In a patient with a complete transection of the spinal cord between the medulla and spinal cord, why is there an initial loss of muscle tone followed by partial recovery that is greater in flexor muscles than extensors, with decreased gamma‑motor neuron activity?

Pathophysiology of Spinal Shock and Subsequent Tone Recovery After Complete Spinal Cord Transection

In a complete spinal cord transection between the medulla and spinal cord, the initial loss of muscle tone (spinal shock) occurs due to sudden loss of descending supraspinal facilitation to spinal reflex circuits, followed by partial recovery with greater tone in flexors than extensors due to differential reorganization of spinal reflex pathways and persistent reduction in gamma motor neuron activity from loss of descending control.

Mechanism of Initial Tone Loss (Spinal Shock)

The immediate flaccid paralysis and areflexia below the lesion results from:

• Sudden loss of descending facilitatory input from supraspinal centers (brainstem reticular formation, vestibulospinal tracts, and corticospinal pathways) that normally maintain baseline excitability of spinal motor neurons and interneurons 1
• Depression of all spinal reflex activity below the injury level, including loss of muscle stretch reflexes, cutaneous reflexes, and autonomic reflexes 1
• Immediate suppression of alpha and gamma motor neuron excitability due to withdrawal of tonic descending drive 2

The spinal shock phase typically lasts days to weeks in humans, with variable duration between patients 3. During this period, F-wave persistence is markedly reduced while H-reflexes may remain elicitable, indicating differential effects on motor neuron pools versus monosynaptic reflex pathways 2.

Mechanisms of Partial Tone Recovery

Recovery from spinal shock involves neuronal adaptation below the lesion level:

• Return of spinal reflex excitability signals the end of spinal shock, beginning with reappearance of cutaneous and muscle spindle reflexes 1, 2
• Reorganization of spinal circuits through denervation supersensitivity, receptor upregulation, and sprouting of remaining axons creates new functional connections 2
• Recovery of F-waves and flexor reflex excitability parallels clinical return of muscle tone and tendon reflexes 2

However, this recovery is incomplete and fundamentally altered from the pre-injury state 1.

Predominance of Flexor Over Extensor Tone

The greater recovery of flexor tone compared to extensors reflects:

• Differential dependence on descending control: Extensor motor neurons require more continuous supraspinal facilitation (particularly from vestibulospinal and reticulospinal tracts) than flexor motor neurons 1
• Flexor reflex dominance: After spinal cord injury, flexor withdrawal reflexes become hyperexcitable and dominate the motor output, while extensor reflexes remain relatively suppressed 2
• Loss of anti-gravity postural control: The vestibulospinal and reticulospinal systems that normally facilitate extensor tone for postural support are permanently disconnected 1

This creates the characteristic pattern where flexor spasms and increased flexor tone develop, while extensors remain relatively hypotonic 2.

Decreased Gamma Motor Neuron Activity

The persistent reduction in gamma motor neuron activity occurs because:

• Gamma motor neurons are heavily dependent on descending supraspinal drive from motor cortex, brainstem reticular formation, and vestibular nuclei for their tonic activity 1
• Loss of fusimotor control means muscle spindles cannot be properly "tuned" to maintain appropriate sensitivity across different muscle lengths 4
• Gamma motor neurons do not undergo the same adaptive reorganization as alpha motor neurons and interneurons in the isolated spinal cord 2

This reduced gamma activity contributes to altered muscle tone quality—the spasticity that develops is primarily from alpha motor neuron hyperexcitability and altered reflex circuits rather than from normal gamma-mediated muscle spindle sensitivity 2.

Clinical Implications

The returning reflex arcs are irrevocably altered and form the substrate for rehabilitation efforts 1. The H-to-M ratio remains relatively stable during recovery, while clinical spasticity continues to evolve, indicating that non-neuronal changes (muscle fiber changes, connective tissue alterations) also contribute significantly to the final clinical picture 2.

In paraplegic patients, secondary degeneration of premotoneuronal circuits and motor neurons may occur months after injury, as evidenced by decreasing M-wave and flexor reflex amplitudes 2. This underscores that spinal cord injury is not a static condition but involves ongoing pathophysiological changes.