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The forebrain somatic sensory locus for input from sensors on the surface of an active prosthesis is an important component of the Brain Machine Interface. We now review the neuronal responses to controlled cutaneous stimuli and the sensations produced by Threshold Stimulation at Microampere current levels (TMIS) in such a locus, the human thalamic Ventral Caudal nucleus (Vc). The responses of these neurons to tactile stimuli mirror those for the corresponding class of tactile mechanoreceptor fiber in the peripheral nerve, and TMIS can evoke sensations like those produced by the stimuli that optimally activate each class. These neuronal responses show a somatotopic arrangement from lateral to medial in the sequence: leg, arm, face and intraoral structures. TMIS evoked sensations show a much more detailed organization into anterior posteriorly oriented rods, approximately 300 microns diameter, that represent smaller parts of the body, such as parts of individual digits. Neurons responding to painful and thermal stimuli are most dense around the posterior inferior border of Vc, and TMIS evoked pain sensations occur in one of two patterns: (i) pain evoked regardless of the frequency or number of spikes in a burst of TMIS; and (ii) the description and intensity of the sensation changes with increasing frequencies and numbers. In patients with major injuries leading to loss of somatic sensory input, TMIS often evokes sensations in the representation of parts of the body with loss of sensory input, e.g., the phantom after amputation. Some patients with these injuries have ongoing pain and pain evoked by TMIS of the representation in those parts of the body. Therefore, thalamic TMIS may produce useful patterned somatotopic feedback to the CNS from sensors on an active prosthesis that is sometimes complicated by TMIS evoked pain in the representation of those parts of the body. [ABSTRACT FROM AUTHOR]

Central pain is neuropathic pain resulting from a lesion of the CNS, such as a stroke [poststroke central pain (CPSP)]. Lesions involving the posterior thalamus lead to reduction or loss of sensation and to CPSP, although the responsible nuclei have not been identified. We now examine the hypotheses that thalamic lesions must extend posterior to the ventral caudal nucleus (Vc) and include ventral medial posterior nucleus (VMpo), to result in loss of cold sensibility and CPSP. Patients with small thalamic strokes associated with CPSP were evaluated by atlas-based mapping of magnetic resonance imaging scans, and by somatosensory testing. All lesions involved posterior Vc; two lesions also involved nuclei posterior to Vc, but not VMpo. All patients tested had alterations of cold pain sensation and tactile sensation, as measured by von Frey hairs. Three patients had altered cool sensation, and the patient with the least involvement of Vc had normal cool thresholds, suggesting that a critical volume of Vc must be involved before cool sensation is impaired. Perception of warm was impaired only in lesions involving nuclei posterior to Vc. Heat pain perception was never affected. In a subject with cold allodynia, a single-subject protocol PET study measured the responses to immersion of either hand in a 20°C waterbath. The scan during stimulation of the affected hand was characterized by intense activation of contralateral sensorimotor cortex. Therefore, there are modality-specific subnuclear structures in the posterior thalamus, but lesions of Vc not involving VMpo are sufficient to impair cold sensibility and to produce CPSP. [ABSTRACT FROM AUTHOR]