Context: Dysfunction of pain circuitry may alter normal pain perception, leading to neuropathic pain. The underlying mechanisms are still unclear, although several animal models of partial nerve injury have been developed. Objectives: This review aimed to describe some essential elements for understanding neuropathic pain after peripheral nerve injury and to discuss its mechanisms with an emphasis on interneuronal disinhibition. Evidence Acquisition: A PubMed search was undertaken with no date restrictions, using a combination of the following keywords: "mechanisms", "allodynia", "peripheral nerve injury", "neuropathic pain", and "interneuronal disinhibition". Then, relevant papers on the underlying mechanisms of neuropathic pain after peripheral nerve injury were selected. Results: Several hypotheses have been proposed to explain neuropathic pain, which are not necessarily independent of each other. Interneuronal disinhibition is one of the most promising hypotheses, which includes several possible mechanisms, such as death of inhibitory interneurons (1), reduced afferent drive to inhibitory interneurons (2), depletion of gamma-aminobutyric acid (GABA) (3), GABA dysfunction (4), altered membrane properties of inhibitory interneurons (5), and specific glycine disruption (6). Currently, only some of these hypotheses are promising. Technical discrepancies among experimental studies are partially responsible for some of these controversial results. Conclusions: Formerly neglected circuitries including the glycinergic system, as well as other disturbances such as shift of GABA activity, currently constitute the most promising hypotheses on neuropathic pain. Additional studies on cell types involved in nociceptive transmission and dorsal horn connectivity of the spinal cord are still needed for a better understanding of pain circuitry and its disorders.
Background: Migraine and epilepsy are both common episodic disorders, typically precipitated or inhibited by some modulatory factors (MFs).Objective: To assess the self-perception of MFs in patients with migraine (PWM) compared to patients with epilepsy (PWE) with a standardized protocol in different countries.Methods: Transcultural multicenter comparative cross-sectional study. All consecutive patients who fulfilled the ICHD-3 criteria for migraine and ILAE's criteria for epilepsy, with at least 1 year of follow-up were interviewed with a semi-structured questionnaire on clinical and epidemiological data and were asked to identify all experienced MFs from a provided list.Results: A total of 608 individuals were surveyed at five university referral centers in Brazil, Guatemala, Lithuania and Turkey. Two hundred and nineteen (91.6%) PWM and 305 (82.7%) PWE identified attack precipitating factors (PFs; p < 0.001). The most frequent three PFs reported by epilepsy patients were: “lack of sleep” (56.6%), “emotional stress” (55.3%), “negative feelings” (53.9%), while among migraine patients “emotional stress” (81.6%), “lack of sleep” (77.8%), “negative feelings” (75.7%) were cited. Inhibitory factors (IFs) for the episodes were reported by 68 (28.5%) PWM and 116 (31.4%) PWE. “Darkness” was the most common one, described by 35.6% of PWM whereas “positive feelings” reported by 10.6% of PWE. Most MFs are concordant across the countries but some transcultural differences were noted.Conclusion: The MFs of migraine and epilepsy attacks and their varying frequencies according to different countries were investigated with the same standardized questionnaire, for the first time. MFs were recognized very often in both migraine and epilepsy cohorts, but in distinct disease-specific prevalence, being more frequent in migraine. Recognition of self-perceived MFs may be helpful for the management of both illnesses.
Conducted the experiments, Acquisition, analysis and interpretation of data; Participated in writing the paper and its critical review; GG: Collection of samples and conduction of the experiments; SMR: Conception and design of the study, Participated in writing the paper and its critical review; SMdA: Conception and design of the study, Participated in writing the paper and its critical review; LAP: Collection of samples and conduction of the experiments; IR: Collection of samples and conduction of the experiments; BMC: Collection of samples and conduction of the experiments; FBM: Collection of samples and conduction of the experiments; CLTD: Collection of samples and conduction of the experiments; GRdAT: Collection of samples and conduction of the experiments; RCRC: Collection of samples and conduction of the experiments, Participated in writing the paper and its critical review; BSS: Collection of samples and conduction of the experiments; LB: Collection of samples and conduction of the experiments; Participated in writing the paper and its critical review; JCdO: Conduction of the experiments, Analysis and interpretation of data, Participated in writing the paper and its critical review; DA: Conduction of the experiments, Analysis and interpretation of data, Participated in writing the paper and its critical review; DFG: Conduction of the experiments, Analysis and interpretation of data, Participated in Participated in writing the paper and its critical review; ACB: Conduction of the experiments, Analysis and interpretation of data, Participated in writing the paper and its critical review; RW: Conduction of the experiments, Analysis and interpretation of data, Participated in writing the paper and its critical review; JMA: Acquisition and organization of clinical data from medical records; RdSP: Acquisition and organization of clinical data from medical records; VJWB: Acquisition and organization of clinical data from medical records; BMMdA: Participated in writing the paper and its critical review; MBN: Conception and design of the study, Conducted the experiments, Acquisition, analysis and interpretation of data, Writing the paper and its critical, Study supervisor.
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