorder (GAD). It has no proven efficacy in smoking cessation. * **Venlafaxine (Option C):** A Serotonin-Norepinephrine Reuptake Inhibitor (SNRI) used for major depression and panic disorders. While it affects neurotransmitters, it is not a first-line agent for nicotine addiction. * **Fluoxetine (Option D):** A Selective Serotonin Reuptake Inhibitor (SSRI). Although it treats depression (which can be comorbid with nicotine dependence), clinical trials have shown it is not effective for smoking cessation. **High-Yield Clinical Pearls for NEET-PG:** * **Varenicline** (a nicotinic α4β2 partial agonist) is currently considered the most effective monotherapy for smoking cessation. * **Contraindication:** Bupropion is strictly contraindicated in patients with **seizure disorders** or **eating disorders** (bulimia/anorexia) as it lowers the seizure threshold. * **Weight Gain:** Bupropion is a preferred choice for smokers concerned about post-cessation weight gain, as it tends to delay weight increase.

Question 343: Ketamine acts on which receptors?

A. GABA
B. Muscarinic
C. 5-HT4
D. NMDA (Correct Answer)

Explanation: **Explanation:** **Ketamine** is a unique intravenous anesthetic agent primarily known for producing **dissociative anesthesia**. 1. **Why NMDA is Correct:** Ketamine acts as a non-competitive antagonist at the **NMDA (N-methyl-D-aspartate) receptors**, which are a subtype of glutamate receptors. By blocking these receptors, ketamine inhibits the excitatory neurotransmitter glutamate. This action interrupts the sensory pathways between the thalamocortical and limbic systems, leading to a state where the patient appears awake (eyes open) but is unconscious and feels no pain. 2. **Why Other Options are Incorrect:** * **GABA:** Most conventional IV anesthetics (like Propofol, Thiopental, and Benzodiazepines) act by potentiating GABA-A receptors. Ketamine is a notable exception as it does not primarily act through the GABA system. * **Muscarinic:** Ketamine actually possesses mild anticholinergic properties (leading to bronchodilation), but this is not its primary mechanism of action. * **5-HT4:** These are serotonin receptors primarily involved in GI motility and memory; they are not the target for ketamine’s anesthetic effects. **High-Yield Clinical Pearls for NEET-PG:** * **Dissociative Anesthesia:** Characterized by profound analgesia, amnesia, and catalepsy while maintaining laryngeal reflexes. * **Sympathomimetic Action:** Unlike other anesthetics, Ketamine increases HR, BP, and Cardiac Output (due to sympathetic stimulation). It is the **DOC for induction in patients with hypovolemic shock.** * **Bronchodilator:** It is the induction agent of choice for patients with **Bronchial Asthma**. * **Emergence Delirium:** A common side effect (hallucinations/vivid dreams) which can be prevented by co-administering **Benzodiazepines**. * **Contraindication:** It increases intracranial pressure (ICP), so it is generally avoided in head injuries.

Question 344: What is the drug of choice for acute migraine?

A. Methysergide
B. Sumatriptan (Correct Answer)
C. Ergotamine
D. Propranolol

Explanation: **Explanation:** The management of migraine is divided into **abortive (acute)** and **prophylactic (preventive)** therapy. **Why Sumatriptan is correct:** Sumatriptan is a selective **5-HT$_{1B/1D}$ receptor agonist**. It works by causing intracranial vasoconstriction and inhibiting the release of pro-inflammatory neuropeptides (like CGRP) from trigeminal nerve endings. Due to its rapid onset, high efficacy, and better side-effect profile compared to older agents, **Triptans are the first-line drugs of choice for moderate-to-severe acute migraine attacks.** **Analysis of Incorrect Options:** * **Methysergide (A):** This is a 5-HT$_2$ antagonist used historically for prophylaxis. It is rarely used now due to the risk of **retroperitoneal, pleuropulmonary, and cardiac valvular fibrosis** with long-term use. * **Ergotamine (C):** A non-selective 5-HT$_1$ agonist. While effective for acute attacks, it has poor oral bioavailability, higher toxicity (nausea, vomiting, and risk of ergotism), and has been largely replaced by Triptans. * **Propranolol (D):** A beta-blocker that is the **drug of choice for migraine prophylaxis** (prevention), not for treating an ongoing acute attack. **High-Yield Clinical Pearls for NEET-PG:** * **Triptan Contraindications:** Avoid in patients with Ischemic Heart Disease (IHD), Prinzmetal angina, or uncontrolled hypertension due to coronary vasoconstriction. * **Mild Migraine:** For mild attacks, **NSAIDs** (like Naproxen or Aspirin) are the initial drug of choice. * **Status Migrainosus:** Defined as an attack lasting >72 hours; the drug of choice is **IV Dihydroergotamine** or **IV Dexamethasone**. * **Newer Agents:** **Lasmiditan** (5-HT$_{1F}$ agonist) is used for acute migraine in patients with cardiovascular contraindications to Triptans.

Question 345: What is the mechanism of action of valproic acid?

A. Inhibition of Na+ channel inactivation
B. Inhibition of GABA
C. Opening of K+ channels
D. Inhibition of 'T' type Ca+2 current (Correct Answer)

Explanation: **Mechanism of Action of Valproic Acid** Valproic acid is a broad-spectrum antiepileptic drug with a multifaceted mechanism of action. The correct answer is **D (Inhibition of 'T' type Ca²⁺ current)** because this specific action in the thalamic neurons is responsible for its efficacy in treating Absence (Petit Mal) seizures [1]. **Detailed Explanation:** 1. **Correct Option (D):** Valproic acid inhibits low-threshold T-type Calcium channels [1]. This action stabilizes the thalamocortical circuitry, preventing the rhythmic 3 Hz spike-and-wave discharges characteristic of absence seizures. 2. **Option A (Inhibition of Na⁺ channel inactivation):** This is technically incorrect as stated. Valproic acid **prolongs** the inactivated state of voltage-gated sodium channels (similar to Phenytoin), thereby limiting high-frequency repetitive firing [1], [2]. It does not "inhibit inactivation." 3. **Option B (Inhibition of GABA):** This is the opposite of its effect. Valproic acid **potentiates** GABAergic transmission by inhibiting GABA-transaminase (the enzyme that breaks down GABA) and stimulating Glutamic Acid Decarboxylase (GAD), which synthesizes GABA. 4. **Option C (Opening of K⁺ channels):** While some newer drugs like Ezogabine act on K⁺ channels, this is not a primary or clinically significant mechanism for Valproic acid. **High-Yield NEET-PG Pearls:** * **Drug of Choice (DOC):** Valproate is the DOC for Generalized Tonic-Clonic Seizures (GTCS), Myoclonic seizures, and Atonic seizures. It is also used for Bipolar Disorder prophylaxis and Migraine prophylaxis. * **Teratogenicity:** It is highly teratogenic, causing **Neural Tube Defects** (Spina Bifida). * **Side Effects:** Remember the mnemonic **VALPROATE**: **V**omiting, **A**lopecia (curly hair), **L**iver toxicity (Hepatotoxicity), **P**ancreatitis, **R**etained fat (Weight gain), **O**edema, **A**norexia, **T**remors, and **E**nzyme inhibitor (unlike most AEDs which are inducers).

Question 346: A 32-year-old woman presents with a 48-hour history of fever, irrelevant talk, and two episodes of successive tonic-clonic seizures. Which of the following drugs can be administered while awaiting further investigations?

A. IV mannitol
B. IV amphotericin B
C. IV penicillin
D. IV acyclovir (Correct Answer)

Explanation: ### Explanation **Correct Option: D. IV Acyclovir** The clinical presentation of fever, altered mental status (irrelevant talk), and seizures in a young adult is highly suggestive of **Herpes Simplex Encephalitis (HSE)**, the most common cause of sporadic fatal encephalitis worldwide. In cases of suspected viral encephalitis, **IV Acyclovir** must be started empirically as soon as possible. Delay in treatment significantly increases mortality and long-term neurological morbidity. HSE typically involves the temporal lobes, leading to psychiatric symptoms and seizures. Because the prognosis depends heavily on the "door-to-needle" time for antiviral therapy, it is administered while awaiting definitive investigations like CSF PCR or MRI. **Analysis of Incorrect Options:** * **A. IV Mannitol:** While mannitol is used to reduce intracranial pressure (ICP), it is an adjunctive symptomatic treatment, not a primary therapy for the underlying pathology. * **B. IV Amphotericin B:** This is the treatment for fungal meningitis (e.g., Cryptococcal). Fungal infections usually present more subacutely and are more common in immunocompromised individuals. * **C. IV Penicillin:** While used for neurosyphilis or certain bacterial meningitides, the combination of acute fever and prominent behavioral changes/seizures points more strongly toward a viral etiology (HSE) than a bacterial one. **Clinical Pearls for NEET-PG:** * **Gold Standard Investigation for HSE:** CSF PCR for HSV DNA. * **Imaging Choice:** MRI is more sensitive than CT; look for "temporal lobe involvement" (hyperintensities). * **EEG Finding:** Periodic Lateralized Epileptiform Discharges (PLEDs) are characteristic of HSE. * **Mechanism of Acyclovir:** It is a guanosine analog that requires viral **thymidine kinase** for initial phosphorylation, making it highly selective for virus-infected cells.

Question 347: Which of the following drugs, proposed for the management of opioid addiction, blocks the action of injected heroin for up to 48 hours with a single dose, and does not activate opioid receptors?

A. Amphetamine
B. Buspirone
C. Methadone
D. Naltrexone (Correct Answer)

Explanation: **Explanation:** The correct answer is **Naltrexone**. **Why Naltrexone is correct:** Naltrexone is a long-acting, competitive **opioid antagonist**. Unlike agonists, it has no intrinsic activity and does not activate opioid receptors (it has zero efficacy). By binding to the $\mu$-opioid receptors with high affinity, it competitively blocks the effects of exogenous opioids like heroin. Its primary clinical advantage in addiction management is its long half-life; a single oral dose can effectively block the "high" of heroin for **48 to 72 hours**, thereby aiding in the prevention of relapse in highly motivated patients. **Why the other options are incorrect:** * **Amphetamine (A):** This is a CNS stimulant that increases synaptic dopamine and norepinephrine. It has no role in blocking opioid receptors and is itself a drug of abuse. * **Buspirone (B):** An anxiolytic that acts as a partial agonist at 5-HT1A receptors. It is used for Generalized Anxiety Disorder (GAD) and does not interact with the opioid system. * **Methadone (C):** While used in opioid addiction, methadone is a **long-acting $\mu$-opioid agonist**. It *does* activate receptors (providing "substitution therapy") to prevent withdrawal symptoms. It does not block heroin via antagonism but rather through cross-tolerance. **High-Yield Clinical Pearls for NEET-PG:** * **Naltrexone vs. Naloxone:** Naloxone is short-acting (30–90 mins) and used for **acute opioid overdose** (IV). Naltrexone is long-acting and used for **maintenance/relapse prevention** and **alcohol dependence** (reduces craving). * **Prerequisite:** Naltrexone must only be started after a patient is opioid-free for 7–10 days to avoid precipitating severe **acute withdrawal syndrome**. * **Vivitrol:** This is the injectable, extended-release formulation of naltrexone administered once monthly.

Question 348: All of the following drugs can be used for the prophylaxis of migraine except?

A. Propranolol
B. Sumatriptan (Correct Answer)
C. Amitriptyline
D. Flunarizine

Explanation: **Explanation:** The management of migraine is divided into two categories: **Abortive (Acute) therapy** and **Prophylactic (Preventive) therapy**. **Why Sumatriptan is the correct answer:** Sumatriptan is a selective **5-HT$_{1B/1D}$ receptor agonist**. Its primary mechanism involves vasoconstriction of dilated cranial blood vessels and inhibition of pro-inflammatory neuropeptide release. Because it has a rapid onset but a short half-life, it is used exclusively for the **acute abortive treatment** of a migraine attack. It is **not** used for prophylaxis because it does not reduce the frequency of future attacks and frequent use can lead to "Medication Overuse Headache." **Analysis of Incorrect Options (Prophylactic Agents):** * **Propranolol (Option A):** A non-selective beta-blocker and the **drug of choice** for migraine prophylaxis. It likely works by stabilizing vascular tone and reducing cortical excitability. * **Amitriptyline (Option B):** A Tricyclic Antidepressant (TCA) that inhibits the reuptake of Norepinephrine and Serotonin. It is highly effective for prophylaxis, especially in patients with co-existing tension-type headaches or depression. * **Flunarizine (Option D):** A non-selective **Calcium Channel Blocker** (CCB) with additional H1-blocking activity. It is specifically used for prophylaxis to prevent the "spreading depression" of cortical activity. **NEET-PG High-Yield Pearls:** * **Prophylaxis is indicated** if attacks occur >2–3 times per month or are severely disabling. * **First-line Prophylaxis:** Beta-blockers (Propranolol), Anticonvulsants (Topiramate, Valproate), or TCAs (Amitriptyline). * **Newer Prophylactic Agents:** CGRP Antagonists (e.g., Erenumab, Galcanezumab) are now frequently tested. * **Contraindication:** Triptans are contraindicated in patients with Ischemic Heart Disease (IHD) or Prinzmetal angina due to their vasoconstrictive properties.

Question 349: Which anticholinergic drug is used in the management of parkinsonism?

A. Benzhexol (Correct Answer)
B. Benzerazide
C. Pirenzepine
D. Atropine

Explanation: **Explanation:** **1. Why Benzhexol is Correct:** Parkinsonism is characterized by a neurochemical imbalance in the basal ganglia: a deficiency of **Dopamine** and a relative excess of **Acetylcholine (ACh)**. To restore this balance, centrally acting anticholinergics are used. **Benzhexol** (also known as Trihexyphenidyl) is a synthetic anticholinergic that crosses the blood-brain barrier. It is particularly effective in reducing **tremors and rigidity**, though it has little effect on bradykinesia. It is also the drug of choice for **Drug-Induced Extrapyramidal Symptoms (EPS)** caused by antipsychotics. **2. Analysis of Incorrect Options:** * **B. Benserazide:** This is a peripheral **Dopa-decarboxylase inhibitor**. It is administered alongside Levodopa to prevent its peripheral conversion to dopamine, thereby increasing CNS availability and reducing systemic side effects. It is not an anticholinergic. * **C. Pirenzepine:** This is a selective **M1-receptor antagonist**. It was historically used to reduce gastric acid secretion in peptic ulcer disease. It does not have a significant role in Parkinsonism. * **D. Atropine:** While Atropine is the prototype anticholinergic, it is a non-selective muscarinic antagonist with significant systemic side effects (tachycardia, urinary retention, blurred vision). It is not used clinically for Parkinsonism due to its poor CNS-to-peripheral side effect ratio. **3. NEET-PG High-Yield Pearls:** * **Other Centrally Acting Anticholinergics:** Biperiden, Procyclidine, and Orphenadrine. * **Drug of Choice (DOC):** For drug-induced parkinsonism/EPS, the DOC is intravenous/intramuscular **Promethazine** or **Benzhexol**. * **Contraindication:** Anticholinergics should be avoided in elderly patients (risk of confusion/dementia) and patients with **Glaucoma** or **Prostatic Hyperplasia**.

Question 350: For the treatment of cerebral edema due to a brain tumor, which corticosteroid is preferred?

A. Hydrocortisone
B. Prednisolone
C. Dexamethasone (Correct Answer)
D. Triamcinolone

Explanation: **Explanation:** **Dexamethasone** is the drug of choice for managing vasogenic cerebral edema associated with brain tumors. The primary reason for its preference is its **minimal mineralocorticoid activity**. Unlike other steroids, dexamethasone does not cause significant sodium and water retention. In the context of increased intracranial pressure (ICP), avoiding fluid retention is critical to prevent further worsening of the edema. Additionally, it has a **long half-life** (36–72 hours) and **high potency**, allowing for effective symptom control with less frequent dosing. It also crosses the blood-brain barrier effectively to reduce capillary permeability. **Analysis of Incorrect Options:** * **A. Hydrocortisone:** It possesses significant mineralocorticoid activity, leading to salt and water retention, which can exacerbate cerebral edema. It is primarily used for replacement therapy in adrenal insufficiency. * **B. Prednisolone:** While it has more potent anti-inflammatory effects than hydrocortisone, it still retains moderate mineralocorticoid activity, making it less ideal than dexamethasone for CNS edema. * **C. Triamcinolone:** Although it has zero mineralocorticoid activity, it is generally used for topical, intra-articular, or intralesional purposes and is not the standard of care for acute reduction of ICP. **High-Yield Clinical Pearls for NEET-PG:** * **Vasogenic Edema:** Dexamethasone is specifically effective for *vasogenic* edema (tumors, abscesses); it is less effective for *cytotoxic* edema (infarction). * **Potency:** Dexamethasone is roughly 25–30 times more potent than hydrocortisone. * **ACTH Suppression:** Due to its long duration of action, dexamethasone causes significant suppression of the Hypothalamic-Pituitary-Adrenal (HPA) axis. * **Diagnostic Use:** It is also used in the **Dexamethasone Suppression Test** to diagnose Cushing’s syndrome.

Practice by Chapter

General Anesthetics

Practice Questions

Local Anesthetics

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Sedative-Hypnotics

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Antiepileptic Drugs

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Antiparkinsonian Drugs

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Opioid Analgesics

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Drugs of Abuse and Addiction

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Psychostimulants

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Hallucinogens

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CNS Stimulants and Cognitive Enhancers

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