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:

Hyperalgesia

This is an increased sensitivity to pain.

Allodynia

This is pain perceived following a non-noxious stimulus which does not normally provoke pain (e.g. touch, heat or non-noxious cold). This is common (90%) in central neuropathic pain (Widar et al. 2002).

Hyperpathia

This is an unpleasant, prolonged post-stimulus reaction.

Dysaesthesia

This is an unpleasant abnormal sensation. For example, burning, wetness, itching, electric shock, pins and needles. This is common in CNP (80%) (Attal et al. 2008).

Paraesthesia

This is an abnormal but not unpleasant sensation.

Behaviour of CNP symptoms

The symptoms of CNP may be spontaneous when they present from no apparent source, evoked as an over-reaction to a wide variety of stimuli, persistent (consistent/permanent) or paroxysmal (temporary).

Distribution of neuropathic pain

Peripheral neuropathic pain: In PNS lesions the pain distribution will conform to the cutaneous innervation of the peripheral nerve, the branches of the brachial or lumbar plexus, or spinal roots (dermatomes).

Central neuropathic pain: In CNS lesions the pain distribution will conform to the topographical representation of the brain area that has been injured by the lesion (i.e. the sensory homunculus). However, as central sensitization is one of the mechanisms that contributes to neuropathic pain, abnormal expansions of the sensory map should be expected.

Central neuropathic pain in neurologically impaired patients

Although neurological conditions result from very different pathophysiology, the pathological processes involved can still be identified as causal in producing CNP. For example, demyelination in MS, compromised circulation in CVA and disruption of spinal cord transmission in SCI can all involve damage to the somatosensory system and therefore produce CNP.

Recent studies have also highlighted a further process that may contribute to CNP which involves the action of glial cells following a CNS lesion. In SCI and MS, inflammatory changes initiated in response to cell damage promote the release of inflammatory mediators and growth hormones by glial cells. If these chemical mediators affect the pain pathway, central sensitization may be enhanced (Svendsen et al. 2005). Although this has not been reported in CVA, it is likely that a similar mechanism takes place following the initial lesion and the resultant inflammatory response.

In PD the mechanism of CNP may be different. In healthy individuals the basal ganglia (S2.11) is now thought to play a significant role in the integration of sensory information and hence the modulation of pain (Juri et al. 2009). In PD the pathophysiology of pain has been linked to a disruption of the basal ganglia’s (striatum) ability to filter the vast amounts of sensory information in order to select an appropriate movement programme. This filtering is normally facilitated by the inhibitory dopaminergic neurons, however as the latter undergoes neurodegeneration in PD its effect is reduced. This may explain why pain may be relieved when in an ‘on’ period (i.e. taking L-Dopa).

Why do I need to assess pain?

While the available knowledge about pain, its physiology and pathophysiology has increased enormously over the last 20 years, it appears to have been largely ignored in respect to patients with neurological deficits. Pain in this population requires recognition as it has been shown to impact significantly on the patient’s quality of life and on the rehabilitative process (Henon 2006).

The incidence of pain in neurologically impaired patients is high, with reports of up to 74% in CVA and SCI; 50–85% in MS and between 40% and 75% in PD. A further breakdown of the different types of pain presented in these conditions can be seen in Tables 29.1–29.3

Table 29.1

Incidence of different types of pain in cerebrovascular accident

Nociceptive pain	5–84%
Shoulder pain	30–40%
Chronic pain	11–55%
Central neuropathic pain	2–35%
Central post-stroke pain	8–46%

Widar et al. 2002; Jönsson et al. 2006; Lindgren et al. 2007; Kong and Woon 2004; Appelros 2006; Kumar and Soni 2009.

Table 29.2

Incidence of different types of pain in Parkinson’s disease

Nociceptive pain	40–70%
Non-dystonic	37.8%
Dystonic	6.7–40%
Peripheral neuropathic pain	10%
Central neuropathic pain	4.5–30%

DeFazio and Tinazzi 2009; Beiske et al. 2009; Djaldetti et al. 2004.

Table 29.3

Incidence of different types of pain in multiple sclerosis

Nociceptive pain	21% (1% related to spasticity)
Peripheral neuropathic pain	1%
Central neuropathic pain	27.5% (87% in LL: 31% in UL)
Abnormal response to pain and temperature	98%

Osterberg et al. 2005.

How do I assess pain?

Pain in the neurologically impaired patient is often complex and should be assessed thoroughly. The following offers a brief overview of the main considerations when assessing pain. Initially the therapist should try to establish the type of pain experienced by the patient, remembering that this population often have pain of more than one type.

Subjective assessment

Onset of pain

Question about the time of onset and any causal event linked to onset.

Area of pain

Identify a location of pain from the patient. This will help to start focusing in on certain structures. However, referred pain away from the origin of the pain means that this information cannot be relied upon completely. If pain reports are diffuse and widespread, the therapist may start to suspect central neuropathic or psychogenic pain.

Behaviour of the symptoms

This questioning should include the pattern of pain in terms of the 24-hour day and any factors that increase or decrease their symptoms (known as aggravating and easing factors). The acronym SIN is often used to represent other information that should be sought:

Severity of the pain (intensity). See visual analogue scale below.

Irritability of the pain, how long does it take for pain to reduce to previous level after a stimulus is removed?

Nature of the pain, a description of the symptoms of pain experienced.

Does the patient describe their pain using adjectives that are typically linked with physiological mechanisms? For example, a dull ache which is difficult to localize (muscle, ligament, joint capsule pain); morning pain that improves with activity (chronic inflammation/oedema); bizarre descriptions of pins and needles; wetness (central neuropathic pain); a sharp or burning pain or a line of pain (peripheral neuropathic pain).

Does the patient report a pattern of pain behaviour? The description of a typical pattern of pain behaviour may help identify a nociceptive origin. No pattern of pain behaviour may indicate a central neuropathic or psychogenic origin.

Does the patient report an irritable condition? The therapist will need to take care during the assessment and treatment not to aggravate their symptoms.

Visual analogue scale (VAS)

The VAS allows the therapist to assess the patient’s perception of their pain in terms of intensity/severity. This test can be carried out on initial assessment and during follow-up treatments to monitor the level of pain in relation to the effectiveness of interventions.

Patient

Patient should be seated comfortably at a table.

Therapist

1. The therapist draws a horizontal line on a piece of paper 10 cm long. The left hand end indicates a 0 score (no pain) and the right hand end a 10 score (the worst pain imaginable) (Fig. 29.2).

Figure 29.2 Visual analogue scale.

2. The patient is requested to rate their perceived pain intensity at that moment in time by making one mark on the line between the two extreme scores.

3. The therapist can then measure along the line from 0 to the point where the patient placed their mark. This value can be used as a quantitative marker for future evaluation.

The Neuropathic Pain Symptom Inventory (NPSI)

The Neuropathic Pain Symptom Inventory (NPSI) (Bouhassira et al. 2004) presents a broad overview of central neuropathic pain symptoms and may be useful to use as a reference source to assist the novice practitioner in identifying the signs of central neuropathic pain from the subjective assessment. Although it is often possible to diagnose neuropathic pain on the basis of history, a clinical examination is also essential (Treede et al. 2008).

Objective assessment

Observation

As the perception of pain is subjective, the therapist should also look for other signs and behaviours which may indicate pain. This process can be ongoing from the time the patient enters the department until the time they leave:

a. Muscle spasm guarding an area

b. Facial grimacing and either increased or decreased vocalizations during movement

c. Poor posture

d. Decreased range or altered patterns of movement

e. Altered muscle tone (S3.21)

f. Dystonia (S3.18)

g. Altered appetite and weight

h. Anxious and stressed. These factors may exacerbate pain

i. Fatigue/exhaustion. This may reflect a lack of sleep due to pain

j. Low mood and poor concentration. Depression may also exacerbate pain

k. Socially withdrawn.

Distribution of pain and other sensations

Assessment of:

• Pin prick testing (S3.23)

• Temperature testing (S3.23)

• Light touch testing (S3.23).

Does the patient exhibit an increased sensitivity to pain? This is hyperalgesia.

Does the patient exhibit a decreased sensitivity to pain? This is hypoalgesia.

Does the patient exhibit an abnormal pain response to a non-noxious stimulus? This is allodynia.

Does the patient report an unpleasant abnormal sensation? (e.g. burning, wetness, itching, electric shock, pins and needles). This is dysaesthesia.

Does the pattern of pain conform to the specific distribution of dermatomes or peripheral nerves? Yes. This is peripheral neuropathic pain. If not it is likely to reflect central neuropathic pain.

Differential diagnosis of nociceptive pain

At this stage the therapist may have made a reasoned decision as to the type of pain (nociceptive, peripheral or central neuropathic) being experienced by the patient.

If the patient’s pain is considered to be of nociceptive origin, a comparison of the findings from AROM (S3.23) and PROM (S3.23) and special clinical tests will allow the therapist to differentiate the structures implicated. In each case, the therapist is evaluating the reproduction of the patient’s pain in order to identify the source. Further comprehensive detail guiding differential diagnosis can be found from a range of musculoskeletal based texts.

Caution