Articles: function.
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The central sensitization inventory (CSI) is a questionnaire that has been widely used as a tool for assessing symptoms associated with sensitization. However, its ability to identify individuals with this phenomenon has recently been questioned. The aim of this study was to assess the correlation of CSI with psychosocial and psychophysical factors in patients with painful TMD diagnosed according to diagnostic criteria for temporomandibular disorders (DC/TMD) and asymptomatic controls, as well as to determine the influence of these variables on the CSI scores variations. ⋯ The research highlights a noteworthy relationship between the central sensitization inventory and psychological factors, emphasizing their substantial influence on inventory values. This correlation offers crucial insights into mental health markers within the questionnaire. Additionally, the lack of connection with pain amplification implies a necessary re-evaluation of the inventory's diagnostic suitability, especially in cases of painful temporomandibular disorders. Thus, caution is urged in its application for identifying CS in these individuals.
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Anesthesia and analgesia · Feb 2025
Interhemispheric and Corticothalamic White-Matter Dysfunction Underlies Affective Morbidity and Impaired Pain Modulation in Chronic Pain.
Although patients with chronic pain show behavioral signs of impaired endogenous pain modulation, responsible cerebral networks have yet to be anatomically delineated. We used diffusion tensor imaging (DTI) to examine the white-matter alterations in patients with chronic pain compared with healthy subjects. We further measured thermal pain modulatory responses using the offset analgesia (OA) paradigm. We tested whether the white-matter indices be associated with psychophysical parameters reflecting morbidity and modulatory responses of pain in patients, and whether they could serve as diagnostic biomarkers of chronic pain. ⋯ Patients with chronic pain showed dysfunction of the white matter concerned with interhemispheric communication of sensorimotor information as well as descending corticothalamic modulation of pain in association with affective morbidity and altered temporal dynamics of pain perception. We suggest that an impaired interhemispheric modulation of pain, through the corpus callosum, might be a novel cerebral mechanism in chronification of pain.
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Spinal cord injury leads to hyperexcitability and dysfunction in spinal sensory processing. As hyperexcitable circuits can become epileptiform, we explored whether such activity emerges in a thoracic spinal cord injury (SCI) contusion model of neuropathic pain. Recordings from spinal sensory axons in multiple below-lesion segmental dorsal roots demonstrated that SCI facilitated the emergence of spontaneous ectopic burst spiking in afferent axons, which were correlated across multiple adjacent dorsal roots. ⋯ We conclude that spinal cord injury promotes the emergence of epileptiform activity in spinal sensory networks that promote profound corruption of sensory signaling. This includes hyperexcitability and bursting by ectopic spiking in afferent axons that propagate bidirectionally by reentrant central and peripheral projections as well as sensory circuit hypoexcitability during the burst refractory period. More broadly, the work links circuit hyperexcitability to epileptiform circuit emergence, further strengthening it as a conceptual basis to understand features of sensory dysfunction and neuropathic pain.