Volume No : Volume: 01 Issue : 4 Year : 2013 Page No: 1-2
Authors : Vishal A. Chakkarwar
Abstract :
Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage (Merskey and Bogduk, 1994). Pain is felt as a result of the brain's response to electrical (neural) and chemical (hormonal) changes in the body as a result of damage, disease or injury. The propagation of pain is initiated with the activation of physiological receptors, called nociceptors, which are free nerve endings and represent the most distal part of a first-order afferent neuron consisting of small-diameter fibers, with little or unmyelinated, of A-delta or C-type, respectively (Almeida et al., 2004). Nociception consists of four processes: transduction, transmission, perception, and modulation. Transduction is the cellular process by which noxious stimuli are changed into the electrical energy necessary to transmit pain (Fine and Ashburn, 1998). Transmission of the pain impulse along the nociceptor fibers (nerve axons) begins when transduction is complete. During the first segment of transmission, the impulse is carried along nociceptor fibers in an ascending fashion to the dorsal horn of the spinal cord. This is followed by transmission from the spinal cord to the brain stem and thalamus. The thalamus, acting as a relay station, sends the impulse to the cortex where it can be processed (Pasero et al., 1999). Modulation (inhibition and alteration) of pain transmission occurs at several locations within the central nervous system (CNS) (Fine and Ashburn, 1998). The neuronal pathways involved in modulation are often referred to as the descending pain system because they originate in the brain stem and descend to the dorsal horn of the spinal cord (Portenoy and Kanner, 1996). These descending pathways release substances, such as endogenous opioids, serotonin (5HT), and norepinephrine (NE), which can inhibit the transmission of noxious stimuli and produce analgesia (Pasero et al., 1999, 2004). In the endorphinergic system, analgesia is mediated by the binding of endogenous opioid compounds to special subsets of receptors: mu, delta, and kappa.
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