Pharmacology Shanbhag-4e: Centrally Acting Muscle Relaxants

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Questions and Answers

What is the reason behind muscle pain after administration?

Hyperkalaemia

Initial fasciculations (correct)

Increased IOP

Sinus bradycardia

Why might aspiration of gastric contents occur after administration?

Hyperkalaemia

Increased IOP

Sinus bradycardia

Fasciculations releasing K+ into the blood (correct)

What can cause prolonged apnoea after administration?

Contraction of external ocular muscles

Initial fasciculations (correct)

Vagal stimulation

Malignant hyperthermia

How is sinus bradycardia explained following the procedure?

Vagal stimulation Signup and view all the answers

What may lead to malignant hyperthermia when using halothane in certain individuals?

Intravenous dantrolene Signup and view all the answers

What is the main reason for succinylcholine (SCh) having a very short duration of action?

Rapid hydrolysis by pseudocholinesterase Signup and view all the answers

Which drug leads to transient apnoea at the peak of its action?

Succinylcholine Signup and view all the answers

What is the main side effect associated with diazepam and other benzodiazepines?

Sedation Signup and view all the answers

Which drug acts on GABAB receptors as its mechanism of action?

Baclofen Signup and view all the answers

In individuals with liver disease or atypical pseudocholinesterase, what complication may arise from succinylcholine administration?

'Prolonged succinylcholine apnoea' Signup and view all the answers

Which drug is primarily used for acute muscle spasm due to trauma and causes drowsiness as a side effect?

Chlorzoxazone Signup and view all the answers

How do centrally acting skeletal muscle relaxants primarily act?

By inhibiting polysynaptic pathways in spinal and supra-spinal sites Signup and view all the answers

What is the main difference between centrally acting skeletal muscle relaxants and neuromuscular blockers?

Effect on neuromuscular transmission Signup and view all the answers

Which type of neuromuscular blocker is Succinylcholine (Suxamethonium)?

Depolarizing blocker Signup and view all the answers

What is the mechanism of action of Succinylcholine at the neuromuscular receptors?

Causes initial fasciculations then flaccid paralysis Signup and view all the answers

What condition can lead to phase II block when exposed to Succinylcholine?

Atypical pseudocholinesterase Signup and view all the answers

Which of the following is NOT a typical use of centrally acting skeletal muscle relaxants?

Post-operative sedation Signup and view all the answers

Study Notes

Centrally Acting Skeletal Muscle Relaxants

Most centrally acting skeletal muscle relaxants are available in combination with nonsteroidal anti-inflammatory drugs (NSAIDs).
They cause certain degree of sedation.
They act by depressing polysynaptic pathways in spinal and supra-spinal sites.
They are used to reduce spasm associated with cerebral palsy, trauma, sprain, tetanus, multiple sclerosis, etc.

Characteristics of Centrally Acting Skeletal Muscle Relaxants

Baclofen: GABAB agonist, used in spinal cord lesions, multiple sclerosis, and amyotrophic lateral sclerosis.
Diazepam and other benzodiazepines: GABAA agonists, used in multiple sclerosis, spinal cord injury or disease.
Tizanidine: Central a2-agonist, used in multiple sclerosis, spinal cord injury or disease.
Chlorzoxazone and methocarbamol: Act on spinal interneurons, used in acute muscle spasm due to trauma.
Riluzole: Inhibits glutamate release, used in amyotrophic lateral sclerosis.
Carisoprodol: Mechanism of action not clearly known, used in muscle sprain.
Thiocolchicoside: Block release of excitatory transmitter in the spinal cord, used in sprain, muscle spasm due to trauma.

Neuromuscular Blockers

They interfere with neuromuscular transmission, do not affect CNS and are administered intravenously.
Include nondepolarizing (competitive) and depolarizing blockers.

Depolarizing Blockers: Succinylcholine (Suxamethonium)

A quaternary ammonium compound, structure resembles two molecules of ACh linked together.
Acts as a partial agonist at NM receptors, causing initial fasciculations and later flaccid paralysis due to prolonged depolarization (phase I block).
With continued exposure, the membrane becomes desensitized, leading to phase II block, which resembles the nondepolarizing block and is partially reversed by anti-cholinesterases.
Adverse effects:
- Muscle pain due to initial fasciculations.
- Increased IOP due to contraction of external ocular muscles.
- Aspiration of gastric contents may occur due to increased intragastric pressure.
- Hyperkalaemia due to fasciculations releasing K+ into the blood.
- Sinus bradycardia due to vagal stimulation.
- SCh apnoea (prolonged apnoea).
- Malignant hyperthermia, especially when used with halothane in genetically susceptible individuals.
Rapidly hydrolysed by pseudocholinesterase, hence has a very short duration of action (3-8 minutes).
Transient apnoea is usually seen at the peak of its action.
In people with liver disease or atypical pseudocholinesterase, the metabolism of SCh becomes slow, leading to severe neuromuscular blockade and respiratory paralysis with prolonged apnoea.

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Description

Learn about centrally acting skeletal muscle relaxants commonly used in combination with NSAIDs. Understand their mechanism of action in depressing polysynaptic pathways and reducing spasm associated with various conditions like trauma and multiple sclerosis.