title: A mechanism of cardiac pain suppression by spinal cord stimulation: implications for patients with angina pectoris.
abstract: Clinical reports show that electrical stimulation of the spinal cord reduces symptoms of angina pectoris, but so far have not provided evidence on the mechanisms involved. The hypothesis for this study was that inhibition of spinothalamic tract transmission may account for this result. Extracellular potentials of 28 spinothalamic tract neurons were recorded in anaesthetized monkeys, and the effects of dorsal column stimulation were determined on activity evoked by cardiac and somatic stimuli. Dorsal column stimulation reduced the number of cell potentials evoked by electrical stimulation of cardiopulmonary sympathetic afferent fibres in 11 spinothalamic tract cells tested. Activity evoked by intracardiac injection of bradykinin was decreased by dorsal column stimulation in six of seven neurons that responded to chemical stimulation of afferents. Differential effects of dorsal column stimulation were correlated to the cell responses to somatic field stimulation. Dorsal column stimulation inhibited activity in 12 of 12 neurons which were excited only by noxious pinch of somatic fields, whereas eight of 16 neurons which were excited by innocuous brushing of somatic fields were unaffected or excited. Transection of the dorsal column showed that the pathway transmitting inhibitory impulses descended from the stimulation site to the spinothalamic tract neurons examined. Results of this study are consistent with the concept that spinal cord stimulation reduces pain by decreasing the firing of spinothalamic tract cells which are activated by small fibre afferents. The paresthesias associated with nerve stimulation techniques may result from activation of spinothalamic tract cells which are excited by large fibre afferents. The clinical decision to employ spinal cord stimulation in patients with angina should balance the obvious benefit of pain relief against the risk of depriving the patient of an important warning signal while active myocardial ischaemia is in progress.
authors.affiliation: Department of Physiology and Biophysics, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City 73190.
authors.forename: M J
authors.initials: MJ
authors.lastname: Chandler
authors.forename: T J
authors.initials: TJ
authors.lastname: Brennan
authors.forename: D W
authors.initials: DW
authors.lastname: Garrison
authors.forename: K S
authors.initials: KS
authors.lastname: Kim
authors.forename: P J
authors.initials: PJ
authors.lastname: Schwartz
authors.forename: R D
authors.initials: RD
authors.lastname: Foreman
mesh_terms: D000344:Afferent Pathways / Q000503:physiopathology; D015360:Analgesia, Epidural / Q000295:instrumentation*; D000787:Angina Pectoris / Q000503:physiopathology / Q000628:therapy*; D000818:Animals; D004599:Electric Stimulation Therapy / Q000295:instrumentation*; D005073:Evoked Potentials, Somatosensory / Q000502:physiology; D005727:Ganglia, Spinal / Q000502:physiology; D005728:Ganglia, Sympathetic / Q000503:physiopathology; D006321:Heart / Q000294:innervation; D008252:Macaca fascicularis; D009619:Nociceptors / Q000503:physiopathology*; D013133:Spinothalamic Tracts / Q000503:physiopathology*