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[This corrects the article DOI: 10.1007/s43465-021-00437-y.].
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BACKGROUND: To determine the optimal direction of the syndesmotic screw and to introduce a consistent landmark for practical application by analyzing three-dimensional (3D) modeling and virtual implantation. METHODS: A total of 105 cadaveric lower legs (50 males and 55 females; average height, 160.6 ± 7.1 cm) were used to reconstruct a 3D model by using the Mimics® software and the joint morphology was evaluated. Syndesmotic cylinders (Ø3.5 mm/Length 100 mm) were transversely placed in the proximal end of the incisura fibularis for simulating screw fixation. The tibial proximal cylinder, which was tangent to the posterior tibial condyles, was traced and the angle between the two cylinders was measured as the tibial torsion angle (TTA). After rotating the syndesmotic cylinder parallel to the ground, the overlapping degree between the proximal fibula and tibia was assessed as a radiologic indicator. RESULTS: Concerning tibial torsion, the TTA was an average of 36.7° (range, 17.2°-54.4°; SD, 8.78) When the syndesmotic cylinder was rotated to be parallel to the ground, the proximal fibula had nonlinear or linear overlap with the lateral border of the tibia, regardless of the joint morphology. In this non-overlapping view, three Weber's indices for normal fibular length could be better visualized than the mortise view. CONCLUSION: The syndesmotic cylinder in the proximal end of the incisura fibularis could be consistently placed parallel to the ground by internally rotating the tibia until there was a nonlinear or linear overlap between the proximal fibula and the tibia, regardless of the joint morphology.
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Spinal cord injury (SCI) frequently results in chronic neuropathic pain (CNP). However, the understanding of brain neural circuits in CNP modulation is unclear. The present study examined the changes of ventral tegmental area (VTA) putative GABAergic and dopaminergic neuronal activity with CNP attenuation in rats. SCI was established by T10 clip compression injury (35 g, 1 min) in rats, and neuropathic pain behaviors, in vivo extracellular single-cell recording of putative VTA gamma-aminobutyric acid (GABA)/dopamine neurons, extracellular GABA level, glutamic acid decarboxylase (GAD), and vesicular GABA transporters (VGATs) were measured in the VTA, respectively. The results revealed that extracellular GABA level was significantly increased in the CNP group (50.5 ± 18.9 nM) compared to the sham control group (10.2 ± 1.7 nM). In addition, expression of GAD65/67, c-Fos, and VGAT exhibited significant increases in the SCI groups compared to the sham control group. With regard to neuropathic pain behaviors, spontaneous pain measured by ultrasound vocalizations (USVs) and evoked pain measured by paw withdrawal thresholds showed significant alteration, which was reversed by intravenous (i.v.) administration of morphine (0.5-5.0 mg/kg). With regard to in vivo electrophysiology, VTA putative GABAergic neuronal activity (13.6 ± 1.7 spikes/sec) and putative dopaminergic neuronal activity (2.4 ± 0.8 spikes/sec) were increased and decreased, respectively, in the SCI group compared to the sham control group. These neuronal activities were reversed by i.v. administration of morphine. The present study suggests that chronic increase of GABAergic neuronal activity suppresses dopaminergic neuronal activity in the VTA and is responsible for negative emotion and motivation for attenuation of SCI-induced CNP.
