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Background Proximal junctional kyphosis is a kyphotic deformity following spine instrumentation, predominantly seen in scoliosis patients. There have been previous attempts to develop classification schema of PJK. We analyzed the factors contributing to PJK based upon our own clinical experience with the goal of developing a clinical guidance tool which took into account both etiology and mechanism of failure. Methods: We performed a retrospective analysis of all re-operation thoracolumbar surgeries at a single institution over a 14-year period. Patients with PJK were identified and categorized based upon the etiology, mechanism of failure, and an indication of revision. Next, we conducted a systematic review on articles emphasizing a classification system for PJK. Results: Fourteen PJK patients were identified out of 121 patients who required revision spine surgery. The average age was 64.9 ± 10.2 years, with 10 males (71%) and 4 females (29%). Three primary etiologies were identified: 6/14 (47%) overcorrection, 6/14 (47%) osteopenia, and 2/14 (14%) ligamentous disruption. The mechanism of failure was likewise divided into three categories: 9/14 (64%) compression fracture, 1/14 (7%) hardware failure, and 4/14 (29%) disc degeneration. The relationship between osteopenia and the development of a compression fracture leading to PJK was statistically significant (p = 0.031). Conclusion: There are multiple current classification systems for PJK. Our study findings were in line with previously published literature and suggest the need for a future classification system combining both etiology, mechanism of failure, and severity of disease.

Patients who present with traumatic brain injury (TBI) combined with blunt cerebrovascular injuries (BCVI) are difficult to manage, in part because treatment for each entity may exacerbate the other. It is necessary to develop a treatment paradigm that ensures maximum benefit while mitigating the opposing risks. A cohort of 150 patients from 2015 to present, with either internal carotid artery (ICA) and/or vertebral artery (VA) dissections or pseudoaneurysms, was cross-referenced with those who had sustained TBI. Of the 38 patients identified with both TBI and BCVI, 25 suffered ICA injuries, 10 had VA injuries and 3 had combined ICA/VA injuries. Unilateral BCVI occurred in 30 patients, while 8 had bilateral BCVI. Two patients required surgical intervention for TBI, and 5 patients required endovascular intervention for BCVI. Positive emboli detection studies (EDS) on transcranial dopplers (TCD) were demonstrated in 19 patients, with 9 patients having radiographic evidence of stroke. Anti-platelet therapy was initiated in 32 patients, and anti-coagulation in 10 patients, without new or worsening intracranial hemorrhages (ICH). Overall, 76% of patients were able to be discharged home or to rehabilitation, with good recovery demonstrated in 73% of the patients who had appropriate follow-up. In the setting of concurrent TBI and BCVI, use of anti-platelet/coagulation to prevent stroke can be safe if monitored closely. Here we describe a treatment paradigm which weighs the risk and benefits of therapies based on severity of ICH and stroke prevention, which tended to result in good disposition and recovery.