Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 701: A 65-year-old gentleman is having tremors, rigidity and reduced mobility. He is likely to be benefited by?

A. Reserpine
B. Bromocriptine (Correct Answer)
C. Acyclovir
D. Alpha methyl dopa

Explanation: ***Bromocriptine*** - The patient's symptoms (tremors, rigidity, reduced mobility) are classic for **Parkinson's disease**, which involves a deficiency of **dopamine** [1]. - **Bromocriptine** is a **dopamine agonist** that directly stimulates dopamine receptors, thereby alleviating Parkinsonian symptoms [2]. *Reserpine* - **Reserpine** depletes **monoamines**, including dopamine, by inhibiting their uptake into synaptic vesicles. - This action would worsen Parkinsonian symptoms rather than improve them. *Acyclovir* - **Acyclovir** is an **antiviral agent** used to treat herpes virus infections. - It has no role in the management of movement disorders like Parkinson's disease. *Alpha methyl dopa* - **Alpha-methyldopa** is an **antihypertensive agent** that reduces sympathetic outflow by acting as an alpha-2 adrenergic agonist. - It does not address the dopamine deficiency seen in Parkinson's disease and is not used to treat movement disorders.

Question 702: The following drugs are used for prophylaxis of migraine except

A. Metoprolol
B. Valproate
C. Topiramate
D. Meperidine (Correct Answer)

Explanation: ***Meperidine*** - **Meperidine** (pethidine) is an **opioid analgesic** primarily used for acute pain relief, not for migraine prophylaxis. - Its use can lead to **opioid dependence** and even worsen headache frequency in the long term, known as medication overuse headache. *Metoprolol* - **Metoprolol** is a **beta-blocker** commonly prescribed for migraine prophylaxis, especially in patients with co-existing hypertension or anxiety. - It works by modulating **adrenergic activity** and is considered a first-line agent for preventing migraine attacks. *Valproate* - **Valproate** (valproic acid/divalproex sodium) is an **anticonvulsant** that is effective in migraine prophylaxis. - It is thought to work by increasing **GABA activity** and modulating neuronal excitability, reducing migraine frequency. *Topiramate* - **Topiramate** is an **anticonvulsant** frequently used for migraine prophylaxis, particularly favored for its potential side effect of **weight loss**. - Its mechanism involves multiple actions, including **GABA potentiation**, glutamate antagonism, and modulation of voltage-gated ion channels.

Question 703: Drugs used for Prophylaxis of migraine include the following except?

A. Valproate
B. Sumatriptan (Correct Answer)
C. TCAs
D. Propranolol

Explanation: ***Sumatriptan*** - **Sumatriptan** is a **triptan** drug class medication (5-HT1B/1D receptor agonist) used for the **acute treatment** of migraine attacks, not for prophylaxis. - It works by causing cranial vasoconstriction and inhibiting neuropeptide release, thereby aborting an active migraine attack. - Triptans are contraindicated in patients with coronary artery disease due to their vasoconstrictive effects. *Valproate* - **Valproate** (sodium valproate/divalproex) is an established **first-line agent for migraine prophylaxis**. - It exerts antimigraine effects through modulation of GABAergic transmission, voltage-gated sodium channels, and possibly NMDA receptor inhibition. - Effective dose for prophylaxis is typically 500-1000 mg/day in divided doses. *Propranolol* - **Propranolol**, a non-selective **beta-blocker**, is one of the most commonly used **first-line prophylactic agents** for migraine. - It reduces migraine frequency through multiple mechanisms including inhibition of norepinephrine, reduction of cortical spreading depression, and stabilization of vascular tone. - Typical prophylactic dose is 80-240 mg/day in divided doses. *TCAs* - **Tricyclic antidepressants (TCAs)**, particularly **amitriptyline**, are highly effective **first-line prophylactic agents** for migraine. - They work through modulation of serotonin and norepinephrine reuptake, as well as effects on ion channels and pain pathways. - Amitriptyline is typically used at doses of 25-150 mg at bedtime for migraine prophylaxis.

Question 704: A female patient of childbearing age is on valproate for JME. Which drug should be used to replace valproate and can be prescribed as monotherapy?

A. Carbamazepine
B. Phenytoin
C. Levetiracetam (Correct Answer)
D. Zonisamide

Explanation: ***Levetiracetam*** - **Levetiracetam** is recommended as a safer alternative to valproate in women of childbearing potential due to its **favorable pregnancy safety profile** and broad-spectrum efficacy against generalized seizures, including those seen in **juvenile myoclonic epilepsy (JME)** [1]. - It can be used as **monotherapy** and has a generally well-tolerated side effect profile [1], making it a suitable long-term option.*Carbamazepine* - **Carbamazepine** is primarily effective for **focal (partial) seizures** and is generally not recommended for **generalized epilepsy syndromes** like JME due to the risk of worsening myoclonic or absence seizures. - It also has significant **teratogenic risks**, including neural tube defects, making it unsuitable for women of childbearing age when safer alternatives exist [2].*Phenytoin* - **Phenytoin** is effective for focal and tonic-clonic seizures but can **exacerbate myoclonic seizures** in JME. - It carries a significant risk of **teratogenicity**, including fetal hydantoin syndrome, making it an inappropriate choice for women of childbearing potential [2].*Zonisamide* - **Zonisamide** is a broad-spectrum antiepileptic drug, but it is often reserved as an **add-on therapy** for refractory epilepsy rather than a first-line monotherapy, particularly if there are safer and more established first-line options. - While generally considered less teratogenic than valproate, its safety profile in pregnancy has fewer established data compared to levetiracetam.

Question 705: Which of the following medications in the treatment of Parkinson's disease is an NMDA antagonist?

A. Amantadine (Correct Answer)
B. Selegiline
C. Entacapone
D. Ropinirole

Explanation: ***Amantadine*** - **Amantadine** is an **NMDA receptor antagonist**, which contributes to its antiparkinsonian effects by modulating glutamatergic neurotransmission. - It works by reducing the **excitatory effects of glutamate**, potentially improving motor fluctuations and dyskinesia in Parkinson's disease. *Selegiline* - **Selegiline** is a **selective irreversible inhibitor of monoamine oxidase B (MAO-B)**, which prevents the breakdown of dopamine. - It enhances the availability of dopamine in the brain but does not act as an NMDA antagonist. *Entacapone* - **Entacapone** is a **catechol-O-methyltransferase (COMT) inhibitor** that prevents the peripheral breakdown of levodopa. - This action increases the bioavailability of levodopa to the brain, but it is not an NMDA antagonist. *Ropinirole* - **Ropinirole** is a **dopamine agonist** that directly stimulates dopamine receptors in the brain. - It mimics the effects of dopamine but does not interact with NMDA receptors.

Question 706: Modafinil is used for

A. Psychogenic erectile dysfunction
B. Narcolepsy (Correct Answer)
C. Orthostatic hypotension
D. OCD

Explanation: ***Narcolepsy*** - **Modafinil** is a **wakefulness-promoting agent** primarily used to improve wakefulness in patients with excessive daytime sleepiness associated with **narcolepsy**. - Its mechanism involves increasing levels of **dopamine** and **norepinephrine** in specific brain regions, promoting alertness without significant cardiovascular or euphoric effects. *Psychogenic erectile dysfunction* - This condition is typically treated with **phosphodiesterase-5 (PDE5) inhibitors** like sildenafil or tadalafil, which improve blood flow to the penis. - Modafinil has no established role in the treatment of erectile dysfunction, as it does not directly affect the physiological mechanisms of erection. *Orthostatic hypotension* - **Orthostatic hypotension** is managed by increasing blood volume and venoconstriction, often using medications like **fludrocortisone** or **midodrine**. - While modafinil has some sympathomimetic properties, it is not a first-line or common treatment for orthostatic hypotension. *OCD* - **Obsessive-compulsive disorder (OCD)** is primarily treated with **selective serotonin reuptake inhibitors (SSRIs)** and cognitive-behavioral therapy (CBT). - Modafinil is not indicated for OCD and would not address the underlying pathology of obsessions and compulsions.

Question 707: Drug of choice in absence seizures:

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

Explanation: ***Valproate*** - **Valproate** is considered a **first-line drug for absence seizures**, particularly effective for **all types of generalized seizures** including absence, myoclonic, and tonic-clonic seizures. - It works by increasing GABA levels and modulating voltage-gated sodium channels, which helps to stabilize neuronal excitability. - **Advantage**: Provides **broad-spectrum coverage**, making it the preferred choice when **mixed seizure types** are present or when **juvenile absence epilepsy** is suspected. - **Note**: **Ethosuximide** is also a first-line drug for **pure typical absence seizures** (especially in children), but valproate is often preferred when broader anticonvulsant coverage is needed. *Carbamazepine* - **Carbamazepine** is effective for **focal (partial) seizures** and **generalized tonic-clonic seizures**. - It can **exacerbate or worsen absence seizures**, making it contraindicated in this seizure type. - Mechanism: Blocks voltage-gated sodium channels, which is ineffective for absence seizures. *Phenytoin* - **Phenytoin** is primarily used for **focal (partial) seizures** and **generalized tonic-clonic seizures**. - Like carbamazepine, **phenytoin can worsen absence seizures** and is contraindicated. - Its mechanism of action (sodium channel blockade) is not suitable for absence seizures. *BZD (Benzodiazepines)* - While benzodiazepines like **clonazepam** can be used as **adjunctive therapy** for refractory absence seizures, they are **not first-line drugs**. - **Limitations**: Sedation, tolerance development, and dependence risk. - **Diazepam** and **lorazepam** are reserved for **acute seizure management** (status epilepticus) rather than chronic seizure control.

Question 708: Drugs used in management of migraine include the following except?

A. Topiramate
B. Valproate
C. Ethosuximide (Correct Answer)
D. Verapamil

Explanation: ***Ethosuximide*** - **Ethosuximide** is an anti-epileptic drug primarily used to treat **absence seizures** by blocking T-type calcium channels [1]. - It has no established role in the **acute** or **prophylactic** management of migraine headaches. *Topiramate* - **Topiramate** is an anti-epileptic drug that is also approved for **migraine prophylaxis**. - Its mechanism of action in migraine includes modulating **GABA receptors**, blocking **voltage-sensitive sodium channels**, and inhibiting **carbonic anhydrase** [2]. *Valproate* - **Valproate** (valproic acid) is an anti-epileptic drug and mood stabilizer commonly used for **migraine prevention**. - Its migraine prophylactic effect is believed to involve increasing **GABA levels** and modulating **neurotransmitter release** [1]. *Verapamil* - **Verapamil** is a **calcium channel blocker** sometimes used off-label for **migraine prophylaxis**, particularly in cases of difficult-to-treat migraines or specific subtypes like **hemiplegic migraine**. - It works by reducing cerebral vasospasm and stabilizing neuronal membranes.

Question 709: What does Parkinsonism treatment primarily involve?

A. Dopamine antagonism
B. Balance of Ach & dopamine in striatum (Correct Answer)
C. Dopamine release
D. Serotonin enhancement

Explanation: ***Balance of Ach & dopamine in striatum*** - Parkinsonism involves a **dopamine deficiency** in the **nigrostriatal pathway**, leading to an imbalance with **acetylcholine (ACh)**. - Treatment aims to restore this **dopamine-ACh balance**, typically by increasing dopamine activity (levodopa, dopamine agonists) or reducing ACh activity (anticholinergics) in the **striatum**. *Dopamine antagonism* - **Dopamine antagonism** would worsen Parkinsonism symptoms by further reducing dopamine's effects. - Antipsychotic medications that are dopamine antagonists can actually induce **drug-induced parkinsonism**. *Dopamine release* - While increasing **dopamine availability** is part of treatment, this option is too narrow and doesn't capture the crucial aspect of balancing it against acetylcholine. - Treatment focuses on the **overall balance** between these neurotransmitter systems rather than just dopamine alone. *Serotonin enhancement* - **Serotonin** is not the primary neurotransmitter involved in Parkinsonism pathophysiology. - The core defect is in the **dopaminergic-cholinergic balance**, not serotonin systems, though serotonin may play a minor role in some non-motor symptoms.

Question 710: Tetanus affects primarily -

A. Neuromuscular junction
B. Muscle fibres
C. Postsynaptic terminal of spinal cord
D. Presynaptic terminal of spinal cord (Correct Answer)

Explanation: **Presynaptic terminal of spinal cord** - The **tetanus toxin (tetanospasmin)**, produced by *Clostridium tetani*, acts on the **presynaptic terminals** of inhibitory interneurons in the spinal cord. - It **blocks the release of inhibitory neurotransmitters** like glycine and GABA, leading to uncontrolled muscle spasms and rigidity. *Neuromuscular junction* - While muscles are the target of tetanus symptoms, the primary action of the toxin is not directly at the neuromuscular junction to affect acetylcholine release or receptor function. - Diseases like **myasthenia gravis** or **Lambert-Eaton myasthenic syndrome** primarily affect the neuromuscular junction. *Muscle fibres* - The tetanus toxin does not directly damage or alter the contractile properties of **muscle fibers** themselves. - Muscle pathology in tetanus is secondary to continuous, uncontrolled contraction due to nerve dysfunction. *Postsynaptic terminal of spinal cord* - The toxin's primary effect is on the **presynaptic release** of neurotransmitters, not on the postsynaptic receptors of spinal cord neurons. - Conditions affecting postsynaptic terminals in the spinal cord would involve issues with neurotransmitter reception or integration.

Practice by Chapter

General Anesthetics

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Local Anesthetics

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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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