Spontaneous neuronal hyperactivity in the medial and intralaminar thalamic nuclei of patients with deafferentation pain

Abstract

Electrical activity was recorded from single cells in the thalamus of 10 patients with chronic pain associated with deafferentation. Under local anesthesia, these patients underwent either electrode implantation or thalamotomy for treatment of their pain. In eight of the 10 patients, single units were identified as discharging spontaneously in high-frequency, often rhythmic, bursts. The discharges were of two types: short bursts comprised of two to six spikes with a burst frequency of one to four per second; and long trains of 30 to 80 spikes of similar frequency. Reconstruction of electrode trajectories indicated that recordings were made from the region corresponding to the lateral aspect of the mediodorsal thalamic nucleus, the central lateral nucleus, a small part of the central median nucleus, and the parafascicular nucleus. In the eight patients in whom spontaneous neuronal burst activity was exhibited, it was impossible to study activity evoked by natural cutaneous stimulation due to the continuous spontaneous neuronal discharges. Both animal and human studies have suggested that pain related to deafferentation is accompanied by spontaneous hyperactivity in the dorsal horn of the spinal cord and in the ventral posterior thalamic nuclei. The authors present evidence of spontaneous neuronal hyperactivity in the intralaminar thalamic nuclei of patients with pain related to deafferentation. The findings suggest that spontaneous neuronal discharge in patients with pain related to deafferentation is more widespread in the central nervous system than has been previously appreciated. The results have important implications for the surgical treatment of chronic pain.

Pain Relief From Preganglionic Injury to the Brachial Plexus by Late Intercostal Nerve Transfer

“…The convulsive pain of injury to the brachial plexus may correlate with the burst pattern of firing. Abnormal bursting patterns after deafferentation are also observed in higher levels of the central nervous system including the thalamus (Rinaldi et al 1991). Transfer of healthy intercostal nerve into trunk nerves of the upper limb may inhibit this abnormal electrical activity.…”

Contribution of central neuroplasticity to pathological pain: review of clinical and experimental evidence

“…Neurons in the somatosensory thalamus of patients with neuropathic pain display high spontaneous firing rates, abnormal bursting activity, and evoked responses to stimulation of body areas that normally do not activate these neurons (Gorecki et a1. 1989;Hirayama et al 1989;Lenz et al 1989;Rinaldi et al 1991). The site of abnormality in thalamic function appears to be somatotopically related to the painful region.…”

Postnatal maturational properties of rat parafascicular thalamic neurons recorded in vitro

“…It is tempting to speculate that perhaps the contribution of It and Ih conductances to Pf cell physiology may change in certain disease states. Several studies have reported changes in the firing properties of Pf cells after deafferentation, such as the loss of intrathalamic and ascending sensory projections (Rinaldi et al, 1991;Pollin et al, 1997;Vaculin et al, 2000). It would be interesting if there were increases in both the expression and/or efficacy of It and Ih channels in Pf cells after deafferentation, or in certain disease pathologies or aberrant developmental paradigms, such that a switch occurs in the electrophysiological properties of these cells results in the expression of a more classic oscillatory thalamic neuron physiology.…”