[Pain]

This text reports the 'introduction remarks' of Professor Ochoa at the inauguration of a Symposium on Pain at the Spanish Neurology Society. Profoundly, but as clearly as possible, the author expounded on the nociceptors to the cerebral cortex, the structures involved in senso-perception--and emotion--which are to be taken into consideration. Some basic facts are: 1. The functional characterization of different nociceptors. 2. The existence of usually 'silent' nociceptors which are only activated under certain conditions. 3. The enumeration of the zones of the posterior horn which are 'specific' for nociception: lamina I and the external zone of lamina II. 4. The great feature of lamina V, with a population of convergent neurones, which receive both tactile and nociceptive stimuli. 5. The contrast between the postero-ventral thalamic nucleus (touch, pain, etc.) and the internal or 'medial' thalamic sectors, which are involved in the most crude and aggravating pain and in the course of impulses which predispose to pathological emotional experiences. This thalamic sector does not generate pain when stimulated under normal conditions, but may do so when the patient has pain of central origin, in which case the condition--sometimes complex--of desafferentization may be assessed. We point out that both the classically named causalgia and the central algias (thalamic, due to pathology of the brainstem and cortico-subcortical lesions) have similar aspects: burning pain with paroxystic exacerbations, sensory defects, hyperpathia and adodynia. We also mention the complex inhibitory effects of impulses conducted by large diameter myelinated fibres or nociceptive effects at different levels. Reference was not made to centrifuge systems (endogenous opiates etc.) which inhibit pain. References 1, 3, 6 and 9 include a considerable quantity of bibliography.