Dissecting central post-stroke pain:a controlled symptom-psychophysical characterization

Central post-stroke pain affects up to 12% of stroke survivors and is notoriously refractory to treatment. However, stroke patients often suffer from other types of pain of non-neuropathic nature (musculoskeletal, inflammatory, complex regional) and no head-to-head comparison of their respective clinical and somatosensory profiles has been performed so far. We compared 39 patients with definite central neuropathic post-stroke pain with two matched control groups: 32 patients with exclusively non-neuropathic pain developed after stroke and 31 stroke patients not complaining of pain. Patients underwent deep phenotyping via a comprehensive assessment including clinical exam, questionnaires and quantitative sensory testing to dissect central post-stroke pain from chronic pain in general and stroke. While central post-stroke pain was mostly located in the face and limbs, non-neuropathic pain was predominantly axial and located in neck, shoulders and knees (P < 0.05). Neuropathic Pain Symptom Inventory clusters burning (82.1%, n = 32, P < 0.001), tingling (66.7%, n = 26, P < 0.001) and evoked by cold (64.1%, n = 25, P < 0.001) occurred more frequently in central post-stroke pain. Hyperpathia, thermal and mechanical allodynia also occurred more commonly in this group (P < 0.001), which also presented higher levels of deafferentation (P < 0.012) with more asymmetric cold and warm detection thresholds compared with controls. In particular, cold hypoesthesia (considered when the threshold of the affected side was <41% of the contralateral threshold) odds ratio (OR) was 12 (95% CI: 3.8–41.6) for neuropathic pain. Additionally, cold detection threshold/warm detection threshold ratio correlated with the presence of neuropathic pain (ρ = −0.4, P < 0.001). Correlations were found between specific neuropathic pain symptom clusters and quantitative sensory testing: paroxysmal pain with cold (ρ = −0.4; P = 0.008) and heat pain thresholds (ρ = 0.5; P = 0.003), burning pain with mechanical detection (ρ = −0.4; P = 0.015) and mechanical pain thresholds (ρ = −0.4, P < 0.013), evoked pain with mechanical pain threshold (ρ = −0.3; P = 0.047). Logistic regression showed that the combination of cold hypoesthesia on quantitative sensory testing, the Neuropathic Pain Symptom Inventory, and the allodynia intensity on bedside examination explained 77% of the occurrence of neuropathic pain. These findings provide insights into the clinical-psychophysics relationships in central post-stroke pain and may assist more precise distinction of neuropathic from non-neuropathic post-stroke pain in clinical practice and in future trials

Imagerie de la douleur

Ce travail reprend les données d’imagerie fonctionnelle cérébrale appliquée à l’étude des phénomènes douloureux chez l’Homme. Contre tous les préjugés qui auraient volontiers désigné le thalamus, l’aire somato-sensorielle primaire (SI) ou le cortex cingulaire antérieur comme des sites principaux d’intégration de la douleur chez l’homme, les phénomènes physiologiques nociceptifs concernent avant tout et de manière constante les aires somato-sensorielles secondaires et insulaires. L’enregistrement de potentiels évoqués à des stimulations laser par le biais d’électrodes implantées directement dans ces aires, mais aussi la stimulation directe de ces aires, qui induit des sensations douloureuses, sont des arguments très forts désignant ces aires comme des sites majeurs pour l’intégration de l’aspect sensoriel de la douleur et de son intensité. De même, les techniques d’imagerie fonctionnelle ont permis d’identifier le recrutement de réponses anormales, excessives, en cas de douleurs neuropathiques chroniques, en particulier dans les aires insulaires et SII, et ce de façon bilatérale. À l’inverse, les processus permettant de soulager ces douleurs impliquent l’activation des structures préfrontales médiales et cingulaires rostrales, qui fait intervenir un système inhibiteur descendant passant par la substance grise péri-aqueducale (SGPA). Les opioïdes endogènes pourraient être impliqués dans ce système inhibiteur

Imagerie fonctionnelle cérébrale appliquée à l’analyse des phénomènes douloureux

Ce travail reprend les données d’imagerie fonctionnelle cérébrale appliquée à l’étude des phénomènes douloureux chez l’homme. Contre tous les préjugés qui auraient volontiers désigné le thalamus, l’aire somato-sensorielle primaire SI ou le cortex cingulaire antérieur comme des sites principaux d’intégration de la douleur chez l’homme, les phénomènes physiologiques nociceptifs concernent avant tout et de manière constante les aires somato-sensorielles secondaires et insulaires. L’enregistrement de potentiels évoqués à des stimulations laser par le biais d’électrodes implantées directement dans ces aires, mais aussi la stimulation directe de ces aires, qui induit des sensations douloureuses, sont des arguments très forts désignant ces aires comme des sites majeurs pour l’intégration de l’aspect sensoriel de la douleur et de son intensité. De même, les techniques d’imagerie fonctionnelle ont permis d’identifier le recrutement de réponses anormales, excessives, en cas de douleurs neuropathiques chroniques, en particulier dans les aires insulaires et SII, et ce de façon bilatérale. À l’inverse, les processus permettant de soulager ces douleurs impliquent l’activation des structures préfrontales médiales et cingulaires rostrales, qui fait intervenir un système inhibiteur descendant passant par la substance grise péri-acqueducale (SGPA). Les opioïdes endogènes pourraient être impliqués dans ce système inhibiteur

Pain matrices and neuropathic pain matrices: A review.

International audience: The pain matrix is conceptualised here as a fluid system composed of several interacting networks. A nociceptive matrix receiving spinothalamic projections (mainly posterior operculoinsular areas) ensures the bodily specificity of pain and is the only one whose destruction entails selective pain deficits. Transition from cortical nociception to conscious pain relies on a second-order network, including posterior parietal, prefrontal and anterior insular areas. Second-order regions are not nociceptive-specific; focal stimulation does not evoke pain, and focal destruction does not produce analgesia, but their joint activation is necessary for conscious perception, attentional modulation and control of vegetative reactions. The ensuing pain experience can still be modified as a function of beliefs, emotions and expectations through activity of third-order areas, including the orbitofrontal and perigenual/limbic networks. The pain we remember results from continuous interaction of these subsystems, and substantial changes in the pain experience can be achieved by acting on each of them. Neuropathic pain (NP) is associated with changes in each of these levels of integration. The most robust abnormality in NP is a functional depression of thalamic activity, reversible with therapeutic manoeuvres and associated with rhythmic neural bursting. Neuropathic allodynia has been associated with enhancement of ipsilateral over contralateral insular activation and lack of reactivity in orbitofrontal/perigenual areas. Although lack of response of perigenual cortices may be an epiphenomenon of chronic pain, the enhancement of ipsilateral activity may reflect disinhibition of ipsilateral spinothalamic pathways due to depression of their contralateral counterpart. This in turn may bias perceptual networks and contribute to the subjective painful experience

ETUDE DES DOULEURS NEUROLOGIQUES PAR LESION DU SYSTEME NERVEUX CENTRAL EN TOMOGRAPHIE D'EMISSION DE POSITONS (TEP) ET EVALUATION DES COMPOSANTES ATTENTIONNELLES DE LA DOULEUR CHEZ LE SUJET SAIN LORS D'UNE STIMULATION NOCIVE

LYON1-BU Santé (693882101) / SudocPARIS-BIUM (751062103) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

Narcolepsy Type 1 as an Autoimmune Disorder: Evidence, and Implications for Pharmacological Treatment

International audienceNarcolepsy type 1 (NT1) is a rare sleep disorder caused by the very specific loss of hypothalamic hypocretin (Hcrt)/orexin neurons. The exact underlying process leading to this destruction is yet unknown, but indirect evidence strongly supports an autoimmune origin. The association with immune-related genetic factors, in particular the strongest association ever reported in a disease with an allele of a human leukocyte antigen (HLA) gene, and with environmental factors (i.e., the H1N1 influenza infection and vaccination during the pandemic in 2009) are in favor of such a hypothesis. The loss of Hcrt neurons is irreversible, and NT1 is currently an incurable and disabling condition. Patients are managed with symptomatic medication, targeting the main symptoms (excessive daytime sleepiness, cataplexy, disturbed nocturnal sleep), and they require a lifelong treatment. Improved diagnostic tools, together with an increased understanding of the pathogenesis of NT1, may lead to new therapeutic and even preventive interventions. One future treatment could include Hcrt replacement, but this neuropeptide does not cross the blood-brain barrier. However, Hcrt receptor agonists may be promising candidates to treat NT1. Another option is immune-based therapies, administered at disease onset, with already some initiatives to slow down or stop the dysimmune process. Whether immune-based therapy could be beneficial in NT1 remains, however, to be proven

Retrieving autobiographical experience of painful events in a phantom limb: brain concomitants in a case report

International audienc

The Challenge of Mastication: Preparing a Bolus Suitable for Deglutition

The Challenge of Mastication: Preparing a Bolus Suitable for Deglutitio

The 'where' and the 'when' of the BOLD response to pain in the insular cortex. Discussion on amplitudes and latencies.

International audienceThe operculo-insular cortex has been recently pointed out to be the main area of the pain matrix to be involved in the integration of pain intensity. This fMRI study specified the pattern of response to laser stimuli by focusing on this cortical area, by optimizing the temporal sampling and by investigating pain-related differences in the amplitudes and latencies of the BOLD responses. Canonical and temporal derivative hemodynamic response function (HRF) and finite impulse response (FIR) modeling provided consistent results. Amplitude of BOLD response discriminated painful from non-painful conditions in posterior and mid-insular cortices, bilaterally. Pain conditions were characterized by a shortened latency (as compared to non-painful conditions) in the anterior insula. In the functional organization of the insula, these results suggest a double dissociation that can be summarized as the 'where' and the 'when' of the BOLD response to pain. These results suggest that differences in the amplitude of the BOLD activity in the posterior and in the mid-insular cortices as well as shortened latency of the response in the anterior insula deal with discriminative processes related to painful conditions