Difference between revisions of "Pain"

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==What is Pain?==
 
==What is Pain?==
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'''''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:
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'''''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==
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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 cortex via several "relay stations", including the [[Forebrain - Anatomy & Physiology|thalamus]], the reticular formation, the [[Hindbrain - Anatomy & Physiology#Pons|pons]] and the amygdala. These modulate the signal on its journey towards conscious perception. Local [[Reflex Arcs - Anatomy & Physiology|reflex arcs]] may also be stimulated in the dorsal horn, producing spinal reflexes such as the withdrawal reflex.
 
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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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Hypersensitisation of the pain transmission can occur at any level of the neuraxis. This can result in two phenomena: '''hyperalgesia''', where an exaggerated response to a noxious stimulus is experienced, and '''allodynia''', where a non-noxious stimulus (such as gentle touch) elicits a painful response.
 
  
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Sensitisation can arise:
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==Physiological Effects==
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* Peripherally, giving '''peripheral sensitisation'''.
 
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** Type A and C peripheral nociceptors are sensitised due to inflammatory mediators released by tissue damage. This lowers the response threshold of the receptors, or a greater response to the same stimulus is produced. Both mechanisms may work in conjunction.
 
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* Centrally, giving '''central sensitisation'''.
 
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** The excitability of spinal nociceptive neurons is enhanced, giving a hypersensitive and hyperactive nociceptive transmission system.
 
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** Central sensitisation may be short-lived when it is associated with transient changes in neurotransmitter activity.
 
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** Central sensitisation may be long-lived when it is associated with phenotypic changes in central neurons.
 
  
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==Physiological Effects==
 
 
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===
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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 immunosuppression. 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.
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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.
 
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===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.
 
  
 
==Assessment of Animal Pain==
 
==Assessment of Animal Pain==
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Assessment of pain in animals is neither easy nor, often, intuitive. Usually, vets make observations of behaviour in order to assess their patients' well-being. They must however bear in mind that pain is a subjective experience that varies greatly between individuals. The expression of pain behaviour is also highly species specific. Pain behaviour is influenced by many extrinsic factors, such as previous conditioning, social dominance and overall health status, which may contort the observations. Finally, since animals cannot verbally describe their pain, bias of the observer is inevitable. Therefore knowledge of an individual's behaviour and the assessor's observational skills and attitude towards pain will influence how pain is assessed and consequently managed.
 
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Pain-associated behaviour differs between species. Physiological variables are useful parameters for giving an indication of pain, but may also be influenced by many other factors such as concurrent disease, stress and drug therepy. They are therefore not reliable measures of pain when used in isolation.
 
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When assessing pain in animals, it is useful to assume that humans an animals are closely related in terms of pain perception and anticipation in order to provide the correct management. Subtle as well as obvious indicators of pain should also be considered, particularly in obtunded animals as invasive procedures, trauma and many medical illnesses may render the animal unable to demonstrate explicit pain behaviour. However, the best diagnostic indicator for pain is response to appropriate [[Analgesic Drugs|analgesia]].
 
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==Analgesics==
 
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Analgesia can be defined as the absence of pain. The term 'analgesics' commonly refers to drugs that produce analgesia. They are categorised into two specific types according to their mode of action:
 
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*[[Systemic Analgesia|Systemic analgesia]] refers to the use of certain analgesic drugs that act at the appropriate receptor found within the entire body. Drug classes include opioids, non-steroidal anti-inflammatories (NSAIDS), as well as ketamine and gabapentin.
 
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*[[Local Analgesia|Local analgesia/anaesthesia]] is used to desensitise a particular region of the body using techniques such as local infiltration, epidurals, paravertebral and specific nerve blocks, and intravenous regional anaesthesia
 
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[[Category:Anaesthesia]]
 
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[[Category:Analgesia]]
 

Revision as of 16:31, 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:

  1. "An unpleasant sensory or emotional experience associated with actual or potential tissue damage." (International Association for the Study of Pain, 1978).
  2. "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

Sensitisation

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

Assessment of Animal Pain

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