The purpose of this study was to examine the effects of TENS application to somatic receptive fields on spontaneous and noxiously evoked dorsal horn cell activity in alpha-chloralose-anesthetized cat. Carbon-filament microelectrodes were used to record extracellular action potentials from 83 spontaneously discharging cells. Using a commercial TENS unit (Medtronic Eclipse Model 7723), spontaneous cell activity was decreased in 54% (65%) of the cells. Twenty-five (30%) did not respond and 4 (5%) increased activity. It was also shown that for 36 cells which were evoked with either manual pinch (19 cells) or manual clamp (17 cells), cell activity decreased during TENS application. This study shows that dorsal horn neurons which can potentially transmit noxious information to supraspinal levels, can have their cell activity decreased during TENS application to somatic receptive fields. This is consistent with the concept of the 'gate control theory of pain' in that less noxious information would be involved in the pain perception process.

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.

No abstract

One objective of this study was to examine a mechanism for the inability of patients to distinguish esophageal pain from cardiac pain. Patients with esophageal disease and angina pectoris often perceive pain as originating from the same somatic fields. Another objective was to compare the effect of esophageal distension between animals with a non-inflamed or with an inflamed esophagus. For this study in anesthetized cats, we recorded extracellular action potentials from T2-T7 spinal neurons that responded to intraluminal distension of an untreated or a turpentine-inflamed distal esophagus. Threshold distension volumes were compared between these 2 groups of animals. Neurons also were examined for effects of intracardiac bradykinin injection and somatic stimuli. Results showed that spinal neurons responded to a smaller threshold distension volume when cells in animals with an inflamed distal esophagus were compared to cells in animals with a non-inflamed distal esophagus. Spinal neurons that received input from the distal esophagus also received convergent input from the heart and somatic fields. Our data supported the hypotheses that (1) referred pain from the distal esophagus resulted from activation of the same spinal neurons by visceral and somatic input, (2) pain originating from the distal esophagus and heart might be difficult to distinguish because of viscerosomatic and viscerovisceral convergence onto the same spinal neurons, and (3) an inflamed distal esophagus might be more sensitive to distension than a non-inflamed esophagus.

No abstract