The neuropsychological assessment battery (NAB) is a valuable tool for evaluating neuropsychological outcome after aneurysmatic subarachnoid hemorrhage

Background!#!Detecting and treating neuropsychological deficits after aneurysmatic subarachnoid hemorrhage (aSAH) play a key role in regaining independence; however, detecting deficits relevant to social and professional reintegration has been difficult and optimal timing of assessments remains unclear. Therefore, we evaluated the feasibility of administering the Neuropsychological Assessment Battery screening module (NAB-S) to patients with aSAH, assessed its value in predicting the ability to return to work and characterized clinical as well as neuropsychological recovery over the period of 24 months.!##!Methods!#!A total of 104 consecutive patients treated for aSAH were recruited. After acute treatment, follow up visits were conducted at 3, 12 and 24 months after the hemorrhage. NAB-S, Montreal Cognitive Assessment (MoCA) and physical examination were performed at each follow up visit.!##!Results!#!The NAB-S could be administered to 64.9, 75.9 and 88.9% of the patients at 3, 12 and 24 months, respectively. Moderate impairment of two or more neuropsychological domains (e.g speech, executive function, etc.) significantly correlated with inability to return to work at 12 and 24 months as well as poor outcome assessed by the extended Glasgow Outcome Scale (GOSE) at 3, 12 and 24 months. The number of patients with favorable outcomes significantly increased from 25.5% at discharge to 56.5 and 57.1% at 3 and 12 months, respectively, and further increased to 74.1% after 24 months.!##!Conclusion!#!The NAB-S can be administered to the majority of patients with aSAH and can effectively detect clinically relevant neuropsychological deficits. Clinical recovery after aSAH continues for at least 24 months after the hemorrhage which should be considered in the design of future clinical trials

The Local Intraarterial Administration of Nimodipine Might Positively Affect Clinical Outcome in Patients with Aneurysmal Subarachnoid Hemorrhage and Delayed Cerebral Ischemia

The effect of the intraarterial administration of nimodipine as a rescue measure to treat delayed vasospasm after aSAH remains understudied; therefore, we evaluated its effect on short- and long-term functional and neuropsychological outcomes after aSAH. In this prospective observational study, a total of 107 consecutive patients treated for aSAH of WFNS grades I–V were recruited. At follow-up visits 3-, 12- and 24-months after the hemorrhage, functional outcome was assessed using the Extended Glasgow Outcome (GOSE) and modified Rankin (mRS) scales, while neurocognitive function was evaluated using the screening module of the Neuropsychological Assessment Battery (NAB-S). The outcome of patients, who had received rescue therapy according to the local standard treatment protocol (interventional group, n = 37), and those, who had been treated conservatively (conservative group, n = 70), were compared. Even though significantly more patients in the interventional treatment group suffered from high-grade aSAH (WFNS Grades IV and V, 54.1% vs. 31.4%, p = 0.04) and required continuous drainage of cerebrospinal fluid at discharge (67.7% vs. 37.7%, p = 0.02) compared to the control group, significant differences in functional outcome were present only at discharge and three months after the bleeding (GOSE > 4 in 8.1% vs. 41.4% and 28.6% vs. 72.7%, p < 0.001 and p = 0.01 for the interventional and control group, respectively). Thereafter, group differences were no longer significant. While significantly more patients in the intervention group had severe neuropsychological deficits (76.3% vs. 36.0% and 66.7% vs. 29.2%, p = 0.04 and 0.05, respectively) and were unable to work (5.9% vs. 38.1%, p = 0.03 at twelve months) at three and twelve months after the hemorrhage, no significant differences between the two groups could be detected at long-term follow-up. The presence of moderate neuropsychological impairments did not significantly differ between the groups at any timepoint. In conclusion, despite initially being significantly more impaired, patients treated with intraarterial administration of nimodipine reached the same functional and neuropsychological outcomes at medium- and long-term follow-up as conservatively treated patients suggesting a potential beneficial effect of intraarterial nimodipine treatment for delayed vasospasm after aSAH

The Single-Dose Application of Interleukin-4 Ameliorates Secondary Brain Damage in the Early Phase after Moderate Experimental Traumatic Brain Injury in Mice

Activation of the interleukin-4 (IL-4) pathway ameliorates secondary injury mechanisms after experimental traumatic brain injury (TBI); therefore, we assessed the effect of a therapeutic IL-4 administration on secondary brain damage after experimental TBI. We subjected 100 C57/Bl6 wildtype mice to controlled cortical impact (CCI) and administered IL-4 or a placebo control subcutaneously 15 min thereafter. Contusion volume (Nissl staining), neurological function (hole board, video open field, and CatWalkXT®), and the immune response (immunofluorescent staining) were analyzed up to 28 days post injury (dpi). Contusion volumes were significantly reduced after IL-4 treatment up to 14 dpi (e.g., 6.47 ± 0.41 mm3 vs. 3.80 ± 0.85 mm3, p = 0.011 3 dpi). Macrophage invasion and microglial response were significantly attenuated in the IL-4 group in the acute phase after CCI (e.g., 1.79 ± 0.15 Iba-1+/CD86+ cells/sROI vs. 1.06 ± 0.21 Iba-1/CD86+ cells/sROI, p = 0.030 in the penumbra 3 dpi), whereas we observed an increased neuroinflammation thereafter (e.g., mean GFAP intensity of 3296.04 ± 354.21 U vs. 6408.65 ± 999.54 U, p = 0.026 in the ipsilateral hippocampus 7 dpi). In terms of functional outcome, several gait parameters were improved in the acute phase following IL-4 treatment (e.g., a difference in max intensity of −7.58 ± 2.00 U vs. −2.71 ± 2.44 U, p = 0.041 3 dpi). In conclusion, the early single-dose administration of IL-4 significantly reduces secondary brain damage in the acute phase after experimental TBI in mice, which seems to be mediated by attenuation of macrophage and microglial invasion