## Distinguishing Feature: Fasciculations **Key Point:** Depolarising muscle relaxants (succinylcholine) produce characteristic visible fasciculations — brief, uncoordinated muscle contractions visible on the skin surface — before onset of paralysis. Non-depolarising agents cause no fasciculations. ## Mechanism Behind Fasciculations Depolarising agents work by: 1. Binding to nicotinic acetylcholine receptors as agonists 2. Causing sustained depolarisation of the muscle membrane 3. Generating uncontrolled action potentials → fasciculations 4. Followed by desensitisation and flaccid paralysis Non-depolarising agents competitively block the receptor without depolarisation, so no fasciculations occur. ## Clinical Significance of Fasciculations | Feature | Depolarising | Non-depolarising | | --- | --- | --- | | Fasciculations | Present (visible) | Absent | | Onset | 30–60 sec | 60–120 sec | | Mechanism | Agonist depolarisation | Competitive antagonism | | Reversibility | Pseudocholinesterase metabolism | Anticholinesterase reversal | | Hyperkalaemia risk | Yes (from fasciculation-induced K⁺ release) | No | **Clinical Pearl:** Fasciculations can cause postoperative myalgia (muscle pain) and dangerous hyperkalaemia in susceptible patients (burns, crush injury, denervation, malignancy). Pre-treatment with a small dose of non-depolarising agent (defasciculation) prevents visible fasciculations. **High-Yield:** Fasciculations are the **hallmark discriminator** between the two classes — no other single feature is as specific and clinically observable.
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