| Abstract: | Afferent neurons from thalamic median and intralaminar (IL) nuclei arise in the spinal cord, brain stem synapses, substantia nigra, internal pallidum and cerebral cortex, directly and through the intermediary of the reticular nucleus of the thalamus (RT). Efferent neurons terminate in the anterior thalamic nuclei, RT, striatum and cerebral cortex. Tracking methods in the rat have demonstrated that some RT neurons which project towards the IL are surrounded by endings from the posterior ventral nucleus (VP). Electrical stimulation of multiple prosencephalic structures (mainly VP) and of sensory pathways induce responses in IL of brief latency followed by inhibition. Whereas the responses appear to be related to activation of excitatory projections (under the tonic facilitating control of cerebral cortex) the inhibition phases could be related to activation of RT, since they disappear after lesion of the RT. This nucleus could act as a common final pathway of inhibitions exerted on IL in the rat. Studies in this species have demonstrated that a lateral lesion of the thalamus that includes the RT provokes the appearance in IL of abnormal neuronal hyperactivity of a tonic nature and yet still exaggerated by stimuli normally capable of inducing responses of brief duration followed by inhibition. Human studies using a tomoscintigraphic method to determine regional blood flow have shown "hyperactivity" of the thalamic region in patients with pain of central origin during a natural stimulus provoking hyperpathia. This was not observed during painful states without hyperpathia. The working hypothesis proposed is that of a central lesion inducing a hyperpathia provoking pathologic hyperactivity in certain thalamic nuclei.(ABSTRACT TRUNCATED AT 250 WORDS) |
