Evidence For a Central Pathway in the Cerebrovascular Effects Of Spinal Cord Stimulation

Abstract

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.

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

“…In another study, spinalization, but not resection of the superior cervical ganglion (SCG), abolished cerebral vasodilation produced by cSCS (Patel et al, 2004). The data support the idea that a vasomotor mechanism in the brainstem is crucial in the production of cSCS-induced cerebral vasodilation.…”

“…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). …”

“…Electrical stimulation of the cerebellar fastigial nucleus can lead to a significant increase in CBF (Mraovitch et al, 1986;Takahashi et al, 1995), which is mainly mediated by rostral ventrolateral nucleus in the medulla (Chida et al, 1990). Therefore, cSCSinduced cerebral vasodilation may initially activate vasomotor centers that include the cerebellar fastigial nucleus and rostral ventrolateral medulla nucleus via ascending spinocerebellar pathways (Patel et al, 2004. Another related theory is that functional activation of the frontal lobe by the ascending reticular pathways mediated via the thalamo-cortical projections during cSCS, is also associated with cSCS-induced cerebral vasodilation (Mazzone et al, 1995(Mazzone et al, , 1996.…”

Roles of dorsal column pathway and transient receptor potential vanilloid type 1 in augmentation of cerebral blood flow by upper cervical spinal cord stimulation in rats

“…Blockade of autonomic ganglia with hexamethonium and blockade of α1-adrenergic receptors can suppress cSCS-induced increases in CBF (Patel et al, 2003;Sagher and Huang, 2000), but muscarinic receptor blockade with atropine had no effect (Garcia-March et al, 1989). Effects on brain vasomotor areas also are presumed to be of importance for increasing CBF (Patel et al, 2004;Sagher and Huang, 2000). In the case of SCS-induced hindlimb vasodilation, the response to SCS depends on TRPV1 containing peripheral fibers, as well as TRPV1 containing neurons in the spinal cord (Wu et al, , 2007b, but it is unknown whether similar pathways are relevant to cSCS effects on CBF.…”

“…In the case of SCS-induced hindlimb vasodilation, the response to SCS depends on TRPV1 containing peripheral fibers, as well as TRPV1 containing neurons in the spinal cord (Wu et al, , 2007b, but it is unknown whether similar pathways are relevant to cSCS effects on CBF. Spinal cord transection in rats and dorsal column section in cats at the cervicomedullary junction abolish effects of cSCS on CBF (Isono et al, 1995;Patel et al 2004). These effects may indicate that dorsal column fibers carry cSCS input to the brain; however, the upper cervical spinal cord also contains spinal neurons with projections to supraspinal structures, including various nuclei in caudal medulla, thalamus, hypothalamus, and periaqueductal gray in rats and cats (Malick et al, 2000;Mouton et al, 2005).…”