The Royal Marsden Hospital Manual of Clinical Nursing Procedures - Lisa Dougherty [330]
Nociceptive pain
Nociceptive pain is the ‘normal’ pain pathway that occurs in response to tissue injury or damage (Figure 9.8). It consists of four components: transduction, transmission, perception and modulation. Nociceptors are free nerve endings found at the end of pain neurones. They are found in skin and subcutaneous tissue, muscle, visceral organs, tendons, fascia, joint capsules and arterial walls (Godfrey 2005). Nociceptors respond to noxious thermal stimuli (heat and cold) and mechanical stimuli (stretching, compression, infiltration) and to the chemical mediators released as part of the inflammatory response to tissue injury. These chemical mediators include prostaglandins, bradykinin, substance P, serotonin and adenosine. As a result of this stimulation process, an action potential is generated in the nerve (transduction).
Figure 9.8 Processing of sensory input and motor output by the spinal cord.
Reproduced from Tortora and Derrickson (2009).
The pain signal is then transmitted along the peripheral nervous system (A delta and C fibres) to the central nervous system, arriving at the dorsal horn of the spinal cord. Neurotransmitters are released to allow the pain signal to be transmitted from the endings of the peripheral nerves to the nociceptors in the dorsal horn. The message is then transmitted to the brain where perception of the pain occurs (transmission). Perception is the end-result of the neuronal activity of pain transmission. The perception of pain includes behavioural, psychological and emotional components as well as physiological processes.
Modulation occurs when the transmission of pain impulses in the spinal cord is changed or inhibited. Modulatory influences on pain perception are complex, involving a gating system which is linked to a descending modulatory pathway. Modulation can occur as a result of a natural release of inhibitory neurotransmitter chemicals that inhibit transmission of pain impulses and therefore produce analgesia. Other interventions, including distraction, relaxation, sense of well-being, heat/cold therapy, massage and TENS, can also help to modulate pain perception. Analgesic medications work by inhibiting some of the chemicals involved in pain transduction and transmission and thus modulating pain perception (Figure 9.9). Pain signals can also be increased by certain factors such as anxiety, fear and low mood/depression.
Figure 9.9 The pain pathway showing key sites for particular analgesic interventions.
Neuropathic pain
Neuropathic pain is not pain that originates as part of ‘normal’ pain pathways. It has been described as pain related to abnormal processing within the nervous system (Mann 2008). Nerve injury or dysfunction can be caused by a range of conditions such as infection, trauma, metabolic disorder, chemotherapy, surgery, radiation, neurotoxins, nerve compression, joint degeneration, tumour infiltration and malnutrition (Mann 2008).
The mechanisms by which neuropathic pain is generated and maintained are not fully understood but the following theories are currently thought to contribute.
Damage or abnormalities in the nerves change the way that nerves communicate with each other.
Pain receptors require less stimulation to initiate pain signals both in peripheral nerves and the central nervous system, where it is often referred to as central sensitization.
Pain transmission is altered from its normal sequence.
There may be an increase in the release of chemical neurotransmitters.
There can be increased and chaotic firing of nerves.
Damaged nerves spontaneously generate impulses in the absence of any stimulation.
The descending inhibitory systems may also be reduced or lost.
These mechanisms result in increased activity or transmission of pain signals despite less input from the peripheral nervous system. Pain can be spontaneous, may be triggered