Autopsy analysis of the safety, efficacy and cartography of electrical stimulation of the central gray in humans
References (20)
Naloxone reversal of analgesia produced by brain stimulation in the human
Pain
(1976)- et al.
A correlative anatomical and clinical study of pain suppression by deep brain stimulation
Pain
(1982) - et al.
Pain reduction by focal electrical stimulation of the brain: an anatomical and behavioral analysis
Brain Research
(1974) - et al.
Central nervous system mechanisms of analgesia
Pain
(1976) - et al.
Appearance of β-endorphin-like immunoreactivity in human ventricular cerebrospinal fluid upon analgesic electrical stimulation
- et al.
Enkephalin-like material elevated in ventricular cerebrospinal fluid of pain patients after analgetic focal stimulation
Science
(1978) - et al.
Contrast medium causes the apparent increase in β-endorphin levels in human cereborspinal fluid following brain stimulation
Pain
(1980) - et al.
Elevated β-endorphin in cerebrospinal fluid after electrical brain stimulation: artifact of contrast infusion?
Science
(1984) - et al.
Selective and prolonged analgesia in monkey resulting from brain stimulation
The current status of analgesic brain stimulation
Acta Neurochir.
(1980)
There are more references available in the full text version of this article.
Cited by (69)
Cell type-specific dissection of sensory pathways involved in descending modulation
2023, Trends in NeurosciencesRole of prefrontal cortical calcium-independent phospholipase A<inf>2</inf> in antinociceptive effect of the norepinephrine reuptake inhibitor antidepresssant maprotiline
2017, NeuroscienceCitation Excerpt :The latter in turn, projects to the dorsolateral pontine tegmentum and the rostral ventromedial medulla, including the nucleus raphe magnus, which projects to the dorsal horn of the spinal cord or spinal trigeminal nucleus to inhibit nociceptive transmission (Lovick and Wolstencroft, 1979; Aimone et al., 1987; Benarroch, 2012). This pathway leads to analgesia when stimulated (Reynolds, 1969; Hosobuchi et al., 1977; Baskin et al., 1986). Thus, inhibition of prefrontal cortical iPLA2 may prevent maprotiline induced activation of the prefrontal cortex, leading to reduced PAG stimulation, and abrogation of antinociceptive effect of the antidepressant.
Copyright © 1986 Published by Elsevier B.V.