Sympathetic neural outflow in spinal man. A preliminary report

Area of Science:

• Neuroscience
• Physiology
• Spinal Cord Injury Research

Background:

• Traumatic spinal cord transection isolates neural circuits below the lesion from supraspinal control.
• Understanding the function of these isolated spinal circuits is crucial for managing complications like autonomic hyperreflexia.

Purpose of the Study:

• To investigate the nature and origin of sympathetic neural activity in patients with spinal cord transection.
• To explore the relationship between peripheral stimuli and sympathetic responses in the absence of supraspinal input.

Main Methods:

• Microelectrode recordings from peroneal skin and muscle fascicles in 11 patients with spinal cord transection.
• Stimulation of the abdomen (bladder pressure), skin (electrical stimulation, pinching) above and below the lesion.
• Pharmacological blockade (local anesthetic) of peripheral nerves.

Main Results:

• Spontaneous neural activity was minimal; bursts of activity were evoked by stimuli below the lesion (e.g., bladder pressure, skin pinch).
• Evoked bursts had a slow conduction velocity (~0.7 m/s) and were abolished by proximal nerve blocks, indicating spinal origin.
• Neural bursts were followed by prolonged vasoconstriction and altered skin resistance, suggesting sympathetic vasoconstrictor and sudomotor outflow.

Conclusions:

• Sympathetic activity in spinal cord injury originates from the isolated spinal cord, comprising vasoconstrictor and sudomotor impulses.
• Less differentiated sympathetic outflow in isolated spinal cords may contribute to exaggerated responses seen in autonomic hyperreflexia.