Articles: neuropathic-pain.
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Pharmacol. Biochem. Behav. · Nov 2014
Establishment and characterization of an optimized mouse model of multiple sclerosis-induced neuropathic pain using behavioral, pharmacologic, histologic and immunohistochemical methods.
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system (CNS) that causes debilitating central neuropathic pain in many patients. Although mouse models of experimental autoimmune encephalomyelitis (EAE) have provided insight on the pathobiology of MS-induced neuropathic pain, concurrent severe motor impairments confound quantitative assessment of pain behaviors over the disease course. To address this issue, we have established and characterized an optimized EAE-mouse model of MS-induced neuropathic pain. ⋯ Single bolus doses of amitriptyline (1-7mg/kg), gabapentin (10-50mg/kg) and morphine (0.1-2mg/kg) evoked dose-dependent analgesia in the bilateral hindpaws of EAE-mice; the corresponding ED50s were 1.5, 20 and 1mg/kg respectively. At day 39 p.i. in EAE-mice exhibiting mechanical allodynia in the hindpaws, there was marked demyelination and gliosis in the brain and lumbar spinal cord, mirroring these pathobiologic hallmark features of MS in humans. Our optimized EAE-mouse model of MS-associated neuropathic pain will be invaluable for future investigation of the pathobiology of MS-induced neuropathic pain and for efficacy profiling of novel molecules as potential new analgesics for improved relief of this condition.
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Understanding the molecular mechanisms associated with disease is a central goal of modern medical research. As such, many thousands of experiments have been published that detail individual molecular events that contribute to a disease. Here we use a semi-automated text mining approach to accurately and exhaustively curate the primary literature for chronic pain states. ⋯ We exploit the contextual data associated with our interactions to analyse subnetworks specific to inflammatory and neuropathic pain, and to various anatomical regions. Here, we identify potential targets for further study and several drug-repurposing opportunities. Finally, the network provides a framework for the interpretation of new data within the field of pain.
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Patients will often visit their primary medical practitioner with orofacial pain complaints. Hence, it is important to recognize and have an understanding of these conditions to properly evaluate and potentially manage these disorders. If the practitioner is uncertain or uncomfortable with these conditions, then patient referral to a knowledgeable health care practitioner should be considered for further evaluation and management. In this article, the evaluation and management of various neuropathic, neurovascular, and vascular pains are discussed.
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Neurosci Biobehav Rev · Nov 2014
ReviewEmotional consequences of neuropathic pain: insight from preclinical studies.
Mood disorders such as depression and anxiety are frequently observed in patients suffering from chronic pain, including neuropathic pain. While this comorbidity is clinically well established, the underlying mechanism(s) remained unclear. The recent development of animal models now allows addressing the consequences of neuropathic pain. ⋯ We present an overview of rodent models of these consequences and we discuss the challenges and parameters to consider for generating these models. We then discuss the possible mechanism(s) underlying anxiodepressive consequences by describing morphological and functional changes. Information is provided concerning neuroanatomical changes and plasticity, including LTP and LTD, in the anterior cingulate cortex, the insula, the hippocampus, the amygdala and the mesolimbic system, neuroendocrine parameters concerning the hypothalamo-pituitary-adrenal axis, neuroimmune response including the role of glial cells and cytokines, monoamine systems and changes in locus coeruleus noradrenergic system, and neurotrophic factors such as BDNF.
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Pain may be the earliest symptom in Fabry disease and presents with a distinct phenotype including triggerable pain attacks, evoked pain, pain crises, and chronic pain. Current pain questionnaires do not reflect the special phenotype of Fabry disease-associated pain, which hampers its systematic evaluation as the basis of correct diagnosis and effective treatment. A questionnaire specifically designed to assess Fabry disease-associated pain is thus urgently needed. ⋯ We determined the test-retest reliability and validity of the FPQ in comparison to data obtained with the Neuropathic Pain Symptom Inventory. The FPQ contains 15 questions on the 4 pain phenotypes of Fabry disease (pain attacks, pain crises, evoked pain, chronic pain) in childhood and adulthood, on pain development during life with and without enzyme replacement therapy, and on everyday life impairment due to pain. This first disease-specific questionnaire is a valuable tool for baseline and follow-up assessment of pain in Fabry disease patients and may guide treatment in this distinct pain phenotype.