Articles: neuralgia.
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Pain assessment and physical examination are the first crucial steps in diagnosis of neuropathic pain disorders because these are still solely diagnosed on clinical grounds. The physical examination should be conducted in such a way that all of the positive sensory phenomena, such as allodynia, hyperalgesia, hyperpathia, summation, and after-sensation are elicited. Other physical examination findings should corroborate the diagnostic impression of neuropathic pain. Specific pain diagnosis should then lead to more specific therapy.
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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.
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This article presents recent observations about different recognized central pain syndromes (CPS) and discusses them in light of contemporary microelectrode and imaging findings. Different theories regarding the generation of CPS are reviewed, with an emphasis on difficulties in diagnosis and treatment. The author discourages destructive procedures for treatment of CPS, favoring, instead, reversible procedures such as stimulation techniques and drug delivery systems.
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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.