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ischemia are prominent pathological features, as occurs in the vasculitides [2]. In painful polyneuropathies, eg, idiopathic small-fiber neuropathy, dia- betic polyneuropathy with predominant small-fiber (Ad- and C-fibers) dam- age, the ‘‘burning,’’ ‘‘lancinating,’’ ‘‘jabbing’’ pains with pins-and-needles sensations are nerve-length dependent and bilaterally symmetric, beginning distally in the feet. With worsening, symptoms ascend to involve more prox- imal portions of the lower extremities and may eventually affect the hands. This centripetal progression can also occur in intercostal nerve distributions, beginning anteriorly over the midline of the torso with later symmetric lat- eral extension to the flanks. Autonomic complaints, eg, abnormal sweating, impotence, orthostatic hypotension, and gastrointestinal symptoms, are frequent.

Clinical examination

Among the more common and important clinical signs in neuropathic pain disorders are positive sensations: stimulus-evoked hypersensitivities such as allodynia to innocuous stimulation, eg, light touch and cold, and hy- peralgesia to noxious stimulation, eg, pinprick. They occur focally in mono- neuropathies and distally and symmetrically in polyneuropathies. Various forms of hyperalgesia have been described, including touch-evoked (or static) mechanical hyperalgesia to gentle pressure, pinprick hyperalgesia, blunt pressure hyperalgesia, and punctate hyperalgesia that increases with repetitive stimulation (windup-like pain) [2,3]. Paradoxically, these hyper- sensitivities can occur in areas in which the patient also complains of and demonstrates loss of sensation. There can be persistence of stimulus-evoked pain after the stimulus has been withdrawn (aftersensation) in the same an- atomic distributions. As with symptoms, spread of allodynia and hyperalge- sia outside the original site of injury is common and may extend to homologous sites in the opposite limb. Focal autonomic abnormalities after nerve injury, especially of sweating, skin temperature, and skin color, in con- junction with the aforementioned pain, fulfill the diagnostic criteria of CRPS (vide infra). With chronicity, trophic changes of the skin and nails de- velop, as do motor symptoms such as weakness, tremor, and dystonia. Nerve percussion at points of compression, entrapment, or irritation can elicit pins-and-needles or ‘‘electrical’’ sensations (Tinel’s sign).

In small-fiber neuropathies, deficits are found in thermal and pain percep- tions and sometimes touch, whereas large-fiber functions, eg, muscle strength, reflexes, and perception of vibratory and proprioceptive stimuli, are normal. In combined large- and small-fiber polyneuropathies, all these functions are compromised. Symmetrical distal autonomic dysfunction is often present but rarely severe.

While it is common for there to be relatively modest demonstrable clin- ical neurological deficits in patients with significant neuropathic pain, in

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