Difference between revisions of "Pain"
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==What is Pain?== | ==What is Pain?== | ||
| − | '''''Nociception''''' is the process of neurotransmission that transmits and processes information relating to tissue damage. It originates from sensory receptors known as ''nociceptors''. | + | |
| + | '''''Nociception''''' is the process of neurotransmission that transmits and processes information relating to tissue damage. It originates from sensory receptors known as ''nociceptors''. ''Pain'', on the other hand, is a conscious experience arising from nociception. It has previously been described as: | ||
# "An unpleasant sensory or emotional experience associated with actual or potential tissue damage." (International Association for the Study of Pain, 1978). | # "An unpleasant sensory or emotional experience associated with actual or potential tissue damage." (International Association for the Study of Pain, 1978). | ||
# "A multidimenstional experience produced from characteristic neurosignature patterns arising from nerve impulses generated by a widely distributed neural network located in the brain. These neurosignatures can be generated independently of somatosensory input". (Melzack, 1999). | # "A multidimenstional experience produced from characteristic neurosignature patterns arising from nerve impulses generated by a widely distributed neural network located in the brain. These neurosignatures can be generated independently of somatosensory input". (Melzack, 1999). | ||
==Physiology and Pathophysiology of Pain Transmission== | ==Physiology and Pathophysiology of Pain Transmission== | ||
| − | Two types of nocieptive fibres (neurons) exist. C-fibres are slow-conducting and unmyelinated, whereas A-delta-fibres are small, fast-conducting, myelinated structures. The cell bodies of these neurons are located in the dorsal root ganglion, and the neurons are bipolar. The sensory nerve endings conduct afferent impulses to the cell body, and fibres then extend to the dorsal horn of the spinal cord. Here, ascending information is transmited to the | + | |
| + | Two types of nocieptive fibres (neurons) exist. C-fibres are slow-conducting and unmyelinated, whereas A-delta-fibres are small, fast-conducting, myelinated structures. The cell bodies of these neurons are located in the dorsal root ganglion, and the neurons are bipolar. The sensory nerve endings conduct afferent impulses to the cell body, and fibres then extend to the dorsal horn of the spinal cord. Here, ascending information is transmited to the cortext via several "relay stations", including the thalamus, the reticular formation, the pons and the amygdala. These modulate the signal on its journey towards conscious perception. Local reflex arcs may also be stimulated in the dorsal horn, producing spinal reflexes such as the withdrawal reflex. | ||
There is a large amount of plasticity in the pain transmission system: modulation of nociceptive transmissions occurs at every level, from the periphery to the cortex. This modulation may be ascending or descending, short-term or [[#Chronic pain|persistent]]. It has the ability to change the pain sensation from a protective, physiological response into a more pathological one, where pain is perceived in the abscence of tissue damage or may persist once the noxious stimulus has subsided. | There is a large amount of plasticity in the pain transmission system: modulation of nociceptive transmissions occurs at every level, from the periphery to the cortex. This modulation may be ascending or descending, short-term or [[#Chronic pain|persistent]]. It has the ability to change the pain sensation from a protective, physiological response into a more pathological one, where pain is perceived in the abscence of tissue damage or may persist once the noxious stimulus has subsided. | ||
===Sensitisation=== | ===Sensitisation=== | ||
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| − | + | Two phenomena may occur: | |
| − | * | + | * '''Hyperalgesia''' - an e |
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==Physiological Effects== | ==Physiological Effects== | ||
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Pain has adverse physiological effects, which include metabolic and cardiac effects. | Pain has adverse physiological effects, which include metabolic and cardiac effects. | ||
===Metabolic Effects=== | ===Metabolic Effects=== | ||
| − | Pain may activate the stress response and hence hormone secretion from the pituitary glands, adrenal glands and pancreas. This leads to substrate mobilisation and catabolism, particularly protein wasting. These effects can impair wound healing, and in the long term result in | + | |
| + | Pain may activate the stress response and hence hormone secretion from the pituitary glands, adrenal glands and pancreas. This leads to substrate mobilisation and catabolism, particularly protein wasting. These effects can impair wound healing, and in the long term result in immunosupression. They can also cause a negative energy balance, giving weight loss or poor growth in young animals. It is important to bear this fact in mind when considering the economics of analgesia in food animal production. | ||
===Cardiovascular Effects=== | ===Cardiovascular Effects=== | ||
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Pain can cause '''hypertension''' and '''tachycardia'''. This is of particular importance in surgical scenarios: poor peri-operative pain management will contribute to poor recovery from anaesthesisa and increase the risk of post-operative complications. | Pain can cause '''hypertension''' and '''tachycardia'''. This is of particular importance in surgical scenarios: poor peri-operative pain management will contribute to poor recovery from anaesthesisa and increase the risk of post-operative complications. | ||
===Chronic Pain=== | ===Chronic Pain=== | ||
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Severe or persistent pain can lease to pathophysiological "chronic" pain. Increased risks of auto-mutilation or wound biting are associated with this, proving proper peri-operative pain relief again to be very important. | Severe or persistent pain can lease to pathophysiological "chronic" pain. Increased risks of auto-mutilation or wound biting are associated with this, proving proper peri-operative pain relief again to be very important. | ||
==Assessment of Animal Pain== | ==Assessment of Animal Pain== | ||
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Revision as of 16:59, 25 February 2009
What is Pain?
Nociception is the process of neurotransmission that transmits and processes information relating to tissue damage. It originates from sensory receptors known as nociceptors. Pain, on the other hand, is a conscious experience arising from nociception. It has previously been described as:
- "An unpleasant sensory or emotional experience associated with actual or potential tissue damage." (International Association for the Study of Pain, 1978).
- "A multidimenstional experience produced from characteristic neurosignature patterns arising from nerve impulses generated by a widely distributed neural network located in the brain. These neurosignatures can be generated independently of somatosensory input". (Melzack, 1999).
Physiology and Pathophysiology of Pain Transmission
Two types of nocieptive fibres (neurons) exist. C-fibres are slow-conducting and unmyelinated, whereas A-delta-fibres are small, fast-conducting, myelinated structures. The cell bodies of these neurons are located in the dorsal root ganglion, and the neurons are bipolar. The sensory nerve endings conduct afferent impulses to the cell body, and fibres then extend to the dorsal horn of the spinal cord. Here, ascending information is transmited to the cortext via several "relay stations", including the thalamus, the reticular formation, the pons and the amygdala. These modulate the signal on its journey towards conscious perception. Local reflex arcs may also be stimulated in the dorsal horn, producing spinal reflexes such as the withdrawal reflex.
There is a large amount of plasticity in the pain transmission system: modulation of nociceptive transmissions occurs at every level, from the periphery to the cortex. This modulation may be ascending or descending, short-term or persistent. It has the ability to change the pain sensation from a protective, physiological response into a more pathological one, where pain is perceived in the abscence of tissue damage or may persist once the noxious stimulus has subsided.
Sensitisation
Two phenomena may occur:
- Hyperalgesia - an e
Physiological Effects
Pain has adverse physiological effects, which include metabolic and cardiac effects.
Metabolic Effects
Pain may activate the stress response and hence hormone secretion from the pituitary glands, adrenal glands and pancreas. This leads to substrate mobilisation and catabolism, particularly protein wasting. These effects can impair wound healing, and in the long term result in immunosupression. They can also cause a negative energy balance, giving weight loss or poor growth in young animals. It is important to bear this fact in mind when considering the economics of analgesia in food animal production.
Cardiovascular Effects
Pain can cause hypertension and tachycardia. This is of particular importance in surgical scenarios: poor peri-operative pain management will contribute to poor recovery from anaesthesisa and increase the risk of post-operative complications.
Chronic Pain
Severe or persistent pain can lease to pathophysiological "chronic" pain. Increased risks of auto-mutilation or wound biting are associated with this, proving proper peri-operative pain relief again to be very important.