Seventeen cases of pancreatic encephalopathy (PE) with acute pancreatitis were studied retrospectively. It was found that on the basis of brain damage caused by pancreatic enzyme, many factor might play a role in the development of PE. It suggests that PE should not be accepted as an operative indication separately in severe acute pancreatitis. Chinese medicine can benefit the patient in the treatment of this disease. Operation is the only choice while patient get worsened even after appropriate and enough nonoperative therapy, as well as while pancreatic necrosis become infected or pancreatic abcess formed. Mortality of PE in this series is 52.9%, slightly less than the level (66.7%-100%) reported by other authors.
Objective To evaluate the efficacy and safety of L-ornithine-L-aspartate (LOLA) in the treatment of hepatic encephalopathy (HE). Methods Such databases as PubMed, EMbase, Web of Science, CENTRAL, Chinese Journals Full-text Database, CBM and WanFang Data were searched from the date of their establishment to November 30, 2011 to collect the randomized controlled trials (RCTs) on LOLA in treating HE. The quality of included studies was evaluated by two reviewers independently, data were extracted and cross-checked, and then meta-analysis was performed using Review Manager 5.0 software. Results Among the total six included RCTs, 432 patients were diagnosed as type-C HE and 185 were diagnosed as type-A HE. Compared with the placebo group, for the patients with type-C HE, LOLA could significantly reduce the serum ammonia level (WMD=16.60, 95%CI 8.34 to 24.85, Plt;0.000 1) and the time of number connection test-A (NCT-A) (WMD=9.6, 95%CI 5.26 to 13.93, Plt;0.00 01), and it could also effectively improve the clinical remission rate (RR=1.36, 95%CI 1.06 to 1.73, P=0.01). However, no significant differences were found between the two groups for the patients with type-A HE (Pgt;0.05). Conclusion LOLA is effective for the patients with type-C hepatic encephalopathy, and it could be regarded as a choice in clinic. However, more high-quality RCTs are needed to further evaluate the effect of LOLA in treating type-A hepatic encephalopathy.
Objective To explore the efficacy and safety of the ketogenic diet (KD) in the treatment of genetic developmental and epileptic encephalopathy (DEE). Methods Clinical data from 42 children with genetically confirmed refractory epileptic encephalopathy treated in the Department of Neurology, Jinan Children’s Hospital, between January 2021 and October 2023 were retrospectively analyzed. A classic KD protocol was implemented, and outcomes including seizure frequency, electroencephalogram (EEG) improvement, and adverse reactions were observed at 3, 6, and 12 months post-treatment. Results Among the 42 children, the seizure-free rates at 3, 6, and 12 months of KD treatment were 16.7%, 16.7%, and 14.3%, respectively, while the effective seizure control rates were 69.0%, 52.4%, and 35.7%. At 3 months, comparison of baseline characteristics between the effective and ineffective groups showed no statistically significant differences in gender (P=0.095), age at onset (P=0.648), age at KD initiation(P=0.768), disease duration before KD (P=0.519), presence of abnormal brain MRI findings (P=0.226), epilepsy syndrome classification(P=0.344), or ion channel gene involvement (P=0.066). EEG improvement rates at 6 and 12 months were 54.2% (24 cases) and 42.8% (14 cases), respectively. Retention rates for KD at 3, 6, and 12 months were 100.0%, 71.4%, and 42.8%. Adverse reactions occurred in 7 patients (16.7%), primarily gastrointestinal symptoms (vomiting, constipation, diarrhea; 6 cases) and elevated uric acid (1 case), with no severe adverse events reported. Conclusion KD is an effective treatment for genetic DEE with favorable short-term safety, though long-term adherence requires attention.
Objective To observe the serumlevel of neuron-specific enolase( NSE) in patients with pulmonary encephalopathy and its changes after treatment with mechanical ventilation. Methods Twentyone patients with pulmonary encephalopathy were enrolled. Glasgow coma scale( GCS) , serumNSE level, and arterial blood gas were evaluated at three time-points: before mechanical ventilation, after 12 hours mechanical ventilation, and the moment of consciousness. Results 18 patients recovered consciousness, and 3 patients remained in persistent coma and died. GCS and arterial blood gas improved obviously after 12 hours mechanical ventilation. Meanwhile, the serumNSE concentration decreased significantly after 12 hours mechanical ventilation [ ( 24. 54 ±6. 65) μg/L] and at the moment of consciousness [ ( 14. 19 ±2. 91) μg/L] compared with before mechanical ventilation( P lt; 0. 05, P lt; 0. 01) . Conclusion Dynamic measurment of serumNSE may be a useful biomarker for assessing the severity of cerebral injury and predicting prognosis.
Severe psychomotor developmental delay resulting from early postnatal (within 3 months) seizures can be diagnosed as Early-Infantile Developmental and Epileptic encephalopathies (EIDEE). Its primary etiologies include structural, hereditary, metabolic and etc. The main pathogenesis may be related to the inhibition of normal physiological activity of the brain by abnormal electrical activity and the damage of the brain neural network. Ohtahara syndrome and Early Myoclonic Encephalopathy (EME) are typical types of EIDEE. The principle of treatment is to improve the cognitive and developmental function by controlling frequent seizures. When the seizure is difficult to control with drugs, surgical evaluation should be performed as soon as possible, and surgical treatment is the first choice for patients suitable for surgery. The types of surgery can be divided into excision surgery, dissociation surgery, neuromodulation surgery and etc. The current status of surgical treatment of EIDEE was described, and the curative effect of surgical treatment was explored, so as to help clinicians choose appropriate treatment methods.
Developmental epileptic encephalopathies (DEEs) are a group of disorders characterized by early-onset seizures, abnormal electroencephalogram (EEG) patterns, and developmental delay or regression. They are characterized by complex etiology and are often refractory to treatment, severely impacting affected children, particularly infants and toddlers, and pose a challenge in pediatric neurology. In recent years, with the rise of precision medicine, an increasing number of pathogenic genes associated with DEEs have been discovered. However, the specific pathogenic mechanisms and signaling pathways of these genes in the body still require further investigation. This article primarily discusses the genetic patterns of DEEs and the selection of genetic testing, emphasizing the timing of genetic testing assisted by the epilepsy phenotype, especially in DEEs associated with single-gene mutations and new therapeutic drugs, to aid in clinical decision-making for DEEs. It also introduces the use of neurobiological models for DEE research to effectively advance epilepsy research, thereby enabling targeted gene therapy.
Objective To construct a nomogram model for predicting delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) in emergency departments. Methods All patients with acute carbon monoxide poisoning who visited the Department of Emergency of Zigong Fourth People’s Hospital between June 1st, 2011 and May 31st, 2023 were retrospectively enrolled and randomly divided into a training set and a testing set in a 6∶4 ratio. LASSO regression was used to screen variables in the training set to establish a nomogram model for predicting DEACMP. The discrimination, calibration, and clinical practicality were compared between the nomogram and Glasgow Coma Scale (GCS) in the training and testing sets. Results A total of 475 patients with acute carbon monoxide poisoning were included, of whom 41 patients had DEACMP. Age, GCS and aspartate aminotransferase were selected as risk factors through LASSO regression, and a nomogram model was constructed based on these factors. The areas under the receiver operating characteristic curves for nomogram and GCS to predict DEACMP in the training set were 0.897 [95% confidence interval (CI) (0.829, 0.966)] and 0.877 [95%CI (0.797, 0.957)], respectively; and those for nomogram and GCS to predict DEACMP in the testing set were 0.925 [95%CI (0.865, 0.985)] and 0.858 [95%CI (0.752, 0.965)], respectively. Compared with GCS, the performance of nomogram in the training set (net reclassification index=0.495, P=0.014; integrated discrimination improvement=0.070, P=0.011) and testing set (net reclassification index=0.721, P=0.004; integrated discrimination improvement=0.138, P=0.009) were both positively improved. The calibration of nomogram in the training set and testing set was higher than that of GCS. The decision curves in the training set and testing set showed that the nomogram had better clinical net benefits than GCS. Conclusion The age, GCS and aspartate aminotransferase are risk factors for DEACMP, and the nomogram model established based on these factors has better discrimination, calibration, and clinical practicality compared to GCS.
目的 探讨5例特重型胰腺炎的特点及治疗方法。方法 我院2001年8月至2003年8月共收治特重型胰腺炎患者5例。其中入院后18 h内心跳、呼吸骤停3次的重症急性胰腺炎（SAP）1例，治疗以及时血液滤过和心、肺、脑复苏为重点； SAP并发胰性脑病2例，以大剂量维生素B1的补充，或足量补给浓缩红细胞为治疗重点； 并发多个器官功能障碍的暴发性胰腺炎（FAP）2例，治疗重点是血液滤过和防治多器官功能衰竭的级联放大反应，其中1例以高渗性糖昏迷为主要表现，治疗重点是内稳态的纠正，血液滤过，重要器官功能维护。结果 5例特重型胰腺炎患者均治愈，平均住院时间为32.2 d。结论 器官功能的复苏和维护、外科ICU监护、短时血液滤过、内稳态的纠正、中西药综合治疗及病因、对症的个体化治疗是特重型胰腺炎的重要治疗措施。