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Background: Undoubtedly, overlooking a stroke can result in severe disability or even death. However, identifying stroke patients in the prehospital setting poses a significant challenge. While the Face–Arm–Speech–Time (FAST) score is widely used, its effectiveness has been questioned because of its focus on symptoms primarily associated with anterior circulation strokes. In response to this limitation, we developed the innovative FAST4D score and conducted a comparative analysis of stroke detection rates between the novel FAST4D score and the FAST score. Methods: This prospective, multicenter proof-of-concept study aimed to assess stroke detection rates using both the FAST score and the new FAST4D score, which incorporates additional items such as the acute onset of diplopic images, deficit in the field of vision, dizziness/vertigo, and dysmetria/ataxia. Following their presentation to emergency medical services, all patients suspected of having a stroke and those diagnosed with a stroke upon discharge were included in this study. The diagnostic performance of the novel FAST4D score was evaluated and compared with that of the FAST score. Results: Between May 2019 and June 2021, a total of 1469 patients (749 female) were enrolled, with 1035 patients discharged with the diagnosis of stroke. Notably, 259 patients were identified solely through the FAST4D score. This resulted in a significantly higher rate of correctly identified as having had a stroke (stroke detection rate, sensitivity) with the new FAST4D score (93%) compared with the established FAST score (78%) (p < 0.001). This resulted in a reduction in false negative diagnoses by 65%. Conclusions: The novel FAST4D score demonstrated a 15-percentage increase in the stroke detection rate. This heightened detection rate holds the potential for more accurate patient allocation to stroke units, consequently reducing the time to revascularization. [ABSTRACT FROM AUTHOR]

This study was designed to investigate the indirect neuroprotective properties of recombinant human erythropoietin (rhEPO) pretreatment in a rat model of transient middle cerebral artery occlusion (MCAO).

Author(s): Marlene Tschernatsch [sup.1] [sup.2] [sup.3], Martin Juenemann [sup.1] [sup.2], Fouad Alhaidar [sup.4], Jasmin El Shazly [sup.1], Marius Butz [sup.1] [sup.2], Marco Meyer [sup.5], Tibo Gerriets [sup.1] [sup.2] [sup.3], Markus [...], Purpose Patients undergoing cardiac surgery often develop delirium which increases the risk of postoperative morbidity and leads to a reduced quality of life. Retrospective studies show a higher incidence of delirium in patients with seizures. However, these studies do not systematically detect subclinical seizures, so the incidence of seizures after cardiac surgery remains speculative. The objective of this study is to determine the prevalence of electrographic seizures after elective open-chamber cardiac surgery. Methods This prospective, blinded, monocentric, observational study investigated patients scheduled for elective open-chamber valve reconstruction or replacement. Anaesthesia, surgery and postoperative treatment were standardized and not influenced by the presented observation. After surgery, all patients arrived at the ICU, and EEG monitoring started within the first hour. EEG recording was continuously performed for up to 24 h, and the results were independently analysed by two blinded EEG board-certified neurologists. Results 100 patients were included. Abnormal EEG patterns were present in 33% of patients, and 9% of all patients showed electrographic seizures. The main EEG activity at the beginning of each recording was suppressed or showed a burst-suppression pattern, and at the end of recording, all patients had an alpha/theta rhythm. An association between electrographic seizures and delirium was found (p.sub.[chi]2 < 0.01). Conclusion This study reveals a surprisingly high incidence of abnormal EEG patterns and electrographic seizures in patients undergoing open-chamber cardiac surgery. As electrographic seizures are associated with the incidence of delirium, this finding is a relevant phenomenon in the post-cardiac surgery ICU population.

Hypoxia triggers reactive microglial inflammation and lipid droplet (LD) accumulation under stroke conditions, although the mutual interactions between these two processes are insufficiently understood. Hence, the involvement of transforming growth factor (TGF)-β1 in inflammation and LD accumulation in cultured microglia exposed to hypoxia were analyzed herein. Primary microglia were exposed to oxygen-glucose deprivation (OGD) injury and lipopolysaccharide (LPS) stimulation. For analyzing the role of TGF-β1 patterns under such conditions, a TGF-β1 siRNA and an exogenous recombinant TGF-β1 protein were employed. Further studies applied Triacsin C, an inhibitor of LD formation, in order to directly assess the impact of LD formation on the modulation of inflammation. To assess mutual microglia-to-neuron interactions, a co-culture model of these cells was established. Upon OGD exposure, microglial TGF-β1 levels were significantly increased, whereas LPS stimulation yielded decreased levels. Elevating TGF-β1 expression proved highly effective in suppressing inflammation and reducing LD accumulation in microglia exposed to LPS. Conversely, inhibition of TGF-β1 led to the promotion of microglial cell inflammation and an increase in LD accumulation in microglia exposed to OGD. Employing the LD formation inhibitor Triacsin C, in turn, polarized microglia towards an anti-inflammatory phenotype. Such modulation of both microglial TGF-β1 and LD levels significantly affected the resistance of co-cultured neurons. This study provides novel insights by demonstrating that TGF-β1 plays a protective role against microglia-mediated neuroinflammation through the suppression of LD accumulation. These findings offer a fresh perspective on stroke treatment, suggesting the potential of targeting this pathway for therapeutic interventions. [ABSTRACT FROM AUTHOR]

Brain injured patients often need deep sedation to prevent or treat increased intracranial pressure. The mainly used IV sedatives have side effects and/or high context-sensitive half-lives, limiting their use. Inhalative sedatives have comparatively minor side effects and a brief context-sensitive half-life. Despite the theoretical advantages, evidence in this patient group is lacking. A Germany-wide survey with 21 questions was conducted to find out how widespread the use of inhaled sedation is. An invitation for the survey was sent to 226 leaders of intensive care units (ICU) treating patients with brain injury as listed by the German Society for Neurointensive Care. Eighty-nine participants answered the questionnaire, but not all items were responded to, which resulted in different absolute counts. Most of them (88%) were university or high-level hospital ICU leaders and (67%) were leaders of specialized neuro-ICUs. Of these, 53/81 (65%) use inhalative sedation, and of the remaining 28, 17 reported interest in using this kind of sedation. Isoflurane is used by 43/53 (81%), sevoflurane by 15/53 (28%), and desflurane by 2. Hypotension and mydriasis are the most common reported side effects (25%). The presented survey showed that inhalative sedatives were used in a significant number of intensive care units in Germany to treat severely brain-injured patients. [ABSTRACT FROM AUTHOR]

Objective: Dysregulation of stress‐reactive neuroendocrine measures, as well as subjective stress, have been found to worsen epilepsy. Transcutaneous vagus nerve stimulation (tVNS) is a relatively new treatment option for epilepsy. We were interested in its effect on the activity of the hypothalamic–pituitary–adrenal (HPA) axis and autonomic nervous system (ANS) as well as subjective stress and tiredness in patients with temporal lobe epilepsy (TLE). Methods: Twenty patients (age 44 ± 11 years, 13 women) were enrolled in the study. They were free of seizures for more than 1 year. All took part in two sessions with 4 h of stimulation (tVNS vs. sham) in a randomized order. Saliva samples and subjective stress and tiredness levels were measured at five time points each session (before and after stimulation and three time points every hour in between). Data were analyzed using repeated measures analysis of variance as well as paired t‐tests. Results: There was a dampened salivary cortisol (sCort) decrease during tVNS (time × condition effect: F[2.38, 38.15] = 6.50, P = 0.002, partial η2 = 0.29). Furthermore, we detected a dampened increase in salivary flow rate during tVNS (time × condition effect: F[3.28, 55.67] = 2.82, P = 0.043, partial η2 = 0.14). There was neither a difference in overall sCort or salivary alpha‐amylase (sAA) levels nor in subjective stress or tiredness levels between conditions. sAA levels at the last measurement point were slightly higher during tVNS (t(19) = 2.26, P = 0.035, d = 0.51), but this effect failed to reach significance when controlled for multiple comparisons. Significance: Our results partially support that tVNS influences the regulation of stress‐reactive neuroendocrine systems (namely the HPA axis and ANS) in epilepsy. More research with larger samples is needed on the difference between short‐term and repeated long‐term stimulation. [ABSTRACT FROM AUTHOR]

Background/Objectives: Comprehensive Geriatric Care (CGC) is a specific multimodal treatment for older patients. In the current study, we aimed to investigate walking performance after CGC in medically ill patients versus those with fractures. Methods: The timed up and go test (TuG), a 5-grade scale assessment (1 = no walking impairment to 5 = no walking ability at all) for evaluating individual walking ability was performed in all patients who underwent CGC prior to and after treatment. Factors associated with improvement in walking ability were analyzed in the subgroup of patients with fractures. Results: Out of 1263 hospitalized patients, 1099 underwent CGC (median age: 83.1 years (IQR 79.0–87.8 years); 64.1% were female). Patients with fractures (n = 300) were older than those without (n = 799), (median 85.6 versus 82.4 years, p = 0.001). Improvement in TuG after CGC was found in 54.2% of the fracture patients compared to just 45.9% of those without fractures. In fracture group patients, TuG improved from median 5 on admission to median 3 on discharge (p = 0.001). In fracture patients, improvement in walking ability was associated with higher Barthel index values on admission (median 45 (IQR: 35–55) versus 35 (IQR: 20–50): p = 0.001) and Tinetti assessment scores (median 9 (IQR: 4–14.25) versus 5 (IQR: 0–13); p = 0.001) and was negatively associated with the diagnosis of dementia (21.4% versus 31.5%; p = 0.058). Conclusion: CGC improved walking ability in more than half of all patients examined. Older patients in particular might benefit from undergoing the procedure after an acute fracture. A better initial functional status favors a positive result following the treatment. [ABSTRACT FROM AUTHOR]

Open in new tab Download slide OBJECTIVES Following cardiac surgery, postoperative cognitive decline (POCD) is a common complication that can impair the quality of life and increase mortality. The aim of this study was to investigate whether early postoperative cognitive training can decrease POCD after cardiac surgery. METHODS The study was a multi-centred, two-arm, randomized (1:1 ratio), controlled trial involving older patients undergoing elective heart valve surgery with extracorporeal circulation. Recruitment took place at the Department of Cardiac Surgery of the Kerckhoff-Clinic in Bad Nauheim (Germany) and the University-Hospital in Giessen (Germany). The patients were randomized to either a paper-and-pencil-based cognitive training group or a standard rehabilitation care control group. The cognitive training started 1 week after surgery and lasted about 3 weeks until discharge from rehabilitation. To detect POCD, neuropsychological functions were assessed prior to surgery, upon discharge from rehabilitation (primary outcome), and 3 months after discharge (secondary outcome). Data were primarily analysed in a per-protocol fashion. RESULTS The frequency of POCD at discharge from rehabilitation (training group, n  = 37; control group, n  = 44) was 50% in the control group and 19% in the training group (χ2[1] = 8.45, P  = 0.004; odds ratio = 4.29, 95% confidence interval [1.56–11.80]). Three months after the cognitive training (training group, n  = 33; control group, n  = 34), POCD frequency was 29% in the control group and 6% in the training group (χ2[1] = 6.21, P  = 0.013; odds ratio = 6.46, 95% confidence interval [1.29–32.28]). CONCLUSIONS Since our cognitive training showed beneficial effects, it could be a promising method to prevent POCD. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is the most common immune-mediated CNS disease, characterised by demyelination and progressive neurological disability. The B-cell activating factor BAFF has been described as one important factor in the pathophysiology of different autoimmune diseases. We measured BAFF levels in the serum and cerebrospinal fluid (CSF) in 50 consecutive patients with MS and 35 patients with infectious CNS disease (ID). 52 patients with other, non-inflammatory disorders (OND), served as controls. BAFF-serum levels in ID patients were higher than in patients diagnosed with MS (ID 0.55 ± 0.24 ng/ml, MS 0.43 ± 0.14 ng/ml, OND 0.45 ± 0.24 ng/ml; p = 0.09). Interestingly, MS patients had lower BAFF CSF levels compared to the controls and ID patients, and the CSF levels in the latter were elevated compared to those of the controls (MS 0.17 ± 0.11 ng/ml, OND 0.25 ± 0.14 ng/ml, ID 0.97 ± 0.78 ng/ml; p < 0.001). The ID patients' having higher absolute BAFF levels in the CSF than in the serum indicates that the increased BAFF CSF levels were caused by intrathecal synthesis rather than passive transfer via a disturbed blood-brain-barrier. The significantly decreased BAFF CSF levels in MS patients were a surprising result of our study. Although it has been reported that astrocytes in active MS lesions can express BAFF, the soluble form was not increased in the CSF of MS patients. It remains unclear whether the inflammatory features of active MS plaques are truly represented by the CSF compartment. [ABSTRACT FROM AUTHOR]

Hereditary Transthyretin-Related Amyloidosis, a clinically heterogeneous autosomal dominant disease caused by pathogenic variants in the TTR gene, is characterized by the deposition of insoluble misfolded protein fibrils. The diagnosis, especially in non-endemic areas, is typically delayed by 4–5 years; a misdiagnosis due to clinical heterogeneity is common. The study objective was to define the prevalence of Hereditary Transthyretin-Related Amyloidosis in patients with polyneuropathy and/or cardiomyopathy of no obvious aetiology. A multicenter observational "Epidemiological analysis for the hereditary Transthyretin-Related AMyloidosis"—TRAM study was performed in Germany, Austria, and Switzerland. A total of 5141 participants were recruited by 50 neurologic and 27 cardiologic specialized centres. Genetic analysis demonstrated a 1.1% Hereditary Transthyretin-Related Amyloidosis positivity rate among patients with polyneuropathy and/or cardiomyopathy of not obvious aetiology. Twenty-one various TTR variants (TTR-positive) were identified. Body Mass Index was lower in the TTR-positive patients as an indicator for the involvement of the autonomic nervous system; the age of onset of clinical manifestations was higher in TTR-positive patients. There were no other genotype-phenotype correlations or the prevalence of specific clinical manifestations in TTR-positive patients. Our data support the fact that Hereditary Transthyretin-Related Amyloidosis is underdiagnosed in polyneuropathy and cardiomyopathy patients. Routine implementation of genetic testing is recommended in patients with unexplained polyneuropathy and/or cardiomyopathy to accelerate the earlier diagnosis and the time-sensitive treatment initiation. More than 5.000 participants with CM and/or PNP of no obvious aetiology were recruited in the observational "Epidemiological analysis for the hereditary Transthyretin-Related AMyloidosis" TRAM study and screened for pathogenic TTR variants. The study demonstrated >1% of patients with CM and/or PNP of unclear aetiology are positive for a pathogenic TTR variant. Routine genetic testing is recommended in patients with unexplained CM and/or PNP to accelerate the initial diagnosis and timely treatment initiation. [ABSTRACT FROM AUTHOR]

Medial medullary infarction (MMI) is a vascular occlusion in the medulla oblongata leading to certain constellations of neurological symptoms and seriously affecting the patient. Effective evidence-based treatment of severe dysphagia as sole symptom of MMI has not yet been reported. This case study aims to report successful effects of evidence-based therapy based on findings of dysphagia symptoms and pathophysiology of swallowing by flexible endoscopic evaluation of swallowing (FEES) in severe isolated dysphagia after MMI. FEES was performed to evaluate swallowing pathophysiology and dysphagia symptoms in a 57-year-old male with severe dysphagia after MMI. On the basis of FEES findings, simple and high-frequent evidence-based exercises for improvement of swallowing were implemented: thermal stimulation of faucial arches, Jaw Opening Exercise, and Jaw Opening Against Resistance. After 7 weeks of high-frequent evidence-based therapy and regular FEES evaluation the patient was set on full oral diet with no evidence of aspiration risk. In a first case report of isolated dysphagia in MMI our case illustrates that high-frequent evidence-based dysphagia therapy in combination with FEES as the method to evaluate and monitor swallowing pathophysiology can lead to successful and quick rehabilitation of severely affected dysphagic patients. [ABSTRACT FROM AUTHOR]