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Despite many authors in psychiatry endorsing a naturalist view of the mind, many still consider that mental dysfunctions cannot be reduced to brain dysfunctions. This paper investigates the main reasons for this view. Some arguments rely on the analogy that the mind is like software while the brain is like hardware. The analogy suggests that just as software can malfunction independently of hardware malfunctions, similarly the mind can malfunction independently of any brain malfunction. This view has been critically examined in recent literature. However, other less discussed reasons suggest that mental dysfunctions cannot be reduced to brain dysfunctions because mental dysfunctions are appropriately ascribed at the level of intentional mental states, while brain dysfunctions are solely related to abnormalities in anatomy and physiological processes. This paper questions why such a view would be upheld. The discussion is framed within the interface problem in the philosophy of cognitive science, which concerns the relationship between personal and subpersonal levels of explanation. The paper examines the view that an autonomist perspective on the personal/subpersonal distinction could justify the separation of mental dysfunctions, described in intentional terms, from brain dysfunctions, described in anatomical or physiological terms. Ultimately, the paper argues that the autonomist view cannot be upheld in psychiatry and, consequently, does not provide a principled justification for rejecting the reduction of mental dysfunctions to brain dysfunctions. [ABSTRACT FROM AUTHOR]

The first clinical case report of the Capgras Delusion in the British literature appeared in 1933, a decade after the seminal article by Capgras and Reboul-Lachaux. The author endeavoured to explain it psychodynamically on the basis of Freud's theory of infantile sexual development, arguing that it was due to a mental mechanism peculiar to women. Despite often ill founded and convoluted, psychodynamic formulations held sway for several decades until cases occurring in toxic-metabolic and structural brain disorders were described. However, by the 1990's it was recognised that the presence of brain dysfunction did not in itself explain the delusion. What was needed in addition was an appropriate cognitive theory of the mechanisms underlying the delusion. The advent of cognitive neuropsychiatry, pioneered by the late Hadyn Ellis, provided a framework for a more systematic and predictive approach to our understanding of delusional misidentification. [ABSTRACT FROM AUTHOR]

Abstract Despite many authors in psychiatry endorsing a naturalist view of the mind, many still consider that mental dysfunctions cannot be reduced to brain dysfunctions. This paper investigates the main reasons for this view. Some arguments rely on the analogy that the mind is like software while the brain is like hardware. The analogy suggests that just as software can malfunction independently of hardware malfunctions, similarly the mind can malfunction independently of any brain malfunction. This view has been critically examined in recent literature. However, other less discussed reasons suggest that mental dysfunctions cannot be reduced to brain dysfunctions because mental dysfunctions are appropriately ascribed at the level of intentional mental states, while brain dysfunctions are solely related to abnormalities in anatomy and physiological processes. This paper questions why such a view would be upheld. The discussion is framed within the interface problem in the philosophy of cognitive science, which concerns the relationship between personal and subpersonal levels of explanation. The paper examines the view that an autonomist perspective on the personal/subpersonal distinction could justify the separation of mental dysfunctions, described in intentional terms, from brain dysfunctions, described in anatomical or physiological terms. Ultimately, the paper argues that the autonomist view cannot be upheld in psychiatry and, consequently, does not provide a principled justification for rejecting the reduction of mental dysfunctions to brain dysfunctions.

Objective: To investigate the effect and mechanism of Rehmannioside A (ReA) on brain dysfunction in cecal ligation and perforation (CLP) -induced sepsis rats. Methods: 56 CLP-induced sepsis rats were randomly divided into CLP group (n=12), CLP+20ReA group (n=11), CLP+40ReA group (n=11), CLP+80ReA group (n=11), and GPX4-IN-3 group (n=11). Ten rats underwent Sham operation as sham group. Rats in Sham group and CLP group were given 1 mL dimethyl sulfoxide (DMSO). Rats in CLP+20ReA group, CLP+40ReA group and CLP+80ReA group were given 1 mL of 20, 40 and 80 mg/kg/d Rehmannioside A, respectively. Rats in GPX4-IN-3 group were simultaneously administrated with 0.5 mL 80 mg/kg/d of Rehmannioside A and 0.5 mL 15 mg/kg/d of the selective inducer of ferroptosis GPX4-IN-3. Each group was given the drug for 3 days. Neural function score and Morris water maze test were used to evaluate brain function. Neuron-specific enolase (NSE) and S100β levels were detected by ELISA. The water content of brain tissue was measured by weighing method. Brain injury was evaluated by HE staining and Nissl staining. The levels of reduced glutathione (GSH) and malondialdehyde (MDA) in brain tissue were detected by micromethods. The levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by ELISA. The content of Fe2+ in brain tissue was determined by micromethod. The levels of nuclear factor E2-related factor 2 (Nrf2), Kelch-like ECH related protein 1 (Keap1) and glutathione peroxidase 4 (GPX4) protein in brain tissue were detected by Western blot. Results: Compared with CLP group, the neural function scores and escape latency of CLP+20ReA group, CLP+40ReA group and CLP+80ReA group decreased (P<0.05), the number of crossing platforms increased (P<0.05), the neuronal damage reduced, the levels of serum NSE and S100β decreased (P<0.05), the level of GSH in brain tissue increased (P<0.05). The water content of brain tissue and levels of MDA, IL-6, TNF-α and the content of Fe2+ in brain tissue decreased(P<0.05), the protein expressions of Nrf2 (nucleus) and GPX4 in brain tissue increased(P<0.05), and the protein expression of Keap1 decreased(P<0.05). Compared with CLP+80ReA group, the brain dysfunction of GPX4-IN-3 group was aggravated, and the Nrf2/GPX4 pathway was inhibited (P<0.05). Conclusion: Rehmannioside A inhibits ferroptosis by activating Nrf2/GPX4 pathway, thereby alleviating brain dysfunction in CLP-induced sepsis rats. [ABSTRACT FROM AUTHOR]

Background: Oxidative stress is a well‐known pathological factor driving neuronal loss and age‐related neurodegenerative diseases. Melatonin, coenzyme Q10 and lecithin are three common nutrients with an antioxidative capacity. Here, we examined the effectiveness of them administrated individually and in combination in protecting against oxidative stress‐induced neuronal death in vitro, and neurodegenerative conditions such as Alzheimer's disease and associated deficits in vivo. Methods: Mouse neuroblastoma Neuro‐2a (N2a) cells were exposed with H2O2 for 6 h, and subsequently treated with melatonin, coenzyme Q10, and lecithin alone or in combination for further 24 h. Cell viability was assessed using the CCK‐8 assay. Eight‐week‐old male mice were intraperitoneally injected with D‐(+)‐galactose for 10 weeks and administrated with melatonin, coenzyme Q10, lecithin, or in combination for 5 weeks starting from the sixth week, followed by behavioral tests to assess the effectiveness in mitigating neurological deficits, and biochemical assays to explore the underlying mechanisms. Results: Exposure to H2O2 significantly reduced the viability of N2a cells and increased oxidative stress and tau phosphorylation, all of which were alleviated by treatment with melatonin, coenzyme Q10, lecithin alone, and, most noticeably, by combined treatment. Administration of mice with D‐(+)‐galactose‐induced oxidative stress and tau phosphorylation, brain aging, impairments in learning and memory, anxiety‐ and depression‐like behaviors, and such detrimental effects were mitigated by melatonin, coenzyme Q10, lecithin alone, and, most consistently, by combined treatment. Conclusions: These results suggest that targeting oxidative stress via supplementation of antioxidant nutrients, particularly in combination, is a better strategy to alleviate oxidative stress‐mediated neuronal loss and brain dysfunction due to age‐related neurodegenerative conditions. [ABSTRACT FROM AUTHOR]

Brain functions are mediated via the complex interplay between several complex factors, and hence, identifying the underlying cause of an abnormality within a certain brain region can be challenging. In mitochondrial disease, abnormalities in brain function are thought to be attributed to accumulation of mitochondrial DNA (mtDNA) with pathogenic mutations; however, only few previous studies have directly demonstrated that accumulation of mutant mtDNA induced abnormalities in brain function. Herein, we examined the effects of mtDNA mutations on brain function via behavioral analyses using a mouse model with an A2748G point mutation in mtDNA tRNALeu(UUR). Our results revealed that mice with a high percentage of mutant mtDNA showed a characteristic trend toward reduced prepulse inhibition and memory-dependent test performance, similar to that observed in psychiatric disorders, such as schizophrenia; however, muscle strength and motor coordination were not markedly affected. Upon examining the hippocampus and frontal lobes of the brain, mitochondrial morphology was abnormal, and the brain weight was slightly reduced. These results indicate that the predominant accumulation of a point mutation in the tRNALeu(UUR) gene may affect brain functions, particularly the coordination of sensory and motor functions and memory processes. These abnormalities probably caused by both direct effects of accumulation of the mutant mtDNA in neuronal cells and indirect effects via changes of systemic extracellular environments. Overall, these findings will lead to a better understanding of the pathogenic mechanism underlying this complex disease and facilitate the development of optimal treatment methods.

Cells in the brain are surrounded by extracellular space (ECS), which forms porous nets and interconnected routes for molecule transportation. Our view of brain ECS has changed from a largely static compartment to dynamic and diverse structures that actively regulate neural activity and brain states. Emerging evidence supports that dysregulation of brain ECS contributes to the pathogenesis and development of many neurological disorders, highlighting the importance of therapeutic modulation of brain ECS function. Here, we aim to provide an overview of the regulation and dysfunction of ECS in healthy and pathological brains, as well as advanced tools to investigate properties of brain ECS. This review emphasizes modulation methods to manipulate ECS with implications to restore their function in brain diseases. Highlights: • Up-to-date overview of the regulation of brain ECS in health and disease. • Recent advances in detecting the biophysical properties, function, and dynamic changes of brain ECS are reviewed. • Advanced pharmacological and physical methods to manipulate brain ECS, which provides therapeutic potentials for treating neurological disorders. [ABSTRACT FROM AUTHOR]

Background: The legalization of cannabis use and false claims about the plant Cannabis sativa to be considered a pharmaceutical product have been found to increase consumption, lower risk perception, and lead to more health problems, without reducing criminal activity. Brain function, typically assessed by neuropsychological tests, shows abnormalities with acute marijuana use, but inconsistent results have been published after abstinence, with a maximum follow-up of 28 days. Our previous research, using neuropsychological tests and brain perfusion single photon emission computed tomography (neuroSPECT), demonstrated consistent abnormalities in brain function among schoolchildren who consume marijuana compared to their non-consuming peers. The aim of this study is to investigate whether brain function changes in 20 adult marijuana users after 6 months of abstinence. Methodology: Comparison of neuropsychological tests (Rey Complex Figure; Porteus Maze; Four subtests of WAIS-IV Intellectual Tests; STROOP; D2) and perfusion neuroSPECT (functional images), obtained in relation to recent consumption and after 6 months of serial drug-screening test confirmed abstinence. Results: In a one-year period (2020-2021) only five compliant participants were recruited. The COVID-19 pandemic was a limiting factor. Preliminary results of neuropsychological tests, functional brain perfusion images and limited statistical analysis are presented. The results of the neuropsychological tests of the three subjects who completed the abstinence period so far show some improvement in working memory and attention after abstinence. NeuroSPECT shows disorganized hypoperfusion of variable severity in relation to recent consumption, involving areas associated with cognitive function such as the posterior cingulate and temporal lobes, in our five initially enrolled patients, when compared to a normal database. Of these, only two participants have already been re-evaluated with neuroSPECT after 6 months of abstinence, one of whom showed some improvement on the post-abstinence images. Conclusion: We analyze the methodological challenges of this research, including the pandemic, to incorporate the appropriate corrections in the next phase of our investigation. Our final findings may provide clinicians and users with information about the long-term effects of marijuana use on brain function. [ABSTRACT FROM AUTHOR]

Approximately one-third of acute ICU patients display atypical sleep patterns that cannot be interpreted by using standard EEG criteria for sleep. Atypical sleep patterns have been associated with poor weaning outcomes in acute ICUs. Do patients being weaned from prolonged mechanical ventilation experience atypical sleep EEG patterns, and are these patterns linked with weaning outcomes? EEG power spectral analysis during wakefulness and overnight polysomnogram were performed on alert, nondelirious patients at a long-term acute care facility. Forty-four patients had been ventilated for a median duration of 38 days at the time of the polysomnogram study. Eleven patients (25%) exhibited atypical sleep EEG. During wakefulness, relative EEG power spectral analysis revealed higher relative delta power in patients with atypical sleep than in patients with usual sleep (53% vs 41%; P <.001) and a higher slow-to-fast power ratio during wakefulness: 4.39 vs 2.17 (P <.001). Patients with atypical sleep displayed more subsyndromal delirium (36% vs 6%; P =.027) and less rapid eye movement sleep (4% vs 11% total sleep time; P <.02). Weaning failure was more common in the atypical sleep group than in the usual sleep group: 91% vs 45% (P =.013). This study provides the first evidence that patients in a long-term acute care facility being weaned from prolonged ventilation exhibit atypical sleep EEG patterns that are associated with weaning failure. Patients with atypical sleep EEG patterns had higher rates of subsyndromal delirium and slowing of the wakeful EEG, suggesting that these two findings represent a biological signal for brain dysfunction. [Display omitted] [ABSTRACT FROM AUTHOR]

Delirium is a potentially severe form of acute encephalopathy. Minocycline has neuroprotective effects in animal models of neurologic diseases; however, data from human studies remain scarce. Does the neuroprotective effect of minocycline prevent delirium occurrence in critically ill patients? This study was a randomized, placebo-controlled, double-anonymized trial conducted in four ICUs. Patients aged 18 years or older were eligible and randomized to receive minocycline (100 mg, twice daily) or placebo. The primary outcome was delirium incidence within 28 days or before ICU discharge. Secondary outcomes included days in delirium during ICU stay, delirium/coma-free days, length of mechanical ventilation, ICU length of stay, ICU mortality, and hospital mortality. The kinetics of various inflammatory (IL-1β, IL-6, IL-10, and C-reactive protein) and brain-related biomarkers (brain-derived neurotrophic factor and S100B) were used as exploratory outcomes. A total of 160 patients were randomized, but one patient in the placebo group died before treatment; thus the data from 159 patients were analyzed (minocycline, n = 84; placebo, n = 75). After the COVID-19 pandemic it was decided to stop patient inclusion early. There was a small but significant decrease in delirium incidence: 17 patients (20%) in the minocycline arm compared with 26 patients (35%) in the placebo arm (P =.043). No other delirium-related outcomes were modified by minocycline treatment. Unexpectedly, there was a significant decrease in hospital mortality (39% vs. 23%; P =.029). Among all analyzed biomarkers, only plasma levels of C-reactive protein decreased significantly after minocycline treatment (F = 0.75, P =.78, within time; F = 4.09, P =.045, group × time). Our findings in this rather small study signal a possible positive effect of minocycline on delirium incidence. Further studies are needed to confirm the benefits of this drug as a preventive measure in critically ill patients. ClinicalTrials.gov ; No.: NCT04219735; URL: www.clinicaltrials.gov [Display omitted] [ABSTRACT FROM AUTHOR]

Background: Sepsis-associated brain dysfunction (SABD) is frequent and is associated with poor outcome. Changes in brain hemodynamics remain poorly described in this setting. The aim of this study was to investigate the alterations of cerebral perfusion pressure and intracranial pressure in a cohort of septic patients. Methods: We conducted a retrospective analysis of prospectively collected data in septic adults admitted to our intensive care unit (ICU). We included patients in whom transcranial Doppler recording performed within 48 h from diagnosis of sepsis was available. Exclusion criteria were intracranial disease, known vascular stenosis, cardiac arrhythmias, pacemaker, mechanical cardiac support, severe hypotension, and severe hypocapnia or hypercapnia. SABD was clinically diagnosed by the attending physician, anytime during the ICU stay. Estimated cerebral perfusion pressure (eCPP) and estimated intracranial pressure (eICP) were calculated from the blood flow velocity of the middle cerebral artery and invasive arterial pressure using a previously validated formula. Normal eCPP was defined as eCPP ≥ 60 mm Hg, low eCPP was defined as eCPP < 60 mm Hg; normal eICP was defined as eICP ≤ 20 mm Hg, and high eICP was defined as eICP > 20 mm Hg. Results: A total of 132 patients were included in the final analysis (71% male, median [interquartile range (IQR)] age was 64 [52–71] years, median [IQR] Acute Physiology and Chronic Health Evaluation II score on admission was 21 [15–28]). Sixty-nine (49%) patients developed SABD during the ICU stay, and 38 (29%) were dead at hospital discharge. Transcranial Doppler recording lasted 9 (IQR 7–12) min. Median (IQR) eCPP was 63 (58–71) mm Hg in the cohort; 44 of 132 (33%) patients had low eCPP. Median (IQR) eICP was 8 (4–13) mm Hg; five (4%) patients had high eICP. SABD occurrence and in-hospital mortality did not differ between patients with normal eCPP and patients with low eCPP or between patients with normal eICP and patients with high eICP. Eighty-six (65%) patients had normal eCPP and normal eICP, 41 (31%) patients had low eCPP and normal eICP, three (2%) patients had low eCPP and high eICP, and two (2%) patients had normal eCPP and high eICP; however, SABD occurrence and in-hospital mortality were not significantly different among these subgroups. Conclusions: Brain hemodynamics, in particular CPP, were altered in one third of critically ill septic patients at a steady state of monitoring performed early during the course of sepsis. However, these alterations were equally common in patients who developed or did not develop SABD during the ICU stay and in patients with favorable or unfavorable outcome. [ABSTRACT FROM AUTHOR]

In her book "Are Mental Disorders Brain Disorders?" (2022), Anneli Jefferson proposes that brain processes that always realize mental dysfunctions are brain dysfunctions. This paper explores possible interpretations of two underdeveloped aspects of this thesis. First, it argues that "realization" should be interpreted as partial rather than full realization. Second, it argues that the "always" should only quantify over biologically normal situations. Taken together, these changes can account for the fact that some psychological dysfunctions are partially realized by functional mechanisms, for the existence of psychological dysfunctions due to mismatches rather than brain dysfunctions, and for the fact that brain dysfunctions do not cease to be brain dysfunctions just because they can be compensated. [ABSTRACT FROM AUTHOR]

Transjugular intrahepatic portosystemic shunt (TIPS) is an established treatment for portal hypertension and its' complications in liver cirrhosis, yet the development of hepatic encephalopathy (HE) remains a significant concern. This review covers the reported incidence, risk factors, and management strategies for post-TIPS HE over the past decade. Incidence varies widely (7–61%), with factors like age, liver function, hyponatremia, and spontaneous portosystemic shunts influencing risk. Procedural aspects, including TIPS timing, indication, and stent characteristics, also contribute. Pharmacological prophylaxis with lactulose and rifaximin shows promise, but current evidence is inconclusive. Procedural preventive measures, such as shunt embolization and monitoring portal pressure gradients, are explored. Treatment involves pharmacological options like lactulose and rifaximin, and procedural interventions like stent diameter reduction. Ongoing studies on novel predictive markers and emerging treatments, such as faecal microbiota transplant, reflect the evolving landscape in post-TIPS HE management. This concise review provides clinicians with insights into the multifaceted nature of post-TIPS HE, aiding in improved risk assessment, prophylaxis, and management for patients undergoing TIPS procedures. [ABSTRACT FROM AUTHOR]

Abstract Sepsis is the most common cause of admission to intensive care units worldwide. Sepsis patients frequently suffer from sepsis-associated encephalopathy (SAE) reflecting acute brain dysfunction. SAE may result in increased mortality, extended length of hospital stay, and long-term cognitive dysfunction. The diagnosis of SAE is based on clinical assessments, but a valid biomarker to identify and confirm SAE and to assess SAE severity is missing. Several blood-based biomarkers indicating neuronal injury have been evaluated in sepsis and their potential role as early diagnosis and prognostic markers has been studied. Among those, the neuroaxonal injury marker neurofilament light chain (NfL) was identified to potentially serve as a prognostic biomarker for SAE and to predict long-term cognitive impairment. In this review, we summarize the current knowledge of biomarkers, especially NfL, in SAE and discuss a possible future clinical application considering existing limitations.

Abstract Background Sepsis-associated encephalopathy (SAE) is frequent in septic patients. Electroencephalography (EEG) is very sensitive to detect early epileptic abnormalities, such as seizures and periodic discharges (PDs), and to quantify their duration (the so-called burden). However, the prevalence of these EEG abnormalities in septic patients, as well as their effect on morbidity and mortality, are still unclear. The aims of this study were to assess whether the presence of electrographic abnormalities (i.e. the absence of reactivity, the presence and burden of seizures and PDs) was associated with functional outcome and mortality in septic patients and whether these abnormalities were associated with sepsis-associated encephalopathy (SAE). Methods We prospectively included septic patients, without known chronic or acute intracranial disease or pre-existing acute encephalopathy, requiring ICU admission in a tertiary academic centre. Continuous EEG monitoring was started within 72 h after inclusion and performed for up to 7 days. A comprehensive assessment of consciousness and delirium was performed twice daily by a trained neuropsychologist. Primary endpoints were unfavourable functional outcome (UO, defined as a Glasgow Outcome Scale-Extended—GOSE—score

Summary: Background: Paediatric Huntington disease with highly expanded mutations (HE-PHD; >80 CAG repeats) presents atypically, compared to adult-onset Huntington disease (AOHD), with neurodevelopmental delay, epilepsy, abnormal brain glucose metabolism, early striatal damage, and reduced lifespan. Since genetic GLUT-1 deficiency syndrome shows a symptom spectrum similar to HE-PHD, we investigated the potential role of the two main glucose transporters, GLUT-1 and GLUT-3, in HE-PHD. Methods: We compared GLUT-1 and GLUT-3 protein expression in HE-PHD, juvenile-onset (JOHD), and AOHD brains (n = 2; n = 3; n = 6) and periphery (n = 3; n = 2; n = 2) versus healthy adult controls (n = 6; n = 6). We also investigated mitochondrial complexes and hexokinase-II protein expression. Findings: GLUT-1 and GLUT-3 expression were significantly lower in HE-PHD frontal cortex (p = 0.009, 95% [CI 13.4, 14.7]; p = 0.017, 95% [CI 14.2, 14.5]) versus controls. In fibroblasts, GLUT-1 and GLUT-3 expression were lower compared to controls (p

Sepsis is the most common cause of admission to intensive care units worldwide. Sepsis patients frequently suffer from sepsis-associated encephalopathy (SAE) reflecting acute brain dysfunction. SAE may result in increased mortality, extended length of hospital stay, and long-term cognitive dysfunction. The diagnosis of SAE is based on clinical assessments, but a valid biomarker to identify and confirm SAE and to assess SAE severity is missing. Several blood-based biomarkers indicating neuronal injury have been evaluated in sepsis and their potential role as early diagnosis and prognostic markers has been studied. Among those, the neuroaxonal injury marker neurofilament light chain (NfL) was identified to potentially serve as a prognostic biomarker for SAE and to predict long-term cognitive impairment. In this review, we summarize the current knowledge of biomarkers, especially NfL, in SAE and discuss a possible future clinical application considering existing limitations. [ABSTRACT FROM AUTHOR]

Background: Sepsis-associated encephalopathy (SAE) is frequent in septic patients. Electroencephalography (EEG) is very sensitive to detect early epileptic abnormalities, such as seizures and periodic discharges (PDs), and to quantify their duration (the so-called burden). However, the prevalence of these EEG abnormalities in septic patients, as well as their effect on morbidity and mortality, are still unclear. The aims of this study were to assess whether the presence of electrographic abnormalities (i.e. the absence of reactivity, the presence and burden of seizures and PDs) was associated with functional outcome and mortality in septic patients and whether these abnormalities were associated with sepsis-associated encephalopathy (SAE). Methods: We prospectively included septic patients, without known chronic or acute intracranial disease or pre-existing acute encephalopathy, requiring ICU admission in a tertiary academic centre. Continuous EEG monitoring was started within 72 h after inclusion and performed for up to 7 days. A comprehensive assessment of consciousness and delirium was performed twice daily by a trained neuropsychologist. Primary endpoints were unfavourable functional outcome (UO, defined as a Glasgow Outcome Scale-Extended—GOSE—score < 5), and mortality collected at hospital discharge and secondary endpoint was the association of PDs with SAE. Mann–Whitney, Fisher's exact and χ2 tests were used to assess differences in variables between groups, as appropriate. Multivariable logistic regression analysis with in-hospital mortality, functional outcome, SAE or PDs as the dependent variables were performed. Results: We included 92 patients. No seizures were identified. Nearly 25% of patients had PDs. The presence of PDs and PDs burden was associated with UO in univariate (n = 15 [41%], p = 0.005 and p = 0.008, respectively) and, for PDs presence, also in multivariate analysis after correcting for disease severity (OR 3.82, IC 95% [1.27–11.49], p = 0.02). The PDs burden negatively correlated with GOSE (Spearman's coefficient ρ = − 0.2, p = 0.047). The presence of PDs was also independently associated with SAE (OR 8.98 [1.11–72.8], p = 0.04). Reactivity was observed in the majority of patients and was associated with outcomes (p = 0.044 for both functional outcome and mortality). Conclusion: Our findings suggest that PDs and PDs burden are associated with SAE and might affect outcome in septic patients. [ABSTRACT FROM AUTHOR]

Brain functions are mediated via the complex interplay between several complex factors, and hence, identifying the underlying cause of an abnormality within a certain brain region can be challenging. In mitochondrial disease, abnormalities in brain function are thought to be attributed to accumulation of mitochondrial DNA (mtDNA) with pathogenic mutations; however, only few previous studies have directly demonstrated that accumulation of mutant mtDNA induced abnormalities in brain function. Herein, we examined the effects of mtDNA mutations on brain function via behavioral analyses using a mouse model with an A2748G point mutation in mtDNA tRNA Leu(UUR) . Our results revealed that mice with a high percentage of mutant mtDNA showed a characteristic trend toward reduced prepulse inhibition and memory-dependent test performance, similar to that observed in psychiatric disorders, such as schizophrenia; however, muscle strength and motor coordination were not markedly affected. Upon examining the hippocampus and frontal lobes of the brain, mitochondrial morphology was abnormal, and the brain weight was slightly reduced. These results indicate that the predominant accumulation of a point mutation in the tRNA Leu(UUR) gene may affect brain functions, particularly the coordination of sensory and motor functions and memory processes. These abnormalities probably caused by both direct effects of accumulation of the mutant mtDNA in neuronal cells and indirect effects via changes of systemic extracellular environments. Overall, these findings will lead to a better understanding of the pathogenic mechanism underlying this complex disease and facilitate the development of optimal treatment methods. [Display omitted] • mtDNA mutations can affect brain function. • Accumulation of mtDNA with A2748G mutation cause reduced prepulse inhibition. • Accumulation of mtDNA with A2748G mutation cause reduced memory-dependent performance. • Abnormal mitochondrial morphology and reduced brain weight were observed in mice. • The results improve understanding of effects of mtDNA mutation on brain function. [ABSTRACT FROM AUTHOR]

Background: Audiovisual stimulation, such as auditory stimulation, light stimulation, and audiovisual combined stimulation, as a non‐invasive stimulation, which can induce gamma oscillation, has received increased attention in recent years, and it has been preliminarily applied in the clinical rehabilitation of brain dysfunctions, such as cognitive, language, motor, mood, and sleep dysfunctions. However, the exact mechanism underlying the therapeutic effect of 40‐Hz audiovisual stimulation remains unclear; the clinical applications of 40‐Hz audiovisual stimulation in brain dysfunctions rehabilitation still need further research. Objective: In order to provide new insights into brain dysfunction rehabilitation, this review begins with a discussion of the mechanism underlying 40‐Hz audiovisual stimulation, followed by a brief evaluation of its clinical application in the rehabilitation of brain dysfunctions. Results: Currently, 40‐Hz audiovisual stimulation was demonstrated to affect synaptic plasticity and modify the connection status of related brain networks in animal experiments and clinical trials. Although its promising efficacy has been shown in the treatment of cognitive, mood, and sleep impairment, research studies into its application in language and motor dysfunctions are still ongoing. Conclusions: Although 40‐Hz audiovisual stimulation seems to be effective in treating cognitive, mood, and sleep disorders, its role in language and motor dysfunctions has yet to be determined. [ABSTRACT FROM AUTHOR]

Background and purpose: Hepatitis C virus (HCV) infection is associated with neuropsychiatric disturbances that impact on functioning and health‐related quality of life (HRQoL). Reversibility at different liver disease stages is unknown, particularly in cirrhosis. We aimed to evaluate cognition, functioning, and HRQoL following HCV eradication at different liver disease stages. Methods: A random sample (n = 152) of consecutive patients treated with direct‐acting antiviral agents (DAAs) between April 2015 and March 2017 were included. A comprehensive neuropsychological assessment, functioning and HRQoL questionnaires were applied at baseline, and 12 and 48 weeks after the end of antivirals. Results: One‐hundred thirty‐five patients who achieved virological response completed the follow‐up, of whom 44 had cirrhosis (27% decompensated). Twenty‐one percent had cognitive impairment before starting DAAs (34.1% cirrhotic vs. 14.4% noncirrhotic, p < 0.011). Viral eradication was associated with a decrease in cognitive impairment to 23% of cirrhotic and 6% of noncirrhotic patients (p < 0.05). Interestingly, older patients (B = 0.11, 95% confidence interval [CI] = 0.03–0.19) with baseline cognitive impairment (B = 3.58, 95% CI = 1.54–5.62) were those with higher cognitive benefit, regardless of liver disease. Persistent cognitive impairment was associated with having higher cardiovascular risk, cirrhosis, lower education, and higher anxiety and depression scores. Functioning and HRQoL also improved after eradication but remained worse in the cirrhotic group. Conclusions: Viral eradication decreases the prevalence of cognitive impairment and improves functioning and HRQoL. Patients with lower brain reserve (older patients) and baseline cognitive impairment may benefit the most. Identification and treatment of HCV patients through screening programs may reduce the burden of cognitive disturbances beyond the prevention of liver disease progression. [ABSTRACT FROM AUTHOR]

Sepsis susceptibility is significantly increased in patients with intracerebral hemorrhage (ICH), owing to immunosuppression and intestinal microbiota dysbiosis. To date, ICH with sepsis occurrence is still difficult for clinicians to deal with, and the mortality, as well as long-term cognitive disability, is still increasing. Actually, intracerebral hemorrhage and sepsis are mutually exacerbated via similar pathophysiological mechanisms, mainly consisting of systemic inflammation and circulatory dysfunction. The main consequence of these two processes is neural dysfunction and multiple organ damages, notably, via oxidative stress and neurotoxic mediation under the mediation of central nervous system activation and blood-brain barrier disruption. Besides, the comorbidity-induced multiple organ damages will produce numerous damage-associated molecular patterns and consequently exacerbate the severity of the disease. At present, the prospective views are about operating artificial restriction for the peripheral immune system and achieving cross-tolerance among organs via altering immune cell composition to reduce inflammatory damage. [ABSTRACT FROM AUTHOR]

Abstract Background Alteration of the mechanisms of cerebral blood flow (CBF) regulation might contribute to the pathophysiology of sepsis-associated encephalopathy (SAE). However, previous clinical studies on dynamic cerebral autoregulation (dCA) in sepsis had several cofounders. Furthermore, little is known on the potential impairment of neurovascular coupling (NVC) in sepsis. The aim of our study was to determine the presence and time course of dCA and NVC alterations in a clinically relevant animal model and their potential impact on the development of SAE. Methods Thirty-six anesthetized, mechanically ventilated female sheep were randomized to sham procedures (sham, n = 15), sepsis (n = 14), or septic shock (n = 7). Blood pressure, CBF, and electrocorticography were continuously recorded. Pearson’s correlation coefficient Lxa and transfer function analysis were used to estimate dCA. NVC was assessed by the analysis of CBF variations induced by cortical gamma activity (Eγ) peaks and by the magnitude-squared coherence (MSC) between the spontaneous fluctuations of CBF and Eγ. Cortical function was estimated by the alpha-delta ratio. Wilcoxon signed rank and rank sum tests, Friedman tests, and RMANOVA test were used as appropriate. Results Sepsis and sham animals did not differ neither in dCA nor in NVC parameters. A significant impairment of dCA occurred only after septic shock (Lxa, p = 0.03, TFA gain p = 0.03, phase p = 0.01). Similarly, NVC was altered during septic shock, as indicated by a lower MSC in the frequency band 0.03–0.06 Hz (p < 0.001). dCA and NVC impairments were associated with cortical dysfunction (reduction in the alpha-delta ratio (p = 0.03)). Conclusions A progressive loss of dCA and NVC occurs during septic shock and is associated with cortical dysfunction. These findings indicate that the alteration of mechanisms controlling cortical perfusion plays a late role in the pathophysiology of SAE and suggest that alterations of CBF regulation mechanisms in less severe phases of sepsis reported in clinical studies might be due to patients’ comorbidities or other confounders. Furthermore, a mean arterial pressure targeting therapy aiming to optimize dCA might not be sufficient to prevent neuronal dysfunction in sepsis since it would not improve NVC.

Objective To investigate the dysregulated genes, pathways and networks involved in type 2 diabetes-derived brain dysfunctions via performing whole transcriptome sequencing on the cerebral cortex of db/db and wild-type (WT) mice. Methods Male db/db and WT mice were divided into two groups (n=9). The body weight and blood glucose were measured at week 8 and 24. The 24-week-old animals were sacrificed for cerebral cortex collection. RNA-sequencing and analysis of differentially expressed genes (DEGs), GO functional enrichment, KEGG pathway enrichment and PPI network were performed. Results A total of 306 differential transcripts, including 178 up-regulated and 128 down-regulated ones were identified in the db/db mice as compared to WT ones. Among all differentially expressed genes, 43 genes (such as Clcnka and Trim17) were found to be up-regulated and 59 genes (such as Arih1 and Nectin-3) were down-regulated. The protein-protein interaction network was constructed with thirteen nodes as hub genes. All the nodes were down-regulated genes and majorly belonged to mitochondrially encoded families. The GO functional enrichment showed changes in various categories as compared to WT. KEGG enrichment analysis revealed that target genes were mainly enriched in metabolic pathways, Parkinson's disease, Alzheimer's disease, and the involved DEGs mainly regulate oxidative phosphorylation process. Conclusions The relationship between type 2 diabetes and central nervous system impairments, and the potentially related genes, pathways and networks are identified.

Sepsis susceptibility is significantly increased in patients with intracerebral hemorrhage (ICH), owing to immunosuppression and intestinal microbiota dysbiosis. To date, ICH with sepsis occurrence is still difficult for clinicians to deal with, and the mortality, as well as long-term cognitive disability, is still increasing. Actually, intracerebral hemorrhage and sepsis are mutually exacerbated via similar pathophysiological mechanisms, mainly consisting of systemic inflammation and circulatory dysfunction. The main consequence of these two processes is neural dysfunction and multiple organ damages, notably, via oxidative stress and neurotoxic mediation under the mediation of central nervous system activation and blood-brain barrier disruption. Besides, the comorbidity-induced multiple organ damages will produce numerous damage-associated molecular patterns and consequently exacerbate the severity of the disease. At present, the prospective views are about operating artificial restriction for the peripheral immune system and achieving cross-tolerance among organs via altering immune cell composition to reduce inflammatory damage.

Aims: To explore the safety and efficacy of normobaric oxygen (NBO) on correcting chronic cerebral ischemia (CCI) and related EEG anomalies. Methods: This prospective randomized trial (NCT03745092) enrolled 50 cases of CCI patients, which were divided into NBO (8 L/min of oxygen supplement) group and control group (room air) randomly, and also enrolled 21 healthy volunteers. Two times of 30‐min EEG recordings with the interval of 45min of NBO or room air were analyzed quantitatively. Results: The CCI‐mediated EEG presented with two patterns of electrical activities: high‐power oscillations (high‐power EEG, n = 26) and paroxysmal slow activities under the normal‐power background (normal‐power EEG, n = 24). The fronto‐central absolute power (AP) of the beta, alpha, theta, and delta in the high‐power EEG was higher than that in healthy EEG (p < 0.05). The fronto‐central theta/alpha, delta/alpha and (delta + theta)/(alpha + beta) ratios in the normal‐power EEG were higher than those in healthy EEG (p < 0.05). The high‐power EEG in NBO group had higher fronto‐central AP reduction rates than those in control group (p < 0.05). NBO remarkably reduced the fronto‐central theta/alpha, delta/alpha, and (delta + theta)/(alpha + beta) ratios in the normal‐power EEG (p < 0.05). Conclusions: NBO rapidly ameliorates CCI‐mediated EEG anomalies, including attenuation of the abnormal high‐power oscillations and the paroxysmal slow activities associated with CCI. [ABSTRACT FROM AUTHOR]

Although COVID-19 affects the respiratory system, extrapulmonary manifestations frequently occur, including encephalopathy and liver damage. Here, we want to call attention to a possible connection between liver and brain dysfunctions, in which ammonia can play a role targeting astrocytes. Importantly, astrocyte dysfunction can produce future and/or long-term neurological consequences.

The article presents a neuropsychological analysis of aggressive manifestations of normal personality and aggression of persons with brain dysfunction. Theoretical analysis of foreign and domestic works on neuropsychological correction of aggressive behavior is carried out. The neuropsychological program on correctional and prophylactic work for persons with affective-personal disorders is offered, considering the peculiarities of determination of aggressive manifestations of personality. The essence of the concept of "aggression" is specified. The types and functions of aggression of personality of different nature are considered: positive, ambivalent, negative. The neuropsychological causes of aggression in connection with the conditionality of aggression by situational and individual and psychological personal factors according to the scheme "personality - aggressive reaction - situation - neuropsychological factor" are clarified. The multifactorial (combination of neuropsychological and social conditions of a formation of aggression) genesis of aggressive behavior in personality disorders, the basis of which is the destructive level of anxiety, which originates from childhood, is analyzed. The integration of neuropsychological and socio-psychological approaches to the study of the problem of aggression is presented. [ABSTRACT FROM AUTHOR]

Cerebral venous outflow disturbance (CVOD) has begun to garner the attention of researches owing to a series of clinical symptoms that impose a significant impact on people's quality of life. Herein, we aimed to investigate whether normobaric oxygen (NBO) can ameliorate CVOD-induced neurological symptoms. This was one part of the prospective trial registered in ClinicalTrials.gov (NCT03373292). A total of 37 CVOD patients were divided into the NBO group (5–8 L/min of oxygen inhalation, 1 h per time, 3 times daily, n = 19) and the control group (without oxygen inhalation, n = 18) randomly. The assessments were performed at admission, 1-week hospitalization, and 6-month follow-up. Quantitative electroencephalogram (qEEG) data were recorded prior to and post 1 h of NBO in some patients. R software was used for data analysis. No NBO-related adverse events were observed during the whole NBO intervention process. The 1-week Patient Global Impression of Change (PGIC) scale showed that the symptom improvement occurred in nine patients in the NBO group (47.4%) while none in the control group (p = 0.001). NBO could improve headache evaluated with visual analog scale (pre-NBO vs. post-NBO: 4.70 ± 2.16 vs. 2.90 ± 2.03, p = 0.024) and Headache Impact Test-6 (53.40 ± 12.15 vs. 50.30 ± 13.04, p = 0.041). As for 6-month PGIC follow-up, eight out of 14 cases (57.1%) in the NBO group reported improvement, while only one out of 12 patients in the control group replied mild improvement (p = 0.014). The qEEG revealed that NBO reduced the ratio of theta to alpha power (0.65 ± 0.38 vs. 0.56 ± 0.35, p = 0.030) over the fronto-central electrodes. To sum up, NBO may be a safe and effective approach to attenuate CVOD-related symptoms (especially for headache) by brain functional improvement resulting from increasing oxygen supply to the brain tissues.

Abstract Background Sepsis-associated brain dysfunction (SABD) is associated with high morbidity and mortality. The pathophysiology of SABD is multifactorial. One hypothesis is that impaired cerebral autoregulation (CAR) may result in brain hypoperfusion and neuronal damage leading to SABD. Methods We studied 100 adult patients with sepsis (July 2012–March 2017) (age = 62 [52–71] years; Acute Physiology and Chronic Health Evaluation II score on admission = 21 [15–26]). Exclusion criteria were acute or chronic intracranial disease, arrhythmias, extracorporeal membrane oxygenation, and known intra- or extracranial supra-aortic vessel disease. The site of infection was predominantly abdominal (46%) or pulmonary (28%). Transcranial Doppler was performed, insonating the left middle cerebral artery with a 2-MHz probe. Middle cerebral artery blood flow velocity (FV) and arterial blood pressure (ABP) signals were recorded simultaneously; Pearson’s correlation coefficient (mean flow index [Mxa]) between ABP and FV was calculated using MATLAB. Impaired CAR was defined as Mxa > 0.3. Results Mxa was 0.29 [0.05–0.62]. CAR was impaired in 50 patients (50%). In a multiple linear regression analysis, low mean arterial pressure, history of chronic kidney disease and fungal infection were associated with high Mxa. SABD was diagnosed in 57 patients (57%). In a multivariable analysis, altered cerebral autoregulation, mechanical ventilation and history of vascular disease were independent predictors of SABD. Conclusions Cerebral autoregulation was altered in half of the patients with sepsis and was associated with the development of SABD. These findings support the concept that cerebral hypoxia could contribute to the development of SABD.

Purpose: We aimed to describe the association between prehospital frailty (PHF), acute organ dysfunction (AOD), and posthospital disability (PHD) outcome in older adults admitted to the intensive care unit (ICU). Methods: In a prospective observational cohort study, we assessed PHF using the Clinical Frailty Scale (CFS) and assessed the level of AOD using Sequential Organ Failure Assessment (SOFA) scores on ICU day 1. We assessed Activities of Daily Living disability levels through to 6 months after discharge and used generalized estimating equations (log link and negative binomial family) to determine the independent association of PHF and AOD with PHD. Results: Of the 302 patients enrolled, 221 (73.1%) survived the hospitalization. Prehospital frailty was associated with PHD (adjusted incident rate ratio [aIRR] 95% confidence interval [95% CI] per unit increase in CFS 1.38 [1.15-1.67], P = .001). Total day 1 SOFA score was weakly associated with PHD, (aIRR [95% CI] 1.05 [1.00-1.10], P = .037) while day 1 SOFA neurologic score was strongly associated with PHD (aIRR [95% CI] 1.42 [1.24-1.62] per unit increase in SOFA neurologic score, P < .001), and these effects were independent of PHF and other premorbid factors. Conclusions: Both PHF and early acute brain dysfunction are important factors associated with increasing PHD in older adults who survive critical illness. [ABSTRACT FROM AUTHOR]

Cerebral venous outflow disturbance (CVOD) has begun to garner the attention of researches owing to a series of clinical symptoms that impose a significant impact on people's quality of life. Herein, we aimed to investigate whether normobaric oxygen (NBO) can ameliorate CVOD-induced neurological symptoms. This was one part of the prospective trial registered in ClinicalTrials.gov (NCT03373292). A total of 37 CVOD patients were divided into the NBO group (5–8 L/min of oxygen inhalation, 1 h per time, 3 times daily, n = 19) and the control group (without oxygen inhalation, n = 18) randomly. The assessments were performed at admission, 1-week hospitalization, and 6-month follow-up. Quantitative electroencephalogram (qEEG) data were recorded prior to and post 1 h of NBO in some patients. R software was used for data analysis. No NBO-related adverse events were observed during the whole NBO intervention process. The 1-week Patient Global Impression of Change (PGIC) scale showed that the symptom improvement occurred in nine patients in the NBO group (47.4%) while none in the control group (p = 0.001). NBO could improve headache evaluated with visual analog scale (pre-NBO vs. post-NBO: 4.70 ± 2.16 vs. 2.90 ± 2.03, p = 0.024) and Headache Impact Test-6 (53.40 ± 12.15 vs. 50.30 ± 13.04, p = 0.041). As for 6-month PGIC follow-up, eight out of 14 cases (57.1%) in the NBO group reported improvement, while only one out of 12 patients in the control group replied mild improvement (p = 0.014). The qEEG revealed that NBO reduced the ratio of theta to alpha power (0.65 ± 0.38 vs. 0.56 ± 0.35, p = 0.030) over the fronto-central electrodes. To sum up, NBO may be a safe and effective approach to attenuate CVOD-related symptoms (especially for headache) by brain functional improvement resulting from increasing oxygen supply to the brain tissues. [ABSTRACT FROM AUTHOR]

Background: Alteration of the mechanisms of cerebral blood flow (CBF) regulation might contribute to the pathophysiology of sepsis-associated encephalopathy (SAE). However, previous clinical studies on dynamic cerebral autoregulation (dCA) in sepsis had several cofounders. Furthermore, little is known on the potential impairment of neurovascular coupling (NVC) in sepsis. The aim of our study was to determine the presence and time course of dCA and NVC alterations in a clinically relevant animal model and their potential impact on the development of SAE. Methods: Thirty-six anesthetized, mechanically ventilated female sheep were randomized to sham procedures (sham, n = 15), sepsis (n = 14), or septic shock (n = 7). Blood pressure, CBF, and electrocorticography were continuously recorded. Pearson's correlation coefficient Lxa and transfer function analysis were used to estimate dCA. NVC was assessed by the analysis of CBF variations induced by cortical gamma activity (Eγ) peaks and by the magnitude-squared coherence (MSC) between the spontaneous fluctuations of CBF and Eγ. Cortical function was estimated by the alpha-delta ratio. Wilcoxon signed rank and rank sum tests, Friedman tests, and RMANOVA test were used as appropriate. Results: Sepsis and sham animals did not differ neither in dCA nor in NVC parameters. A significant impairment of dCA occurred only after septic shock (Lxa, p = 0.03, TFA gain p = 0.03, phase p = 0.01). Similarly, NVC was altered during septic shock, as indicated by a lower MSC in the frequency band 0.03–0.06 Hz (p < 0.001). dCA and NVC impairments were associated with cortical dysfunction (reduction in the alpha-delta ratio (p = 0.03)). Conclusions: A progressive loss of dCA and NVC occurs during septic shock and is associated with cortical dysfunction. These findings indicate that the alteration of mechanisms controlling cortical perfusion plays a late role in the pathophysiology of SAE and suggest that alterations of CBF regulation mechanisms in less severe phases of sepsis reported in clinical studies might be due to patients' comorbidities or other confounders. Furthermore, a mean arterial pressure targeting therapy aiming to optimize dCA might not be sufficient to prevent neuronal dysfunction in sepsis since it would not improve NVC. [ABSTRACT FROM AUTHOR]

ADHD is nowadays a relatively wellestablished diagnostic category that has been in the literature for nearly 150 years. This review provides an overview of the development of this term from the first mentions of related symptomatology starting at the turn from the 18th to 19th century, over concepts in 20th century, especially in the sense of Minimal brain damage and Minimal brain dysfunction up to the present. It focuses in depth on the concepts that went beyond the actual definition of ADHD in DSM-III in 1980. The development of this diagnostic category from DSM-II to the current definition in DSM-5 is also described. As well as development of the diagnostical category "Hyperkinetic disorder" published in ICD 10. The article summarises complex overview of advances in understanding and diagnostical definition of neurodevelopmental disorder ADHD. [ABSTRACT FROM AUTHOR]

Objective: The objective was to compare the executive functions between hypertensive and non-hypertensive middle-aged Mexican adults. Methods: An observational and analytic study was designed. Participants were men and women residents of Southeastern Mexico, aged between 40 and 60 years, with at least 5 years of hypertension diagnosis. The control group was people without hypertension. All participants completed a digit symbol substitution test (DSST), clinical and epidemiological data. Statistical analysis unpaired Student's t-test, p < 0.05. Results: DSST score in control men was 37.78 ± 11.94, control women: 42.96 ± 11.19, hypertensive men: 16.81 ± 9.82, and hypertensive women: 26.88 ± 12.04. Significant differences were found between hypertensive and non-hypertensive groups. Men had worse scores than women. No difference between normotensive men and women. Inverse correlation was found between DSST score and age, values of systolic and diastolic blood tension in the hypertension group. Conclusion: Hypertension decreases the executive function in middle-aged people, mainly in men. This dysfunction could be an early indicator of brain deterioration. [ABSTRACT FROM AUTHOR]

Background: Sepsis-induced brain dysfunction (SIBD) is often encountered in sepsis patients and is related to increased morbidity. No specific tests are available for SIBD, and neuroimaging findings are often normal. In this study, our aim was to analyze the diagnostic value of volumetric analysis of the brain structures and to find out its significance as a prognostic measure.Methods: In this prospective observational study, brain magnetic resonance imaging (MRI) sections of 25 consecutively enrolled SIBD patients (17 with encephalopathy and 8 with coma) and 22 healthy controls underwent volumetric evaluation by an automated segmentation method.Results: Ten SIBD patients had normal MRI, and 15 patients showed brain lesions or atrophy. The most prominent volume reduction was found in cerebral and cerebellar white matter, cerebral cortex, hippocampus, and amygdala, whereas deep gray matter regions and cerebellar cortex were relatively less affected. SIBD patients with normal MRI showed significantly reduced volumes in hippocampus and cerebral white matter. Caudate nuclei, putamen, and thalamus showed lower volume values in non-survivor SIBD patients, and left putamen and right thalamus showed a more pronounced volume reduction in coma patients.Conclusions: Volumetric analysis of the brain appears to be a sensitive measure of volumetric changes in SIBD. Volume reduction in specific deep gray matter regions might be an indicator of unfavorable outcome. [ABSTRACT FROM AUTHOR]

Objective: Acute brain dysfunction is common in sepsis patients and is associated with increased mortality. This study aimed to investigate the clinical and electroencephalographic (EEG) findings of patients with acute neurological dysfunction due to sepsis and to evaluate their relationship with prognosis. Methods: Sixty-one patients with sepsis were included in this prospective observational study. All patients underwent a daily neurological examination. EEG monitoring was performed in patients with delirium, coma, clinical seizures, and focal neurological findings. The patients were divided into two groups as survivors and non-survivors. Results: Sixty-one patients included in the study had a median age of 60 years (range=21 to 81), Acute Physiology and Chronic Health Evaluation 2 score of 24 (range=14 to 39), and Sepsis-related Organ Failure Assessment score of 10 (range=3 to 24). During the EEG examination, coma was detected in 23 patients (38%), delirium/confusion in 20 patients (33%), clinical seizures in 16 patients (26%) and focal neurological findings in two patients (3%). The overall mortality rate was 42% (n=26). The EEG examination showed slowing of background activity in all patients. Also, among three patients who had seizure activity, two showed findings of an electrophysiological seizure. The EEG examination revealed a relationship between low-amplitude non-reactive background activity and mortality. Conclusion: EEG monitoring may be indicated in the follow-up of encephalopathy in sepsis, the determination of the severity of the disease, the presence of an accompanying seizure or status, and prognosis. [ABSTRACT FROM AUTHOR]

It has been known that infants less than 1 year develop cerebral white matter (WM) lacerations associated with head trauma, however, there has been no report of similar WM lesions over 1 year. We report three teenage boys (11, 12, and 18 years at final MRI studies) with acquired WM lacerations associated with recurrent head trauma who developed neurologic symptoms such as spastic paralysis, afebrile convulsions, and cognitive impairment. Two of them (patients 1 and 2) were given a diagnosis of autism spectrum disorder and had a history of repeated severe self-inflicted head trauma from preschool age. Patient 3, who practiced karate and boxing from preschool age, showed gradual declining intellectual ability. Brain MRI of the three patients revealed severe lacerations in the bilateral cerebral WM. Previous neuroimaging showed no WM lacerations at 4 and 5 years in patients 1 and 2, or mild WM lacerations at 17 years in patient 3, indicating the WM lacerations could have been acquired in childhood. It is suggested that repetition of head trauma in children can cause cerebral WM lacerations and brain dysfunction. [ABSTRACT FROM AUTHOR]