Identification of pain processing systems by electrical stimulation of the brain.
Much can be learned about the brain's function in pain processing through electrical stimulation. The spinothalamic tract which is conceived to be the chief pathway for nociceptive pain and whose interruption induces dissociated sensory loss can be recognized from the anterolateral columns of the spinal cord to the posterior thalamus by the induction of feelings of chiefly contralateral, somatotopographically organized, warm, cool, or cold sensations, less often burning and rarely pain. The spinoreticulothalamic tract, whose function in normal pain processing is controversial and whose interruption produces no clinically detectable sensory loss, is normally silent to stimulation. However, in patients with deafferentation pain, it appears to become sensitive to electrical stimulation, both in the anterolateral columns and in midbrain and medial thalamus, giving rise to chiefly contralateral, non-somatotopographically organized, burning or painful sensations which often reproduce fairly accurately the patient's pain. This phenomenon, which does not appear to occur in patients with nociceptive pain, may reflect denervation neuronal hypersensitivity which is a possible pathophysiological mechanism explaining deafferentation pain. The dorsal column/lemniscal system can be recognized by electrical stimulation from the spinal cord to the somatosensory cortex by the induction of paraesthesiae. Its chronic stimulation at the level of the dorsal column, the ventrocaudal nucleus or the internal capsule appears capable of suppressing deafferentation pain. The arc of neuronal tissue extending from the septal area through hypothalamus and periventricular grey to the periaqueductal grey, which acts as a receptor area for opiates and endorphins, thereby exerting an inhibitory effect on access to the spinothalamic tract, can also be exploited through chronic stimulation for the control of pain. Stimulation of the periventricular area gives rise to feelings of warmth, comfort and relaxation, of the hypothalamus, horror and autonomic effects while that of the periaqueductal grey induces discomfort, distress, anxiety and weeping, and of the septal area flushing, paraesthesiae, nausea, nystagmus and a feeling of warmth. Thus four brain systems involved in pain signalling can be recognized by electrical stimulation, one which conveys nociceptive pain to consciousness, another that suppresses it, one that may undergo denervation neuronal hypersensitivity and bring deafferentation pain into consciousness, possibly by establishing novel connectivity and one that is presumably capable of suppressing that hyperactivity.
D000344:Afferent Pathways / Q000502:physiology; D000818:Animals; D001921:Brain / Q000502:physiology*; D001931:Brain Mapping; D001933:Brain Stem / Q000502:physiology; D002552:Cerebral Ventricles / Q000502:physiology; D004292:Dominance, Cerebral / Q000502:physiology; D004558:Electric Stimulation; D006801:Humans; D007031:Hypothalamus / Q000502:physiology; D009619:Nociceptors / Q000502:physiology*; D010487:Periaqueductal Gray / Q000502:physiology; D051381:Rats; D012154:Reticular Formation / Q000502:physiology; D012688:Septum Pellucidum / Q000502:physiology; D013116:Spinal Cord / Q000502:physiology; D013133:Spinothalamic Tracts / Q000502:physiology; D013787:Thalamic Nuclei / Q000502:physiology