A farmer presents with trismus, opisthotonus, and violent generalized muscle spasms triggered by minor stimuli, following a contaminated puncture wound. The toxin producing these spasms acts by:

• A Causing massive acetylcholine release at the neuromuscular junction
• B Directly depolarizing alpha motor neurons via glutamate receptor activation
• C Blocking glycine and GABA release from inhibitory interneurons in the spinal cord and brainstem ✓
• D Blocking calcium channels at the presynaptic motor nerve terminal

Explanation

Tetanospasmin undergoes retrograde axonal transport to the spinal cord and brainstem, where it cleaves synaptobrevin in inhibitory interneurons (Renshaw cells and glycinergic/GABAergic cells). Loss of recurrent and reciprocal inhibition leaves alpha motor neurons unrestrained, so opposing muscles co-contract and stimuli trigger spasms. Option A resembles the effect of black widow spider venom, which causes flaccid then cramping phases, not fixed rigid spasms.

Reference: Ganong's Review of Medical Physiology, 26th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.