Traumatic Brain Injury: A Comprehensive Review of Biomechanics and Molecular Pathophysiology.

Traumatic brain injury (TBI) is a critical public health concern with profound consequences for affected individuals. This comprehensive literature review delves into TBI intricacies, encompassing primary injury biomechanics and the molecular pathophysiology of the secondary injury cascade. Primary TBI involves a complex interplay of forces, including impact loading, blast overpressure, and impulsive loading, leading to diverse injury patterns. These forces can be categorized into inertial (e.g., rotational acceleration causing focal and diffuse injuries) and contact forces (primarily causing focal injuries like skull fractures). Understanding their interactions is crucial for effective injury management. The secondary injury cascade in TBI comprises multifaceted molecular and cellular responses, including altered ion concentrations, dysfunctional neurotransmitter networks, oxidative stress, and cellular energy disturbances. These disruptions impair synaptic function, neurotransmission, and neuroplasticity, resulting in cognitive and behavioral deficits. Moreover, neuroinflammatory responses play a pivotal role in exacerbating damage. As we endeavor to bridge the knowledge gap between biomechanics and molecular pathophysiology, further research is imperative to unravel the nuanced interplay between mechanical forces and their consequences at the molecular and cellular levels, ultimately guiding the development of targeted therapeutic strategies to mitigate the debilitating effects of TBI. In this study, we aim to provide a concise review of the bridge between biomechanical processes causing primary injury and the ensuing molecular pathophysiology of secondary injury, while detailing the subsequent clinical course for this patient population. This knowledge is crucial for advancing our understanding of TBI and developing effective interventions to improve outcomes for those affected.

Middle Fossa Approach for Resection of a Petrous Bone Hemangioma Compressing the Geniculate Ganglion.

Facial nerve hemangiomas are a rare entity of skull base lesions that arise within the temporal bone and affect the seventh cranial nerve.1 They are vascular malformations arising from the vascular plexuses surrounding the nerve. Although slow growing and overall benign in nature, they can cause significant facial nerve dysfunction even at small sizes.2 Facial nerve hemangiomas can arise within different segments of the facial nerve within the temporal bone, but most commonly arise near the geniculate ganglion.3 We describe the case of a 34-year-old female who presented with progressive right facial palsy (House-Brackmann 4) and a calcified lesion arising from the petrous temporal bone. Resection of the lesion was performed with a posterior to anterior middle fossa approach, with identification of the greater superficial petrosal nerve and geniculate ganglion, sectioning of the middle meningeal artery, and identification of V2 and V3 segments of the trigeminal nerve (Video 1). The bony mass was peeled off the petrous temporal bone and the geniculate ganglion without sacrifice of the facial nerve. Postoperative imaging showed gross total resection, and the patient's facial palsy improved to House-Brackmann 1. A comprehensive literature review on surgical approaches and outcomes for the resection of hemangiomas involving the geniculate ganglion or the facial nerve is also provided.2,4-18 The case presentation, surgical anatomy, operative nuances with technical considerations, and postoperative course with imaging are reviewed. The patient and family provided informed consent for the procedure and publication of patient images.