UNASSIGNED: Following aneurysmal subarachnoid hemorrhage, 40-50% of survivors experience cognitive dysfunction, which affects their quality of life. Anesthetic agents play a pivotal role in aneurysm surgeries. However, substantial evidence regarding their effects on neurocognitive function is lacking. This study evaluated the effects of propofol and desflurane on postoperative neurocognitive function and serum S-100B levels.
UNASSIGNED: One hundred patients were equally randomized to receive either propofol (Group P) or desflurane (Group D). Cognitive function was assessed using the Montreal Cognitive Assessment scale at three different time points: Preoperatively, at the time of discharge, and one month after surgery. Perioperative serum levels of S-100B were also measured.
UNASSIGNED: The preoperative mean cognitive score in Group P was 21.64 + 4.46 and in Group D was 21.66 + 4.07 (P = 0.79). At discharge, a significant decrease in cognitive scores was observed compared to preoperative scores (Group P- 20.91 + 3.94, P = 0.03 and Group D-19.28 + 4.22, P = 0.00); however, scores were comparable between the two groups (P = 0.09). One month following surgery, mean cognitive scores were 22.63 + 3.57 in Group P and 20.74 + 3.89 in Group D, and the difference was significant (P = 0.04). Higher memory and orientation scores were observed in Group P than in Group D at one month (P < 0.05) in the subgroup analysis. Both groups had similar serum S-100B levels.
UNASSIGNED: The mean cognitive scores one month after surgery improved significantly with propofol compared with desflurane, but without clinical significance. Individual domain analysis demonstrated that orientation and memory scores were better preserved with propofol.

We aimed to investigate the impact of prolonged targeted temperature management (TTM) in cardiac arrest patients on release of serum levels of NSE and S-100b and their prognostic performances.
This is a substudy of the Targeted Temperature Management for 24 vs 48h trial. NSE and S-100b levels were analysed retrospectively in serum samples collected upon admission, at 24, 48, and 72h after reaching the target temperature of 33±1°C. The primary outcome was biomarker serum concentrations and secondary outcome was the cerebral performance category score after 6 months.
115 patients from two centres were analysed. NSE and S-100b levels did not differ between TTM groups at any single time-point. Poor outcome patients had higher biomarker levels at 24, 48, and 72h: NSE: 9.73 (7.2; 10.9) versus 20.40 (12.7; 27.2), 8.86 (6.6; 9.6) versus 17.47 (11.1; 37.3) and 6.23 (5.3; 8.5) versus 31.05 (12.8; 52.5) respectively and S-100b: 0.09 (0.07; 0.11) versus 0.23 (0.19; 0.39), 0.08 (0.07; 0.09) versus 0.18 (0.15; 0.33) and 0.07 (0.06; 0.08) versus 0.13 (0.09; 0.23). The daily changes in NSE from admission to Day 2 after the cardiac arrest (CA) were also related to the outcome (p=0.003 and p=0.02). The best prediction of outcome was found at 72h for NSE and at 24h as well as 48h for S100b.
No clinically relevant differences were found in the levels of NSE or S-100b between standard and prolonged TTM. Prognostic reliability of NSE and S-100b was unaltered by prolonged TTM.

OBJECTIVE: Factors affecting neurological outcome and the usefulness of neuron-specific enolase (NSE), S-100B, glial fibrillary acidic protein (GFAP), and procalcitonin (PCT) in predicting neurological outcomes were assessed in patients who survived at least 24 h after cardiopulmonary resuscitation (CPR).
METHODS: Thirty successfully resuscitated cardiac arrest patients were included in this prospective clinical study. The initial cardiac arrest rhythm, duration of CPR, return of spontaneous circulation time, administered doses of adrenaline, base excess, blood sugar, and hemodynamic parameters were recorded. Patients with Glasgow Outcome Scale (GOS) scores of 1-3 were defined as Group I and patients with GOS scores of 4-5 were defined as Group II. Serum NSE, GFAP, S-100B, and PCT levels were compared between the two groups shortly after CPR (hour 0) and at hours 12 and 24 of the postresuscitation period.
RESULTS: Serum S-100B was significantly higher (P = 0.009) in Group II immediately after CPR. Serum S-100B and NSE after CPR at hours 0, 12, and 24 were significantly lower in patients who survived to hospital discharge. Serum PCT at hours 12 and 24 and serum S-100B after CPR at 0, 12, and 24 h reached 94.7% sensitivity. Serum NSE, GFAP, S-100B, and PCT specificities were lower than 50%.
CONCLUSIONS: In predicting neurological outcomes, serum S-100B has high sensitivity and low specificity immediately after CPR.

Epilepsy is the most common neurologic disorder of childhood. In approximately 6-14% of all patients with epilepsy, complete seizure control is difficult to achieve with current antiepileptic treatments. Several current studies have shown in both animals and people that the lengthening of epileptic seizures and frequent recurrence increases the likelihood of neuronal damage. S-100B protein is the most analyzed brain derived peripheral biochemical marker in brain damage. This study aimed to evaluate interictal serum S-100B protein levels in children diagnosed with intractable epilepsy. A group of 32 patients with intractable epilepsy and 25 healthy controls were recruited. Serum S-100B protein levels were measured using a commercially available electrochemiluminescence immunoassay (ECLIA kit, as supplied and according to the manufacturer\'s standards. The serum S-100B protein levels of the patient group in the study were found to be 0.094±0.011 μm/L, and 0.083±0.014 μm/L in the age-matched control group. The difference between the groups was determined to be statistically significant (P=0.004). In conclusions, it can be said that as the serum S-100B protein levels of the patients with focal epilepsy were high compared to those of the control group, this can be reliable peripheral biomarker for neuronal damage in patients with focal intractable epilepsy.

BACKGROUND: Previous studies have suggested that affective disorders are characterized by glial pathology. In this context, it has been hypothesized that elevated S100B serum and cerebrospinal fluid levels may represent a suitable surrogate marker. However, brain studies on the cellular distribution pattern of S100B in depressed patients are lacking so far. Such analyses are crucial, since S100B has been detected in various other cell types, even outside the central nervous system.
METHODS: Therefore, we performed a first postmortem analysis on this topic in the hippocampus--which is of major importance for emotional and cognitive aspects of affective disorders. S100B-immunopositive astrocytes and oligodendrocytes were evaluated in the alveus and the CA1 pyramidal layer of patients with major depressive disorder (MDD) or bipolar I disorder (BD) compared to controls.
RESULTS: As revealed by the optical disector cell-counting method, the numerical density of S100B-immunopositive astrocytes was bilaterally decreased in the CA1 pyramidal layer of MDD and BD patients compared to controls, whereas only the bipolar group showed a decreased density of S100B-immunopositive oligodendrocytes in the left alveus. These results were not confounded by gender, age, duration of disease, medication dosage, or autolysis time.
CONCLUSIONS: Confirming the idea of previous S100B serum and cerebrospinal fluid studies, our data suggest that S100B-immunopositive glia is dysregulated in the brains of depressed patients. These findings are in accordance with animal experiments in rodents showing a reduced astrocytic S100B-immunoreactivity in the hippocampus after pharmacological serotonin depletion (modeling depression).