The Devor lab 
research on neuropathic pain and pain-free surgery

Identification of a critical period for regeneration of severed axons in the olfactory cortex and related patterns of neuroplastic axonal reorganization.

Among the first research on collateral sprouting in the skin following nerve injury as a mechanisms of recovery of sensory function, in rats and human patients.

Discovery of neuroplastic reorganization of somatosensory maps in the spinal dorsal horn and cortex following peripheral nerve injury in rodents and cats. Findings later extended by others to primates and humans.

Research on ectopic discharge in nerve-end neuromas as a fundamental factor in neuropathic pain.

Demonstration that corticosteroids and anticonvulsants suppress ectopia and hence neuropathic pain.

Discovery of “sympathetic-sensory coupling" as a factor in neuropathic pain, and its association with sympathetic sprouting in the cut nerve end and associated dorsal root ganglia (DRGs).

Establishment of the first animal model of chronic neuropathic pain, the “neuroma model” (autotomy) in rats and mice.

First demonstration of Na+ channel accumulation in severed axons in fish and later in rodents, a key mechanism of hyperexcitability in neuromas.

Documentation of ephaptic (electrical) crosstalk at nerve injury sites, including ultrastructural correlates, previously only a medical speculation.

Established that susceptibility to neuropathic pain may be heritable, based on the development of selection-line rat strains; a foundational discovery in the emergence of "Pain Genetics".

A new approach to defining fundamental pain “types” using correlational analysis across multiple inbred mouse strains.

Identification of Cacng2 (stargazin) as a susceptibility gene for neuro-pathic pain, among the first known “pain genes”, in animals and man.

Novel mechanism and potential treatment of osteoarthritic pain based intrinsic subchondral bone innervation and a dental root canal analogy.

“Ignition Hypothesis” of pain paroxysms in Trigeminal Neuralgia. 

Discovery of chemically-mediated non-ephaptic/ non-synaptic crosstalk among injured afferent axons and DRG somata.

Discovered neuropathic hyperexcitability in DRG neurons and the role of subthreshold oscillations in DRG ectopia.

Identification of primary afferent "algoneurons", neurons whose activity evokes the experience of pain (contrasting with "nociceptors", defined by their high-threshold receptive field).

Found the brainstem MPTA (mesopontine tegmental anesthesia area), a key node in the neuronal network sub-serving brain-state transitioning between wake and unconsciousness induced by GABAergic anesthetics.

First direct evidence that phantom limb sensation and phantom limb pain (PLP) in human amputees aredriven primarily by DRG ectopia, including a potential therapeutic approach to relieving PLP.

Novel hypothesis concerning the causes of pain in herpes zoster and postherpetic neuralgia.

Assembly of evidence suggesting that consciousness may be seated subcortically, perhaps in the brainstem, rather than the cerebral cortex.

Identified the cellular and molecular targets of GABAergic general anesthetics in the MPTA.

Honorary member of both the International Association for the Study of Pain (IASP) and the World Insitute of Pain (WIP).