Lenz Fred A, Gracely Richard H, Hope Earl J, Baker Frank H, Rowland Lance H, Dougherty Patrick M, Richardson Russell T
Department of Neurosurgery, Johns Hopkins University, Baltimore, MD 21287 USA Department of Cardiology, Johns Hopkins University, Baltimore, MD 21287 USA Department of Ophthalmology, Johns Hopkins University, Baltimore, MD 21287 USA Department of Neuroscience, Johns Hopkins University, Baltimore, MD 21287 USA Department of Zanvyl Krieger Mind-Brain Institute, Johns Hopkins University, Baltimore, MD 21287 USA Neurobiology and Anesthesiology Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 21287 USA.
Pain. 1994 Oct;59(1):119-125. doi: 10.1016/0304-3959(94)90055-8.
We have performed single-neuron recording and microstimulation in the region of the thalamic principal sensory nucleus (ventrocaudal nucleus, Vc) prior to implantation of a deep brain-stimulating electrode in a patient with pain secondary to arachnoiditis and with a past history of unstable angina. Cells located in the 16 mm lateral plane had cutaneous receptive fields on the chest wall. At and posterior to the location of these cells stimulation coincided precisely with the sensation of angina (stimulation-associated angina). The description of stimulation-associated angina was measured using a questionnaire and was identical to the patient's usual angina except that it began and terminated suddenly. Stimulation-associated angina was coincident with a tingling sensation in the leg. Clinical, hemodynamic, electrophysiologic and biochemical measures of cardiac function showed no evidence of myocardial strain or injury related to stimulation-associated angina. Since cells in the region of the principle sensory nucleus of thalamus respond to cardiac injury in animals, the present results suggest that this region mediates the sensation of angina.
