Spinal reflexes: tetanus: practice question

A Physiology question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Physiology · Spinal reflexes: tetanus

Sample item

A farmer with a puncture wound of the foot develops trismus, risus sardonicus and painful generalised spasms triggered by noise. Which neural mechanism accounts for the spasms?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

D. Blockade of glycine and GABA release from spinal inhibitory interneurons, with disinhibition of motor neurons

Tetanospasmin is carried by retrograde axonal transport to the spinal cord and brainstem, where it cleaves synaptobrevin in inhibitory interneurons. Release of glycine and GABA is blocked, so motor neurons fire unchecked and produce tonic spasm and exaggerated reflexes. Treatment includes human tetanus immunoglobulin, wound care, muscle relaxants and ventilatory support.

Option by option

  • A. Blockade of acetylcholine release at the neuromuscular junction

    Blockade of acetylcholine release is the action of botulinum toxin and produces flaccid paralysis.

  • B. Destruction of anterior horn cells by viral infection

    Anterior horn cell destruction by poliovirus causes flaccid paralysis without spasms.

  • C. Irreversible inactivation of acetylcholinesterase at the end plate

    Cholinesterase inhibition by organophosphates causes fasciculations and cholinergic features, not trismus.

  • D. Blockade of glycine and GABA release from spinal inhibitory interneurons, with disinhibition of motor neurons (correct)

    Loss of inhibitory transmitter release leaves motor neurons unrestrained, giving spasm.

Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.

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Questions about this Physiology question

What is the answer to this Physiology question?

The best answer is D, Blockade of glycine and GABA release from spinal inhibitory interneurons, with disinhibition of motor neurons. Tetanospasmin is carried by retrograde axonal transport to the spinal cord and brainstem, where it cleaves synaptobrevin in inhibitory interneurons.

Why is "Blockade of acetylcholine release at the neuromuscular junction" not the answer?

Blockade of acetylcholine release is the action of botulinum toxin and produces flaccid paralysis.

Why is "Destruction of anterior horn cells by viral infection" not the answer?

Anterior horn cell destruction by poliovirus causes flaccid paralysis without spasms.

Why is "Irreversible inactivation of acetylcholinesterase at the end plate" not the answer?

Cholinesterase inhibition by organophosphates causes fasciculations and cholinergic features, not trismus.

What concept does this question test?

It tests Spinal reflexes: tetanus in Physiology. Release of glycine and GABA is blocked, so motor neurons fire unchecked and produce tonic spasm and exaggerated reflexes. Treatment includes human tetanus immunoglobulin, wound care, muscle relaxants and ventilatory support.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Spinal reflexes: tetanus?

For each system, sketch the key graph (pressure–volume loop, oxygen dissociation curve, nephron handling) and explain it aloud. Then use the flashcards and the other Physiology questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.