Disease/Anatomy-based Classification
It is common clinical practice to classify NP according to the underlying aetiology of the disorder and the anatomical location of the specific lesion.¹ The majority of patients fall into three broad classes: painful peripheral neuropathies (focal, multifocal or generalised, e.g. traumatic, ischaemic, inflammatory, toxic, metabolic, hereditary); central pain syndromes (e.g. stroke, multiple sclerosis, spinal cord injury); and mixed pain syndromes (a combination of nociceptive and neuropathic pain, e.g. chronic low-back pain with radiculopathy) and complex painful neuropathic disorders (complex regional pain syndromes [CRPS]) (see Table 1). One important subgroup of painful polyneuropathies is characterised by a predominant or, in some cases, even isolated affection of small afferent fibres, i.e. unmyelinated Cfibres and small myelinated Aδ-fibres. It is important to realise that conventional electrophysiological techniques assess only the function of myelinated peripheral axonal systems; the affection of small fibres is missed. Therefore, especially in small-fibre neuropathies, alternative diagnostic procedures have to be used).

Signs and Symptoms of Neuropathic Pain
NP is characterised by a variety of sensory symptoms that can be present by themselves or in different combinations. The most typical traits of NP that are often described by patients are burning pain, shooting, electric-shock-like pain and evoked pain (hyperalgesia, allodynia). There is almost always an area of abnormal sensation, and the patient’s maximum pain is often co-extensive with the area of sensory deficit. This is an important diagnostic feature for neuropathic pain. The sensory deficit is usually to noxious and thermal stimuli, which indicates damage to small-diameter afferent fibres or to thespinothalamic tract.

As well as the existence of negative somatosensory signs (deficit in function), there are also positive signs that are characteristic of neuropathic conditions. Paresthesias (ant crawling, tingling) are symptoms typically described by patients that are bothersome but not painful. Painful positive signs are spontaneous (not stimulus-induced) or evoked types of pain (stimulus-induced pain, hypersensitivity). Spontaneous pain is separated into spontaneous ongoing pain, which often has a burning character, and spontaneous shooting, electricshock- like sensations. Evoked types of pain include mechanical hypersensitivity and hypersensitivity to heat and cold. Two types of hypersensitivity can be distinguished. First, allodynia is defined as pain in response to a non-nociceptive stimulus. The most common example is dynamic mechanical allodynia, which means that even gentle stroking of the skin may cause severe pain. Second, hyperalgesia is defined as increased pain sensitivity to a nociceptive stimulus. Another evoked feature is summation, which is the progressive worsening of pain evoked by slow, repetitive stimulation with mildly noxious stimuli, for example a pinprick. A small percentage of patients with peripheral nerve injury have a nearly pure hypersensitive syndrome in which no sensory deficit is demonstrable. Although all of these characteristics are neither universally present in nor absolutely diagnostic of neuropathic pain, the diagnosis of NP is likely when they are present.