Reorganization of sensory modalities evoked by microstimulation in region of the thalamic principal sensory nucleus in patients with pain due to nervous system injury

Abstract

Stimulation of the somatosensory system is more likely to evoke pain in patients with chronic pain after nervous system injury than in patients without somatosensory abnormalities. We now describe results of stimulation through a microelectrode at microampere thresholds (threshold microstimulation; TMIS) in the region of the human thalamic principal sensory nucleus (ventral caudal; Vc) during operations for treatment of movement disorders or of chronic pain. Patients were trained preoperatively to use a standard questionnaire to describe the location (projected field) and quality of sensations evoked by TMIS intraoperatively. The region of Vc was divided on the basis of projected fields into areas representing the part of the body where the patients experienced chronic pain (pain affected) or did not experience chronic pain (pain unaffected) and into a control area located in the thalamus of patients with movement disorders and no experience of chronic pain. The region of the Vc was also divided into a core region and a posterior-inferior region. The core was defined as the region above a standard radiologic horizontal line (anterior commissure-posterior commissure line; ACPC line) where the majority of cells responded to innocuous somatosensory stimulation. The posterior-inferior area was a cellular area posterior and inferior to the core. In both the core and the posterior-inferior regions, the proportion of sites where TMIS evoked pain was larger in pain-affected and unaffected areas than in control areas. The number of sites where thermal (warm or cold) sensations were evoked was correspondingly smaller, so that the total of pain-plus-thermal (sensation of warmth or cold) sites was the same in all areas. Therefore, sites pain where stimulation evoked pain in patients with neuropathic pain (i.e., pain following an injury to the nervous system) may correspond to sites where thermal sensations were evoked by stimulation in patients without somatosensory abnormality.

Human Thalamic Somatosensory Nucleus (Ventral Caudal, Vc) as a Locus for Stimulation by INPUTS from Tactile, Noxious and Thermal Sensors on an Active Prosthesis

“…However, such bursting could cause pain if stimulation in the vicinity of the bursting cellular activity produced the sensation of pain. This finding has been reported in studies of sensations evoked by stimulation of the region of Vc in patients with chronic pain secondary to neural injury [82,111]. …”

“…The PFs show an increased representation of the stump contrasted with that for the same part of the body in controls [37,82], which is evidence for a change in the representation of the arm embedded in thalamic-cortical assemblies [83,84]. …”

“…We have examined the modalities of the sensation produced by TMIS in patients with chronic neuropathic pain due to several diagnoses versus patients with movement disorders [82]. These results showed that patients with chronic pain had more sites at which TMIS evoked pain and fewer at which warm and cold (thermal) sensations were evoked.…”

Pathophysiologic mechanisms of neuropathic pain

“…Although data is limited, nerve injury may increase the excitability of and reorganize the connections of neurons in these supraspinal centers [84]. For example, patients with neuropathic pain demonstrate a dramatic reorganization of sensory modalities in the thalamus [85]. Also, the phantom limb pain following arm amputation is associated with a spatial reorganization of somatosensory cortical mapping [86].…”

Mechanisms of Pain and Itch Caused by Herpes Zoster (Shingles)

“…Ectopic hyperexcitability is a fundamental nonspecific injury response of neurons, and ectopic firing of pain neurons and expanded receptive fields have been documented at every level of the pain pathway in humans as well as in experimental animals. 25,27 Functional brain imaging has documented somatotopic plasticity of somatosensory cortex in neuropathic pain patients 30 and widespread changes in cerebral blood flow. 6 Microneurographic recordings from single fibers within nerves of humans with painful small-fiber polyneuropathies have provided indisputable evidence of pathological activity of peripheral nociceptive axons.…”