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A medical error is a preventable adverse effect of medical care. Errors can happen in the hospital at the doctor’s office, at the pharmacy, laboratory and ward. These can also occur at home by the patient or the attendant. These errors may lead to death or major/minor injuries or can also be harmless. However these should be recorded, analysed and remedial measures implemented to reduce the risk of being committed in the future. We are reporting the medical care of our patient in persistent vegetative state over nineteen years due to medical error at our hospital resulting in brain anoxia. The key issues faced during the care were recurrent respiratory and urinary tract infections and in last one year kidney calculi leading to chronic kidney disease and its complications. There are no contractures or thrombo-embolic events and above all no bed sore over this period.

Supplemental Digital Content is available in the text., Objectives: Recovery from coma might critically depend on the structural and functional integrity of frontoparietal networks. We aimed to measure this integrity in traumatic brain injury and anoxo-ischemic (cardiac arrest) coma patients by using an original multimodal MRI protocol. Design: Prospective cohort study. Setting: Three Intensive Critical Care Units affiliated to the University in Toulouse (France). Patients: We longitudinally recruited 43 coma patients (Glasgow Coma Scale at the admission < 8; 29 cardiac arrest and 14 traumatic brain injury) and 34 age-matched healthy volunteers. Exclusion criteria were disorders of consciousness lasting more than 30 days and focal brain damage within the explored brain regions. Patient assessments were conducted at least 2 days (5 ± 2 d) after complete withdrawal of sedation. All patients were followed up (Coma Recovery Scale-Revised) 3 months after acute brain injury. Interventions: None. Measurements and Main Results: Functional and structural MRI data were recorded, and the analysis was targeted on the posteromedial cortex, the medial prefrontal cortex, and the cingulum. Univariate analyses and machine learning techniques were used to assess diagnostic and predictive values. Coma patients displayed significantly lower medial prefrontal cortex–posteromedial cortex functional connectivity (area under the curve, 0.94; 95% CI, 0.93–0.95). Cardiac arrest patients showed specific structural disturbances within posteromedial cortex. Significant cingulum architectural disturbances were observed in traumatic brain injury patients. The machine learning medial prefrontal cortex–posteromedial cortex multimodal classifier had a significant predictive value (area under the curve, 0.96; 95% CI, 0.95–0.97), best combination of subregions that discriminates a binary outcome based on Coma Recovery Scale-Revised). Conclusions: This exploratory study suggests that frontoparietal functional disconnections are specifically observed in coma and their structural counterpart provides information about brain injury mechanisms. Multimodal MRI biomarkers of frontoparietal disconnection predict 3-month outcome in our sample. These findings suggest that fronto-parietal disconnection might be particularly relevant for coma outcome prediction and could inspire innovative precision medicine approaches.

International audience; We developed a new rodent model of reversible brain anoxia and performed continuous electrocorticographic (ECoG) and intracellular recordings of neocortical neurons to identify in real-time the cellular and network dynamics that successively emerge throughout the dying-to-recovery process. Along with a global decrease in ECoG amplitude, deprivation of oxygen supply resulted in an early surge of beta-gamma activities, accompanied by rhythmic membrane depolarizations and regular firing in pyramidal neurons. ECoG and intracellular signals were then dominated by low-frequency activities which progressively declined towards isoelectric levels. Cortical neurons during the isoelectric state underwent a massive membrane potential depolarizing shift, captured in the ECoG as a large amplitude triphasic wave known as the "wave-of-death" (WoD). This neuronal anoxic depolarization, associated with a block of action potentials and a loss of cell integrative properties, could however be reversed if brain re-oxygenation was rapidly restored (within 2-3.5 min). The subsequent slow repolarization of neocortical neurons resulted in a second identifiable ECoG wave we termed "wave-of-resuscitation" since it inaugurated the progressive regaining of pre-anoxic synaptic and firing activities. These results demonstrate that the WoD is not a biomarker of an irremediable death and unveil the cellular correlates of a novel ECoG wave that may be predictive of a successful recovery. The identification of real-time biomarkers of onset and termination of cell anoxic insult could benefit research on interventional strategies to optimize resuscitation procedures.

Purpose: evaluation of the clinical significance of parametric monitoring of the effectiveness of intensive care and rehabilitation based on the analysis of the functional state of the autonomous nervous system in patients with brain damage of different genesis.Materials and methods. The study included 66 patients on day 20—50 after the traumatic brain injury; anoxic damage; and stroke consequences. The isolation of clinical groups and subsequent analysis of clinical status is based on the analysis of the functional state of the autonomic nervous system based on the dynamics of the heart rate variability (HRV) parameters. Findings obtained in studies of 500 patients in the postoperative period with a 5-minute HRV were tested as normal and abnormal ANS parameters [1]. Parasympathetic hyperactivity was measured within the limits for SDNN (standard deviation of all normal-to-normal R-R intervals) > 41.5 ms; for rMSSD (root-meansquare of the successive normal sinus R-R interval difference) > 42.4 ms; for pNN50% (the percentage of interval differences in successive NN intervals greater than 50 ms (NN50) / total number of NN intervals) > 8.1%; for SI (Baevsky stress index, in normalized units) < 80 n. u.; for TP (total power of variance of all NN intervals) > 2000 ms2. Sympathetic hyperactivity was determined within the limits for following parameters: SDNN, < 4.54 ms; rMSSD, < 2.25 ms; pNN50%, < 0.109%; SI, > 900 n. u.; TP < 200 ms2. Normal HRV parameters were selected within the limits of the values for: SDNN [13.31-41.4ms]; rMSSD [5.78—42.3 ms]; pNN50% [0.110—8.1%]; SI [80—900 nu]; for TP [200—2000 ms2]. To verify the parasympathetic or sympathetic hyperactivity within these limits, 3 of 5 parameters were chosen [1].Results. Based on the dynamics of the HRV parameters before the intensive care and on days 30—60 of the intensive therapy and rehabilitation of patients with traumatic and non-traumatic brain injuries, 5 main clinical groups of patients were identified. Group 1 (n=27) consisted of patients with normal parameters of the ANS functional activity (both at the time of admission to the hospital and on the 30—60th day of the intensive therapy and rehabilitation). Group 2 (n=9) included patients with the baseline sympathetic hyperactivity of the ANS at admission to the intensive care unit and normal functional activity of the ANS on the 30—60th day of the intensive care and rehabilitation. Group 3 (n=8) included patients with baseline normal functional state of the ANS and the signs of sympathetic hyperactivity of the ANS on the 30—60th day of the intensive care and rehabilitation. Group 4 (n=15) consisted of patients with signs of sympathetic hyperactivity of the ANS both initially and on the 30—60th day of the intensive care and rehabilitation. Group 5 (n=7) included patients with signs of parasympathetic hyperactivity of the ANS (according to the parameters of HRV) both at baseline, at admission to the intensive care unit, and on the 30—60th day of the intensive care and rehabilitation.Conclusion: The normalization of HRV parameters is accompanied by patients’ recovery from the vegetative state and coma to minimal consciousness or normal consciousness; the index of disability rate decreases, the social reintegration grows, according to the DRS scale (M. Rappaport, 1982); dependence on mechanical ventilation reduces, and the muscle tone normalizes.

We studied slow (≤2.5Hz) non-evolving generalized periodic epileptiform discharges (GPED) in the EEG of comatose patients after cardiac arrest (CA) in search of evidence that could assist early diagnosis of possible hypoxic non-convulsive status epilepticus (NCSE) and its differentiation from terminal brain anoxia (BA) that can present with similar EEG pattern. We investigated the topography of the GPED in the first post-CA EEGs of 13 patients, using voltage-mapping and compared findings between 2 patients with NCSE and GPED >2.5Hz (group 1), and 11 with GPED ≤2Hz, of whom 6 had possible NCSE (group 2) and 5 terminal BA (group 3). Voltage mapping showed frontal maximum for the negative phase of the GPED in all patients of groups 1 and 2, but not in any of the patients of group 3, who invariably showed posterior maximum of the negative phase. Morphology, amplitude and duration of the GPED varied across the groups without distinctive features for possible NCSE. These findings provide evidence that, in hypoxic coma after CA with slow GPED, anterior topography of the maximum GPED negativity on voltage mapping may be a distinctive biomarker for possible NCSE contributing to the coma. This article is protected by copyright. All rights reserved.

Background We recently showed that electroencephalography (EEG) patterns within the first 24 hours robustly contribute to multimodal prediction of poor or good neurological outcome of comatose patients after cardiac arrest. Here, we confirm these results and present a cost-minimization analysis. Early prognosis contributes to communication between doctors and family, and may prevent inappropriate treatment. Methods A prospective cohort study including 430 subsequent comatose patients after cardiac arrest was conducted at intensive care units of two teaching hospitals. Continuous EEG was started within 12 hours after cardiac arrest and continued up to 3 days. EEG patterns were visually classified as unfavorable (isoelectric, low-voltage, or burst suppression with identical bursts) or favorable (continuous patterns) at 12 and 24 hours after cardiac arrest. Outcome at 6 months was classified as good (cerebral performance category (CPC) 1 or 2) or poor (CPC 3, 4, or 5). Predictive values of EEG measures and cost-consequences from a hospital perspective were investigated, assuming EEG-based decision- making about withdrawal of life-sustaining treatment in the case of a poor predicted outcome. Results Poor outcome occurred in 197 patients (51% of those included in the analyses). Unfavorable EEG patterns at 24 hours predicted a poor outcome with specificity of 100% (95% CI 98–100%) and sensitivity of 29% (95% CI 22–36%). Favorable patterns at 12 hours predicted good outcome with specificity of 88% (95% CI 81–93%) and sensitivity of 51% (95% CI 42–60%). Treatment withdrawal based on an unfavorable EEG pattern at 24 hours resulted in a reduced mean ICU length of stay without increased mortality in the long term. This gave small cost reductions, depending on the timing of withdrawal. Conclusions Early EEG contributes to reliable prediction of good or poor outcome of postanoxic coma and may lead to reduced length of ICU stay. In turn, this may bring small cost reductions.

EEG and serum neuron-specific enolase (NSE) are used for outcome prognostication in patients with postanoxic coma; however, it is unclear if EEG abnormalities reflect transient neuronal dysfunction or neuronal death. To assess this question, EEG abnormalities were correlated with NSE. Moreover, NSE cutoff values and hypothermic EEG features related with poor outcome were explored.In a prospective cohort of 61 adults treated with therapeutic hypothermia (TH) after cardiac arrest (CA), multichannel EEG recorded during TH was assessed for background reactivity and continuity, presence of epileptiform transients, and correlated with serum NSE collected at 24-48 hours after CA. Demographic, clinical, and functional outcome data (at 3 months) were collected and integrated in the analyses.In-hospital mortality was 41%, and 82% of survivors had good neurologic outcome at 3 months. Serum NSE and EEG findings were strongly correlated (Spearman rho = 0.45; p0.001). Median NSE peak values were higher in patients with unreactive EEG background (p0.001) and discontinuous patterns (p = 0.001). While all subjects with nonreactive EEG died, 5 survivors (3 with good outcome) had NSE levels33 μg/L.The correlation between EEG during TH and serum NSE levels supports the hypothesis that early EEG alterations reflect permanent neuronal damage. Furthermore, this study confirms that absent EEG background reactivity and presence of epileptiform transients are robust predictors of poor outcome after CA, and that survival with good neurologic recovery is possible despite serum NSE levels33 μg/L. This underscores the importance of multimodal assessments in this setting.

Numerous strategies exist for preoperative cardiac testing before patients undergo vascular operations. Potential adverse effects of evaluation and cardiac intervention should be considered before undertaking screening studies. We recently analyzed the adverse outcomes of preoperative cardiac evaluation and intervention before vascular operations in patients treated at the Denver Department of Veterans Affairs Medical Center. During the 12 month study period, 161 patients were scheduled to undergo major vascular operations; 153 patients came to operation. The decision to pursue a cardiac evaluation was made without a defined protocol. Forty two men. aged 68±9 years underwent comprehensive preoperative cardiac evaluations Sixteen (38%) patients had untoward events related to cardiac evaluation, Including eight patients (19%) who refused vascular surgery after cardiac screening and/or intervention. Other complications included prosthetic graft infection, pseudoaneurysms (2), sternal wound infections (2) amputations (2), renal failure and brain anoxia. Extensive cardiac evaluation prior to vascular operations can result in morbidity, delays, and refusal to undergo vascular surgery. The underlying indication for vascular operations and the local iatrogenic cardiac complication rates must be considered before ordering special studies.

Clinical signs, laboratory tests, EEG or evoked potentials only permit an indirect estimation of the extent of structural brain damage following severe global brain anoxia. Positron emission tomography (PET) permits additional insights into the extent of neuronal damage in acute and persistent postanoxic vegetative states (VS). PET documents a severe and irreversible damage of supratentorial cortical structures in postanoxic VS and allows its differential diagnosis from related disorders, e.g. the locked-in-syndrome. PET clearly distinguishes functional alterations in VS from those in non-REM sleep and documents that patients in VS are not in a sleep-like condition, but in a state closely related to deep anesthesia. Furthermore, the extent of impairment of the residual cortical glucose consumption yields information concerning the possible recovery of consciousness and neuronal function in VS. In combination with clinical, laboratory and neurophysiological findings, PET may be helpful to establish the individual prognosis in acute VS.

Lactic acid is one of metabolisms from the glycolysis. Brain anoxia and ischemia will cause accumulation of lactate. Noninvasive detection of lactate using MR spectroscopy has played an important role in diagnosis and treatments of diseases. But lactate is usually difficult to be detected in most of cases. The purpose of present study was to obtain optimal detection and quantitative analysis of lactate by changing a series of parameters used in the sequences. The experiment was carried out in a glass model containing lactate and 12 patients with brain diseases. The MR scanner is a 1.5T system (Signa MR/i, GE). The spectra were obtained by using both PRESS and STEAM sequences. The spectra were processed using a GE software. The curves of lactate peaks versus TE obtained by the model exhibited waveform characteristic. The up doublets were recorded with their maximum peak heights using TE values of 26 ms and 270 ms, whereas the down doublets were recorded at their peaks using a TE value between 135 to 160 ms. All the peaks recorded by STEAM sequence were weaker than those by PRESS sequence. The results indicate that the optimized sequences are useful for better detection of lactate in clinical examinations.

Editors' Note: In reference to “Anti-JC virus antibodies in a large German natalizumab-treated MS cohort” by Trampe et al., Mr. Zahednasab discusses why testing for anti-JC virus antibodies in urine may be more effective than serum sampling. He also comments that patients taking IFN-β should have been excluded as it can falsely decrease those patients' JCV titers. The authors uphold …

This essay presents a case of a study of a young veterinary student (FR), that suffered a cardio-respiratory arrest resulted in brain anoxia. The study aims to understand, in consonance with the Lurian neuropsychology and with the Discursive Neurolinguistics, the effects caused by the neurological lesion and to contribute to the clinical practice with brain-damaged subjects, principally in the Speech Therapy. KEYWORDS: Attention. Memory. Neurolinguistics. Speech pathology., Este trabalho apresenta o estudo de caso de um jovem FR que sofreu uma parada cárdio-respiratória ocasionando anóxia cerebral. O estudo visa a compreender, de acordo com a Neuropsicologia luriana e com a Neurolingüística Discursiva, os efeitos causados pela lesão neurológica e a contribuir para a prática clínica com sujeitos cérebro-lesados, sobretudo na Fonoaudiologia.PALAVRAS-CHAVE: Atenção. Memória. Neurolingüística. Fonoaudiologia.ABSTRACTThis essay presents a case of a study of a young veterinary student (FR), that suffered a cardio-respiratory arrest resulted in brain anoxia. The study aims to understand, in consonance with the Lurian neuropsychology and with the Discursive Neurolinguistics, the effects caused by the neurological lesion and to contribute to the clinical practice with brain-damaged subjects, principally in the Speech Therapy. KEYWORDS: Attention. Memory. Neurolinguistics. Speech pathology.

The association of truncal ataxia with a number of different factors has been studied in a group of 95 epileptic outpatients on chronic anticonvulsant treatment. The 28 patients showing truncal ataxia had been epileptic for a longer period of time, received a significantly larger number of drugs, and had higher serum levels of phenobarbital than the non-ataxic group. Serum folate levels were significantly lower in the ataxic group. A role is postulated for anticonvulsant-induced folate deficiency in the appearance of truncal ataxia presenting after prolonged anti-convulsant therapy, either by increasing the serum levels of the anticonvulsants or through other, unknown mechanisms. The presence of tonic-clonic seizures, presumably associated with brain anoxia, was not associated with the appearance of truncal ataxia.

A hypothesis was made that hyperactivity as stated by others was not a direct result of brain anoxia produced in pre and post-natal factors, but that they share a common genetic cause. A comparison between four Mz. and six Dz. sets of twins were made. It was found that all Mz. pairs were male and concordant to hyperactivity. In the Dz. group all pairs were discordant except one male-male combination. Also in the Dz. group hyperactivity was always present in the male partners but for one discordant pair where the syndrome was present in the female. The importance of genetics as a causative factor was not obviously due to the small amount of hyperactive females studied in this project.

The selection and classification by airborne electroencephalography of pilots in high performance aircrafts were carried out. Film-strips of the pilots' reaction were made at the time of a stressful turn and five minutes later, during bombruns at a target range. EEG, ECG and flight patterns recordings were made from take-off to landing; movies, for technical reasons, only for brief periods. The pilots rated as A, with only minimal changes in the airborne EEG test, appeared unaffected on the movie. The B-group has short episodes of high voltage delta-theta-activity in the EEG. The movie revealed an eight seconds convulsion. The pilots in the C category showed major EEG abnormalities. The movie revealed them unconscious for thirty seconds. During the study more than 100 subjects were tested. The study underlines the value of airborne EEG testing as an objective method to evaluate the pilots' ability to act and react when subjected to flight stress and fatigue in the high performance aircrafts and space vehicles. An unknown number of pilots have convulsions during 'black-outs' and brain anoxia, as a secondary response in spite of good 02 supply.