How Is Neuropathic Pain Assessed?

Today's post from paineurope.com (see link below) is a slightly difficult to understand look at how neuropathy is currently assessed. If you can take the time to work your way through it, there is quite a bit of useful information. The conclusion is that communication between scientists/researchers and doctors/clinicians should be better, to achieve an optimum treatment path for patients and the suggestion is that current assessment techniques based on pain-scales could benefit from being refined and modernised.

Assessment of neuropathic pain
Written by Dr Mike Bennett Published 1 July 2013

Neuropathic pain is pain that arises from a disturbance of function or pathological change in a nerve, explains Dr Mike Bennett

Neuropathy is a disturbance of function or pathological change in a nerve.1 Neuropathic pain, therefore, is pain that arises from this process and occurs as a result of dysfunction or injury to peripheral nerves, posterior roots, spinal cord and the brain2,3 (Table 1). Evidence suggests that it is a result of various pathophysiological mechanisms. The most important of these relate to ectopic impulse formation, hyperexcitability and loss of inhibitory control.

Clinical features

A clinical diagnosis of neuropathic pain should be made only when the distribution of pain and the associated sensory abnormalities point to a neurological condition in a clinical context.4 Put simply, neuropathic pain is pain that often occurs in an area of abnormal or absent sensation. Classically, patients complain of spontaneous pains (without detectable stimulation) and evoked pains (abnormal responses to stimuli).

Spontaneous pains can be continuous (steady and ongoing) or paroxysmal (episodic and intermittent). Descriptions of cutaneous pain are often in terms of dysaesthesias (pain from stimuli not usually painful), ie burning, cutting, pricking, tingling and stabbing. However, deep pains can be described ascramping, aching, throbbing and crushing. Paroxysmal pain is usually described in terms of shooting,stabbing, lancinating or jabbing. The incidence of these features is variable and ranges from absence in some to a full spectrum of descriptions in others.

Evoked pains have been summarised as exaggerated responses to stimuli with either reduced pain threshold (allodynia), normal pain threshold (hyperalgesia) or increased pain threshold (hyperpathia).5

Put simply, neuropathic pain is pain that often occurs in an area of abnormal or absent sensation

Allodynia is a common feature and three types of neuropathic allodynia are thought to exist based on the initiating stimulus – mechanical (tactile), thermal (warm and cold) and movement. Mechanical and thermal allodynia are exclusively disorders of cutaneous sensibility. Mechanical allodynia can be induced by punctate stimuli (static mechanical allodynia) or more commonly by stroking movements (dynamic mechanical allodynia). Hyperalgesia is a painful sensation of abnormal severity following a noxious stimulus and is an augmented response to the same modality stimulus (a quantitative abnormality).1

Allodynia and hyperalgesia frequently co-exist and it can be difficult to differentiate the two.6 Both are reported to be pathognomonic of neuropathic pain, but are in fact also associated with tissue damage and inflammation.7 However, when associated with chronic pain, these phenomena are most likely to represent a neuropathic mechanism. Hyperpathia is characterised by temporal abnormalities such as increased reaction to a stimulus, particularly a repetitive stimulus, as well as an increased threshold. Prolonged painful after sensations are also a feature. Spatial abnormalities such as dyslocalisation and radiation are other features of
neuropathic pain.4

Autonomic dysfunction can result in a wide range of vasomotor and sudomotor signs. Blood flow, skin temperature and sweating can all be increased or decreased and vary within, as well as between, patients. Trophic changes are late signs of autonomic dysfunction.

Diagnosis of neuropathic pain

The demonstration of nerve dysfunction is important corroborating evidence in the diagnosis of neuropathic pain. Nerve dysfunction in this context can be represented by sensory, motor or autonomic dysfunction attributable to a discrete neurological lesion.2 In order to make sense of neuropathic signs, Ochoa has suggested that the features of a neuropathy depend on whether the process produces positive or negative phenomena8 (Figure 1). Positive phenomena in neuropathic pain are diverse and are a combination of evoked pains and sensations.

Figure 1. Organisational chart of clinical features of neuropathic pain
 
Clinicians base their diagnosis of neuropathic pain on a combination of symptoms and examination evidence suggestive of nerve dysfunction. The latter has proved challenging because pain is a subjective phenomenon and traditional tests, such as vibrametry and nerve conduction studies have only measured function in large myelinated fibres. More recently, neurophysiological tests have been developed that enable clinical assessment of the peripheral and central nociceptive system. However, abnormalities detected by these tests only provide the clinician with a surrogate marker of neuropathic pain.

Alternative approaches for investigation have focused on the development of standardised assessment tools largely based on a patient’s symptoms. Although verbal descriptor lists have been used to identify specific neuropathic pain descriptors, these have not been successfully tested for their discriminatory ability.9

The Neuropathic Pain Scale (NPS) consists of 10 verbal descriptions each rated on an 11-point numerical rating scale.10 It was developed from clinical experience and used single descriptors to discriminate between four diagnostic categories of neuropathic pain. Only postherpetic neuralgia could be distinguished from the other diagnostic groups (reflex sympathetic dystrophy, diabetic neuropathy and peripheral nerve injury). The NPS was not used to discriminate between neuropathic pain and nociceptive pain symptoms. More recently it had been shown to be sensitive to treatment changes.11

The Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) pain scale is a seven-item pain scale consisting of five symptom items and two examination items administered by a clinician in an interview format.12 Its purpose is to assess the probability that a patient’s pain is dominated by neuropathic mechanisms and does not assess severity. It is the only published tool with discriminant validity in the setting of neuropathic and nociceptive pain irrespective of disease-based diagnostic categories.
Relating pain assessment to treatment

The identification of neuropathic pain mechanisms has long been considered important to direct treatment. Specific neuropathic pain scales have been important in this quest, but much work remains to be done on relating specific symptoms to specific mechanisms. This will rely on more dialogue between basic scientists and clinicians. Until this is achieved, we await a consensus on the classification and assessment of neuropathic pain.13,14
Dr Mike Bennett, senior clinical lecturer in palliative medicine at St Gemma’s Hospice and University of Leeds, Leeds, UK

http://www.paineurope.com/articles/assessment-of-neuropathic-pain