Cefepime-Induced Encephalopathy in Patients Treated for Urinary Tract Infection.

Cefepime is a fourth-generation cephalosporin antibiotic administered intravenously used to treat various bacterial infections, including urinary tract infections. Administering cefepime to patients should be done with caution, understanding both potential risks and side effects. A 74-year-old female presented to the family medicine clinic with abdominal pain and a history of urinary tract infections. The workup included a CT scan that showed bowel obstruction and bladder wall thickening. Due to a history of urinary tract infections, three days following the presentation, the patient underwent an explorative laparotomy. Following the laparotomy, the patient was started on cefepime, a fourth-generation cephalosporin antibiotic. Five days following the initial presentation, the patient became confused and was nonverbal. An encephalopathy workup showed a negative MRI, but an EEG was consistent with encephalopathy. Cefepime was discontinued. Forty-eight hours after cefepime was discontinued, the patient returned to baseline with normal cognitive function. It is crucial that clinicians understand the different classifications of antibiotics, as well as the drugs and potential side effects of prescriptions. Cefepime can be used in gram-negative infections with resistance to more generic antibiotics. It has the ability to cross the blood-brain barrier, making it effective in treating meningitis. It has also been shown to cause encephalopathy as a side effect. It is important that clinicians understand the different generations of cephalosporins, as well as the cross-reactions and potential side effects of prescriptions. These factors must be considered when prescribing broad-spectrum antibiotics, such as cefepime.

Clinician Stakeholder Experience With Telemedicine Consults to Assess Neonatal Encephalopathy in a Rural State.

BACKGROUND: Serial neonatal encephalopathy (NE) examinations are difficult to perform in rural community hospitals as on-site experts are not readily available. We implemented a synchronous, acute care model of teleconsultation-the Maine Neonatal Encephalopathy Teleconsultation program (Maine NET)-to provide remote, joint assessment of NE by pediatric neurology and neonatology at nine community hospitals and one tertiary care center. We performed a qualitative study to interview clinicians about their experience of this program. METHODS: From April 2018 to October 2022, we employed a semistructured interview format with 16 clinicians representing all participating hospitals. We utilized deductive analysis to assign a set of predefined codes to the transcribed interviews. RESULTS: Thematic analysis supported the anticipated benefits of Maine NET, demonstrating that clinicians felt resource utilization, collaborative decision making, communication, and continuity of care were improved. Clinicians overwhelmingly supported the program: "This program has truly saved babies' lives and future function. I have not met any parents through this journey, who aren't incredibly grateful for the care that is provided" and emphasized the benefit of collaboration between all care team members. Teleconsultation was felt to be "more than adequate to [assess] NE." Connectivity issues were cited as a limitation. CONCLUSIONS: Maine NET has positively impacted care delivery for newborns with clinical concerns for NE. Additionally, the program has improved resource allocation, collaborative decision making, communication, and equity of care. Addressing technological challenges will be vital to the success and sustainability of the planned Maine NET expansion.

A case report of spastic diplegic cerebral palsy in a late preterm child with hypoplastic left heart syndrome.

Background: Congenital heart disease (CHD) is the most common birth defect, affecting 1% of children who are born in the United States each year. Children with hypoplastic left heart syndrome, a type of critical CHD, are at high risk for neurodevelopmental disabilities, which are conditions that can affect motor, language, and cognitive development. In children with critical CHD, the severity and prevalence of their motor delays is most pronounced in infancy. Case Description: We present a case of a former late preterm male with hypoplastic left heart syndrome and history of hypoxic ischemic encephalopathy, who was diagnosed with spastic diplegic cerebral palsy in the setting of periventricular leukomalacia. Like many children with critical CHD, this child had gross motor delays and tone abnormalities in infancy. However, unlike many children with CHD, he continued to have neurologic differences that prompted additional evaluation through a Cardiac Neurodevelopmental Program. He was diagnosed with spastic diplegic cerebral palsy based upon clinical history and physical examination. Ancillary testing showed periventricular leukomalacia on brain magnetic resonance imaging (MRI); this finding was consistent with his clinical diagnosis. Conclusions: This is an interesting case report of spastic diplegic cerebral palsy in a late preterm infant with critical CHD. When making a diagnosis of cerebral palsy, it is important to consider the etiology of the motor impairment. Selective vulnerability may have played a factor in this child's condition. The most vulnerable part of the neonatal brain is the periventricular white matter; cerebral hypoxia can lead to periventricular leukomalacia. Children with CHD have brain dysmaturity beginning in-utero. Thus, it is possible that this child's brain dysmaturity may have increased his susceptibility to periventricular leukomalacia. Because most children with CHD have gross motor delays in infancy, it may be challenging to make a definitive diagnosis of cerebral palsy in an infant with critical CHD. Children with cerebral palsy have early motor delays that persist throughout life. It is the identification of persistent motor impairments through repeat evaluations that enabled this child's cerebral palsy diagnosis. This illustrates the importance of developmental surveillance in children with critical CHD.

Bibliometrics and knowledge mapping of the pathogenesis of hepatic encephalopathy in patients with liver cirrhosis.

Background: Hepatic encephalopathy is a common and serious complication of decompensated cirrhosis. It can considerably contribute to economic burden and impaired quality of life. However, its pathogenesis remains unclear. Method: In this study, we aimed to visually analyse the research status and development trends in hepatic encephalopathy pathogenesis using bibliometrics and knowledge mapping. Information regarding publications between 1978 and 2022 were obtained from the Web of Science Core Collection. CiteSpace was used to analyse and present data by year, author, institution, country, journal, reference, and keyword. Results: A total of 1578 publications on hepatic encephalopathy pathogenesis in patients with cirrhosis were retrieved from Web of Science Core Collection. A gradual increasing trend in annual publications has occurred. The collaborative network analysis results suggest the United States of America, the University of London, and Bajaj, Jasmohan S as the most influential country, institution, and author, respectively, in this research field. Notably, China appeariiuis to be the most promising country. Research on 'hepatology' garners the most significant papers in the field. Combined with reference co-citation and keyword co-occurrence analyses, we found that ammonia metabolism, gut microbiota, sarcopenia, and trace elements will become future research frontiers that are likely to be explored for a considerable length of time. Conclusion: Future research directions in HE pathogenesis may target modulating the ammonia metabolism, the gut microbiota, sarcopenia, and trace elements.

Intestinal dysbacteriosis contributes to persistent cognitive impairment after resolution of acute liver failure.

Regulating the gut microbiota alleviates hepatic encephalopathy (HE). It remains unclear whether it is imperative to withhold treatment for microbial imbalance after liver functional recovery. This work aims to elucidate the alterations in cognitive behavior, liver function, synaptic transmission, and brain metabolites in acute liver failure(ALF) mice before and after hepatic function recovery. Here, thioacetamide was injected intraperitoneally to establish an ALF mouse model, which induced HE. By performing hierarchical clustering analysis, we found that the liver functions normalized, but cognitive dysfunction and intestinal dysbacteriosis were found in the ALF mice 14 days after thioacetamide injection. Additionally, fecal microbiota transplant from the ALF mice with liver function recovery could induce liver injury and cognitive impairment. Moreover, we found alterations in synaptic transmission in the ALF mice with liver function improvement, and the correlations between the gut bacteria and synaptic transmission in the cortex were significant. Finally, we detected apparent alterations in the brain metabolic profiles of the ALF mice after liver function improvement by performing 1H nuclear magnetic resonance spectroscopy, suggesting a risk of HE. These results showed that intestinal dysbacteriosis in ALF mice with liver function recovery is sufficient to induce liver injury and cognitive impairment. These results indicated continuous care may be necessary for monitoring microbial imbalance even in ALF-induced HE patients whose liver function has recovered significantly.

Combined use of the Montreal Cognitive Assessment and Symbol Digit Modalities Test improves neurocognitive screening accuracy after cardiac arrest: A validation sub-study of the TTM2 trial.

AIM: To assess the merit of clinical assessment tools in a neurocognitive screening following out-of-hospital cardiac arrest (OHCA). METHODS: The neurocognitive screening that was evaluated included the performance-based Montreal Cognitive Assessment (MoCA) and Symbol Digit Modalities Test (SDMT), the patient-reported Two Simple Questions (TSQ) and the observer-reported Informant Questionnaire on Cognitive Decline in the Elderly-Cardiac Arrest (IQCODE-CA). These instruments were administered at 6-months in the Targeted Hypothermia versus Targeted Normothermia after Out-of-Hospital Cardiac Arrest (TTM2) trial. We used a comprehensive neuropsychological test battery from a TTM2 trial sub-study as a gold standard to evaluate the sensitivity and specificity of the neurocognitive screening. RESULTS: In our cohort of 108 OHCA survivors (median age = 62, 88% male), the most favourable cut-off scores were: MoCA <26; SDMT z ≤-1; IQCODE-CA ≥3.04. The MoCA (sensitivity 0.64, specificity 0.85) and SDMT (sensitivity 0.59, specificity 0.83) had a higher classification accuracy than the TSQ (sensitivity 0.28, specificity 0.74) and IQCODE-CA (sensitivity 0.42, specificity 0.60). When using the cut-points for MoCA or SDMT in combination to identify neurocognitive impairment, sensitivity improved (0.74, specificity 0.81), area under the curve = 0.77, 95% CI [0.69, 0.85]. The most common unidentified impairments were within the episodic memory and executive functions domains, with fewer false negative cases on the MoCA or SDMT combined. CONCLUSION: The MoCA and SDMT have acceptable diagnostic accuracy for screening for neurocognitive impairment in an OHCA population, and when used in combination the sensitivity improves. Patient and observer-reports correspond poorly with neurocognitive performance. CLINICALTRIALS: gov Identifier: NCT03543371.

Impact of inhaled sedation on delirium incidence and neurological outcome after cardiac arrest - a propensity-matched control study (Isocare).

RATIONALE: poor neurological outcome is common following a cardiac arrest. The use of volatile anesthetic agents has been proposed during post-resuscitation to improve outcome. OBJECTIVES: to determine the effects of inhaled isoflurane on neurological outcome, delirium incidence, ICU length-of-stay, ventilation duration, mortality during post-resuscitation care of ICU patients. PATIENTS: 510 patients were admitted within our medical ICU following a cardiac arrest during the study period, 401 of them being sedated using intravenous sedation prior to 2017 and 109 of them using inhaled isoflurane according to a standardized protocol following 2017. RESULTS: matched-pair analysis depicted a delirium incidence decrease, without improved neurologic outcome on ICU discharge (CPC ≤ 2) for isoflurane patients (16.1% vs 32.2%, p 0.03 and 29% vs 23%, p 0.47, respectively). Ventilation duration and ICU length of stay were shorter for isoflurane patients (78 vs 167 hrs, p 0.01 and 7.9 vs 8.5 days, p 0.01 respectively). Isoflurane had no impact on mortality. CONCLUSION: in this propensity-matched control study, isoflurane sedation during the post-resuscitation care of ICU patients was associated with a lower incidence of delirium, a shorter duration of mechanical ventilation and a reduced ICU length of stay. Prospective data are needed before its widespread use.

Unraveling neuroimaging insights in developmental epileptic encephalopathy type 25: a comprehensive review of reported cases and a novel SLC13A5 variant.

Developmental and epileptic encephalopathy type 25 with amelogenesis imperfecta (DEE25) is a rare autosomal recessive disorder caused by homozygous or compound heterozygous disease-causing variants in the SLC13A5. These variants can disrupt energy production and delay brain development, leading to DEE25. Key symptoms include refractory seizures, often manifesting in neonates or infants, alongside global developmental delay, intellectual disability, progressive microcephaly, ataxia, spasticity, and speech difficulties. Dental anomalies related to amelogenesis imperfecta are common. Previous studies have typically reported normal or minimally altered early-life brain magnetic resonance imaging (MRI) findings in DEE25. However, our investigation identified a homozygous splice donor variant (NM_177550.5: c.1437 + 1G >T) in SLC13A5 through whole-exome sequencing in two affected siblings (P1 and P2). They displayed developmental delay, cerebral hypotonia, speech delay, recurrent seizures, mild but constant microcephaly, and motor impairments. Significantly, P1 exhibited novel findings on brain magnetic resonance imaging at age 5, including previously unreported extensive persistent hypomyelination. Meanwhile, P2 showed substantial loss of cerebral white matter in the frontoparietal region and delayed myelination at 18 months old. These discoveries broaden the DEE25 imaging spectrum and highlight the clinical heterogeneity even within siblings sharing the same variants.

[Posterior reversible encephalopathy syndrome in autoimmune disorders]. / Sindrom zadnei obratimoi entsefalopatii pri autoimmunnykh narusheniyakh.

Posterior reversible encephalopathy syndrome (PRES) is characterized by nonspecific symptoms, including not only pronounced non-focal and various focal neurological signs but also specific neuroimaging features, including vasogenic edema affecting predominantly the posterior area. PRES usually develops in the setting of acute arterial hypertension. However, it is not uncommon for PRES to develop in non-hypertensive patients, including people with autoimmune disorders (multiple sclerosis, neuromyelitis optica spectrum disorder, etc). PRES could also be due to the toxic effects of drugs or other substances. The pathophysiological mechanisms of PRES include impaired autoregulation of cerebral blood flow due to acute arterial hypertension and toxic endotheliotropic effects of endogenous and exogenous factors.

Acute onset of hypertensive encephalopathy in a dog with right adrenal pheochromocytoma and neoplastic invasion of the caudal vena cava: Case report and review of the literature.

Background: Canine pheochromocytomas (PCCs) are rare tumors of the adrenal medulla. Clinical signs are often vague, resulting in intermittent catecholamine over secretion or neoplastic invasion of adjacent structures. Case Description: A 12-year-old Epagneul Breton dog with a 1-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 the 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 PCC, with caval invasion. Conclusion: To the authors' conclusions, acute hypertensive encephalopathy is a peculiar manifestation of PCCs. Ultrasound is a useful, and rapid test to suspect PCC as it can detect adrenal alterations, caval invasion, metastasis, and cardiac sequelae consistent with the condition. PCC 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 reminds us to include PCC also in the differential diagnosis of dogs with an acute onset of severe neurological signs.

Analysis of the risk factors of the radiation-induced encephalopathy in nasopharyngeal carcinoma: A retrospective cohort study.

To analyze the related factors of radiation-induced encephalopathy in nasopharyngeal carcinoma (NPC) to identify the risk factors and their clinical significance. This retrospective cohort study included 707 NPC patients. They had undergone conventional and enhanced computed tomography or magnetic resonance imaging scans. They were divided into the radiation-induced encephalopathy group and the no encephalopathy group according to the imaging examination. Detailed clinical information was collected. The incidence of radiation-induced encephalopathy in NPC was 22.2%, in which 124 were radiation-induced encephalopathy and 33 were reirradiation patients. We found that age, pathological type, radiation method, hypertension, radiation course, relapse, carotid/cerebral arteriosclerosis, clinical stage, and radiotherapy dose were statistically significant between the two groups (p < 0.05). Multiple logistic regression showed that clinical stage, age, radiotherapy method, hypertension, carotid/cerebral arteriosclerosis, and radiation courses after a reoccurrence of NPC were risk factors for radiation-induced encephalopathy. The more advanced the clinical stage was and the older the patient, the greater the risk. Radiotherapy method, radiation course, hypertension, carotid/cerebral arteriosclerosis, age, and clinical stage were the risk factors associated with radiation-induced encephalopathy in NPC.

Neurological Complications of COVID-19 Infection: A Comprehensive Review.

The COVID-19 pandemic is well on its way to reaching endemic status across the globe. While the medical community's understanding of the respiratory complications induced by COVID-19 is improving, there is still much to be learned about the neurological manifestations associated with COVID-19 infection. This review aimed to compile relevant, available evidence of COVID-19-induced neurological complications and to provide information for each complication regarding symptomology, progression patterns, demographic risk factors, treatment, and causative mechanism of action when available. Data for this review was collected using a confined search on PubMed using the keywords ["COVID-19" OR "SARS-CoV-2"] AND ["neurological complications" OR "olfactory symptoms" OR "gustatory symptoms" OR "myalgia" OR "headache" OR "dizziness" OR "stroke" OR "seizures" OR "meningoencephalitis" OR "cerebellar ataxia" OR "acute myelitis" OR "Guillain Barré Syndrome" OR "Miller Fisher Syndrome" OR "Posterior Reversible Encephalopathy Syndrome"] between 2019 and 2023. A wide range of neurological manifestations impact a significant percentage of COVID-19 patients, and a deeper understanding of these manifestations is necessary to ensure adequate management. The most common neurological complications identified consist of olfactory and gustatory dysfunctions, myalgia, headache, and dizziness, while the most severe complications include stroke, seizures, meningoencephalitis, Guillain-Barré syndrome, Miller Fisher syndrome, acute myelitis, and posterior reversible encephalopathy syndrome. While this review effectively provides a roadmap of the neurological risks posed to COVID-19 patients, further research is needed to clarify the precise incidence of these complications and to elucidate the mechanisms responsible for their manifestation.

Protective effect of menthol against thioacetamide-induced hepatic encephalopathy by suppressing oxidative stress and inflammation, augmenting expression of BDNF and α7-nACh receptor, and improving spatial memory.

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that can occur in people with acute or chronic liver disease. Here, we investigated the effects of menthol, a natural monoterpene, on HE induced by thioacetamide (TA) in male Wistar rats. The rats received 200 mg/kg of TA twice a week for four weeks and were administered 10 mg/kg of menthol intraperitoneally daily for the same period. The results showed that menthol treatment reduced oxidative stress and inflammation in the livers and hippocampi of the rats that received TA. It also lowered the levels of ammonium and liver enzymes AST, ALT, ALP, and GGT in the serum of these animals and prevented liver histopathological damage. In addition, the expression and activity of acetylcholinesterase in the hippocampus of HE model rats were decreased by menthol. Likewise, this monoterpene reduced the expression of TLR4, MyD88, and NF-κB in the hippocampus while increasing the expression of BDNF and α7-nACh receptor. Menthol also reduced neuronal death in the hippocampal cornu ammonis-1 and dentate gyrus regions and reduced astrocyte swelling, which led to improved learning and spatial memory in rats with HE. In conclusion, the study suggests that menthol may have strong protective effects on the liver and brain, making it a potential treatment for HE and neurodegenerative diseases.

A Comprehensive Review on Current Insights Into Epileptic Encephalopathy: Pathogenesis and Therapeutic Strategies.

Epileptic encephalopathy (EE) represents a challenging group of disorders characterized by severe epilepsy and significant cognitive, behavioral, and neurological impairments. This comprehensive review aims to elucidate the current insights into the pathogenesis and therapeutic strategies for these disorders. Pathogenesis involves a complex interplay of genetic factors, neurobiological mechanisms, and environmental influences that contribute to the severity and progression of symptoms. Clinical manifestations are diverse, encompassing various seizure types, cognitive and behavioral impairments, and developmental delays. Current therapeutic strategies include pharmacological treatments, nonpharmacological interventions, and emerging therapies such as gene and stem cell therapy. Despite advancements, significant challenges and limitations remain, highlighting the need for ongoing research and innovation. This review synthesizes existing knowledge, identifies research gaps, and proposes future directions, emphasizing the potential for personalized medicine to improve patient outcomes and quality of life.

Dynamic A-to-I RNA editing during acute neuroinflammation in sepsis-associated encephalopathy.

Introduction: The activation of cerebral endothelial cells (CECs) has recently been reported to be the earliest acute neuroinflammation event in the CNS during sepsis-associated encephalopathy (SAE). Importantly, adenosine-to-inosine (A-to-I) RNA editing mediated by ADARs has been associated with SAE, yet its role in acute neuroinflammation in SAE remains unclear. Methods: Our current study systematically analyzed A-to-I RNA editing in cerebral vessels, cerebral endothelial cells (CECs), and microglia sampled during acute neuroinflammation after treatment in a lipopolysaccharide (LPS)-induced SAE mouse model. Results: Our results showed dynamic A-to-I RNA editing activity changes in cerebral vessels during acute neuroinflammation. Differential A-to-I RNA editing (DRE) associated with acute neuroinflammation were identified in these tissue or cells, especially missense editing events such as S367G in antizyme inhibitor 1 (Azin1) and editing events in lincRNAs such as maternally expressed gene 3 (Meg3), AW112010, and macrophage M2 polarization regulator (Mm2pr). Importantly, geranylgeranyl diphosphate synthase 1 (Ggps1) and another three genes were differentially edited across cerebral vessels, CECs, and microglia. Notably, Spearman correlation analysis also revealed dramatic time-dependent DRE during acute neuroinflammation, especially in GTP cyclohydrolase1 (Gch1) and non-coding RNA activated by DNA damage (Norad), both with the editing level positively correlated with both post-LPS treatment time and edited gene expression in cerebral vessels and CECs. Discussion: The findings in our current study demonstrate substantial A-to-I RNA editing changes during acute neuroinflammation in SAE, underlining its potential role in the disease.

Effective knockdown-replace gene therapy in a novel mouse model of DNM1 developmental and epileptic encephalopathy.

Effective gene therapy for gain-of-function or dominant-negative disease mutations may require eliminating expression of the mutant copy together with wild-type replacement. We evaluated such a knockdown-replace strategy in a mouse model of DNM1 disease, a debilitating and intractable neurodevelopmental epilepsy. To challenge the approach robustly, we expressed a patient-based variant in GABAergic neurons-which resulted in growth delay and lethal seizures evident by postnatal week three-and delivered to newborn pups an AAV9-based vector encoding a ubiquitously expressed, Dnm1-specific interfering RNA (RNAi) bivalently in tail-to-tail configuration with a neuron-specific, RNAi-resistant, codon-optimized Dnm1 cDNA. Pups receiving RNAi or cDNA alone fared no better than untreated pups, whereas the vast majority of mutants receiving modest doses survived with almost full growth recovery. Synaptic recordings of cortical neurons derived from treated pups revealed that significant alterations in transmission from inhibitory to excitatory neurons were rectified by bivalent vector application. To examine the mutant transcriptome and impact of treatment, we used RNA sequencing and functional annotation clustering. Mutants displayed abnormal expression of more than 1,000 genes in highly significant and relevant functional clusters, clusters that were abrogated by treatment. Together these results suggest knockdown-replace as a potentially effective strategy for treating DNM1 and related genetic neurodevelopmental disease.

[Efficacy of therapeutic hypothermia on mild neonatal hypoxic-ischemic encephalopathy: a prospective randomized controlled study]. / æ–°ç”Ÿå„¿è½»åº¦ç¼ºæ°§ç¼ºè¡€æ€§è„‘ç— äºšä½Žæ¸©æ²»ç–—æ•ˆæžœçš„å‰çž»æ€§éšæœºå¯¹ç §ç ”ç©¶.

OBJECTIVES: To investigate the efficacy of therapeutic hypothermia on mild neonatal hypoxic-ischemic encephalopathy (HIE). METHODS: A prospective study was performed on 153 neonates with mild HIE who were born from September 2019 to September 2023. These neonates were randomly divided into two groups: therapeutic hypothermia (n=77) and non-therapeutic hypothermia group (n=76). The short-term clinical efficacy of the two groups were compared. Barkovich scoring system was used to analyze the severity of brain injury shown on magnetic resonance imaging (MRI) between the two groups. RESULTS: There were no significant differences in gestational age, gender, birth weight, mode of birth, and Apgar score between the therapeutic hypothermia and non-therapeutic hypothermia groups (P>0.05). There were no significant differences in the incidence rates of sepsis, arrhythmia, persistent pulmonary hypertension and pulmonary hemorrhage and the duration of mechanical ventilation within the first 72 hours after birth between the two groups. The therapeutic hypothermia group had longer prothrombin time within the first 72 hours after birth and a longer hospital stay (P<0.05). Compared with the non-therapeutic hypothermia group, the therapeutic hypothermia group had lower incidence rates of MRI abnormalities (30% vs 57%), moderate to severe brain injury on MRI (5% vs 28%), and watershed injury (27% vs 51%) (P<0.05), as well as lower medium watershed injury score (0 vs 1) (P<0.05). CONCLUSIONS: Therapeutic hypothermia can reduce the incidence rates of MRI abnormalities and watershed injury, without obvious adverse effects, in neonates with mild HIE, suggesting that therapeutic hypothermia may be beneficial in neuroprotection in these neonates.

The causal effect of gut microbiota on hepatic encephalopathy: a mendelian randomization analysis.

BACKGROUND: There is growing evidence for a relationship between gut microbiota and hepatic encephalopathy (HE). However, the causal nature of the relationship between gut microbiota and HE has not been thoroughly investigated. METHOD: This study utilized the large-scale genome-wide association studies (GWAS) summary statistics to evaluate the causal association between gut microbiota and HE risk. Specifically, two-sample Mendelian randomization (MR) approach was used to identify the causal microbial taxa for HE. The inverse variance weighted (IVW) method was used as the primary MR analysis. Sensitive analyses were performed to validate the robustness of the results. RESULTS: The IVW method revealed that the genus Bifidobacterium (OR = 0.363, 95% CI: 0.139-0.943, P = 0.037), the family Bifidobacteriaceae (OR = 0.359, 95% CI: 0.133-0.950, P = 0.039), and the order Bifidobacteriales (OR = 0.359, 95% CI: 0.133-0.950, P = 0.039) were negatively associated with HE. However, no causal relationship was observed among them after the Bonferroni correction test. Neither heterogeneity nor horizontal pleiotropy was found in the sensitivity analysis. CONCLUSION: Our MR study demonstrated a potential causal association between Bifidobacterium, Bifidobacteriaceae, and Bifidobacteriales and HE. This finding may provide new therapeutic targets for patients at risk of HE in the future.

Co-occurrence of anti-phospholipid syndrome and posterior reversible encephalopathy syndrome in a patient with Autoimmune hepatitis: A case report.

Posterior reversible encephalopathy syndrome (PRES) is a neurological disease characterized by a variety of neurological findings, in accordance with radiological characteristics. PRES is commonly secondary to elevated BP and/or conditions such as autoimmune patients receiving immunosuppressive drugs. Our case involves a 36-year-old female with a history of autoimmune hepatitis (AIH), who presented with sudden onset headaches from 3 weeks prior, and a single episode of seizure attack the morning before admission. In the initial examination she had highly elevated blood pressure (BP) (190/116). Her neurological examination revealed decline in force of limbs in addition to mild paresthesia. After primary stabilization, she underwent brain magnetic resonance imaging. Due to the clinical and radiological findings, the patient was diagnosed with PRES. In the following work-up of BP elevation, abdominopelvic sonography and subsequent computed tomography scan, multiple lesions were observed in spleen and both kidneys consistent with infarction. In further evaluation, Lupus-like anticoagulants were found to be elevated, which, in conjunction with the confirmed antiphospholipid syndrome (APS), suggested a possible role for APS-nephropathy as the missing link between PRES and APS. However, despite the role of an autoimmune disease in increasing the risk of developing other autoimmune conditions, APS and AIH have been rarely observed together. Our study indicates that developing APS in the context of AIH is a rare occurrence. However, APS could serve as a critical intermediary, potentially facilitating the onset of PRES despite lower BP.

Early onset of posterior reversible encephalopathy syndrome (PRES) following postpartum eclampsia-A case report.

Early screening and management of postpartum posterior reversible encephalopathy syndrome (PRES) can reduce hospital stay and complications. Obstetricians, gynecologists, ophthalmologists, and even general physicians should be aware of PRES since its presentation is variable.