Cervical spinal cord stimulation may prevent cerebral vasospasm by modulating sympathetic activity of the superior cervical ganglion at lower cervical spinal level.

Cervical spinal cord stimulation (SCS) has been for many years hypothesized to be of use in treatment of cerebral vasospasm after subarachnoid hemorrhage. Experiments in animals and research in humans have demonstrated increase in cerebral blood flow (CBF), and different theories have been tried to explain these observations. Although there are many claims of circulatory improvements in these circumstances, no clinical application has yet been established. A complete understanding of physiological and anatomic correlation between CBF modulation and SCS remain unclear. We strongly believe that the main objective is not to treat vasospasm by increasing blood flow but to prevent vasoconstriction of the cerebral arteries by a functional sympathectomy. SCS may, at least theoretically, work in different ways at the same time: (1) preventing vasoconstriction of cerebral arteries by functional sympathectomy, acting at the lower cervical levels; and (2) increasing CBF through central pathways, perhaps involving brainstem connections, at the upper cervical levels. One of the practical implications of this hypothesis would be differential placement of cervical spinal cord stimulation electrodes in patients with subarachnoid hemorrhage depending on the timing of electrode insertion and presence or absence of vasospasm at the time of initial intervention.