Despite extensive research on aneurysm treatment and neurocritical care, aneurysmal subarachnoid hemorrhage (SAH) is still a life-threatening disease, often leaving survivors with lasting neurological and cognitive impairments. Early brain injury (EBI) and delayed cerebral ischemia (DCI) are the main contributors to brain damage, with neuroinflammation being a critical shared pathophysiological process. While numerous inflammatory markers and their temporal profiles in cerebrospinal fluid (CSF) have already been identified, comparisons with age- and sex-matched controls are limited. This study analyzed CSF from 17 SAH patients requiring an external ventricular drain (EVD) due to symptomatic hydrocephalus, sampled on days 4 and 10 post-ictus. An age- and sex-matched control group included 17 cerebrovascularly healthy patients requiring lumbar drains during aortic surgery. Chemokines and cytokines were quantified using immunoassays. Significantly elevated markers in SAH patients across both time points included MCP-1, CXCL-13, Eotaxin-1, CXCL-10, IL-8, and MIF. MIP-1α and MIP-1β showed significant differences at particular time points, indicating a distinct temporal profile for each parameter. These findings highlight neuroinflammation’s key role in intracranial and systemic pathophysiology following SAH, emphasizing its complexity and individual variability. Knowing demographic factors impact the specific manifestations of pathophysiological processes, the comparison with an age- and sex-matched control group is meaningful.

This study investigated supra- and infratentorial structural gray and white matter (GM, WM) alterations in patients with degenerative cervical myelopathy (DCM) as an indicator of secondary harm due to chronic cervical cord compression and micro trauma. With MRI-based anatomical assessment and subsequent voxel-based morphometry analyses, pre- and postoperative volume alterations in the primary motor cortex (MI), the primary somatosensory cortex (SI), the supplementary motor area (SMA), and the cerebellum were analyzed in 43 DCM patients and 20 controls. We assessed disease-related symptom severity by the modified Japanese Orthopaedic Association scale (mJOA). The study also explored symptom severity-based brain volume alterations as well as their association with clinical status. Patients had lower mJOA scores (p = .000) and lower GM volume than controls in SI (p = .016) and cerebellar regions (p = .001). Symptom severity-based subgroup analyses revealed volume reductions in almost all investigated GM ROIs (MI: p = .001; CB: p = .040; SMA: p = .007) in patients with severe clinical symptoms as well as atrophy already present in patients with moderate symptom severity. Clinical symptoms in DCM were associated with cortical and cerebellar volume reduction. GM volume alterations may serve as an indicator of both disease severity and ongoing disease progression in DCM, and should be considered in further patient care and treatment monitoring.

Background Our objective was to investigate the effect of intraoperative dexamethasone administration on wound healing, complications, and clinical outcome in patients with posterior surgery for cervical spondylotic myelopathy (CSM). Methods We conducted a retrospective study of patients with CSM undergoing dorsal instrumentation and decompression of the cervical spine. The senior surgeon decided if administration of dexamethasone (40 mg intravenously) was indicated. Patients were divided into two groups: dexamethasone group (DG) and non-dexamethasone group (nDG). All patients were monitored for pre- and postoperative neurologic symptoms and complications. Clinical follow-up was evaluated with the Neck Disability Index (NDI) and the modified Japanese Orthopaedic Association (mJOA) score. Results A total of 49 patients were included (DG, 25; nDG, 24). DG and nDG patients showed no significant differences in pre- and postoperative findings. Five patients in the DG had wound healing complications compared with patients in the nDG (p = 0.021), and one died due to infection. Apart from that, we did not observe any significant differences between the two groups regarding complications, neurologic symptoms, and follow-up (NDI and mJOA). Conclusion Intraoperative dexamethasone administration had no influence on the postoperative outcome and follow-up. A significantly higher rate of wound infections was detected in the DG. These data support the hypothesis that intraoperative dexamethasone bolus application in CSM lacks benefit.

Endogenous immune mediated reactions of inflammation and angiogenesis are components of the spinal cord injury in patients with degenerative cervical myelopathy (DCM). The aim of this study was to identify alteration of certain mediators participating in angiogenetic and inflammatory reactions in patients with DCM. A consecutive series of 42 patients with DCM and indication for surgical decompression were enrolled for the study. 28 DCM patients were included, as CSF samples were taken preoperatively. We enrolled 42 patients requiring surgery for a thoracic abdominal aortic aneurysm (TAAA) as neurologically healthy controls. In 38 TAAA patients, CSF samples were taken prior to surgery and thus included. We evaluated the neurological status of patients and controls prior to surgery including NDI and mJOA. Protein-concentrations of factors with a crucial role in inflammation and angiogenesis were measured in CSF via ELISA testing (pg/ml): Angiopoietin 2, VEGF-A and C, RANTES, IL 1 beta and IL 8. Additionally, evaluated the status of the blood-spinal cord barrier (BSCB) by Reibers´diagnostic in all participants. Groups evidently differed in their neurological status (mJOA: DCM 10.1 ± 3.3, TAAA 17.3 ± 1.2, p < .001; NDI: DCM 47.4 ± 19.7, TAAA 5.3 ± 8.6, p < .001). There were no particular differences in age and gender distribution. However, we detected statistically significant differences in concentrations of mediators between the groups: Angiopoietin 2 (DCM 267.1.4 ± 81.9, TAAA 408.6 ± 177.1, p < .001) and VEGF C (DCM 152.2 ± 96.1, TAAA 222.4 ± 140.3, p = .04). DCM patients presented a mild to moderate BSCB disruption, controls had no signs of impairment. In patients with DCM, we measured decreased concentrations of angiogenic mediators. These results correspond to findings of immune mediated secondary harm in acute spinal cord injury. Reduced angiogenic activity could be a relevant part of the pathogenesis of DCM and secondary harm to the spinal cord.