The initial injury or damage to the body begins the transduction process where an electrical signal from the nociceptors relays information of tissue damage through to the grey matter from the spinal cord to the thalamus and the cerebral cortex in the brain, all via the ascending pathway. (Renn and Dorsey, 2005:280) During this process neurotransmitters have the ability to increase or decrease the perception of pain experienced by the individual. (Brigg, 2010:35) This initial injury causes cells to release a number of chemical mediators such as histamine, bradykinin, prostaglandins, serotonin and endorphins (Briggs, 2010:35). These neurotransmitters cause nerve endings to become sensitized to the pain signal which result in an inflammatory response and assist in the wound healing process. (Crisp and Taylor, 2005:1185).
The second stage in the pain pathway is the transmission stage where the pain signal is relayed to the dorsal.
horn in the spinal cord via both the A-delta and C-delta fibres which are both types of peripheral nerve fibres that ascend to the brain (Briggs, 2010:36) Type A – delta fibres are myelinated and carry the sensation of fast pain, known as acute pain. This sensation transmits Pin impulses rapidly which directly results in sharp, stabbing pain experience. C –delta fibres are smaller, unmyelinated fibres that conduct much slower transmission and generally create a dull, persistent, aching pain, also known as chronic pain. Transmission of the pain stimulus continues until it reaches the dorsal horn in the spinal cord. The dorsal horn processes the pain signals and can enhance or inhibit it. The neurotransmitters assist the pain impulse travel between nerves by excitation of the synapses between neurons and also by increasing depolarization of cells. (Crisp and Taylor, 2005: 1186) .
The third stage of the pain pathway is modulation, which can be influenced by a number of mechanisms that either decrease or increase the pain impulse (Kuttner, 2010).
