Spinal reflexes
Spinal reflexes, muscle spindle, Golgi tendon organ, spinal shock, clonus and posture
The muscle spindle senses length and drives the monosynaptic stretch reflex; the Golgi tendon organ senses tension and relaxes the muscle. Covers gamma motor neurones, reciprocal inhibition, glycine, clonus, spinal shock, reflex roots, primitive reflexes and areflexia.
The muscle spindle
- Lies in parallel with the main (extrafusal) fibres, inside a capsule.
- Intrafusal fibres: nuclear bag fibres (dynamic and static) and nuclear chain fibres (static).
- Sensory endings: group Ia (primary, annulospiral) respond to the rate and amount of stretch; group II (secondary, flower-spray) signal sustained length.
- Motor supply: gamma motor neurones contract the polar ends of intrafusal fibres, keeping the central sensory region taut. During voluntary contraction gamma neurones fire with alpha neurones (alpha–gamma coactivation), so the spindle stays sensitive while the muscle shortens. Gamma neurones produce no useful force; they set sensitivity.
- Spindles are densest in muscles needing fine control (hand, extraocular, neck).
The stretch (myotatic) reflex
Tapping a tendon stretches the muscle; spindle Ia afferents fire; they make monosynaptic excitatory synapses on alpha motor neurones of the same muscle, which contracts. At the same time Ia afferents excite Ia inhibitory interneurones that release glycine onto motor neurones of the antagonist, which relaxes: reciprocal inhibition (quadriceps contracts while hamstrings relax).
- The stretch reflex is the only monosynaptic reflex; it tests a specific segment.
- Strychnine (from kuchla, nux vomica seeds) blocks glycine receptors on motor neurones; tetanus toxin blocks glycine (and GABA) release from inhibitory interneurones. Both remove inhibition, so agonists and antagonists contract together: violent spasms triggered by noise or touch, opisthotonus and trismus, with full consciousness. Treatment is benzodiazepines, a quiet room and support.
| Reflex | Root |
|---|---|
| Ankle jerk | S1 (S1–S2) |
| Knee jerk | L3–L4 |
| Biceps | C5–C6 |
| Brachioradialis (supinator) | C5–C6 |
| Triceps (radial nerve) | C7 (C6–C7) |
| Finger flexion | C8 |
Loss of lateral arm sensation, triceps weakness and an absent triceps jerk point to a C7 root (or radial nerve) lesion.
The Golgi tendon organ
- Lies in series at the musculotendinous junction and senses tension, mainly from active contraction.
- Group Ib afferents excite inhibitory interneurones that relax the same muscle (autogenic or inverse stretch reflex), limiting force. This is a disynaptic reflex.
- It contributes to the clasp-knife response in spasticity: resistance to passive stretch suddenly gives way.
Spindle and tendon organ compared
| Feature | Muscle spindle | Golgi tendon organ |
|---|---|---|
| Arrangement | Parallel to muscle fibres | In series (tendon) |
| Senses | Length and rate of change | Tension |
| Afferent | Ia and II | Ib |
| Effect on same muscle | Contraction | Relaxation |
| Synapses | Monosynaptic | Disynaptic |
| Efferent control | Gamma motor neurones | None |
Other spinal reflexes
- Withdrawal (flexor) reflex: polysynaptic flexion away from a painful stimulus.
- Crossed extensor reflex: the opposite limb extends to bear weight.
- Superficial reflexes: abdominal (T8–T12), cremasteric (L1–L2), anal wink (S2–S4); lost in UMN lesions.
- Bulbocavernosus reflex (S2–S4): squeezing the glans or tugging a catheter contracts the anal sphincter. It is a sacral cord reflex and is the first to return, marking the end of spinal shock.
Reinforcement and reflex timing
- Jendrassik manoeuvre (pulling hooked fingers apart, clenching teeth) raises excitability of the reflex arc, partly through gamma drive and reduced presynaptic inhibition, bringing out a reflex that seemed absent. Healthy elderly people may have reduced ankle jerks, so reinforce first.
- Slow-relaxing reflexes in hypothyroidism: the contraction is normal but relaxation is slow because calcium reuptake into the sarcoplasmic reticulum (and myosin ATPase activity) is slowed. Hypothermia does the same.
Hyperreflexia and clonus after UMN lesions
- Descending pathways, especially reticulospinal, normally restrain gamma motor neurones and spinal interneurones. When they are lost, spindles become hypersensitive and inhibitory circuits weaken: tone and reflexes rise and the plantar becomes extensor.
- Clonus: a brisk dorsiflexion stretches the calf, the hyperactive stretch reflex contracts it, relaxation stretches it again, and the stretch reflex repeats itself rhythmically. Sustained clonus (for example with thoracic cord compression) is pathological; a few unsustained beats can be normal.
- Baclofen is a GABA-B agonist in the spinal cord that reduces excitatory transmitter release onto motor neurones, relieving spasticity (MS). Abrupt withdrawal, especially intrathecal, causes seizures, hallucinations and hyperthermia.
Spinal shock
Immediately after cord transection, everything below the lesion is flaccid and areflexic, because spinal neurones suddenly lose their tonic descending facilitation. Over days to weeks they become hyperexcitable: spasticity, hyperreflexia, extensor plantars and a small spastic reflex bladder appear. Return of the bulbocavernosus reflex marks the end of shock; do not call an injury complete before then.
Lost reflexes
- LMN or afferent lesions break the arc: peripheral neuropathy, tabes dorsalis, root lesions.
- Diabetic polyneuropathy is length-dependent: the longest axons degenerate first, so ankle jerks go before knee jerks and sensory loss starts in the feet.
- Guillain–Barré syndrome: early demyelination desynchronises and blocks the reflex volley, so reflexes are lost even while power is fair. Brisk reflexes in suspected GBS should prompt imaging for cord compression.
Primitive reflexes
Newborn reflexes (Moro, asymmetric tonic neck, grasp, rooting) are brainstem and spinal patterns that disappear by about 4–6 months as cortical inhibition matures. Their persistence at 10 months with stiff, scissoring legs after birth asphyxia indicates cerebral palsy. An asymmetric Moro in a newborn suggests brachial plexus injury or fractured clavicle.
Posture
Posture relies on stretch reflexes in antigravity muscles, with vestibular, visual and neck inputs integrated in the brainstem and cerebellum. The lateral vestibular (Deiters) nucleus, through the lateral vestibulospinal tract, and the pontine reticulospinal tract excite antigravity extensors; lesions above the vestibular nuclei release this drive (decerebrate rigidity).
Remember Spindle: parallel, length, Ia, contract. Tendon organ: series, tension, Ib, relax. Gamma sets the gain.
Exam trap The stretch reflex is monosynaptic; reciprocal inhibition of the antagonist uses a glycinergic Ia interneurone.
Exam trap Immediately after cord injury reflexes are absent (spinal shock), not brisk.
How FCPS asks about this
- Alpha–gamma coactivation: keeps spindles sensitive during shortening; gamma neurones make no useful force.
- Hamstrings relax during the knee jerk: Ia inhibitory interneurone (glycine); strychnine blocks glycine receptors.
- Golgi tendon organ: in series, senses tension, Ib afferents relax the same muscle.
- End of spinal shock: return of the bulbocavernosus reflex.
- Clonus: a self-repeating stretch reflex in UMN lesions.
- Ankle jerks lost before knee jerks in diabetes: longest axons degenerate first.
- Main nucleus for antigravity posture: lateral vestibular nucleus.
Test yourself on this topic
5 of the 90 questions in our bank on this topic. Choose an answer to see why every option is right or wrong.
A tendon jerk is obtained with a brisk tap but not with slow pressure on the tendon. Which of the following receptor properties explains this?
Answer: Ia endings respond to rate of stretch
Muscle spindle primary (group Ia) endings, wrapped around the intrafusal fibres, have a strong dynamic response: they fire intensely while muscle length is changing, in proportion to the rate of stretch. A brisk tendon tap gives a sudden, tiny stretch that produces a synchronous burst of Ia impulses and a monosynaptic contraction. A slow stretch of the same size produces only a small static response, which is not enough. Secondary (group II) endings signal mainly static length.
Dynamic spindle response
- Ia endings: rate of stretch
- Brisk tap: synchronous Ia burst
- Group II: static length
- Tendon organs: tension
Remember The tap must be quick because spindles sense speed.
Exam trap Poor tapping technique is a common cause of apparently absent reflexes.
Why the other options are wrong
- Golgi tendon organs need fast stretch Tendon organs signal tension and inhibit the muscle.
- Pacinian corpuscles in tendon fire Pacinian corpuscles do not drive the stretch reflex.
- Slow stretch activates Renshaw cells Renshaw cells give recurrent inhibition, not this effect.
- Ia endings respond only to tension Golgi tendon organs, not Ia endings, signal tension.
A man in a coma after a midbrain haemorrhage holds all four limbs rigidly extended. Which of the following pathways, now released from higher control, mainly drives this extensor tone?
Answer: Lateral vestibulospinal tract
A lesion between the red nucleus and the vestibular nuclei removes cortical and rubrospinal input, which favour flexion, and releases the vestibular and pontine reticular nuclei from inhibition. The lateral vestibulospinal tract, from the lateral (Deiters) vestibular nucleus, powerfully excites extensor (antigravity) motor neurones, together with the pontine reticulospinal tract. The result is decerebrate posturing with extended arms and legs. In normal life the same pathway keeps the body upright against gravity.
Extensor tone
- Lateral vestibular (Deiters) nucleus
- Excites antigravity extensors
- Released in decerebrate lesions
- Rubrospinal input favours flexion
Remember The vestibulospinal tract keeps you upright against gravity.
Exam trap Decerebrate posturing after head injury carries a worse outlook than decorticate posturing.
Why the other options are wrong
- Lateral corticospinal tract The corticospinal input is cut off by this lesion.
- Rubrospinal tract The rubrospinal tract favours flexion and is lost here.
- Tectospinal tract The tectospinal tract turns the head towards visual stimuli.
- Medial longitudinal fasciculus The MLF links the eye movement nuclei.
When a man steps on a nail, his injured leg flexes and his other leg straightens to bear his weight. What causes the second response?
Answer: Crossed extensor reflex
Painful input from the foot triggers a polysynaptic flexor withdrawal reflex in the same limb. Collaterals of the same afferent volley cross the cord through commissural interneurones to excite extensor motor neurones and inhibit flexors of the opposite limb, the crossed extensor reflex, so the other leg can take the extra weight. Both responses are organised in the spinal cord and do not need the brain. Reverberating interneurone circuits give them a long after-discharge.
Crossed extensor reflex
- Pain: flexor withdrawal on the same side
- Opposite limb: extensors excited
- Polysynaptic, via commissural interneurones
- Keeps balance during withdrawal
Remember One leg pulls away; the other holds you up.
Exam trap Crossed extensor responses persist after complete spinal cord transection, showing the circuit is spinal.
Why the other options are wrong
- Stretch reflex The stretch reflex is monosynaptic and acts on the stretched muscle only.
- Inverse stretch reflex The inverse stretch reflex relaxes a muscle under high tension.
- Positive supporting reaction This extends a limb when its own sole is pressed, not in response to pain on the other side.
- Righting reflex Righting reflexes restore head and body position.
A 6-year-old with spastic diplegic cerebral palsy has selective dorsal rhizotomy, in which some lumbosacral dorsal rootlets are cut. His leg tone falls markedly, though his brain lesion is unchanged. What does this show about his spasticity?
Answer: It depends on stretch-reflex afferent input
Spasticity is an exaggerated stretch reflex: muscle spindle Ia afferents entering through the dorsal roots excite motor neurones that have lost normal descending inhibition. Cutting part of the dorsal rootlets reduces this afferent drive, so tone falls even though the brain lesion is unchanged. The same principle was shown in decerebrate animals, whose extensor rigidity disappears after dorsal root section because it depends on overactive γ motor neurones driving the spindles. Fixed contractures do not improve with rhizotomy.
Spasticity and the reflex arc
- Spasticity is an exaggerated stretch reflex
- Needs Ia afferent input
- Cutting dorsal rootlets lowers tone
- Decerebrate rigidity is γ-driven
Remember No sensory input, no spasticity.
Exam trap Rhizotomy reduces spasticity but cannot restore lost strength or selective motor control.
Why the other options are wrong
- It arises from damaged muscle fibres The muscle fibres are normal in spasticity.
- It is generated directly by the cortex The cortex is damaged, not generating the tone.
- It is caused by fixed joint contractures Contractures would persist after rhizotomy.
- It is driven by efferent γ fibres alone γ fibres work through spindle afferents, which were cut.
After a spinal cord injury, the patient is in spinal shock with flaccid paralysis and absent reflexes. Return of which reflex usually marks the end of spinal shock?
Answer: Bulbocavernosus reflex
Spinal shock is a temporary loss of all reflex activity below an acute cord injury, lasting hours to weeks. The bulbocavernosus reflex (anal sphincter contraction on squeezing the glans or tugging a catheter, S2–S4) is usually the first to return, marking its end. Only then can the injury be judged complete or incomplete. Spinal shock differs from neurogenic shock, which is haemodynamic (hypotension with bradycardia).
Spinal shock
- Loss of all reflexes below injury
- Ends: bulbocavernosus reflex returns
- Then judge complete vs incomplete
- Not the same as neurogenic shock
Remember Bulbocavernosus back, spinal shock over.
Exam trap Do not call an injury complete until spinal shock has ended.
Why the other options are wrong
- Knee (patellar) jerk Returns later.
- Ankle (Achilles) jerk Returns later.
- Biceps jerk Upper limb; not the marker.
- Corneal reflex Brainstem reflex.
Where this sits in the CPSP syllabus
- Paper 1: Nervous system, Spinal reflexes, muscle spindle, Golgi tendon organ, posture
- Surgery & Allied, Paper 2: Nervous system, Spinal reflexes, muscle spindle, Golgi tendon organ, posture
- Medicine & Allied, Paper 2: Nervous system, Spinal reflexes, muscle spindle, Golgi tendon organ, posture