Articles: neuralgia.
-
Painful polyneuropathy is one of the most common chronic pain syndromes neurologists are asked to assess for diagnostic and therapeutic purposes. This article reviews the most current clinical guidelines, including history, pain assessment, physical examination findings, treatment recommendations, and pathophysiologic pain mechanisms underlying this condition. As a result of recent advances, the understanding and therapy of pain associated with polyneuropathy has evolved over the past several years and will continue to do so in the years to come.
-
Neurobiology of disease · Oct 1998
ReviewPostherpetic neuralgia: irritable nociceptors and deafferentation.
Postherpetic neuralgia (PHN) is a common and often devastatingly painful condition. It is also one of the most extensively investigated of the neuropathic pains. Patients with PHN have been studied using quantitative testing of primary afferent function, skin biopsies, and controlled treatment trials. ⋯ Other deafferentation patients have severe spontaneous pain without hyperalgesia or allodynia and presumably have lost both large and small diameter fibers. In this group the pain is likely due to increased spontaneous activity in deafferented central neurons and/or reorganization of central connections. These three types of mechanism may coexist in individual patients and each offers the possibility for developing new therapeutic interventions.
-
Randomized Controlled Trial Comparative Study Clinical Trial
Nortriptyline versus amitriptyline in postherpetic neuralgia: a randomized trial.
OBJECTIVE (BACKGROUND): Amitriptyline (AT) is a standard therapy for postherpetic neuralgia (PHN). Our hypothesis was that nortriptyline (NT), a noradrenergic metabolite of AT, may be more effective. ⋯ We concluded that this study provides a scientific basis for an analgesic action of NT in PHN because pain relief occurred without an antidepressant effect, and that although there were fewer side effects with NT, AT and NT appear to have a similar analgesic action for most individuals.
-
J Pain Symptom Manage · Oct 1998
Randomized Controlled Trial Clinical TrialProlonged treatment with transdermal fentanyl in neuropathic pain.
Forty-eight patients with noncancer neuropathic pain who had participated in a randomized controlled trial with intravenous fentanyl (FENiv) infusions received prolonged transdermal fentanyl (FENtd) in an open prospective study. Pain relief, side effects, tolerance, psychological dependence, mood changes, and quality of life were evaluated. The value of clinical baseline characteristics and the response to FENiv also was evaluated in terms of the outcome with long-term FENtd. ⋯ In only one patient did tolerance emerge. There was a significant positive correlation between the pain relief obtained with FENiv and that with prolonged FENtd (r = 0.59, P < 0.0001). We conclude that (1) long-term transdermal fentanyl may be effective in noncancer neuropathic pain without clinically significant management problems and (2) A FENiv-test may assist in selecting neuropathic pain patients who might benefit from prolonged treatment with FENtd.
-
Recent evidence indicates that neuropathic pain from partial peripheral nerve injury is maintained by electrophysiologically abnormal signals from injured sensory neurons. To gain an insight into the mechanisms underlying this electrophysiological abnormality, we examined the effects of S1 spinal nerve transection on the membrane properties of S1 dorsal root ganglion neurons one to two weeks after injury. This injury produced significant action potential broadening [40% (1 ms) in C-, 149% (1.5 ms) in A delta- and 84% (0.5 ms) in A alpha/beta-cells], which was primarily due to the enhancement of the "shoulder" appearing on the falling phase of the action potential in C- and A delta-cells and the emergence of a shoulder in A alpha/beta-cells, and significant cell-type specific changes in the time-course of the rising phase of the action potential; i.e. an increase in rise time (A delta: 35%, 0.15 ms; A alpha/beta: 13%, 0.04 ms) and a decrease in the maximal rate of rise (A delta: 17%, 77 V/s; A alpha/beta: 13%, 79 V/s). ⋯ The nerve injury-induced reduction of rheobase was not accompanied by related change in input resistance or threshold potential in any of the cell populations. The present results indicate that chronic peripheral axotomy of dorsal root ganglion neurons, which gives rise to neuropathic pain, produces profound changes in the action potential waveform of dorsal root ganglion neurons in a cell type-specific fashion. Furthermore, the results suggest that the axotomy increases the excitability of dorsal root ganglion neurons not by altering input resistance (i.e. leak conductance) or threshold potential, but by increasing apparent input resistance near the resting membrane potential in A-cells and decreasing the resting membrane potential in C-cells.