Tasker R R
Hum Neurobiol. 1982;1(4):261-72.
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.
通过电刺激，可以了解到大脑在疼痛处理过程中的许多功能。脊髓丘脑束被认为是伤害性疼痛的主要传导通路，其阻断会导致分离性感觉丧失，通过诱导主要为对侧、躯体感觉定位组织的温暖、凉爽或寒冷感觉（较少为灼痛，极少为疼痛），可以从脊髓前外侧柱一直识别到丘脑后部。脊髓网状丘脑束在正常疼痛处理中的功能存在争议，其阻断不会产生临床上可检测到的感觉丧失，通常对刺激无反应。然而，在去传入性疼痛患者中，它似乎对电刺激变得敏感，在前外侧柱以及中脑和内侧丘脑均如此，会产生主要为对侧、非躯体感觉定位组织的灼痛或疼痛感觉，这些感觉常常相当准确地再现患者的疼痛。这种现象在伤害性疼痛患者中似乎不会出现，可能反映了去神经支配神经元的超敏反应，这是解释去传入性疼痛的一种可能的病理生理机制。通过诱导感觉异常，电刺激可以从脊髓一直识别到躯体感觉皮层的背柱/内侧丘系系统。在背柱、腹尾核或内囊水平对其进行慢性刺激似乎能够抑制去传入性疼痛。从隔区经下丘脑和室周灰质延伸至导水管周围灰质的神经元组织弧，作为阿片类药物和内啡肽的受体区域，从而对脊髓丘脑束的传入发挥抑制作用，也可以通过慢性刺激来控制疼痛。刺激室周区域会产生温暖、舒适和放松的感觉，刺激下丘脑会产生恐惧和自主神经效应，刺激导水管周围灰质会导致不适、痛苦、焦虑和哭泣，刺激隔区会引起脸红、感觉异常、恶心、眼球震颤和温暖感。因此，通过电刺激可以识别出四个参与疼痛信号传导的脑系统，一个将伤害性疼痛传递至意识，另一个抑制疼痛，一个可能会经历去神经支配神经元超敏反应并将去传入性疼痛带入意识，可能是通过建立新的连接，还有一个大概能够抑制这种过度活动。
