Segmental Recovery of Amino Acid Neurotransmitters During Posterior Epidural Stimulation After Spinal Cord Injury

Abstract

Epidural spinal cord stimulation (SCS) has been used as an effective method for managing pain and spasticity for over two decades. However, the mechanisms of these beneficial effects are largely unknown. Since neurotransmitters are likely to be involved, we examined the relationship between SCS and local segmental amino acid release into the spinal cord extracellular space. Microdialysis was performed during continuous epidural SCS in animals subjected to ischemic spinal cord injury. Recovery of amino acid neurotransmitters from stimulated, injured animals was compared to that from a control group. Evoked potentials from the cortex and spinal cord were recorded to insure adequate stimulation and stable cord function. A significant increase in the concentrations of glycine and taurine was seen before, during, and after 90 minutes of continuous stimulation and was independent of the degree of injury. Levels of the other putative amino acid neurotransmitters were not significantly elevated. These results suggest that amelioration of pain or spasticity by epidural SCS may result from maintenance of post-injury elevation in baseline glycine and taurine levels.

Activity-dependent plasticity in spinal cord injury

“…ESCS appears to produce significant plastic changes. These changes include altering the electrophysiological properties of spinal motor pattern-generating circuitry [115,[123][124], altering amino acid neurotransmitter levels in the spinal cord (glycine and taurine) [125], and altering blood flow (both centrally and peripherally) [126][127][128].…”

Mapping the Iceberg of Autonomic Recovery: Mechanistic Underpinnings of Neuromodulation following Spinal Cord Injury

“…The gate control theory ( Melzack and Wall 1965 ) explains the potential mechanism as follows: primary afferent inputs activate inhibitory interneurons to close the gate to the visceral and/or noxious afferent inputs of the small diameter fibers at the spinal cord level. There is evidence on the effect of SCS on increased GABA ( Cui and others 1997 ) and glycine ( Simpson and others 1993 ), potentially indicating the activation of inhibitory neurons in the spinal cord. The inhibition of the sympathetic outflow could result from blocking the spinal transmissions of visceral/noxious afferent impulses in the primary afferent neurons or from pre- and postsynaptic inhibition of SPNs via spinal interneurons ( Figure 2B , spinal interneurons in blue).…”

Management of Chronic Limb Pain with Spinal Cord Stimulation

“…Various aminoacid neurotransmitters have been shown to participate in nociception. Inhibitory transmitters like taurine and glycine have been studied in relation to SCS‐induced analgesia, using microdyalisis has demonstrated SCS increases the concentration of glycine in spinal cord tissue, and proposes glycine as a reasonable candidate to explain SCS‐induced analgesia 29,30 . Another neuro‐transmitter, gama‐amino butyric acid(GABA), is increased with SCS 31,32 .…”