Stretch Reflex: Regulation and Applied Aspects

1. Definition and Basic Circuit

1. Muscle stretch → activates muscle spindle (Ia afferents)
2. Ia afferent enters dorsal root → synapses directly on alpha (α) motor neurons in anterior horn
3. α motor neuron fires → contracts the same (homonymous) muscle
4. Muscle shortens → spindle unloads → Ia firing returns to baseline

• Contraction of synergistic muscles
• Relaxation of antagonistic muscles (reciprocal inhibition via inhibitory interneurons)

2. Structure of the Muscle Spindle

• Nuclear bag fibers (dynamic and static subtypes) - contain many nuclei in a dilated central area
• Nuclear chain fibers - thinner, shorter, no bag

3. Dynamic vs. Static Stretch Reflex

4. Regulation: The Gamma Motor (Fusimotor) System

Two types of gamma motor neurons:

• Supply dynamic nuclear bag fibers
• Increase the phasic/dynamic sensitivity of Ia endings
• Enhance the response to rate of stretch (velocity)

• Supply static nuclear bag fibers + nuclear chain fibers
• Increase tonic/steady-state firing of both Ia and Group II afferents
• Decrease dynamic sensitivity of Ia afferents
• Prevent silencing of Ia afferents during maintained stretch

Alpha-Gamma Coactivation:

1. Keeps the spindle taut (prevents "unloading") during whole-muscle contraction - maintains reflex sensitivity
2. Maintains the damping/smoothing function of the spindle regardless of muscle length changes

Brain Areas Controlling the Gamma System:

• Bulboreticular facilitatory area (brain stem) - primary driver; concerned with antigravity contractions
• Cerebellum - modulates via bulboreticular area
• Basal ganglia - modulates via bulboreticular area
• Cerebral cortex - transmits impulses into bulboreticular area

5. Damping and Stabilization Functions

6. Inverse Stretch Reflex (Golgi Tendon Organ)

7. Clinical Applications

Deep Tendon Reflexes (DTRs)

• Biceps: C5, C6
• Triceps: C7
• Patellar (knee jerk): L4
• Achilles (ankle jerk): S1
• Masseter: trigeminal nerve

Hyporeflexia / Absent Reflexes

• Muscle spindle damage
• Ia afferent neuropathy (most common cause: peripheral neuropathy from diabetes, alcoholism, toxins)
• Alpha motor neuron lesion (lower motor neuron lesion)

Hyperreflexia and Spasticity

• Cerebral cortex lesions (strokes, brain tumors) - affects contralateral muscles
• Upper motor neuron lesions at any level
• Increased excitation of the bulboreticular facilitatory area

Clonus

• Example (ankle clonus): sudden plantarflexion stretch → gastrocnemius reflex contracts → body rises → spindle unloads → relaxes → body drops → cycle repeats
• Clonus indicates high facilitation of the spinal cord (upper motor neuron pathology)
• Clinicians test by applying sudden, maintained stretch and observing for sustained oscillation

Physiologic Tremor

Summary Table

• Guyton and Hall Textbook of Medical Physiology, Ch. 55
• Ganong's Review of Medical Physiology, 26th Edition, Ch. 12
• Costanzo Physiology, 7th Edition, Ch. 3

Q1. Cerebellar Haemorrhage - Model Answer

• Jerky eye movements (nystagmus)
• Sways when standing (disequilibrium/truncal ataxia)
• Drunken gait (wide-based ataxic gait)

(a) Which Part of the Cerebellum is Most Likely Affected? (2 marks)

"The major dysfunction seen after damage to the vestibulocerebellum is ataxia, disequilibrium, and nystagmus." - Ganong's Review of Medical Physiology, 26th Ed.

(b) Features Seen in Cerebellar Lesion (5 marks)

1. Dysdiadochokinesia

• Inability to perform rapidly alternating opposite movements (e.g., repeated pronation/supination of the hands)
• Due to inability to stop one movement and start the opposite rapidly

2. Ataxia

• Wide-based, unsteady, "drunken" gait
• Incoordination due to errors in rate, range, force, and direction of movement
• Manifest also as scanning/staccato speech (slurred, slow, dysarthric)

3. Nystagmus

• Jerky oscillatory eye movements
• Particularly associated with vestibulocerebellar lesions
• Due to loss of smooth coordination of eye movements

4. Intention Tremor (+ Dysmetria)

• Tremor that worsens on approaching a target (unlike resting tremor of Parkinsonism)
• Dysmetria: overshooting or undershooting a target (e.g., finger-nose test)
• The correction itself overshoots, causing the finger to oscillate (intention tremor)

5. Slurred (Scanning) Speech

• Dysarthria due to incoordination of speech muscles
• Speech is broken into syllables with inappropriate pauses

6. Hypotonia

• Decreased resistance to passive movement of joints
• Due to loss of cerebellar facilitatory drive on alpha motor neurons

Additional Signs:

• Rebound phenomenon: inability to check movement suddenly (forearm flies back when resistance is removed)
• Decomposition of movement: multi-joint tasks are broken down and performed one joint at a time
• Delay in initiating movement (especially with cerebrocerebellum damage)
• Pendular knee jerk: reflex oscillates instead of a single jerk, due to hypotonia

Note: Cerebellar signs are ipsilateral to the lesion (because cerebellar output crosses twice - once in the cerebellum and once in the brainstem - ending up ipsilateral).

(c) Comparator Servo Mechanism of the Cerebellum (3 marks)

The Mechanism - Step by Step:

Motor Cortex
    |
    |---- Motor Command (efference copy/"reference signal")
    |           ↓
    |        CEREBELLUM  ← Actual movement feedback (from proprioceptors,
    |           |            vestibular system, visual system)
    |           |
    |    Compares intended vs. actual
    |           |
    |    Generates ERROR SIGNAL
    |           |
    ←-----------+--- Corrective output (via thalamus → motor cortex,
                      or brainstem → spinal cord)

Three Inputs to the Comparator:

1. Motor plan (intended movement) - from motor cortex via corticopontine-pontocerebellar fibers (mossy fibers) → what movement is desired
2. Peripheral sensory feedback (actual movement) - from proprioceptors, vestibular apparatus, visual system (via spinocerebellar tracts, vestibular inputs)
3. Ongoing motor commands - collateral copies of signals going to muscles

How the Cerebellum Corrects Errors:

• If actual movement deviates from intended: cerebellum detects the discrepancy
• Purkinje cell outputs (inhibitory, via GABA) modulate the deep cerebellar nuclei
• Deep nuclei send excitatory corrections via:
  • Dentate nucleus → VL thalamus → motor cortex (for voluntary movement)
  • Fastigial nucleus → vestibulospinal/reticulospinal tracts (for posture/balance)
  • Interposed nucleus → red nucleus → rubrospinal tract (for limb coordination)

Why is this called a "Servo" mechanism?

• Set point = intended movement (motor plan)
• Actual output = real limb movement (sensory feedback)
• Error signal = difference between the two
• Correction = cerebellar output adjusting ongoing motor commands

When the Comparator Fails (Cerebellar Lesion):

• The error cannot be detected and corrected in real time
• Result: dysmetria (overshooting), intention tremor (repeated failed corrections oscillate), ataxia
• The patient cannot execute smooth goal-directed movements

"The spinocerebellum receives proprioceptive input from the body as well as a copy of the motor plan from the motor cortex" - allowing it to compare intended vs. actual movement (Ganong's Review, 26th Ed.)