Is it correct that a complete spinal cord transection below the medulla causes an initial loss of muscle tone during spinal shock, followed by partial recovery with predominance of flexor tone over extensor tone and reduced gamma‑motor neuron activity?

Spinal Animal Model: Accuracy of Described Physiological Changes

The description is partially correct but contains a critical error: gamma motor neuron activity is typically INCREASED, not decreased, following spinal cord transection after the resolution of spinal shock. 1

Initial Spinal Shock Phase

The initial loss of muscle tone following complete spinal cord transection below the medulla is accurate and well-established 2:

• Immediate flaccid paralysis occurs below the level of injury with complete loss of reflexes and muscle tone
• This represents the acute phase of "spinal shock," lasting from hours to weeks (typically up to 72 hours in the acute phase) 2
• During this period, all spinal reflexes are suppressed due to sudden loss of descending supraspinal input 1

Recovery Phase and Tone Patterns

The partial recovery of tone with predominance in flexors is generally accurate 1:

• Tone gradually returns as spinal shock resolves, though not to pre-injury levels
• Flexor spasms and reflexes predominate over extensor responses in most cases of complete spinal cord injury
• This flexor predominance reflects the reorganization of spinal circuits below the lesion 3
• Complete transection of the spinal cord is actually rare even in clinically complete injuries—most retain some anatomical continuity 1

Critical Error: Gamma Motor Neuron Activity

The statement about decreased gamma motor activity is incorrect:

• Gamma motor neuron activity is typically INCREASED, not decreased, following spinal cord injury after spinal shock resolves 1
• This increased gamma activity contributes to the development of spasticity and hyperreflexia characteristic of upper motor neuron lesions 1
• The exaggerated responsiveness of spinal neurons after injury includes amplification of peripheral inputs, which involves heightened gamma motor neuron function 3

Mechanism of Changes

The physiological reorganization involves several key processes 1, 3:

• Loss of descending inhibitory control from supraspinal centers (reticulospinal, vestibulospinal pathways)
• Sprouting and reorganization of remaining spinal circuits below the lesion
• Increased neuronal excitability in the isolated spinal cord segments
• Amplification of peripheral sensory inputs contributing to both motor and sensory abnormalities 3

Clinical Implications

These changes have important functional consequences 2, 1:

• Development of spasticity (increased muscle tone with velocity-dependent resistance to stretch)
• Flexor withdrawal reflexes become exaggerated and may be triggered by minimal stimuli
• Risk of autonomic dysreflexia in injuries above T6 due to reorganization of autonomic pathways 3
• Potential for neuropathic pain related to the amplified sensory processing 3, 4