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Item Atlanto-axial rotary instability (Fielding type 1): characteristic clinical and radiological findings, and treatment outcomes following alignment, fusion, and stabilization(Springer, 2021) Henderson, Fraser C.; Rosenbaum, Robert; Narayanan, Malini; Koby, Myles; Tuchman, Kelly; Rowe, Peter C.; Francomano, Clair; Medical and Molecular Genetics, School of MedicineAtlanto-axial instability (AAI) is common in the connective tissue disorders, such as rheumatoid arthritis, and increasingly recognized in the heritable disorders of Stickler, Loeys-Dietz, Marfan, Morquio, and Ehlers-Danlos (EDS) syndromes, where it typically presents as a rotary subluxation due to incompetence of the alar ligament. This retrospective, IRB-approved study examines 20 subjects with Fielding type 1 rotary subluxation, characterized by anterior subluxation of the facet on one side, with a normal atlanto-dental interval. Subjects diagnosed with a heritable connective tissue disorder, and AAI had failed non-operative treatment and presented with severe headache, neck pain, and characteristic neurological findings. Subjects underwent a modified Goel-Harms posterior C1-C2 screw fixation and fusion without complication. At 15 months, two subjects underwent reoperation following a fall (one) and occipito-atlantal instability (one). Patients reported improvement in the frequency or severity of neck pain (P < 0.001), numbness in the hands and lower extremities (P = 0.001), headaches, pre-syncope, and lightheadedness (all P < 0.01), vertigo and arm weakness (both P = 0.01), and syncope, nausea, joint pain, and exercise tolerance (all P < 0.05). The diagnosis of Fielding type 1 AAI requires directed investigation with dynamic imaging. Alignment and stabilization is associated with improvement of pain, syncopal and near-syncopal episodes, sensorimotor function, and exercise tolerance.Item Demystifying Airline Syncope(Baishideng Publishing Group, 2020-03-26) Kingsley, Thomas; Kirchoff, Robert; Newman, James S.; Chaudhary, Rahul; Kelley School of Business - IndianapolisSyncope forms a major part of medical in-flight emergencies contributing one-in-four in-flight medical events accounting to 70% of flight diversions. In such patients, it is important to elucidate the pathophysiology of syncope prior to diversion. Postural hypotension is the most common etiology of in-flight syncopal events. However, individuals without any underlying autonomic dysfunction can still experience syncope from hypoxia also known as airline syncope. Initial steps in managing such patients include positioning followed by the airway, breathing and circulation of resuscitation. These interventions need to be in close coordination with ground control to determine decision for flight diversion. Interventions which have been tried for prevention include mental challenge and increased salt and fluid intake. The current paper enhances the understanding of airline syncope by summarizing the associated pathophysiologic mechanisms and the management medical personnel can initiate with limited resources.Item Skin Sympathetic Nerve Activity as a Biomarker for Syncopal Episodes during a Tilt Table Test(Elsevier, 2020-05) Kumar, Awaneesh; Wright, Keith; Uceda, Domingo E.; Vasallo, Peter A., III.; Rabin, Perry L.; Adams, David; Wong, Johnson; Das, Mithilesh; Lin, Shien-Fong; Chen, Peng-Sheng; Everett, Thomas H., IV.; Medicine, School of MedicineBackground: Autonomic imbalance is the proposed mechanism of syncope during a tilt table test (TTT). We have recently demonstrated that skin sympathetic nerve activity (SKNA) can be noninvasively recorded using electrocardiographic electrodes. Objective: The purpose of this study was to test the hypothesis that increased SKNA activation precedes tilt-induced syncope. Methods: We studied 50 patients with a history of neurocardiogenic syncope undergoing a TTT. The recorded signals were band-pass filtered at 500-1000 Hz to analyze nerve activity. Results: The average SKNA (aSKNA) value at baseline was 1.38 ± 0.38 μV in patients without syncope and 1.42 ± 0.52 μV in patients with syncope (P = .77). On upright tilt, aSKNA was 1.34 ± 0.40 μV in patients who did not have syncope and 1.39 ± 0.43 μV in patients who had syncope (P = .65). In all 14 patients with syncope, there was a surge of SKNA before an initial increase in heart rate followed by bradycardia, hypotension, and syncope. The peak aSKNA immediately (<1 minute) before syncope was significantly higher than baseline aSKNA (2.63 ± 1.22 vs 1.39 ± 0.43 μV; P = .0005). After syncope, patients were immediately placed in the supine position and aSKNA dropped significantly to 1.26 ± 0.43 μV; (P = .0004). The heart rate variability during the TTT shows a significant increase in parasympathetic tone during syncope (low-frequency/high-frequency ratio: 7.15 vs 2.21; P = .04). Conclusion: Patients with syncope do not have elevated sympathetic tone at baseline or during the TTT except immediately before syncope when there is a transient surge of SKNA followed by sympathetic withdrawal along with parasympathetic surge.