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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article describes the effects of topically applied capsaicin (a nociceptive substance-P suppressor) in patients with neuropathic periocular or facial pain. Peripheral neuropathic pain is a major cause of periocular or facial discomfort and usually follows injury to a subcutaneous peripheral nerve. Though the damage is local, the pain tends to radiate. We studied three patients who complained of a 2- to 30-year history of fluctuating pain in the periocular area. All three had an area of point tenderness that responded to the topical application of capsaicin cream.
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PMID:The treatment of periocular and facial pain with topical capsaicin. 953 33

Peripheral neuropathic pain is produced by multiple etiological factors that initiate a number of diverse mechanisms operating at different sites and at different times and expressed both within, and across different disease states. Unraveling the mechanisms involved requires laboratory animal models that replicate as far as possible, the different pathophysiological changes present in patients. It is unlikely that a single animal model will include the full range of neuropathic pain mechanisms. A feature of several animal models of peripheral neuropathic pain is partial denervation. In the most frequently used models a mixture of intact and injured fibers is created by loose ligation of either the whole (Bennett GJ, Xie YK. A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man. Pain 1988;33:87-107) or a tight ligation of a part (Seltzer Z, Dubner R, Shir Y. A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury. Pain 1990;43:205-218) of a large peripheral nerve, or a tight ligation of an entire spinal segmental nerve (Kim SH, Chung JM. An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat. Pain 1992;50:355-363). We have developed a variant of partial denervation, the spared nerve injury model. This involves a lesion of two of the three terminal branches of the sciatic nerve (tibial and common peroneal nerves) leaving the remaining sural nerve intact. The spared nerve injury model differs from the Chung spinal segmental nerve, the Bennett chronic constriction injury and the Seltzer partial sciatic nerve injury models in that the co-mingling of distal intact axons with degenerating axons is restricted, and it permits behavioral testing of the non-injured skin territories adjacent to the denervated areas. The spared nerve injury model results in early (<24 h), prolonged (>6 months), robust (all animals are responders) behavioral modifications. The mechanical (von Frey and pinprick) sensitivity and thermal (hot and cold) responsiveness is increased in the ipsilateral sural and to a lesser extent saphenous territories, without any change in heat thermal thresholds. Crush injury of the tibial and common peroneal nerves produce similar early changes, which return, however to baseline at 7-9 weeks. The spared nerve injury model may provide, therefore, an additional resource for unraveling the mechanisms responsible for the production of neuropathic pain.
Pain 2000 Aug
PMID:Spared nerve injury: an animal model of persistent peripheral neuropathic pain. 1092 8

Peripheral neuropathic pain syndromes (PNPS) are difficult to treat because commonly used analgesics are often ineffective when, for example, touch-evoked allodynia, hyperalgesia, and pain paroxysms are present. To investigate whether lidocaine patch 5% treatment is also effective in postherpetic neuropathy (PHN) and in other PNPS, 40 patients with various forms and localizations of PNPS completed a prospective, randomized, placebo-controlled, two-way, cross-over study in three medical hospitals. Patients suffering from pain in a localized skin area with intensity above 40 mm visual analog scale (VAS) and a stable consumption of pain medication were included in this study. The study was divided into four phases: 3-day run-in phase, treatment phase 1, wash-out period, and treatment phase 2, each lasting 1 week. At the discretion of the patients, up to four patches (covering a maximum of 560 cm2) were applied onto the maximally painful area for 12 consecutive hours daily, always either by day or at night. Throughout the four phases, ongoing pain, allodynia, quality of neuropathic symptoms, quality of sleep, and adverse events were assessed. When, after the wash-out period, the pain intensity scores did not return to the pre-treatment values (+/-20%), these patients were excluded from the study. The present study revealed that, as an add-on therapy, the lidocaine patch 5% was clearly effective in reducing ongoing pain (P=0.017) and allodynia (P=0.023) during the first 8 h after application and that the patches also worked well over a period of 7 days (P=0.018) in diverse focal PNPS. Calculation of the numbers needed to treat (NNT) to obtain one patient with more than 50% relief of ongoing pain revealed that the NNT of 4.4 in the present study compared reasonably well with other studies of PHN, such as topically applied capsaicin (NNT: 5.3-infinity) or systemic treatment with gabapentin (NNT: 3.2-5.0).
Pain 2003 Nov
PMID:Efficacy of lidocaine patch 5% in the treatment of focal peripheral neuropathic pain syndromes: a randomized, double-blind, placebo-controlled study. 1458 Nov 22

Peripheral neuropathic pain, that clinical pain syndrome associated with lesions to the peripheral nervous system, is characterized by positive and negative symptoms. Positive symptoms include spontaneous pain, paresthesia and dysthesia, as well as a pain evoked by normally innocuous stimuli (allodynia) and an exaggerated or prolonged pain to noxious stimuli (hyperalgesia/hyperpathia). The negative symptoms essentially reflect loss of sensation due to axon/neuron loss, the positive symptoms reflect abnormal excitability of the nervous system. Diverse disease conditions can result in neuropathic pain but the disease diagnosis by itself is not helpful in selecting the optimal pain therapy. Identification of the neurobiological mechanisms responsible for neuropathic pain is leading to a mechanism-based approach to this condition, which offers the possibility of greater diagnostic sensitivity and a more rational basis for therapy. We are beginning to move from an empirical symptom control approach to the treatment of pain to one targeting the specific mechanisms responsible. This review highlights some of the mechanisms underlying neuropathic pain and the novel targets they reveal for future putative analgesics.
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PMID:Dissecting out mechanisms responsible for peripheral neuropathic pain: implications for diagnosis and therapy. 1504 42

Peripheral neuropathic pain is a unique form of chronic pain that afflicts up to 50% of persons with AIDS. The purpose of this pilot study was to examine the effects of ice massage to reduce neuropathic pain and improve sleep quality and to determine the feasibility of a larger study. A repeated measures design was used. The three treatments consisted of ice massage, dry-towel massage, and presence. Consecutive sampling was used to select 33 persons with AIDS who had neuropathic pain. Although the results of the study were negative, there was a decrease in pain intensity over time with both the ice massage and towel massage, suggesting that the intervention has some clinical benefit.
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PMID:Effects of ice massage on neuropathic pain in persons with AIDS. 1697 11

Peripheral neuropathic pain is a common clinical problem with few existing treatments. Previously, we constructed rAAV bearing GAD65 and demonstrated that GAD65 and GABA can be constitutively produced in the CNS. To investigate the beneficial effects of GAD65 produced by rAAV and resulting GABA release in peripheral neuropathic pain, we established a neuropathic pain rat model. The direct administration of rAAV-GAD65 to dorsal root ganglion induced constitutive GAD65 expression, which was readily detected by immunohistochemistry. Both allodynic and hyperalgeic behavior tests suggested that neuropathic pain was noticeably reduced, along with the transgenic GAD65 expression. Moreover, the magnitude of pain relief was maintained during the entire experimental period. Concomitantly, the significant enhancement in GABA release following transgenic GAD65 expression was identified in vivo. Taken all together, these results provide evidence that persistent GAD65 and subsequent GABA expression in DRGs via rAAV effectively attenuates peripheral neuropathic pain for long period of time.
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PMID:Constitutive GABA expression via a recombinant adeno-associated virus consistently attenuates neuropathic pain. 1746 64

Peripheral neuropathic pain (PNP) frequently occurs as a consequence of nerve injury and may differ depending upon the type of insult and the individual patient. Progress in our knowledge of PNP induction mechanisms depends upon the utilization of appropriate experimental models in rodents based on various types of peripheral nerve lesions. In this review, we draw attention to current knowledge on basic cellular and molecular events in various experimental models used to induce the PNP symptoms. Spontaneous ectopic activity of axotomized and non-axotomized primary sensory neurons, the bodies of which are located in the dorsal root ganglion (DRG), seems to be a key mechanism of PNP induction. The primary sensory neurons are directly affected by nerve injury or indirectly by activated satellite glial cells and adjoining immune cells that release a variety of molecules changing the microenvironment of the neurons. Recently, it has become clear that molecules produced during Wallerian degeneration play an important role not only in axon-promoting conditions distal to nerve injury but also in initiation of neuropathic pain. The molecules, transported by the blood, influence afferent neurons and their axons not only in DRG associated, but also those not directly associated with the injured nerve (i.e., in the contralateral DRG or at different spinal segments). Generally, all experimental PNP models based on a partial injury of peripheral nerve segments contain mechanisms initiated by signal molecules of Wallerian degeneration.
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PMID:Experimental models of peripheral neuropathic pain based on traumatic nerve injuries - an anatomical perspective. 1940 84

Thalidomide and bortezomib are remarkably efficacious in the treatment of multiple myeloma. Unfortunately, their use can cause sensory neuropathy, a common and serious adverse event that frequently limits dose and duration of treatment. Although the relationship between peripheral neuropathy and therapeutic dose is controversial, many authors have demonstrated a positive correlation between neuropathy and cumulative dose, dose intensity, and length of therapy. Peripheral neuropathic pain is the most troublesome symptom of neuropathy. Spontaneous pain, allodynia, hyperalgesia, and hyperpathia are often associated with decreased physical activity, increased fatigue, mood, and sleep problems. Symptoms are often difficult to manage, and available treatment options rarely provide total relief. Moreover, the adverse effects of these treatments often limit their use. Several studies have demonstrated the efficacy of acupuncture, with fewer adverse effects than analgesic drugs, in the treatment of painful diabetic and human immunodeficiency virus-related neuropathy. However, the effectiveness of acupuncture in treating toxic neuropathy has not been assessed. Although its putative mechanisms remain elusive, acupuncture has strong potential as an adjunctive therapy in thalidomide- or bortezomib-induced painful neuropathy, and a better understanding might guide its use in the management of chemotherapy-induced neuropathic pain. Well-designed clinical trials with adequate sample size and power are warranted.
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PMID:Multiple myeloma, painful neuropathy, acupuncture? 1988 92

Peripheral neuropathic pain is a severe chronic pain condition which may result from trauma to sensory nerves in the peripheral nervous system. The spared nerve injury (SNI) model induces symptoms of neuropathic pain such as mechanical allodynia i.e. pain due to tactile stimuli that do not normally provoke a painful response [1]. The SNI mouse model involves ligation of two of the three branches of the sciatic nerve (the tibial nerve and the common peroneal nerve), while the sural nerve is left intact [2]. The lesion results in marked hypersensitivity in the lateral area of the paw, which is innervated by the spared sural nerve. The non-operated side of the mouse can be used as a control. The advantages of the SNI model are the robustness of the response and that it doesn't require expert microsurgical skills. The threshold for mechanical pain response is determined by testing with von Frey filaments of increasing bending force, which are repetitively pressed against the lateral area of the paw [3], [4]. A positive pain reaction is defined as sudden paw withdrawal, flinching and/or paw licking induced by the filament. A positive response in three out of five repetitive stimuli is defined as the pain threshold. As demonstrated in the video protocol, C57BL/6 mice experience profound allodynia as early as the day following surgery and maintain this for several weeks.
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PMID:The spared nerve injury (SNI) model of induced mechanical allodynia in mice. 2187 24

Peripheral neuropathic pain arises from trauma to sensory nerves. Other types of acute neurotrauma such as stroke and spinal cord injury are treated immediately, largely to prevent secondary damage. To pursue the possibility that neuropathic pain may also be amenable to early treatment, a rat model of neuropathic pain was induced using a 2-mm polyethylene cuff implanted around one sciatic nerve. Within 24 hours, hypersensitivity to von Frey hair stimulation appeared, as indicated by decreased paw withdrawal thresholds. When the cuff was removed 24 hours after implantation, readings returned to pre-implantation levels starting as early as day 18. When the cuff was removed after 4 days, there was a period of initial hypersensitivity, and then an increase toward baseline at two time points near the end of the study; therefore, only a partial recovery toward pre-implantation values occurred. Having established that a temporal reversal can occur, the next step examined possible pharmacological reversal. The tachykinin NK(1) receptor antagonist, CP-96,345, produced a minor increase in withdrawal thresholds in animals with the cuff left permanently implanted. To determine the effect of early and repeated administration of CP-96,345, it was given daily on days 1-4. The cuff was removed on day 4. Six days later, readings showed reversal of tactile hypersensitivity. We suggest that persistent neuropathic pain occurs from processes that develop over several hours and days, and that some of these processes may be prevented by early medical intervention. Thus, nerve injury in the context of chronic neuropathic pain should be treated in a similar manner to nerve injury resulting from stroke, spinal cord injury, and other types of neurotrauma. We suggest that effective medical intervention within the first few hours after nerve injury may spare a patient from a chronic debilitating pain that may be refractory to later therapies.
J Pain Res 2011
PMID:Neuropathic pain as a process: reversal of chronification in an animal model. 2200 5


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