The theory of the specificity of sensation, proposed at the end of the last century, maintains that each type of sensation is conveyed by a separate anatomical pathway. This theory has been repeatedly questioned. Sir Henry Head postulated the existence of two sets of sensory inputs to the central nervous system (CNS), the epicritic and the protopathic inputs. Epicritic sensation allowed discrimination of touch, temperature, and pain, whereas protopathic sensation was a poorly localized, unpleasant, and long-lasting sensation. This protopathic sensation was physiologically inhibited in the central nervous system by the epicritic system. Head based his conclusions on careful observations of the recovery of sensation after experimental division of his own cutaneous nerves. Later, Trotter and Davies dismissed the theory of epicritic and protopathic sensations after performing equally careful experiments on themselves, maintaining that Head's findings could all be attributed to activity in the regenerating nerve fibers. The debate continues about whether sensation, particularly pain, is the result of a pattern of activity in the afferent sensory pathways or of activity in separate specific channels.
Pain is the consequence of stimulation of pain-sensitive structures and is often an early sign of disease or tissue damage. When pain is the result of physiological activity in the normal pain receptors, and there is no primary dysfunction of the nervous system, it is called nociceptive pain. Nociceptive pain may indicate a disorder in any other system or organ, and its diagnosis and treatment involve different medical specialties. Pain resulting from the dysfunction of the central or peripheral nervous system is called neuropathic pain, ^ and its treatment usually involves the neurological team. Neuropathic pain actually involves different kinds of pain and reflects different pathophysiological mechanisms (see later discussion).
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