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1.
Eur J Neurol ; 30(1): 204-214, 2023 01.
Artículo en Inglés | MEDLINE | ID: mdl-36148823

RESUMEN

BACKGROUND AND PURPOSE: Advanced analysis of electroencephalography (EEG) data has become an essential tool in brain research. Based solely on resting state EEG signals, a data-driven, predictive and explanatory approach is presented to discriminate painful from non-painful diabetic polyneuropathy (DPN) patients. METHODS: Three minutes long, 64 electrode resting-state recordings were obtained from 180 DPN patients. The analysis consisted of a mixture of traditional, explanatory and machine learning analyses. First, the 10 functional bivariate connections best differentiating between painful and non-painful patients in each EEG band were identified and the relevant receiver operating characteristic was calculated. Later, those connections were correlated with selected clinical parameters. RESULTS: Predictive analysis indicated that theta and beta bands contain most of the information required for discrimination between painful and non-painful polyneuropathy patients, with area under the receiver operating characteristic curve values of 0.93 for theta and 0.89 for beta bands. Assessing statistical differences between the average magnitude of functional connectivity values and clinical pain parameters revealed that painful DPN patients had significantly higher cortical functional connectivity than non-painful ones (p = 0.008 for theta and p = 0.001 for alpha bands). Moreover, intra-band analysis of individual significant functional connections revealed a positive correlation with average reported pain in the previous 3 months in all frequency bands. CONCLUSIONS: Resting state EEG functional connectivity can serve as a highly accurate biomarker for the presence or absence of pain in DPN patients. This highlights the importance of the brain, in addition to the peripheral lesions, in generating the clinical pain picture. This tool can probably be extended to other pain syndromes.


Asunto(s)
Polineuropatías , Humanos , Biomarcadores , Encéfalo , Electroencefalografía , Dolor , Polineuropatías/diagnóstico
2.
Pain ; 163(5): 827-833, 2022 05 01.
Artículo en Inglés | MEDLINE | ID: mdl-34371518

RESUMEN

ABSTRACT: Endogenous pain modulation, as tested by the conditioned pain modulation (CPM) protocol, is typically less efficient in patients with chronic pain compared with healthy controls. We aimed to assess whether CPM is less efficient in patients with painful diabetic polyneuropathy (DPN) compared with those with nonpainful DPN. Characterization of the differences in central pain processing between these 2 groups might provide a central nervous system explanation to the presence or absence of pain in diabetic neuropathy in addition to the peripheral one. Two hundred seventy-one patients with DPN underwent CPM testing and clinical assessment, including quantitative sensory testing. Two modalities of the test stimuli (heat and pressure) conditioned to cold noxious water were assessed and compared between patients with painful and nonpainful DPN. No significant difference was found between the groups for pressure pain CPM; however, patients with painful DPN demonstrated unexpectedly more efficient CPMHEAT (-7.4 ± 1.0 vs -2.3 ± 1.6; P = 0.008). Efficient CPMHEAT was associated with higher clinical pain experienced in the 24 hours before testing (r = -0.15; P = 0.029) and greater loss of mechanical sensation (r = -0.135; P = 0.042). Moreover, patients who had mechanical hypoesthesia demonstrated more efficient CPMHEAT (P = 0.005). More efficient CPM among patients with painful DPN might result from not only central changes in pain modulation but also from altered sensory messages coming from tested affected body sites. This calls for the use of intact sites for proper assessment of pain modulation in patients with neuropathy.


Asunto(s)
Dolor Crónico , Diabetes Mellitus , Neuropatías Diabéticas , Neuralgia , Humanos , Dolor Crónico/complicaciones , Neuropatías Diabéticas/complicaciones , Neuralgia/complicaciones , Umbral del Dolor/fisiología , Sensación
3.
Pain Rep ; 5(3): e821, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32903910

RESUMEN

INTRODUCTION AND OBJECTIVES: Chronic pain is a common postcollision consequence. Wherein, a clearer understanding of acute pain can help stem the acute-to-chronic pain transition. However, the variability of acute pain is only partially explained by psychophysical pain characteristics as measured by quantitative sensory testing. The Pain Sensitivity Questionnaire (PSQ) may reflect inherent psychocognitive representations of patient's sensitivity and thus may reveal less-explored pain dimensions. In the vein of the biopsychosocial approach, this study aimed to explore whether PSQ holds additive value in explaining head and neck pain reports in very early acute-stage mild traumatic brain injury (mTBI) after collision, above the use of psychophysical assessment. METHODS: Study cohort (n = 130) consisted of mTBI patients (age range 19-66, 57 F) after accident with area-of-injury pain of at least 20 on the day of testing (mean pain 58.4 ± 21.6, range 20-100 Numerical Pain Scale) who underwent clinical, psychophysical, and pain-related psychological assessment within 72-hour after injury. RESULTS: Pain Sensitivity Questionnaire scores were significantly correlated with acute clinical, psychophysical, and pain-related psychological measures. Regression model (R 2 = 0.241, P < 0.001) showed that, together, age, sex, high PSQ, enhanced temporal summation, and less-efficient conditioned pain modulation explained head and neck pain variance. This model demonstrated that the strongest contribution to degree of postinjury pain was independently explained by PSQ (ß = 0.32) and then pressure pain threshold-conditioned pain modulation (ß = -0.25). CONCLUSION: Appraisal of cognitive daily-pain representations, by way of memory and imagination, provides an additional important dispositional facet to explain the variability in the acute mTBI postcollision clinical pain experience, above assessing nociceptive responsiveness to experimentally induced pain.

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