Background: The cavernous sinus (CS) is a highly vulnerable anatomical space, mainly for the neurovascular structures which it contains, therefore a detailed knowledge of its anatomy is mandatory for the surgical unlocking. To compare the anatomy of this region from different endoscopic and microsurgical operative corridors, also focusing on the corresponding anatomic landmarks met along these routes. Furthermore, we tried to define the safe entry zones to this venous space from these three different operative corridors and provide indications regarding the optimal approach according to the lesion location. Methods: Five embalmed and injected adult cadaveric specimens (10 sides) separately underwent dissection and exposure of the CS via superior eyelid endoscopic transorbital (SETOA), extended endoscopic endonasal transsphenoidal-transethmoidal (EEEA) and microsurgical transcranial fronto-temporo-orbito-zygomatic (FTOZ) approaches. The anatomical landmarks and the content of this venous space have been described and compared from these surgical perspectives. Results: The SETOA allowed the exposure of the entire lateral wall of the CS without entering its neurovascular structures and part of the posterior wall; furthermore, thanks to its anteroposterior trajectory, it allowed to disclose in a minimally invasive fashion, also the posterior ascending segment of the cavernous ICA with the related sympathetic plexus through the Mullan’s triangle. Through the anterolateral triangle, the transorbital corridor allowed to expose the lateral 180 degrees of vidian nerve and artery in the homonymous canal, the anterolateral aspect of the lacerum segment of the ICA, at its the transition zone from the petrous horizontal to the ascending posterior cavernous segment, surrounded by the carotid sympathetic plexus, and the medial Meckel’s cave. Conclusion: Different regions of the cavernous sinus are better exposed by different surgical corridors. The relationship of tumor and cranial nerves in the lateral wall guides the selection of the approach to cavernous sinus lesions. The transorbital endoscopic approach can be considered a safe and minimally invasive complementary surgical corridor to the well-established transcranial and endoscopic endonasal routes in the exposure of the cavernous sinus. Nevertheless, peer knowledge of the anatomy and a surgical learning curve are required.

Extreme atrophy of the maxilla poses still challenging for the clinicians. Some of the techniques used could be complex, risky, expensive, time consuming and should be performed, preferably, only by skilled surgeons. Most the commonly used techniques have been reported to have very high success percentages; however, sometimes complications may occur. In this regard, Premaxillary Device (PD) is a technique that has been devised to render more simple the reconstruction of extremely atrophic maxilla, trying to avoid more complicated and risky surgical procedures. Finite Element Analysis (FEA) allows evaluation of several differen aspects of dental implant biomechanics. Our results showed that the use of PD allows an optimal distribution of the stresses on the basal bone, avoiding tension peaks that could determine bone resorption or, even, implant failure. ANSYS has been used to perform this type of localized finite element analysis; with this type of analysis, it was possible to analyze the peri-crestal area of the plant more precisely and the PD through a more accurate reconstruction of the mesh element, which allowed us to mathematically solve the FEA solution. A most favorable biomechanical behavior has been found for the materials such as titanium alloys and reduce stress levels for bone, implants, screws, and abutments. Moreover, the stress values did not exceed bone strength limits for basal bone and titanium alloy. In conclusion, from a biomechanical point of view, PD could be considered a viable alternative for rehabilitation of severe atrophic maxilla.

The orbitofrontal cortex (OFC) area plays a critical role in human brain functions. However, susceptibility differences between paranasal sinuses and nasal cavity tissues often cause local field variations in the OFC during MRI, resulting in image distortions and signal loss. In this paper, we introduce a subject-friendly neck passive shim solution aimed at enhancing field homogeneity in the brain, specifically in the OFC region. Utilizing 3D gradient-echo pulse sequences, main magnetic field (B0) maps of four subjects’ brains were acquired at 4T MRI. Subsequently, these maps were decomposed into spherical harmonic coefficients and averaged. Optimal positions for placing shim elements on a semi-cylindrical surface, positioned slightly above the neck and below the chin, were computed. The findings indicate a substantial enhancement in B0 homogeneity, particularly within the OFC region, through the integration of this semi-cylindrical passive shim system in conjunction with first and second-order active shimming.

Spinocerebellar ataxia type 2 (SCA2) is caused by polyglutamine expansion in Ataxin-2 (ATXN2). This factor binds RNA/proteins to modify metabolism after stress, and to control calcium (Ca2+) homeostasis after stimuli, thus exerting crucial neuroprotection for cerebellar ataxias and corticospinal motor neuron degeneration. Our Atxn2-CAG100-Knock-In mouse faithfully models features observed in patients at pre-onset, early and terminal stages. Here, its cerebellar global RNA profiling revealed downregulation of signaling cascades to precede motor deficits. Validation work at mRNA/protein level defined alterations that were independent of constant physiological ATXN2 functions, but specific for RNA/aggregation toxicity, and progressive across the short lifespan. Earliest changes were detected at 3 months among Ca2+ channels/transporters (Itpr1, Ryr3, Atp2a2, Atp2a3, Trpc3), IP3 metabolism (Plcg1, Inpp5a, Itpka), and Ca2+-Calmodulin dependent kinases (Camk2a, Camk4). CaMKIV–Sam68 control over alternative splicing of Nrxn1, an adhesion component of glutamatergic synapses between granule and Purkinje neurons, was found affected. Systematic screening of pre/post-synapse components, with dendrite morphology assessment, suggested early impairment of CamKIIα abundance together with weakening of parallel fiber connectivity. These data reveal molecular changes due to ATXN2 pathology, impacting communication and excitability of cerebellar neurons. Discovery of such risk versus progression markers improves the assessment of pre-symptomatic treatments in SCA2 and related disorders.