Central Nervous System Pharmacology Practice Questions

Q: Which of the following anti-Parkinson drugs acts by decreasing brain cholinergic activity?

Biperiden. **Explanation:** **Underlying Concept:** Parkinson’s disease is characterized by a neurochemical imbalance in the basal ganglia: a **deficiency of Dopamine** (inhibitory) and a relative **excess of Acetylcholine** (excitatory). To restore balance, treatment strategies either increase dopaminergic tone or decrease cholinergic activity. **Why Biperiden is Correct:** **Biperiden** is a **centrally acting anticholinergic** drug. It works by blocking muscarinic receptors in the striatum, thereby decreasing the relative cholinergic overactivity. These drugs are particularly useful for treating tremors and managing drug-induced parkinsonism (extrapyramidal symptoms). **Analysis of Incorrect Options:** * **Levodopa (A):** A precursor of dopamine. It acts by increasing dopamine levels in the brain, not by decreasing acetylcholine. * **Benserazide (B):** A peripheral dopa-decarboxylase inhibitor. It does not cross the blood-brain barrier; its role is to prevent the peripheral metabolism of Levodopa, increasing its central bioavailability. * **Selegiline (C):** A selective MAO-B inhibitor. It acts by inhibiting the breakdown of dopamine in the CNS, thus prolonging dopaminergic action. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC):** For drug-induced parkinsonism (caused by antipsychotics), centrally acting anticholinergics like **Biperiden** or **Trihexyphenidyl (Benzhexol)** are the drugs of choice. * **Contraindication:** Anticholinergics should be avoided in elderly patients due to the risk of confusion, urinary retention, and glaucoma. * **Benztropine** is another common central anticholinergic used in this category.

Q: All of the following drugs are used for managing status epilepticus except?

Carbamazepine. **Explanation:** **Status Epilepticus (SE)** is a medical emergency defined as a continuous seizure lasting more than 5 minutes or recurrent seizures without recovery of consciousness between episodes. The management requires **rapid-acting, injectable medications** to terminate electrical activity immediately. **Why Carbamazepine is the correct answer:** Carbamazepine is primarily used for long-term maintenance therapy in focal and generalized tonic-clonic seizures. It is **not used** in status epilepticus for two main reasons: 1. **Lack of IV formulation:** It is traditionally administered orally, which is impractical in an unconscious, seizing patient. 2. **Slow onset of action:** Even if absorbed, its pharmacokinetics are not suited for emergency seizure termination. Furthermore, it can potentially worsen certain seizure types like absence or myoclonic seizures. **Analysis of other options:** * **Diazepam (Option B):** A benzodiazepine that acts as the first-line emergency drug (along with Lorazepam). It has high lipid solubility, allowing it to cross the blood-brain barrier rapidly to enhance GABAergic inhibition. * **Phenytoin (Option A):** Used as a second-line agent to prevent the recurrence of seizures after the initial benzodiazepine dose. It is administered via slow IV infusion. * **Thiopentone sodium (Option C):** An ultra-short-acting barbiturate used in **refractory status epilepticus**. It induces deep sedation/anesthesia to suppress resistant electrical discharges. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (Initial):** IV Lorazepam (preferred over Diazepam due to longer duration of action in the brain). * **Drug of Choice (Maintenance/Secondary):** IV Fosphenytoin (preferred over Phenytoin as it causes less injection-site irritation/Purple Glove Syndrome). * **Refractory SE:** Defined as failure of first and second-line drugs; managed with Midazolam infusion, Propofol, or Thiopentone.

Q: A psychiatric patient taking medication develops a tremor, thyroid enlargement, and leucocytosis. Which drug is most likely implicated?

Lithium. **Explanation:** The clinical triad of **tremor, thyroid enlargement (goiter), and leucocytosis** is a classic presentation of **Lithium** side effects. Lithium is the gold standard mood stabilizer used for Bipolar Affective Disorder (BPAD). * **Why Lithium is correct:** 1. **Tremors:** Fine tremors are the most common side effect of Lithium. (Coarse tremors indicate toxicity). 2. **Thyroid Enlargement:** Lithium inhibits the release of thyroid hormones ($T_3$ and $T_4$) by interfering with thyroglobulin iodination, leading to compensatory TSH rise and goiter/hypothyroidism. 3. **Leucocytosis:** Lithium stimulates granulopoiesis in the bone marrow, causing a harmless increase in the White Blood Cell (WBC) count. This is sometimes used therapeutically in Felty’s syndrome. **Analysis of Incorrect Options:** * **Clomipramine:** A Tricyclic Antidepressant (TCA). While it can cause tremors, it is more commonly associated with anticholinergic effects (dry mouth, blurred vision) and cardiac arrhythmias. * **Haloperidol:** A typical antipsychotic. It causes Extrapyramidal Symptoms (EPS) like dystonia and parkinsonism (resting tremor), but does not cause goiter or leucocytosis. * **Olanzapine:** An atypical antipsychotic. Its primary side effects are significant weight gain, metabolic syndrome, and sedation. **High-Yield Clinical Pearls for NEET-PG:** * **Therapeutic Index:** Lithium has a narrow therapeutic index (0.6–1.2 mEq/L). * **Renal Effects:** Causes Nephrogenic Diabetes Insipidus (treated with Amiloride). * **Teratogenicity:** Associated with **Ebstein’s Anomaly** (atrialization of the right ventricle). * **Drug Interactions:** Thiazides, NSAIDs, and ACE inhibitors increase Lithium levels, potentially leading to toxicity.

Q: Which of the following structures is not used in the treatment of epilepsy?

Atropine. **Explanation:** The correct answer is **Atropine** because it is a **muscarinic antagonist** (anticholinergic) and has no intrinsic anticonvulsant activity. In fact, in very high doses, atropine can cause central nervous system excitation, restlessness, and even seizures, making it contraindicated for epilepsy management. **Analysis of Options:** * **Barbiturates (e.g., Phenobarbitone):** These act by increasing the duration of GABA-A chloride channel opening. Phenobarbitone is a classic enzyme inducer used primarily in generalized tonic-clonic seizures (GTCS) and status epilepticus. * **Hydantoins (e.g., Phenytoin):** These are first-line agents that work by blocking voltage-gated sodium channels in their inactivated state. Phenytoin is a mainstay for GTCS and focal seizures but is notorious for its zero-order kinetics and side effects like gingival hyperplasia. * **Acetylurea (e.g., Phenacemide):** Though rarely used today due to severe toxicity (hepatotoxicity and bone marrow suppression), this class historically belongs to the anticonvulsant category, specifically for refractory complex partial seizures. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Valproate is the DOC for most seizures (GTCS, Myoclonic, Absence), except in women of childbearing age (where Levetiracetam or Lamotrigine is preferred). * **Ethosuximide:** Specifically used for Absence seizures; it blocks T-type Ca²⁺ channels. * **Phenytoin Side Effects:** Remember the mnemonic **HOT MALAR** (Hirsutism, Osteomalacia, Teratogenicity, Megaloblastic anemia, Ataxia, Lymphadenopathy, Acne, Rigidity/Gingival Hyperplasia). * **Status Epilepticus:** The immediate DOC is IV Lorazepam.

Q: Coenzyme Q10 is recommended for the management of which condition?

Parkinson disease. **Explanation:** **Correct Option: A. Parkinson disease** Coenzyme Q10 (Ubiquinone) is a vital component of the mitochondrial electron transport chain (Complex I and II). In Parkinson’s disease (PD), mitochondrial dysfunction and oxidative stress play a central role in the degeneration of dopaminergic neurons in the substantia nigra. Coenzyme Q10 acts as a potent **antioxidant and mitochondrial enhancer**. Clinical trials (such as the QE2 study) have suggested that high-dose Coenzyme Q10 may slow the functional decline in patients with early-stage PD by protecting against neurotoxicity. **Analysis of Incorrect Options:** * **B. Guillain-Barré Syndrome (GBS):** This is an acute inflammatory demyelinating polyneuropathy. Management focuses on immunomodulation (IVIG or Plasmapheresis), not mitochondrial support. * **C. Lewy Body Dementia (LBD):** While pathologically related to PD (alpha-synucleinopathy), the primary management involves cholinesterase inhibitors (e.g., Rivastigmine). Coenzyme Q10 is not a standard recommendation for LBD. * **D. Amyotrophic Lateral Sclerosis (ALS):** Although oxidative stress is involved in ALS, Coenzyme Q10 has not shown significant clinical benefit in major trials. The standard drugs for ALS are Riluzole (glutamate antagonist) and Edaravone (antioxidant). **High-Yield Facts for NEET-PG:** * **Statins and CoQ10:** HMG-CoA reductase inhibitors (Statins) inhibit the synthesis of mevalonate, a precursor to both cholesterol and Coenzyme Q10. This depletion is a hypothesized cause of statin-induced myopathy. * **Mitochondrial Cocktails:** CoQ10 is frequently used in "mitochondrial cocktails" for treating mitochondrial encephalomyopathies like **MELAS** and **Kearns-Sayre syndrome**. * **Other uses:** It is also used as an adjuvant in heart failure and migraine prophylaxis.

Q: Which of the following is true about benzodiazepines?

Lorazepam has a shorter duration of action than temazepam. ### Explanation **1. Why Option C is Correct:** Benzodiazepines (BZDs) are classified based on their duration of action, which is determined by their metabolism and the presence of active metabolites. **Lorazepam** is an intermediate-acting BZD with a half-life of 10–20 hours and **no active metabolites**. In contrast, **Temazepam**, while also intermediate-acting, typically exhibits a longer clinical duration of action in the context of sedative effects compared to Lorazepam. More importantly, Lorazepam is preferred in patients with liver dysfunction (along with Oxazepam and Temazepam—the "LOT" group) because it undergoes direct conjugation without phase I oxidative metabolism, leading to a predictable, shorter clearance profile. **2. Why Other Options are Incorrect:** * **Options A & B:** Benzodiazepines do not increase or antagonize the *release* of GABA. Instead, they act as **positive allosteric modulators**. They bind to the BZD site on the $GABA_A$ receptor, increasing the **frequency** of chloride channel opening in the presence of GABA. * **Option D:** **Flumazenil** is the specific competitive antagonist for benzodiazepines. Atropine is a muscarinic antagonist used for organophosphate poisoning or bradycardia. **3. High-Yield NEET-PG Pearls:** * **Mechanism of Action:** BZDs increase the **frequency** of $Cl^-$ channel opening; Barbiturates increase the **duration**. * **Metabolism (LOT):** **L**orazepam, **O**xazepam, and **T**emazepam are metabolized via glucuronidation (Phase II) only. They are safe in the elderly and those with liver failure. * **Drug of Choice:** * Status Epilepticus: **Lorazepam** (IV). * Alcohol Withdrawal: **Chlordiazepoxide** (or Lorazepam if liver is damaged). * Panic Disorder: **Alprazolam**. * **Antidote:** Flumazenil can precipitate seizures in BZD-dependent patients or in mixed TCA overdoses.

Q: Which of the following is NOT a side effect of prolonged phenytoin therapy?

Gynaecomastia. **Explanation:** Phenytoin is a widely used antiepileptic drug known for its extensive side-effect profile, often remembered by the mnemonic **"HOT MALAYALAM."** **Why Gynaecomastia is the correct answer:** Gynaecomastia is **not** a side effect of phenytoin. It is, however, a well-known side effect of other drugs like Spironolactone, Cimetidine, Ketoconazole, and Digitalis. Phenytoin primarily affects connective tissue, bone metabolism, and folate levels rather than estrogen/androgen balance. **Analysis of incorrect options:** * **Osteomalacia:** Phenytoin induces hepatic microsomal enzymes (CYP450), which increases the metabolism of Vitamin D. This leads to Vitamin D deficiency, reduced calcium absorption, and subsequent osteomalacia or rickets. * **Megaloblastic Anemia:** Phenytoin interferes with the absorption and metabolism of dietary folate. Chronic use can lead to folate deficiency, manifesting as macrocytic/megaloblastic anemia. * **Gum Hyperplasia:** This is one of the most common side effects (occurring in ~20% of patients). It is caused by the overgrowth of gingival collagen due to the inhibition of calcium influx in gingival fibroblasts and increased expression of Platelet-Derived Growth Factor (PDGF). **High-Yield Clinical Pearls for NEET-PG:** * **Teratogenicity:** Phenytoin causes **Fetal Hydantoin Syndrome** (hypoplastic phalanges, cleft lip/palate, microcephaly). * **Zero-Order Kinetics:** At therapeutic or high doses, phenytoin follows non-linear (saturation) kinetics, meaning small dose increases can lead to toxicity. * **Other Side Effects:** Hirsutism, Lymphadenopathy (Pseudolymphoma), Peripheral neuropathy, and Ataxia (sign of toxicity). * **Drug Choice:** It is the drug of choice for Generalized Tonic-Clonic Seizures (GTCS) but can **exacerbate Absence Seizures.**

Q: Which of the following is not a mood stabilizer?

Fluoxetine. **Explanation** The correct answer is **Fluoxetine**. **1. Why Fluoxetine is the correct answer:** Fluoxetine is a **Selective Serotonin Reuptake Inhibitor (SSRI)**, classified as an **antidepressant**, not a mood stabilizer. While mood stabilizers are used to treat Bipolar Disorder (BD) by preventing both manic and depressive "poles," antidepressants like Fluoxetine can actually trigger **manic switching** (inducing a manic episode) in patients with Bipolar I disorder if used without a mood stabilizer. **2. Why the other options are incorrect:** * **Lithium (Option A):** The "Gold Standard" mood stabilizer. It is the drug of choice for classic mania and has a proven anti-suicidal effect. * **Valproate (Option B):** An anticonvulsant that is now the first-line treatment for **Acute Mania** and **Rapid Cycling Bipolar Disorder**. It acts by increasing GABA levels. * **Carbamazepine (Option C):** An anticonvulsant used as a second-line mood stabilizer, particularly effective in patients who do not respond to Lithium or Valproate. **3. NEET-PG High-Yield Pearls:** * **Mood Stabilizers vs. Antipsychotics:** While atypical antipsychotics (e.g., Quetiapine, Olanzapine) are used in Bipolar Disorder, the "classic" mood stabilizers are Lithium, Valproate, Carbamazepine, and **Lamotrigine** (specifically for bipolar depression prophylaxis). * **Lithium Toxicity:** Therapeutic range is narrow (**0.6–1.2 mEq/L**). Toxicity occurs >1.5 mEq/L. * **Teratogenicity:** Lithium causes **Ebstein’s Anomaly**; Valproate causes **Neural Tube Defects** (highest risk). * **Drug of Choice for Rapid Cyclers:** Valproate.

Q: Which of the following skeletal muscle relaxants undergoes Hoffman's elimination?

Atracurium. ### Explanation **Atracurium** is a benzylisoquinolinium neuromuscular blocking agent (NMBA) that is unique because it does not rely on hepatic or renal metabolism. Instead, it undergoes **Hoffman’s elimination**, a spontaneous, non-enzymatic chemical degradation that occurs at physiological pH and temperature. #### Why the Correct Answer is Right: * **Hoffman’s Elimination:** This process involves the breakdown of the molecule into laudanosine and quaternary monoacrylate. Because it is independent of organ function, Atracurium (and its isomer **Cisatracurium**) is the **drug of choice for patients with liver or kidney failure.** #### Why the Other Options are Wrong: * **B. Succinylcholine:** This is a depolarizing muscle relaxant metabolized by **pseudocholinesterase** (plasma cholinesterase). * **C. Mivacurium:** A short-acting non-depolarizing NMBA that is also metabolized by **pseudocholinesterase**. * **D. Vecuronium:** An aminosteroid NMBA primarily eliminated through **biliary excretion** (hepatic metabolism) and, to a lesser extent, renal excretion. #### High-Yield Clinical Pearls for NEET-PG: * **Laudanosine Toxicity:** A major metabolite of Atracurium is laudanosine. In high concentrations (prolonged infusions), it can cross the blood-brain barrier and act as a **CNS stimulant**, potentially causing **seizures**. * **Cisatracurium:** It is 3x more potent than Atracurium, undergoes Hoffman's elimination, but produces significantly **less laudanosine** and does not cause histamine release. * **Temperature/pH Sensitivity:** Since Hoffman’s elimination is spontaneous, the rate of degradation **increases with hyperthermia and alkalosis**, and decreases with hypothermia and acidosis.

Question 1

Which of the following statements about anti-epileptics is false?

Accepted Answer

Lamotrigine mainly acts by causing GABA mediated Cl- channel opening.

Answer

Phenytoin and carbamazepine act by prolonging the inactivated state of Na+ channels.

Answer

Carbamazepine can be used in trigeminal neuralgias.

Answer

Diazepam is an anticonvulsant drug.

Question 2

Which of the following anti-Parkinson drugs acts by decreasing brain cholinergic activity?

Accepted Answer

Biperiden

Answer

Levodopa

Answer

Benserazide

Answer

Selegiline

Question 3

All of the following drugs are used for managing status epilepticus except?

Accepted Answer

Carbamazepine

Answer

Phenytoin

Answer

Diazepam

Answer

Thiopentone sodium

Question 4

A psychiatric patient taking medication develops a tremor, thyroid enlargement, and leucocytosis. Which drug is most likely implicated?

Accepted Answer

Lithium

Answer

Clomipramine

Answer

Haloperidol

Answer

Olanzapine

Question 5

Which of the following structures is not used in the treatment of epilepsy?

Accepted Answer

Atropine

Answer

Barbiturates

Answer

Hydantoins

Answer

Acetylurea

Question 6

Coenzyme Q10 is recommended for the management of which condition?

Accepted Answer

Parkinson disease

Answer

Guillain-Barré syndrome

Answer

Lewy body dementia

Answer

Amyotrophic lateral sclerosis

Question 7

Which of the following is true about benzodiazepines?

Accepted Answer

Lorazepam has a shorter duration of action than temazepam

Answer

Increased release of GABA

Answer

Antagonizing release of GABA

Answer

Atropine is its antagonist

Question 8

Which of the following is NOT a side effect of prolonged phenytoin therapy?

Accepted Answer

Gynaecomastia

Answer

Osteomalacia

Answer

Megaloblastic anemia

Answer

Gum hyperplasia

Question 9

Which of the following is not a mood stabilizer?

Accepted Answer

Fluoxetine

Answer

Lithium

Answer

Valproate

Answer

Carbamazepine

Question 10

Which of the following skeletal muscle relaxants undergoes Hoffman's elimination?

Accepted Answer

Atracurium

Answer

Succinylcholine

Answer

Mivacurium

Answer

Vecuronium

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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