The psychological burden of disease among patients undergoing cervical spine surgery: Are we underestimating our patients' inherent disability?

BACKGROUND: Studies have utilized psychological questionnaires to identify the psychological distress among certain surgical populations. RESEARCH QUESTION: Is there an additional psychological burden among patients undergoing surgical treatment for their symptomatic degenerative cervical disease? MATERIALS AND METHODS: Patients>18 years of age with symptomatic, degenerative cervical spine disease were included and prospectively enrolled. Correlations and multivariable logistic regression analysis assessed the relationship between these mental health components (PCS, FABQ) and the severity of disability described by the NDI, EQ-5D, and mJOA score. Patient distress scores were compared to previously published benchmarks for other diagnoses. RESULTS: 47 patients were enrolled (age: 56.0 years,BMI: 29.7kg/m2). Increasing neck disability and decreasing EQ-5D were correlated with greater PCS and FABQ(all P<0.001). Patients with severe psychological distress at baseline were more likely to report severe neck disability, while physician-reported mJOA had weaker associations. Compared to historical controls of lumbar patients, patients in our study had greater levels of psychological distress, as measured by FABQ (40.0 vs. 17.6; P<0.001) and PCS (27.4 vs. 19.3;P<0.001). DISCUSSION AND CONCLUSION: Degenerative cervical spine patients seeking surgery were found to have a significant level of psychological distress, with a large portion reporting severe fear avoidance beliefs and catastrophizing pain at baseline. Strong correlation was seen between patient-reported functional metrics, but less so with physician-reported signs and symptoms. Additionally, this population demonstrated higher psychological burden in certain respects than previously identified benchmarks of patients with other disorders. Preoperative treatment to help mitigate this distress, impact postoperative outcomes, and should be further investigated. LEVEL OF EVIDENCE: Level III.

Disrupted autophagy after spinal cord injury is associated with ER stress and neuronal cell death.

Autophagy is a catabolic mechanism facilitating degradation of cytoplasmic proteins and organelles in a lysosome-dependent manner. Autophagy flux is necessary for normal neuronal homeostasis and its dysfunction contributes to neuronal cell death in several neurodegenerative diseases. Elevated autophagy has been reported after spinal cord injury (SCI); however, its mechanism, cell type specificity and relationship to cell death are unknown. Using a rat model of contusive SCI, we observed accumulation of LC3-II-positive autophagosomes starting at posttrauma day 1. This was accompanied by a pronounced accumulation of autophagy substrate protein p62, indicating that early elevation of autophagy markers reflected disrupted autophagosome degradation. Levels of lysosomal protease cathepsin D and numbers of cathepsin-D-positive lysosomes were also decreased at this time, suggesting that lysosomal damage may contribute to the observed defect in autophagy flux. Normalization of p62 levels started by day 7 after SCI, and was associated with increased cathepsin D levels. At day 1 after SCI, accumulation of autophagosomes was pronounced in ventral horn motor neurons and dorsal column oligodendrocytes and microglia. In motor neurons, disruption of autophagy strongly correlated with evidence of endoplasmic reticulum (ER) stress. As autophagy is thought to protect against ER stress, its disruption after SCI could contribute to ER-stress-induced neuronal apoptosis. Consistently, motor neurons showing disrupted autophagy co-expressed ER-stress-associated initiator caspase 12 and cleaved executioner caspase 3. Together, these findings indicate that SCI causes lysosomal dysfunction that contributes to autophagy disruption and associated ER-stress-induced neuronal apoptosis.