Pain

Published on 03/03/2015 by admin

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Last modified 03/03/2015

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Chapter 29

Pain

What is pain?

Pain is highly complex with many interactive dimensions, including physiological, sensory, affective, cognitive, behavioural and psychosocial. The evidence base related to pain is often confusing for the novice therapist because of the different terminology used in different areas of speciality and a lack of clarification between types of pain, the physiological processes involved and the signs and symptoms presented. This section will attempt to summarize the issues surrounding pain, related to the neurologically impaired patient. For more in depth reading, the therapist is referred to the International Association for the Study of Pain (IASP) website (www.iasp-pain.org).

Types of pain

There are three main types of pain experienced by neurologically impaired patients, with patients often presenting with more than one type.

Nociceptive

This type of pain is physiological and arises as a consequence of the activation of nociceptors (pain receptors) following a chemical, thermal or mechanical event. The activation of primary nociceptive afferents by actual or potentially tissue-damaging stimuli is then processed within the nociceptive system (Treede et al. 2008). This type of pain may involve the musculoskeletal system but can also be from a visceral origin. It is important to note that not all nociceptive activation is perceived by the individual as ‘pain’. The perception of an unpleasant experience (pain) is highly subjective. Dystonic pain is associated with abnormal sustained muscle contraction (S3.18), which mediates the activation of nociceptive afferents in the muscles.

Symptoms associated with pain

Central neuropathic pain (CNP)

Unfortunately there are no uniform predictable signs with regard to the clinical presentation of CNP and the descriptions often vary greatly between patients. As a result it is often diagnosed through exclusion of any other source.

The symptoms of CNP occur as a result of CNS damage particularly to the somatosensory system which may lead to disinhibition and central sensitization (Fig. 29.1). With the pain pathway now inappropriately active, activity dependent neural plastic changes occur at the synapses within the whole pathway and may lead to an increase in the cortical representation (sensory homunculus) of the painful part. The timescales within which these neural changes take place and in which the symptoms develop is not clear with different studies stating from 1 month to 5–6 years.

The symptoms produced as a result of disinhibition and central sensitization include: