Objective To analyze the changes in biomarkers associated with sleep disorders in anti-leucine-rich glioma-inactivated 1 (LGI1) antibody-associated encephalitis, and to preliminarily explore the mechanism of sleep disorders. Methods Fifty patients with anti-LGI1 antibody-associated encephalitis who admitted He'nan Provincial People's Hospital from April 2015 to September 2022 were selected. Serum and cerebrospinal fluid (CSF) samples were collected for biomarkers detection, and Pittsburgh Sleep Quality Index (PSQI) was used to evaluate the presence of sleep disorders. Results The 50 patients were divided into the sleep disorders (>7) group (n=28) and the no sleep disorders (≤7) group (n=22) based on PSQI score. Compared with the no sleep disorders group, the sleep disorders group in serum and CSF showed higher levels of neurofilament light chain (NfL; t=6.690, P=0.000; t=2.356, P=0.023), glial fibrillary acidic protein (GFAP; t=3.713, P=0.000; t=2.768, P = 0.008), ionized calcium-binding adapter molecule 1 (Iba1; t = 5.042, P = 0.000; t = 3.472, P = 0.001), orexin A (t = 3.250, P = 0.002; t = 5.376, P = 0.000), cortisol (t = 2.487, P = 0.016; t=5.779, P=0.000), tumor necrosis factor-α (TNF-α; t=3.832, P=0.000; t=5.122, P=0.000) and chemokine (C-X-C motif) ligand 13 (CXCL13; t=2.483, P=0.017; t=4.116, P=0.000), while only interleukin-1β (IL-1β) increased in CSF (t=2.526, P=0.015). Conclusions Sleep disorders associated with anti-LGI1 antibody-associated encephalitis is elevated in levels of neuroinjury markers, neuroendocrine markers and neuroimmune markers, suggesting that sleep disorders associated with anti-LGI1 antibody-associated encephalitis is not a single mechanism and may be related to the extensive involvement of the neuro-endocrine-immune network.

Longitudinal cognitive changes in Parkinson’s disease (PD) exhibit considerable heterogeneity.Predicting cognitive trajectories in early PD patients can improve prognostic counseling and guide clinical trials. This study included 337 early PD patients with 6-year follow-up in the Parkinson's Progression Markers Initiative (PPMI) database.Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) to identify subtypes of longitudinal cognitive trajectories, and a nomogram predictive model was constructed using baseline clinical variables. The 337 PD patients had a mean age of 61.0 years, mean disease duration of 0.55 years, and mean MoCA score of 27.1 points. Latent class mixed models (LCMM) identified two longitudinal cognitive subtypes: cognitive stable (276 cases, 81.9

OBJECTIVE:Parkinson's disease (PD) is marked by a high incidence of neuropsychiatric symptoms that significantly impact the patients' quality of life. Biomarkers for monitoring anxiety and depressive symptoms in patients with PD are currently scarce. Epidermal growth factor (EGF), a neuroprotective growth factor, is linked to mood disorders and cognitive decline in patients with PD. This longitudinal study aimed to assess whether baseline plasma EGF levels can forecast the advancement of anxiety and depressive symptoms in patients with PD. METHODS:We examined clinical and biomarker data from 154 drug-naïve patients with PD enrolled in the Parkinson's Progression Markers Initiative cohort, with annual follow-up assessments spanning seven years. Baseline plasma EGF concentrations were measured using a sandwich enzyme-linked immunosorbent assay. Participants were categorized into tertiles (low, medium, and high) based on their EGF levels. Linear mixed-effects models (LME) were utilized to investigate the relationships between baseline EGF (evaluated as both continuous and categorical variables) and changes over time in State-Trait Anxiety Inventory (STAI) and Geriatric Depression Scale (GDS) scores. RESULTS:The median age of the cohort was 63.74 years, and the median disease duration at baseline was 0.38 years. No significant differences were observed in the baseline STAI/GDS scores or motor symptom severity among the EGF tertiles. Covariate-adjusted LME analyses indicated that the medium and high EGF groups showed significantly lower annual increases in STAI (β = -0.94 to -1.20, P < 0.05) and GDS (β = -0.14 to -0.22, P < 0.05) scores compared to the low EGF group. Baseline EGF, when considered as a continuous variable, exhibited no correlation with STAI/GDS scores at baseline but displayed significant negative interactions with time for both scales (STAI: β = -0.01, P = 0.017; GDS: β = -0.001, P = 0.020). The sensitivity analyses validated these results. CONCLUSIONS:Elevated baseline plasma EGF levels correlate with a decelerated advancement of anxiety and depressive symptoms in PD, supporting EGF's dual potential as a monitoring biomarker and therapeutic target for the neuropsychiatric aspects of PD.

Parkinson’s disease (PD) demonstrates considerable heterogeneity in the manifestation of clinical symptoms and disease progression. Recently, six clinical milestones have been proposed to evaluate disease severity in PD. However, the identification of PD progression subtypes based on these milestone events has not yet been performed. Latent class analysis (LCA) was employed to identify subtypes of PD progression based on the timing of the first occurrence of six milestones within a 6-year follow-up period in Parkinson’s Progression Markers Initiative (PPMI) database. The study cohort consisted of 354 early PD patients, of whom 42.9

While the previous studies have discussed the association of narcolepsy with autoimmune diseases, autoimmune thyroid disease (IATD) has rarely been described in patients with narcolepsy. The association of narcolepsy with thyroid disease is intriguing for speculating the causal or coexisting autoimmune disorder. We report a case of narcolepsy Type 1 with IATD, presenting with excessive daytime sleepiness (EDS), cataplexy attacks, and unexplainable weight gain. Oral modafinil and sodium oxybate were used for treatment and prevention. During the 1-year follow-up, the patient’s EDS and cataplexy attacks improved. However, the patient developed hypothyroidism and was subsequently prescribed with thyroid replacement therapy.

Objective To quantitatively analyze the difference in the content of plasma exosome α-synuclein(α-syn)be-tween Parkinson disease(PD)and idiopathic rapid eye movement sleep behavior disorder(iRBD),and to identify predictable biological markers.Methods A total of 20 patients with iRBD(iRBD group),21 PD patients without RBD(PD-nRBD group),and 20 healthy controls matched for age and sex(HC group)were enrolled.Rapid-Eye-Movement Sleep Behavior Dis-order Questionnaire-Hong Kong(RBDQ-HK)was used to evaluate the nocturnal symptoms of all subjects,and the motor section of Unified Parkinson Disease Rating Scale Ⅲ(UPDRS Ⅲ)was used to evaluate motor impairment.ELISA was used to measure the content of plasma exosome α-syn,and the three groups were analyzed in terms of the content of plasma exosome α-syn and its correlation with RBDQ-HK score and UPDRS Ⅲ score.Results There was a significant difference in UPDRS Ⅲ score be-tween the iRBD group,the PD-nRBD group,and the HC group(P=0.000 1),with a significant difference between any two groups(P<0.05);there was also a significant difference in RBDQ-HK score between the three groups(P=0.000 1),and the iRBD group had a significantly higher score than the other two groups(P=0.000 1).The iRBD group and the PD-nRBD group had a significantly higher content of plasma exosome α-syn than the HC group(P=0.001),and the iRBD group had a lower con-tent of plasma exosome α-syn than the PD-nRBD group(P>0.05).In the iRBD group,plasma exosome α-syn was positively correlated with RBDQ-HK score(r=0.842,P=0.000 1),and in the PD-nRBD group,plasma exosome α-syn was positively cor-related with UPDRS Ⅲ score(r=0.817,P=0.000 1)and H-Y staging(r=0.592,P=0.005).Conclusion The presence of plasma exosome α-syn is observed in iRBD patients,which is similar to that in PD-nRBD patients,and the content of plasma exosome α-syn is associated with the motor score of PD-nRBD and the nocturnal symptom score of iRBD.Therefore,plasma exo-some α-syn is expected to become an early biomarker for predicting the conversion of iRBD to PD.

Background:Chronic insomnia disorder (CID) is considered a major public health problem worldwide. Therefore, innovative and effective technical methods for studying the pathogenesis and clinical comprehensive treatment of CID are urgently needed.Methods:Real-time fMRI neurofeedback (rtfMRI-NF), a new intervention, was used to train 28 patients with CID to regulate their amygdala activity for three sessions in 6 weeks. Resting-state fMRI data were collected before and after training. Then, voxel-based degree centrality (DC) method was used to explore the effect of rtfMRI-NF training. For regions with altered DC, we determined the specific connections to other regions that most strongly contributed to altered functional networks based on DC. Furthermore, the relationships between the DC value of the altered regions and changes in clinical variables were determined.Results:Patients with CID showed increased DC in the right postcentral gyrus, Rolandic operculum, insula, and superior parietal gyrus and decreased DC in the right supramarginal gyrus, inferior parietal gyrus, angular gyrus, middle occipital gyrus, and middle temporal gyrus. Seed-based functional connectivity analyses based on the altered DC regions showed more details about the altered functional networks. Clinical scores in Pittsburgh sleep quality index, insomnia severity index (ISI), Beck depression inventory, and Hamilton anxiety scale decreased. Furthermore, a remarkable positive correlation was found between the changed ISI score and DC values of the right insula.Conclusions:This study confirmed that amygdala-based rtfMRI-NF training altered the intrinsic functional hubs, which reshaped the abnormal functional connections caused by insomnia and improved the sleep of patients with CID. These findings contribute to our understanding of the neurobiological mechanism of rtfMRI-NF in insomnia treatment. However, additional double-blinded controlled clinical trials with larger sample sizes need to be conducted to confirm the effect of rtfMRI-NF from this initial study.

Idiopathic rapid eye movement sleep behavior disorder (iRBD) is an important non-motor complication of Parkinson's disease. At the same time, iRBD is considered to be the prodromal stage of α-synucleinopathy. This high risk of conversion suggests that iRBD becomes a nerve It is a window for early research on degenerative diseases and is the best candidate for neuroprotection trials. A wide range of neuroimaging techniques has improved our understanding of iRBD as a prodromal stage of the disease. In addition, neuroimaging of abnormal iRBD is expected to be a potential biomarker for predicting clinical phenotypic transformation. This article reviews the research progress of neuromolecular imaging in patients with iRBD from the perspective of iRBD transforming synucleinopathies.

BackgroundThe study aims to investigate the role of serum albumin (ALB) and creatinine (CRE), bilirubin (BIL), and uric acid (UA) as major intravascular antioxidants in migraine.MethodsWe enrolled 148 patients with migraine and 150 age- and sex-matched healthy controls. The serum levels of ALB, TBIL, CRE, and UA were measured in patients with migraine of different subtypes. The risk of migraine was assessed by multiple stepwise logistic regression analysis.ResultsThe serum levels of ALB, total BIL (TBIL), CRE, and UA were significantly lower in the migraine group than in the HC group (p < 0.05). The ALB and UA levels were lower during migraine attack periods (p < 0.05). There were no statistically significant differences observed in serum ALB, TBIL, CRE, and UA levels between aura/without aura and episodic/chronic migraine subtypes (p > 0.05). The multiple stepwise logistic regression revealed that ALB [odds ratio (OR) 0.79, 95% confidence interval (CI) 0.69–0.89, p < 0.001], TBIL (OR 0.61, 95% CI 0.5–0.75, p < 0.001), and UA (OR 0.97, 95% CI 0.96–0.99, p = 0.014) were independently associated with migraine. In addition, the serum levels of ALB, TBIL, and UA were significantly lower in the migraine group when compared by sex.ConclusionThe serum levels of UA, TBIL, ALB, and CRE were lower in the patients with migraine, indicating a lower antioxidant status. In addition, ALB, TBIL, and UA were independently related to migraine. These results could provide insights into the possible role of oxidative stress in the pathogenesis of migraine.

Background: Restless Legs Syndrome (RLS) can be defined as a sleep disorder. However, whether changes in the serum vitamin B12 levels are involved in the pathophysiological mechanism of RLS remains unclear. Our study aimed to determine whether vitamin B12 levels are independently related to the occurrence of RLS. Methods: The serum vitamin B12 levels of 80 patients with RLS and 80 age- and gender-matched healthy controls (HC) were retrospectively analyzed. Results: Serum vitamin B12 levels in the RLS group were significantly reduced, while the levels of creatinine, and homocysteine were higher (P < 0.05). In addition, multivariate logistic regression revealed serum vitamin B12 to be independently associated with RLS (p < 0.05; odds ratio=0.97; 95 % confidence interval: 0.96-0.98). Pearson correlation analysis indicated that serum vitamin B12 level was negatively correlated with the International Restless Legs Scales (IRLS) score, and the 24-item Hamilton Depression Rating Scale (HAMD(24)) score (r = 0.025, P = 0.023, r = 0.295, P = 0.001). Conclusion: Patients with RLS had significant vitamin B12 deficiency compared to HC. Such deficiency significantly affects severity of symptoms and depression symptoms. In addition, decreased serum vitamin B12 levels are independently associated with the development of RLS, which illustrates the complex relationship between vitamin B12 and RLS. Prospective vitamin B12 treatment studies are needed to confirm this relationship and to evaluate the efficacy of vitamin B12 as a treatment for RLS patients.

Background Restless Legs Syndrome (RLS) is a common neurological disorder. Growing evidence shows that dopaminergic dysfunction and iron deficiency are associated with the pathogenesis of RLS. Additionally, the dopaminergic system is linked with the hypothalamic-pituitary-thyroid (HPT) axis. Thus, the current study aimed to compare thyroid function between RLS patients and healthy subjects and investigate the associations with clinical characteristics of RLS. Methods Serum levels of thyroid hormones were investigated in 102 first-episode drug-naïve RLS patients and 80 matched healthy controls (HCs). Baseline data and clinical characteristics were performed by professional personnel. In addition, multivariate regression was used to analyze the relationship between thyroid function and RLS. Results Compared with control group, RLS patients had significantly higher serum thyroid-stimulating hormone (TSH) levels (p < 0.001), and higher prevalence of subclinical hypothyroidism [Odds ratio (OR) 8.00; 95% confidence interval (CI) = 3.50–18.30; p < 0.001]. The Subclinical hypothyroidism rate (47.1 vs. 10%, p < 0.001) in RLS patients was higher than the HCs group. Regression analysis revealed that serum TSH (OR = 1.77; 95% CI = 1.41–2.23; p < 0.001) was independently associated with RLS. There was a statistically significant positive correlation between TSH and the Pittsburgh sleep quality index (PSQI) scores (r = 0.728, p < 0.001), and the International Restless Legs Scales (IRLS) points (r = 0.627, p < 0.001). Spearman correlation analysis showed that FT3 was positive correlated with HAMA14 score (r = 0.239, p = 0.015). In addition, compared with the good-sleeper group, poor-sleeper patients had significantly higher serum TSH levels (p < 0.001). Conclusion Serum levels of TSH and the prevalence of subclinical hypothyroidism were higher in RLS patients, indicating the imbalance between thyroid hormones (TH) and the dopaminergic system may contribute to the development of primary RLS. Additionally, the TH axis may influence the quality of sleep in RLS patients.

Acute intermittent porphyria (AIP) is an autosomal, dominant, hereditary metabolic disease caused by an inherited deficiency of hydroxymethylbilane synthase (HMBS), a crucial enzyme in the heme biosynthetic pathway. It can affect the central, peripheral, and autonomic nervous systems. We report a 23-year Chinese woman who presented with severe abdominal pain, convulsions, constipation, tachycardia, quadriparesis, and hyponatremia, accompanied by posterior reversible encephalopathy syndrome (PRES). The clinical diagnosis of AIP was made after positive urine Watson-Schwartz test for porphobilinogen (PBG). Genetic testing is important for AIP patients in confirming the diagnosis. We identified a new insertion mutation in intron 14 [c.1005dupC (p.I336Hfs*23)] of the HMBS in her genomic DNA. Timely and accurate treatment of AIP may improve disease prognosis. Key Words: Acute intermittent porphyria, Mutation, Posterior reversible encephalopathy syndrome.

Background: Migraine is the second most common neurological disorder. Inflammation plays an important role in the pathology and symptoms of migraine. Although, many studies have analyzed the levels of peripheral cytokines in migraine patients, the conclusions of these studies were not consistent. Meta-analysis for peripheral cytokine levels in migraine is necessary to solve the inconsistency in clinical conclusion. Methods: We conducted a systematic search to July 2021, to identify the literatures that measured peripheral cytokine levels in migraine patients and compared them with healthy controls. Results: 10 studies were finally included in the meta-analysis: 6 for C-reactive protein (CRP), 2 for interleukin (IL)1 beta, 5 for IL-6, 3 for tumor necrosis factor alpha (TNF-alpha), 1 for IL-2, 2 for IL-10. Compared with healthy controls, we found that the patients with migraine had higher serum levels of CRP (standardized mean difference, SMD = 1.48; P < 0.001), IL-1 beta (SMD = 0.75; P < 0.001), IL-6(SMD = 1.18; P<0.001) and TNF-alpha (SMD = 0.69; P = 0.003), while did not have significant difference in serum IL-2(SMD = -0.24; P = 0.25) and IL-10 (SMD = -0.17; P = 0.88). Conclusions: The findings of the meta-analysis provide evidence for higher serum of CRP, IL-1 beta, IL-6 and TNF-alpha in migraine patients compared with healthy controls. Our results support that inflammation play a role in the pathophysiology of migraine. However, there was no significant difference in serum IL-2 and IL-10.

Purpose Idiopathic rapid eye movement Sleep Behavior Disorder (iRBD) is considered as a prodromal and most valuable warning symptom for Parkinson’s disease (PD). Although iRBD and PD without RBD (nRBD-PD) are both α-synucleinopathies, whether they share the same neurodegeneration process is not clear enough. In this study, the pattern and extent of neurodegeneration were investigated and compared between early-stage nRBD-PD and iRBD from the perspective of whole-brain functional network changes. Methods Twenty-one patients with iRBD, 23 patients with early-stage nRBD-PD, and 22 matched healthy controls (HCs) were enrolled. Functional networks were constructed using resting-state functional MRI (fMRI) data. Network topological properties were analyzed and compared among groups by graph theory approaches. Correlation analyses were performed between network topological properties and cognition in the iRBD and nRBD-PD groups. Results Both patients with iRBD and patients with early-stage nRBD-PD had attention, executive function, and some memory deficits. On global topological organization, iRBD and nRBD-PD groups still presented small-worldness, but both groups exhibited decreased global/local efficiency and increased characteristic path length. On regional topological organization, compared with HC, nRBD-PD presented decreased nodal efficiency, decreased degree centrality, and increased nodal shortest path length, while iRBD presented decreased nodal efficiency and nodal shortest path. For iRBD, brain regions with decreased nodal efficiency were included in the corresponding regions of nRBD-PD. Nodal shortest path changes were significantly different in terms of brain regions and directions between nRBD-PD and iRBD. Attention deficits were correlated with local topological properties of the occipital lobe in both iRBD and nRBD-PD groups. Conclusion Both global and local efficiency of functional networks declined in nRBD-PD and iRBD groups. The overlaps and differences in local topological properties between nRBD-PD and iRBD indicate that iRBD not only shares functional changes of PD but also presents distinct features.

Background: The relationship between uric acid and patients with type 1 (NT1) remains unclear. UA may contribute to the development of depression. Depression is also common in NT1. Our study aimed to evaluate serum levels of UA, creatinine, and UA/Cr ratio, and examine the association of serum UA levels with psychological status in NT1 patients. Methods: This is a case-control study conducted on 48 patients diagnosed with NT1 and 40 healthy controls (HC). The 17-item Hamilton Depression Rating (HAMD-17) was used as screening tools for depressive symptoms for patients with NT1. Serum UA, creatinine, and UA/Cr ratio were measured. In addition, the correction of UA status and scores of depressive scales was statistically analyzed. Results: Approximately 70% of all subjects with NT1 had depression or depressive symptoms compared with the HC group, the serum UA levels and UA/Cr ratios were higher in patients with NT1 (p < 0.05). In addition, there was a negative correlation between UA levels and HAMD-17 scores in NT1 patients (r = -0.334; p = 0.020). Conclusion: We found that serum UA levels were higher in patients with NT1, and the serum UA levels were negatively correlated with depressive symptom scores. Further well-designed prospective cohort studies are needed to determine the causality of the correlation and to further clarify the pathophysiological mechanisms of UA in NT1 patients.

BackgroundChronic insomnia disorder (CID) is a highly prevalent sleep disorder, which influences people's daily life and is even life threatening. However, whether the resting-state regional homogeneity (ReHo) of disrupted brain regions in CID can be reshaped to normal after treatment remains unclear. MethodsA novel intervention real-time functional magnetic resonance imaging neurofeedback (rtfMRI-NF) was used to train 28 CID patients to regulate the activity of the left amygdala for three sessions in 6 weeks. The ReHo methodology was adopted to explore its role on resting-state fMRI data, which were collected before and after training. Moreover, the relationships between changes of clinical variables and ReHo value of altered regions were determined. ResultsResults showed that the bilateral dorsal medial pre-frontal cortex, supplementary motor area (SMA), and left dorsal lateral pre-frontal cortex had decreased ReHo values, whereas the bilateral cerebellum anterior lobe (CAL) had increased ReHo values after training. Some clinical scores markedly decreased, including Pittsburgh Sleep Quality Index, Insomnia Severity Index, Beck Depression Inventory, and Hamilton Anxiety Scale (HAMA). Additionally, the ReHo values of the left CAL were positively correlated with the change in the Hamilton depression scale score, and a remarkable positive correlation was found between the ReHo values of the right SMA and the HAMA score. ConclusionOur study provided an objective evidence that amygdala-based rtfMRI-NF training could reshape abnormal ReHo and improve sleep in patients with CID. The improved ReHo in CID provides insights into the neurobiological mechanism for the effectiveness of this intervention. However, larger double-blinded sham-controlled trials are needed to confirm our results from this initial study.

Purpose:This study investigates the topological properties of brain functional networks in patients with isolated rapid eye movement sleep behavior disorder (iRBD). Participants and Methods:A total of 21 patients with iRBD (iRBD group) and 22 healthy controls (HCs) were evaluated using resting-state functional MRI (rs-fMRI) and neuropsychological measures in cognitive and motor function. Data from rs-fMRI were analyzed using graph theory, which included small-world properties, network efficiency, network local efficiency, nodal shortest path, node efficiency, and network connectivity, as well as the relationship between behavioral characteristics and altered brain topological features. Results:Rey-Osterrieth complex figure test (ROCFT-copy), symbol digital modalities test (SDMT), auditory verbal learning test (AVLT)-N1, AVLT-N2, AVLT-N3, and AVLT-N1-3 scores were significantly lower in patients with iRBD than in HC (P < 0.05), while trail making test A (TMT-A), TMT-B, and Unified Parkinson's Disease Rating Scale Part-III (UPDRS-III) scores were higher in patients with iRBD (P < 0.05). Compared with the HCs, patients with iRBD had no difference in the small-world attributes (P > 0.05). However, there was a significant decrease in network global efficiency (P = 0.0052) and network local efficiency (P = 0.0146), while an increase in characteristic path length (P = 0.0071). There was lower nodal efficiency in occipital gyrus and nodal shortest path in frontal, parietal, temporal lobe, and cingulate gyrus. Functional connectivities were decreased between the nodes of occipital with the regions where they had declined nodal shortest path. There was a positive correlation between TMT-A scores and the nodal efficiency of the right middle occipital gyrus (R = 0.602, P = 0.014). Conclusion:These results suggest that abnormal behaviors may be associated with disrupted brain network topology and functional connectivity in patients with iRBD and also provide novel insights to understand pathophysiological mechanisms in iRBD.

BackgroundRestless Legs Syndrome (RLS) is a common sleep disorder. Polysomnographic (PSG) studies have been used to explore the night sleep characteristics of RLS, but their relationship with RLS has not been fully analyzed and researched.MethodsWe searched the Cochrane Library electronic literature, PubMed, and EMBASE databases to identify research literature comparing the differences in polysomnography between patients with RLS and healthy controls (HCs).ResultsThis review identified 26 studies for meta-analysis. Our research found that the rapid eye movement sleep (REM)%, sleep efficiency (SE)%, total sleep time (TST) min, and N2 were significantly decreased in patients with RLS compared with HCs, while sleep latency (SL) min, stage shifts (SS), awakenings number (AWN), wake time after sleep onset (WASO) min, N1%, rapid eye movement sleep latency (REML), and arousal index (AI) were significantly increased. Additionally, there was no significant difference among N3%, slow wave sleep (SWS)%, and apnea-hypopnea index (AHI).ConclusionOur findings demonstrated that architecture and sleep continuity had been disturbed in patients with RLS, which further illustrates the changes in sleep structure in patients with RLS. In addition, further attention to the underlying pathophysiological mechanisms of RLS and its association with neurodegenerative diseases is needed in future studies.

目的 特发性快眼动睡眠行为障碍(idopathic rapid eye movement sleep behavior disorder,iRBD)又称帕金森病临床前期,为寻找其早期损害的证据,利用功能核磁共振探查其早期大脑自发活动性的改变,以提供其脑损害的影像证据.方法 选取符合诊断标准的iRBD 21例,性别、年龄匹配的健康对照组22例,进行认知量表及统一帕金森病等级评分-运动部分(Unified Parkinson's Disease Rating Scale motor section,UPDRSⅢ)测评,并进行功能磁振扫描,利用局部一致性(region homogeneity,ReHo)方法进行数据分析;结果 与正常对照组相比,iRBD组Rey-Osterrieth复杂图形测验(ROCFT)、听词语学习测验(AVLT)N1、N2、N3、符号数字模式测验(SDMT)、数字排序测验-注意力部分(DOT-A)得分均下降(U=133.5、t=-2.416、t=-2.873、U=134.5、U=81.0、U=144.5,P<0.05),连线测验B(TMT-B)及UPDRSⅢ得分明显增加(U=138.0、U=121.0,P<0.05);与对照组比较,iRBD组基底节区右尾状核、左壳核、右壳核及右苍白球局部一致性明显下降(t=-4.611、t=-4.360、t=-4.298、t=-3.422,P<0.05).结论 iRBD患者存在视空间、记忆、执行、注意及运动方面损害,其基底节区神经团块内部自发活动一致性明显下降,提示基底节区功能活动异常,可能是iRBD早期基底节损害的标记.

BACKGROUND:Narcolepsy can be defined as a sleep disorder. However, whether changes in the serum vitamin B12 levels are involved in the pathophysiological mechanism of narcolepsy remains unclear. Our study aimed to assess whether vitamin B12 levels are independently related to the occurrence of narcolepsy. METHODS:The serum folate, vitamin B12, and homocysteine levels of 40 patients with narcolepsy and 40 age- and gender-matched healthy controls (HC) were retrospectively analyzed. According to the results of the univariate logistic analysis, a multiple logistic regression model was constructed to predict the independent influencing indicators. RESULTS:Serum folic acid and vitamin B12 levels in the narcolepsy group were significantly reduced. Moreover, through the sex subgroup, males in the narcolepsy group had lower serum vitamin B12 levels. Multivariate logistic regression revealed serum vitamin B12 to be independently associated with narcolepsy (p < 0.05; odds ratio=0.97; 95% confidence interval: 0.95-0.98). CONCLUSION:Decreased serum vitamin B12 levels are independently associated with the development of narcolepsy, which illustrates the complex relationship between vitamin B12 and narcolepsy. Future studies should explore whether vitamin B12 supplementation can improve the symptoms of patients.