Immersive Surgical Anatomy of the Far-Lateral Approach.

The far-lateral (FL) approach is a classic neurosurgical technique that enables access to the craniocervical junction, which includes the lower clivus, the anterior foramen magnum, and the first two cervical vertebrae. The FL approach also provides access to the inferior cranial nerves (i.e., CN IX, CN X, CN XI, and CN XII), distal portions of the vertebral artery (VA), and inferior basilar trunk. Recent advances in three-dimensional (3D) technology as well as dissections allow for a better understanding of the spatial relationships between anatomical landmarks and neurovascular structures encountered during neurosurgical procedures. This study aims to create a collection of volumetric models (VMs) obtained from cadaveric dissections that depict the FL approach's relevant anatomy and surgical techniques. We describe the relevant multilayer anatomy involved in the FL approach and discuss modifications of this approach as well. Five embalmed heads and two dry skulls were used to record and simulate the FL approach. Relevant steps and anatomy of the FL approach were recorded using 3D scanning technology (e.g., photogrammetry and structured light scanning) to construct high-resolution VMs. Images and VMs were generated to demonstrate major anatomical landmarks for the FL approach. The interactive models allow for clear visualization of the surgical anatomy and windows in 3D and extended reality, rendering a closer look at the nuances of the topography experienced in the laboratory. VMs can be valuable resources for surgical planning and anatomical education by accurately depicting important landmarks.

Immersive Surgical Anatomy of the Craniocervical Junction.

With the advent and increased usage of posterior, lateral, and anterior surgical approaches to the craniocervical junction (CCJ), it is essential to have a sound understanding of the osseous, ligamentous, and neurovascular layers of this region as well as their three-dimensional (3D) orientations and functional kinematics. Advances in 3D technology can be leveraged to develop a more nuanced and comprehensive understanding of the CCJ, classically depicted via dissections and sketches. As such, this study aims to illustrate - with the use of 3D technologies - the major anatomical landmarks of the CCJ in an innovative and informative way. Photogrammetry, structured light scanning, and 3D reconstruction of medical images were used to generate these high-resolution volumetric models. A clear knowledge of the critical anatomical structures and morphometrics of the CCJ is crucial for the diagnosis, classification, and treatment of pathologies in this transitional region.

Anterior cervical discectomy and fusion performed using structural allograft or polyetheretherketone: pseudarthrosis and revision surgery rates with minimum 2-year follow-up.

OBJECTIVE: Both structural allograft and PEEK have been used for anterior cervical discectomy and fusion (ACDF). There are reports that PEEK has a higher pseudarthrosis rate than structural allograft. The authors compared pseudarthrosis, revision, subsidence, and loss of lordosis rates in patients with PEEK and structural allograft. METHODS: The authors performed a retrospective review of patients who were treated with ACDF at their hospital between 2005 and 2017. Inclusion criteria were adult patients with either PEEK or structural allograft, anterior plate fixation, and a minimum 2-year follow-up. Exclusion criteria were hybrid PEEK and allograft cases, additional posterior surgery, adjacent corpectomies, infection, tumor, stand-alone or integrated screw and cage devices, bone morphogenetic protein use, or lack of a minimum 2-year follow-up. Demographic variables, number of treated levels, interbody type (PEEK cage vs structural allograft), graft packing material, pseudarthrosis rates, revision surgery rates, subsidence, and cervical lordosis changes were collected. These data were analyzed by Pearson's chi-square test (or Fisher's exact test, according to the sample size and expected value) and Student t-test. RESULTS: A total of 168 patients (264 levels total, mean follow-up time 39.5 ± 24.0 months) were analyzed. Sixty-one patients had PEEK, and 107 patients had structural allograft. Pseudarthrosis rates for 1-level fusions were 5.4% (PEEK) and 3.4% (allograft) (p > 0.05); 2-level fusions were 7.1% (PEEK) and 8.1% (allograft) (p > 0.05); and ≥ 3-level fusions were 10% (PEEK) and 11.1% (allograft) (p > 0.05). There was no statistical difference in the subsidence magnitude between PEEK and allograft in 1-, 2-, and ≥ 3-level ACDF (p > 0.05). Postoperative lordosis loss was not different between cohorts for 1- and 2-level surgeries. CONCLUSIONS: In 1- and 2-level ACDF with plating involving the same number of fusion levels, there was no statistically significant difference in the pseudarthrosis rate, revision surgery rate, subsidence, and lordosis loss between PEEK cages and structural allograft.

Speciation Theory of Carcinogenesis Explains Karyotypic Individuality and Long Latencies of Cancers.

It has been known for over 100 years that cancers have individual karyotypes and arise only years to decades after initiating carcinogens. However, there is still no coherent theory to explain these definitive characteristics of cancer. The prevailing mutation theory holds that cancers are late because the primary cell must accumulate 3⁻8 causative mutations to become carcinogenic and that mutations, which induce chromosomal instability (CIN), generate the individual karyotypes of cancers. However, since there is still no proven set of mutations that transforms a normal to a cancer cell, we have recently advanced the theory that carcinogenesis is a form of speciation. This theory predicts carcinogens initiate cancer by inducing aneuploidy, which automatically unbalances thousands of genes and thus catalyzes chain-reactions of progressive aneuploidizations. Over time, these aneuploidizations have two endpoints, either non-viable karyotypes or very rarely karyotypes of new autonomous and immortal cancers. Cancer karyotypes are immortalized despite destabilizing congenital aneuploidy by clonal selections for autonomy-similar to those of conventional species. This theory predicts that the very low probability of converting the karyotype of a normal cell to that of a new autonomous cancer species by random aneuploidizations is the reason for the karyotypic individuality of new cancers and for the long latencies from carcinogens to cancers. In testing this theory, we observed: (1) Addition of mutagenic and non-mutagenic carcinogens to normal human and rat cells generated progressive aneuploidizations months before neoplastic transformation. (2) Sub-cloning of a neoplastic rat clone revealed heritable individual karyotypes, rather than the non-heritable karyotypes predicted by the CIN theory. (3) Analyses of neoplastic and preneoplastic karyotypes unexpectedly identified karyotypes with sets of 3⁻11 new marker chromosomes without detectable intermediates, consistent with single-step origins. We conclude that the speciation theory explains logically the long latencies from carcinogen exposure and the individuality of cancers. In addition, the theory supports the single-step origins of cancers, because karyotypic autonomy is all-or-nothing. Accordingly, we propose that preneoplastic aneuploidy and clonal neoplastic karyotypes provide more reliable therapeutic indications than current analyses of thousands of mutations.