Background: We investigated the association between oxcarbazepine (OXC)-induced maculopapular eruption (MPE) and HLA-B alleles in a northern Han Chinese population, and conducted an analysis of clinical risk factors for OXC-MPE.Methods: Forty-two northern Han Chinese patients who had been treated with OXC in Changchun, China were genotyped. Among them were 14 cases with OXC-induced MPE; the remaining 28 were OXC-tolerant. The HLA-B allele frequencies of the normal control group were found in the Allele Frequency Net Database. Polymerase chain reaction-sequence specific primer( PCR-SSP )was used for HLA-B*1502 testing and direct sequencing for four-digit genotype determination.Results: Four-digit allele sequencing showed that there was no statistically significant difference in the frequency of the HLA-B*1502 allele between the OXC-MPE and OXC-tolerant controls (3.6% versus 7.5%, OR = 0.38, 95% CI = 0.04–3.40, P = 0.65), as well as between OXC-MPE and normal controls (3.6% versus 2.4%, OR = 1.54, 95% CI = 0.20–11.73, P = 0.49). However, a significant difference in the frequency of HLA-B*3802 alleles was found between the MPE group and normal controls (10.7% versus 1.9%, OR = 6.329, 95% CI = 1.783-22.460, P = 0.018). There was no significant difference in terms of age, gender, or final OXC dose between the OXC-MPE and OXC-tolerant groups.Conclusions: There was no significant association between OXC-MPE and HLA-B*1502 in the northern Han Chinese population in our study. Instead, HLA-B*3802 was found to be a potential risk factor for OXC-MPE.

This study's purpose was to determine the sensitivity, false-positive and false-negative of seizure detection in adult intensive care by amplitude-integrated electroencephalography (aEEG) and color density spectral array (CDSA). 30 continuous electroencephalogram (EEG) recordings were randomly performed in 3 digital EEG-recording machines, 3 specialized neurophysiologists participated in this study, underwent 4 hours of training of CDSA and aEEG, marked any epochs suspected to be seizures without access to the raw EEG. The results will be compared and analyzed with continuous EEG reading to consider sensitivity, positive or negative rate. The recordings in this study, comprised 720 hours of EEG containing a total of 435 seizures. The median sensitivity for seizure identification was 80% of CDSA and 81.3% of aEEG, Median false-positive was 4 per 24 hours of CDSA, and 2 per 24 hours of aEEG display, Median false-negative was 4 per 24 hours of CDSA, and 4 per 24 hours of aEEG display. The time spent in identification of seizures by CDSA and aEEG was much time-saving than continuous EEG-reading. In this study, both CDSA and aEEG have a higher sensitivity but lower false-positive or missed rate in the interpretation of seizure identification in adult NICU.

Epigenetics underlying refractory epilepsy is poorly understood. DNA methylation may affect gene expression in epilepsy patients without affecting DNA sequences. Herein, we investigated the association between Carbamazepine-resistant (CBZ-resistant) epilepsy and EPHX1 methylation in a northern Han Chinese population, and conducted an analysis of clinical risk factors for CBZ-resistant epilepsy. Seventy-five northern Han Chinese patients participated in this research. 25 cases were CBZ-resistant epilepsy, 25 cases were CBZ-sensitive epilepsy and the remaining 25 cases were controls. Using a CpG searcher was to make a prediction of CpG islands; bisulfite sequencing PCR (BSP) was applied to test the methylation of EPHX1. We then did statistical analysis between clinical parameters and EPHX1 methylation. There was no difference between CBZ-resistant patients, CBZ-sensitive patients and healthy controls in matched age and gender. However, a significant difference of methylation levels located in NC_000001.11 (225,806,929.....225807108) of the EPHX1 promoter was found in CBZ-resistant patients, which was much higher than CBZ-sensitive and controls. Additionally, there was a significant positive correlation between seizure frequency, disease course and EPHX1 methylation in CBZ-resistant group. Methylation levels in EPHX1 promoter associated with CBZ-resistant epilepsy significantly. EPHX1 methylation may be the potential marker for CBZ resistance prior to the CBZ therapy and potential target for treatments.

Sleep staging has always been a hot topic in the field of sleep medicine, and it is the cornerstone of research on sleep problems. At present, sleep staging heavily relies on manual interpretation, which is a time-consuming and laborious task with subjective interpretation factors. In this paper, we propose an automatic sleep stage classification model based on the Bidirectional Recurrent Neural Network (BiRNN) with data bundling augmentation and label redirection for accurate sleep staging. Through extensive analysis, we discovered that the incorrect classification labels are primarily concentrated in the transition and nonrapid eye movement stage I (N1). Therefore, our model utilizes a sliding window input to enhance data bundling and an attention mechanism to improve feature enhancement after label redirection. This approach focuses on mining latent features during the N1 and transition periods, which can further improve the network model’s classification performance. We evaluated on multiple public datasets and achieved an overall accuracy rate of 87.3%, with the highest accuracy rate reaching 93.5%. Additionally, the network model’s macro F1 score reached 82.5%. Finally, we used the optimal network model to study the impact of different EEG channels on the accuracy of each sleep stage.

Diagnosis of Creutzfeldt-Jakob disease (CJD) is often challenging in elderly individuals, not only because of its variable clinical features but also because of nonspecific changes on the electroencephalogram (EEG) in the early stages of the disease. Here we report on a patient who presented with progressive cognitive dysfunction, psychiatric symptoms, involuntary facio-brachio-crural movement, and an abnormal EEG. We provide a detailed analysis and differential diagnosis between anti-leucine-rich glioma inactivated 1 (LGI1) limbic encephalitis versus CJD, in the hope of providing a new understanding of CJD. A 65-year-old Chinese man presented with slowly progressive cognitive decline with psychiatric symptoms. On admission, he presented with facial grimacing and brief left upper limb dystonic posturing lasting 1–2 seconds, with hyponatremia that was difficult to rectify. Neurological examination showed increased muscle tension in the left limb but without pathological reflexes. His early EEG showed focal periodic wave complexes. Diffusion-weighted magnetic resonance imaging showed a suspected “lace sign” in the occipital cortex. His cerebrospinal fluid was negative for LGI1 antibodies and positive for 14-3-3 brain protein. Therefore, we made a presumptive diagnosis of CJD. At the following visit, a second EEG showed paroxysmal sharp wave complexes, but the patient had a poor prognosis. Atypical facio-brachio-crural movement and nonspecific EEG changes may occasionally be found in patients with CJD or anti-LGI1 encephalitis. Clinicians should not be dissuaded from a diagnosis of CJD where the EEG does not show paroxysmal sharp wave complexes in the early stages but abnormal facio-brachio-crural movement is present.