Evidence of an association between brain cellular injury and cognitive decline after non-cardiac surgery.

BACKGROUND: Postoperative cognitive dysfunction (POCD) is common after non-cardiac surgery, but the mechanism is unclear. We hypothesized that decrements in cognition 1 month after non-cardiac surgery would be associated with evidence of brain injury detected by elevation of plasma concentrations of S100ß, neuron-specific enolase (NSE), and/or the brain-specific protein glial fibrillary acid protein (GFAP). METHODS: One hundred and forty-nine patients undergoing shoulder surgery underwent neuropsychological testing before and then 1 month after surgery. Plasma was collected before and after anaesthesia. We determined the relationship between plasma biomarker concentrations and individual neuropsychological test results and a composite cognitive functioning score (mean Z-score). RESULTS: POCD (≥-1.5 sd decrement in Z-score from baseline) was present in 10.1% of patients 1 month after surgery. There was a negative relationship between higher plasma GFAP concentrations and lower postoperative composite Z-scores {estimated slope=-0.14 [95% confidence interval (CI) -0.24 to -0.04], P=0.005} and change from baseline in postoperative scores on the Rey Complex Figure Test copy trial (P=0.021), delayed recall trial (P=0.010), and the Symbol Digit Modalities Test (P=0.004) after adjustment for age, sex, history of hypertension and diabetes. A similar relationship was not observed with S100ß or NSE concentrations. CONCLUSIONS: Decline in cognition 1 month after shoulder surgery is associated with brain cellular injury as demonstrated by elevated plasma GFAP concentrations.

Effects of ethanol on axon outgrowth and branching in developing rat cortical neurons.

Humans exposed prenatally to ethanol can exhibit brain abnormalities and cognitive impairment similar to those seen in patients expressing mutant forms of the L1 cell adhesion molecule (L1CAM). The resemblance suggests that L1CAM may be a target for ethanol, and consistent with this idea, ethanol can inhibit L1CAM adhesion in cell lines and L1CAM-mediated outgrowth and signaling in cerebellar granule neurons. However, it is not known whether ethanol inhibits L1CAM function in other neuron types known to require L1CAM for appropriate development. Here we asked whether ethanol alters L1CAM function in neurons of the rat cerebral cortex. We find that ethanol does not alter axonal polarization, L1CAM-dependent axon outgrowth or branching, or L1CAM recycling in axonal growth cones. Thus, ethanol inhibition of L1CAM is highly dependent on neuronal context.

A randomized blinded comparison of two methods used for venous antistasis in tetraplegia.

OBJECTIVE: The hemodynamic effects of slow sequential compression (SCD) were compared with rapid intermittent pulsatile compression (IPC) in subjects with complete tetraplegia. METHODS: Twenty subjects underwent Doppler examination of the bilateral popliteal and femoral veins. Resting volume flow per minute (VFM), average venous velocity (AVV), and maximal venous velocity (MVV) were measured in both veins. SCD and IPC were then randomly applied to one limb each, followed by repeat Doppler measurements under compression conditions. Doppler spectral recordings were stored for future analysis, and then measured by an investigator blinded to testing conditions (rest versus compression) and device (SCD versus IPC). RESULTS: Sequential compression and IPC compression both increased popliteal and femoral vein VFM, AVV, and MVV above resting levels (all p's < 0.001). In the femoral vein VFM (p < 0.05) and MVV (p < 0.05) were augmented during IPC compared to SCD compression. CONCLUSION: As MVV best reflects performance effectiveness of compression devices, these data find IPC more effective than SCD for stimulating venous blood flow in subjects with tetraplegia.