Evidence for a central pathway in the cerebrovascular effects of spinal cord stimulation

Cervical spinal cord stimulation (SCS) augments cerebral blood flow (CBF) in a number of animal models. The mechanisms underlying the cerebrovascular effects of SCS are not yet well delineated. In this study, we analyzed two alternative pathways in CBF alterations induced by SCS in rats, one involving direct modulation of sympathetic outflow and the other through central vasomotor influence.

Resection of the superior cervical ganglion (SCG), SCS alone, or SCS after SCG removal was performed in adult male Sprague-Dawley rats. CBF was measured with (14)C-inosine monophosphate radiotracer studies. In another set of experiments, SCS was performed after spinalization at the cervicomedullary junction or after laminectomy alone.

Baseline CBF in the SCG removal group was 71 +/- 8 ml/100 g/min, similar to controls. SCS alone significantly increased blood flow to 100 +/- 10 ml/100 g/min (P < 0.05). Animals that underwent SCS after SCG removal demonstrated a similar robust augmentation in CBF. SCS-induced changes in CBF were completely attenuated by spinalization.

The profound effects of spinal cord transection on SCS-induced CBF augmentation, together with the lack of effect of surgical sympathectomy, suggest that the mechanisms underlying the effects of SCS involve central influences rather than cervical sympathetic outflow. These findings suggest a possible role for brainstem vasomotor centers in the cerebrovascular effects of SCS.