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Background: Intensive care unit (ICU) acquired weakness is a major contributor to poor functional outcome of ICU patients. Quantification of temporal muscle volume assessed on routine computed tomography (CT) scans may serve as a biomarker for muscle wasting in patients suffering from acute brain injury. Methods: This is a retrospective analysis of prospectively collected data. Temporal muscle volume was assessed on head CT scans of consecutive patients with spontaneous subarachnoid hemorrhage within prespecified time frames (on admission, then weekly ± 2 days). Whenever possible, temporal muscle volume was assessed bilaterally and averaged for the analysis. Poor functional outcome was defined as a 3-month modified Rankin Scale Score ≥ 3. Statistical analysis was performed using generalized estimating equations to handle repeated measurements within individuals. Results: The analysis comprised 110 patients with a median Hunt & Hess score of 4 (interquartile range 3–5). Median age was 61 (50–70) years, 73 patients (66%) were women. Baseline temporal muscle volume was 18.5 ± 0.78 cm3 and significantly decreased over time (p < 0.001) by a mean of 7.9% per week. Higher disease severity (p = 0.002), hydrocephalus (p = 0.020), pneumonia (p = 0.032), and bloodstream infection (p = 0.015) were associated with more pronounced muscle volume loss. Patients with poor functional outcome had smaller muscle volumes 2 and 3 weeks after subarachnoid hemorrhage compared with those with good outcome (p = 0.025). The maximum muscle volume loss during ICU stay was greater in patients with poor functional outcome (− 32.2% ± 2.5% vs. − 22.7% ± 2.5%, p = 0.008). The hazard ratio for poor functional outcome was 1.027 (95% confidence interval 1.003–1.051) per percent of maximum muscle volume loss. Conclusions: Temporal muscle volume, which is easily assessable on routine head CT scans, progressively decreases during the ICU stay after spontaneous subarachnoid hemorrhage. Because of its association with disease severity and functional outcome, it may serve as a biomarker for muscle wasting and outcome prognostication. [ABSTRACT FROM AUTHOR]

Background: The amount of intracranial blood is a strong predictor of poor outcome after subarachnoid hemorrhage (SAH). Here, we aimed to measure iron concentrations in the cerebral white matter, using the cerebral microdialysis (CMD) technique, and to associate iron levels with the local metabolic profile, complications, and functional outcome. Methods: For the observational cohort study, 36 patients with consecutive poor grade SAH (Hunt & Hess grade of 4 or 5, Glasgow Coma Scale Score ≤ 8) undergoing multimodal neuromonitoring were analyzed for brain metabolic changes, including CMD iron levels quantified by graphite furnace atomic absorption spectrometry. The study time encompassed 14 days after admission. Statistical analysis was performed using generalized estimating equations. Results: Patients were admitted in a poor clinical grade (n = 26, 72%) or deteriorated within 24 h (n = 10, 28%). The median blood volume in the subarachnoid space was high (SAH sum score = 26, interquartile range 20–28). Initial CMD iron was 44 µg/L (25–65 µg/L), which significantly decreased to a level of 25 µg/L (14–30 µg/L) at day 4 and then constantly increased over the remaining neuromonitoring days (p < 0.01). A higher intraventricular hemorrhage sum score (≥ 5) was associated with higher CMD iron levels (Wald-statistic = 4.1, df = 1, p = 0.04) but not with the hemorrhage load in the subarachnoid space (p = 0.8). In patients developing vasospasm, the CMD iron load was higher, compared with patients without vasospasm (Wald-statistic = 4.1, degree of freedom = 1, p = 0.04), which was not true for delayed cerebral infarction (p = 0.4). Higher iron concentrations in the brain extracellular fluid (34 µg/L, 36–56 µg/L vs. 23 µg/L, 15–37 µg/L) were associated with mitochondrial dysfunction (CMD lactate to pyruvate ratio > 30 and CMD-pyruvate > 70 µM/L, p < 0.001). Brain extracellular iron load was not associated with functional outcome after 3 months (p > 0.5). Conclusions: This study suggests that iron accumulates in the cerebral white matter in patients with poor grade SAH. These findings may support trials aiming to scavenger brain extracellular iron based on the hypothesis that iron-mediated neurotoxicity may contribute to acute and secondary brain injury following SAH. [ABSTRACT FROM AUTHOR]

Background/objective: Monitoring of brain tissue oxygen tension (PbtO2) provides insight into brain pathophysiology after intracerebral hemorrhage (ICH). Integration of probe location is recommended to optimize data interpretation. So far, little is known about the importance of PbtO2 catheter location in ICH patients. Methods: We prospectively included 40 ICH patients after hematoma evacuation (HE) who required PbtO2-monitoring. PbtO2-probe location was evaluated in all head computed tomography (CT) scans within the first 6 days after HE and defined as location in the healthy brain tissue or perilesional when the catheter tip was located within 1 cm of a focal lesion (hypodense or hyperdense). Generalized estimating equations were used to investigate levels of PbtO2 in relation to different probe locations. Results: Patients were 60 [51–66] years old and had a median ICH-volume of 47 [29–60] mL. Neuromonitoring probes remained for a median of 6 [2–11] days. PbtO2-probes were located in healthy brain tissue in 18/40 (45%) patients and in perilesional brain tissue in 22/40 (55%) patients. In the acute phase after HE (0–72 h), PbtO2 levels were significantly lower (21 ± 12 mmHg vs. 29 ± 10 mmHg, p = 0.010) and brain tissue hypoxia (BTH) was more common in the perilesional area as compared to healthy brain tissue (46% vs. 19%, adjOR 4.0, 95% CI 1.54–10.58, p = 0.005). Episodes of BTH significantly decreased over time in patients with probes in perilesional location (p = 0.001) but remained stable in normal appearing area (p = 0.485). A significant association between BTH and poor functional outcome was only found when probes were located in the perilesional brain tissue (adjOR 6.6, 95% CI 1.3–33.8, p = 0.023). Conclusions: In the acute phase, BTH was more common in the perilesional area compared to healthy brain tissue. The improvement of BTH in the perilesional area over time may be the result of targeted treatment interventions and tissue regeneration. Due to the localized measurement of invasive neuromonitoring devices, integration of probe location in the clinical management of ICH patients and in research protocols seems mandatory. [ABSTRACT FROM AUTHOR]

Background: Despite the tremendous impact of swallowing disorders on outcome following ischemic stroke, little is known about the incidence of dysphagia after subarachnoid hemorrhage (SAH) and its contribution to hospital complications, length of intensive care unit stay, and functional outcome.Methods: This is a retrospective analysis of an ongoing prospective cohort study. Swallowing ability was assessed in consecutive non-traumatic SAH patients admitted to our neurological intensive care unit using the Bogenhausen Dysphagia Score (BODS). A BODS > 2 points indicated dysphagia. Functional outcome was assessed 3 months after the SAH using the modified Rankin Scale with a score > 2 defined as poor functional outcome.Results: Two-hundred and fifty consecutive SAH patients comprising all clinical severity grades with a median age of 57 years (interquartile range 47-67) were eligible for analysis. Dysphagia was diagnosed in 86 patients (34.4%). Factors independently associated with the development of dysphagia were poor clinical grade on admission (Hunt & Hess grades 4-5), SAH-associated parenchymal hematoma, hydrocephalus, detection of an aneurysm, and prolonged mechanical ventilation (> 48 h). Dysphagia was independently associated with a higher rate of pneumonia (OR = 4.32, 95% CI = 2.35-7.93), blood stream infection (OR = 4.3, 95% CI = 2.0-9.4), longer ICU stay [14 (8-21) days versus 29.5 (23-45) days, p < 0.001], and poor functional outcome after 3 months (OR = 3.10, 95% CI = 1.49-6.39).Conclusions: Dysphagia is a frequent complication of non-traumatic SAH and associated with poor functional outcome, infectious complications, and prolonged stay in the intensive care unit. Early identification of high-risk patients is needed to timely stratify individual patients for dysphagia treatment. [ABSTRACT FROM AUTHOR]

The numbers of migrants, refugees and asylum seekers reached an unprecedented high in Europe in 2015 and 2016 but in 2019 they are back to the average numbers of the last 30 years. In contrast, frequencies of international and intercontinental travelers have continuously increased over the past decades and will continue to do so in the coming years. In 2018 more than 1.35 billion incoming travelers were reported worldwide by international organizations. Detailed knowledge of the epidemiology, transmission types, risk behavior and clinical presentation of acute and chronic central nervous system (CNS) infections enables timely diagnosis and initiation of potentially life-saving emergency treatment. Acute infections of the CNS, e.g. cerebral Plasmodium falciparum malaria or arboviral encephalitis, are seen most frequently and almost exclusively in travelers returning from tropical countries, whereas chronic CNS infections, e.g. tuberculous meningitis or neurocysticercosis, are typically seen in migrants and refugees. Beside CNS infections genetic diseases, environment-associated, nutrition-related, metabolic or cerebrovascular diseases also need to be considered when discussing differential diagnostic possibilities. [ABSTRACT FROM AUTHOR]

Background: There is no uniform definition for cerebral microdialysis (CMD) probe location with respect to focal brain lesions, and the impact of CMD-probe location on measured molecule concentrations is unclear.Methods: We retrospectively analyzed data of 51 consecutive subarachnoid hemorrhage patients with CMD-monitoring between 2010 and 2016 included in a prospective observational cohort study. Microdialysis probe location was assessed on all brain computed tomography (CT) scans performed during CMD-monitoring and defined as perilesional in the presence of a focal hypodense or hyperdense lesion within a 1-cm radius of the gold tip of the CMD-probe, or otherwise as normal-appearing brain tissue.Results: Probe location was detected in normal-appearing brain tissue on 53/143 (37%) and in perilesional location on 90/143 (63%) CT scans. In the perilesional area, CMD-glucose levels were lower (p = 0.003), whereas CMD-lactate (p = 0.002), CMD-lactate-to-pyruvate-ratio (LPR; p < 0.001), CMD-glutamate (p = 0.002), and CMD-glycerol levels (p < 0.001) were higher. Neuroglucopenia (CMD-glucose < 0.7 mmol/l, p = 0.002), metabolic distress (p = 0.002), and mitochondrial dysfunction (p = 0.005) were more common in perilesional compared to normal-appearing brain tissue. Development of new lesions in the proximity of the CMD-probe (n = 13) was associated with a decrease in CMD-glucose levels, evidence of neuroglucopenia, metabolic distress, as well as increasing CMD-glutamate and CMD-glycerol levels. Neuroglucopenia was associated with poor outcome independent of probe location, whereas elevated CMD-lactate, CMD-LPR, CMD-glutamate, and CMD-glycerol levels were only predictive of poor outcome in normal-appearing brain tissue.Conclusions: Focal brain lesions significantly impact on concentrations of brain metabolites assessed by CMD. With the exception of CMD-glucose, the prognostic value of CMD-derived parameters seems to be higher when assessed in normal-appearing brain tissue. CMD was sensitive to detect the development of new focal lesions in vicinity to the neuromonitoring probe. Probe location should be described in the research reporting brain metabolic changes measured by CMD and integrated in statistical models. [ABSTRACT FROM AUTHOR]

Background: Nimodipine is the only drug approved in the treatment of aneurysmal subarachnoid hemorrhage (aSAH) in many countries. EG-1962, a product developed using the Precisa™ platform, is an extended-release microparticle formulation of nimodipine that can be administered intraventricularly or intracisternally. It was developed to test the hypothesis that delivering higher concentrations of extended-release nimodipine directly to the cerebrospinal fluid would provide superior efficacy compared to systemic administration.Results: A Phase 1/2a multicenter, controlled, randomized, open-label, dose-escalation study determined the maximum tolerated dose and supported the safety and tolerability of EG-1962 in patients with aSAH. EG-1962, 600 mg, was selected for a pivotal, Phase 3 multicenter, randomized, double-blind, placebo-controlled, parallel-group efficacy, and safety study comparing it to standard of care oral nimodipine in adults with aSAH. Key inclusion criteria are patients with a ruptured saccular aneurysm repaired by clipping or coiling, World Federation of Neurological Surgeons grade 2-4, and modified Fisher score of > 1. Patients must have an external ventricular drain as part of standard of care. Patients are randomized to receive intraventricular investigational product (EG-1962 or NaCl solution) and an oral placebo or oral nimodipine in the approved dose regimen (active control) within 48 h of aSAH. The primary objective is to determine the efficacy of EG-1962 compared to oral nimodipine.Conclusions: The primary endpoint is the proportion of subjects with favorable outcome (6-8) on the Extended Glasgow Outcome Scale assessed 90 days after aSAH. The secondary endpoint is the proportion of subjects with favorable outcome on the Montreal Cognitive Assessment 90 days after aSAH. Data on safety, rescue therapy, delayed cerebral infarction, and health economics will be collected. Trail registration NCT02790632. [ABSTRACT FROM AUTHOR]

The posterior reversible encephalopathy syndrome (PRES) is a neurological disorder of (sub)acute onset characterized by varied neurological symptoms, which may include headache, impaired visual acuity or visual field deficits, disorders of consciousness, confusion, seizures, and focal neurological deficits. In a majority of patients the clinical presentation includes elevated arterial blood pressure up to hypertensive emergencies. Neuroimaging, in particular magnetic resonance imaging, frequently shows a distinctive parieto-occipital pattern with a symmetric distribution of changes reflecting vasogenic edema. PRES frequently develops in the context of cytotoxic medication, (pre)eclampsia, sepsis, renal disease or autoimmune disorders. The treatment is symptomatic and is determined by the underlying condition. The overall prognosis is favorable, since clinical symptoms as well as imaging lesions are reversible in most patients. However, neurological sequelae including long-term epilepsy may persist in individual cases. [ABSTRACT FROM AUTHOR]

Introduction: Vasospasm still is a major cause of morbidity after aneurysmal subarachnoid hemorrhage. The purpose of this report is to describe the successful management of severe refractory vasospasm with continuous intra-arterial nimodipine (IAN) treatment. Case description: A 72-year old right handed woman was admitted with non-traumatic SAH WFNS grade 1. Cerebral computed tomography demonstrated thick blood filling of the basal cisterns, and intraventricular hemorrhage. Cerebral angiogram failed to detect a vascular abnormality. After an uneventful initial course the patient developed symptomatic left middle cerebral artery vasospasm with aphasia and corresponding restriction in diffusion weighted images in the left frontal lobe. Bolus IAN only transiently improved cerebral circulation and clinical signs and symptoms. Continuous-IAN was started and led to full clinical recovery and normalisation of MRI diffusion restrictions. Discussion and conclusions: Continuous selective intra-arterial infusion of nimodipine may be an option in selected patients with symptomatic vasospasm refractory to conventional treatment after careful consideration of benefits and procedure-related risks. [ABSTRACT FROM AUTHOR]

We recently reported a novel neurological syndrome characterized by a unique NREM and REM parasomnia with sleep apnea and stridor, accompanied by bulbar dysfunction and specific association with antibodies against the neuronal cell-adhesion protein IgLON5. All patients had the HLA-DRB1*1001 and HLA-DQB1*0501 alleles. Neuropathological findings in two patients revealed a novel tauopathy restricted to neurons and predominantly involving the hypothalamus and tegmentum of the brainstem. The aim of the current study is to describe the neuropathological features of the anti-IgLON5 syndrome and to provide diagnostic levels of certainty based on the presence of associated clinical and immunological data. The brains of six patients were examined and the features required for the neuropathological diagnosis were established by consensus. Additional clinical and immunological criteria were used to define 'definite', 'probable' and 'possible' diagnostic categories. The brains of all patients showed remarkably similar features consistent with a neurodegenerative disease with neuronal loss and gliosis and absence of inflammatory infiltrates. The most relevant finding was the neuronal accumulation of hyperphosphorylated tau composed of both three-repeat (3R) and four-repeat (4R) tau isoforms, preferentially involving the hypothalamus, and more severely the tegmental nuclei of the brainstem with a cranio-caudal gradient of severity until the upper cervical cord. A 'definite' diagnosis of anti-IgLON5-related tauopathy is established when these neuropathological features are present along with the detection of serum or CSF IgLON5 antibodies. When the antibody status is unknown, a 'probable' diagnosis requires neuropathological findings along with a compatible clinical history or confirmation of possession of HLA-DRB1*1001 and HLA-DQB1*0501 alleles. A 'possible' diagnosis should be considered in cases with compatible neuropathology but without information about a relevant clinical presentation and immunological status. These criteria should help to identify undiagnosed cases among archival tissue, and will assist future clinicopathological studies of this novel disorder. [ABSTRACT FROM AUTHOR]

Introduction: Viral encephalitis is an emerging disease requiring intensive care management in severe cases. Underlying pathophysiologic mechanisms are incompletely understood and may be elucidated using invasive multimodal neuromonitoring techniques in humans.Methods: Two otherwise healthy patients were admitted to our neurological intensive care unit with altered level of consciousness necessitating mechanical ventilation. Brain imaging and laboratory workup suggested viral encephalitis in both patients. Invasive neuromonitoring was initiated when head computed tomography revealed generalized brain edema, including monitoring of intracranial pressure, brain metabolism (cerebral microdialysis; CMD), brain tissue oxygen tension (in one patient), and cerebral blood flow (in one patient).Results: Brain metabolism revealed episodes of severe neuroglucopenia (brain glucose <0.7 mM/l) in both patients, which were not attributable to decreased cerebral perfusion or hypoglycemia. CMD-glucose levels changed depending on variations in insulin therapy, nutrition, and systemic glucose administration. The metabolic profile, moreover, showed a pattern of non-ischemic metabolic distress suggestive for mitochondrial dysfunction. Both patients had a prolonged but favorable clinical course and improved to a modified Rankin Scale Score of 1 and 0 three months later.Conclusion: Invasive multimodal neuromonitoring is feasible in poor-grade patients with viral meningoencephalitis and may help understand pathophysiologic mechanisms associated with secondary brain injury. The detection of neuroglucopenia and mitochondrial dysfunction may serve as treatment targets in the future. [ABSTRACT FROM AUTHOR]

Background: Cerebral edema and delayed cerebral infarction (DCI) are common complications after aneurysmal subarachnoid hemorrhage (aSAH) and associated with poor functional outcome. Experimental data suggest that the amino acid taurine is released into the brain extracellular space secondary to cytotoxic edema and brain tissue hypoxia, and therefore may serve as a biomarker for secondary brain injury after aSAH. On the other hand, neuroprotective mechanisms of taurine treatment have been described in the experimental setting.Methods: We analyzed cerebral taurine levels using high-performance liquid chromatography in the brain extracellular fluid of 25 consecutive aSAH patients with multimodal neuromonitoring including cerebral microdialysis (CMD). Patient characteristics and clinical course were prospectively recorded. Associations with CMD-taurine levels were analyzed using generalized estimating equations with an autoregressive process to handle repeated observations within subjects.Results: CMD-taurine levels were highest in the first days after aSAH (11.2 ± 3.2 µM/l) and significantly decreased over time (p < 0.001). Patients with brain edema on admission or during hospitalization (N = 20; 80 %) and patients developing DCI (N = 5; 20 %) had higher brain extracellular taurine levels compared to those without (Wald = 7.3, df = 1, p < 0.01; Wald = 10.1, df = 1, p = 0.001, respectively) even after adjusting for disease severity and CMD-probe location. There was no correlation between parenteral taurine supplementation and brain extracellular taurine (p = 0.6). Moreover, a significant correlation with brain extracellular glutamate (r = 0.82, p < 0.001), lactate (r = 0.56, p < 0.02), pyruvate (r = 0.39, p < 0.01), potassium (r = 0.37, p = 0.01), and lactate-to-pyruvate ratio (r = 0.24, p = 0.02) was found.Conclusions: Significantly higher CMD-taurine levels were found in patients with brain edema or DCI after aneurysmal subarachnoid hemorrhage. Its value as a potential biomarker deserves further investigation. [ABSTRACT FROM AUTHOR]

Background: Neuroprotection through targeted temperature management is currently investigated in patients with severe brain injury in multiple trials. Feedback devices have been shown to precisely reach and maintain target temperature by constantly adjusting cooling activity. We analyzed the association between cooling activity expressed as cool bath temperatures and functional neurological outcome. Methods: Data were retrospectively analyzed from a prospective randomized trial on controlled prophylactic normothermia (i.e., 36.5 °C) in patients with severe cerebrovascular disease. Body core temperature of patients who had been randomized to the endovascular group, was controlled using an endovascular cooling device. Cool bath temperature was analyzed over a period of 168 h. Functional neurological outcome was evaluated at 180 days using the modified Rankin Scale. Results: 51 of 102 patients included were randomized to the endovascular group. Cool bath temperature data were available from 47/51 patients. Patients with lower cool bath temperatures reflecting high cooling activity had a more favorable neurological outcome at 180 days (mRS 0-2) than patients with low cooling activity ( p < 0.05). We did not find a significant correlation between cool bath temperature and inflammatory markers. Conclusion: High cooling activity of an endovascular feedback device is associated with favorable outcome in patients with severe cerebrovascular disease. [ABSTRACT FROM AUTHOR]

In acute bacterial meningitis long-term morbidity and mortality are still high, in particular, in low and middle income countries where meningococci are the most frequent causative agents of this disease. If at all, dexamethasone has been shown to be helpful in pneumococcal meningitis, i.e., in elderly Europeans and not in adolescent African, Asian or South American patients. Since deranged glucose, in particular, glucose variability and deranged coagulation homeostasis are known to be deleterious in patients with bacterial meningitis, dexamethasone-being capable to cause both-might add to morbidity and mortality. After more than 20 prospective trials evidence still lacks that dexamethasone improves outcome in the majority of patients. Dexamethasone only exerts a positive effect, if given prior to the first dose of antibiotic; therefore, the introduction of empiric antimicrobial chemotherapy into the emergency (= pre-hospital) management of patients with suspected bacterial meningitis, the discussion on dexamethasone in acute bacterial meningitis is rendered almost futile. [ABSTRACT FROM AUTHOR]

Background: Little is known about endothelial activation under the influence of endovascular temperature management. This analysis was designed to measure the endothelial markers Angiopoietin-1 (Ang-1) and -2 (Ang-2) in endovascularly based prophylactic normothermia versus conventional temperature management. Methods: In this randomized controlled trial patients with spontaneous subarachnoid or spontaneous intracerebral hemorrhage were prospectively enrolled and randomized in two treatment arms: (a) prophylactic normothermia group with target core temperature 36.5°C using endovascular cooling, (b) active control group with conventional stepwise predefined fever management using antipyretic medication and surface cooling. Blood samples were obtained on days 1, 4, and 7. In a substudy Ang-1 and -2 were measured in 63 patients for whom samples on consecutive days were available. Results: The median total fever burden during the course of treatment was 0.0°C and 5.9°C h in the endovascular and the conventional group, respectively ( P < 0.0001). Angiopoietin serum levels did not yield a statistical difference when comparing the two treatment arms. Ang-1 was significantly lowered, whereas Ang-2 levels were significantly elevated on day 4 compared to baseline levels irrespective of group allocation ( P < 0.0001). The application of non-steroidal anti-inflammatory drugs (NSAIDs) was associated with significantly increased Ang-1 ( P < 0.05) and lower Ang-2 levels on day 7 ( P < 0.05). Conclusions: Endovascular long-term temperature management did not alter Ang-1 and -2 levels compared to the control group indicating that the endovascular cooling technique itself does not lead to additional endothelial impairment. However, application of NSAIDs led to lower Ang-2 serum concentrations in the endovascular group. [ABSTRACT FROM AUTHOR]

Although metabolic abnormalities have been linked with poor outcome after subarachnoid hemorrhage, there are limited data addressing the impact of glycemic control or benefits of glucose management after aneurysmal subarachnoid hemorrhage. A systematic literature search was conducted of English-language articles describing original research on glycemic control in patients with subarachnoid hemorrhage. Case reports and case series were excluded. A total of 22 publications were selected for this review. Among the 17 studies investigating glucose as an outcome predictor, glucose levels during hospitalization were more likely to predict outcome than admission glucose. In general, hyperglycemia was linked to worse outcome. While insulin therapy in subarachnoid hemorrhage patients was shown to effectively control plasma glucose levels, plasma glucose control was not necessarily reflective of cerebral glucose such that very tight glucose control may lead to neuroglycopenia. Furthermore, tight glycemic control was associated with an increased risk for hypoglycemia which was linked to worse outcome. [ABSTRACT FROM AUTHOR]

Subarachnoid hemorrhage (SAH) is an acute cerebrovascular event which can have devastating effects on the central nervous system as well as a profound impact on several other organs. SAH patients are routinely admitted to an intensive care unit and are cared for by a multidisciplinary team. A lack of high quality data has led to numerous approaches to management and limited guidance on choosing among them. Existing guidelines emphasize risk factors, prevention, natural history, and prevention of rebleeding, but provide limited discussion of the complex critical care issues involved in the care of SAH patients. The Neurocritical Care Society organized an international, multidisciplinary consensus conference on the critical care management of SAH to address this need. Experts from neurocritical care, neurosurgery, neurology, interventional neuroradiology, and neuroanesthesiology from Europe and North America were recruited based on their publications and expertise. A jury of four experienced neurointensivists was selected for their experience in clinical investigations and development of practice guidelines. Recommendations were developed based on literature review using the GRADE system, discussion integrating the literature with the collective experience of the participants and critical review by an impartial jury. Recommendations were developed using the GRADE system. Emphasis was placed on the principle that recommendations should be based not only on the quality of the data but also tradeoffs and translation into practice. Strong consideration was given to providing guidance and recommendations for all issues faced in the daily management of SAH patients, even in the absence of high quality data. [ABSTRACT FROM AUTHOR]

Background: Aortic coarctation (AC) rarely remains undiagnosed until adulthood. Intracranial aneurysms and spontaneous subarachnoid hemorrhage (SAH) are more frequent in patients with AC than in the general population. Methods: The purpose of this report is to describe the management of a poor grade SAH patient with previously undiagnosed AC using advanced monitoring techniques of the brain and the cardiovascular system. Results: A 28-year-old man with previously unknown AC was admitted with aneurysmal SAH WFNS grade 5. Head computed tomography demonstrated thick blood filling the basal cisterns, mild hydrocephalus, and global cerebral edema. The ruptured aneurysm of the anterior communicating artery was successfully coiled on the same day. Echocardiography revealed high grade isthmus stenosis with a pressure gradient of 60 mm Hg. Hospital course was complicated by prerenal failure and severe vasospasm. Neuromonitoring data (cerebral metabolism, brain tissue oxygenation, cerebral blood flow and intracranial pressure) were used as endpoint to define the optimal blood pressure to meet the cerebral metabolic and oxygen demand in each phase. Conclusions: Cerebral aneurysm rupture associated with coarctation of the aorta is rare. The aim of this report is to call attention to AC in, particularly, young patients presenting with SAH and to discuss advanced multimodal neuromonitoring techniques used to optimize intensive care management. [ABSTRACT FROM AUTHOR]

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Copyright of Wiener Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The prevalence of Parkinson’s disease (PD) in sub-Saharan Africa is still a matter of debate. The few studies that have been conducted have shown prevalences lower than those in the western world. Whether this represents a genuine finding is unclear to date. In northern Tanzania, we have conducted a hospital-based evaluation and a community-based door-to-door study to assess the prevalence of Parkinsonism, including that of PD. Over a period of 8 months, all patients admitted to a mid-size rural hospital were screened for PD. In parallel, 1,569 people aged ≥50 years were recruited from the communities and assessed for PD with standard questions. Sampling was performed according to the method of “multistage cluster sampling.” The questions had previously been tested in a pilot study prior to the survey. People who screened positive were examined by a specialist neurologist. In the hospital, eight of 740 people with neurological diagnoses had Parkinsonism, of whom three patients had a diagnosis of PD. In the community-based study, 18 people answered positively to least one of the 12 screening questions. However, the diagnosis of PD could not be confirmed by further examination in any of them. The prevalence of PD in northern Tanzania was found to be very low. This result would need confirmation in studies with larger populations, ideally of different African ethnicities. [ABSTRACT FROM AUTHOR]

Background: Acanthamoeba sp. are known to cause fatal granulomatous Acanthamoeba encephalitis (GAE) in immunocompromised patients.Methods: The case of a 17 year old immunocompetent patient with acute purulent meningoencephalitis is reported.Results: After substantial improvement of cerebrospinal fluid under conventional antimicrobial treatment the patient was suffering several relapses. The causative agent was identified as Acanthamoeba lenticulata T5 which entered the CNS through a bone dehiscence of ethmoidal cells. Due to severe vasospasm the patient developed multiple strokes, which led to marked neurologic sequels.Conclusions: This case report demonstrates successful treatment of usually lethal GAE in an immunocompetent patient with high dose meropenem, linezolid, moxifloxacin and fluconazole followed by a partially adapted antimicrobial combination therapy. [ABSTRACT FROM AUTHOR]

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Abstract Introduction  Neurocritical care patients requiring external ventricular drainage are at risk for the development of a device-related infection. Infection rate of external ventriculostomy catheters is high with reported incidences ranging from 5% up to more than 20%. Nosocomial ventriculitis or ventriculomeningitis are potential life-threatening conditions which may contribute to a permanent adverse outcome of the patient. Reducing morbidity and mortality is strongly dependent on prompt diagnosis and on the initiation of appropriate antiinfective therapy. Scientific Background  Management of nosocomial ventriculitis is challenging and needs to consider the most likely pathogens involved, local resistance patterns, the nature of the underlying disease, patient factors such as age, comorbidity, and immune status. Further, decisions on catheter exchange and the type and duration of systemic or local antimicrobial therapy have to be made. Because so many factors have to be taken into account, it is evident that the diagnostic and therapeutic approach to nosocomial ventriculitis is difficult to standardize. Staphylococci are the pathogens most frequently identified in nosocomial ventriculitis. Therefore, initial treatment with an antistaphylococcal agent with adequate cerebrospinal fluid penetration may be considered as first-line therapy for this infection. Conclusion  In the review of a contemporary case we will discuss important issues in the management of device-related ventriculitis. [ABSTRACT FROM AUTHOR]

Chronic meningitis is an inflammation of the meninges with subacute onset and persisting cerebrospinal fluid (CSF) abnormalities lasting for at least one month. Several non-infectious and infectious etiologies are known to be causative. The wide range of different etiologies renders the approach to patients with this syndrome particularly difficult. There is no standardized diagnostic procedure, thus, taking an in depth history combined with a complete physical examination is mandatory in every patient. This review aims to present the current knowledge on etiology, neurological course of disease, diagnostic and therapeutic management steps of patients presenting with clinical signs and symptoms of chronic meningitis and meningoencephalitis. Still, the etiology of one third of patients remains unclear, reflecting the diagnostic challenge of this syndrome for each physician or neurologist, respectively. However, most patients with idiopathic chronic meningitis have a relatively good outcome. [ABSTRACT FROM AUTHOR]

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Copyright of Wiener Klinische Wochenschrift is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: Patients sustaining facial fractures are at risk for accompanying traumatic intracranial hematomas, which are a major cause of morbidity and mortality. Prompt recognition is crucial in improving patient survival and recovery. This study examined which simple clinical signs identify facial fracture patients at risk for intracranial hemorrhage before the performance of computed tomography.Design and Methods: Retrospective study of 2,195 patients with facial fractures during a period of 7 years. By means of univariate and multivariate analysis clinical features potentially predictive for (a) intracranial hemorrhage and (b) surgery for intracranial hemorrhage were identified.Setting: Critical care units of anesthesiology and neurology, general traumatology, and oral and maxillofacial surgery in a level I trauma university hospital.Results: Seizures (OR 22.1) and vomiting/nausea (OR 20.2) were the strongest independent predictors of intracranial bleeding in facial fracture patients. For intracranial hemorrhages requiring surgical intervention closed head injuries (OR 9.75) and cranial vault fractures (OR 5.0) were the most significant risk factors. However, among those patients without vomiting/nausea and without seizures and without closed head injury ( n=1,628), 20 patients (1.2%) suffered intracranial hemorrhage, and six (0.37%) of them required surgical intervention.Conclusions: Simple clinical symptoms, such as seizures, vomiting/nausea, history of a closed head injury or cranial vault fractures are strong predictors for intracranial hemorrhage in facial fracture patients. The early consideration of such important indicators allows us to detect patients at elevated risk of an intracranial hematoma requiring surgical intervention. [ABSTRACT FROM AUTHOR]

Within the past decade the management of acute HSV I encephalitis has been improved dramatically by the advent of the polymerase chain reaction (PCR), a method which has become the gold standard of diagnosis of HSV I encephalitis, replacing diagnostic uncertainties and, avoiding, in particular, invasive brain biopsy. Early detection of HSV II in the neonate is mandatory; however, prevention by Caesarean section and/or prenatal therapy of the mother are for this the best option. Very recently the causative agent of Mollaret's meningitis has proved to be, at least in part, HSV I or II. So far prospective randomized therapeutic trials are awaited for the treatment of Mollaret's meningitis using intravenous acyclovir or the more modern oral forms of virostatics (famciclovir, valaciclovir). For decades the causative agent of facial palsy (Bell's palsy) has been sought; only with the advent of PCR has this question been answered. Although one single study indicates the superiority of a combination of acyclovir plus prednisone, this finding has to be confirmed by a large scale prospective randomised double blind study. Nevertheless, if other causes for the clinical/neurological syndrome of peripheral facial palsy have been excluded, a combination therapy with acyclovir plus prednisone seems to be indicated in a patient with Bell's palsy. [ABSTRACT FROM AUTHOR]

The amino-acids tryptophan, phenylalanine and tyrosine seem to play an important role in the pathophysiology of depressive disorders. We measured daily brain extracellular levels of these amino-acids using cerebral microdialysis (CMD) and high performance liquid chromatography in 26 consecutive subarachnoid hemorrhage (SAH) patients and associated them with the presence of depressive disorders. Patients were grouped as follows: medical history of depression (prior to SAH), antidepressant intake 12 months after SAH (but not before), or neither. CMD-tryptophan, CMD-phenylalanine and CMD-tyrosine levels were significantly lower in patients with preexisting depressive disorders compared to those without depression (p < 0.01). Disease severity and SAH-related complications were not associated with amino-acid concentrations. We found a positive correlation between nutritionally administered and brain interstitial levels of tryptophan and phenylalanine in non-depressed patients (R = 0.26 and R = 0.24, p < 0.05), which was not present in patients with preexisting depression (p > 0.1). In conclusion, brain interstitial levels of tryptophan, phenylalanine and tyrosine measured in the context of the clinical management of SAH were significantly decreased in patients with a medical history of depression. This study supports the hypothesis that the availability of these neurotransmitter precursor amino-acids in the human brain may play an important role in the pathophysiology of depressive disorders. [ABSTRACT FROM AUTHOR]

A letter to the editor discussing a case of a 16-year-old girl diagnosed with encephalitis lethargica is presented.