Central Nervous System Pharmacology Practice Questions

Q: Which drug acts on the receptor X shown below in skeletal muscle?

Dantrolene. ***Correct: Dantrolene*** - **Dantrolene** acts directly on the **ryanodine receptor (RyR1)** shown as receptor X in the sarcoplasmic reticulum of skeletal muscle - It **blocks calcium release** from the sarcoplasmic reticulum by inhibiting the ryanodine receptor - **Mechanism**: Prevents excitation-contraction coupling by reducing intracellular calcium availability - **Clinical use**: Treatment of **malignant hyperthermia** and spasticity of central origin - This is the only drug among the options that directly targets the intracellular calcium release channel *Incorrect: Tubocurarine* - Acts on **nicotinic receptors at the neuromuscular junction** (postsynaptic membrane), not on intracellular receptors - Non-depolarizing neuromuscular blocker that prevents acetylcholine binding - Does not affect calcium release from sarcoplasmic reticulum *Incorrect: Baclofen* - Acts on **GABA-B receptors** in the spinal cord (presynaptic and postsynaptic) - Reduces muscle spasticity by inhibiting excitatory neurotransmitter release at spinal level - Does not directly act on skeletal muscle calcium channels or ryanodine receptors *Incorrect: Vecuronium* - Acts on **nicotinic receptors at the neuromuscular junction**, similar to tubocurarine - Non-depolarizing neuromuscular blocker used for muscle relaxation during anesthesia - Blocks neuromuscular transmission, not intracellular calcium release mechanisms

Q: A patient of hemiplegic stroke is having extreme stiffness of arm and truncal musculature. Which drug marked X will act on GABA-B receptors to reduce symptoms? (Recent NEET Pattern 2016-17)

Baclofen. ***Baclofen*** - The image shows a drug 'X' acting on **GABA-B receptors** on both pre- and post-synaptic terminals, which is the mechanism of action for **baclofen**. - Baclofen is a centrally acting **muscle relaxant** often used to treat spasticity, stiffness, and muscle spasms, consistent with the symptoms in a patient with a hemiplegic stroke. *Diazepam* - Diazepam is a **benzodiazepine** that acts as an allosteric modulator primarily on **GABA-A receptors**, increasing the frequency of chloride channel opening. - While it has muscle relaxant properties, its primary mechanism is not via GABA-B receptors, and it has more pronounced sedative effects compared to baclofen. *Tizanidine* - Tizanidine is an **alpha-2 adrenergic agonist** that reduces spasticity by increasing presynaptic inhibition of motor neurons. - It does not primarily act on GABA-B receptors, distinguishing it from the drug depicted in the image. *Dantrolene* - Dantrolene acts directly on **skeletal muscle** by inhibiting calcium release from the sarcoplasmic reticulum, thereby uncoupling excitation-contraction. - It does not work on GABA receptors in the central nervous system; its effects are peripheral.

Q: A 6-year-old child has poor school performance. On scolding by teacher abnormal behavior is noted. EEG is performed. Which of the following drugs will cause worsening of the patient?

Carbamazepine. ***Carbamazepine*** - The EEG image shows **generalized spike-wave complexes at 3 Hz**, which are characteristic of **absence seizures** (also known as petit mal seizures). - **Carbamazepine** is known to **exacerbate absence seizures** and should be avoided in patients with this diagnosis. *Ethosuximide* - This is a **first-line drug** specifically for treating **absence seizures**. - It works by blocking **T-type calcium channels** in the thalamus, effectively reducing spike-wave discharges. *Valproate* - **Valproate** is a broad-spectrum anticonvulsant effective against various seizure types, including **absence seizures**, generalized tonic-clonic seizures, and myoclonic seizures. - It is an appropriate choice if ethosuximide is ineffective or if other seizure types coexist. *Clonazepam* - **Clonazepam** is a **benzodiazepine** that can be used as an add-on therapy for **absence seizures**, especially in refractory cases. - While it has sedative side effects, it does not typically worsen absence seizures; rather, it helps control them.

Q: Which anti-epileptic drug marked X will act at the site shown?

Tiagabine. ***Tiagabine*** - The image shows site 'X' as a **GABA reuptake transporter** that actively removes GABA from the synaptic cleft back into the presynaptic neuron or glial cells - **Tiagabine** specifically inhibits **GABA reuptake transporters (GAT-1)**, thereby increasing GABA concentration in the synaptic cleft and enhancing its inhibitory effect - This is the mechanism directly targeting the site shown in the diagram *Vigabatrin* - Irreversible inhibitor of **GABA transaminase (GABA-T)**, the enzyme responsible for catabolizing GABA - Acts intracellularly to prevent GABA breakdown, not at the synaptic reuptake transporter shown - Different mechanism from the site depicted *Gabapentin* - GABA analog but does not bind to GABA receptors or interfere with GABA reuptake - Primary mechanism involves modulating **voltage-gated calcium channels (α2δ subunit)**, reducing excitatory neurotransmitter release - Does not act at GABA transporters *Rufinamide* - Prolongs the inactive state of **voltage-dependent sodium channels**, reducing neuronal excitability - Mechanism is distinct from GABA reuptake or metabolism - Does not act at the site shown in the diagram

Q: Which anti-epileptic drug marked X will act at the site shown?

Tiagabine. ***Tiagabine*** - The image shows the reuptake of **GABA** from the synaptic cleft, and "X" points to this reuptake mechanism. Tiagabine is an anti-epileptic drug that acts by **inhibiting GABA reuptake**. - By inhibiting GABA reuptake, tiagabine increases the concentration of **GABA** in the synapse, enhancing its inhibitory effects and reducing neuronal excitability. *Valproate* - Valproate has multiple mechanisms of action, including inhibiting **GABA transaminase** (GABA-T) which leads to increased GABA levels, but it does not directly act on GABA reuptake. - It also blocks voltage-gated **sodium channels** and T-type calcium channels. *Gabapentin* - Gabapentin is an analogue of GABA but does not act directly on GABA receptors or GABA reuptake. - Its mechanism of action is primarily by binding to the **α2δ subunit of voltage-gated calcium channels**, reducing calcium influx and neurotransmitter release. *Vigabatrin* - Vigabatrin primarily works by irreversibly inhibiting **GABA transaminase (GABA-T)**, the enzyme responsible for the breakdown of GABA. - This leads to a persistent increase in **GABA** levels in the brain, thereby enhancing inhibitory neurotransmission.

Q: A 70-year-old man is diagnosed with Parkinsonism. Which is the drug at site marked as X?

Tolcapone. ***Tolcapone*** - The diagram shows 'X' inhibiting **COMT (catechol-O-methyltransferase)** in the periphery - **Tolcapone** is a COMT inhibitor that works both peripherally and centrally - It prevents the methylation of levodopa to 3-O-methyldopa, increasing levodopa availability to cross the blood-brain barrier - Tolcapone is more potent than entacapone but has potential hepatotoxicity risk requiring liver function monitoring *Entacapone* - Also a COMT inhibitor, but works only peripherally (not centrally) - While it does inhibit peripheral COMT like the site shown, tolcapone is the more comprehensive COMT inhibitor - Entacapone is safer with no hepatotoxicity concerns *Selegiline* - This is a selective **MAO-B (monoamine oxidase-B) inhibitor**, not a COMT inhibitor - Works by preventing dopamine breakdown in the brain - Does not act at the COMT site shown in the diagram *Rasagiline* - Also a selective **MAO-B inhibitor**, not a COMT inhibitor - Prevents dopamine degradation in the CNS - Does not inhibit COMT as shown at site X

Q: Which one of the following drugs is a long acting local anaesthetic agent ?

Bupivacaine. ***Bupivacaine***- **Bupivacaine** is the **classic and most widely recognized long-acting amide local anesthetic** with a duration of action typically ranging from **2 to 8 hours** depending on the concentration and site of administration. [1]- Its prolonged action is due to its high **lipid solubility** and **protein binding** (95%), allowing it to penetrate nerves effectively and stay bound within tissues for extended periods. [1]- It is the **prototypical long-acting local anesthetic** and has been the gold standard for decades in regional anesthesia and pain management. [1]*Lignocaine*- **Lignocaine** (also known as **lidocaine**) is an **intermediate-acting amide local anesthetic**, with a duration of action of **1-2 hours** (much shorter than bupivacaine). [1]- It is frequently used for **infiltration anesthesia**, **nerve blocks**, and **topical anesthesia** but is **not considered long-acting**. *Prilocaine*- **Prilocaine** is an **intermediate-acting amide local anesthetic**, similar to lignocaine, with a duration of action of approximately **1-2 hours**. [1]- A notable side effect of prilocaine, especially at high doses, is the potential for **methemoglobinemia** due to its metabolite o-toluidine. [1]*Ropivacaine*- **Ropivacaine** is a **newer long-acting amide local anesthetic** (duration 2-6 hours) introduced in the 1990s as an alternative to bupivacaine. [1]- While it has a **similar duration of action**, it is distinguished by its **lower cardiotoxicity** and **greater motor-sensory separation** compared to bupivacaine. [1]- However, **bupivacaine remains the classic textbook example** of a long-acting local anesthetic and is the expected answer in most examination contexts. [1]- Ropivacaine is often preferred in obstetric and pediatric anesthesia due to its better safety profile.

Q: The anticonvulsant of choice in the treatment of generalized tonic-clonic seizures is

Phenytoin. ***Phenytoin*** - **Historical Context (2012):** Phenytoin was traditionally considered a first-line anticonvulsant for **generalized tonic-clonic seizures** due to its ability to stabilize neuronal membranes and prevent seizure propagation by **blocking voltage-gated sodium channels**. - **Current Guidelines:** While phenytoin remains effective, it is now generally considered a **second-line agent** due to its narrow therapeutic index, significant side effects (gingival hyperplasia, hirsutism, osteomalacia), and multiple drug interactions. **Valproate, levetiracetam, and lamotrigine** are now preferred first-line options per modern ILAE guidelines. - **Note:** This question reflects the 2012 exam standards when phenytoin was still widely taught as first-line therapy. *Diazepam* - **Diazepam** is a **benzodiazepine** primarily used for the **acute termination of seizures** (status epilepticus), not as long-term maintenance therapy for generalized tonic-clonic seizures. - It acts by enhancing **GABA-A receptor** activity, leading to rapid CNS depression and seizure termination. *Phenobarbital* - **Phenobarbital** is a **barbiturate** that can be used for generalized tonic-clonic seizures but is generally a **second or third-line agent** due to significant sedative effects, cognitive impairment, and potential for drug interactions. - Its mechanism involves increasing **GABA-mediated chloride influx**, causing neuronal hyperpolarization. *Magnesium sulphate* - **Magnesium sulfate** is specifically indicated for the prevention and treatment of seizures in **eclampsia and preeclampsia**, not for generalized tonic-clonic seizures in other contexts. - It exerts anticonvulsant effects by acting as an **NMDA receptor antagonist** and reducing neuronal excitability.

Q: Which of the following local anaesthetics causes irreversible cardiac arrest if it is given intravenously ?

Bupivacaine. ***Bupivacaine*** - Bupivacaine is known for its **cardiotoxicity**, which can lead to severe and often irreversible **cardiac arrest** if inadvertently administered intravenously. - This is due to its high potency, slow dissociation from cardiac sodium channels, and increased lipid solubility, leading to prolonged cardiac depression. *Lignocaine* - While lignocaine (lidocaine) can cause cardiac toxicity in overdose, it is generally considered less cardiotoxic than bupivacaine, and cardiac arrest is more readily reversible. - It is commonly used intravenously as an antiarrhythmic, indicating a safer cardiac profile at therapeutic doses. *Cocaine* - Cocaine is a vasoconstrictor and stimulant; its primary cardiovascular effects are **tachycardia**, hypertension, and arrhythmias due to inhibition of norepinephrine reuptake, rather than direct myocardial depression leading to irreversible cardiac arrest from intravenous injection in the same manner as bupivacaine. - Cocaine toxicity can cause myocardial ischemia and infarction, but not the same profound, irreversible cardiac depression seen with bupivacaine. *Prilocaine* - Prilocaine is associated with **methemoglobinemia** as a dose-dependent side effect, especially in large doses, due to its metabolite o-toluidine. - While it can cause cardiovascular depression at very high doses, it does not have the same potent and often irreversible direct negative inotropic effects on the heart as bupivacaine.

Q: The first drug approved for Rett syndrome is?

Trofinetide. ***Trofinetide*** - **Trofinetide** (marketed as Daybue) is the first drug specifically approved by the FDA for the treatment of Rett syndrome, receiving approval in March 2023. - It is an analog of the **N-terminal tripeptide of insulin-like growth factor-1 (IGF-1)** and is thought to reduce neuroinflammation and support synaptic function in the brain, improving core symptoms of Rett syndrome. *L-carnitine* - **L-carnitine** is a nutritional supplement that has been studied in Rett syndrome for potential mitochondrial dysfunction, but it is not a primary treatment or an FDA-approved drug for the condition. - While sometimes used adjunctively, there is limited evidence for its efficacy as a standalone therapy in Rett syndrome. *Naltrexone* - **Naltrexone** is an opioid antagonist typically used to treat opioid and alcohol dependence. - It has been explored in some neurodevelopmental disorders, but it is not approved for or considered a primary treatment for Rett syndrome. *Folinic acid* - **Folinic acid** is a form of folic acid that can bypass metabolic blocks in folate pathways, sometimes used in conditions with cerebral folate deficiency. - While metabolic abnormalities can occur in Rett syndrome, folinic acid is not an FDA-approved drug for Rett syndrome.

Question 1

Which drug acts on the receptor X shown below in skeletal muscle?

Accepted Answer

Dantrolene

Answer

Tubocurarine

Answer

Baclofen

Answer

Vecuronium

Question 2

A patient of hemiplegic stroke is having extreme stiffness of arm and truncal musculature. Which drug marked X will act on GABA-B receptors to reduce symptoms? (Recent NEET Pattern 2016-17)

Accepted Answer

Baclofen

Answer

Dantrolene

Answer

Diazepam

Answer

Tizanidine

Question 3

A 6-year-old child has poor school performance. On scolding by teacher abnormal behavior is noted. EEG is performed. Which of the following drugs will cause worsening of the patient?

Accepted Answer

Carbamazepine

Answer

Ethosuximide

Answer

Valproate

Answer

Clonazepam

Question 4

Which anti-epileptic drug marked X will act at the site shown?

Accepted Answer

Tiagabine

Answer

Vigabatrin

Answer

Gabapentin

Answer

Rufinamide

Question 5

Which anti-epileptic drug marked X will act at the site shown?

Accepted Answer

Tiagabine

Answer

Vigabatrin

Answer

Valproate

Answer

Gabapentin

Question 6

A 70-year-old man is diagnosed with Parkinsonism. Which is the drug at site marked as X?

Accepted Answer

Tolcapone

Answer

Entacapone

Answer

Selegiline

Answer

Rasagiline

Question 7

Which one of the following drugs is a long acting local anaesthetic agent ?

Accepted Answer

Bupivacaine

Answer

Lignocaine

Answer

Prilocaine

Answer

Ropivacaine

Question 8

The anticonvulsant of choice in the treatment of generalized tonic-clonic seizures is

Accepted Answer

Phenytoin

Answer

Diazepam

Answer

Phenobarbital

Answer

Magnesium sulphate

Question 9

Which of the following local anaesthetics causes irreversible cardiac arrest if it is given intravenously ?

Accepted Answer

Bupivacaine

Answer

Lignocaine

Answer

Cocaine

Answer

Prilocaine

Question 10

The first drug approved for Rett syndrome is?

Accepted Answer

Trofinetide

Answer

L-carnitine

Answer

Naltrexone

Answer

Folinic acid

Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology — MCQs

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