Define Tone in cns

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Tone (Muscle Tone) in the CNS

Definition

Muscle tone (tonus) is defined as the resistance of a muscle to passive stretch at rest. It represents the baseline level of tension maintained in skeletal muscles even when no voluntary movement is occurring. Somewhere between the extremes of complete flaccidity (zero resistance) and spasticity (exaggerated resistance) lies the ill-defined zone of normal tone.
"The resistance of a muscle to stretch is often referred to as its tone or tonus."
  • Ganong's Review of Medical Physiology, 26th Ed.

Neural Basis of Tone - The Key Components

Tone depends on the integrity of a reflex arc involving:
ComponentRole
Alpha (α) motor neuronsLarge anterior horn cells - innervate extrafusal muscle fibers; their discharge produces actual contraction
Gamma (γ) motor neuronsSmaller anterior horn cells - innervate intrafusal fibers of the muscle spindle; tonically active at rest, keeping spindles taut and sensitive
Muscle spindlesSensory receptors within muscle; detect changes in muscle length
Ia afferent fibersCarry stretch signals from spindles to α motor neurons (monosynaptic arc)
Golgi tendon organs (GTOs)Detect tension - mediate the inverse stretch reflex to prevent overstretching
Descending supraspinal pathwaysModulate the α and γ motor neurons from above
Patellar reflex arc and gamma efferent system - Adams and Victor's
The stretch reflex arc. (A) Patellar reflex; (B) γ efferent fibers maintain spindle sensitivity via intrafusal muscle fibers. - Adams & Victor's Principles of Neurology, 12th Ed.
Alpha and gamma motor neurons and the muscle spindle system
α motor neurons innervate extrafusal fibers; γ motor neurons innervate intrafusal (spindle) fibers. Together they regulate tone and stretch reflexes. - Harrison's Principles of Internal Medicine, 22nd Ed.

Mechanism of Normal Tone

  1. γ motor neurons fire tonically at rest, keeping the intrafusal fibers of muscle spindles under continuous mild tension.
  2. This tonic stretch keeps the spindle Ia afferents active, delivering a low-level excitatory drive to α motor neurons.
  3. α motor neurons respond with a low level of efferent firing, maintaining background muscle contraction - this is tone.
  4. Descending supraspinal pathways (corticospinal, reticulospinal, vestibulospinal, rubrospinal) continuously modulate this loop from above.
"Some gamma motor neurons are tonically active at rest, keeping the intrafusal muscle fibers taut and more sensitive to active and passive changes in muscle length."
  • Adams & Victor's Principles of Neurology, 12th Ed.

CNS Control - Supraspinal Influences on Tone

PathwayEffect on Tone
Corticospinal (pyramidal)Facilitatory to distal muscles; lesion causes initial hypotonia followed by spasticity
ReticulospinalMedullary reticulospinal - inhibitory; Pontine reticulospinal - facilitatory (to extensors)
VestibulospinalStrongly facilitatory - excites extensor (antigravity) tone
RubrospinalFacilitatory to flexors of distal limbs
Basal gangliaModulate tone via thalamo-cortical loop; lesions cause rigidity
CerebellumFacilitates γ motor neuron activity; lesions cause hypotonia
"Bulbospinal upper motor neurons influence strength and tone but are not part of the pyramidal system. The descending ventromedial bulbospinal pathways originate in the tectum, vestibular nuclei, and reticular formation and are involved in the maintenance of posture."
  • Harrison's Principles of Internal Medicine, 22nd Ed.

Abnormalities of Tone

1. Hypotonia (Decreased Tone)

  • Definition: Reduced resistance to passive movement; muscles feel "floppy."
  • Causes:
    • Lower motor neuron (LMN) lesion: peripheral nerve or anterior horn cell damage
    • Posterior column / proprioceptive pathway damage
    • Acute upper motor neuron (UMN) lesions - spinal shock phase
    • Cerebellar lesions (ipsilateral hypotonia)
    • Severe hypotonia allows passive hyperextension of joints.

2. Spasticity (UMN type Hypertonia)

  • Definition: Velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks.
  • Mechanism: Loss of descending inhibitory (mainly reticulospinal) influence on α motor neurons → hyperactive stretch reflex.
  • Clasp-knife phenomenon: On rapid passive stretch, there is initial resistance, then sudden release - caused by activation of the inverse stretch reflex (GTOs) and Ib inhibitory interneurons.
  • Features: Increased tone with free interval, velocity-dependent, brisk tendon reflexes, Babinski sign.
  • Causes: Stroke, spinal cord injury, cerebral palsy, multiple sclerosis.
"Rapid passive displacement of the extremity results in increased resistance followed by relaxation (clasp-knife phenomenon). Resistance varies with the speed and direction of passive motion."
  • Bradley & Daroff's Neurology in Clinical Practice

3. Rigidity (Extrapyramidal type Hypertonia)

  • Definition: Increased resistance to passive movement that is uniform throughout the range of motion and not velocity-dependent, affecting both flexors and extensors equally.
  • Lead-pipe rigidity: Smooth, uniform resistance like bending a lead pipe.
  • Cogwheel rigidity: Ratchet-like, rhythmically interrupted resistance - represents tremor superimposed on rigidity (seen in Parkinson's disease).
  • Mechanism: Overactivity of the stretch reflex due to loss of basal ganglia inhibition on the thalamo-cortical loop; γ motor neuron hyperactivity.
  • Features: No free interval, not velocity-dependent, tendon reflexes NOT enhanced, limb does not resume original position after manipulation.
  • Causes: Parkinson's disease, Wilson's disease, neuroleptic drugs, MSA, PSP.
"The increased resistance on passive movement that characterizes rigidity is not preceded by an initial free interval and has an even or uniform quality throughout the range of movement, like bending a lead pipe."
  • Adams & Victor's Principles of Neurology, 12th Ed.

4. Paratonia (Gegenhalten)

  • The patient appears to actively resist passive movement in any direction.
  • Seen in frontal lobe disease, dementia, confusional states.
  • Reflects inability to relax, not a true basal ganglia disorder.

Comparison: Spasticity vs. Rigidity

FeatureSpasticity (UMN)Rigidity (Extrapyramidal)
Velocity dependenceYes (faster = more resistance)No
DistributionFlexors > extensors (UL); extensors > flexors (LL)Both flexors and extensors equally
Free intervalYesNo
Clasp-knifePresentAbsent
Tendon reflexesExaggeratedNormal or mildly increased
BabinskiPresentAbsent
CogwheelingNoCommon (Parkinson's)
Lesion siteCorticospinal tractBasal ganglia / extrapyramidal

Clinical Examination of Tone

  1. Inspection: Spontaneous posture - spasticity causes fixed flexed posture of upper limbs.
  2. Palpation: Hypertonic muscles feel firm; hypotonic muscles feel "doughy."
  3. Passive movement: Ask the patient to relax completely. Move the limb passively through its full range at varying speeds.
    • Normal: uniform, low-level resistance throughout, same at all velocities.
    • Spastic: resistance increases with faster movement; clasp-knife release.
    • Rigid: even, "lead-pipe" resistance at all velocities.
    • Hypotonic: abnormally easy passive movement; joints may hyperextend.
  4. Heel-dragging test (lower limb): In a supine patient, grasp behind the knee and lift briskly. Normally the heel stays in contact with the table; in spasticity the heel rises off the table.

Summary

Tone in the CNS is the background resistance of muscle to stretch, arising from tonic activity of γ motor neurons maintaining spindle sensitivity, feeding back through Ia afferents onto α motor neurons, all under continuous modulation by supraspinal pathways. When CNS pathways are disrupted, tone becomes either excessively increased (spasticity from corticospinal lesions, or rigidity from extrapyramidal lesions) or decreased (hypotonia from cerebellar, acute UMN, or LMN lesions).

Sources: Adams & Victor's Principles of Neurology, 12th Ed. | Ganong's Review of Medical Physiology, 26th Ed. | Bradley & Daroff's Neurology in Clinical Practice | Harrison's Principles of Internal Medicine, 22nd Ed.
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