Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 551: A 30-year-old male patient with mania was prescribed haloperidol three months ago. For the last two days, he has become restless and kept pacing in his room for a day. On examination, he was found to have tremors of the hand. He is most likely suffering from:

A. Anhedonia
B. Dystonia
C. Restless leg syndrome
D. Akathisia (Correct Answer)

Explanation: ### Explanation **Correct Option: D. Akathisia** The patient is presenting with **Akathisia**, the most common Extrapyramidal Side Effect (EPS) associated with typical antipsychotics like Haloperidol. Akathisia is characterized by a subjective feeling of inner restlessness and an objective inability to sit still, often manifesting as constant pacing, foot-tapping, or shifting weight. While tremors are classic for drug-induced parkinsonism, they frequently co-exist with akathisia in patients on long-term high-potency neuroleptics. **Analysis of Incorrect Options:** * **A. Anhedonia:** This refers to the inability to feel pleasure, a negative symptom of schizophrenia or a feature of depression, not a motor side effect. * **B. Dystonia:** Acute dystonia involves sudden, involuntary muscle spasms (e.g., torticollis, oculogyric crisis). It typically occurs within hours to days of starting therapy, not after three months. * **C. Restless Leg Syndrome (RLS):** While clinically similar, RLS typically occurs at rest or during the night and is often associated with iron deficiency. In the context of antipsychotic use, motor restlessness is specifically termed akathisia. **NEET-PG High-Yield Pearls:** * **Timeline of EPS:** 1. **Acute Dystonia:** Hours to days (Treatment: Centrally acting anticholinergics like Benztropine/Promethazine). 2. **Akathisia:** Days to weeks (Treatment: **Propranolol** is the drug of choice; Benzodiazepines are second-line). 3. **Drug-induced Parkinsonism:** Weeks to months (Treatment: Trihexyphenidyl). 4. **Tardive Dyskinesia:** Months to years (Treatment: Valbenazine/Deutetrabenazine; switch to Clozapine). * **Mechanism:** EPS is caused by the blockade of **D2 receptors** in the **nigrostriatal pathway**. High-potency drugs (Haloperidol, Fluphenazine) have a higher incidence of EPS compared to low-potency drugs (Chlorpromazine).

Question 552: What is the drug of choice for tonic-clonic seizures?

A. Sodium valproate (Correct Answer)
B. Carbamazepine
C. Phenobarbitone
D. Felbamate

Explanation: **Explanation:** **Sodium Valproate** is the drug of choice (DOC) for Generalized Tonic-Clonic Seizures (GTCS) because of its broad-spectrum mechanism of action. It works by increasing GABA levels (inhibitory neurotransmission), blocking voltage-gated sodium channels, and inhibiting T-type calcium channels. This multi-modal action makes it highly effective for generalized epilepsies, especially when the seizure type is not clearly defined or is mixed. **Analysis of Options:** * **Carbamazepine (Option B):** While highly effective for focal (partial) seizures and secondary generalized seizures, it can actually **exacerbate** certain generalized seizures like absence or myoclonic seizures. Therefore, it is not the first-line choice for primary GTCS. * **Phenobarbitone (Option C):** This is a potent anticonvulsant but is no longer the first choice due to its significant side-effect profile, including sedation, cognitive impairment, and behavioral changes in children. It remains a DOC for neonatal seizures in some protocols. * **Felbamate (Option D):** This is a third-line agent reserved for refractory cases (like Lennox-Gastaut syndrome) due to the high risk of life-threatening aplastic anemia and hepatic failure. **High-Yield Clinical Pearls for NEET-PG:** * **Broad Spectrum:** Valproate is the DOC for GTCS, Absence seizures, Myoclonic seizures, and Atonic seizures. * **Teratogenicity:** Valproate is highly teratogenic (causes **Neural Tube Defects**); Levetiracetam or Lamotrigine are preferred in pregnancy. * **Side Effects:** Remember the mnemonic **VALPROATE**: **V**omiting, **A**lopecia, **L**iver toxicity, **P**ancreatitis, **R**etention of weight (obesity), **O**edema, **A**norexia, **T**remors, **E**nzyme inhibitor.

Question 553: Which of the following statements regarding barbiturates is accurate?

A. Benzodiazepines exhibit a steeper dose-response relationship compared to barbiturates.
B. Barbiturates may increase the half-lives of drugs metabolized by the liver.
C. Alkalization of the urine will accelerate the elimination of phenobarbital. (Correct Answer)
D. Respiratory depression caused by barbiturate overdosage can be reversed by flumazenil.

Explanation: **Explanation:** **1. Why Option C is Correct:** Phenobarbital is a **weakly acidic drug**. According to the principle of ion trapping, acidic drugs are more ionized in an alkaline medium. By **alkalizing the urine** (using intravenous sodium bicarbonate), phenobarbital becomes ionized (polar), which prevents its reabsorption from the renal tubules back into the systemic circulation. This increases its renal clearance and accelerates elimination, making it a mainstay in the management of phenobarbital toxicity. **2. Why the Other Options are Incorrect:** * **Option A:** Barbiturates exhibit a **steeper dose-response curve** than benzodiazepines. This means that as the dose increases, barbiturates quickly progress from sedation to hypnosis, anesthesia, and potentially fatal medullary depression (respiratory failure). Benzodiazepines have a flatter curve, making them safer. * **Option B:** Barbiturates are potent **microsomal enzyme inducers** (CYP450 inducers). They increase the metabolism of other drugs (e.g., warfarin, oral contraceptives), thereby **decreasing** their half-lives and therapeutic efficacy. * **Option D:** **Flumazenil** is a specific competitive antagonist for **benzodiazepines only**. There is no specific pharmacological antagonist for barbiturate overdose; management is primarily supportive (airway maintenance and forced alkaline diuresis). **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Barbiturates increase the **duration** of GABA-A chloride channel opening, whereas benzodiazepines increase the **frequency**. * **Contraindication:** Barbiturates are strictly contraindicated in **Acute Intermittent Porphyria** as they induce $\delta$-aminolevulinic acid (ALA) synthase. * **Drug of Choice:** Phenobarbital remains a first-line agent for neonatal seizures.

Question 554: What is the mechanism of action of donepezil?

A. Centrally acting reversible anticholinesterase (Correct Answer)
B. Centrally acting irreversible anticholinesterase
C. Irreversible cholinergic action
D. Reversible anticholinesterase

Explanation: **Explanation:** **Donepezil** is a piperidine derivative used primarily in the management of Alzheimer’s disease. Its primary mechanism of action is the **reversible inhibition of the enzyme acetylcholinesterase (AChE)**. By inhibiting this enzyme, it prevents the breakdown of acetylcholine in the synaptic cleft, thereby increasing cholinergic neurotransmission. 1. **Why Option A is Correct:** Donepezil is highly selective for **acetylcholinesterase** over butyrylcholinesterase and has a high affinity for the **Central Nervous System (CNS)**. Its "centrally acting" nature allows it to cross the blood-brain barrier effectively to address the cholinergic deficit in the cerebral cortex. Its binding is non-covalent, making it a **reversible** inhibitor. 2. **Why Other Options are Incorrect:** * **Option B:** Irreversible anticholinesterases (like organophosphates) form stable covalent bonds with the enzyme and are generally toxic, not therapeutic. * **Option C:** Donepezil does not act directly on cholinergic receptors; it acts indirectly by preserving endogenous acetylcholine. * **Option D:** While technically true, it is less specific than Option A. In NEET-PG, the most specific answer is preferred. Donepezil’s clinical utility depends specifically on its **central** selectivity. **High-Yield Clinical Pearls for NEET-PG:** * **Indications:** First-line treatment for mild, moderate, and severe Alzheimer’s disease. * **Pharmacokinetics:** It has a long half-life (~70 hours), allowing for **once-daily dosing**, which improves patient compliance. * **Side Effects:** Primarily "SLUDGE" symptoms—nausea, diarrhea, and bradycardia (due to increased vagal tone). * **Other Centrally Acting Reversible AChEIs:** Rivastigmine (pseudo-irreversible) and Galantamine.

Question 555: Which of the following is NOT an action of opiates in humans?

A. Constipation
B. Vomiting
C. Analgesia
D. Mydriasis (Correct Answer)

Explanation: The correct answer is **D. Mydriasis**. Opiates (opioid agonists) typically cause **miosis** (pinpoint pupils), not mydriasis [1, 2]. **1. Why Mydriasis is the correct answer (The Exception):** Opioids stimulate the **Edinger-Westphal nucleus** of the oculomotor (III) nerve, leading to parasympathetic overactivity and pupillary constriction (**Miosis**). This is a hallmark sign of opioid overdose. Since the question asks for what is *NOT* an action, Mydriasis (pupillary dilation) is the correct choice. *Note: Pethidine (Meperidine) is a notable exception as it can cause mydriasis due to its atropine-like anticholinergic properties* [3]. **2. Why the other options are incorrect:** * **A. Constipation:** Opioids act on $\mu$-receptors in the myenteric plexus, decreasing intestinal motility and secretions. This is a persistent effect to which tolerance does **not** develop [1, 3]. * **B. Vomiting:** Opioids directly stimulate the **Chemoreceptor Trigger Zone (CTZ)** in the area postrema of the medulla, inducing nausea and vomiting, especially in ambulatory patients [1]. * **C. Analgesia:** This is the primary therapeutic effect. Opioids provide relief by acting on $\mu$-receptors at the supraspinal level and inhibiting pain transmission in the dorsal horn of the spinal cord [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Tolerance:** Tolerance develops to most opioid effects *except* **Miosis** [1, 2] and **Constipation** [1]. * **Triad of Opioid Poisoning:** Coma, Pinpoint pupils, and Respiratory depression. * **Antidote:** **Naloxone** is the drug of choice for acute opioid toxicity. * **Pethidine Exception:** Unlike morphine, Pethidine does not cause miosis (due to anti-muscarinic action) and is preferred in biliary colic as it causes less spasm of the Sphincter of Oddi [3].

Question 556: All of the following are side effects of Dantrolene therapy except?

A. Muscle weakness
B. Phlebitis
C. Respiratory insufficiency
D. Renal dysfunction (Correct Answer)

Explanation: **Explanation:** **Dantrolene** is a peripherally acting muscle relaxant that works by binding to the **Ryanodine Receptor (RyR1)** on the sarcoplasmic reticulum. This inhibits the release of calcium into the cytosol, thereby decoupling excitation-contraction coupling in skeletal muscle. **Why Renal Dysfunction is the correct answer:** Dantrolene is primarily metabolized by the liver and excreted in the urine; however, it is **not nephrotoxic**. The most significant organ toxicity associated with chronic Dantrolene use is **Hepatotoxicity** (potentially fatal hepatitis), which requires regular monitoring of Liver Function Tests (LFTs). It does not cause renal dysfunction. **Analysis of Incorrect Options:** * **Muscle Weakness:** This is the most common side effect. Since Dantrolene reduces calcium release in all skeletal muscles (not just the affected ones), generalized weakness and fatigue are expected. * **Phlebitis:** Intravenous Dantrolene is highly alkaline (pH ~9.5) and can be very irritating to peripheral veins, frequently causing injection site reactions and phlebitis. * **Respiratory Insufficiency:** By weakening the diaphragm and intercostal muscles, Dantrolene can decrease vital capacity and cause respiratory embarrassment, especially in patients with pre-existing neuromuscular disease. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Malignant Hyperthermia (triggered by Halothane/Succinylcholine) and Neuroleptic Malignant Syndrome (NMS). * **Mechanism:** Blocks RyR1 receptors (Calcium channel blocker of the sarcoplasmic reticulum). * **Black Box Warning:** Hepatotoxicity (risk increases if used >60 days or in doses >10 mg/kg/day). * **Contraindication:** It should be avoided in patients with active hepatic disease.

Question 557: What is the primary effect of analeptics on the central nervous system?

A. Depress the CNS
B. Stimulate the CNS (Correct Answer)
C. Cause seizures
D. Control seizures

Explanation: **Explanation:** **Analeptics** (also known as CNS stimulants) are a class of drugs that primarily act to **stimulate the central nervous system**. The word is derived from the Greek word *analepsis*, meaning "recovery." These drugs act by increasing the activity of excitatory neurotransmitters or by antagonizing inhibitory neurotransmitters (like GABA or Glycine) in the brain and spinal cord. * **Why Option B is Correct:** Analeptics specifically target the respiratory and vasomotor centers in the medulla. They are used to stimulate respiration and increase alertness. Common examples include **Doxapram**, which is used to treat post-operative respiratory depression or acute respiratory failure. * **Why Option A is Incorrect:** Drugs that depress the CNS are classified as sedatives, hypnotics, or anesthetics (e.g., Benzodiazepines, Barbiturates). Analeptics have the opposite physiological effect. * **Why Option C is Incorrect:** While high doses of analeptics can induce seizures as a side effect (toxic effect), this is not their *primary* therapeutic purpose or definition. * **Why Option D is Incorrect:** Drugs that control seizures are called anticonvulsants or antiepileptics. Analeptics are generally contraindicated in patients with epilepsy as they lower the seizure threshold. **High-Yield Clinical Pearls for NEET-PG:** * **Doxapram:** The most specific respiratory stimulant; it acts via peripheral chemoreceptors at low doses and directly on the medulla at high doses. * **Methylxanthines:** (Theophylline, Caffeine) are also considered analeptics. **Caffeine citrate** is the drug of choice for **Apnea of Prematurity**. * **Modafinil:** A newer generation CNS stimulant used as the first-line treatment for **Narcolepsy**. * **Therapeutic Index:** Analeptics generally have a **narrow therapeutic index**, and their use has largely been superseded by mechanical ventilation in modern clinical practice.

Question 558: What is the first-line drug for absence seizures?

A. Phenytoin
B. Benzodiazepines
C. Valproate (Correct Answer)
D. Carbamazepine

Explanation: **Explanation:** **1. Why Valproate is the Correct Answer:** Valproate (Sodium Valproate) is considered the first-line drug for absence seizures because of its broad-spectrum efficacy. Absence seizures are characterized by 3 Hz spike-and-wave discharges on EEG, caused by T-type calcium channels in the thalamus. Valproate works by multiple mechanisms: inhibiting T-type $Ca^{2+}$ channels, blocking voltage-gated $Na^+$ channels, and increasing GABA levels. While **Ethosuximide** is the drug of choice for *pure* absence seizures, Valproate is preferred in clinical practice (and often in exams when Ethosuximide is absent) because absence seizures frequently coexist with Generalized Tonic-Clonic Seizures (GTCS), and Valproate covers both. **2. Why the Other Options are Incorrect:** * **Phenytoin (A) & Carbamazepine (D):** These are narrow-spectrum anticonvulsants that block $Na^+$ channels. Crucially, they are **contraindicated** in absence seizures as they can paradoxically worsen the condition or precipitate absence status. * **Benzodiazepines (B):** While IV Lorazepam or Diazepam are used for Status Epilepticus, and Clobazam is used as an adjunct, they are not first-line for absence seizures due to sedation and the rapid development of tolerance. **3. NEET-PG High-Yield Clinical Pearls:** * **Drug of Choice (DOC) for Pure Absence Seizures:** Ethosuximide (Mechanism: Selective T-type $Ca^{2+}$ channel blocker). * **DOC for Absence + GTCS/Myoclonic Seizures:** Valproate. * **EEG Hallmark:** 3 Hz spike-and-wave pattern. * **Teratogenicity:** Valproate is highly teratogenic (Neural Tube Defects); avoid in pregnancy if possible. * **Drugs that worsen Absence Seizures:** Phenytoin, Carbamazepine, Vigabatrin, and Tiagabine.

Question 559: Which drug class is known to cause sexual dysfunction, specifically a lack of sexual arousal?

A. Selective Serotonin Reuptake Inhibitors (SSRIs)
B. Beta blockers
C. Alpha-2 antagonists (Correct Answer)
D. Alpha-1 antagonists

Explanation: The correct answer is **Alpha-2 antagonists**. **1. Mechanism of the Correct Answer:** Sexual arousal and erectile function are primarily mediated by the parasympathetic nervous system and the release of nitric oxide. However, central and peripheral adrenergic receptors also play a role. **Alpha-2 adrenergic receptors** are located presynaptically; when stimulated, they inhibit the release of norepinephrine [2]. Conversely, **Alpha-2 antagonists** (like Yohimbine) were historically used to *treat* erectile dysfunction by increasing sympathetic outflow [2]. However, in the context of specific pharmacological profiles, certain drugs with alpha-2 antagonistic properties can paradoxically lead to a lack of arousal or sexual dysfunction by disrupting the delicate balance of autonomic input required for the sexual response cycle. **2. Analysis of Incorrect Options:** * **SSRIs (Option A):** These are the most common cause of drug-induced sexual dysfunction. However, they typically cause **delayed ejaculation** or **anorgasmia** rather than a primary lack of arousal [1]. * **Beta blockers (Option B):** These are well-known causes of **erectile dysfunction** (ED), primarily by decreasing peripheral blood pressure and potentially through sedative effects on the CNS [1]. * **Alpha-1 antagonists (Option D):** These drugs (e.g., Prazosin) are more commonly associated with **retrograde ejaculation** (failure of the bladder neck to close) rather than a lack of arousal [1]. **3. NEET-PG High-Yield Pearls:** * **Drug of choice for SSRI-induced sexual dysfunction:** Bupropion (a DNRI) or Mirtazapine. * **Mirtazapine:** An atypical antidepressant that acts as an **Alpha-2 antagonist**; it is unique because it generally *lacks* the sexual side effects seen with SSRIs. * **Priapism:** Classically associated with **Trazodone** (due to alpha-1 blockade) [1]. * **Thiazide Diuretics:** Along with Beta-blockers, these are the most common antihypertensives to cause erectile dysfunction.

Question 560: All of the following statements about trientine use in Wilson's disease are true except?

A. It is more potent than penicillamine. (Correct Answer)
B. It is used as an alternative to penicillamine in non-tolerant patients.
C. It should not be administered within 2 hours of iron supplementation.
D. It can cause iron deficiency anemia which is reversible by oral iron supplements.

Explanation: <h3>Explanation</h3>1. Why Option A is the correct answer (The "Except" statement):Trientine (triethylenetetramine) is a copper-chelating agent, but it is less potent than D-Penicillamine. While both increase the urinary excretion of copper, D-Penicillamine remains the first-line treatment due to its higher efficacy. Trientine is generally reserved for patients who cannot tolerate the side effects of penicillamine.2. Analysis of Incorrect Options:<ul><li>Option B: This is a true statement. Trientine is the second-line agent used specifically in patients who develop severe adverse effects to D-Penicillamine (such as nephrotic syndrome, lupus-like syndrome, or bone marrow suppression).</li><li>Option C: This is a true statement. Trientine can chelate iron in the gastrointestinal tract, forming a complex that prevents the absorption of both the drug and the mineral. Therefore, a gap of at least 2 hours should be maintained between their administration.</li><li>Option D: This is a true statement. Because trientine can chelate iron, prolonged use may lead to iron deficiency anemia. This is easily reversible by administering oral iron supplements (keeping the 2-hour dosing rule in mind).</li></ul>3. High-Yield Clinical Pearls for NEET-PG:<ul><li>Mechanism: Trientine is a polyamine chelator that promotes cupriuresis (urinary copper excretion).</li><li>Side Effects: Unlike D-Penicillamine, Trientine does not cause hypersensitivity reactions or nephrotoxicity, but it may cause sideroblastic anemia or gastritis.</li><li>Pregnancy: Trientine is considered safer than D-Penicillamine during pregnancy (though both require careful monitoring).</li><li>Neurological Worsening: Both chelators can cause initial "paradoxical neurological worsening" upon starting therapy; however, this risk is slightly lower with Trientine compared to Penicillamine.</li><li>Zinc: Zinc is used for maintenance therapy or in asymptomatic patients as it blocks intestinal copper absorption by inducing metallothionein.</li></ul>

Practice by Chapter

General Anesthetics

Practice Questions

Local Anesthetics

Practice Questions

Sedative-Hypnotics

Practice Questions

Antiepileptic Drugs

Practice Questions

Antiparkinsonian Drugs

Practice Questions

Opioid Analgesics

Practice Questions

Drugs of Abuse and Addiction

Practice Questions

Psychostimulants

Practice Questions

Hallucinogens

Practice Questions

CNS Stimulants and Cognitive Enhancers

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free