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OBJECTIVE: To develop a predictive model for thiamine responsive disorders (TRDs) among infants and young children hospitalized with signs or symptoms suggestive of thiamine deficiency disorders (TDDs) based on response to therapeutic thiamine in a high-risk setting. STUDY DESIGN: Children aged 21 days to

Key points The optimal rate of rewarming after therapeutic hypothermia is unclear. Slow rewarming may reduce cardiovascular instability and rebound seizures, but there is little controlled evidence to support this. The present study aimed to determine whether slow rewarming can improve neuroprotection after 72 h of hypothermia. Fetal sheep (0.85 gestation) received sham occlusion (n = 8) or 30 min of global cerebral ischaemia followed by normothermia (n = 7), or hypothermia from 3 to 72 h with either fast, spontaneous rewarming within 1 h (n = 8) or slow rewarming at 0.5°C h−1 over 10 h (n = 8). Hypothermia improved EEG and spectral edge recovery, with no significant difference between fast and slow rewarming. Hypothermia reduced the number of seizures, with no significant difference in seizure activity between fast and slow rewarming. Hypothermia improved neuronal survival in the cortex, CA1, CA3, CA4 and dentate gyrus regions of the hippocampus, with no significant difference between fast and slow rewarming. Hypothermia attenuated microglia counts in the cortex, with no significant difference between fast and slow rewarming. The rate of rewarming after a clinically relevant duration of hypothermia did not affect neurophysiological recovery, neuronal survival or attenuation of microglia after global cerebral ischaemia in term‐equivalent fetal sheep. The rate of rewarming after 72 h of hypothermia did not affect recovery of EEG or spectral edge. There was no difference in the occurrence of seizures as a result of the rate of rewarming after hypothermia. The rate of rewarming after 72 h of hypothermia did not affect neuronal survival in the cortex or hippocampus. [ABSTRACT FROM AUTHOR]

Patatin-like phospholipase domain-containing lipase 8 (PNPLA8), one of the calcium-independent phospholipase A2 enzymes, is involved in various physiological processes through the maintenance of membrane phospholipids. Biallelic variants in PNPLA8 have been associated with a range of paediatric neurodegenerative disorders. However, the phenotypic spectrum, genotype–phenotype correlations and the underlying mechanisms are poorly understood. Here, we newly identified 14 individuals from 12 unrelated families with biallelic ultra-rare variants in PNPLA8 presenting with a wide phenotypic spectrum of clinical features. Analysis of the clinical features of current and previously reported individuals (25 affected individuals across 20 families) showed that PNPLA8 -related neurological diseases manifest as a continuum ranging from variable developmental and/or degenerative epileptic–dyskinetic encephalopathy to childhood-onset neurodegeneration. We found that complete loss of PNPLA8 was associated with the more profound end of the spectrum, with congenital microcephaly. Using cerebral organoids generated from human induced pluripotent stem cells, we found that loss of PNPLA8 led to developmental defects by reducing the number of basal radial glial cells and upper-layer neurons. Spatial transcriptomics revealed that loss of PNPLA8 altered the fate specification of apical radial glial cells, as reflected by the enrichment of gene sets related to the cell cycle, basal radial glial cells and neural differentiation. Neural progenitor cells lacking PNPLA8 showed a reduced amount of lysophosphatidic acid, lysophosphatidylethanolamine and phosphatidic acid. The reduced number of basal radial glial cells in patient-derived cerebral organoids was rescued, in part, by the addition of lysophosphatidic acid. Our data suggest that PNPLA8 is crucial to meet phospholipid synthetic needs and to produce abundant basal radial glial cells in human brain development. [ABSTRACT FROM AUTHOR]

Patients in delirium require trustful communication and re‐orientation. We developed a flyer with positive, re‐orientating suggestions for families of delirious patients in intensive care units. Suggestions include creating a safe environment, interpreting unusual behaviours positively and fostering mental resilience. Additionally, families are encouraged to prioritize their own well‐being, recognizing their crucial role in supporting their loved ones. This flyer offers practical strategies across four key areas: ensuring security and orientation, reframing noises and body experiences, managing agitation and reshaping perceptions. By equipping families with knowledge and tools, this resource aims to promote understanding, resilience and strength to humanize delirium care. [ABSTRACT FROM AUTHOR]

Encephalopathy is part of the clinical triad of Susac syndrome, but a detailed understanding of the neurocognitive and neuropsychiatric profile of this condition is lacking. Existing literature indicates that cognitive deficits range in severity from subtle to profound. Executive function and short-term recall are affected frequently. Psychiatric manifestations may be absent or may include anxiety, mood disorders or psychosis. If psychiatric phenomena develop during the disease course, it can be hard to disentangle whether symptoms directly relate to the pathology of Susac syndrome or are secondary to treatment-related side effects. In this article, we review what is known about the cognitive and psychiatric morbidity of Susac syndrome and identify areas where knowledge is deficient. Importantly, we also provide a framework for future research, arguing that better phenotyping, understanding of pathophysiology, evaluation of treatments on cognitive and psychiatric outcomes, and longitudinal data capture are vital to improving patient outcomes. [ABSTRACT FROM AUTHOR]

Background: Mild encephalitis/encephalopathy with reversible splenial lesion (MERS) is a clinical-radiological syndrome characterized by transient central nervous system symptoms and a reversible lesion in the splenium of the corpus callosum (SCC) on magnetic resonance (MR). We reported a case of adult-onset MERS with uncommon presentation and reviewed the existing literature. Methods: We described a case of adult-onset MERS with uncommon symptoms and signs and performed a systematic review of case series including more than four patients of adult-onset (> 14 years old) MERS, from January 2000 to December 2022. We summarized the clinical, laboratory, imaging and therapy data. Results: We included seven eligible studies for a total of 51 adult-onset MERS patients. Neurological manifestations were preceded by prodromal symptoms in most of the patients (88%), mainly with fever (78%). Headache was the most common symptom (50%), followed by seizures (22%) and disturbance of consciousness (22%). Inflammatory changes on cerebrospinal fluid were present in a half of patient, so defining encephalitis cases. Clinal recovery, was achieved in all patients but two with severe disturbance of consciousness who required ventilator support in the acute phase. MR showed isolated lesion in the SCC in 92% of patients, while 8% of patients showed also extracallosal lesions, all the lesions resolved or improved on follow-up imaging. Conclusions: MERS is a form of encephalitis/encephalopathy with a broad range of central nervous system manifestation, often with mild symptoms, such as headache alone, that can lead to overlooked some cases, with an excellent prognosis in most patient. [ABSTRACT FROM AUTHOR]

Neuroinflammation and oxidative stress contribute to the progression of sepsis-associated encephalopathy (SAE). Angiotensin-converting enzyme 2 (ACE2) is considered to be a neuroprotective factor due to its anti-inflammatory and antioxidant properties. However, the role of ACE2 on myeloid cells in regulating SAE and the underlying mechanism warrants further exploration. SAE was induced in ACE2 transgenic (TG), knockout (KO), and bone marrow (BM) chimeric mice by cecal ligation and puncture (CLP). The expression levels of apoptosis-, oxidation- and neuroinflammation-associated mediators and morphological changes were monitored by quantitative real-time PCR analyses and histological examinations in the cortex of septic mice. The contents of angiotensin (Ang) II and Ang-(1–7) along with the activity of ACE2 were examined with commercial kits. The expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and Sestrin2 was detected by immunoblotting analysis. Our results indicated that the expression of cortical ACE2 was significantly reduced in the early phase of CLP-induced sepsis. Moreover, ACE2 overexpression in TG mice conferred neuroprotection against sepsis, as evidenced by alleviated neuronal apoptosis, oxidative stress, and proinflammatory M1-like microglial polarization, accompanied by upregulation of the Ang-(1–7), Nrf2, and Sestrin2 protein levels. Conversely, ACE2 deficiency in KO mice exacerbated SAE. The neuroprotective effects of ACE2 were further confirmed in wild-type mice transplanted with ACE2-TG and KO BM cells. Therefore, our data suggest that myeloid ACE2 exerts a protective role in the pathogenesis of SAE, potentially by activating Ang-(1–7)-Nrf2/sestrin2 signaling pathway, and highlight that upregulating ACE2 expression and activity may represent a promising approach for the treatment of SAE in patients with sepsis. [ABSTRACT FROM AUTHOR]

Copyright of Monatsschrift Kinderheilkunde is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Lead encephalopathy, while thankfully rare, is a devastating and potentially fatal consequence of lead intoxication. Owing to successful public health measures, severe lead toxicity is not often encountered by most practicing physicians in the United States, making both its recognition and management challenging. Article summary: A case study of a 4-year-old female presenting in refractory status epilepticus, found to have severe microcytic anemia and lead level > 100 mcg/dL. Case presentation: We report a case of a 4-year-old girl who presented with refractory seizures, severe microcytic anemia, and a history of developmental delay who was ultimately diagnosed with lead encephalopathy, requiring multiple courses of calcium disodium ethylenediaminetetraacetic acid (EDTA) and succimer for rebounding lead levels. Conclusion: Rapid recognition and appropriate management is essential to ensure neurologically intact survival. This case documents one of the first cases of successful lead chelation after multiple courses of calcium disodium EDTA and succimer dual therapy since the removal of dimercaprol from the United States market. This case also highlights the importance of using body surface area dosing for chelation therapy in order to prevent under-dosing in young children. [ABSTRACT FROM AUTHOR]

Sepsis-associated encephalopathy (SAE) is a frequent and severe complication in septic patients, characterized by diffuse brain dysfunction resulting from systemic inflammation. Accurate prediction of long-term mortality in these patients is critical for improving clinical outcomes and guiding treatment strategies. We conducted a retrospective cohort study using the MIMIC IV database to identify adult patients diagnosed with SAE. Patients were randomly divided into a training set (70%) and a validation set (30%). Least absolute shrinkage and selection operator regression and multivariate logistic regression were employed to identify significant predictors of 1-year mortality, which were then used to develop a prognostic nomogram. The model's discrimination, calibration, and clinical utility were assessed using the area under the receiver operating characteristic curve (AUC), calibration plots, and decision curve analysis, respectively. A total of 3,882 SAE patients were included in the analysis. The nomogram demonstrated strong predictive performance with AUCs of 0.881 (95% CI: 0.865, 0.896) in the training set and 0.859 (95% CI: 0.830, 0.888) in the validation set. Calibration plots indicated good agreement between predicted and observed 1-year mortality rates. The decision curve analysis showed that the nomogram provided greater net benefit across a range of threshold probabilities compared to traditional scoring systems such as Glasgow Coma Scale and Sequential Organ Failure Assessment. Our study presents a robust and clinically applicable nomogram for predicting 1-year mortality in SAE patients. This tool offers superior predictive performance compared to existing severity scoring systems and has significant potential to enhance clinical decision-making and patient management in critical care settings. [ABSTRACT FROM AUTHOR]

Here we critique recent arguments proposing to distinguish ictal from non‐ictal generalized periodic discharges (GPDs) based on etiology and stimulation response, arguing that these are unreliable. We advocate for an empirical approach to GPDs: describe objectively, interpret through medication trials, and base further treatment on response. We call for evidence‐based approaches considering meaningful clinical outcomes. [ABSTRACT FROM AUTHOR]

Case Presentation: This case report documents a unique presentation of hepatic encephalopathy induced by the reactivation of chronic hepatitis B due to Cytomegalovirus (CMV) infection in a 76-year-old female patient. The patient was admitted with a diminished level of consciousness subsequent to a week of anorexia, intermittent fever, chills, postprandial nausea, and vomiting. Laboratory tests revealed significant hepatocellular injury, while imaging suggested cirrhosis. The presence of hepatitis B surface antigen and a detectable hepatitis B virus DNA qualitative analysis was noted, alongside an elevated CMV viral load, indicating the reactivation of chronic hepatitis due to CMV infection. Therapeutic interventions included Ganciclovir for CMV infection, Colistin for an Enterococcus urinary infection, and Tenofovir for hepatitis. Upon stabilization, the patient was discharged for continued medical management. Conclusion: This case highlighted the significance of considering the reactivation of chronic viral hepatitis in the differential diagnosis of hepatic encephalopathy. It underscored the critical role of comprehensive diagnostic investigation in patients presenting with reduced consciousness, especially those with a history of liver disease. Moreover, it emphasized the importance of managing concurrent infections in the context of liver disease and served as a reminder of the potential for CMV to reactivate chronic hepatitis, leading to serious complications, such as hepatic encephalopathy. [ABSTRACT FROM AUTHOR]

Neuronal intranuclear inclusion disease (NIID) is a neurodegenerative disorder represented by eosinophilic intranuclear inclusions (EIIs) and GGC/CGG repeat expansion in the NOTCH2NLC gene. We report here two adult cases of NIID, genetically confirmed, with manifestation of encephalopathy‐like symptoms and address the histopathologic findings obtained by brain biopsies, with a focus on "astrocytic" intranuclear inclusions (AIIs). Case 1 presented with paroxysmal restlessness, vertigo, or fever and was later involved in severe dementia and tetraparesis. Case 2 presented with forgetfulness and then with paroxysmal fever and headache. In both cases, delimited areas with gadolinium enhancement on magnetic resonance imaging and corresponding hyperperfusion were detected, leading to brain biopsies of the cortex. On histology, Case 1 showed an abnormal lamination, where the thickness of layers was different from usual. Both neurons and astrocytes showed some dysmorphologic features. Notably, astrocytes rather than neurons harbored EIIs. Case 2 showed a cortex, where neurons tended to be arrayed in a columnar fashion. Astrocytes showed some dysmorphologic features. Notably, much more astrocytes than neurons harbored EIIs. By a double‐labeling immunofluorescence study for p62/NeuN and p62/glial fibrillary acidic protein, the predominance of AIIs was confirmed in both cases. Considering the physiological functions of astrocytes for the development and maintenance of the cortex, the encephalopathy‐like symptoms, dynamic change of cerebral blood flow, and cortical dysmorphology can reasonably be explained by the dysfunction of EII‐bearing astrocytes rather than EII‐bearing neurons. This study suggests the presence of a subtype of NIID where AIIs rather than "neuronal" intranuclear inclusions are likely a key player in the pathogenesis of NIID, particularly in cases with encephalopathy‐like symptoms. The importance of AIIs ("gliopathy") should be more appreciated in future studies of NIID. [ABSTRACT FROM AUTHOR]

Many coronavirus disease 2019 (COVID‐19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting "brain fog" and mild cognitive impairments even months after the acute phase of infection. Resting‐state EEG abnormalities include EEG slowing (reduced alpha rhythm; increased slow waves) and epileptiform activity. An expert panel conducted a systematic review to present compelling evidence that cognitive deficits due to COVID‐19 and to Alzheimer's disease and related dementia (ADRD) are driven by overlapping pathologies and neurophysiological abnormalities. EEG abnormalities seen in COVID‐19 patients resemble those observed in early stages of neurodegenerative diseases, particularly ADRD. It is proposed that similar EEG abnormalities in Long COVID and ADRD are due to parallel neuroinflammation, astrocyte reactivity, hypoxia, and neurovascular injury. These neurophysiological abnormalities underpinning cognitive decline in COVID‐19 can be detected by routine EEG exams. Future research will explore the value of EEG monitoring of COVID‐19 patients for predicting long‐term outcomes and monitoring efficacy of therapeutic interventions. Highlights: Abnormal intrinsic electrophysiological brain activity, such as slowing of EEG, reduced alpha wave, and epileptiform are characteristic findings in COVID‐19 patients. EEG abnormalities have the potential as neural biomarkers to identify neurological complications at the early stage of the disease, to assist clinical assessment, and to assess cognitive decline risk in Long COVID patients.Similar slowing of intrinsic brain activity to that of COVID‐19 patients is typically seen in patients with mild cognitive impairments, ADRD. Evidence presented supports the idea that cognitive deficits in Long COVID and ADRD are driven by overlapping neurophysiological abnormalities resulting, at least in part, from neuroinflammatory mechanisms and astrocyte reactivity.Identifying common biological mechanisms in Long COVID‐19 and ADRD can highlight critical pathologies underlying brain disorders and cognitive decline. It elucidates research questions regarding cognitive EEG and mild cognitive impairment in Long COVID that have not yet been adequately investigated. [ABSTRACT FROM AUTHOR]

Objective: This systematic review aimed to evaluate the published cases with miliary brain lesions and their etiological factors, clinical manifestations, diagnostic procedures, and outcomes. Methods: A comprehensive search of PubMed, Scopus, Embase, and Google Scholar was conducted using the specified search strategy. Eligibility criteria included cases with miliary lesions in the brain confirmed through neuroimaging and various diagnostic procedures. The PRISMA guidelines were followed, and the PROSPERO registration number for the protocol is CRD42023445849. Results: Data from 130 records provided details of 140 patients. Tuberculosis was the primary cause in 93 cases (66.4%), malignancies in 36 cases (25.7%), and other causes accounted for the remaining 11% cases. Tuberculosis patients averaged 35.7 years old, while those with malignancies averaged 55.44 years. Tuberculosis symptoms primarily included fever, headache, and altered sensorium, whereas malignant cases often exhibited progressive encephalopathy, headache, and specific neurological deficits. Distinctive indicators for CNS tuberculosis were choroidal tubercles and paradoxical reactions. Additionally, 63 tuberculosis patients showed miliary lung shadows and 49 had abnormal CSF findings. For the malignancy group, 13 exhibited miliary lung lesions, and 8 had CSF abnormalities. Regarding outcomes, a significant mortality disparity was observed, with 58.3% in the malignancy group, compared to 10.8% in the tuberculosis group and 27.3% in other cases. Conclusion: Miliary brain lesions are a crucial imaging abnormality that necessitates prompt work up. In an immunocompromised state, diagnostic possibilities of miliary brain lesions are more varied and often pose a bigger challenge. [ABSTRACT FROM AUTHOR]

Aim: COVID‐19 can lead to encephalopathy and loss of consciousness. This double‐blinded randomized clinical trial conducted in Tehran, Iran, aimed to assess the potential effectiveness of modafinil in patients with COVID‐19‐related encephalopathy. Methods: Nineteen non‐intubated COVID‐19 patients with encephalopathy were randomized into two groups: a treatment group receiving crushed modafinil tablets and a placebo group receiving starch powder. Modafinil was administered at a dose of 100 mg every 2 h, reaching a peak dosage of 400 mg. The level of consciousness was assessed using the Glasgow Coma Score (GCS) at multiple time points on the day of medication administration. The trial was registered under IRCT20170903036041N3 on 23/5/2021. Results: The average age in the modafinil and placebo groups was 75.33 and 70 years, respectively. No significant differences were observed between the two groups in terms of chronic conditions, clinical symptoms, or laboratory data. GCS scores were similar between the groups at baseline (p‐value = 0.699). After four doses of modafinil, GCS scores were slightly higher in the treatment group, but this difference was not statistically significant (p‐value = 0.581). GCS scores after each round of drug administration didn't significantly differ between the treatment and placebo groups (p‐value = 0.908). Conclusion: Modafinil exhibited a slight improvement in the level of consciousness among COVID‐19 patients with encephalopathy, although this improvement did not reach statistical significance when compared to the control group. Further research with larger sample sizes and longer treatment durations is recommended to explore modafinil's potential benefits in managing altered consciousness in COVID‐19 patients. [ABSTRACT FROM AUTHOR]

Cytokine release syndrome (CRS) occurs frequently after haplo-identical allogeneic stem cell transplantation (alloSCT) with post-transplant cyclophosphamide (PTCy), increasing nonrelapse mortality (NRM) and decreasing survival. Data on CRS in HLA-matched alloSCT are limited and effects of specific HLA-mismatches on CRS development unknown. We hypothesized that in HLA-matched alloSCT increasing degrees of HLA-mismatching influence CRS incidence, NRM and survival. Retrospective analysis of 126 HLA-matched PTCy-alloSCT patients showed that higher degrees of HLA-mismatching significantly increased CRS incidence (26%, 75% and 90% CRS with 12/12, 10/10 and 9/10 matched donors, respectively). Maximum temperature during CRS increased with higher HLA-mismatch. Specific associations between HLA-mismatches and CRS could be determined. Grade 2 CRS and CRS-induced grade 3 fever were associated with significantly increased NRM (p < 0.001 and p = 0.003, respectively) and inferior survival (p < 0.001 and p = 0.005, respectively). NRM was mainly caused by disease conditions that may be considered CRS-induced inflammatory responses (encephalopathy, cryptogenic organizing pneumonia and multi-organ failure). [ABSTRACT FROM AUTHOR]

Background: Neurodevelopmental disorders (NDDs) encompass a diverse group of disorders characterized by impaired cognition, behavior, and motor skills. Genetic factor is the leading cause in about 35% of NDDs patients. Mutations of UFC1, an E2 enzyme participating in the post-translational modification of proteins through attachment of ubiquitin-like proteins, were recently reported to be associated with NDDs. However, the UFC1 associated NDDs are rare and the data are scarce, thus making it difficult to identify this disease. Objective: This study reported a novel compound heterozygous mutation of UFC1 in a Chinese patient with NDD. Methods: Detailed clinical data were recorded. Whole exome sequencing (WES) was performed to determine the genetic cause of the patient. The candidate mutation was verified using Sanger sequencing. Results: WES analysis identified a novel compound heterozygous mutation of UFC1 (c.19 C > T, p.Arg7* and c.164G > A, p.Arg55Gln). The nonsense mutation c.19 C > T (p.Arg7*) led to a premature truncation of UFC1 and nonsense-mediated RNA decay. Arg55 is highly conserved among orthologues. Molecular modeling predicted that mutation c.164G > A (p.Arg55Gln) may influence the correct folding of UFC1. These two mutations were evaluated as likely pathogenic based on the ACMG guideline. Moreover, neurodevelopmental delay, microcephaly, and epilepsy were confirmed as major phenotypes of UFC1 mutation. Conclusion: This study expands the mutational spectrum of NDDs. We reported the nonsense mutation of UFC1 for the first time. We also confirmed the major phenotypes that may guide clinical identification of UFC1 mutation. Ubiquitination mechanism is highlighted in NDDs pathogenesis. [ABSTRACT FROM AUTHOR]

Copyright of Namık Kemal Tıp Dergisi is the property of Galenos Yayinevi Tic. LTD. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose of Review: This review provides a concise update on recent developments in liver and brain interactions traversing encephalopathy in acute, acute on chronic liver failure, and non-cirrhotic liver disease. Recent Findings: An interconnected axis of gut-microbiota changes, systemic inflammation, and mediators of neuroinflammation impact liver-brain interaction. Encephalopathy in acute on chronic liver failure has its own trajectories. Newer drugs and techniques show promise, while established therapies have newer indications. Summary: Neurogliovascular unit dysfunction and cross-talk abnormalities play an important role in brain dysfunction in liver disease. Ammonia is central to pathogenesis and has different implications in different settings of liver failure (acute/chronic/acute on chronic). Beyond cirrhosis, neurological dysfunction is common in non-cirrhotic portal hypertension, chronic viral hepatitis, and metabolic dysfunction associated steatotic liver disease. Newer therapies are promising, and future research should focus on further refinement of the pathophysiological basis for targeted therapies according to the type of encephalopathy. [ABSTRACT FROM AUTHOR]

Background and Objectives: Hepatic cirrhosis is a disease with an increasing frequency globally, but its mechanisms of disease development are not yet completely known. The aim of this study was to evaluate the relationship between thyroid hormone levels (T3, fT4, and TSH) and survival in patients with chronic liver disease. Materials and Methods: A total of 419 patients diagnosed with liver cirrhosis were included in the study. The MELD score was computed, and TSH, T3, and fT4 were collected from each patient using the ELISA procedure. Signs and symptoms of liver failure and portal hypertension confirmed the clinical diagnosis of liver cirrhosis, and biological tests and imaging methods confirmed the diagnosis. Results: The MELD score was positively associated with TSH on admission and TSH on discharge and negatively associated with T3 at discharge. TSH levels were higher in non-survivors than in survivors. The values of T3 and fT4 present no significant changes to be considered as prognostic factors. Conclusions: Although the differences between the median TSH values of the patients who died and those who survived are not very large, the statistical significance of the data obtained demonstrates that there are changes in metabolism of the thyroid hormones during the progression of liver cirrhosis. It is possible that TSH is the one which maintains the normal balance of thyroid activity for patients with liver cirrhosis, so it can be considered as an important marker of evolution of these patients. [ABSTRACT FROM AUTHOR]

Objectives: To describe the clinical profile and determine the factors affecting mortality of children admitted with adenovirus infection in a tertiary care centre in South India. Methods: In this observational study, respiratory specimens (nasopharyngeal swab / endotracheal aspirate) were collected from all hospitalized pediatric patients presenting with fever, cough, breathlessness, gastrointestinal symptoms, unexplained encephalopathy or multisystem involvement, between February 2023 and August 2023. Infection with adenovirus was determined by viral pathogen panel based on polymerase chain reaction (PCR) technique. Those referred from elsewhere with positive adenovirus report but nonavailability of treatment details and children with coinfections were excluded. The clinical and laboratory profile of children with adenovirus infection were collected and predictors for in-hospital mortality were determined by logistic regression analysis. Results: Out of 527 children who were screened, 130 children with a median (IQR) age of 18 (10, 48) months, had adenovirus infection. 84.5% were aged below 5 years. 62 (41.33%) children required intensive care admission. Abnormal chest radiograph, multisystem involvement and non-respiratory illness were present in 90 (69.2%), 97 (74.62%) and 26 (20%) children. Complications included acute respiratory distress syndrome (n = 8), hemophagocytic lymphohistiocytosis (n = 7), left ventricular dysfunction (n = 11), acute liver cell failure (n = 7), acute kidney injury (n = 13), and multiorgan dysfunction (n = 16). Overall mortality was 13%. Acute kidney injury, left ventricular dysfunction and pancytopenia were identified as factors that may be significantly associated with death. Conclusions: Multisystem involvement was observed in majority of children presenting with adenovirus infection. Non-respiratory presentation is seen in a fifth of children with adenovirus infection. [ABSTRACT FROM AUTHOR]

Susac syndrome is a rare microangiopathy of unclear etiology, likely autoimmune, characterized by a characteristic clinical triad of encephalopathy, retinopathy, and hypoacusis. The majority of cases reported in the literature involve adult patients, with its occurrence in the pediatric population being extremely rare. Magnetic resonance imaging (MRI) is essential for diagnosis and patient monitoring, revealing nearly pathognomonic features, particularly valuable given the typically incomplete clinical triad and the consistent presence of encephalopathy, often as the initial symptom. We report the case of an 11-year-old child diagnosed with Susac syndrome, highlighting the importance of considering this diagnosis in cases of childhood encephalopathy and initiating treatment as early as possible to prevent irreversible sequelae.

Abstract Background Lead encephalopathy, while thankfully rare, is a devastating and potentially fatal consequence of lead intoxication. Owing to successful public health measures, severe lead toxicity is not often encountered by most practicing physicians in the United States, making both its recognition and management challenging. Article summary A case study of a 4-year-old female presenting in refractory status epilepticus, found to have severe microcytic anemia and lead level > 100 mcg/dL. Case presentation We report a case of a 4-year-old girl who presented with refractory seizures, severe microcytic anemia, and a history of developmental delay who was ultimately diagnosed with lead encephalopathy, requiring multiple courses of calcium disodium ethylenediaminetetraacetic acid (EDTA) and succimer for rebounding lead levels. Conclusion Rapid recognition and appropriate management is essential to ensure neurologically intact survival. This case documents one of the first cases of successful lead chelation after multiple courses of calcium disodium EDTA and succimer dual therapy since the removal of dimercaprol from the United States market. This case also highlights the importance of using body surface area dosing for chelation therapy in order to prevent under-dosing in young children.

Abstract Sepsis-associated encephalopathy (SAE) is a frequent and severe complication in septic patients, characterized by diffuse brain dysfunction resulting from systemic inflammation. Accurate prediction of long-term mortality in these patients is critical for improving clinical outcomes and guiding treatment strategies. We conducted a retrospective cohort study using the MIMIC IV database to identify adult patients diagnosed with SAE. Patients were randomly divided into a training set (70%) and a validation set (30%). Least absolute shrinkage and selection operator regression and multivariate logistic regression were employed to identify significant predictors of 1-year mortality, which were then used to develop a prognostic nomogram. The model’s discrimination, calibration, and clinical utility were assessed using the area under the receiver operating characteristic curve (AUC), calibration plots, and decision curve analysis, respectively. A total of 3,882 SAE patients were included in the analysis. The nomogram demonstrated strong predictive performance with AUCs of 0.881 (95% CI: 0.865, 0.896) in the training set and 0.859 (95% CI: 0.830, 0.888) in the validation set. Calibration plots indicated good agreement between predicted and observed 1-year mortality rates. The decision curve analysis showed that the nomogram provided greater net benefit across a range of threshold probabilities compared to traditional scoring systems such as Glasgow Coma Scale and Sequential Organ Failure Assessment. Our study presents a robust and clinically applicable nomogram for predicting 1-year mortality in SAE patients. This tool offers superior predictive performance compared to existing severity scoring systems and has significant potential to enhance clinical decision-making and patient management in critical care settings.

The beginning of neonatal neurology dates back to the fifties of the last century, when the criterion of normality or optimal functioning of the central nervous system on the one hand and abnormalities on the other were set. This was followed by the development of imaging methods, which made it possible to recognize bleeding in the cerebral ventricles and damage to the white matter of the brain - periventricular cystic leukomalacia; later on magnetic resonance imaging significantly contributed to the understanding of the complexity of brain injury in premature and term infants. The development of electroencephalography has provided insight into the brain maturation and has made a key contribution to the understanding of the nature of neonatal seizures. Advances in basic science have contributed to the understanding of the mechanisms of brain damage at the cellular level and to the initiation of neuroprotection. The current era of neonatal neurology has focused on the concept of neonatal injury leading to impaired brain development - secondary dysmaturation and on new options of neuroprotection. In the future, we primarily expect an improvement in the level of neuroprotection, additional development of genetic diagnostics and treatment, and thus the development of the personalized medicine.

Abstract Aim COVID‐19 can lead to encephalopathy and loss of consciousness. This double‐blinded randomized clinical trial conducted in Tehran, Iran, aimed to assess the potential effectiveness of modafinil in patients with COVID‐19‐related encephalopathy. Methods Nineteen non‐intubated COVID‐19 patients with encephalopathy were randomized into two groups: a treatment group receiving crushed modafinil tablets and a placebo group receiving starch powder. Modafinil was administered at a dose of 100 mg every 2 h, reaching a peak dosage of 400 mg. The level of consciousness was assessed using the Glasgow Coma Score (GCS) at multiple time points on the day of medication administration. The trial was registered under IRCT20170903036041N3 on 23/5/2021. Results The average age in the modafinil and placebo groups was 75.33 and 70 years, respectively. No significant differences were observed between the two groups in terms of chronic conditions, clinical symptoms, or laboratory data. GCS scores were similar between the groups at baseline (p‐value = 0.699). After four doses of modafinil, GCS scores were slightly higher in the treatment group, but this difference was not statistically significant (p‐value = 0.581). GCS scores after each round of drug administration didn't significantly differ between the treatment and placebo groups (p‐value = 0.908). Conclusion Modafinil exhibited a slight improvement in the level of consciousness among COVID‐19 patients with encephalopathy, although this improvement did not reach statistical significance when compared to the control group. Further research with larger sample sizes and longer treatment durations is recommended to explore modafinil's potential benefits in managing altered consciousness in COVID‐19 patients.

Diagnosis of chronic Lyme disease is a challange for a clinician, even if there is modern laboratory and instrumental facilities at the hospital. Borreliosis is known for polysystemic and variable clinical picture. This article describes the clinical feachures and diagnosis of chronic borreliosis with central nervous system involvement. Various clinical variants of the disease and available methods of specific and nonspecific diagnosis are listed. The theoretical part of the work was carried out based on materials from 34 publications devoted to the problem of chronic neuroborreliosis. Also we describe the clinical case that illustrates the difficulties of managing this group of patients.

Aim: Sepsis remains a leading cause of mortality among the older hospitalized patients, particularly those with complex comorbidities. This study investigates the prognostic factors influencing one-year mortality in patients aged 65 years and over, who were hospitalized with sepsis, emphasizing the role of sepsis-associated encephalopathy (SAE) in long-term outcomes. Materials and Methods: In a retrospective cohort of 207 older patients treated for sepsis, clinical and laboratory data were meticulously recorded. Demographic details, comorbidity indices, and specific treatment interventions were analyzed. The association between these variables and one-year mortality was evaluated using univariate and multivariate Cox regression models. The Kaplan-Meier curves, complemented by the Log-rank test, assessed the survival probabilities. Results: The cohort consisted of patients with a nearly equal gender distribution, with a mean age of 73.7 years. The study found that SAE, increased international normalized ratio (INR), and advanced age were significantly associated with higher one-year mortality (p

Delirium has been recognized, documented, and examined for centuries. In 500 BC Hippocrates described hyper- and hypoactive forms of delirium. As medicine, surgery, and critical care have accelerated over the last century, so too has our understanding of delirium and its profound risks to patients, families, and health care teams. It has also been increasingly understood that it is the accumulation of risk factors that ultimately precipitates delirium and nonpharmacological interventions to reduce these risks remain the cornerstone of delirium prevention and management. However, over the last three decades, these nonpharmacological strategies have moved from a single-component approach to a multicomponent approach, targeting multiple risk factors. Additionally, our understanding of what constitutes a risk factor for delirium has evolved, and in particular, it has been recognized that delirium can sometimes be a byproduct of our interventions and health care systems. In the surgical setting, for example, optimization of risk factors prior to surgery, when possible, is now seen as a key way to prevent postoperative delirium. Similarly, critical care medicine now operates with the appreciation of the profound risk to patients of prolonged mechanical ventilation, sedation, and immobilization and seeks to minimize each to reduce the risk of delirium, among other negative effects. The future of delirium prevention and management lies in both better implementation of best practices that have been defined over the last three decades as well as taking more of a whole patient view. This includes harnessing the electronic medical record, artificial intelligence, and so on to risk assess and individualize care for each patient; restructuring care to reduce deliriogenic practices and care environments; redefining what usual care looks like (e.g., utilizing music and involving loved ones, etc.); policy changes to change systematic priorities. In this paper, we will explore the past, present, and future of nonpharmacological prevention and management of delirium across care settings. [ABSTRACT FROM AUTHOR]

Acute encephalopathy is a common presenting symptom in the emergency room and complicates many hospital and intensive care unit admissions. The evaluation of patients with encephalopathy poses several challenges: limited history and examination due to the patient's mental status, broad differential diagnosis of systemic and neurologic etiologies, low yield of neurodiagnostic testing due to the high base rate of systemic causes, and the importance of identifying less common neurologic causes of encephalopathy that can be life-threatening if not identified and treated. This article discusses the differential diagnosis of acute encephalopathy, presents an approach to the history and examination in a patient with encephalopathy, reviews the literature on the yield of neurodiagnostic testing in this population, and provides a diagnostic framework for the evaluation of patients with altered mental status. [ABSTRACT FROM AUTHOR]

The evaluation and diagnosis of altered mental status in the pregnant or postpartum patient largely parallels the approach used for any other patient; however, there are several critical differences including that some neuroobstetric diagnoses require emergent delivery of the fetus. Being familiar with the physiological changes and medical complications of pregnancy and delivery is therefore essential. This review first addresses pregnancy-specific disorders that may result in altered mental status, such as the hypertensive disorders of pregnancy and pregnancy-related metabolic and endocrinopathies. The focus then shifts to the complex physiologic changes in pregnancy and how these changes contribute to the distinct epidemiology of pregnancy-related cerebrovascular complications like intracranial hemorrhage, ischemic stroke, and reversible cerebral vasoconstriction syndrome. Medical disorders that are not unique to pregnancy, such as infections and autoimmune conditions, may present de novo or worsen during pregnancy and the peripartum period and require a thoughtful approach to diagnosis and management. Finally, the unique nervous system complications of obstetric anesthesia are explored. In each section, there is a focus not only on diagnosis and syndrome recognition but also on the emergent treatment needed to reverse these complications, bearing in mind the unique physiology of the pregnant patient. [ABSTRACT FROM AUTHOR]

Altered mental status (AMS) is a syndrome posing substantial burden to patients in the intensive care unit (ICU) in both prevalence and intensity. Unfortunately, ICU patients are often diagnosed merely with syndromic labels, particularly the duo of toxic–metabolic encephalopathy (TME) and delirium. Before applying a nonspecific diagnostic label, every patient with AMS should be evaluated for specific, treatable diseases affecting the central nervous system. This review offers a structured approach to increase the probability of identifying specific causal etiologies of AMS in the critically ill. We provide tips for bedside assessment in the challenging ICU environment and review the role and yield of common neurodiagnostic procedures, including specialized bedside modalities of diagnostic utility in unstable patients. We briefly review two common etiologies of TME (uremic and septic encephalopathies), and then review a selection of high-yield toxicologic, neurologic, and infectious causes of AMS in the ICU, with an emphasis on those that require deliberate consideration as they elude routine screening. The final section lays out an approach to the various etiologies of AMS in the critically ill. [ABSTRACT FROM AUTHOR]

A case involving a 29-year-old female patient with a known case of hypothyroidism at 38 weeks gestation. She developed a fronto-occipital, postural type of headache. This ensued on the second postoperative day after undergoing an unintended dural puncture with the introducer needle during spinal anesthesia for an elective cesarean section. It was initially treated as a post-dural puncture headache until she developed generalized tonic–clonic seizures the next day. Magnetic resonance imaging (MRI) of the brain exhibited features of posterior reversible encephalopathy syndrome (PRES). With anticonvulsants and antibiotics, the neurological symptoms subsided, and the patient was discharged home symptom-free. We call attention to the importance of suspecting PRES in obstetric cases with an inadvertent dural puncture in a normotensive patient. Neuroimaging plays a crucial role in making a diagnosis of headaches, especially during the peripartum period. Lastly, keeping in view, the potential medicolegal implications in such cases, further research seems vital, especially in the Asian population.

Introduction: Combined immuno-oncology (IO) regimens are the cornerstone of the current front-line systemic therapy for metastatic renal cell carcinoma (mRCC). Despite the fact that combined IO regimens show high efficacy, they are often accompanied by a wide spectrum of immune-related adverse effects (irAEs). Case Presentation: We describe a case of rare irAEs manifested as giant cell temporal arteritis (GCA) followed by severe encephalopathy occurring after continuing immunotherapy in a 66-year-old man with mRCC receiving a combination of ipilimumab and nivolumab in the first line of systemic therapy. GCA occurred 4 months after the initiation of IO and responded promptly to the low-dose prednisone therapy. Four months after the continuation of nivolumab maintenance, the patient was hospitalized due to severe irAE encephalopathy which presented as psycho-behavioral abnormalities and progressive cognitive decline. He was treated with high-dose methylprednisolone which led to complete resolution of the symptoms and IO was permanently discontinued. The patient achieved a durable partial response. Conclusion: Both GCA and the subsequent encephalopathy in our patient responded well to the corticosteroid therapy, leading to the complete resolution of the symptoms and the patient achieved a durable partial response. Although the risk of severe neurologic irAEs affecting the central nervous system induced by IO re-administration, following previous discontinuation due to irAE, is not well-defined because of their rarity, this case highlights the need for caution, particularly in cases with a history of previous irAE-associated GCA.

Background: Hypereosinophilic syndrome is characterized by a peripheral blood eosinophil count >1.5 × 103/μL on two different examinations within a month of each other and/or a 20% or higher percentage of eosinophils in a bone marrow section, associated with organ damage. Rarely, neurological manifestations may occur, even in the early stages. We report a case of idiopathic hypereosinophilic syndrome with Loeffler endocarditis presenting with multiple bilateral strokes and encephalopathy as the first clinical manifestations. Summary: Hypereosinophilia and echocardiographic findings suggested a Loeffler’s endocarditis. Blood hyperviscosity and small vessels inflammation induced by the hypereosinophilia itself, the embolization of intracardiac thrombus, along with the impaired clearance of microthrombi in the watershed areas, are the main mechanisms involved in the pathophysiology of stroke in the hypereosinophilic syndrome. Additionally, encephalopathy could be considered as a consequence of multiple cerebral infarcts and neurotoxicity induced by hypereosinophilia since our patient’s confusion and aggressive behavior gradually remitted after steroid therapy was started. Key Messages: To the best of our knowledge, our case report is a rare instance highlighting neurological involvement as the earliest manifestation of hypereosinophilia. We aimed to elucidate the central nervous system involvement in this intriguing disorder, with the goal of encouraging clinicians to consider hypereosinophilic syndrome in the diagnostic assessment of rare stroke etiologies.

Abstract Background Both dengue and Leptospira infections are endemic to tropical and subtropical regions, with their prevalence increasing in recent decades. Coinfection with these pathogens presents significant diagnostic challenges for clinicians due to overlapping clinical manifestations and laboratory findings. This case report aims to elucidate two clinical scenarios where the coinfection of dengue and leptospirosis complicates the disease course, creating a diagnostic conundrum. Case presentation We present the clinical scenarios of two Bangladeshi males, aged 25 and 35 years, who were admitted to our hospital with acute febrile illness. The first patient exhibited hepatic and renal involvement, while the second presented with symptoms initially suggestive of meningoencephalitis. Both cases were initially managed under the presumption of dengue infection based on positive serology. However, further evaluation revealed coinfection with Leptospira, complicating the disease course. Both patients received appropriate treatment for dengue and antibacterial therapy for leptospirosis, ultimately resulting in their recovery. Conclusion These case scenarios underscore the critical importance for clinicians in regions where dengue and Leptospira are endemic to consider both diseases when evaluating patients presenting with acute febrile illness.

Abstract Objective To determine the effectiveness of phase-change-material mattress (PCM) during transportation of newborns with hypoxic ischemic encephalopathy (HIE). Study design Randomized controlled trial of newborns with HIE from June 2016 to December 2019. Patients were randomized to transport with PCM or without PCM (control) when transferred to a cooling center in northern Vietnam. Primary outcome measure was mortality rate, secondary outcomes including temperature control and adverse effects. Result Fifty-Two patients in PCM-group and 61 in control group. Median rectal temperature upon arrival was 34.5 °C (IQR 33.5–34.8) in PCM-group and 35.1 °C (IQR 34.5–35.9) in control group (p = 0.023). Median time from birth to reach target temperature was 5.0 ± 1.4 h and 5.5 ± 1.2 h in the respective groups (p = 0.065). 81% of those transported with PCM versus 62% of infants transported without (p = 0.049) had reached target temperature within the 6-h timeframe. There was no record of overcooling ( 0.05)). Conclusion Phase-change-material can be used as a safe and effective cooling method during transportation of newborns with HIE in low-resource settings. Trial registration The study was retro-prospectively registered in Clinical Trials (04/05/2022, NCT05361473).

Wernicke encephalopathy (WE) is a rare but severe neurological syndrome characterized, in its classic form, by the acute onset of ocular disturbances, ataxia, and cognitive impairment. It is caused by a deficiency of thiamine (vitamin B1) and mainly affects chronic alcoholics, although it can also affect patients with pathologies that lead to malnutrition. We present a case of a 58-year-old woman, who presented with significant weight loss over the past 6 months and who came to the emergency department for episodes of repetitive vomiting and a sleepy state. The patient underwent blood chemistry tests and a brain CT scan, which revealed symmetrical and bilateral hypodensity of the medial portion of the thalamus, tectal plate, and periaqueductal gray matte, suggestive of WE. She was subsequently referred to the Department of Neurology and underwent a brain MRI, which confirmed the clinical suspicion. She also had an abdominal CT scan and ileo-colonoscopy and was diagnosed with Crohn's disease. Immediately after the clinical diagnosis of WE, a replacement therapy based on intravenous thiamine at high doses was promptly set up, and the patient improved from a clinical point of view.Wernicke encephalopathy can be difficult to diagnose when it occurs in non-alcoholic patients; WE associated with IBD is a rare condition, and it can present with atypical and more subtle symptoms. Radiologists and physicians must be aware of this condition and imaging findings for rapid diagnosis and treatment.

Background: Canine pheochromocytomas are rare tumors of adrenal medulla. Clinical signs are often vague, resulting of intermittent catecholamine over secretion or neoplastic invasion of adjacent structures. Case Description: A 12 years old Epagneul Breton dog with a one-year history of chronic kidney disease, was examined for acute onset of severe neurological signs. Based on clinical and instrumental data, hypertensive encephalopathy was suspected. Cardiac and abdominal ultrasound were performed. Severe hypertensive cardiopathy and a right adrenal gland mass with invasion of caudal vena cava were diagnosed. Computed tomography imaging confirmed the suspect of invasive malignant neoplasia. Emergency pharmacological therapy was started to reduce systemic pressure, improve clinical signs, and stabilize the dog in view of surgical resolution. After initial improvement, patient conditions abruptly worsened, and euthanasia was elected. Histology examination confirmed a right adrenal pheochromocytoma, with caval invasion. Conclusion: To authors conclusions, acute hypertensive encephalopathy is a peculiar manifestation for pheochromocytomas. Ultrasound is a useful, and rapid test to suspect pheochromocytoma as it can detect adrenal alterations, caval invasion, metastasis, and cardiac sequelae consistent with the condition. Pheochromocytoma can mimic multiple affections, and be misinterpreted, especially when a concurrent disease has already been diagnosed. Veterinarians need to be aware that comorbidities could mask clinical signs and delay diagnosis. Furthermore, this clinical case remind to include pheochromocytoma also in the differential diagnosis of dogs with an acute onset of severe neurological signs. [Open Vet J 2024; 14(7.000): 1716-1725]

Abstract Background To understand the clinical characteristics and prognosis of respiratory syncytial virus (RSV)-related encephalopathy in children. Methods A retrospective analysis of the data of children who were diagnosed with RSV-related encephalopathy and admitted to the paediatric intensive care unit (PICU) of Beijing Children’s Hospital between November 2016 and November 2023 was performed. Results Four hundred and sixty-four children with RSV infection were treated in the PICU, and eight of these patients (1.7%) were diagnosed with RSV-related encephalopathy. The mean age of the patients was 24.89 (5.92 ∼ 36.86) months. Two patients had underlying diseases. The time from the onset of illness to impaired consciousness was 3 (1.88–3.75) days. Five patients had convulsions, and three patients had an epileptic status. The serum procalcitonin (PCT) level was 1.63 (0.24, 39.85) ng/ml for the eight patients, and the cerebrospinal fluid (CSF) protein level was 232 (163 ∼ 848) g/L. Among the 8 patients, four patients underwent electroencephalogram (EEG) monitoring or examination. One patient showed continuous low-voltage, nonresponsive activity, and another patient displayed persistent slow waves, the remaining two patients had negative results. One patient had a combination of acute necrotizing encephalopathy (ANE) and acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). Additionally, one patient had ANE, and another had acute brain swelling (ABS). One patient died in the hospital, and the other seven patients were discharged with improvement. Routine follow-up was conducted for 4.58(0.5 ∼ 6.50) years, and all patients fully recovered. Conclusions RSV-related encephalopathy could have varying clinical manifestations, and some types, such as ANE and ABS, are dangerous and can lead to death.

Introduction: Combined immuno-oncology (IO) regimens are the cornerstone of the current front-line systemic therapy for metastatic renal cell carcinoma (mRCC). Despite the fact that combined IO regimens show high efficacy, they are often accompanied by a wide spectrum of immune-related adverse effects (irAEs). Case Presentation: We describe a case of rare irAEs manifested as giant cell temporal arteritis (GCA) followed by severe encephalopathy occurring after continuing immunotherapy in a 66-year-old man with mRCC receiving a combination of ipilimumab and nivolumab in the first line of systemic therapy. GCA occurred 4 months after the initiation of IO and responded promptly to the low-dose prednisone therapy. Four months after the continuation of nivolumab maintenance, the patient was hospitalized due to severe irAE encephalopathy which presented as psycho-behavioral abnormalities and progressive cognitive decline. He was treated with high-dose methylprednisolone which led to complete resolution of the symptoms and IO was permanently discontinued. The patient achieved a durable partial response. Conclusion: Both GCA and the subsequent encephalopathy in our patient responded well to the corticosteroid therapy, leading to the complete resolution of the symptoms and the patient achieved a durable partial response. Although the risk of severe neurologic irAEs affecting the central nervous system induced by IO re-administration, following previous discontinuation due to irAE, is not well-defined because of their rarity, this case highlights the need for caution, particularly in cases with a history of previous irAE-associated GCA. [ABSTRACT FROM AUTHOR]

Background: Both dengue and Leptospira infections are endemic to tropical and subtropical regions, with their prevalence increasing in recent decades. Coinfection with these pathogens presents significant diagnostic challenges for clinicians due to overlapping clinical manifestations and laboratory findings. This case report aims to elucidate two clinical scenarios where the coinfection of dengue and leptospirosis complicates the disease course, creating a diagnostic conundrum. Case presentation: We present the clinical scenarios of two Bangladeshi males, aged 25 and 35 years, who were admitted to our hospital with acute febrile illness. The first patient exhibited hepatic and renal involvement, while the second presented with symptoms initially suggestive of meningoencephalitis. Both cases were initially managed under the presumption of dengue infection based on positive serology. However, further evaluation revealed coinfection with Leptospira, complicating the disease course. Both patients received appropriate treatment for dengue and antibacterial therapy for leptospirosis, ultimately resulting in their recovery. Conclusion: These case scenarios underscore the critical importance for clinicians in regions where dengue and Leptospira are endemic to consider both diseases when evaluating patients presenting with acute febrile illness. [ABSTRACT FROM AUTHOR]

Objective: To determine the effectiveness of phase-change-material mattress (PCM) during transportation of newborns with hypoxic ischemic encephalopathy (HIE). Study design: Randomized controlled trial of newborns with HIE from June 2016 to December 2019. Patients were randomized to transport with PCM or without PCM (control) when transferred to a cooling center in northern Vietnam. Primary outcome measure was mortality rate, secondary outcomes including temperature control and adverse effects. Result: Fifty-Two patients in PCM-group and 61 in control group. Median rectal temperature upon arrival was 34.5 °C (IQR 33.5–34.8) in PCM-group and 35.1 °C (IQR 34.5–35.9) in control group (p = 0.023). Median time from birth to reach target temperature was 5.0 ± 1.4 h and 5.5 ± 1.2 h in the respective groups (p = 0.065). 81% of those transported with PCM versus 62% of infants transported without (p = 0.049) had reached target temperature within the 6-h timeframe. There was no record of overcooling (< 32 °C) in any of the groups. The was no difference in mortality rate between the two groups (33% and 34% respectively (p > 0.05)). Conclusion: Phase-change-material can be used as a safe and effective cooling method during transportation of newborns with HIE in low-resource settings. Trial registration: The study was retro-prospectively registered in Clinical Trials (04/05/2022, NCT05361473). [ABSTRACT FROM AUTHOR]

Contrast-induced encephalopathy (CIE) is a rare complication of angiography. According to our knowledge, the majority of CIE reports is imaging observations and rarely includes results of cerebrospinal fluid (CSF) tests. Furthermore, among the cases reporting the data for CSF testing, most of the results were normal. Here, we report a case of CIE presenting with significantly elevated levels of CSF protein. We found that the course of improvement in brain imaging findings was not consistent with the severity of clinical manifestations. The diffusion-weighted imaging (DWI) and apparent diffusion coefficient (ADC) sequences were normal. Considering the lack of convenient direct indicators to observe blood-brain barrier (BBB) function, changes in the levels of CSF protein may be related to BBB permeability and recovery and may serve as a potential prognostic marker. [ABSTRACT FROM AUTHOR]

Rasmussen's encephalitis (RE) stands as a rare neurological disorder marked by progressive cerebral hemiatrophy and epilepsy resistant to medical treatment. Despite extensive study, the primary cause of RE remains elusive, while its histopathological features encompass cortical inflammation, neuronal degeneration, and gliosis. The underlying molecular mechanisms driving disease progression remain largely unexplored. In this case study, we present a patient with RE who underwent hemispherotomy and has remained seizure-free for over six months, experiencing gradual motor improvement. Furthermore, we conducted molecular analysis on the excised brain tissue, unveiling a decrease in the expression of cell-cycle-associated genes coupled with elevated levels of BDNF and TNF-α proteins. These findings suggest the potential involvement of cell cycle regulators in the progression of RE. [ABSTRACT FROM AUTHOR]

• A large proportion of patients had normal neuroimaging (CT 40.8 %, MRI 53.1 %). • CT abnormalities included cortical/subarachnoid hyperattenuation (42.1 %), cerebral oedema/sulcal effacement (26.3 %), and loss of grey-white differentiation (7.9 %). • MRI abnormalities included brain parenchymal MRI signal change (40.8 %) and cerebral oedema (12.2 %). • Characterisation of imaging findings according to anatomical location and clinical symptoms has been conducted. Contrast-induced neurotoxicity (CIN), is an increasingly recognised complication of endovascular procedures, presenting as a spectrum of neurological symptoms that mimic ischaemic stroke. The diagnosis of CIN remains a clinical challenge, and stereotypical imaging findings are not established. This study was conducted to characterise the neuroimaging findings in patients with CIN, to raise diagnostic awareness and improve decision making. We performed a systematic review of PubMed and Embase databases from inception (1946/1947) to June 2023 for reports of CIN following administration of iodinated contrast media. Studies with a final diagnosis of CIN, which provided details of neuroimaging were included. All included cases were pooled and descriptive analysis was conducted. A total of 84 patients were included, with a median age of 64 years. A large proportion of patients had normal imaging (CT 40.8 %, MRI 53.1 %). CT abnormalities included cortical/subarachnoid hyperattenuation (42.1 %), cerebral oedema/sulcal effacement (26.3 %), and loss of grey-white differentiation (7.9 %). Frequently reported MRI abnormalities included brain parenchymal MRI signal change (40.8 %) and cerebral oedema (12.2 %), most commonly observed on FLAIR sequences (26.5 %). Characterisation of imaging findings according to anatomical location and clinical symptoms has been conducted. Neuroimaging is an essential part of the diagnostic workup of CIN. Analysis of the anatomical location and laterality of imaging abnormalities may suggest relationship between radiological features and actual clinical symptoms, although this remains to be confirmed with dedicated study. Radiological abnormalities, particularly CT, appear to be transient and reversible in most patients. [ABSTRACT FROM AUTHOR]

Background: To understand the clinical characteristics and prognosis of respiratory syncytial virus (RSV)-related encephalopathy in children. Methods: A retrospective analysis of the data of children who were diagnosed with RSV-related encephalopathy and admitted to the paediatric intensive care unit (PICU) of Beijing Children's Hospital between November 2016 and November 2023 was performed. Results: Four hundred and sixty-four children with RSV infection were treated in the PICU, and eight of these patients (1.7%) were diagnosed with RSV-related encephalopathy. The mean age of the patients was 24.89 (5.92 ∼ 36.86) months. Two patients had underlying diseases. The time from the onset of illness to impaired consciousness was 3 (1.88–3.75) days. Five patients had convulsions, and three patients had an epileptic status. The serum procalcitonin (PCT) level was 1.63 (0.24, 39.85) ng/ml for the eight patients, and the cerebrospinal fluid (CSF) protein level was 232 (163 ∼ 848) g/L. Among the 8 patients, four patients underwent electroencephalogram (EEG) monitoring or examination. One patient showed continuous low-voltage, nonresponsive activity, and another patient displayed persistent slow waves, the remaining two patients had negative results. One patient had a combination of acute necrotizing encephalopathy (ANE) and acute encephalopathy with biphasic seizures and late reduced diffusion (AESD). Additionally, one patient had ANE, and another had acute brain swelling (ABS). One patient died in the hospital, and the other seven patients were discharged with improvement. Routine follow-up was conducted for 4.58(0.5 ∼ 6.50) years, and all patients fully recovered. Conclusions: RSV-related encephalopathy could have varying clinical manifestations, and some types, such as ANE and ABS, are dangerous and can lead to death. [ABSTRACT FROM AUTHOR]

Cefepime is a fourth-generation cephalosporin with extended antimicrobial coverage. Concerns have been raised about the side effects of cefepime including myoclonus, encephalopathy, and seizures, especially when renal impairment is present. There have been reports of cases of adverse neurological consequences despite appropriate renal adjustment. Here, we present a case of a 69-year-old patient initially diagnosed with pneumonia and treated with cefepime. The patient later developed altered mental status, leading to differential diagnoses including stroke, drug overdose, or non-convulsive seizures. Following a comprehensive workup, it was determined that she had cefepime-induced encephalopathy, despite having normal kidney function, which resolved completely after discontinuing the medication. In addition, we include similar cases retrieved from PubMed up to the present date, to the best of our knowledge. [ABSTRACT FROM AUTHOR]