Narcolepsy is a central sleep disorder with the core symptom of excessive daytime sleepiness. Recent studies have shown a significant increase in the risk of comorbid metabolic syndrome in patients with narcolepsy， with a prevalence rate of approximately 30%. This article systematically reviews the research advances in the comorbidity between narcolepsy and the components of metabolic syndrome， including obesity， abnormal glucose metabolism， hypertension， and dyslipidemia. The underlying pathophysiological mechanisms involve reduced energy expenditure， insulin resistance， lipid metabolism disorders， and impaired autonomic regulation， all resulting from orexin deficiency； endocrine hormone imbalances and reduced physical activity due to excessive daytime sleepiness are also involved. Clinical management should be based on systematic screening and assessment， with lifestyle intervention as the core strategy， supplemented by cautious selection of medications and enhanced monitoring. Future longitudinal studies are needed to clarify the key pathways through which orexin deficiency mediates metabolic disorders and to establish an evidence-based comprehensive prevention and treatment system.

Paradoxical insomnia is a sleep disorder characterized by a substantial discrepancy between subjective perceptions and objective measurements of sleep parameters， and this article systematically summarizes the conceptual evolution， mechanisms， and advances in diagnosis and treatment of paradoxical insomnia. The mechanisms of paradoxical insomnia involve cortical hyperarousal， sleep microstructure fragmentation， impaired sleep-protective mechanisms， and dysregulation of the gut-brain axis， and it is also affected by psychological factors including anxiety， depression， nightmares， and cognitive biases. Cognitive behavior therapy， pharmacotherapy， and physical therapy may be more effective in patients with marked discrepancies between subjective perceptions and objective measurements of sleep parameters. Future research will adopt a longitudinal， multi-night， multi-modal design and establish standardized diagnostic criteria， so as to achieve individualized， stratified precision treatment of paradoxical insomnia.

Objective To investigate the association of anxiety symptoms with thalamic GABA+ （the composite signal comprising γ-aminobutyric acid [GABA] and co-edited macromolecules） and glutamate-glutamine complex （Glx）-related metabolite markers in college students with moderate-to-severe insomnia. Methods A total of 34 college students who met the diagnostic criteria for insomnia disorder and had an Insomnia Severity Index score of ≥15 were enrolled， and according to the score of 7-item Generalized Anxiety Disorder Scale （GAD-7）， they were divided into anxiety symptom group （23 patients with a GAD-7 score of >4） and non-anxiety symptom group （11 patients with a GAD-7 score of ≤4）. Proton magnetic resonance spectroscopy was used to measure GABA+/creatine （Cr）， Glx/Cr， and GABA+/Glx ratios in both thalami， which were compared between groups， and the Spearman correlation analysis was used to investigate the correlation between GAD-7 score and the above metabolite markers. Results Compared with the non-anxiety symptom group， the anxiety symptom group had a significantly lower mean GABA+/Cr ratio in the left thalamus and in both thalami （Z=-2.43， P=0.015； Z=-2.31， P=0.021）， and there were no significant differences in Glx/Cr and GABA+/Glx ratios between the two groups （P>0.05）. GAD-7 score was not significantly correlated with any thalamic metabolite marker （P>0.05）. Conclusion Anxiety symptoms in college students with moderate-to-severe insomnia are associated with lower thalamic GABA+/Cr ratios， suggesting that thalamic GABA+-related metabolic alterations may be involved in the co-occurrence of insomnia and anxiety symptoms. Since this is an exploratory cross-sectional study with a small sample size and P-values are not adjusted for multiple comparisons， prospective studies with a larger sample size are needed in the future for further validation.

Objective To investigate the clinical and neuroelectrophysiological features of patients with comorbid narcolepsy and schizophrenia. Methods The database of the Electroencephalography Monitoring Center， Department of Neurology， Xijing Hospital， Air Force Medical University， was searched using the keywords “narcolepsy” and “schizophrenia” for the period from January 2018 to January 2026. The clinical and neuroelectrophysiological data of patients with comorbid narcolepsy and schizophrenia were analyzed， and the patients were followed up. Results A total of 130 patients with narcolepsy were identified， and 4 （2 females） of these patients were diagnosed with comorbid narcolepsy type 1 （NT1） and schizophrenia. The ages at NT1 onset were 8， 13， 10， and 22 years， respectively. The ages at schizophrenia onset in cases 1， 3， and 4 were 8， 18， and 25 years， respectively. Case 2 had exhibited psychiatric， psychological， and behavioral abnormalities since early childhood. All four patients experienced nocturnal nightmares. Case 1 developed psychiatric symptoms after methylphenidate administration， which did not resolve after discontinuation of the medication. All four patients underwent video-polysomnography and the multiple sleep latency test. The mean sleep latency was 1.3 min， and the mean number of sleep-onset rapid eye movement periods was 4.3. Conclusion Patients with comorbid NT1 and schizophrenia exhibit extremely short mean sleep latency， with sleep-onset rapid eye movement periods occurring in nearly every nap trial during the multiple sleep latency test. Nightmares may be common among patients with comorbid NT1 and schizophrenia； however， the potential clinical significance of nightmares remains unclear.

Objective To investigate the risk factors for sleep disorders in patients with chronic subjective dizziness （CSD）， and to construct a nomogram prediction model. Methods A total of 60 patients with CSD who were treated in Nanyang Second People’s Hospital from October 2023 to April 2024 and developed sleep disorders within the 6-month follow-up after treatment were enrolled as an occurrence group， while 60 patients with CSD who did not develop sleep disorders were enrolled as a non-occurrence group； these two groups formed the modeling set （n=120）. A total of 60 patients with CSD who were treated in our hospital from May to October 2024 and developed sleep disorders within the 6-month follow-up after treatment and 60 patients with CSD who did not develop sleep disorders were enrolled to form the validation set （n=120）. The baseline data of all patients were analyzed， and the receiver operating characteristic （ROC） curve was used to analyze the predictive value of continuous variables； univariate and logistic regression analyses were used to identify related risk factors； R software was used to construct a nomogram prediction model， and the goodness-of-fit test was conducted. Results There were significant differences between the two groups in age， number of comorbidities， disease duration， severity of dizziness， Self-Rating Anxiety Scale （SAS） score， Self-Rating Depression Scale （SDS） score， proportion of N3 stage， proportion of REM stage， and interleukin-6 （IL-6） level （P<0.05）. Age， disease duration， SAS score， SDS score， proportion of N3 stage， proportion of REM stage， and IL-6 level had a certain value in predicting sleep disorders in patients with CSD， with an area under the ROC curve of 0.630， 0.897， 0.696， 0.728， 0.832， 0.705， and 0.668， respectively （P<0.05）. The multivariate analysis showed that ≥3 comorbidities， a longer disease course， severe dizziness， a higher SDS score， and a lower proportion of N3 stage might increase the risk of sleep disorders （P<0.05）. The nomogram model constructed in this study showed good performance， with a C-index of 0.972 （95% CI 0.949-0.995）. The calibration curve showed that the model had a high consistency between the observed data and the predicted data. The decision curve showed that when the risk threshold was set at a value of >0.04， this model could effectively provide standardized net benefit. The Hosmer-Lemeshow goodness-of-fit test showed a 2 value of 4.039 and a P value of 0.854， indicating that this model had good prediction accuracy. Conclusion A number of ≥3 comorbidities， a longer disease course， severe dizziness， a higher SDS score， and a lower proportion of N3 stage may increase the risk of sleep disorders. In addition， the model has good discriminatory ability and calibration， suggesting that it holds promise for clinical application.

Objective To investigate the role and mechanism of dexmedetomidine （DEX） in regulating the function of the hypothalamic-pituitary-adrenocortical （HPA） axis in a rat model of postpartum sleep disorders （PPSD）. Methods A rat model of PPSD was established， and the rats were divided into control group， PPSD model group， low-dose DEX group （5 μg/kg）， and high-dose DEX group （25 μg/kg）. The open field test and the elevated plus maze test were used to assess behavioral changes； ELISA was used to measure the serum levels of adrenocorticotropic hormone （ACTH） and corticosterone （CORT）； qPCR and Western blotting were used to measure the mRNA and protein expression levels of glucocorticoid receptor （GR） and mineralocorticoid receptor （MR） in the hippocampus； immunohistochemistry was used to measure the expression of c-Fos in the hypothalamus； chemical genetics techniques were used to verify the effect of DEX on CRH neuronal activity in the hypothalamic paraventricular nucleus. Results Compared with the PPSD model group， DEX treatment significantly improved anxiety-like behavior and locomotor activity in PPSD rats （P<0.05）， reduced the serum levels of ACTH and CORT（P<0.05）， upregulated the mRNA and protein expression levels of GR and MR in the hippocampus （P<0.05）， and inhibited the expression of c-Fos in the hypothalamus （P<0.05）. Chemical genetics experiments showed that activation of CRH neurons could reverse the reductions in ACTH and CORT induced by DEX （P<0.05）. Conclusion DEX can inhibit CRH neuronal activity in the hypothalamus， regulate the function of the HPA axis， and thus improve anxiety-like behaviors and neuroendocrine disorders in rats with PPSD， possibly by regulating the expression of GR and MR in the hippocampus. DEX is expected to become a potential drug for the treatment of PPSD.

Objective To compare the histomorphological characteristics and collagen remodeling between plaque-containing and plaque-free intracranial arteries from the same donors with intracranial atherosclerosis. Methods Eight autopsy donors were included. Plaque-containing and plaque-free intracranial arteries from the same donors were used to establish eight paired samples. Serial sections were stained with hematoxylin and eosin， Masson trichrome， and picrosirius red. The intima-to-media area ratio and intimal collagen burden were compared between the paired plaque-containing and plaque-free arteries. Using the plaque shoulders as anatomical boundaries， medial thickness， medial collagen area fraction， and the proportions of type Ⅰ and type Ⅲ collagen-related fibers were compared between the regions inside and outside the plaque shoulders. Results Compared with the plaque-free arteries from the same donors， plaque-containing arteries showed intimal thickening， disruption of the internal elastic lamina， inflammatory cell infiltration， and foam cell accumulation. Both the intima-to-media area ratio and intimal collagen burden were significantly increased in plaque-containing arteries （both P<0.05）. Within the plaque-containing arteries， medial thickness was significantly lower inside the plaque shoulders than outside the plaque shoulders， whereas the medial collagen area fraction was significantly higher inside the plaque shoulders （both P<0.001）. There was no significant difference in the proportion of medial type Ⅰ collagen-related fibers between the two regions （P>0.05）. In contrast， the proportion of type Ⅲ collagen-related fibers was significantly higher inside the plaque shoulders （P<0.001）. Conclusion Intracranial atherosclerotic plaque formation is accompanied by increased intimal burden and collagen deposition. Medial thinning， relative collagen enrichment， and an increased proportion of type Ⅲ collagen-related fibers inside the plaque shoulders suggest more pronounced localized extracellular matrix remodeling in this region.

Objective To investigate the association between ABCG2 rs2231142 gene polymorphism and the severity of white matter hyperintensity （WMH） in patients with ischemic stroke （IS）. Methods A cross-sectional study was conducted among 498 patients with IS who were admitted to Department of Neurology， Affiliated Hospital of Guangdong Medical University， from January 2022 to July 2025. MassARRAY nucleic acid mass spectrometry was used to detect ABCG2 rs2231142 genotypes， and Fazekas scale was used to assess the severity of WMH. Clinical data were compared between the groups with different genotypes， and the ordinal logistic regression analysis was used to investigate the association between T allele dosage and WMH severity. Results Among the 498 patients， 252 （50.6%） carried the GG genotype， 200 （40.2%） carried the GT genotype， and 46 （9.2%） carried the TT genotype， suggesting that the genotype distribution was consistent with Hardy-Weinberg equilibrium （P=0.489）. With the increase in T allele dosage， there was an increase in serum uric acid and a reduction in estimated glomerular filtration rate （eGFR）， and there was a significant difference in the distribution of WMH severities between the groups with different genotypes （P=0.043）. After adjustment for age， sex， body mass index， hypertension， diabetes， hyperlipidemia， smoking， drinking， and serum uric acid， T allele dosage remained associated with the increase in WMH severity （OR=1.331， 95% CI 1.019-1.740， P=0.036）， and this association remained after further adjustment for eGFR （OR=1.311， 95%CI 1.002-1.714， P=0.048）. Conclusion ABCG2 rs2231142 T allele dosage is associated with the increase in WMH severity in patients with IS， suggesting that this locus may be involved in post-stroke cerebral small vessel injury burden through abnormal uric acid metabolism and renal function-related changes.

Objective To investigate the dynamic changes of plasma biomarkers in patients with acute ischemic stroke， and to assess their clinical value in the early differential diagnosis of stroke subtypes. Methods The patients with suspected stroke who were referred to emergency department were enrolled， and the cohort for analysis was determined after screening based on inclusion and exclusion criteria. All patients underwent standardized clinical assessments and blood sampling at predefined time points， and according to imaging findings and clinical diagnosis， they were divided into acute ischemic stroke （AIS） group， hemorrhagic stroke （HS） group， and stroke mimics （SM） group. The plasma levels of glial fibrillary acidic protein （GFAP） and total Tau protein （Tau） were measured at multiple time windows， including prehospital initial sampling， in-hospital secondary sampling， and sampling on the following morning. Data were compared between different stroke subtypes， and the dynamic changes of biomarkers from onset to sampling were analyzed， as well as the performance of GFAP level and GFAP release rate in the differential diagnosis of stroke subtypes. Results A total of 272 patients were enrolled， among whom there were 203 patients with AIS， 60 patients with HS， and 9 patients with SM. Comparison of baseline characteristics showed a significant difference in the distribution of National Institutes of Health Stroke Scale （NIHSS） score between the patients with different stroke subtypes. Multi-timepoint analyses showed that compared with the AIS group， the HS group had a significantly higher GFAP level at prehospital initial sampling （<1 hour and <3 hours）， in-hospital secondary sampling （at 3 hours）， and sampling on the following morning （P<0.001）， with greater differences between the two groups over time. In contrast， there was no significant difference in plasma Tau level between the HS group and the AIS group at each time point （P>0.05）. The analysis of dynamic changes showed that GFAP level in AIS patients gradually increased with the increase in onset-to-sampling time， while GFAP level in HS patients showed a steeper non-linear changing pattern， and Tau showed no clear time-dependent changing pattern in either stroke subtype. The receiver operating characteristic curve analysis showed that GFAP had good performance for identifying different stroke subtypes during prehospital sampling and in-hospital secondary sampling， and GFAP obtained by secondary sampling had the largest area under the curve. The combined distribution of prehospital GFAP release rate and GFAP level formed relatively distinct clusters between AIS and HS patients. Conclusion There is a significant increase in the plasma level of GFAP in the ultra-early stage in patients with HS， and it shows good performance for identifying different stroke subtypes across multiple time windows； Tau has a limited value in the early differential diagnosis of stroke subtypes. Temporal assessment of GFAP level and GFAP release rate can improve the accuracy of early stroke classification and provide an objective reference for clinical decision-making when imaging is unavailable or delayed.

Objective To investigate the changing trend of the disease burden of intracerebral hemorrhage （ICH） in the labor force population aged 20‒54 years in China from 1990 to 2023， to predict the level of disease burden from 2024 to 2038， and to quantify the contribution of population aging and disease risk changes to the change of disease burden. Methods The 2023 Global Disease Burden Database was used to extract the incidence， mortality， disability-adjusted life years （DALY） data， and age-standardized rates of ICH for the 20‒54 age group in China from 1990 to 2023. Average annual percentage change was calculated； the Kitagawa decomposition method was used to quantify the contribution of age structure effects and risk change effects to disease burden changes； an Autoregressive Integrated Moving Average model was constructed to predict the disease burden from 2024 to 2038. Results From 1990 to 2023， the absolute number of incident cases of ICH among the labor force population aged 20-54 years in China remained essentially stable， whereas mortality and DALY numbers decreased by approximately 40% and 41%， respectively； the age-standardized incidence rate （ASIR）， age-standardized mortality rate （ASMR）， and age-standardized DALY rate （ASDR） all continued to decline. The decomposition analysis showed that approximately 65%‒70% of the growth in absolute case numbers could be attributed to population aging， whereas the reduction in standardized rates by more than 95% was driven by the reduction in disease risks across age groups. The disease burden increased sharply with the increase in age， and the burden rate of male individuals remained 1.3‒1.8 times that of female individuals across all age groups. The prediction analysis showed that ASIR， ASMR， and ASDR will continue to decline from 2024 to 2038， but the decline rate in men will be slower than that in women， potentially widening the gender gap in disease burden. Conclusion From 1990 to 2023， there was a significant improvement in the age-standardized burden of ICH in the labor force population in China， while the limited decline in absolute case numbers associated with population aging remains a persistent challenge.Middle-aged male individuals （especially those aged 40-54 years） tend to have the heaviest disease burden and a relatively slow improvement. Primary prevention and disease management should be strengthened for this population in the future to address the public health pressure brought by demographic changes.

Objective To investigate the relationships between the fluctuation amplitude of mean arterial pressure （MAP） during endovascular therapy and the 90-day neurological outcomes in patients with acute anterior circulation large vessel occlusion， and provide evidence for refined intraoperative blood pressure management. Methods This single-center retrospective cohort study categorized patients into a blood pressure stability group （fluctuation≤20%） and a blood pressure variability group （fluctuation>20%） based on whether their intraoperative maximum and minimum MAP remained within ±20% of the mean intraoperative MAP. The primary outcome was modified Rankin Scale （mRS） score at 90 days post-procedure. Multinomial and binary logistic regression models were employed to assess the independent impact of blood pressure variability on outcomes， with adjustment for confounding factors including age， baseline NIH Stroke Scale score， and post-procedure intracranial hemorrhage. Results Among the 209 enrolled patients， the stability group showed a significantly higher probability of achieving an excellent neurological outcome （mRS 0-1） compared to the variability group （OR=2.37，95%CI 1.09‒5.14，P=0.029）. Multinomial regression analysis further indicated that stable blood pressure specifically reduced the risk of progression to mild disability （mRS=2）， moderate disability （mRS=3）， and death （mRS=6）， with adjusted ORs of 0.19， 0.16， and 0.04， respectively （all P<0.05）. When functional independence （mRS 0-2） was used as the outcome， the adjusted OR for blood pressure stability group was 1.72 （95% CI 0.74‒3.98），The result did not reach statistical significance （P=0.206）. Conclusion Maintaining intraoperative MAP fluctuations within ±20% of the mean level during endovascular therapy is significantly associated with increased odds of excellent neurological outcomes and reduces the risks of mild-to-moderate disability （mRS 2‒3） and death （mRS=6）. Intraoperative blood pressure stability serves as a critical modifiable factor for improving the long-term outcomes of acute ischemic stroke.

Anti-myelin-associated glycoprotein antibody-positive peripheral neuropathy （MAG-PN） is a rare paraproteinemia-associated peripheral neuropathy. This article reports a male patient， aged 73 years， who initially presented with numbness and weakness of both lower limbs and gait instability， accompanied by tremor and autonomic symptoms such as frequent urination， incomplete bladder emptying， and alternating constipation and diarrhea. He was initially misdiagnosed with lumbar disc herniation. Based on the results of neural electrophysiological examination， serum immunofixation electrophoresis， and detection of anti-myelin-associated glycoprotein antibodies， the patient was finally diagnosed with MAG-PN. The clinical symptoms of the patient were significantly improved after treatment with rituximab combined with glucocorticoids. This report reviews the clinical data of this case and performs a literature review to improve awareness of the atypical clinical manifestations， differential diagnosis， and therapeutic strategies of this disease among clinicians.

Hereditary diffuse leukoencephalopathy with spheroids （HDLS） is a rare autosomal dominant genetic disease caused by mutations in the colony-stimulating factor 1 receptor （CSF1R） gene， and it is characterized by diverse clinical and radiological manifestations， leading to the difficulty in early diagnosis. This article reports a case of a young female HDLS patient with the initial manifestations of prominent mental and behavioral disorders and spastic paralysis. A retrospective analysis was performed for the diagnosis and treatment process， and head magnetic resonance imaging showed symmetric hyperintensities on diffusion-weighted imaging in the bilateral frontoparietal white matter， accompanied by thinning of the corpus callosum and brain atrophy. Whole-exome sequencing identified a heterozygous missense mutation， c.2350T>C （p.I994T）， in exon 19 of the CSF1R gene， and the pedigree analysis confirmed that the mutation was inherited from her mother. This case expands the clinical phenotypic spectrum of HDLS and reports a novel pathogenic mutation site， underscoring the importance of CSF1R gene screening in young patients presenting with neuropsychiatric symptoms. At present， symptomatic/supportive treatment remains the main treatment method for HDLS， and this study provides new ideas for exploration of targeted therapies and genetic counseling in the future.

Parkinson disease （PD） is a neurodegenerative disease characterized by abnormal aggregation of α-synuclein. PD-related orthostatic hypotension （OH） is a typical non-motor symptom that seriously affects the quality of life of patients. The main cause of OH is autonomic dysfunction， which is caused by the coexistence of two mechanisms： peripheral sympathetic degeneration and dysregulation of the central autonomic network. Head-up tilt test， as the currently recognized gold standard for the evaluation of orthostatic blood pressure regulation ability， can accurately determine the presence of OH by standardized postural stimulation. The test can classify OH into different subtypes according to hemodynamic parameters and reflect the degree of autonomic dysfunction， thereby facilitating the exploration of the pathogenesis of OH in PD patients and guiding the selection of clinical treatment strategies. This article discusses the mechanisms of peripheral and central autonomic dysfunction and the diagnostic classification by head-up tilt test in PD complicated with OH. On this basis， combined with the development of novel multimodal technologies in recent years， it proposes future research directions， aiming to provide a theoretical basis and practical guidance for the precise diagnosis and treatment of PD-OH.

The etiological profile of young-onset ischemic stroke （aged 18‒50 years） differs from that of the elderly population， and the disease burden has been steadily increasing. This article systematically reviews the research advances in etiological heterogeneity and multidisciplinary team （MDT）-based targeted management strategies for young-onset ischemic stroke. Among the young patients with ischemic stroke， there is a relatively high proportion of patients with stroke of other determined etiology or stroke of undetermined etiology， while there is a relatively low proportion of the patients with large-artery atherosclerosis， and such marked heterogeneity poses challenges to the traditional single-discipline diagnostic and therapeutic model. Therefore， this article proposes to establish a diagnostic and therapeutic approach under the MDT framework， which prioritizes the identification and standardized management of common etiologies and identifies rare etiologies through collaboration， covering tiered etiological screening pathways， individualized intervention strategies based on etiological subtypes， and life-course rehabilitation management. Standardization of the MDT-based diagnostic and therapeutic model for young-onset ischemic stroke can help to identify the etiology and formulate standardized individualized treatment and secondary prevention regimens， thereby improving prognosis， reducing disability and recurrence rates， enhancing quality of life， and alleviating economic and psychological burdens on families and society.