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Regulation of Tone and Posture

MBBS 1st Year Physiology - Exam Notes

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1. MUSCLE TONE - Definition & Basics

• High γ-motor discharge → Hypertonia
• Low γ-motor discharge → Hypotonia

Exam tip: Gamma motor neurons innervate intrafusal (spindle) fibers; alpha motor neurons innervate extrafusal (working) fibers.

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2. MUSCLE SPINDLE & STRETCH REFLEX (Basis of Tone)

Muscle Spindle Structure

• Intrafusal fibers - innervated by γ-motor neurons
• Nuclear bag fibers - detect rate of change (dynamic)
• Nuclear chain fibers - detect static stretch
• Ia afferents - primary endings (both bag + chain) → monosynaptic reflex
• II afferents - secondary endings (mainly chain) → polysynaptic reflex

Stretch Reflex Arc (Monosynaptic)

Muscle stretched → Spindle Ia afferent activated → Enters dorsal horn
→ Directly synapses on α-motor neuron (ventral horn)
→ Same muscle contracts (homonymous)
→ Reciprocal inhibition of antagonist (via Ia inhibitory interneuron)

• γ-motor neuron fires → contracts intrafusal fiber → sensitizes spindle → increases Ia firing → increases α-motor neuron discharge → muscle tone rises

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3. INVERSE STRETCH REFLEX (Golgi Tendon Organ Reflex)

• Receptor: Golgi tendon organ (GTO) - in series with muscle fibers (at musculotendinous junction)
• Afferent: Ib afferent fibers
• Effect: When tension is HIGH → GTO fires → inhibits α-motor neurons of same muscle + excites antagonist

Clasp-Knife Effect (clinically important!)

1. Moderate passive stretch → muscle contracts (stretch reflex)
2. Further stretch → GTO fires → muscle suddenly relaxes
3. Resistance followed by sudden give = Clasp-knife effect

Resembles closing a pocket knife - seen in upper motor neuron lesions

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4. ROLE OF SUPRASPINAL CENTERS IN TONE & POSTURE

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5. DECEREBRATE vs. DECORTICATE RIGIDITY

Decerebrate Rigidity (Lower midbrain/Upper pons transection)

• Level of lesion: Between red nucleus and vestibular nucleus (lower midbrain/upper pons)
• Mechanism: Red nucleus (rubrospinal - flexor facilitating) is disconnected; Vestibulospinal (extensor facilitating) is intact → unopposed extensor facilitation
• Posture:
  • All 4 limbs → extended (opisthotonos)
  • Neck and back → arched backward
  • Upper limbs: extended + pronated + fingers flexed
  • Lower limbs: extended + plantar flexed + toes inward
• Abolished by: Cutting dorsal roots (γ-loop dependent)

Decorticate Rigidity (Upper midbrain lesion / Cortical lesion)

• Level of lesion: Above the red nucleus (rostral to superior colliculus)
• Mechanism: Corticospinal inhibition lost; red nucleus and rubrospinal intact → flexor drive to arms preserved; vestibulospinal still facilitates leg extensors
• Posture:
  • Upper limbs: flexed (elbows, wrists)
  • Lower limbs: extended
  • Head: extended

Memory Trick

"De-CER-ebrate = all Extended" (CER sounds like "stiff") "De-COR-ticate = arms CORE/Curled in" (arms flex inward)

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6. SPINAL SHOCK

• Complete flaccid paralysis below the lesion
• Loss of ALL reflexes (areflexia) - even stretch reflexes disappear
• Loss of sensation
• Loss of bladder/bowel control
• Hypotension

• Reflexes return - first flexor reflexes then extensor
• Hyperreflexia and spasticity eventually develop
• Babinski sign positive
• Mass reflex may develop

Why does spinal shock occur? Sudden removal of tonic facilitatory impulses (especially from vestibulospinal and reticulospinal tracts) → temporary inexcitability of spinal neurons.

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7. POSTURAL REFLEXES

A. Static Reflexes (Tonic Reflexes)

B. Statokinetic Reflexes (Righting Reflexes)

Integration centers for righting reflexes: Midbrain (and higher centers). In decerebrate animals, righting reflexes are lost.

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8. VESTIBULAR CONTRIBUTION TO POSTURE

• Lateral vestibular nucleus (Deiters' nucleus) → Vestibulospinal tract → ipsilateral extensor facilitation (anti-gravity muscles)
• Medial vestibular nucleus → Medial vestibulospinal tract → Cervical motor neurons (head/neck posture)
• Input from: Otolith organs (linear acceleration, gravity) + Semicircular canals (angular acceleration)

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9. CEREBELLUM & POSTURE

• Anterior lobe (spinocerebellum/paleocerebellum): Receives proprioceptive input; regulates muscle tone - lesion causes hypotonia
• Flocculonodular lobe (vestibulocerebellum/archicerebellum): Equilibrium and vestibular responses - lesion causes truncal ataxia
• Cerebellar lesions cause ipsilateral deficits

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10. BASAL GANGLIA & POSTURE

• Regulate background tone for voluntary movements
• Substantia nigra (dopamine) → striatum
• Lesions: Parkinson's disease - cogwheel/lead-pipe rigidity + akinesia
• Huntington's disease - hypotonia + chorea

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QUICK REVISION SUMMARY TABLE

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HIGH-YIELD EXAM POINTS

1. Clasp-knife = GTO (Ib afferents) = upper motor neuron lesion (vs. cogwheel = basal ganglia = Parkinson's)
2. Decerebrate = all extended; Decorticate = arms flexed, legs extended
3. Decerebrate rigidity is abolished by cutting dorsal roots - proves it depends on the γ-loop/muscle spindle
4. Gamma motor neurons set spindle sensitivity → regulates tone
5. Vestibulospinal = major extensor facilitator (anti-gravity)
6. Medullary reticulospinal = inhibitory; Pontine reticulospinal = facilitatory
7. Spinal shock: Flaccid first, then spastic - due to loss of supraspinal facilitation
8. Righting reflexes are integrated at the midbrain level
9. Anterior lobe of cerebellum damage → hypotonia (not ataxia)
10. Positive supporting reaction = limb becomes weight-bearing pillar on foot contact

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