Articles: neuralgia.
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Better tools are required for the earlier identification and management of orofacial pain with different aetiologies. The painDETECT questionnaire is a patient-completed screening tool with utility for identification of neuropathic pain in a range of contexts. 254 patients, referred from primary care for management of orofacial pain and attending a secondary care centre, were prospectively recruited, and completed the painDETECT prior to consultation. The aim of this study was to determine the accuracy of the painDETECT to detect neuropathic components of orofacial pain, when compared to a reference standard of clinical diagnosis by experienced physicians, in a cohort of hospital-based patients. ⋯ In secondary care settings, the painDETECT performed modestly at identifying neuropathic components, and underestimates the complexity of orofacial pain in its mixed presentations and with multiple diagnoses. Prior to clinical applications or research use, the painDETECT and other generic screening tools must be adapted and revalidated for orofacial pain patients, and separately in primary care, where orofacial pain is considerably less common.
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Opioids remain a mainstay in the treatment of acute and chronic pain, despite numerous and potentially dangerous side effects. There is a great unmet medical need for alternative treatments for patients suffering from pain that do not result in addiction or adverse side effects. Anticonvulsants have been shown to be effective in managing pain, though high systemic levels and subsequent side effects limit their widespread usage. Our goal was to determine if the incorporation of an anticonvulsant, carbamazepine, into a biodegradable microparticle for local sustained perineural release would be an efficacious analgesic following a peripheral injury. ⋯ This formulation reduced systemic exposure to carbamazepine over 1,000-fold relative to traditional analgesic dosing regimens. This 2-component drug delivery system has been specifically engineered to release a controlled amount of carbamazepine over a 14-day period, providing significant pain relief with no toxicological or observable adverse events via behavioral or histochemical analysis.
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To investigate if a combination of anticonvulsant and antidepressant, two primary therapies for neuropathic pain, is associated with improved pain control compared to individual therapy. ⋯ The initiation of a combination of anticonvulsant and antidepressant shortly after SCI was not associated with improved pain control at 6 months compared to individual therapy. Adherent patients reported lower levels of pain; further analysis is warranted to elucidate this association.
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Two well-known spinal cord stimulation (SCS) paradigms, conventional (Con) and burst SCS, are hypothesized to exert their antinociceptive effects through different stimulation-induced mechanisms. We studied the course of the behavioral antinociceptive effect during 60 minutes of SCS and 30 minutes post-SCS in a rat model of chronic neuropathic pain. ⋯ To conclude, biphasic burst SCS results in a delayed antinociceptive effect after onset of the stimulation, as compared with Con SCS, in a chronic neuropathic pain model. Furthermore, biphasic burst SCS seems to exhibit a delayed wash-out of analgesia after stimulation is turned off.
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Anticonvulsant drugs such as pregabalin (PGB) and lacosamide (LCM), exhibit potent analgesic effects in diabetic neuropathy; however, their possible role/mechanisms in paclitaxel (PTX)-induced peripheral neuropathy have not been elucidated, which is the aim of the present study. Neuropathic pain was induced in rats by injecting PTX (2 mg/kg, i. p) on days 0, 2, 4 and 6. Forty eight hours after the last dose of PTX, rats were treated orally with 30 mg/kg/day of either PGB or LCM for 21 days. ⋯ Treatment with PGB or LCM restored the sciatic nerve content of the depleted total antioxidant capacity (TAC) and nerve growth factor (NGF), and lessened the elevated contents of nuclear factor kappa B p65 (NF-kB p65), tumor necrosis factor-α (TNF-α), and active caspase-3. On the molecular level, the drugs reduced the protein expression of Notch1 receptor, phosphorylated p38 mitogen-activated protein kinase (p-p38-MAPK), and the trajectory interleukin-6/phosphorylated janus kinase 2/phosphorylated signal transducer and activator of transcription 3 (IL-6/p-JAK2/p-STAT3). Therefore, the current study demonstrated a pivotal role for LCM in the management of PTX-induced peripheral neuropathy similar to PGB, but without motor adverse effects via the inhibition of oxidative stress, inflammation and apoptosis, as well as IL-6/JAK/STAT pathway and Notch1 receptor over-expression.