Reflex Integration and Posture
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Direct answer
Tap the patellar tendon and the leg extends within roughly 20-25 milliseconds: spindle Ia afferents enter the dorsal root, synapse monosynaptically on the quadriceps alpha motor neuron, and collaterals excite inhibitory interneurons for the antagonistic hamstrings — reciprocal inhibition. This is the body's only monosynaptic arc and the building block of posture, since standing is a continuous conversation between gravity and stretch reflexes whose gain is set from above. The gamma efferent system adjusts spindle sensitivity, and alpha-gamma coactivation keeps spindles loaded as muscles shorten. Above the cord, posture is built in tiers: tonic neck and vestibulospinal reflexes in the medulla, righting reflexes in the midbrain, and corticobulbar control above that. Section the brainstem between the colliculi and all four limbs extend — decerebrate rigidity from released gamma drive; section above the red nucleus and the arms flex while the legs extend — the decorticate pattern.
What you must remember
- Arc anatomy: receptor, afferent, centre, efferent, effector; the stretch reflex is the sole monosynaptic arc, with a latency near 20-25 ms at the knee.
- Segmental roots: biceps C5-6, triceps C7-8, knee L3-4, ankle S1-2; abdominals T8-T12, cremasteric L1-2, plantar S1-2 — the levels examiners expect without pause.
- Gamma loop: static and dynamic gamma motor neurons set spindle gain; the Jendrassik manoeuvre reinforces absent jerks by raising gamma drive; alpha-gamma coactivation prevents off-loading during shortening.
- Inverse stretch reflex: Golgi tendon organ Ib afferents inhibit the agonist motor neuron through an interneuron — autogenic inhibition, felt as the clasp-knife release of spasticity.
- Protective arcs: the flexor withdrawal reflex is polysynaptic and crosses segments; the crossed extensor reflex supports the body while the hurt limb flexes.
- Righting hierarchy: labyrinthine, neck and body righting reflexes integrate at midbrain level; visual righting needs the cortex — a midbrain animal can stand, a decorticate one can walk, a spinal one cannot.
- Spinal shock: transection silences reflexes below the lesion for minutes in frogs, days in dogs, one to six weeks in humans, after which reflexes return exaggerated — the species gradient is a viva one-liner worth money.
A levels-of-lesion walk
Work upward from the cord. A complete transection at T10 first produces spinal shock: flaccid paralysis, areflexia, autonomic disturbance; in humans this lasts days to weeks. Reflexes then reappear, flexor responses first, then extensor tone climbs into the mass reflex state — a bladder stimulus can trigger flexion and sweating below the lesion because every arc now fires without descending control. Move up to an intercollicular brainstem section and the picture is decerebrate rigidity: opisthotonus, all four limbs extended, gamma drive maximal, classically seen clinically in pontine compression. Section higher, above the red nucleus, and the rubrospinal tract survives to flex the upper limbs — decorticate posture with arms flexed, legs extended, the familiar picture of a diffuse cortical injury. Each level adds a surviving pathway, and each posture names the last surviving descending influence — which is why the pattern itself is the localisation.
Where students slip
Jendrassik is described as "distracting the patient"; the real answer is gamma bias — increased fusimotor drive pre-contracts intrafusal fibres so the same tap yields a bigger Ia volley. The clasp-knife phenomenon is credited to "spasticity giving way" rather than to the Golgi tendon organ's inverse myotatic reflex firing at high tension — naming Ib inhibition is what scores. The UMN-LMN boundary confuses reflex and tone direction: below a cord lesion reflexes are initially absent (shock) then exaggerated (release), and only the LMN level itself keeps areflexia permanently — a temporal distinction candidates forget. Finally, plantar response latencies: the flexor plantar is a polysynaptic withdrawal; the extensor (Babinski) is the released flexor-withdrawal pattern of infancy, re-emerging when the pyramidal tract is damaged — framing it as a primitive reflex return is the answer examiners wait to hear.
Frequently asked questions
Why is the stretch reflex called monosynaptic?
The Ia afferent synapses directly on the alpha motor neuron without an interneuron, making it the only monosynaptic reflex in the body, with reciprocal inhibition running through separate interneurons.
What does the Jendrassik manoeuvre actually do?
It increases gamma motor neuron discharge, pre-loading muscle spindles so a standard tendon tap produces a larger afferent volley and a visible reflex.
What is the inverse stretch reflex?
Golgi tendon organ Ib afferents, activated by rising tension, inhibit the homonymous alpha motor neuron through an interneuron — autogenic inhibition that protects muscle and produces clasp-knife phenomenon.
How do decerebrate and decorticate rigidity differ?
Decerebrate (intercollicular section) shows extension of all four limbs from unopposed gamma drive; decorticate (section above red nucleus) shows flexed upper limbs with extended lower limbs as rubrospinal flexor influence survives.
How long does spinal shock last across species?
Minutes in frogs, days in dogs, and one to six weeks in humans — reflexes return below the lesion, eventually exaggerated as descending inhibition stays lost.