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The relationship between osteogenesis and angiogenesis is complex. Normal bone development requires angiogenesis, mediated by vascular endothelial growth factor A (VEGFA). Studies have demonstrated through systemic inhibition or genetic modification that VEGFA is indispensable for several types of bone repair, presumably via its role in supporting angiogenesis. But a direct role for VEGFA within osteoblasts, in the absence of angiogenesis, has also been suggested. To address the question of whether VEGFA from osteoblasts supports bone formation directly, we applied anabolic loading to induce lamellar bone formation in mice, a process shown to be independent of angiogenesis. We hypothesized that VEGFA from osteoblasts is required for lamellar bone formation. To test this hypothesis, we applied axial tibial compression to inducible Cre/LoxP mice from three lines. Vegfa fl/fl mice were crossed with Ubiquitin C (UBC), Osterix (Osx) and Dentin-Matrix Protein 1 (DMP1) Cre-ERT2 mice to target all cells, (pre)osteoblast-lineage cells, and mature osteoblasts and osteocytes, respectively. Genotype effects were determined by comparing control (Vegfa fl/fl ) and Cre+ (VegfaΔ) mice for each line. At 5 months of age tamoxifen was injected for 5 days followed by a 3-week clearance prior to loading. Female and male mice (N = 100) were loaded for 5 days to peak forces to engender -3100 με peak compressive strain and processed for dynamic histomorphometry (day 12). Percent MS/BS increased 20-70 % as a result of loading, with no effect of genotype in Osx or Dmp1 lines. In contrast, the UBC groups had a significant decrease in relative periosteal BFR/BS in VegfaΔ vs. Vegfa fl/fl mice. The UBC line did not have any cortical bone phenotype in non-loaded femurs. In summary, dynamic histomorphometry data confirmed that tibial loading induces lamellar bone formation. Contrary to our hypothesis, there was no decrease in loading-induced bone formation in the Osx or Dmp1 lines in the absence of VEGFA. There was a decrease in bone formation in the UBC line where all cells were targeted. This result indicates that VEGFA from a non-osteoblast cell source supports loading-induced lamellar bone formation, although osteoblast/osteocyte VEGFA is dispensable. These findings support a paracrine model whereby non-osteoblast VEGFA supports lamellar bone formation, independent of angiogenesis., (Copyright © 2022 Elsevier Inc. All rights reserved.)

Trigeminal neuralgia (TN), one of the most intense forms of facial pain, has been the subject of great clinical interest. Significant advances have been made in its management, including surgical treatment and imaging of the trigeminal nerve and associated neurovascular compression. The different options for surgical treatment, recent advances in each as well as novel methods of imaging of the trigeminal nerve focusing on diffusion tensor imaging/tractography will be discussed.

Object: Maximal resection of symptomatic cavernous angioma (CA), including its surrounding gliosis if possible, has been recommended to minimize the risk of seizures or (re)bleeding. However, despite recent neurosurgical advances, such extensive CA removal is still a challenge in eloquent areas. The authors report a consecutive series of patients who underwent awake surgery for CA within the left dominant hemisphere in which intraoperative cortical-subcortical electrical stimulation was used., Methods: Nine patients harboring a CA that was revealed by seizures in 6 cases and bleeding in 3 cases underwent resection. All CAs were located in the left dominant hemisphere: 3 temporal, 2 insular, 2 parietal, and 2 in the parietotemporal region. Awake mapping was performed in all cases by using intraoperative cortical-subcortical electrical stimulation and ultrasonography (except in 1 insular CA in which a neuronavigation system was used)., Results: Total removal of the CA was achieved in all patients, with identification and preservation of language and sensory-motor structures. In addition, the pericavernomatous gliosis was removed in 7 cases, according to the functional boundaries provided by intraoperative subcortical stimulation. In 2 cases, subcortical mapping revealed eloquent areas within the surrounding gliosis, which was voluntarily avoided. There was no postsurgical permanent deficit, no rebleeding, and no epilepsy in 7 cases (2 patients had rare seizures in the 1st year or two after surgery, and then complete arrest), with a mean follow-up of 28.5 months (range 3-64 months)., Conclusions: These results suggest that intraoperative cortical-subcortical stimulation in awake patients represents a valuable adjunct to image-guided surgery with the aim of selecting the safer surgical approach for CAs involving eloquent areas. Moreover, such online mapping can be helpful when removing the pericavernomatous gliosis while preserving functional structures, which can persist within the hemosiderin rim. Thus, the authors propose that awake surgery be routinely considered, both to optimize the resection and to improve the quality of life through seizure control and avoidance of (re)bleeding for CAs located in the left dominant hemisphere.

Object: There are no specific studies about cranial nerve (CN) injury following mild head trauma (Glasgow Coma Scale Score 14-15) in the literature. The aim of this analysis was to document the incidence of CN injury after mild head trauma and to correlate the initial CT findings with the final outcome 1 year after injury., Methods: The authors studied 49 consecutive patients affected by minor head trauma and CN lesions between January 2000 and January 2006. Detailed clinical and neurological examinations as well as CT studies using brain and bone windows were performed in all patients. Based on the CT findings the authors distinguished 3 types of traumatic injury: no lesion, skull base fracture, and other CT abnormalities. Patients were followed up for 1 year after head injury. The authors distinguished 3 grades of clinical recovery from CN palsy: no recovery, partial recovery, and complete recovery., Results: Posttraumatic single nerve palsy was observed in 38 patients (77.6%), and multiple nerve injuries were observed in 11 (22.4%). Cranial nerves were affected in 62 cases. The most affected CN was the olfactory nerve (CN I), followed by the facial nerve (CN VII) and the oculomotor nerves (CNs III, IV, and VI). When more than 1 CN was involved, the most frequent association was between CNs VII and VIII. One year after head trauma, a CN deficit was present in 26 (81.2%) of the 32 cases with a skull base fracture, 12 (60%) of 20 cases with other CT abnormalities, and 3 (30%) of 10 cases without CT abnormalities., Conclusions: Trivial head trauma that causes a minor head injury (Glasgow Coma Scale Score 14-15) can result in CN palsies with a similar distribution to moderate or severe head injuries. The CNs associated with the highest incidence of palsy in this study were the olfactory, facial, and oculomotor nerves. The trigeminal and lower CNs were rarely damaged. Oculomotor nerve injury can have a good prognosis, with a greater chance of recovery if no lesion is demonstrated on the initial CT scan.