Articles: hyperalgesia.
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Cold hyperalgesia is a common side effect of oxaliplatin treatment; still, the pathophysiological and molecular mechanisms as well as the contribution of different primary afferent fiber systems are unclear. Therefore, patients with oxaliplatin-induced acute neuropathy with (n = 6) and without (n = 7) cold hyperalgesia were tested by applying a preferential blockade of peripheral myelinated A-fiber afferents in combination with quantitative sensory testing. Additionally, an interview-based questionnaire assessed the severity of symptoms and the impact on daily activities. ⋯ This suggests that oxaliplatin-induced cold hyperalgesia is mediated by A-fibers and that a deficit in A-fiber function might prevent the development of cold hyperalgesia. The work supports findings in rodents and in human sural nerve biopsies indicating that oxaliplatin interferes with axonal ion conductance in intact A-fibers by sensitizing potassium and/or sodium channels. Drugs that act on these molecular targets might be of potential value to treat oxaliplatin-induced cold hyperalgesia.
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Intraoperative remifentanil anesthesia exaggerates postoperative pain sensitivity. Recent studies recapitulate the significance of protein kinase Mζ in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor-mediated pathologic pain. Kalirin-7, a Rho guanine nucleotide exchange factor, coordinates AMPA receptor trafficking and dendritic spine plasticity. This study examines whether protein kinase Mζ and Kalirin-7 contribute to remifentanil-induced postincisional hyperalgesia via AMPA receptor. ⋯ Spinal protein kinase Mζ regulation of GluA1-containing AMPA receptor trafficking and spine morphology via Kalirin-7 overexpression is a fundamental pathogenesis of remifentanil-induced hyperalgesia in rats.
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Chronic stress produces maladaptive pain responses, manifested as alterations in pain processing and exacerbation of chronic pain conditions including irritable bowel syndrome. Female predominance, especially during reproductive years, strongly suggests a role of gonadal hormones. However, gonadal hormone modulation of stress-induced pain hypersensitivity is not well understood. ⋯ In addition, the presence of estradiol during stress increased spinal brain-derived neurotrophic factor (BDNF) expression independent of sex. In contrast, testosterone blocked the stress-induced increase in BDNF expression in female rats. These data suggest that estradiol facilitates and testosterone attenuates SIVH by modulating spinal excitatory and inhibitory glutamatergic receptor expression.
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Hyperalgesia and allodynia are typical signs of neuropathic pain. Quantitative sensory testing (QST) is a validated tool to clinically assess these phenomena. However, whether QST reveals findings that are reported by the patients is unclear. The aim of this study was therefore to investigate the association between self-reported symptoms assessed with the painDETECT questionnaire (PDQ) with results of validated QST. ⋯ Results demonstrate that self-reported PDQ symptoms cannot predict abnormal QST values. The poor predictive power of the PDQ may depend on several factors based on possibility of comparison between PDQ and QST and also on methodical issues. Both, symptoms (questionnaires) and signs address complementary aspects of the pain experience and should be considered for diagnosis and treatment of neuropathic pain.
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Physiology & behavior · Jul 2018
Anxiety- but not depressive-like behaviors are related to facial hyperalgesia in a model of trigeminal neuropathic pain in rats.
Trigeminal neuralgia (TN) is a painful condition characterized by excruciating facial pain, which has a serious impact on quality of life. Depression and anxiety have been commonly associated with TN, but clinical studies report that these comorbidities are frequently underdiagnosed and undertreated in TN patients. Herein it was investigated if rats submitted to the infraorbital nerve constriction (CION), a model of trigeminal neuropathic pain, would display anxiety- and depressive-like behaviors in addition to the facial sensory changes in different time points after the nerve injury. ⋯ The depressive-like behavior was assessed by measuring the time of immobility on the forced swim test (FST) and sucrose preference (SP) in rats previously tested for heat (day 5) and mechanical allodynia (days 15, 30 and 45) induced by CION. The evaluation of immobility time on FST and sucrose preference consumption revealed that both CION rats did not displayed depressive- and anhedonic-like behavior at any time point evaluated. Altogether, these results demonstrate that trigeminal neuropathic pain in rats leads to the development of anxiety-, but not depressive-like behavior, suggesting that the CION model represents a methodology that allows the study of drugs targeting both pain and anxiety.