Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0423716 (Neuropathic pain)
 1,417 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Neuropathic pain may respond poorly to morphine and is often difficult to relieve. Recent attention has been drawn to the role of the N-methyl-D-aspartate (NMDA) receptor in the potentiation of neuropathic pain. Magnesium is known to block the NMDA receptor. It reduces the neuropathic pain response in animals, and attenuates postoperative pain and migraine in humans. We have examined the safety, tolerability, and efficacy of two intravenous doses of magnesium sulfate in 12 patients with neuropathic pain due to malignant infiltration of the brachial or lumbosacral plexus. The first six patients received 500 mg, the remainder 1 g. Apart from a mild feeling of warmth at the time of the injection, both doses were well tolerated. After receiving 500 mg, three patients experienced complete pain relief and two experienced partial pain relief for up to 4 hours duration; pain was unchanged in one patient. After receiving 1 g, one patient experienced complete relief and four experienced partial pain relief of similar duration; pain was unchanged in one patient. Intravenous magnesium sulfate in these doses appears to be safe and well tolerated. A useful analgesic effect may be obtained in some patients and further evaluation is warranted.
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PMID:The safety and efficacy of a single dose (500 mg or 1 g) of intravenous magnesium sulfate in neuropathic pain poorly responsive to strong opioid analgesics in patients with cancer. 1101 12

Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system". Neuropathic orofacial pain has previously been known as "atypical odontalgia" (AO) and "phantom tooth pain". The patient afflicted with neuropathic oral/orofacial pain may present to the dentist with a persistent, severe pain, yet there are no clearly identifiable clinical or radiographic abnormalities. Accordingly, multiple endodontic procedures may be instigated to remove the likely anatomical source of the pain, yet the pain persists. There have been few studies and limited patient numbers investigating the condition. Two retrospective studies revealed the incidence of persistent pain following endodontic treatment to be 3-6% and 5% of patients; one author with wide experience in assessing the condition estimated its prevalence at 125,000 individuals in the USA alone. In one study, 50% of neuropathic orofacial pain patients reported persistent pain specifically following endodontic treatment. Patients predisposed to the condition may include those suffering from recurrent cluster or migraine headaches. Neuropathic pain states include postherpetic neuralgia (shingles) and phantom limb/stump pain. The aberrant developmental neurobiology leading to this pain state is complex. Neuropathic pain serves no protective function, in contrast to physiological pain that warns of noxious stimuli likely to result in tissue damage. The relevant clinical features of neuropathic pain include: (i) precipitating factors such as trauma or disease (infection), and often a delay in onset after initial injury (days-months), (ii) typical complaints such as dysaesthesias (abnormal unpleasant sensations), pain that may include burning, and paroxysmal, lancinating or sharp qualities, and pain in an area of sensory deficit, (iii) on physical examination there may be hyperalgesia, allodynia and sympathetic hyperfunction, and (iv) the pathophysiology includes deafferentation, nerve sprouting, neuroma formation and sympathetic efferent activity.
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PMID:Neuropathic orofacial pain part 1--prevalence and pathophysiology. 1135 93

B vitamins have been used as analgesic drugs to treat pain disorders associated with their deficiency. More recently it has been claimed that B vitamins are useful to relieve different pain states as carpal tunnel, migraine and premenstrual tension. In Latin America, B vitamins are commonly used to treat neuropathic pain; however, there is no data to support this indication. In the present work we assessed the possible analgesic activity of vitamin B12 alone and combined with diclofenac in a neuropathic pain model in the rat. Neuropathic pain was induced by ligation of the left L5 and L6 spinal nerves of female Wistar rats. Tactile allodynia was determined by measuring paw withdrawal in response to probing with a series of calibrated von Frey filaments. Vitamin B12 (0.75-6 mg/kg), but not diclofenac (1-10 mg/kg), reduced in a dose-dependent manner tactile allodynia induced by spinal nerve ligation. Diclofenac (3.2 mg/kg) was not able to further increase vitamin B12-induced antiallodynia. Results indicate that vitamin B12, but not diclofenac, produces antiallodynic effects in the rat and suggest that this vitamin could be a potential treatment for neuropathic pain in humans.
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PMID:Effect of diclofenac on the antiallodynic activity of vitamin B12 in a neuropathic pain model in the rat. 1563 22

Neuropathic pain is a phenomenon characterized by a high population prevalence by possessing several etiologies. In contrast to nociceptive pain, painful signals in neuropathic pain are originated in the nervous system, present poor responses to conventional treatments and may worsen the quality of life. Antiepileptic drugs are increasingly used for different purposes including migraine, neuropathic pain, tremor or psychiatric disorders and they have started to be called neuromodulators. These drugs may act on very different targets such as sodium, potassium or calcium channels, purinergic, GABAergic, glutamatergic or vanilloid receptors and different cytokines including IL-6 or TNF, each if which may be important in managing some aspects of neuropathic pain. Antiepileptic drugs have demonstrated effectiveness in the treatment of this pathology, and owing to the important development of these drugs in the last years, they may become a very effective tool. On the other hand, the increasing knowledge of the pathophysiology of nociception is leading to new channels and receptors as potential targets for treatment. In this paper we try to review the different potential therapeutic targets and role of antiepileptic drugs in the treatment of this pathology.
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PMID:Neuromodulators and therapeutic targets in neuropathic pain: from molecules to man. 1960 15

Neuropathic pain is a complicated symptomatic disease as migraine in recent years. Not because the pain character differed from the nociceptive inflammatory symptoms but because of its complexity of mechanisms. Though peripheral sensitization, ectopic discharge, central sensitization, central re-organization and loss of inhibition play part of roles in mechanisms, however, based on this mechanistic treatment, the outcome still disappointed physicians and patients, exampled as central post-stroke central pain (CPSP). The pain reduction is far less than the expectation from patients and physician's under-treatment frequently occur due to the fear of adverse effects or off-label use of these anti-neuropathic pain drugs. Therefore, a multidisciplinary procedure including non-pharmacological management, rehabilitation program, careful explanation, stepwise pain reduction, daily diary record, and tailored individual planning for medications are helpful in treating this kind of sufferers. Pharmacological treatment is the mainstream in post-herpetic neuralgia (PHN), diabetic peripheral neuropathic pain (DPNP), central post-stroke pain (CPSP), trigeminal neuralgia (TN), complex regional pain syndrome (CRPS), cancer pain, failed back syndrome etc, while polypharmacy is still the major prescriptions facing such kind of miserable patients. The tricyclic antidepressants (TCA), gamma- aminobutyric acid (GABA), voltage-dependent calcium channel blockers, selective non-epinephrine reuptake inhibitor (SNRI), opioid or morphine etc, are still evidence-based medicines (EBM) but with different outcome for individuals. Acupuncture is to some extend effective in Taiwanese people with perceived evidence or placebo. The Taiwan guidance for total pain management and review of EBM in treating neuropathic pain from neurological point of view will be introduced in this manuscript.
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PMID:[Guideline of neuropathic pain treatment and dilemma from neurological point of view]. 2319 35

Despite the fact that neurophysiological evaluation is not useful for primary headache diagnosis, the nociceptive system exploration through reflexes and evoked potentials procedures may give an aid in understanding the pathophysiological mechanism subtending pain. Neuropathic pain is caused by a lesion or disease of the somatosensory nervous system, which is supported by clinical evaluation and instrumental assessment by trigeminal and nociceptive reflexes and laser evoked potentials. The same methods, applied to migraine and cluster headache, together with evidences coming from structural and functional neuroimaging, excluded the neuropathic origin of pain, which is attaining to symptomatic and idiopathic trigeminal neuralgia, but confirmed a complex dysfunction of pain processing. Tension-type headache fits with a model of non-nociceptive and non-neuropathic pain, subtended by a complex interaction of peripheral muscular and central neuronal factors. The presence of altered modulation of pain concurs with migraine and tension-type headache, and should be taken into account for the choice of the best therapeutic approach.
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PMID:Primary headaches and trigeminal neuralgia: neuropathic pain yes or not? Evidences from neurophysiological procedures. 2395 54

The patients with multiple sclerosis (MS) are at greater risk of pain than people without the disease; however, the occurrence and characteristics of pain among these patients are incompletely described. We aimed to assess characteristics of pain amongst MS patients using MS patients who were recruited to participate in 3 studies in Sweden (n = 3877) and were matched with individuals without MS (n = 4548) by sex, year of birth, and region of residence. The Prescribed Drugs Register identified prescribed pain medication, overall and restricted to those given 4 or more prescriptions in 1 year to assess chronic pain. Anatomical therapeutic chemical codes classified whether pain was neuropathic, musculoskeletal, or migraine. Cox-proportional hazard models were used to estimate associations. Our findings showed the patients with MS were at increased risk of pain treatment, with a hazard ratio (HR) of 2.52 (95% confidence interval 2.38-2.66). The largest magnitude HR was for neuropathic pain (5.73, 5.07-6.47) for which 34.2% (n = 1326) of the MS and 7.15% (n = 325) of the non-MS cohort were prescribed a treatment. The HR for chronic pain treatment was 3.55 (3.27-3.84), indicating an increased effect size relative to any pain treatment. Chronic neuropathic pain showed the largest HR at 7.43 (6.21-8.89). Neuropathic pain was shown to be the primary mechanism leading to increased risk of pain in patients with MS.
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PMID:The association between multiple sclerosis and pain medications. 3088 19

To investigate the physiopathology of pain in chronic inflammatory rheumatic diseases (CIRDs), we assessed the prevalence of migraine and neuropathic pain in 499 patients with CIRDs. We studied 238 patients with rheumatoid arthritis, 188 with spondyloarthritis (SpA), 72 with psoriatic arthritis (PsA), and 1 unclassified. Migraine was diagnosed according to IHS migraine diagnostic criteria. Neuropathic pain was diagnosed when patients scored at least 3 on the DN4 questionnaire. Participants completed a validated self-assessment questionnaire. Migraine prevalence was 34% (165/484), and it was highest in PsA. Risk factors for migraine were a high level of anxiety, female sex, young age, and TNF-alpha inhibitor treatment (OR = 1.90 (1.13-3.25)). Besides, high disease activity was a risk factor in SpA. Blood CRP level was not significantly associated with migraine. Of 493 patients with CIRDs, 21.5% had chronic pain with neuropathic characteristics. Compared to the French general population, these patients had significantly higher prevalences of migraine (two-fold) and neuropathic pain (three-fold). This study showed that migraine and neuropathic pain frequently occurred in patients with rheumatic diseases. Therefore, upon reporting residual pain, these patients should be checked for the presence of migraine or neuropathic pain, despite adequate clinical control of rheumatic disease.
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PMID:Prevalence of Migraine and Neuropathic Pain in Rheumatic Diseases. 3256 Mar 21