Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 591: A 55-year-old man with dementia was given a natural alkaloid. Which of the following could it be?

A. Tacrine
B. Donepezil
C. Galantamine (Correct Answer)
D. Rivastigmine

Explanation: **Explanation:** The question focuses on the pharmacological management of Alzheimer’s disease using Acetylcholinesterase (AChE) inhibitors. The key differentiator here is the **source** of the drug. **Why Galantamine is correct:** **Galantamine** is a tertiary amine and a **natural alkaloid** originally extracted from the bulbs of the Caucasian snowdrop (*Galanthus woronowii*) and the Red spider lily (*Lycoris radiata*). In addition to being a reversible AChE inhibitor, it also acts as an allosteric modulator of nicotinic acetylcholine receptors, enhancing the action of acetylcholine. **Why the other options are incorrect:** * **Tacrine (A):** This was the first centrally acting AChE inhibitor. However, it is a **synthetic** compound and is no longer used clinically due to significant hepatotoxicity. * **Donepezil (B):** This is a **synthetic** piperidine derivative. It is the most commonly used drug for Alzheimer’s due to its once-daily dosing and lack of hepatotoxicity. * **Rivastigmine (D):** This is a **synthetic** carbamate derivative. It is unique because it inhibits both Acetylcholinesterase and Butyrylcholinesterase and is available as a transdermal patch. **NEET-PG High-Yield Pearls:** * **Mechanism:** All four drugs increase cholinergic transmission in the CNS by inhibiting the breakdown of Acetylcholine. * **Rivastigmine:** Preferred in patients with **Parkinson’s Disease Dementia (PDD)**. * **Memantine:** An NMDA receptor antagonist used for moderate-to-severe Alzheimer’s; it is NOT an AChE inhibitor. * **Side Effects:** Common side effects include GI distress (nausea, vomiting, diarrhea) and bradycardia due to increased parasympathetic activity.

Question 592: Which of the following statements is not true about domperidone?

A. It rarely causes extrapyramidal side effects.
B. It is a D2 receptor antagonist.
C. Its antiemetic efficacy is higher than metoclopramide. (Correct Answer)
D. It causes loose stool.

Explanation: **Explanation:** Domperidone is a dopamine (D2) receptor antagonist primarily used as a prokinetic and antiemetic. The statement that its efficacy is higher than metoclopramide is **incorrect**, making it the right answer for this "not true" question. **1. Why Option C is the correct answer (False statement):** While both drugs are D2 antagonists, **metoclopramide** is generally considered more potent as an antiemetic. This is because metoclopramide crosses the blood-brain barrier (BBB) and acts on both the Chemoreceptor Trigger Zone (CTZ) and the solitary tract nucleus, and at higher doses, it also provides 5-HT3 receptor antagonism. Domperidone has lower systemic potency and does not cross the BBB effectively. **2. Analysis of other options:** * **Option A (True):** Domperidone has poor penetration across the BBB. Since it does not reach the basal ganglia in significant concentrations, it **rarely causes extrapyramidal side effects** (EPS) like dystonia or parkinsonism, unlike metoclopramide. * **Option B (True):** Its primary mechanism of action is the blockade of **D2 receptors** in the CTZ (which lies outside the BBB) and the upper gastrointestinal tract. * **Option D (True):** As a prokinetic agent, domperidone increases gastric motility and speeds up gastric emptying. A common side effect of increased GI motility is **loose stools** or diarrhea. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Domperidone is the preferred antiemetic for **Levodopa-induced vomiting** in Parkinson’s disease because it does not worsen motor symptoms (due to poor BBB penetration). * **Cardiac Warning:** Domperidone is associated with a risk of **QT interval prolongation** and cardiac arrhythmias; it should be used with caution in elderly patients. * **Hyperprolactinemia:** Since the pituitary gland lies outside the BBB, domperidone can cause galactorrhea and gynecomastia by blocking dopamine's inhibitory effect on prolactin.

Question 593: Which of the following is the most common side effect seen with fluoxetine therapy?

A. Seizure
B. Anxiety (Correct Answer)
C. Hypotension
D. Loose stools

Explanation: **Explanation:** Fluoxetine is a **Selective Serotonin Reuptake Inhibitor (SSRI)**. While SSRIs are generally better tolerated than older antidepressants, they are associated with specific side effects due to increased serotonergic activity in various pathways. **Why Anxiety is the Correct Answer:** Fluoxetine is unique among SSRIs because it has a **stimulatory/activating effect**. In the initial stages of therapy, increased serotonin levels in the limbic system can lead to **anxiety, agitation, restlessness, and insomnia**. This "jitteriness syndrome" is the most frequently reported side effect during early treatment. Because of its long half-life and activating nature, it is typically dosed in the morning to avoid sleep disturbances. **Analysis of Incorrect Options:** * **A. Seizure:** While some antidepressants (like Bupropion or Maprotiline) significantly lower the seizure threshold, SSRIs like fluoxetine carry a very low risk of seizures at therapeutic doses. * **C. Hypotension:** Unlike Tricyclic Antidepressants (TCAs), which cause orthostatic hypotension due to alpha-1 adrenergic blockade, SSRIs have negligible effects on blood pressure. * **D. Loose stools:** Gastrointestinal upset (nausea, diarrhea) is a common class effect of SSRIs due to stimulation of 5-HT3 receptors in the gut. However, in the specific clinical profile of fluoxetine, CNS activation (anxiety/insomnia) is more characteristically prominent. **High-Yield NEET-PG Pearls:** * **Drug of Choice:** SSRIs are the first-line treatment for Depression, OCD, Panic Disorder, and Bulimia Nervosa. * **Longest Half-life:** Fluoxetine has the longest half-life (2–4 days) and its active metabolite, **norfluoxetine**, lasts up to 7–10 days. This reduces withdrawal symptoms but requires a longer "washout period" (5 weeks) before starting an MAOI to avoid **Serotonin Syndrome**. * **Weight:** Fluoxetine is often preferred in patients with obesity or Bulimia as it may cause initial weight loss (unlike other SSRIs like Paroxetine which cause weight gain).

Question 594: Central muscle relaxants act by:

A. Decreased nerve conduction
B. Inhibiting spinal polysynaptic reflexes (Correct Answer)
C. Blocking conduction across the neuromuscular junction
D. Central nervous system depression

Explanation: **Explanation:** Central muscle relaxants (e.g., Diazepam, Baclofen, Tizanidine, and Mephenesin congeners) reduce skeletal muscle tone by acting primarily on the **spinal cord and subcortical levels** of the Central Nervous System (CNS). **Why Option B is Correct:** The primary mechanism of these drugs is the **selective inhibition of polysynaptic reflexes** in the spinal cord. They increase the activity of inhibitory neurotransmitters (like GABA) or inhibit excitatory interneurons. By depressing these polysynaptic pathways, they reduce the excitatory input to alpha-motor neurons, thereby decreasing muscle spasticity without significantly affecting voluntary muscle strength. **Why Other Options are Incorrect:** * **Option A:** Decreased nerve conduction is the mechanism of **Local Anesthetics**, which block voltage-gated sodium channels. * **Option C:** Blocking conduction across the neuromuscular junction (NMJ) is the mechanism of **Peripheral Muscle Relaxants** (e.g., Succinylcholine, Vecuronium). These act on nicotinic receptors ($N_m$), not the CNS. * **Option D:** While many central muscle relaxants cause sedation as a side effect, "CNS depression" is a generalized effect of hypnotics/anesthetics. The specific therapeutic action for muscle relaxation is the targeted inhibition of spinal reflexes. **High-Yield Clinical Pearls for NEET-PG:** * **Baclofen:** A $GABA_B$ agonist; the drug of choice for spasticity in Multiple Sclerosis. * **Tizanidine:** An $\alpha_2$ adrenergic agonist (similar to Clonidine) that reduces spasticity with less muscle weakness than Baclofen. * **Diazepam:** Acts via $GABA_A$ receptors to increase chloride conductance. * **Dantrolene:** Often confused with central relaxants, but it is a **directly acting** muscle relaxant that inhibits calcium release from the sarcoplasmic reticulum (used in Malignant Hyperthermia).

Question 595: Which antiepileptic drug is used in petit mal epilepsy?

A. Phenobarbitone
B. Dilantin sodium
C. Dilantin sodium
D. Ethosuximide (Correct Answer)

Explanation: **Explanation:** **Petit mal epilepsy**, now clinically referred to as **Absence Seizures**, is characterized by brief lapses of consciousness and a classic **3 Hz spike-and-wave pattern** on EEG. **Why Ethosuximide is the Correct Answer:** Ethosuximide is the **drug of choice** for absence seizures. Its mechanism of action involves the inhibition of **T-type Calcium channels** in thalamic neurons. Since these channels are responsible for generating the rhythmic cortical discharges seen in absence seizures, blocking them effectively suppresses the seizure activity without significant sedation. **Analysis of Incorrect Options:** * **Phenobarbitone (Option A):** A barbiturate that acts via GABA-A receptors. While used for Generalized Tonic-Clonic Seizures (GTCS) and status epilepticus, it is ineffective for absence seizures and may even exacerbate them. * **Dilantin Sodium (Phenytoin) (Options B & C):** Phenytoin works by blocking voltage-gated sodium channels. It is a first-line drug for GTCS and focal seizures but is **contraindicated** in absence seizures as it can worsen the condition. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (DOC):** Ethosuximide is the DOC for *pure* absence seizures. However, if absence seizures coexist with GTCS, **Valproate** becomes the DOC. * **Side Effects of Ethosuximide:** Remember the mnemonic **EFGHI** – **E**thosuximide causes **F**atigue, **G**I distress, **H**eadache, **I**tching (Urticaria), and Stevens-Johnson Syndrome. * **EEG Hallmark:** 3 Hz spike-and-wave discharge is a frequent "image-based" or "fact-based" question associated with this topic.

Question 596: What is the drug of choice for petit mal seizures?

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

Explanation: **Explanation:** **Petit mal seizures**, also known as **Absence seizures**, are characterized by brief lapses in consciousness and a classic **3 Hz spike-and-wave pattern** on EEG. **1. Why Valproate is the Correct Choice:** While Ethosuximide is the drug of choice for *isolated* absence seizures [1], **Sodium Valproate** is considered the overall drug of choice for petit mal seizures in clinical practice and competitive exams like NEET-PG because: * It is a **broad-spectrum antiepileptic** effective against multiple seizure types [2]. * Absence seizures often coexist with Generalized Tonic-Clonic Seizures (GTCS) or Myoclonic seizures; Valproate covers all these [2], whereas Ethosuximide only covers absence seizures [1]. * **Mechanism:** It increases GABA levels, inhibits T-type $Ca^{2+}$ channels, and prolongs the inactivated state of $Na^+$ channels. **2. Why Other Options are Incorrect:** * **Ethosuximide (Option A):** It is the drug of choice for *pure* absence seizures (no other seizure types present) [1]. However, in a general context, Valproate is preferred due to its broader coverage. * **Carbamazepine (Option B) & Phenytoin (Option C):** These are narrow-spectrum agents [2]. Crucially, they are **contraindicated** in absence seizures as they can paradoxically **aggravate** or worsen petit mal attacks. **3. High-Yield Clinical Pearls for NEET-PG:** * **DOC for Pure Absence:** Ethosuximide [1] (Mechanism: Blocks T-type $Ca^{2+}$ channels in thalamic neurons). * **DOC for Atypical Absence/Myoclonic/GTCS:** Valproate [2]. * **Teratogenicity:** Valproate is highly teratogenic (Neural Tube Defects); avoid in pregnancy if possible. * **EEG Hallmark:** 3 Hz spike-and-wave discharge is the pathognomonic finding for Absence seizures.

Question 597: All of the following are side effects of clozapine, except:

A. Granulocytopenia
B. Seizures
C. Sedation
D. Extrapyramidal side effects (Correct Answer)

Explanation: **Explanation:** Clozapine is the prototype **Atypical Antipsychotic** (Second Generation Antipsychotic). The correct answer is **Extrapyramidal side effects (EPS)** because clozapine is uniquely characterized by its minimal to absent risk of EPS. **1. Why EPS is the correct answer:** Unlike typical antipsychotics (e.g., Haloperidol) which strongly block $D_2$ receptors in the nigrostriatal pathway, Clozapine has a **low affinity for $D_2$ receptors** and a high affinity for $5-HT_{2A}$ receptors. This "loose" binding to $D_2$ receptors allows it to treat psychosis without causing significant Parkinsonian symptoms, dystonia, or akathisia. It is, in fact, the drug of choice for patients who develop severe EPS or tardive dyskinesia from other antipsychotics. **2. Analysis of incorrect options:** * **Granulocytopenia (A):** This is the most serious side effect of Clozapine. It can progress to **Agranulocytosis** (1% risk), necessitating mandatory weekly blood monitoring (ANC counts). * **Seizures (B):** Clozapine causes a dose-dependent reduction in the seizure threshold. The risk is approximately 3-5% at high doses. * **Sedation (C):** Clozapine has potent H1-histaminergic and $\alpha_1$-adrenergic blocking activity, making sedation and orthostatic hypotension very common side effects. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** Treatment-resistant schizophrenia and suicidal behavior in schizophrenia. * **Sialorrhea:** Paradoxically, Clozapine causes excessive salivation (hypersalivation) despite its anticholinergic profile. * **Metabolic Syndrome:** It carries the highest risk among antipsychotics for weight gain, hyperlipidemia, and new-onset diabetes. * **Myocarditis:** A rare but potentially fatal side effect requiring monitoring during the first two months of therapy.

Question 598: Risperidone increases the risk of which of the following?

A. Cerebrovascular accidents
B. Extrapyramidal symptoms (Correct Answer)
C. Agranulocytosis
D. Diabetes insipidus

Explanation: **Explanation:** Risperidone is a **Second-Generation (Atypical) Antipsychotic**. While atypical antipsychotics generally have a lower risk of Extrapyramidal Symptoms (EPS) compared to first-generation drugs (like Haloperidol), **Risperidone is unique** because it exhibits dose-dependent EPS. At higher therapeutic doses (>6 mg/day), its potent D2 receptor antagonism outweighs its 5-HT2A antagonism, significantly increasing the risk of akathisia, dystonia, and parkinsonism. **Analysis of Options:** * **Extrapyramidal Symptoms (Correct):** Risperidone has the highest propensity for EPS among all atypical antipsychotics. It also frequently causes hyperprolactinemia due to D2 blockade in the tuberoinfundibular pathway. * **Cerebrovascular accidents:** While there is an increased risk of stroke in elderly patients with dementia-related psychosis taking atypicals, it is a "Black Box Warning" for the class rather than the primary side effect associated with Risperidone in general pharmacology. * **Agranulocytosis:** This is a classic, life-threatening side effect specifically associated with **Clozapine**, requiring mandatory WBC monitoring. * **Diabetes insipidus:** Nephrogenic Diabetes Insipidus is a classic side effect of **Lithium**, not antipsychotics. **High-Yield NEET-PG Pearls:** 1. **"The Typical Atypical":** Risperidone is the atypical antipsychotic most likely to cause EPS and prolactin elevation (amenorrhea, galactorrhea). 2. **Metabolic Syndrome:** Atypicals (especially Clozapine and Olanzapine) are high-risk for weight gain, dyslipidemia, and Type 2 Diabetes. 3. **Ziprasidone:** Notable for causing QT interval prolongation but has the least weight gain. 4. **Aripiprazole:** A D2 partial agonist, often called a "dopamine stabilizer."

Question 599: What is the drug of choice for an acute attack of migraine?

A. Sumatriptan (Correct Answer)
B. NSAIDS
C. Bromocriptine
D. Corticosteroids

Explanation: **Explanation:** The drug of choice for a moderate to severe acute attack of migraine is **Sumatriptan**. **1. Why Sumatriptan is correct:** Sumatriptan is a selective **5-HT$_{1B/1D}$ receptor agonist**. Its therapeutic effect is mediated through three mechanisms: * **Vasoconstriction:** It stimulates 5-HT$_{1B}$ receptors on intracranial blood vessels, reversing the vasodilation associated with migraine. * **Inhibition of Neuropeptides:** It acts on pre-junctional 5-HT$_{1D}$ receptors to inhibit the release of pro-inflammatory neuropeptides (like CGRP and Substance P) from trigeminal nerve endings. * **Central Inhibition:** It reduces pain transmission within the trigeminal nucleus caudalis. **2. Why other options are incorrect:** * **NSAIDS:** While drugs like Naproxen or Aspirin are first-line for *mild to moderate* attacks, they are generally less effective than triptans for severe acute migraine. * **Bromocriptine:** This is a dopamine (D2) agonist used in Parkinson’s disease and hyperprolactinemia; it has no role in treating acute migraine. * **Corticosteroids:** These are not used for acute attacks but may be used to break "Status Migrainosus" (a debilitating attack lasting >72 hours). **Clinical Pearls for NEET-PG:** * **Triptan Side Effects:** "Triptan sensations" include chest tightness and paresthesia. They are **contraindicated** in patients with Ischemic Heart Disease (IHD) or Prinzmetal angina due to coronary vasospasm. * **Prophylaxis:** The drug of choice for migraine *prophylaxis* is **Propranolol** (Beta-blocker). * **Newer Agents:** **Lasmiditan** (5-HT$_{1F}$ agonist) is a newer "ditan" that does not cause vasoconstriction, making it safer for cardiac patients. **Gepants** (e.g., Rimegepant) are CGRP antagonists used for both acute treatment and prophylaxis.

Question 600: Which antiparkinsonian drug is known to cause cardiac valvular fibrosis?

A. Levodopa
B. Ropinirole
C. Pramipexole
D. Pergolide (Correct Answer)

Explanation: **Explanation:** The correct answer is **Pergolide**. **1. Why Pergolide is correct:** Pergolide is an older, **ergot-derived** dopamine receptor agonist. The mechanism behind cardiac valvular fibrosis is its high affinity and potent agonist activity at the **5-HT2B receptors** located on heart valves. Activation of these receptors stimulates fibroblast proliferation, leading to valvulopathy (similar to the pathology seen in Carcinoid syndrome). Due to this serious adverse effect, pergolide was voluntarily withdrawn from the US market and its use is severely restricted worldwide. **2. Why the other options are incorrect:** * **Levodopa (A):** A precursor to dopamine. Its primary side effects are peripheral (nausea, arrhythmias, orthostatic hypotension) and central (dyskinesias, hallucinations), but it does not cause valvular fibrosis. * **Ropinirole (B) & Pramipexole (C):** These are **non-ergot** dopamine agonists. Unlike ergot derivatives, they are highly selective for D2/D3 receptors and have negligible affinity for 5-HT2B receptors. Therefore, they do not carry the risk of cardiac fibrosis and are preferred in clinical practice. **3. NEET-PG High-Yield Pearls:** * **Ergot-derived drugs** associated with fibrosis (cardiac, pulmonary, or retroperitoneal) include **Pergolide, Cabergoline, and Methysergide**. * **Bromocriptine** is also an ergot derivative but has a much lower risk of valvulopathy compared to Pergolide. * **Pramipexole** is unique as it may have neuroprotective properties by scavenging free radicals. * **Apomorphine** is the dopamine agonist used as a "rescue" therapy for "off" episodes in Parkinson’s disease (administered SC).

Practice by Chapter

General Anesthetics

Practice Questions

Local Anesthetics

Practice Questions

Sedative-Hypnotics

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Antiepileptic Drugs

Practice Questions

Antiparkinsonian Drugs

Practice Questions

Opioid Analgesics

Practice Questions

Drugs of Abuse and Addiction

Practice Questions

Psychostimulants

Practice Questions

Hallucinogens

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CNS Stimulants and Cognitive Enhancers

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