Obesity risk is associated with altered cerebral glucose metabolism and decreased µ-opioid and CB1 receptor availability.

BACKGROUND: Obesity is a pressing public health concern worldwide. Novel pharmacological means are urgently needed to combat the increase of obesity and accompanying type 2 diabetes (T2D). Although fully established obesity is associated with neuromolecular alterations and insulin resistance in the brain, potential obesity-promoting mechanisms in the central nervous system have remained elusive. In this triple-tracer positron emission tomography study, we investigated whether brain insulin signaling, µ-opioid receptors (MORs) and cannabinoid CB1 receptors (CB1Rs) are associated with risk for developing obesity. METHODS: Subjects were 41 young non-obese males with variable obesity risk profiles. Obesity risk was assessed by subjects' physical exercise habits, body mass index and familial risk factors, including parental obesity and T2D. Brain glucose uptake was quantified with [18F]FDG during hyperinsulinemic euglycemic clamp, MORs were quantified with [11C]carfentanil and CB1Rs with [18F]FMPEP-d2. RESULTS: Subjects with higher obesity risk had globally increased insulin-stimulated brain glucose uptake (19 high-risk subjects versus 19 low-risk subjects), and familial obesity risk factors were associated with increased brain glucose uptake (38 subjects) but decreased availability of MORs (41 subjects) and CB1Rs (36 subjects). CONCLUSIONS: These results suggest that the hereditary mechanisms promoting obesity may be partly mediated via insulin, opioid and endocannabinoid messaging systems in the brain.

Coronary artery disease and its impact on the pulsatile brain: A functional NIRS study.

Recent studies have reported that optical indices of cerebral pulsatility are associated with cerebrovascular health in older adults. Such indices, including cerebral pulse amplitude and the pulse relaxation function (PRF), have been previously applied to quantify global and regional cerebral pulsatility. The aim of the present study was to determine whether these indices are modulated by cardiovascular status and whether they differ between individuals with low or high cardiovascular risk factors (LCVRF and HCVRF) and coronary artery disease (CAD). A total of 60 older adults aged 57-79 were enrolled in the study. Participants were grouped as LCVRF, HCVRF, and CAD. Participants were asked to walk freely on a gym track while a near-infrared spectroscopy (NIRS) device recorded hemodynamics data. Low-intensity, short-duration walking was used to test whether a brief cardiovascular challenge could increase the difference of pulsatility indices with respect to cardiovascular status. Results indicated that CAD individuals have higher global cerebral pulse amplitude compared with the other groups. Walking reduced global cerebral pulse amplitude and PRF in all groups but did not increase the difference across the groups. Instead, walking extended the spatial distribution of cerebral pulse amplitude to the anterior prefrontal cortex when CAD was compared to the CVRF groups. Further research is needed to determine whether cerebral pulse amplitude extracted from data acquired with NIRS, which is a noninvasive, inexpensive method, can provide an index to characterize the cerebrovascular status associated with CAD.

Monitoring and modifying brain oxygenation in patients at risk of hypoxic ischaemic brain injury after cardiac arrest.

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2021. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2021 . Further information about the Annual Update in Intensive Care and Emergency Medicine is available from https://link.springer.com/bookseries/8901 .

Unilateral Spatial Neglect without Hemiplegia: The Output-Mode Effect Revisited.

BACKGROUND: The occurrence of unilateral spatial neglect (USN) in non-hemiplegic right-hemisphere damaged patients is rare. Earlier studies of such patients revealed a significant advantage when typical neglect tests were performed by the patient's left hand as compared to the dominant right hand. The mechanism underlying this "output-mode effect" remains elusive. METHODS: We analyzed the temporal dynamics of this effect using line-bisection task in 9 non-hemiplegic stroke patients with left-USN. RESULTS: In 4 patients tested shortly after stroke onset (≤ 6 weeks), the impact of hand laterality was variable (left-hand advantage in one patient; right-hand advantage in 2 patients; similar performance in both hands in one patient). Only later (> 6 weeks) a clear advantage of the left hand emerged in the majority of patients, similar to the earlier reports which were all based on late testing. CONCLUSIONS: We found variable dynamics in the expression of the output-mode effect in the first weeks following stroke onset, which may reflect changes of inter-hemispheric balance, related to recovery processes. We propose that therapeutic interventions aiming to manipulate the inter-hemispheric balance (e.g., by non-invasive brain stimulation) take into account the existence of such dynamics and their highly variate nature.

Right Hemispheric Homologous Language Pathways Negatively Predicts Poststroke Naming Recovery.

Background and Purpose- Stroke is the leading cause of disability in United States, and aphasia is a common sequela after a left hemisphere stroke. Functional imaging and brain stimulation studies show that right hemisphere structures are detrimental to aphasia recovery but evidence from diffusion tensor imaging is lacking. We investigated the role of homologous language pathways in naming recovery after left hemispheric stroke. Methods- Patients with aphasia after a left hemispheric stroke underwent naming assessment using the Boston Naming Test and diffusion tensor imaging at the acute and chronic time points. We analyzed diffusion tensor imaging of right arcuate fasciculus and frontal aslant tracts. We used Wilcoxon rank-sum test to evaluate structural lateralization patterns and partial Spearman correlation/multivariate generalized linear model to determine the role of right arcuate fasciculus and frontal aslant tracts in naming recovery after controlling for confounders. Results were corrected for multiple comparisons. Results- On average, the structural integrity of left language pathways deteriorated more than their right homologs, such that there was rightward lateralization in the chronic stage. Regression/correlation analyses showed that greater preservation of tract integrity of right arcuate fasciculus was associated with poorer naming recovery. Conclusions- Our study provides preliminary evidence that preservation of right homologs of language pathways is associated with poor recovery of naming after a left hemispheric stroke, consistent with previous evidence that maintaining greater reliance on left hemisphere structures is associated with better language recovery.

Common and separable neural alterations in substance use disorders: A coordinate-based meta-analyses of functional neuroimaging studies in humans.

Delineating common and separable neural alterations in substance use disorders (SUD) is imperative to understand the neurobiological basis of the addictive process and to inform substance-specific treatment strategies. Given numerous functional MRI (fMRI) studies in different SUDs, a meta-analysis could provide an opportunity to determine robust shared and substance-specific alterations. The present study employed a coordinate-based meta-analysis covering fMRI studies in individuals with addictive cocaine, cannabis, alcohol, and nicotine use. The primary meta-analysis demonstrated common alterations in primary dorsal striatal, and frontal circuits engaged in reward/salience processing, habit formation, and executive control across different substances and task-paradigms. Subsequent sub-analyses revealed substance-specific alterations in frontal and limbic regions, with marked frontal and insula-thalamic alterations in alcohol and nicotine use disorders respectively. Examining task-specific alterations across substances revealed pronounced frontal alterations during cognitive processes yet stronger striatal alterations during reward-related processes. Finally, an exploratory meta-analysis revealed that neurofunctional alterations in striatal and frontal reward processing regions can already be determined with a high probability in studies with subjects with comparably short durations of use. Together the findings emphasize the role of dysregulations in frontostriatal circuits and dissociable contributions of these systems in the domains of reward-related and cognitive processes which may contribute to substance-specific behavioral alterations.

Dysregulation of inflammation, neurobiology, and cognitive function in PTSD: an integrative review.

Compelling evidence from animal and human research suggest a strong link between inflammation and posttraumatic stress disorder (PTSD). Furthermore, recent findings support compromised neurocognitive function as a key feature of PTSD, particularly with deficits in attention and processing speed, executive function, and memory. These cognitive domains are supported by brain structures and neural pathways that are disrupted in PTSD and which are implicated in fear learning and extinction processes. The disruption of these supporting structures potentially results from their interaction with inflammation. Thus, the converging evidence supports a model of inflammatory dysregulation and cognitive dysfunction as combined mechanisms underpinning PTSD symptomatology. In this review, we summarize evidence of dysregulated inflammation in PTSD and further explore how the neurobiological underpinnings of PTSD, in the context of fear learning and extinction acquisition and recall, may interact with inflammation. We then present evidence for cognitive dysfunction in PTSD, highlighting findings from human work. Potential therapeutic approaches utilizing novel pharmacological and behavioral interventions that target inflammation and cognition also are discussed.

Advantages of methohexital over amobarbital in determining hemispheric language and memory lateralization in the Wada test - A retrospective study.

OBJECTIVE: Due to supply shortage, amobarbital, the traditional anesthetic agent in Wada testing, was replaced by methohexital in many epilepsy centers. This study aimed to compare the two barbiturates to identify possible advantages or disadvantages of methohexital as compared to amobarbital with regard to the adequacy of language and memory testing during the Wada test. METHODS: Data from 75 patients with temporal lobe epilepsy who underwent bilateral Wada tests using either amobarbital (n = 53) or methohexital (n = 22) as part of presurgical work-up were analyzed retrospectively. The two subgroups were compared regarding hemispheric language and memory lateralization results and Wada testing characteristics, and the adequacy of language and memory testing was assessed. RESULTS: We observed shorter durations of motor-, speech-, and EEG recovery after each injection in patients receiving methohexital compared to amobarbital. In addition, significantly more items could be presented during effective hemispheric inactivation in the methohexital group. Moreover, significant correlations of Wada memory scores with standard neuropsychological memory test scores could be found in the methohexital group. SIGNIFICANCE: Our findings confirm that methohexital is not only equally suitable for Wada testing but has several advantages over amobarbital. Wada testing can be performed more efficiently and under more constant hemispheric inactivation using methohexital. Furthermore, the adequacy of language and memory testing during the Wada test might be affected by the anesthetic agent used.

Prognostic information of gaze deviation in acute ischemic stroke patients.

INTRODUCTION: Gaze deviation (GD) in acute ischemic stroke patients has been suggested to be associated with poor outcome and with the presence of large vessel occlusion. Our aim was to study the prognostic significance of GD in ischemic stroke patients submitted to acute revascularization treatments. METHODS: Retrospective single-center study of consecutive anterior circulation ischemic stroke patients submitted to thrombolysis and/or endovascular revascularization between 2007 and 2017. The groups of patients with and without GD were compared concerning baseline clinical and imagiological variables, functional outcome at 3 months, and survival at 1 year. RESULTS: Among a study population of 711 patients, 332 (46.7%) presented GD. Patients with GD were more frequently of female sex (p = 0.048), had higher baseline NIHSS scores (p < 0.001), had lower ASPECTS on baseline CT (p < 0.001), more frequently had ischemia of the right hemisphere (p < 0.001), presented higher NIHSS 24 hours after treatment (p < 0.001), and more frequently presented cardioembolic stroke (p = 0.003). In the unadjusted analyses, GD was associated with decreased 3-month functional independence and increased 1-month and 1 year mortality (p < 0.001). After adjustment for variables of interest, namely, for NIHSS 24 hours after treatment, GD was no longer associated with functional outcome or survival. CONCLUSIONS: GD in patients with acute ischemic stroke is associated with increased clinical and imagiological severity at baseline. However, in patients submitted to acute revascularization treatments, this does not appear to be independent predictor of functional outcome or survival.

Correlation Between Speech Repetition Function and the Arcuate Fasciculus in the Dominant Hemisphere Detected by Diffusion Tensor Imaging Tractography in Stroke Patients with Aphasia.

BACKGROUND Repetition disorder can be used as an important criterion for aphasia classification, and damaged arcuate fasciculus in the dominate hemisphere has been reported to be closely related to repetition disorder, but the underlying neurological mechanism remains unclear. MATERIAL AND METHODS Fifteen stroke patients with poststroke aphasia and 9 healthy controls were included in the study. The value of fractional anisotropy (FA) in the dominate arcuate fasciculus in stroke patients and healthy controls were measured using DTI. We also assessed their repetition dysfunction with the Aphasia Battery of Chinese (ABC) assessment and calculated the correlation between the FA values in the dominate arcuate fasciculus and ABC scores of word repetition and sentence repetition. RESULTS There was a moderate correlation between the total score of repetition evaluation and the FA value of injured arcuate fasciculus in the dominant hemisphere (r=0.551, P=0.033). We found no correlation between the score of word repetition and the FA value of injured arcuate fasciculus in the dominant hemisphere (r=0.330, P=0.230), but there was a strong correlation between the score of sentence repetition and the FA value of injured arcuate fasciculus in the dominant hemisphere (r=0.795, P≤0.001). CONCLUSIONS We found that unintegrated left arcuate fasciculus might be related to the repetition dysfunction after stroke, especially sentence repetition deficit, which suggests that sentence repetition evaluation could be used to indicate the integrity of the arcuate fasciculus in the dominant hemisphere after stroke.

Effects of Bihemispheric Transcranial Direct Current Stimulation on Upper Extremity Function in Stroke Patients: A randomized Double-Blind Sham-Controlled Study.

BACKGROUND AND PURPOSE: Transcranial direct current stimulation (tDCS) is a treatment used in the rehabilitation of stroke patients aiming to improve functionality of the plegic upper extremity. Currently, tDCS is not routinely used in post stroke rehabilitation. The aim of this study was to establish the effects of bihemspheric tDCS combined with physical therapy (PT) and occupational therapy (OT) on upper extremity motor function. METHODS: Thirty-two stroke inpatients were randomised into 2 groups. All patients received 15 sessions of conventional upper extremity PT and OT over 3 weeks. The tDCS group (n = 16) also received 30 minutes of bihemispheric tDCS and the sham group (n = 16) 30 minutes of sham bihemispheric tDCS simultaneously to OT. Patients were evaluated before and after treatment using the Fugl Meyer upper extremity (FMUE), functional independence measure (FIM), and Brunnstrom stages of stroke recovery (BSSR) by a physiatrist blind to the treatment group RESULTS: The improvement in FIM was higher in the tDCS group compared to the sham group (P = .001). There was a significant within group improvement in FMUE, FIM and BSSR in those receiving tDCS (P = .001). There was a significant improvement in FIM in the chronic (> 6months) stroke sufferers who received tDCS when compared to those who received sham tDCS and when compared to subacute stroke (3-6 months) sufferers who received tDCS/sham. CONCLUSIONS: Upper extremity motor function in hemiplegic stroke patients improves when bihemispheric tDCS is used alongside conventional PT and OT. The improvement in functionality is greater in chronic stroke patients.

Network abnormalities among non-manifesting Parkinson disease related LRRK2 mutation carriers.

Non-manifesting carriers (NMC) of the G2019S mutation in the LRRK2 gene represent an "at risk" group for future development of Parkinson's disease (PD) and have demonstrated task related fMRI changes. However, resting-state networks have received less research focus, thus this study aimed to assess the integrity of the motor, default mode (DMN), salience (SAL), and dorsal attention (DAN) networks among this unique population by using two different connectivity measures: interregional functional connectivity analysis and Dependency network analysis (DEP NA). Machine learning classification methods were used to distinguish connectivity between the two groups of participants. Forty-four NMC and 41 non-manifesting non-carriers (NMNC) participated in this study; while no behavioral differences on standard questionnaires could be detected, NMC demonstrated lower connectivity measures in the DMN, SAL, and DAN compared to NMNC but not in the motor network. Significant correlations between NMC connectivity measures in the SAL and attention were identified. Machine learning classification separated NMC from NMNC with an accuracy rate above 0.8. Reduced integrity of non-motor networks was detected among NMC of the G2019S mutation in the LRRK2 gene prior to identifiable changes in connectivity of the motor network, indicating significant non-motor cerebral changes among populations "at risk" for future development of PD.

Multimodal imaging reveals a complex pattern of dysfunction in corticolimbic pathways in major depressive disorder.

Major depressive disorder (MDD) is highly prevalent and associated with considerable morbidity, yet its pathophysiology remains only partially understood. While numerous studies have investigated the neurobiological correlates of MDD, most have used only a single neuroimaging modality. In particular, diffusion tensor imaging (DTI) studies have failed to yield uniform results. In this context, examining key tracts and using information from multiple neuroimaging modalities may better characterize potential abnormalities in the MDD brain. This study analyzed data from 30 participants with MDD and 26 healthy participants who underwent DTI, magnetic resonance spectroscopy (MRS), resting-state functional magnetic resonance imaging (fMRI), and magnetoencephalography (MEG). Tracts connecting the subgenual anterior cingulate cortex (sgACC) and the left and right amygdala, as well as connections to the left and right hippocampus and thalamus, were examined as target areas. Reduced fractional anisotropy (FA) was observed in the studied tracts. Significant differences in the correlation between medial prefrontal glutamate concentrations and FA were also observed between MDD and healthy participants along tracts connecting the sgACC and right amygdala; healthy participants exhibited a strong correlation but MDD participants showed no such relationship. In the same tract, a correlation was observed between FA and subsequent antidepressant response to ketamine infusion in MDD participants. Exploratory models also suggested group differences in the relationship between DTI, fMRI, and MEG measures. This study is the first to combine MRS, DTI, fMRI, and MEG data to obtain multimodal indices of MDD and antidepressant response and may lay the foundation for similar future analyses.

Predicting recovery in acute poststroke aphasia.

OBJECTIVE: Many stroke patients show remarkable recovery of language after initial severe impairment, but it is difficult to predict which patients will show good recovery. We aimed to identify patient and lesion characteristics that together predict the best naming outcome in 4 studies. METHODS: We report 2 longitudinal studies that identified 2 variables at onset that were strongly associated with good recovery of naming (the most common residual deficit in aphasia) in the first 6 months after stroke: damage to left posterior superior temporal gyrus (pSTG) and/or superior longitudinal fasciculus/arcuate fasciculus (SLF/AF), and selective serotonin reuptake inhibitor (SSRI) use. We then tested these variables in 2 independent cohorts of chronic left hemisphere stroke patients, using chi-square tests and multivariate logistic regression for dichotomous outcomes and t tests for continuous outcomes. RESULTS: Lesion load in left pSTG and SLF/AF was associated with poorer naming outcome. Preservation of these areas and use of SSRIs were associated with naming recovery, independent of lesion volume, time since stroke, and depression. Patients with damage to these critical areas showed better naming outcome if they took SSRIs for 3 months after stroke. Those with preservation of these critical areas achieved good recovery of naming regardless of SSRI use. INTERPRETATION: Lesion load in left pSTG and SLF/AF at onset predicts later naming performance. Although based on a small number of patients, our preliminary results suggest outcome might be modulated by SSRIs, but these associations need to be confirmed in a larger randomized controlled trial. Ann Neurol 2018;83:612-622.

Near-infrared spectroscopy after out-of-hospital cardiac arrest.

BACKGROUND: Cerebral hypoperfusion may aggravate neurological damage after cardiac arrest. Near-infrared spectroscopy (NIRS) provides information on cerebral oxygenation but its relevance during post-resuscitation care is undefined. We investigated whether cerebral oxygen saturation (rSO2) measured with NIRS correlates with the serum concentration of neuron-specific enolase (NSE), a marker of neurological injury, and with clinical outcome in out-of-hospital cardiac arrest (OHCA) patients. METHODS: We performed a post hoc analysis of a randomised clinical trial (COMACARE, NCT02698917) comparing two different levels of carbon dioxide, oxygen and arterial pressure after resuscitation from OHCA with ventricular fibrillation as the initial rhythm. We measured rSO2 in 118 OHCA patients with NIRS during the first 36 h of intensive care. We determined the NSE concentrations from serum samples at 48 h after cardiac arrest and assessed neurological outcome with the Cerebral Performance Category (CPC) scale at 6 months. We evaluated the association between rSO2 and serum NSE concentrations and the association between rSO2 and good (CPC 1-2) and poor (CPC 3-5) neurological outcome. RESULTS: The median (inter-quartile range (IQR)) NSE concentration at 48 h was 17.5 (13.4-25.0) µg/l in patients with good neurological outcome and 35.2 (22.6-95.8) µg/l in those with poor outcome, p < 0.001. We found no significant correlation between median rSO2 and NSE at 48 h, rs = - 0.08, p = 0.392. The median (IQR) rSO2 during the first 36 h of intensive care was 70.0% (63.5-77.0%) in patients with good outcome and 71.8% (63.3-74.0%) in patients with poor outcome, p = 0.943. There was no significant association between rSO2 over time and neurological outcome. In a binary logistic regression model, rSO2 was not a statistically significant predictor of good neurological outcome (odds ratio 0.99, 95% confidence interval 0.94-1.04, p = 0.635). CONCLUSIONS: We found no association between cerebral oxygenation measured with NIRS and NSE concentrations or outcome in patients resuscitated from OHCA. TRIAL REGISTRATION: ClinicalTrials.gov, NCT02698917 . Registered on 26 January 2016.

Cerebral metabolism is not affected by moderate hyperventilation in patients with traumatic brain injury.

BACKGROUND: Hyperventilation-induced hypocapnia (HV) reduces elevated intracranial pressure (ICP), a dangerous and potentially fatal complication of traumatic brain injury (TBI). HV decreases the arteriolar diameter of intracranial vessels, raising the risk of cerebral ischemia. The aim of this study was to characterize the effects of moderate short-term HV in patients with severe TBI by using concomitant monitoring of cerebral metabolism, brain tissue oxygen tension (PbrO2), and cerebral hemodynamics with transcranial color-coded duplex sonography (TCCD). METHODS: This prospective trial was conducted between May 2014 and May 2017 in the surgical intensive care unit (ICU) at the University Hospital of Zurich. Patients with nonpenetrating TBI older than 18 years of age with a Glasgow Coma Scale (GCS) score < 9 at presentation and with ICP monitoring, PbrO2, and/or microdialysis (MD) probes during ICU admission within 36 h after injury were included in our study. Data collection and TCCD measurements were performed at baseline (A), at the beginning of moderate HV (C), after 50 min of moderate HV (D), and after return to baseline (E). Moderate HV was defined as arterial partial pressure of carbon dioxide 4-4.7 kPa. Repeated measures analysis of variance was used to compare variables at the different time points, followed by post hoc analysis with Bonferroni adjustment as appropriate. RESULTS: Eleven patients (64% males, mean age 36 ± 14 years) with an initial median GCS score of 7 (IQR 3-8) were enrolled. During HV, ICP and mean flow velocity (CBFV) in the middle cerebral artery decreased significantly. Glucose, lactate, and pyruvate in the brain extracellular fluid did not change significantly, whereas PbrO2 showed a statistically significant reduction but remained within the normal range. CONCLUSION: Moderate short-term hyperventilation has a potent effect on the cerebral blood flow, as shown by TCCD, with a concomitant ICP reduction. Under the specific conditions of this study, this degree of hyperventilation did not induce pathological alterations of brain metabolites and oxygenation. TRIAL REGISTRATION: NCT03822026 . Registered on 30 January 2019.

Scary symptoms? Functional magnetic resonance imaging evidence for symptom interpretation bias in pathological health anxiety.

Patients with pathological health anxiety (PHA) tend to automatically interpret bodily sensations as sign of a severe illness. To elucidate the neural correlates of this cognitive bias, we applied an functional magnetic resonance imaging adaption of a body-symptom implicit association test with symptom words in patients with PHA (n = 32) in comparison to patients with depression (n = 29) and healthy participants (n = 35). On the behavioral level, patients with PHA did not significantly differ from the control groups. However, on the neural-level patients with PHA in comparison to the control groups showed hyperactivation independent of condition in bilateral amygdala, right parietal lobe, and left nucleus accumbens. Moreover, patients with PHA, again in comparison to the control groups, showed hyperactivation in bilateral posterior parietal cortex and left dorsolateral prefrontal cortex during incongruent (i.e., harmless) versus congruent (i.e., dangerous) categorizations of body symptoms. Thus, body-symptom cues seem to trigger hyperactivity in salience and emotion processing brain regions in PHA. In addition, hyperactivity in brain regions involved in cognitive control and conflict resolution during incongruent categorization emphasizes enhanced neural effort to cope with negative implicit associations to body-symptom-related information in PHA. These results suggest increased neural responding in key structures for the processing of both emotional and cognitive aspects of body-symptom information in PHA, reflecting potential neural correlates of a negative somatic symptom interpretation bias.

Near-infrared spectroscopy monitoring during out-of-hospital cardiac arrest: can the initial cerebral tissue oxygenation index predict ROSC?

STUDY OBJECTIVES: Near-infrared spectroscopy is a modality that can monitor tissue oxygenation index (TOI) and has potential to evaluate return of spontaneous circulation (ROSC) during cardiopulmonary resuscitation (CPR). This study's objectives were to evaluate whether TOI could be associated with ROSC and used to help guide the decision to either terminate CPR or proceed to extracorporeal CPR (ECPR). METHODS: In this observational study, we assessed the patients with out-of-hospital cardiac arrest with non-traumatic cause receiving CPR on arrival at our ED between 2013 and 2016. TOI monitoring was discontinued either on CPR termination after ROSC was reached or on patient death. Patients were classified into two groups: ROSC and non-ROSC group. RESULTS: Out of 141 patients, 24 were excluded and the remaining 117 were classified as follows: ROSC group (n=44) and non-ROSC group (n=73). ROSC group was significantly younger and more likely to have their event witnessed and bystander CPR. ROSC group showed a higher initial TOI than non-ROSC group (60.5%±17.0% vs 37.9%±13.7%: p<0.01). Area under the curve analysis was more accurate with the initial TOI than without it for predicting ROSC (0.88, 95% CI 0.82 to 0.95 vs 0.79, 95% CI 0.70 to 0.87: p<0.01). TOI cut-off value ≥59% appeared to favour survival to hospital discharge whereas TOI ≤24% was associated with non-ROSC. CONCLUSIONS: This study demonstrated an association between higher initial TOI and ROSC. Initial TOI could increase the accuracy of ROSC prognosis and may be a clinical factor in the decision to terminate CPR and select patients who are to proceed to ECPR.

Right in Comparison to Left Cerebral Hemisphere Damage by Stroke Induces Poorer Muscular Responses to Stance Perturbation Regardless of Visual Information.

OBJECTIVE: Fast and scaled muscular activation is required to recover body balance following an external perturbation. An issue open to investigation is the extent to which the cerebral hemisphere lesioned by stroke leads to asymmetric deficits in postural reactive responses. In this experiment, we aimed to compare muscular responses to unanticipated stance perturbations between individuals who suffered unilateral stroke either to the right or to the left cerebral hemisphere. METHODS: Stance perturbations were produced by releasing a load attached to the participant's trunk, inducing fast forward body oscillation. Electromyography was recorded from the gastrocnemius medialis and biceps femoris muscles. Muscular activation from age-matched healthy individuals was taken as reference. RESULTS: Analysis indicated that damage to the right hemisphere induced delayed activation onset, and lower rate and magnitude of activation of the proximal and distal muscles of the paretic leg. Those deficits were associated with stronger activation of the nonparetic leg. Comparisons between left hemisphere damage and controls showed deficits limited to activation of the biceps femoris of the paretic leg. Manipulation of visual information led to no significant effects on muscular responses. CONCLUSIONS: These results suggest that right cerebral hemisphere damage by stroke leads to more severe deficits in the generation of reactive muscular responses to stance perturbation than damage to the left cerebral hemisphere regardless of visual information.

Functional State of Various Types of Regeneration-Competent Cells in the Nervous Tissue in Ethanol-Induced Neurodegeneration.

The in vitro and in vivo models of ethanol-induced neurodegeneration were used to evaluate the content and functional activity of various types of regeneration-competent cells in subventricular zone of the cerebral hemispheres in C57Bl/6JY mice. In nervous tissue culture, ethanol (65 mM) produced no effect on formation of neurospheres. When administered per os in a daily dose of 3 g/kg for 8 weeks, ethanol produced no effect on the number of neural CFU in situ. In both cases, ethanol reduced proliferative activity of neural CFU. Long-term administration of ethanol in vivo suppressed differentiation of neural stem cells and decreased the number of committed precursors (neural cluster-forming units) in the subventricular zone of cerebral hemispheres. In vitro application of ethanol stimulated secretion of humoral growth factors by the cluster-forming neural glial cells. In contrast, in vivo administration of ethanol suppressed this secretion.