Effects of cervical spinal cord stimulation on cerebral blood flow in the rat

Abstract

<jats:p content-type="fine-print"><jats:italic>Object.</jats:italic> Spinal cord stimulation (SCS) is frequently used for the treatment of chronic pain. Although the mechanisms by which SCS alleviates pain are unclear, they are believed to involve changes within the dorsal horn of the spinal cord. Spinal cord stimulation has also been found to cause significant vasodilation in the peripheral vasculature. The mechanisms underlying this effect are thought to involve sympathetic blockade. A rostral vasodilatory effect has also been described, but changes in cerebral blood flow (CBF) have been poorly delineated. Using laser Doppler flowmetry (LDF), the authors examined the effects of cervical SCS on CBF in rats.</jats:p> <jats:p content-type="fine-print"><jats:italic>Methods.</jats:italic> Cervical SCS was found to result in a significant increase in cortical LDF values (83 ± 11% [mean ± standard error of the mean]). The increase in cortical LDF values was not accompanied by a significant increase in systemic blood pressure. Stimulation of the upper cervical spinal cord was more effective in inducing LDF changes than was that of the lower cervical cord. Changes in SDS-induced LDF values were significantly attenuated after spinal cord transection at the cervicomedullary junction and by the administration of the sympathetic blocker hexamethonium.</jats:p> <jats:p content-type="fine-print"><jats:italic>Conclusions.</jats:italic> These results indicate that cervical SCS may induce cerebral vasodilation and that this effect may involve indirect effects on vasomotor centers in the brainstem as well as an alteration in sympathetic tone.</jats:p>

Putative mechanisms behind effects of spinal cord stimulation on vascular diseases: A review of experimental studies

“…Intravenous administration of hexamethonium (10 mg/Kg) prior to the initiation of cSCS in the rats abolished the cSCS-induced cerebral vasodilation (Sagher et al, 2000). Another study also showed that cSCS-induced cerebral vasodilation was abolished by both a high-dose of hexamethonium (20 mg/Kg) and prazosin (a selective α-1 receptor blocker, 1 mg/Kg) (Patel et al, 2003).…”

“…Effects of cSCS on the cerebral vascular system include an increase in CBF (Meglio et al, 1991 a;Ebel et al, 2001;Robaina et al, 2004;Karadag et al, 2005) combined with a decrease in cerebral vascular resistance and an increase in blood flow velocity (Meglio et al, 1991 b), leading to an enhancement of the local-regional delivery of oxygen (Clavo et al, 2002(Clavo et al, , 2003, Further effects of cSCS on the cerebral vascular system also include a decrease in induced vasospasms Gurelik et al, 2005) and an improvement of neurological dysfunction , a modification of glucose metabolism (Momose et al, 1989;Clavo et al, 2006), and the prevention of early spasm due to subarachnoid hemorrhage (SAH) . cSCS effects on cerebral vasodilation depend on a decrease of sympathetic tone (Sagher et al, 2000;Patel et al, 2003), activation of vasomotor centers (Sagher et al, 2000;Patel et al, 2004) and release of neurohumoral factors (Hosobuchi, 1985;Goksel et al, 2001). …”

“…Rats are used to study the cSCS effects under the normal physiological conditions (Sagher et al, 2000Patel et al, 2003). The effects of cSCS in pathological conditions are studied with several vasospasm models that have been established in the larger animals such as rabbits (Visocchi et al, 1994;Goksel et al, 2001) and cats Isono et al, 1994).…”

“…In brief, fresh autologous blood (1 ml/Kg) from each animal's femoral artery was injected into cisterna magna (CM). The locations of cSCS can range from C1 to C6 and the optimal placements of the stimulating electrode is on segments C1-C3 (Patel et al, 2003;Goksel et al, 2001;Sagher et al, 2000). It showed that CBF was increased by more than 80% above baseline with the amplitude of 1.5 mA (Zhong et al, 2004).…”

“…2.3.3 Sympathetic mechanisms-Sagher was the first to assess the role of sympathetic tone in cSCS-induced cerebral vasodilation (Sagher et al, 2000), although the earlier studies suggested this mechanism (Broseta et al, 1994;Isono et al, 1994;Visocchi et al, 1994). Intravenous administration of hexamethonium (10 mg/Kg) prior to the initiation of cSCS in the rats abolished the cSCS-induced cerebral vasodilation (Sagher et al, 2000).…”