THALAMIC STIMULATION-EVOKED SENSATIONS IN CHRONIC PAIN PATIENTS AND IN NONPAIN (MOVEMENT DISORDER) PATIENTS

1. Little is known about the effect of central and peripheral nervous system injury on the processing of somatosensory information at the th alamic level in humans. The role of the human thalamic ventrocaudal nu cleus (Vc) in nociception is not well understood because reports of no ciceptive neuronal responses and stimulation-evoked pain are rare. In this study, we have characterized effects of microstimulation in the t actile region of Vc. Specifically, we investigated the incidence of pa inful sensations evoked by thalamic microstimulation in patients with and without chronic pain. 2. Data were obtained during stereotactic th alamic procedures for relief of pain or motor disorders. Patients were divided into three groups, those with 1) central poststroke pain (PSP , n = 13); 2) nonstroke pain (NSP, n = 23); and 3) movement disorders (controls, n = 24). Most (15 of 23) of the NSP patients had peripheral nerve damage. Tungsten microelectrodes were used to record neuronal r esponses in the thalamus and to deliver stimuli. Localization of tacti le Vc was determined according to stereotactic coordinates and neurona l responses to innocuous somatic stimuli. At selected sites, microstim ulation (1-s trains, 300 Hz, 0.1-0.2 ms pulses, <100 mu A) was perform ed and the patient was requested to describe the quality of the sensat ion and its peripheral location (projected field, PF). 3. Microstimula tion in tactile Vc commonly evoked paresthesia-type sensations. Thresh old stimulation never evoked pain in the NSP patients and evoked pain at only 2% of Vc sites in the movement disorder patients. In these lat ter 2 groups of patients, stimulation at >98% of Vc sites evoked pares thesia. By contrast, in the PSP patients, 28% of Vc sites stimulated e voked painful sensations at threshold. Suprathreshold stimuli evoked p ainful sensations at 46% of Vc sites in the PSP patients but at only 8 % of Vc sites in NSP patients and 12% of Vc sites in the movement diso rder patients. 4. The thresholds to evoke paresthesia in the NSP and m ovement disorder patients were significantly lower than the thresholds in the PSP patients. However, stimulation thresholds to elicit pain w ere similar in all patient groups. 5. All patients were capable of dif ferentiating stimulation-evoked paresthesia from pain. Stimulation-evo ked painful sensations in the PSP patients were often described as bur ning and sometimes as ''sharp,'' ''shocking,'' or ''unpleasant.'' By c ontrast, the quality of pain evoked in the other patient groups was ty pically described as unpleasant or shocking. Pain could be evoked at s ites throughout tactile Vc, although most sites were located in the ve ntral 2/3 of the nucleus. 6. In the movement disorder patients, the lo cation of the projected sensation usually corresponded to the location of the receptive fields of the tactile neurons recorded at the same s ite. By contrast, in both groups of pain patients there was a high inc idence of mismatches between the projected and receptive fields. 7. Th ese results suggest that the effective thalamic output from Ve to the cortex is affected by somatosensory deafferentation in pain patients. In addition, in the PSP patients there are also changes in the thalamo cortical processing of noxious information. The increased incidence of thalamic-evoked pain in PSP patients may be due to 1) loss of low-thr eshold mechanoreceptive thalamic neurons such that nociceptive neurona l output is now prominent, 2) reduced tonic inhibition of thalamic or cortical nociceptive neurons, and/or 3) unmasking or strengthening of nociceptive pathways.