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Initial healthcare delivery after warfront injury is unpredictably challenging for military forces. As preparatory training, healthcare providers use simulation to improve their performance in stressful critical situations. This study investigated whether a digital CA held by the team leader improved performance in simulated combat casualty care.This randomized controlled trial was performed during a combat casualty training course for military physicians and nurses in France. Each pair of care providers completed 2 scenarios randomized to be undertaken either with or without a digital CA. The primary end point was the technical performance evaluated from a video recording by 2 independent raters using a pre-established score grid (up to 100%) according to military protocols. The secondary end point was the nontechnical performance (TEAM scale, maximum: 54 points).Thirty-six pairs of participants were included. Use of the digital CA improved both technical (74% vs 53%, P0.001) and nontechnical (42 vs 32, P0.001) performance.The digital CA improved technical and nontechnical performance during training of medical care for military combat casualties. Use of a dedicated digital CA might improve care in a combat environment.This study is a randomized controlled trial.

Resume Le diagnostic d’encephalite est parfois difficile, alors que le delai de traitement notamment pour les origines infectieuses conditionne le pronostic. Tout signe de dysfonction neurologique associe a une fievre, sans explication, doit faire evoquer une infection neuro-meningee qui constitue une urgence therapeutique et diagnostique. L’absence de fievre oriente vers la recherche d’une cause extra neurologique a l’atteinte des fonctions cerebrales avant de debuter un traitement anti-infectieux. Le bilan de premiere ligne repose sur l’elimination de facteurs confondants, la mise en evidence d’une inflammation du systeme nerveux central (ponction lombaire), la recherche d’un agent pathogene, le bilan des lesions (IRM), et la recherche de complication, comme par exemple l’epilepsie. Les encephalites les plus frequemment rencontrees en reanimation ont une origine infectieuse (HSV, VZV, listeria ou tuberculose), ou dysimmunitaire postinfectieuse (acute disseminated encephalomyelitis). Les objectifs de la reanimation reposent sur l’adaptation du traitement etiologique, le monitorage et le traitement des crises d’epilepsie, d’une hydrocephalie ou d’une transformation hemorragique et la prise en charge des defaillances extra neurologiques (respiratoire et dysautonomie). Le traitement initial repose sur l’administration d’acyclovir et d’amoxicilline et sera reevalue en fonction des resultats de l’enquete etiologique. Lorsque les resultats du bilan de premiere ligne sont negatifs a 48 h, une deuxieme ponction lombaire sera realisee au moins 4 j apres le debut des symptomes afin d’eliminer formellement une encephalite a HSV ou VZV ; le bilan sera aussi complete en fonction du contexte a la recherche d’autres causes infectieuse ou dysimmunitaire (auto-immune, paraneoplasique ou postinfectieuse). Aucune cause n’est retrouvee dans un tiers des cas, mais la decouverte de nouveaux anticorps diriges contre le systeme nerveux central reduira sans doute ce nombre dans le futur.

Severe traumatic brain injury (TBI) is a multifactorial injury process involving respiratory, cardiovascular and immune functions in addition to the brain. Thus, live animal models are needed to study the molecular, cellular and systemic mechanisms of TBI. The ethical use of laboratory animals requires that the benefits of approaches be carefully weighed against potential harm to animals. Welfare assessments adapted to severe TBI research are lacking. Here, we introduce a scoresheet to describe and monitor potential distress in animals, which includes general welfare (body weight, general appearance and spontaneous behaviour) and TBI-specific indices (respiratory function, pain, locomotor impairment, wound healing). Implementation of this scoresheet in Sprague–Dawley rats subjected to severe lateral fluid percussion TBI revealed a period of suffering limited to four days, followed by a recovery to normal welfare scores within 10–15 days, with females showing a worse impact than males. The scores indicate that animal suffering in this model is transitory compared with TBI consequences in humans. The scoresheet allows for the implementation of refinement measures including (1) analgesia during the initial period following TBI and (2) humane endpoints set (30% weight loss, score ≥90 and/or respiratory problems). This animal scoresheet tailored to TBI research provides a basis for further refinement of animal research paradigms aimed at understanding or treating the sequelae of severe TBI.

Introduction High-fidelity simulation is widely used in the ongoing education of caregivers. However, the complex high-stakes simulated crisis environment affects memorization. This study investigated whether participants would remember more key training messages 3 months after a simulated complex emergency situation if they had used a digital cognitive aid (CA) during the simulations. Materials and Methods This randomized controlled trial was performed during a combat casualty training course for military physicians and nurses. Each pair of care providers completed two scenarios randomized to be undertaken either with or without a digital CA. At the end of each debriefing, instructors gave five scenario-specific key messages aloud. Three months later, learners were asked to recall the messages from their two scenarios and were scored for each scenario. The primary endpoint was the number of key messages recalled. The secondary endpoints were the influence on the results of the profession and the scenario block and age of the leader. Results Thirty-six pairs of participants were included. Due to operational constraints, only 34 completed the study. The use of the digital CA was associated with a positive effect on memorization at 3 months (F = 82.2, P Conclusions The digital CA allowed learners to remember twice as many key elements 3 months after simulated training of medical care for military combat casualties. A dedicated digital CA might be an asset for better care in a combat environment and for learning and memorizing critical care procedures following complex emergency situations.

Only a few clinical cases of cerebral arterial gas embolism during spinal surgery are published. It seems important not to overlook this diagnosis in order to initiate rapid appropriate treatment. This was a suspected case of paradoxical gas embolism revealed postoperatively by neurological deficits and whose recovery was noted during hyperbaric oxygen treatment. Unfortunately, no complementary examination showed gas embolism and only the context, the clinical picture and the case evolution evoke this diagnosis. The diagnostic difficulty in the immediate postoperative period is highlighted.

Resume L’ischemie cerebrale retardee (ICR) reste une complication frequente et dramatique de l’hemorragie meningee anevrismale, dont l’incidence, elevee avant le onzieme jour post-saignement, impose une surveillance continue. Le diagnostic clinique d’une anomalie de perfusion avec un deficit neurologique peut etre rendu difficile chez les patients qui ont des troubles de la conscience. La surveillance clinique seule est a risque de diagnostic trop tardif pour une prevention efficace de la lesion cerebrale definitive. Une approche multimodale pour un diagnostic precoce du risque d’ICR peut associer le Doppler transcrânien, de l’electrophysiologie, de l’oxymetrie ou du metabolisme cerebral, ou encore un biomarqueur plasmatique, qui devra etre confirme par une imagerie de perfusion. Cette difficulte diagnostique reflete la complexite des mecanismes a l’origine de l’ICR que les etudes experimentales ont bien mis en evidence. En accord avec cette complexite, differentes strategies de prevention therapeutique ont cible la spasticite vasculaire, l’inflammation, l’agregation plaquettaire, le metabolisme cerebral, ou l’elimination du sang dans les espaces sous-arachnoidiens. Les resultats inconstants des etudes cliniques ont confirme la complexite de la lesion d’ICR. La nimodipine reste le seul traitement preventif recommande avec un impact sur le devenir neurologique. Plus recemment, l’antagoniste du recepteur a l’endotheline semblait efficace sur la vasomotricite des arteres cerebrales sans amelioration du devenir neurologique. Les prochaines etudes cliniques devraient preciser l’interet des inhibiteurs des phosphodiesterases ou du drainage du liquide cephalorachidien. La encore, une approche multimodale des therapeutiques devrait permettre la prevention optimale de cette complication redoutable.

Objective To compare old patients hospitalized in ICU for respiratory distress due to COVID-19 with old patients hospitalized in ICU for a non-COVID-19-related reason in terms of autonomy and quality of life. Design Comparison of two prospective multi-centric studies. Setting This study was based on two prospective multi-centric studies, the Senior-COVID-Rea cohort (COVID-19-diagnosed ICU-admitted patients aged over 60) and the FRAGIREA cohort (ICU-admitted patients aged over 70). Patients We included herein the patients from both cohorts who had been evaluated at day 180 after admission (ADL score and quality of life). Interventions None. Measurements and main results A total of 93 COVID-19 patients and 185 control-ICU patients were included. Both groups were not balanced on age, body mass index, mechanical ventilation, length of ICU stay, and ADL and SAPS II scores. We modeled with ordered logistic regression the influence of COVID-19 on the quality of life and the ADL score. After adjustment on these factors, we observed COVID-19 patients were less likely to have a loss of usual activities (aOR [95% CI] 0.47 [0.23; 0.94]), a loss of mobility (aOR [95% CI] 0.30 [0.14; 0.63]), and a loss of ADL score (aOR [95% CI] 0.30 [0.14; 0.63]). On day 180, 52 (56%) COVID-19 patients presented signs of dyspnea, 37 (40%) still used analgesics, 17 (18%) used anxiolytics, and 14 (13%) used antidepressant. Conclusions COVID-19-related ICU stay was not associated with a lower quality of life or lower autonomy compared to non-COVID-19-related ICU stay.

International audience; INTRODUCTION: With the spread of COVID-19 epidemic, health plans must be adapted continuously. There is an urgent need to define the best care courses of patients with COVID-19, especially in intensive care units (ICUs), according to their individualised benefit/risk ratio. Since older age is associated with poorer short-term and long-term outcomes, prediction models are needed, that may assist clinicians in their ICU admission decision. Senior-COVID-Rea was designed to evaluate, in patients over 60 years old admitted in ICU for severe COVID-19 disease, the impact of age and geriatric and paraclinical parameters on their mortality 30 days after ICU admission. METHODS AND ANALYSIS: This is a multicentre survey protocol to be conducted in seven hospitals of the Auvergne-Rhône-Alpes region, France. All patients over 60 years old admitted in ICU for severe COVID-19 infection (or their legally acceptable representative) will be proposed to enter the study and to fill in a questionnaire regarding their functional and nutritional parameters 1 month before COVID-19 infection. Paraclinical parameters at ICU admission will be collected: lymphocytes and neutrophils counts, high-fluorescent lymphoid cells and immature granulocytes percentages (Sysmex data), D-dimers, C-reactive protein, lactate dehydrogenase (LDH), creatinine, CT scan for lung extension rate as well as clinical resuscitation scores, and the delay between the first signs of infection and ICU admission. The primary outcome will be the overall survival at day 30 post-ICU admission. The analysis of factors predicting mortality at day 30 will be carried out using univariate and multivariate logistic regressions. Multivariate logistic regression will consider up to 15 factors.The ambition of this trial, which takes into account the different approaches of geriatric vulnerability, is to define the respective abilities of different operational criteria of frailty to predict patients' outcomes. ETHICS AND DISSEMINATION: The study protocol was ethically approved. The results of the primary and secondary objectives will be published in peer-reviewed journals. TRIAL REGISTRATION NUMBER: NCT04422340.

In situ simulation sessions can be useful to test a new organization and detect latent safety threats. Here we report two cases of routine in situ interprofessional simulation sessions in an intensive care unit that unexpectedly revealed latent safety threats in our emergency trolley. These latent safety threats included drug mislabeling, secondary to a recent change in stored medications. Corrective actions have been put in place. In doing so, we highlight that simulation can increase the patient safety.

Early or primary injury due to brain aggression, such as mechanical trauma, hemorrhage or is-chemia, triggers the release of damage-associated molecular patterns (DAMPs) in the extracellular space. Some DAMPs, such as S100B, participate in the regulation of cell growth and survival but may also trigger cellular damage as their concentration increases in the extracellular space. When DAMPs bind to pattern-recognition receptors, such as the receptor of advanced glycation end-products (RAGE), they lead to non-infectious inflammation that will contribute to necrotic cell clearance but may also worsen brain injury. In this narrative review, we describe the role and ki-netics of DAMPs and RAGE at the acute phase of brain injury. We searched the MEDLINE database for “DAMPs” or “RAGE” or “S100B” and “traumatic brain injury” or “subarachnoid hemorrhage” or “stroke”. We selected original articles reporting data on acute brain injury pathophysiology, from which we describe DAMPs release and clearance upon acute brain injury, and the implication of RAGE in the development of brain injury. We will also discuss the clinical strategies that emerge from this overview in terms of biomarkers and therapeutic perspectives

The International Conference on Spreading Depolarizations (iCSD) held in Boca Raton, Florida, in the September of 2018 devoted a section to address the question, “What should a clinician do when spreading depolarizations are observed in a patient?” Discussants represented a wide range of expertise, including neurologists, neurointensivists, neuroradiologists, neurosurgeons, and pre-clinical neuroscientists, to provide both clinical and basic pathophysiology perspectives. A draft summary of viewpoints offered was then written by a multidisciplinary writing group of iCSD members, based on a transcript of the session. Feedback of all discussants was formally collated, reviewed, and incorporated into the final document which was subsequently approved by all authors.

Background: Current SARS-COV2 pandemic induces tensions on the health systems and ethical dilemmas. A triage tool is needed to define older patients with individual advantage to be considered for intensive care unit (ICU) transfer. Methods: This multicentre observational cohort study included patients over 60 admitted into 7 ICUs between 7th March and 7th May 2020. The primary objective was to evaluate age impact on 30-day mortality, to construct a multivariate prognostic model. This analysis explores the prediction value of geriatric parameters 1 month before ICU admission. This trial is registered with ClinicalTrials.gov, number NCT04422340. Findings: Among 290 screened patients, 231 were included in the cohort. In univariate analysis, factors associated with decreased day-30 survival were: age>75 (OR 4·82 [95%CI: 2·56-9·06]), three or more CIRS-G grade ≥2 comorbidities (OR 2·49 [95%CI: 1·36-4·56]), impaired ADL (Activities of Daily Living), (OR 4·86 [95%CI: 2·44-9·72]), impaired IADL8 (Instrumental ADL, 8 variables, OR 6·33 [95%CI: 3·31-12·10], p 75 (OR 4·64 [95%CI: 2·36-9·39], p

Background High-fidelity simulation is known to improve participant learning and behavioral performance. Simulation scenarios generate stress that affects memory retention and may impact future performance. The authors hypothesized that more participants would recall three or more critical key messages at three months when a relaxation break was performed before debriefing of critical event scenarios. Methods Each resident actively participated in one scenario and observed another. Residents were randomized in two parallel-arms. The intervention was a 5-min standardized relaxation break immediately before debriefing; controls had no break before debriefing. Five scenario-specific messages were read aloud by instructors during debriefings. Residents were asked by telephone three months later to recall the five messages from their two scenarios, and were scored for each scenario by blinded investigators. The primary endpoint was the number of residents participating actively who recalled three or more messages. Secondary endpoints included: number of residents observing who recalled three or more messages, anxiety level, and debriefing quality. Results In total, 149 residents were randomized and included. There were 52 of 73 (71%) residents participating actively who recalled three or more messages at three months in the intervention group versus 35 of 76 (46%) among controls (difference: 25% [95% CI, 10 to 40%], P = 0.004). No significant difference was found between groups for observers, anxiety or debriefing quality. Conclusions There was an additional 25% of active participants who recalled the critical messages at three months when a relaxation break was performed before debriefing of scenarios. Benefits of relaxation to enhance learning should be considered for medical education.

Background Cognitive aids improve the technical performance of individuals and teams dealing with high-stakes crises. Hand-held electronic cognitive aids have rarely been investigated. A randomized controlled trial was conducted to investigate the effects of a smartphone application, named MAX (for Medical Assistance eXpert), on the technical and non-technical performance of anaesthesia residents dealing with simulated crises. Methods This single-centre randomized, controlled, unblinded trial was conducted in the simulation centre at Lyon, France. Participants were anaesthesia residents with >1 yr of clinical experience. Each participant had to deal with two different simulated crises with and without the help of a digital cognitive aid. The primary outcome was technical performance, evaluated as adherence to guidelines. Two independent observers remotely assessed performance on video recordings. Results Fifty-two residents were included between July 2015 and February 2016. Six participants were excluded for technical issues; 46 participants were confronted with a total of 92 high-fidelity simulation scenarios (46 with MAX and 46 without). Mean ( sd ) age was 27 (1.8) yr and clinical experience 3.2 (1.0) yr. Inter-rater agreement was 0.89 (95% confidence interval 0.85–0.92). Mean technical scores were higher when residents used MAX [82 (11.9) vs 59 (10.8)%; P Conclusion The use of a hand-held cognitive aid was associated with better technical performance of residents dealing with simulated crises. These findings could help digital cognitive aids to find their way into daily medical practice and improve the quality of health care when dealing with high-stakes crises. Clinical trial registration NCT02678819.

Traumatic brain injury causes widespread neurological lesions that can be reproduced in animals with the lateral fluid percussion (LFP) model. The characterization of the pattern of neuronal death generated in this model remains unclear, involving both cortical and subcortical brain regions. Here, 7 days after moderate (3 atmospheres absolute [ATA]) or severe (3.8 ATA) LFP, we estimated neuronal loss by using immunohistochemistry together with a computer-assisted automated method for quantifying neuronal density in brain sections. Neuronal counts were performed ipsilateral to the impact, in the parietal cortex ventral to the site of percussion, in the temporal cortex, in the dorsal thalamus, and in the hippocampus. These results were compared with the counts observed at similar areas in sham animals. We found that neuronal density was severely decreased in the temporal cortex (-60%), in the dorsal thalamus (-63%), and in area CA3 of the hippocampus (-36%) of injured animals compared with controls but was not significantly modified in the cortices located immediately ventral to the impact. Total cellular density increased in brain structures displaying neuronal death, suggesting the presence of gliosis. The increase in the severity of LFP did not change the pattern of neuronal injury. This automated method simplified the study of neuronal loss following traumatic brain injury and allowed the identification of a pattern of neuronal loss that spreads from the dorsal thalamus to the temporal cortex, with the most severe lesions being in brain structures remote from the site of impact.

International audience; Monitoring the chemical composition of the brain interstitial fluid is an important challenge for both pre-clinical and clinical research on brain injury. Microelectrode biosensors are a promising technique with a temporal resolution in the order of seconds. Here, ultra-microelectrodes based on platinized carbon fibers were fabricated to obtain biosensors with less than 15 µm external diameter. Platinization was achieved by sputtering a 10 nm Cr adhesion layer followed by 100 nm of platinum. Platinized carbon fibers were then encased in a glass micropipette and covered with electropolymerized poly-phenylenediamine for selectivity, and covalently immobilized oxidase enzymes (glucose oxidase, lactate oxidase, D-amino acid oxidase or glutamate oxidase). After implantation in the rat parietal cortex, such biosensors detected a smaller basal lactate concentration and a slower diffusion of glucose and D-serine through the blood brain barrier compared to more conventional biosensors with 100 µm external diameter. Interestingly, spreading depolarization (SD) produced a smaller increase in lactate, a larger decrease in glucose, and a larger increase in D-serine at platinized carbon fibers microelectrode biosensors compared to larger sensors. Therefore, the neurochemical signature of SDs was significantly different when estimated with these new minimally invasive biosensors. Such small devices avoid major mechanical injury to blood vessels, preserve the blood brain barrier at the site of implantation, and therefore, provide more accurate measurements from the brain interstitial fluid. Developing smaller, less invasive probes for brain monitoring is therefore an important challenge in order to obtain meaningful information about the cellular mechanisms at work during brain injury.

Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.

Spreading depolarizations are waves of near-complete breakdown of neuronal transmembrane ion gradients, free energy starving, and mass depolarization. Spreading depolarizations in electrically inactive tissue are associated with poor outcome in patients with traumatic brain injury. Here, we studied changes in regional cerebral blood flow and brain oxygen (PbtO2), glucose ([Glc]b), and lactate ([Lac]b) concentrations in rats, using minimally invasive real-time sensors. Rats underwent either spreading depolarizations chemically triggered by KCl in naïve cortex in absence of traumatic brain injury or spontaneous spreading depolarizations in the traumatic penumbra after traumatic brain injury, or a cluster of spreading depolarizations triggered chemically by KCl in a remote window from which spreading depolarizations invaded penumbral tissue. Spreading depolarizations in noninjured cortex induced a hypermetabolic response characterized by a decline in [Glc]b and monophasic increases in regional cerebral blood flow, PbtO2, and [Lac]b, indicating transient hyperglycolysis. Following traumatic brain injury, spontaneous spreading depolarizations occurred, causing further decline in [Glc]b and reducing the increase in regional cerebral blood flow and biphasic responses of PbtO2 and [Lac]b, followed by prolonged decline. Recovery of PbtO2 and [Lac]b was significantly delayed in traumatized animals. Prespreading depolarization [Glc]b levels determined the metabolic response to clusters. The results suggest a compromised hypermetabolic response to spreading depolarizations and slower return to physiological conditions following traumatic brain injury-induced spreading depolarizations.

Introduction Les depolarisations corticales envahissantes (DCE) sont des processus pathologiques se propageant sur le cortex. Leur survenue apres un traumatisme crânien grave (TCG) est associee a un mauvais pronostique [1] surtout lorsque celle-ci surviennent en groupe (cluster). Cependant, leur pathogenicite et leurs consequences sur le metabolisme cerebral ne sont pas bien etablie [2] . Cette etude a pour objectif de definir les modifications metaboliques secondaires aux DCE sur un tissu sain ou apres un TCG chez le rat. Materiel et methodes Le TCG experimental a ete realise selon le modele de percussion laterale de fluide (LFPI, 3,8 ATA) chez des rat Wistar adultes sous anesthesie (isoflurane dans 30 % d’oxygene) et ventilation mecanique. Des DCE etaient induites soit spontanement apres un LFPI severe (DCE isolee, n = 6), soit repetees (toutes les 3 a 5 min) par apposition de KCl apres un LFPI (DCE cluster, n = 6), soit par apposition de KCl sur un tissu sain (temoins, n = 6). Les DCE etaient enregistrees a l’aide d’electrodes d’argents dans une micropipette de verre (3–5 μm). Les concentrations cerebrales de glucose et de lactate etaient mesurees a l’aide de biocapteurs enzymatiques (40 μm), et la concentration d’oxygene (tpO 2 ) par une electrode de clarck (10 μm). Ces technologies peu invasives offrent une resolution temporelle d’une seconde. Des enregistrements laser-Doppler (LDF) ont ete menes de maniere concomitante. Les capteurs ont ete places dans la region du cortex parietal montrant le maximum de pertes neuronales apres LFPI. Resultats Les concentrations cerebrales basales de glucose et de lactates n’etaient pas differentes dans la situation controle et apres LFPI, de meme que la glycemie la lactatemie et la tPO 2 . Dans le groupe temoin une DCE entrainait une chute du glucose cerebrale de 0,7 ± 0,45 mM avec un retour aux concentrations basales en 30 minutes. Cette diminution du glucose etait associee a une liberation de 0,52 ± 0,58 mM de lactate ( Fig. 1 A) ainsi qu’a une augmentation de la tPO 2 et du LDF. Dans le groupe DCE isolee une chute similaire du glucose de 1,45 ± 0,87 mM ( p = 0,068) etait au contraire associee a une diminution du lactate de 0,39 ± 0,55 mM ( p = 0,004), une variation bi-phasique du LDF et de la tPO 2 . Enfin dans le groupe DCE cluster il existait une chute prolongee du glucose cerebrale et de la tPO 2 associee a une alternance de liberation et de consommation de lactate ( Fig. 1 B). Discussion Les DCEs induisent des modifications metaboliques differentes en fonction de l’etat du cortex sous-jacent (controle ou LFPI). Ainsi le couplage neurovasculaire et le metabolisme cerebral etaient alteres apres LPFI, en particulier en cas de cluster de DCE ou les concentrations de glucose et d’oxygene etaient profondement abaissees. Ces observations sont comparables a celles de crises metaboliques avec effondrements des concentrations de glucoses observees chez l’homme a l’aide de catheter de microdialyse cerebrale [3] , placant les clusters de DCE comme un substrat physiopathologique potentiel de la mauvaise evolution des TCG.

La detection precoce d’une souffrance cerebrale est un element cle de la prise en charge des patients victimes d’une hemorragie sous arachnoidienne (HSA). Certains parametres d’analyse quantifiee de l’electroencephalogramme (EEG), tel que le ratio des puissances alpha/delta (A/D), sont modifies lors de la survenue d’une nouvelle ischemie [1] , [2] , [3] . Cependant, ces variations sont peu specifiques [2] , [3] , ce qui limite leur utilisation en pratique pour guider la prise en charge. Notre objectif a ete de caracteriser les modifications de l’A/D associees ou non a une ischemie cerebrale retardee (ICR). Le monitoring EEG a ete realise avec une frequence d’echantillonnage de 256 Hz et des filtres passe haut et bas a 0,5 et 60 Hz, respectivement. Une bande « alpha » elargie etait definie entre 6 et 12 Hz car la frequence de base des patients etait de 5,5 ± 1,7 Hz, et la bande delta entre 1 et 4 Hz. L’index A/D a ete calcule sur des derivations bipolaires correspondant aux territoires vasculaires anterieurs (Fp1/2–F3/4), moyens (C3/4–T3/4) et posterieurs (P3/4–O1/2). Le deficit ischemique a ete defini retrospectivement sur les controles scannographiques. Dix HSA, âges de 48,5 ± 5,6 ans ont ete monitores pendant 4,5 ± 3,9 jours, a partir de 3,2 ± 3,2 jours apres l’accident initial. Nous avons observe trois patterns d’evolution differents de l’A/D : une diminution transitoire inferieure a 2 h, aucune diminution ou une augmentation progressive, et une diminution prolongee superieure a 2 h. Tous les patients (n = 4) avec diminution prolongee de l’A/D ont presente une ICR. Chez un patient la diminution de l’A/D etait asymetrique, limitee au territoire de l’ICR, sans modification de la pression intracrânienne ou la PtiO2. Ces parametres ont ete modifies de facon retardee dans deux autres cas. Les patients n’ayant pas presente de diminution prolongee de l’A/D n’ont pas eu d’ICR (n = 5). Parmi les 3 profils de variation de l’A/D, une diminution prolongee pourrait etre un argument precoce en faveur d’une ICR.