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Following publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pubmed. Below the collaborators names full list: The TBI collaborative group: Long K (Intensive Care Unit, Royal Melbourne Hospital, Parkville, Victoria, Australia), Rodrigues A (Department of Anesthesia and Surgical Intensive Care, CHU de Bicetre, Le Kremlin Bicêtre, France), Lozano A (Department of Intensive Care, Erasme Hospital, Université Libre de Bruxelles, Brussels, Belgium), Saxby E (Intensive Care Unit, The Alfred Hospital, Melbourne, Victoria, Australia), Vargiolu A (School of Medicine and Surgery, University Milano Bicocca-Neurointensive Care, San Gerardo Hospital, ASSTMonza, Monza, Italy), Quintard H (Université Côte d’Azur, Centre hospitalier Universitaire de Nice, Service de Réanimation polyvalente, Hôpital Pasteur 2. Nice, France), Robba C (Department of Anesthesiology and Surgical-Trauma Intensive Care, Hospital Clinic Universitari de Valencia, University of Valencia, Valencia, Spain), Sisson A (Adult Critical Care Unit, The Royal London Hospital, Barts Health NHS Trust, London, UK), Allen G (Neurosciences and Trauma Critical Care Unit, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK), Baro N (Department of Neurosurgery, Charité Universitätsmedizin Berlin), Kofler M (Neurological Intensive Care Unit, Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria).

There has been much debate concerning whether startling sensory stimuli can activate a fast-neural pathway for movement triggering (StartReact) which is different from that of voluntary movements. Activity in sternocleidomastoid (SCM) electromyogram is suggested to indicate activation of this pathway. We evaluated whether SCM activity can accurately identify trials which may differ in their neurophysiological triggering and assessed the use of cumulative distribution functions (CDFs) of reaction time (RT) data to identify trials with the shortest RTs for analysis. Using recent data sets from the StartReact literature, we examined the relationship between RT and SCM activity. We categorised data into short/longer RT bins using CDFs and used linear mixed-effects models to compare potential conclusions that can be drawn when categorising data on the basis of RT versus on the basis of SCM activity. The capacity of SCM to predict RT is task-specific, making it an unreliable indicator of distinct neurophysiological mechanisms. Classification of trials using CDFs is capable of capturing potential task- or muscle-related differences in triggering whilst avoiding the pitfalls of the traditional SCM activity-based classification method. We conclude that SCM activity is not always evident on trials that show the early triggering of movements seen in the StartReact phenomenon. We further propose that a more comprehensive analysis of data may be achieved through the inclusion of CDF analyses. These findings have implications for future research investigating movement triggering as well as for potential therapeutic applications of StartReact.

Background: In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP). Aim: In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients. Methods: We obtained data from 14 neurotrauma ICUs in Europe, Australia and UK for severe TBI patients (GCS≤8) requiring ICP monitoring. We identifed patients who received any desmopressin and recorded daily dose, 6-hourly serum sodium, and 6-hourly ICP. Results: We studied 262 severe TBI patients. Of these, 39 patients (14.9%) received desmopre

Following publication of the original article [1], we were notified that the collaborators’ names part of the “The TBI Collaborative” group has not been indexed in Pubmed. Below the collaborators names full list: The TBI collaborative group: Long K (Intensive Care Unit, Royal Melbourne Hospital, Parkville, Victoria, Australia), Rodrigues A

Following publication of the original article [1], we were notified that the collaborators' names part of the "The TBI Collaborative" group has not been indexed in Pubmed. Below the collaborators names full list.

BACKGROUND: In traumatic brain injury (TBI) patients desmopressin administration may induce rapid decreases in serum sodium and increase intracranial pressure (ICP). AIM: In an international multi-centre study, we aimed to report changes in serum sodium and ICP after desmopressin administration in TBI patients. METHODS: We obtained data from 14 neurotrauma ICUs in Europe, Australia and UK for severe TBI patients (GCS ≤ 8) requiring ICP monitoring. We identified patients who received any desmopressin and recorded daily dose, 6-hourly serum sodium, and 6-hourly ICP. RESULTS: We studied 262 severe TBI patients. Of these, 39 patients (14.9%) received desmopressin. Median length of treatment with desmopressin was 1 [1-3] day and daily intravenous dose varied between centres from 0.125 to 10 mcg. The median hourly rate of decrease in serum sodium was low (- 0.1 [- 0.2 to 0.0] mmol/L/h) with a median period of decrease of 36 h. The proportion of 6-h periods in which the rate of natremia correction exceeded 0.5 mmol/L/h or 1 mmol/L/h was low, at 8% and 3%, respectively, and ICPs remained stable. After adjusting for IMPACT score and injury severity score, desmopressin administration was independently associated with increased 60-day mortality [HR of 1.83 (1.05-3.24) (p = 0.03)]. CONCLUSIONS: In severe TBI, desmopressin administration, potentially representing instances of diabetes insipidus is common and is independently associated with increased mortality. Desmopressin doses vary markedly among ICUs; however, the associated decrease in natremia rarely exceeds recommended rates and median ICP values remain unchanged. These findings support the notion that desmopressin therapy is safe.