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Unfortunately, the diagnosis of neuropathic pain is often problematic. Clinically, a distinction between nociceptive and neuropathic types of pain is not precise and conditions such as diabetes mellitus, cancer, and neuro- logic diseases with dystonia or spasticity can produce mixed pain pictures [2]. As with other pains, the perception of neuropathic pain is purely subjec- tive, not easily described, nor directly measured. Also, pain pathway re- sponses to damage are not static, but dynamic; signs and symptoms change with pathway activation and responsiveness, and with chronicity. Further, the multiplicity of disorders that have neuropathic pain as a compo- nent of their clinical presentations makes a single underlying pathophysio- logic mechanism unlikely; more than one type of pain, and therefore probably more than one pain mechanism, can occur in a single patient, and some symptoms can be attributed to multiple mechanisms [2,3]. For these and other reasons the current management of neuropathic pain should be mechanistic in approach rather than disease-based [1]. Existing disease- based symptom palliation strategies should be supplemented with ‘‘targeted’’ mechanism-specific pharmacologic management [4].


Despite these complexities, there are several unique features to the clini- cal presentation of neuropathic pain that can be used to support its diagno- sis and should be sought during history taking. In the case of mononeuropathies secondary to trauma, the severity of the pain often ex- ceeds the severity of the inciting injury. CRPS can follow minor skin or joint trauma, bone fractures, or injections. The pain is stimulus-independent and described as ‘‘burning,’’ ‘‘lancinating,’’ ‘‘electric shock–like,’’ ‘‘jabbing,’’ or ‘‘cramping’’; it is often accompanied by pins-and-needles sensations and sometimes by intractable itching (these are considered positive symptoms). These symptoms don’t adhere to specific peripheral nerve distributions and often begin and remain most pronounced distally. The pain may be worse at night or during cold, damp weather, and is exacerbated by move- ment of the affected limb. Multiple types of pain (constant pain with parox- ysms and stimulus-evoked pains) can be experienced simultaneously. It is useful to separate stimulus-independent and stimulus-evoked pains to differ- entiate ongoing from provoked activities [3]. Spread of symptoms outside the initial site of injury is common; in the case of unilateral pain there may be spread to homologous sites in the opposite limb (mirror pain). Pos- itive and negative (numbness, loss of sensation) symptoms can occur con- currently and can be accompanied by autonomic symptoms. Spontaneous pain, often without complaints of sensory loss, is a feature of the cranial mononeuralgiasdtrigeminal, glossopharyngeal, and post-herpetic. Of course, location, intensity, and duration of pain are extremely important.

In generalized polyneuropathies, rapid progression solely affecting sen- sory fibers is more likely to be painful, especially if inflammation and

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