Central Nervous System Pharmacology — MCQs

Central Nervous System Pharmacology Indian Medical PG Practice Questions and MCQs

Question 711: Drugs used in Alzheimer's disease are all EXCEPT:

A. Biperidin (Correct Answer)
B. Memantine
C. Rivastigmine
D. Donepezil

Explanation: ***Biperidin*** - **Biperidin** is an **anticholinergic drug** primarily used to treat **Parkinson's disease** and **drug-induced extrapyramidal symptoms**. - Its **anticholinergic effects** can worsen cognitive function in Alzheimer's patients, making it unsuitable for their treatment. *Memantine* - **Memantine** is an **NMDA receptor antagonist** that helps regulate glutamate activity in the brain. - It is used to treat **moderate to severe Alzheimer's disease** by preventing overstimulation of neurons. *Rivastigmine* - **Rivastigmine** is a **cholinesterase inhibitor** used to treat mild to moderate Alzheimer's disease. - It works by increasing levels of **acetylcholine** in the brain, improving communication between nerve cells. *Donepezil* - **Donepezil** is another **cholinesterase inhibitor** commonly prescribed for mild to moderate Alzheimer's disease. - It helps to improve **cognitive function** by enhancing cholinergic neurotransmission.

Question 712: Prophylaxis for migraine -

A. Amitriptyline (Correct Answer)
B. Sumatriptan
C. Diazepam
D. Nifedipine

Explanation: ***Amitriptyline*** - **Amitriptyline**, a **tricyclic antidepressant**, is commonly used for migraine prophylaxis due to its neuromodulatory effects that can reduce headache frequency and severity. - It works by affecting neurotransmitters like **serotonin** and **norepinephrine**, which play a role in migraine pathophysiology. *Nifedipine* - **Nifedipine** is a **calcium channel blocker** primarily used for hypertension and angina, not typically for migraine prophylaxis. - While other calcium channel blockers like **verapamil** can be used for migraine, nifedipine is not a first-line or common choice. *Sumatriptan* - **Sumatriptan** is an **abortive medication** used to treat acute migraine attacks once they have started. - It works by constricting blood vessels and blocking pain pathways in the brain, but it is not used for chronic prevention. *Diazepam* - **Diazepam** is a **benzodiazepine** primarily used for anxiety, muscle spasms, and seizures due to its sedative and anxiolytic properties. - It is not indicated for migraine prophylaxis and can sometimes worsen headaches with chronic use or withdrawal.

Question 713: Drug of choice for myasthenia gravis -

A. D. tubocurare
B. Gallamine
C. Pyridostigmine (Correct Answer)
D. Succinylcholine

Explanation: ***Pyridostigmine*** - **Pyridostigmine** is an **acetylcholinesterase inhibitor** that increases the amount of acetylcholine at the neuromuscular junction, improving muscle strength in myasthenia gravis. - It is the **first-line symptomatic treatment** for generalized myasthenia gravis, helping to alleviate muscle weakness and fatigue. *Succinylcholine* - **Succinylcholine** is a **depolarizing neuromuscular blocker** often used in anesthesia to induce paralysis by mimicking acetylcholine. - In myasthenia gravis patients, its effects can be unpredictable and potentially prolonged due to altered acetylcholine receptor sensitivity, making it a poor choice for treatment and dangerous in surgical settings. *D. tubocurare* - **D-tubocurarine** is a **non-depolarizing neuromuscular blocker** that competitively inhibits acetylcholine at the neuromuscular junction, leading to muscle paralysis. - Patients with myasthenia gravis are highly sensitive to non-depolarizing blockers, and even small doses can cause profound and prolonged paralysis, making it contraindicated in their management. *Gallamine* - **Gallamine** is also a **non-depolarizing neuromuscular blocker** that works by antagonizing acetylcholine receptors at the neuromuscular junction. - Similar to D-tubocurarine, it can cause severe and prolonged neuromuscular blockade in patients with myasthenia gravis, making it an inappropriate and dangerous drug for treatment.

Question 714: Which of the following drugs can cause neuropsychiatric side effects due to its lipophilic nature and ability to cross the blood-brain barrier?

A. Propranolol (Correct Answer)
B. Clozapine
C. Clonidine
D. Disulfiram

Explanation: ***Propranolol*** - Propranolol is a **lipophilic (fat-soluble) non-selective beta-blocker** that readily crosses the **blood-brain barrier (BBB)**, leading to significant central nervous system penetration - This CNS penetration results in **neuropsychiatric side effects** including **depression, nightmares, hallucinations, vivid dreams, fatigue, memory impairment, and confusion** - These neuropsychiatric features are more prominent with **lipophilic beta-blockers** (propranolol, metoprolol) compared to hydrophilic ones (atenolol, nadolol) - This makes propranolol a notable example of an **unexpected neuropsychiatric adverse effect** from a cardiovascular drug *Clozapine* - Clozapine is an **atypical antipsychotic** that does cross the BBB (as it must to exert its therapeutic effect on schizophrenia) - However, it is **not lipophilic** in the same manner as propranolol and works through different mechanisms (dopamine D2 and serotonin 5-HT2A antagonism) - While it causes CNS effects like **sedation and seizures**, these are expected effects of a psychiatric medication, not unexpected neuropsychiatric side effects from a non-CNS drug *Clonidine* - Clonidine is a **centrally-acting alpha-2 agonist** that must cross the BBB to exert its therapeutic antihypertensive effect - It causes **sedation and drowsiness** as part of its primary mechanism of action (reducing sympathetic outflow from the CNS) - These are **expected CNS effects** rather than unexpected neuropsychiatric side effects from peripheral drug action *Disulfiram* - Disulfiram is an **aldehyde dehydrogenase inhibitor** used for alcohol dependence treatment - Its primary side effects relate to the **disulfiram-ethanol reaction** (acetaldehyde accumulation causing flushing, nausea, tachycardia) - While it can cause neuropsychiatric effects in some cases, it is **not particularly lipophilic** and this is not its characteristic adverse effect profile

Question 715: Abuse of which of the following is the most common cause of seizures:

A. Short term barbiturates
B. Opioids
C. Cocaine (Correct Answer)
D. Short term benzodiazepines

Explanation: ***Cocaine*** - **Cocaine** is a potent **central nervous system stimulant** that can induce seizures through neuronal excitation, vasoconstriction, and direct neurotoxicity. - Its abuse is frequently linked to a variety of neurological complications, including **ischemic stroke** and **intracranial hemorrhage**, both of which can also lower seizure threshold. *Short term barbiturates* - **Barbiturates** are **CNS depressants** often prescribed for sedation or seizure control; their withdrawal, not short-term abuse, is a more common cause of seizures. - While acute intoxication with very high doses could cause seizures, their primary effect is general CNS depression rather than excitation. *Opioids* - **Opioids primarily cause CNS depression** and are not typically associated with inducing seizures. - **Opioid withdrawal** can sometimes lead to seizures, but this is less common than with other substances and is not directly due to abuse itself. *Short term benzodiazepines* - **Benzodiazepines** are **anticonvulsants** and are commonly used to treat seizures; acute abuse is unlikely to cause seizures. - Similar to barbiturates, **benzodiazepine withdrawal** is a significant cause of seizures, but this is distinct from short-term abuse.

Question 716: Which of the following muscle relaxants causes pain on injection?

A. Succinylcholine
B. Rocuronium (Correct Answer)
C. Vecuronium
D. Pancuronium

Explanation: ***Rocuronium*** - **Rocuronium** is known to cause pain on injection, especially when administered in **small veins**, due to its **low pH** and high osmolarity. - This discomfort can be mitigated by injecting into a **larger vein** or by pre-treating with a small dose of **lidocaine**. *Succinylcholine* - **Succinylcholine** typically does not cause pain on injection, but it can lead to **muscle fasciculations** and subsequent **post-operative myalgia**. - Its mechanism of action involves initial depolarization of the neuromuscular junction, which can transiently increase **intracranial pressure** and **intraocular pressure**. *Vecuronium* - **Vecuronium** is a nondepolarizing neuromuscular blocker that is generally well-tolerated and **does not frequently cause pain on injection**. - It is known for its relatively **short duration of action** and minimal cardiovascular effects. *Pancuronium* - **Pancuronium** is a long-acting, nondepolarizing neuromuscular blocker that does **not typically cause pain on injection**. - It can, however, cause **tachycardia** due to its vagolytic effects, which is a significant differentiating characteristic.

Question 717: Increase in ICP is due to:

A. Procaine
B. Ketamine (Correct Answer)
C. Prilocaine
D. Bupivacaine

Explanation: ***Ketamine*** - **Ketamine** is known to increase **cerebral blood flow** and metabolic rate, which can lead to an increase in **intracranial pressure (ICP)**. - This effect makes ketamine generally contraindicated in patients with pre-existing elevated ICP or neurotrauma. *Prilocaine* - **Prilocaine** is a **local anesthetic** that does not directly cause increases in ICP. - Its metabolism can produce **o-toluidine**, which can cause **methemoglobinemia**, a side effect unrelated to ICP. *Procaine* - **Procaine** is an **ester-type local anesthetic** that primarily functions by blocking nerve impulses. - It does not have a direct mechanism that would lead to increased **intracranial pressure**. *Bupivacaine* - **Bupivacaine** is a **long-acting local anesthetic** commonly used for regional anesthesia. - While it can cause **cardiovascular depression** and **CNS toxicity** in high doses, it does not typically increase **intracranial pressure**.

Question 718: 30 year old female with partial seizure. Drug of choice:

A. Phenytoin
B. Carbamazepine (Correct Answer)
C. Phenobarbitone
D. Na+ valproate

Explanation: ***Carbamazepine*** - **Carbamazepine** is a first-line drug of choice for treating **partial seizures** due to its efficacy in controlling seizure activity with a generally favorable side effect profile. - It works by blocking **voltage-gated sodium channels**, thereby stabilizing the inactivated state of Na+ channels and preventing repetitive firing of action potentials. *Phenytoin* - While **phenytoin** is effective for partial seizures by blocking **sodium channels**, its use is often limited by its non-linear kinetics and significant side effects, including **gingival hyperplasia**, hirsutism, and cerebellar atrophy with chronic use. - Due to these side effects and monitoring difficulties, it's often considered a second-line option or for acute seizure control rather than initial monotherapy. *Phenobarbitone* - **Phenobarbitone** is an older antiepileptic drug that enhances **GABAergic neurotransmission**, but it is generally not a first-line agent for partial seizures due to its sedative properties, cognitive side effects, and potential for drug interactions. - Its use has largely been replaced by newer, better-tolerated drugs as a primary treatment. *Na+ valproate* - **Sodium valproate** is a broad-spectrum antiepileptic drug effective for both partial and generalized seizures, but it is typically not the first-line drug of choice specifically for partial seizures in female patients of childbearing age due to concerns about **teratogenicity and PCOS risk**. - Its mechanism involves multiple actions, including enhancing GABA activity, blocking sodium channels, and blocking T-type calcium channels.

Question 719: The mechanism of action of botulinum toxin A is best described by:

A. Slowing of myelinated nerve fiber transmission
B. Postsynaptic receptor blockade
C. Acetylcholinesterase inhibition
D. Presynaptic blockade of acetylcholine release (Correct Answer)

Explanation: ***Presynaptic blockade of acetylcholine release*** - **Botulinum toxin A** acts by cleaving specific proteins (**SNARE proteins** like SNAP-25, synaptobrevin, and syntaxin) essential for the fusion of **acetylcholine-containing vesicles** with the presynaptic membrane. - This prevents the release of acetylcholine into the **neuromuscular junction**, leading to muscle paralysis. *Slowing of myelinated nerve fiber transmission* - This describes the action of agents that affect **myelin sheaths** (e.g., demyelinating diseases) or ion channels involved in action potential propagation, not the mechanism of botulinum toxin. - Botulinum toxin specifically targets the **synaptic transmission**, not the speed of nerve conduction itself. *Postsynaptic receptor blockade* - This mechanism is seen with drugs like **curare** or **neuromuscular blockers** (e.g., rocuronium, vecuronium), which compete with acetylcholine for binding to **nicotinic acetylcholine receptors** on the muscle endplate. - Botulinum toxin does not affect the postsynaptic receptors directly; its action is entirely presynaptic. *Acetylcholinesterase inhibition* - **Acetylcholinesterase inhibitors** (e.g., neostigmine, pyridostigmine) prevent the breakdown of acetylcholine in the synaptic cleft, increasing its concentration and prolonging its action. - This mechanism would enhance, rather than block, muscle contraction, which is opposite to the effect of botulinum toxin.

Question 720: Most common drug used in Spasticity in patients with spinal cord injury is:

A. Salicylates
B. Tizanidine
C. Baclofen (Correct Answer)
D. Diazepam

Explanation: ***Baclofen*** - **Baclofen** is the most commonly prescribed muscle relaxant for spasticity, especially in cases related to **spinal cord injury** and multiple sclerosis. - It acts as a **GABA-B receptor agonist**, reducing excitatory neurotransmitter release and thus decreasing muscle tone. *Salicylates* - **Salicylates** (e.g., aspirin) primarily act as **analgesics** and **anti-inflammatory** agents. - They are not used for treating spasticity. *Tizanidine* - **Tizanidine** is an **alpha-2 adrenergic agonist** used for spasticity, but it is generally considered a second-line agent compared to baclofen. - It works by reducing the release of excitatory amino acids, thereby enhancing presynaptic inhibition. *Diazepam* - **Diazepam** is a **benzodiazepine** that acts as a **GABA-A receptor agonist**, enhancing inhibitory neurotransmission. - While it can reduce spasticity, its sedative effects and potential for dependence make it less preferred than baclofen for chronic management in spinal cord injury.

Practice by Chapter

General Anesthetics

Practice Questions

Local Anesthetics

Practice Questions

Sedative-Hypnotics

Practice Questions

Antiepileptic Drugs

Practice Questions

Antiparkinsonian Drugs

Practice Questions

Opioid Analgesics

Practice Questions

Drugs of Abuse and Addiction

Practice Questions

Psychostimulants

Practice Questions

Hallucinogens

Practice Questions

CNS Stimulants and Cognitive Enhancers

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free