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Painful diabetic peripheral neuropathy (DPN) is described as a superficial burning pain associated with other positive and/or negative sensory systems affecting the feet and lower extremities. It is one of the most commonly encountered neuropathic pain syndromes in clinical practice. Presentation may be complicated by multiple symptoms, including allodynia, hyperalgesia, other less well characterized dysesthesias, and serious disruption of social functioning and mood. Peripheral nerve function may deteriorate, which can account for patient reports of diminution of pain after several years of follow-up. Although current understanding holds that the pathogenesis of DPN is multifactorial in nature, long-term studies have shown that rigorous glycemic control is the most relevant factor in clinical intervention and can delay the onset and slow the progression of neuropathy. In addition to glycemic control, other treatment approaches must be examined in order to restore quality of life for patients experiencing painful DPN. Differential diagnosis is required to isolate DPN from other unexplained chronic pain. Neurologic testing in painful DPN is an area of active research and is used to assess the neurologic pathways giving rise to the pain, the degree of neural damage and the degree of subclinical damage. Current treatment options for DPN include mainly antidepressants and anticonvulsants, with other agents such as tramadol, dextromethorphan and memantine being employed or studied. This review article includes a case study of a patient with painful DPN to demonstrate the current management strategies for this neuropathic pain syndrome.

An exceptional case of long-standing central pain temporarily relieved by a focal stroke in the primary somatosensory area is reported. This case highlights the focal nature of central pain mechanisms and the possible value of selective subparietal leukotomies in the management of central pain.

It is estimated that at least one out of four patients with cancer complains of pain originating from nerve injury. Nerve injury may result from direct invasion/compression by tumour, or by remote effect of the cancer such as paraneoplastic polyneuropathy. In many cases, the nerve injury is caused by medical therapy, or surgical interventions. Pain generated by drugs or medical acts is called iatrogenic. A common iatrogenic neuralgia is chemotherapy induced painful polyneuropathy. This neuropathy typically affects mostly the small myelinated and unmyelinated nerve fibres. Surgical and anaesthesiological interventions also frequently cause direct nerve stretch or section. Some interventions, particularly those requiring extended resection, have a higher incidence of painful sequelae. Limb and colon amputation, nerve dissection, mastectomy and thoracotomy are the most common interventions for cancer known to cause nerve injury. As pain clinicians, we focus attention on the painful consequences of surgical interventions because there is evidence that a more accurate surgical approach and possibly a prophylactic prevention of the neuralgia may reduce the painful sequelae of nerve injury.

Four patients with pancoast's syndrome had burning pain in the axilla and abnormal sensation in the intercostobrachial nerve territory. The intercostobrachial nerve is the first component of the brachial plexus to be invaded by lung tumours.

Ten patients with organic nerve injury causing chronic neuropathic pain were tested for the effects of intravenous lidocaine versus saline upon psychophysical somatosensory variables. The variables assessed were the subjective magnitude of pain, area of mechanical hyperalgesia and presence and magnitude of thermal heat/cold hyperalgesia. The study methods applied to evaluate these conditions were the conventional testing of somatosensory submodalities with area mapping and the subjective magnitude estimation of spontaneous pain. It was found that spontaneous pain and mechanical hyperalgesia were consistently improved, transiently, by intravenous administration of lidocaine in all 10 patients; areas of hyperalgesia which extended beyond the territory of the nerve also improved transiently. Spontaneous pain and mechanical hyperalgesia, but not hypoesthesia, were transiently improved by injection of saline in only 1 of the 10 patients. This outcome is probably due to a placebo effect. This improvement is in keeping with the inhibition of anomalous neural impulses which can be generated anywhere along the sensory channels responsible for generating spontaneous pain and hyperalgesia. Thus, intravenous lidocaine is proposed as a diagnostic aid in the examination of patients complaining of complex sensory disorders associated with nerve injury. The transient pain relief may allow a fuller identification of the area of sensory loss.

Painful neurogenic syndromes commonly diagnosed as reflex sympathetic dystrophy (RSD) may not be the consequence of sympathetic dysfunction. Recent experimental data on the mechanism of hyperalgesia indicate that the primary pathophysiological mechanism of RSD may be sensitization of either peripheral nociceptors, or central neurons, or both. The sympathetic system might be involved in maintaining this condition, but this is not always the case. This presentation is an attempt to interpret clinical neuropathic syndromes on the basis of new scientific knowledge.

Recent studies have described abnormalities of visual evoked potentials and pattern electroretinography in diabetics without retinopathy. The visual contrast sensitivity, determined by psychophysical tests, has proved to be abnormal in diabetic patients with and without clinical retinopathy. In this study we evaluated contrast sensitivity function using both electrophysiologic and psychophysical methods. The objective assessment of functional visual contrast sensitivity was superior to psychophysical evaluation in the detection of contrast sensitivity alterations. No relationships were found between contrast sensitivity dysfunction and abnormalities of pattern electroretinography or fluorescein angiography. Our data suggest that functional visual deficits might precede background retinopathy and that the involvement of foveal function is early and very frequent in diabetic patients, even if they have normal visual acuity.