Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 791: Which of the following is not true about benzodiazepines?

A. Can produce ataxia
B. Has GABA facilitatory but no GABA mimetic action
C. Produces muscle relaxation by action on spinal cord
D. REM, and Stage 3 and 4 sleep is increased (Correct Answer)

Explanation: **REM, and Stage 3 and 4 sleep is increased** - Benzodiazepines actually **decrease REM sleep** and **slow-wave sleep** (Stages 3 and 4) while increasing Stage 2 sleep. - This alteration in sleep architecture contributes to less restorative sleep despite inducing sedation. *Can produce ataxia* - Benzodiazepines can cause **ataxia**, especially at higher doses, due to their depressant effects on the **cerebellum** and motor coordination centers. - This side effect is a common concern, particularly in older adults, increasing the risk of falls. *Has GABA facilitatory but no GABA mimetic action* - Benzodiazepines **facilitate the action of GABA** by increasing the *frequency* of chloride channel opening, leading to enhanced inhibitory neurotransmission. - They do not directly activate GABA receptors in the absence of GABA, meaning they have no direct **GABA mimetic action**. *Produces muscle relaxation by action on spinal cord* - Benzodiazepines exert their **muscle relaxant effects** primarily by enhancing *GABAergic inhibition* in the **spinal cord** and **brainstem**. - This leads to a reduction in skeletal muscle tone and can be beneficial in treating muscle spasms.

Question 792: Which of the following drug pairs is correctly matched?

A. Peripheral decarboxylase inhibitor - Benserazide (Correct Answer)
B. Dopamine agonist - Amantadine
C. COMT inhibitor - Rasagiline
D. MAO-A inhibitor - Selegiline

Explanation: ***Peripheral decarboxylase inhibitor - Benserazide*** - **Benserazide** is a **peripheral decarboxylase inhibitor** that is commonly co-administered with **levodopa** to prevent its metabolism in the periphery. - By inhibiting the breakdown of levodopa outside the brain, **more levodopa can cross the blood-brain barrier**, where it is then converted to dopamine. *MAO-A inhibitor - Selegiline* - **Selegiline** is an **MAO-B inhibitor**, not an MAO-A inhibitor. It selectively inhibits the enzyme **monoamine oxidase B**, which is responsible for dopamine breakdown in the brain. - **MAO-A inhibitors** (like moclobemide) are primarily used as antidepressants, as they inhibit the breakdown of serotonin and norepinephrine. *COMT inhibitor - Rasagiline* - **Rasagiline** is an **MAO-B inhibitor**, similar to selegiline, used in the treatment of **Parkinson's disease** to reduce the breakdown of dopamine. - **COMT inhibitors** (like entacapone and tolcapone) block the enzyme **catechol-O-methyltransferase**, another enzyme involved in the peripheral and central metabolism of levodopa and dopamine. *Dopamine agonist - Amantadine* - **Amantadine** is an **antiviral drug** that also has **anti-Parkinsonian effects**, primarily through its influence on dopamine release and reuptake, as well as NMDA receptor antagonism. - While it modulates dopamine, it is not classified as a direct **dopamine agonist**; true dopamine agonists (like pramipexole and ropinirole) directly stimulate dopamine receptors.

Question 793: Which of the following is true about barbiturates?

A. Limbic system is most sensitive to the depressive action of barbiturates to CNS
B. Shows GABA facilitatory action (Correct Answer)
C. Enhances GABAergic activity by mimicking GABA's effects
D. Primarily acts by blocking voltage gated Na+ and K+ channels

Explanation: ***Shows GABA facilitatory action*** - Barbiturates enhance the effect of **GABA** (gamma-aminobutyric acid), the primary inhibitory neurotransmitter in the central nervous system, by increasing the **duration** of chloride channel opening. - This facilitatory action leads to **hyperpolarization** of neurons, making them less excitable and resulting in CNS depression. - This is the **primary mechanism** of action of barbiturates at therapeutic doses. *Enhances GABAergic activity by mimicking GABA's effects* - While barbiturates enhance GABAergic activity, they do not **mimic GABA's effects** in the same direct way that full agonists do. - Instead of acting as direct agonists, barbiturates **allosterically modulate** the GABA<sub>A</sub> receptor, increasing the receptor's affinity for GABA and prolonging the opening time of the associated chloride channel. *Limbic system is most sensitive to the depressive action of barbiturates to CNS* - The **reticular activating system (RAS)** in the brainstem, which plays a crucial role in regulating wakefulness and arousal, is generally considered the most sensitive area to the depressive effects of barbiturates. - While the limbic system is affected, its sensitivity is not uniquely highest compared to other CNS regions like the RAS, which is critical for the sedative and hypnotic effects observed. *Primarily acts by blocking voltage gated Na+ and K+ channels* - This is **incorrect**. The primary mechanism of barbiturates is through **GABA<sub>A</sub> receptor modulation**, not by blocking voltage-gated ion channels. - While barbiturates can have non-specific membrane effects on voltage-gated channels at very high (toxic) concentrations, this is not their primary or therapeutic mechanism of action.

Question 794: Which of the following is used for the patient on antiparkinsonian medication levodopa + carbidopa, but patient showing marked on-off effect?

A. Bromocriptine
B. Amantadine
C. Selegiline (Correct Answer)
D. Rimonabant

Explanation: ***Selegiline*** - **Selegiline** is a **MAO-B inhibitor** that slows the breakdown of dopamine in the brain, thus extending the therapeutic effect of **levodopa** and reducing motor fluctuations including "on-off" phenomena. - It works by inhibiting the enzyme monoamine oxidase type B, which metabolizes dopamine, thereby preserving both endogenous and levodopa-derived dopamine for more sustained dopaminergic stimulation. - **MAO-B inhibitors** are established adjuncts to levodopa therapy for managing motor complications and reducing "off" time. *Bromocriptine* - **Bromocriptine** is a **dopamine agonist** that directly stimulates dopamine receptors (particularly D2 receptors) and has a longer half-life than levodopa, providing more continuous dopaminergic stimulation [1]. - While dopamine agonists are also effective for motor fluctuations, **Selegiline** is often preferred as an initial adjunct due to its better tolerability profile and lower risk of inducing dyskinesias. - Bromocriptine can cause more side effects including **dyskinesias**, **hallucinations**, and **nausea**, particularly in elderly patients [1]. *Amantadine* - **Amantadine** is an **NMDA receptor antagonist** primarily used to treat **levodopa-induced dyskinesia** rather than motor fluctuations. - While it has mild antiparkinsonian effects, it is not the preferred agent for managing "on-off" phenomena specifically. - Its mechanism does not directly prolong levodopa's effect or prevent dopamine breakdown. *Rimonabant* - **Rimonabant** is a **cannabinoid receptor 1 (CB1) antagonist** that was previously marketed for obesity and smoking cessation but was **withdrawn from the market** due to serious psychiatric adverse effects including depression and suicidality. - It has **no role** in the management of **Parkinson's disease** or its motor complications.

Question 795: Modafinil is a drug used in which of the following conditions?

A. Shift work disorder (Correct Answer)
B. Chronic fatigue syndrome
C. Chronic pain syndrome
D. Insomnia

Explanation: ***Shift work disorder*** - **Modafinil** is a **wake-promoting agent** approved by the FDA for improving wakefulness in patients with excessive sleepiness associated with **shift work sleep disorder**. - It helps individuals maintain alertness during atypical work hours, overcoming disruption to their natural circadian rhythm. - **Note:** Modafinil's **primary indication is narcolepsy**, but among the given options, shift work disorder is the correct answer. *Chronic fatigue syndrome* - While fatigue is a primary symptom of **chronic fatigue syndrome**, modafinil is generally **not recommended** as a standard treatment. - Its efficacy in this condition is limited and inconsistent, and management focuses on symptom control and lifestyle adjustments. *Chronic pain syndrome* - **Modafinil has no direct analgesic properties** and is not indicated for **chronic pain syndrome**. - Treatment for chronic pain involves addressing underlying causes with appropriate analgesics or interventional therapies. *Insomnia* - **Modafinil is a wakefulness-promoting agent** and would be **contraindicated in insomnia**, as it would worsen the inability to sleep. - Insomnia is treated with sleep hygiene, cognitive behavioral therapy, or sedative-hypnotics.

Question 796: All of the following are CNS stimulants except?

A. Cocaine
B. Methylphenidate
C. Benzodiazepines (Correct Answer)
D. Amphetamines

Explanation: ***Correct Answer: Benzodiazepines*** - **Benzodiazepines** are the correct answer because they are central nervous system (CNS) **depressants**, NOT stimulants. - They enhance the effect of the neurotransmitter **GABA** at the GABA-A receptor, leading to decreased neuronal excitability. - They cause sedation, anxiolysis, muscle relaxation, and anticonvulsant effects. *Incorrect: Amphetamines* - **Amphetamines** are potent CNS **stimulants** that increase the release of dopamine and norepinephrine, leading to increased alertness, energy, and focus. - They are commonly prescribed for conditions like attention-deficit/hyperactivity disorder (ADHD) and narcolepsy, but also have high potential for abuse. *Incorrect: Cocaine* - **Cocaine** is a powerful CNS **stimulant** that blocks the reuptake of dopamine, norepinephrine, and serotonin in the brain, resulting in a rapid onset of euphoria, increased energy, and heightened sensory perception. - Its effects are short-lived, leading to a strong craving for more, and it has significant cardiovascular and neurological risks. *Incorrect: Methylphenidate* - **Methylphenidate** is a CNS **stimulant** structurally similar to amphetamines, primarily used in the treatment of ADHD and narcolepsy. - It works by blocking the reuptake of dopamine and norepinephrine, increasing the concentration of these neurotransmitters in the synaptic cleft, and improving attention and focus.

Question 797: Which of the following is the most commonly prescribed first-line medication for ADHD?

A. Atomoxetine
B. Dextroamphetamine
C. Methylphenidate (Correct Answer)
D. Guanfacine

Explanation: ***Methylphenidate*** - **Methylphenidate** is a central nervous system stimulant and is widely considered a **first-line treatment** for ADHD in both children and adults. - It works by increasing the levels of **dopamine** and **norepinephrine** in the brain, improving attention and reducing impulsivity. - Most commonly prescribed due to extensive clinical experience, proven efficacy, and favorable safety profile. *Atomoxetine* - **Atomoxetine** is a **non-stimulant** medication used for ADHD, but it is typically considered second-line due to slower onset of action compared to stimulants. - It selectively inhibits the reuptake of **norepinephrine**, taking several weeks to show full therapeutic effect. - Preferred when stimulants are contraindicated or not tolerated. *Dextroamphetamine* - **Dextroamphetamine** is an effective **stimulant** medication for ADHD, but it is often reserved as an alternative if methylphenidate is not well-tolerated or effective. - It also increases **dopamine** and **norepinephrine** but has a slightly different pharmacological profile and duration of action. *Guanfacine* - **Guanfacine** is an **alpha-2 adrenergic agonist** used as adjunctive or alternative therapy for ADHD. - It is **not a first-line medication** and is typically used when stimulants are ineffective, contraindicated, or for specific symptom management (especially hyperactivity/impulsivity). - Has a different mechanism of action focusing on prefrontal cortex modulation.

Question 798: Which of the following is not a use of Thiopentone?

A. Induction of anesthesia
B. As antidepressant (Correct Answer)
C. Medically induced coma
D. As truth serum

Explanation: As antidepressant - **Thiopentone** is a short-acting **barbiturate** and a potent central nervous system depressant, with no known antidepressant properties. [1] - Its mechanism of action involves enhancing **GABAergic inhibition**, leading to sedation and anesthesia, not mood elevation. *Induction of anesthesia* - **Thiopentone** is a classic intravenous anesthetic, often used for **rapid induction of general anesthesia** due to its fast onset of action. [2], [4] - It quickly crosses the **blood-brain barrier** to produce unconsciousness, making it effective for this purpose. [4] *Medically induced coma* - **Thiopentone** can be used to induce and maintain a **medically induced coma**, particularly in cases of severe head injury or status epilepticus, to reduce metabolic demand and cerebral edema. [3] - Its ability to significantly suppress brain activity makes it suitable for **neuroprotection** in critical care settings. [3] *As truth serum* - Historically, **thiopentone** (often referred to as **sodium pentothal**) has been colloquially known as a **"truth serum"** due to its ability to lower inhibitions and make subjects more loquacious. - While it can facilitate questioning by making individuals less guarded, its effectiveness as a reliable truth serum is largely unsubstantiated and ethically controversial.

Question 799: Which among the following is a depolarising muscle relaxant?

A. Decamethonium (Correct Answer)
B. D-tubocurarine
C. Doxacurium
D. Atracurium

Explanation: **Correct: Decamethonium** - **Decamethonium** is a **depolarizing neuromuscular blocker** that mimics acetylcholine at the neuromuscular junction, leading to initial muscle fasciculations followed by paralysis. - It binds to and activates **nicotinic acetylcholine receptors**, causing persistent depolarization and preventing further muscle contraction. - While historically important, it is rarely used clinically today compared to succinylcholine. *Incorrect: D-tubocurarine* - **D-tubocurarine** is a **non-depolarizing neuromuscular blocker** that acts as a competitive antagonist at the nicotinic acetylcholine receptors. - It prevents acetylcholine from binding, thereby inhibiting muscle contraction without initial depolarization. *Incorrect: Doxacurium* - **Doxacurium** is a **non-depolarizing neuromuscular blocker** of the long-acting benzylisoquinolinium class. - It functions by competitively blocking acetylcholine at the neuromuscular junction, leading to muscle relaxation. *Incorrect: Atracurium* - **Atracurium** is an **intermediate-acting, non-depolarizing neuromuscular blocker** also of the benzylisoquinolinium class. - It undergoes unique elimination pathways, including **Hofmann elimination** and ester hydrolysis, making it suitable for patients with renal or hepatic impairment.

Question 800: Which of the following serotonin receptors is classified as an ionotropic receptor?

A. 5-HT1A
B. 5-HT1B
C. 5-HT2A
D. 5-HT3 (Correct Answer)

Explanation: ***5-HT3*** - The 5-HT3 receptor is unique among serotonin receptors as it is the **only ionotropic receptor**, meaning it directly gates an ion channel upon ligand binding. - Activation of 5-HT3 receptors leads to rapid **depolarization** of the neuronal membrane through the influx of **sodium and potassium ions**, mediating fast excitatory neurotransmission. *5-HT1A* - The 5-HT1A receptor is a **G-protein coupled receptor (GPCR)** and is inhibitory, primarily located pre- and post-synaptically in the brain. - Activation leads to a decrease in **cAMP** levels and opening of **potassium channels**, resulting in hyperpolarization. *5-HT1B* - The 5-HT1B receptor is also a **GPCR**, primarily found on presynaptic terminals where it acts as an **autoreceptor** to inhibit serotonin release. - Similar to 5-HT1A, its activation inhibits adenylyl cyclase activity, leading to reduced **cAMP** levels. *5-HT2A* - The 5-HT2A receptor is a **GPCR** that couples to the Gq protein, leading to increased **inositol triphosphate (IP3)** and **diacylglycerol (DAG)**. - This pathway activates protein kinase C and mobilizes intracellular calcium, typically leading to **excitatory effects** in various brain regions.

Practice by Chapter

General Anesthetics

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Local Anesthetics

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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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