Central neuropathic pain

Rosner, Jan; de Andrade, Daniel C.; Davis, Karen D.; Gustin, Sylvia M.; Kramer, John L. K.; Seal, Rebecca P.; Finnerup, Nanna B.

doi:10.1038/s41572-023-00484-9

Cited by 25 publications

(7 citation statements)

References 235 publications

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“…Previous studies investigating whether TGI is enhanced or reduced in specific clinical populations failed to account for the inter-individual differences in thermal sensitivity (e.g., [21,22]). Given the proposed role of TGI as a model for chronic pain in conditions such as central neuropathic [37,38] and nociplastic pain [11,29], adopting an approach that captures the entire spectrum of individual responses to TGI is crucial for elucidating its significance in clinical settings.…”

Section: Discussionmentioning

confidence: 99%

Assessing Individual Sensitivity to the Thermal Grill Illusion: A Two-Dimensional Adaptive Psychophysical Approach

Sardeto Deolindo,

Ehmsen,

Courtin

et al. 2024

Preprint

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In the thermal grill illusion (TGI), the spatial alternation of non-noxious warm and cold temperatures elicits burning sensations that resemble the presence of noxious stimuli. Previous research has largely relied on the use of specific temperature values (i.e., 20°C and 40°C) to study this phenomenon in both healthy individuals and patient populations. However, this methodology fails to account for inter-individual differences in thermal sensitivity, limiting the precision with which TGI responses can be evaluated across diverse populations. To address this gap, we created a Two-Dimensional Thermal Grill Calibration (2D-TGC) protocol, enabling an efficient and precise estimation of the combinations of warm and cold temperatures needed to elicit burning sensations tailored to each individual. By applying the 2D-TGC protocol in 43 healthy participants, we demonstrated key findings: (1) The TGI can be thresholded using an adaptive psychophysical method. (2) Multiple combinations of warm and cold temperatures can elicit this phenomenon. (3) The protocol facilitated the identification of temperature combinations that elicit TGI with varying levels of probability, intensity, and perceived quality ranging from freezing cold to burning hot. (4) TGI responsivity can be quantified as a continuous variable, moving beyond the conventional classification of individuals as responders vs. non-responders based on arbitrary temperature values. The 2D-TGC offers a comprehensive approach to investigate the TGI across populations with altered thermal sensitivity, and can be integrated with other methods (e.g., neuroimaging) to elucidate the mechanisms responsible for perceptual illusions in the thermo-nociceptive system.

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Section: Discussionmentioning

confidence: 99%

Assessing Individual Sensitivity to the Thermal Grill Illusion: A Two-Dimensional Adaptive Psychophysical Approach

Sardeto Deolindo,

Ehmsen,

Courtin

et al. 2024

Preprint

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“…Neuropathic pain presents a signi cant global health challenge, impacting around 6.9-10% of the global population, necessitating novel treatment approaches (Orhurhu et al 2020;Rosner et al 2023). Mitochondria play a crucial role in regulating cell death, and various forms of cell death have been linked to neuroimmune mechanisms in neuropathic pain (Bock & Tait 2020; L. Li et al 2024).…”

Section: Discussionmentioning

confidence: 99%

“…Neuropathic pain (NP) refers to pain that arises from damage or dysfunction in the somatosensory nerve system (Rosner et al 2023). Risk factors associated with NP include conditions such as diabetes, nerve compression, traumatic events, oxidative stress, cancer, and in ammation (Gilron et al 2015; Ouyang et al 2024).…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction and Disulfidptosis Co-regulate Neuronal cell in Neuropathic Pain Based on Bioinformatics Analysis

Ge,

Song,

Tao

et al. 2024

Preprint

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Neuropathic pain affects approximately 6.9-10% of the world's population and necessitates the development of novel treatments. Mitochondria are essential in the regulation of cell death. Neuroimmune mechanisms are implicated in various forms of cell death associated with neuropathic pain. However, the specific involvement of mitochondrial dysfunction and disulfidptosis in neuropathic pain remains uncertain. Further research is required to gain a better understanding of their combined contribution. Our comprehensive study employs a variety of bioinformatic analysis methods, including differential gene analysis, weighted gene co-expression network analysis, machine learning, functional enrichment analysis, immune infiltration, sub-cluster analysis, single-cell dimensionality reduction and cell-cell communicationto gain insight into the molecular mechanisms behind these processes. Our study rationally defines a list of key gene sets for mitochondrial dysfunction and disulfidptosis. 6 hub mitochondrial genes and 3 disulfidptosis-related genes (DRGs) were found to be associated with NP. The key genes were predominantly expressed in neurons and were lowly expressed in the NP group compared to SHAM. In addition, our macrophages used the APP-CD74 pathway to interact with neurons. These results suggest that NP is interconnected with the mechanistic processes of mitochondrial dysfunction and disulfidptosis, which may contribute to clinically targeted therapies.

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“…Several reasons could explain this. Patients with more severe injuries can be reasonably assumed to have a higher risk of experiencing headache, both from peripheral sources such as the dura mater and bone, which are innervated by pain receptors called nociceptors [ 4 ], and from central sources, such as lesions in the central somatosensory nervous system [ 41 ]. Additionally, PTH is widely prevalent after mild TBI, which may be attributed to differences in its diagnosis among studies, the length of time between the injury and evaluation, and the specific population being tested (e.g.…”

Section: Discussionmentioning

confidence: 99%

Frequency and predictors of headache in the first 12 months after traumatic brain injury: results from CENTER-TBI

Howe,

Andelic,

Brunborg

et al. 2024

J Headache Pain

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Background Headache is a prevalent and debilitating symptom following traumatic brain injury (TBI). Large-scale, prospective cohort studies are needed to establish long-term headache prevalence and associated factors after TBI. This study aimed to assess the frequency and severity of headache after TBI and determine whether sociodemographic factors, injury severity characteristics, and pre- and post-injury comorbidities predicted changes in headache frequency and severity during the first 12 months after injury. Methods A large patient sample from the Collaborative European NeuroTrauma Effectiveness Research in Traumatic Brain Injury (CENTER-TBI) prospective observational cohort study was used. Patients were stratified based on their clinical care pathway: admitted to an emergency room (ER), a ward (ADM) or an intensive care unit (ICU) in the acute phase. Headache was assessed using a single item from the Rivermead Post-Concussion Symptoms Questionnaire measured at baseline, 3, 6 and 12 months after injury. Mixed-effect logistic regression analyses were applied to investigate changes in headache frequency and associated predictors. Results A total of 2,291 patients responded to the headache item at baseline. At study enrolment, 59.3% of patients reported acute headache, with similar frequencies across all strata. Female patients and those aged up to 40 years reported a higher frequency of headache at baseline compared to males and older adults. The frequency of severe headache was highest in patients admitted to the ICU. The frequency of headache in the ER stratum decreased substantially from baseline to 3 months and remained from 3 to 6 months. Similar trajectory trends were observed in the ICU and ADM strata across 12 months. Younger age, more severe TBI, fatigue, neck pain and vision problems were among the predictors of more severe headache over time. More than 25% of patients experienced headache at 12 months after injury. Conclusions Headache is a common symptom after TBI, especially in female and younger patients. It typically decreases in the first 3 months before stabilising. However, more than a quarter of patients still experienced headache at 12 months after injury. Translational research is needed to advance the clinical decision-making process and improve targeted medical treatment for headache. Trial registration ClinicalTrials.gov NCT02210221.

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Central neuropathic pain

Cited by 25 publications

References 235 publications

Assessing Individual Sensitivity to the Thermal Grill Illusion: A Two-Dimensional Adaptive Psychophysical Approach

Assessing Individual Sensitivity to the Thermal Grill Illusion: A Two-Dimensional Adaptive Psychophysical Approach

Mitochondrial Dysfunction and Disulfidptosis Co-regulate Neuronal cell in Neuropathic Pain Based on Bioinformatics Analysis

Frequency and predictors of headache in the first 12 months after traumatic brain injury: results from CENTER-TBI

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