Search

Traumatic brain injury is a global public health problem associated with chronic neurological complications and long-term disability. Biomarkers that map onto the underlying brain pathology driving these complications are urgently needed to identify individuals at risk for poor recovery and to inform design of clinical trials of neuroprotective therapies. Neuroinflammation and neurodegeneration are two endophenotypes potentially associated with increases in brain extracellular water content, but the nature of extracellular free water abnormalities after neurotrauma and its relationship to measures typically thought to reflect traumatic axonal injury are not well characterized. The objective of this study was to describe the relationship between a neuroimaging biomarker of extracellular free water content and the clinical features of a cohort with primarily complicated mild traumatic brain injury. We analyzed a cohort of 59 adult patients requiring hospitalization for non-penetrating traumatic brain injury of all severities as well as 36 healthy controls. Patients underwent brain MRI at two-weeks (n = 59) and six-months (n = 29) post-injury period, and controls underwent a single MRI. Of the participants with TBI, 50 underwent clinical neuropsychological assessment at two weeks and 28 at six months. For each subject, we derived a summary score representing deviations in whole brain white matter (1) extracellular free water volume fraction (VF) and (2) free water-corrected fractional anisotropy (fw-FA). The summary specific anomaly score (SAS) for VF was significantly higher in TBI patients at two-weeks and six-months post-injury relative to controls. SAS for VF exhibited moderate correlation with neuropsychological functioning, particularly on measures of executive function. These findings indicate abnormalities in whole brain white matter extracellular water fraction in patients with TBI and are an important step toward identifying and validating noninvasive biomarkers that map onto the pathology driving disability after TBI.

BACKGROUND: Intraoperative hypotension (IOH) has been found to be associated with organ damage, including cardiac injury and acute kidney injury (AKI). However, to our knowledge, this relationship has not been studied in a neurosurgery-specific patient population. In this report, we review our institutional experience to understand the magnitude of association between IOH in spinal fusion operations and incidence of postoperative AKI. METHODS: This retrospective cohort study included 910 patients who underwent posterior spinal fusion procedures performed in the prone position. Intraoperative variables collected and analyzed include minute-by-minute mean arterial pressure (MAP) from an arterial catheter, intermittent blood pressure cuff readings, volume of administered intravenous fluids, urine output, and all relevant vitals and administered medications. The electronic medical record was queried for additional patient data. IOH was defined as MAP 10 minutes, and total IOH time) and any outcome metrics, including AKI, except for vasopressor usage and estimated blood loss. Patient age at surgery was not associated with any outcome variables. The lack of association between IOH and AKI contrasts with existing literature; this could be due to underlying differences in our patient population or could highlight a more complex relationship between IOH and AKI than previously understood. CONCLUSION: Occurrence and duration of IOH were not associated with AKI, postoperative ileus, troponin leak, length of stay, or any other major outcome variables in spinal fusion patients. CLINICAL RELEVANCE: These findings depart from previous literature showing a correlation between IOH and AKI and provide level 3 evidence clinically relevant to spinal surgery. Further research is needed to better understand the exact nature of this relationship. LEVEL OF EVIDENCE: 3.

The course of Alzheimer’s disease is associated with an increase in oxidative stress associated with an increase in the production of reactive oxygen species against the background of neurodegenerative inflammation, and a simultaneous depletion of the antioxidant defense capabilities of brain cells. The result is the oxidative modification of macromolecules: proteins, lipids, nucleic acids. Protein carbonylation products accumulate not only in neurons, and in direct correlation with the degree of increase in amyloidosis and neurodegeneration, but also in extra-neuronal tissues, including leukocytes. In the course of this study, the levels of spontaneous and induced oxidative modification of proteins were determined in the blood plasma and fractionated leukocytes of peripheral blood of patients with different durations of Alzheimer’s disease, and the value of the reserve-adaptive potential was assessed as markers of the severity of oxidative stress. It has been established that the course of Alzheimer’s disease has a greater effect on the accumulation of carbonyl derivatives in blood plasma. In patients with a disease duration of 5–10 years, the total level of aldehyde and ketone derivatives of modified plasma proteins exceeds the same indicator in subgroups with a shorter duration of the disease. This tendency is less typical for mononuclear leukocytes. The level of induced oxidative modification of proteins increases to a greater extent in blood plasma than in fractionated leukocytes. This indicates the depletion of the reserve-adaptive potential of plasma antioxidant capabilities, which is more pronounced in patients with a long course of Alzheimer’s disease. For polymorphonuclear leukocytes, such a pattern was not revealed, which is probably associated with a short cell life. In mononuclear leukocytes, as well as in plasma, there is a tendency to depletion of the reserve-adaptive potential, but to a lesser extent.