Articles: cations.
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Cervical laminoplasty is commonly used to treat cervical spondylotic myelopathy (CSM) and ossification of the posterior longitudinal ligament (OPLL). Postoperative kyphotic changes can restrict spinal cord dorsal shift, leading to poor neurological outcomes. This study analyzes risk factors for loss of cervical lordosis (LCL) after laminoplasty in 3 groups: CSM, continuous OPLL, and other OPLL. It also evaluates postoperative changes in cervical spine parameters: C2-7 sagittal vertical axis, C2-7 Cobb angle (CA), T1 slope, and C2 slope. ⋯ The continuous OPLL group had a lower likelihood of postoperative kyphosis due to structural support. K-line tilt, dynamic extension reserve, and extensor muscle volume were significant predictors of LCL in CSM and segmental OPLL groups. K-line tilt is a valuable radiographic parameter for predicting outcomes and guiding surgical decisions in cervical laminoplasty patients.
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A well-recognized molecular entity involved in pain-related neuroplasticity is the N-methyl-D-aspartate receptor (NMDAR), which is crucial for developing chronic pain. Likewise, the pannexin 1 (Panx1) channel has been described as necessary for initiating and maintaining neuropathic pain, driving nociceptive signals dependent on spinal NMDAR through several possible mechanisms. Through behavioral, pharmacological, and molecular approaches, our study in male rats has revealed several key findings: (1) neurons located in spinal cord laminae I and II express functional Panx1 channels in both neuropathic and sham rats. ⋯ Notably, while 10Panx successfully alleviates hyperalgesia, it does not alter pSrc expression; and (4) NMDA-stimulated YOPRO-1 uptake in neurons of laminae I-II of spinal cord slices were prevented by the NMDAR antagonist D-AP5, the Src inhibitor PP2 (but not PP3), as well as with the 10Panx and carbenoxolone. Therefore, NMDAR activation in dorsal horn neurons triggers an NMDAR-Src-Panx1 signaling pathway, where Panx1 acts as an enhancing effector in neuropathic pain. This implies that disrupting the NMDAR-Panx1 communication (eg, through Src inhibitors and/or Panx1 blockers) may offer a valuable strategy for managing some forms of chronic pain.
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The spread of pain across body locations remains poorly understood but may provide important insights into the encoding of sensory features of noxious stimuli by populations of neurons. In this psychophysical experiment, we hypothesized that more intense noxious stimuli would lead to spread of pain, but more intense light stimuli would not produce perceptual radiation. Fifty healthy volunteers (27 females, 23 males, ages 14-44 years) participated in this study wherein noxious stimuli (43, 45, 47, and 49°C) were applied to glabrous (hand) and hairy skin (forearm) skin with 5-second and 10-second durations. ⋯ Pain radiation was more pronounced in hairy than glabrous skin (P < 0.05) and was more pronounced with longer stimulus duration (P < 0.001). Pain intensity explained only 14% of the pain radiation variability. The relative independence of the pain radiation from pain intensity indicates that distinct components of population coding mechanisms may be involved in the spatial representation of pain vs intensity coding.
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Adult trauma centers, including combined pediatric/adult centers (CPACs), see high volumes of penetrating trauma. Few studies have compared outcomes of adolescents presenting with gunshot wounds (GSWSs) at CPACs vs. pediatric only hospitals (POHs). This study aimed to compare injury patterns, complications, and mortality for adolescents sustaining GSWs presenting to CPACs vs POHs, hypothesizing decreased associated risk of complications and mortality at CPACs. ⋯ Adolescent GSW patients had similar associated risk of mortality and complications when comparing POHs to CPACs. This suggests that adolescents with GSWs receive similar care at both CPACs and POHs. Additional research is warranted to corroborate these findings.