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BACKGROUND: This report describes the use of hyperbaric oxygen therapy for the acute management of an intraoperative air embolism encountered during a neurosurgical procedure. Furthermore, the authors highlight the concomitant diagnosis of tension pneumocephalus requiring evacuation prior to hyperbaric therapy. OBSERVATIONS: A 68-year-old male developed acute ST-segment elevation and hypotension during elective disconnection of a posterior fossa dural arteriovenous fistula. The semi-sitting position had been used to minimize cerebellar retraction, raising the concern for acute air embolism. Intraoperative transesophageal echocardiography was utilized to establish the diagnosis of air embolism. The patient was stabilized on vasopressor therapy, and immediate postoperative computed tomography revealed air bubbles in the left atrium along with tension pneumocephalus. He underwent urgent evacuation for the tension pneumocephalus followed by hyperbaric oxygen therapy to manage the hemodynamically significant air embolism. The patient was eventually extubated and went on to fully recover; a delayed angiogram revealed complete cure of the dural arteriovenous fistula. LESSONS: Hyperbaric oxygen therapy should be considered for an intracardiac air embolism resulting in hemodynamic instability. In the postoperative neurosurgical setting, care should be taken to exclude pneumocephalus requiring operative intervention prior to hyperbaric therapy. A multidisciplinary management approach facilitated expeditious diagnosis and management for the patient.
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Mild traumatic brain injury (mTBI) is impossible to detect with standard neuroradiological assessment such as structural magnetic resonance imaging (MRI). Injury does, however, disrupt the dynamic repertoire of neural activity indexed by neural oscillations. In particular, beta oscillations are reliable predictors of cognitive, perceptual, and motor system functioning, as well as correlating highly with underlying myelin architecture and brain connectivity-all factors particularly susceptible to dysregulation after mTBI. We measured local and large-scale neural circuit function by magnetoencephalography (MEG) with a data-driven model fit approach using the fitting oscillations and one-over f algorithm in a group of young adult men with mTBI and a matched healthy control group. We quantified band-limited regional power and functional connectivity between brain regions. We found reduced regional power and deficits in functional connectivity across brain areas, which pointed to the well-characterized thalamocortical dysconnectivity associated with mTBI. Furthermore, our results suggested that beta functional connectivity data reached the best mTBI classification performance compared with regional power and symptom severity [measured with Sport Concussion Assessment Tool 2 (SCAT2)]. The present study reveals the relevance of beta oscillations as a window into neurophysiological dysfunction in mTBI and also highlights the reliability of neural synchrony biomarkers in disorder classification.NEW & NOTEWORTHY Mild traumatic brain injury (mTBI) disrupts the dynamic repertoire of neural oscillations, but so far beta activity has not been studied. In mTBI, we found reductions in frontal beta and large-scale beta networks, indicative of thalamocortical dysconnectivity and disrupted information flow through cortico-basal ganglia-thalamic circuits. Relatively, connectivity more accurately classifies individual mTBI cases compared with regional power. We show the relevance of beta oscillations in mTBI and the reliability of these markers in classification.