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ObjectiveAmong adolescents with depression, the occurrence of non-suicidal self-injury (NSSI) behavior is prevalent, constituting a high-risk factor for suicide. However, there has been limited research on the neuroimaging mechanisms underlying adolescent depression and NSSI behavior, and the potential association between the two remains unclear. Therefore, this study aims to investigate the alterations in functional connectivity (FC) of the regions in the prefrontal cortex with the whole brain, and elucidates the relationship between these alterations and NSSI behavior in adolescents with depression.MethodsA total of 68 participants were included in this study, including 35 adolescents with depression and 33 healthy controls. All participants underwent assessments using the 17-item Hamilton Depression Rating Scale (17-HAMD) and the Ottawa Self-Harm Inventory. In addition, functional magnetic resonance imaging (fMRI) data of the participants’ brains were collected. Subsequently, the FCs of the regions in the prefrontal cortex with the whole brain was calculated. The FCs showing significant differences were then subjected to correlation analyses with 17-HAMD scores and NSSI behavior scores.ResultCompared to the healthy control group, the adolescent depression group exhibited decreased FCs in several regions, including the right frontal eye field, left dorsolateral prefrontal cortex, right orbitofrontal cortex, left insula and right anterior cingulate coetex. The 17-HAMD score was positively correlated with the frequency of NSSI behavior within 1 year (rs = 0.461, p = 0.005). The FC between the right anterior cingulate cortex and the right precuneus showed a negative correlation with the 17-HAMD scores (rs = −0.401, p = 0.023). Additionally, the FC between the right orbitofrontal cortex and the right insula, demonstrated a negative correlation with the frequency of NSSI behavior within 1 year (rs = −0.438, p = 0.012, respectively).ConclusionAdolescents with depression showed decreased FCs of the prefrontal cortex with multiple brain regions, and some of these FCs were associated with the NSSI frequency within 1 year. This study provided neuroimaging evidence for the neurophysiological mechanisms underlying adolescent depression and its comorbidity with NSSI behavior.

Background: Major depressive disorder (MDD) patients face an increased risk of developing cognitive impairments. One of the prominent cognitive impairments in MDD patients is verbal fluency deficit. Nonetheless, it is not clear which vulnerable brain region in MDD is interactively linked to verbal fluency deficit. It is important to gain an improved understanding for verbal fluency deficit in MDD.Methods: Thirty-four MDD patients and 34 normal controls (NCs) completed resting-state fMRI (rs-fMRI) scan and a set of verbal fluency tests (semantic VFT and phonemic VFT). Fourteen brain regions from five brain networks/systems (central executive network, default mode network, salience network, limbic system, cerebellum) based on their vital role in MDD neuropathology were selected as seeds for functional connectivity (FC) analyses with the voxels in the whole brain. Finally, correlations between the z-score of the FCs from clusters showing significant between-group difference and z-score of the VFTs were calculated using Pearson correlation analyses.Results: Increased FCs in MDD patients vs. NCs were identified between the bilateral posterior cingulate cortex (PCC) and the right inferior frontal gyrus (triangular part), in which the increased FC between the right PCC and the right inferior frontal gyrus (triangular part) was positively correlated with the z score of phonemic VFT in the MDD patients. Moreover, decreased FCs were identified between the right hippocampal gyrus and PCC, as well as left cerebellum Crus II and right parahippocampal gyrus in MDD patients vs. NCs.Conclusions: The MDD patients have altered FCs among key brain regions in the default mode network, the central executive network, the limbic system, and the cerebellum. The increased FC between the right PCC and the right inferior frontal gyrus (triangular part) may be useful to better characterize pathophysiology of MDD and functional correlates of the phonemic verbal fluency deficit in MDD.

Objective: This study aims to evaluate the efficacy of music-supported therapy for stroke patients' hand function.Methods: The databases used included Cumulative Index to Nursing and Allied Health Literature (CINAHL), MEDLINE, PubMed, Embase, Music Index, and Google Scholar. Studies published between January 2010 and August 2020 were included. The searching key terms included “music-supported therapy,” “music therapy,” “hand function,” “hand dysfunction,” “stroke,” “ischemic,” and “hemorrhagic.” Randomized controlled trials or controlled trials involving adults who have hand function problems caused by stroke are included in this study. The methodological quality and risk of bias of the included studies were rated by two independent assessors under the guidance of Cochrane collaboration's risk of bias tool.Results: Twelve studies that met the inclusion criteria were included in this study. Totally, the data included 598 stroke patients (345 male, 253 female) with recruited time from 1.7 months to 3 years, and the mean age of the participants were 61.09 years old. Based on the Cochrane risk of bias tool, study quality ranged from three to seven out of seven points. Compared with the control group, outcomes including hand strength, range of joint motion, dexterity of hands, arm function, and quality of life were significantly superior with music-supported therapy. Five studies reported improved dexterity of hands, and one study reported the improvement of range of motion and strength of patients' hands, which supported the therapy has positive effects on patients' hand function and improving their quality of life after the therapy. The therapy ranged over a period of 4–8 weeks, with an average duration of 30 min/session and an average of three times per week.Conclusion: Based on the results, music-supported therapy could be a useful treatment for improving hand function and activities of daily living in patients with stroke, especially for patients within 6 months after stroke. However, the low certainty of evidence downgrades our confidence to practice in hospital. More and more randomized controlled trials and larger sample sizes are required for a deeper review.

Background: DBS has been shown to significantly affect motor symptoms in Parkinson's disease (PD). However, some studies have suggested that it may have adverse effects on patients' neurocognitive function. To clarify this operation's effect on neurocognitive function, we collected studies containing neurocognitive function evaluation for qualitative and quantitative analysis.Methods: We searched relevant clinical studies through Pubmed and Embase databases and extracted and sorted out information such as sample size, post-operative scores, pre-operative and post-operative evaluation interval, PD course, and exclusion criteria, from articles meeting the standards. The magnitude and variance of the DBS group's combined effects and the drug therapy group in each neurocognitive domain were calculated and analyzed by the random-effects model.Results: Compared with the drug treatment group, the verbal fluency of patients in the experimental group was significantly decreased at least moderately (ES = −0.553), in which the phonemic fluency declines greatly (ES = −0.842), learning and memory ability was slightly decreased (ES = −0.305), and other neurocognitive functions were not significantly decreased.Conclusion: STN-DBS can affect verbal fluency and damage learning and memory. There was no significant correlation between the above effects and disease progression itself, and it was more likely to be associated with STN-DBS. It is suggested that post-operative patients should be trained and evaluated regularly for their verbal fluency and learning and memory ability. The safety of STN-DBS is acceptable for the majority of patients with motor symptoms.

Background: Major depressive disorder (MDD) is one of the most common and costly psychiatric disorders. In addition to significant changes in mood, MDD patients face an increased risk of developing cognitive dysfunction. It is important to gain an improved understanding of cognitive impairments and find a biomarker for cognitive impairment diagnosis in MDD.Methods: One hundred MDD patients and 100 normal controls (NCs) completed resting-state fMRI (rs-fMRI) scan, in which 34 MDD patients and 34 NCs had scores in multiple cognitive domains (executive function, verbal fluency, and processing speed). Twenty-seven regions of interest from the default mode network (DMN), central executive network (CEN), salience network (SN), and limbic system (LS) were selected as seeds for functional connectivity (FC) analyses with the voxels in the whole brain. Finally, partial correlations were conducted for cognitive domain scores and FCs with significant differences between the MDD and NC groups.Results: Significant FC differences between groups were identified among the seeds and clusters in the DMN, CEN, LS, visual network, somatomotor network, ventral attention network, and dorsal attention network. In the MDD patients, the magnitude of the Stroop interference effect was positively correlated with the illness duration, and the illness duration was negatively correlated with the FC between the right ventral hippocampal gyrus and the left inferior frontal gyrus. However, the correlation between the Stroop interference effect and the FC of the right anterior prefrontal cortex with the left cerebellum_4_5 was disrupted in these patients.Conclusions: The MDD patients have altered FCs among multiple brain networks and a disrupted correlation between the FC of prefrontal cortex and executive function. The disrupted correlation could present before the symptoms develop and may be the core process in the development of executive function impairment.

Objectives: The lesion topography of medullary infarction (MI) is heterogeneous and its correlation with stroke etiology remains elusive. We aim to clarify the lesion pattern of MI and to assess its correlation with stroke etiology. Material and Methods: Of 1129 subjects with available DWI in SMART study (a multi-center trial concerning secondary stroke prevention in China) between April 2008 and December 2010, 43 patients with DWI confirmed MI (3.8%) were retrospectively evaluated. Lesions were categorized as lateral and medial medullary infarction (LMI and MMI, 33 and 10 subjects respectively) at 3 levels rostro-caudally and correlated with the stroke etiology. Clinical profiles and long-term prognosis were analyzed. Results: Large artery atherosclerosis, small vessel occlusion, cardiogenic embolism and artery dissection accounted for 29, 11, 1, and 2 infarcts, respectively. Large artery disease was the most common cause in LMI (24 of 33, 72.7%) whereas small vessel occlusion was not uncommon in MMI (5 of 10, 50.0%). Though the difference of infarct pattern between large artery atherosclerosis and small vessel occlusion was insignificant, two distinct lesion patterns were considered to be relevant: (1) Rostral MMI with continuous medial pontine infarctions were more likely attributed to small vessel occlusion than large artery atherosclerosis. Kameda et al. (2) MMI with ventral to dorsal extension were more often caused by large artery disease than small vessel occlusion. Median NIHSS at admission was 4. During a median follow-up of 17 months, 2 patients died and 2 experienced recurrent ischemic events, 39 of 41 subjects (95.1%) were functional independent (mRS 0-2). Conclusions: This multi-center study demonstrates that MI has distinct lesion pattern depending on various stroke etiologies andmechanisms. Future investigations with larger sample size should establish the lesion pattern of MI and validate its correlation with the stroke etiology and mechanisms, which might improve stroke management. [ABSTRACT FROM AUTHOR]

Background: Few studies have investigated structural imaging findings of cerebral venous thrombosis (CVT) in China. The structural imaging [head computed tomography (CT) and routine brain magnetic resonance imaging (MRI)] can assess any parenchymal lesion secondary to the venous thrombosis and reveal direct signs of intraluminal thrombus. In recent years, many patients can be diagnosed with CVT more rapidly and directly by structural imaging. The aim of the present study is to determine the performance of structural imaging in the diagnosis and outcome of CVT in a large cohort single center of Chinese patients. Methods: We evaluated consecutive patients admitted to our hospital with CVT receiving structural imaging from 1991 to 2015. A neuroradiologist, blinded to clinical data, independently reviewed the structural imaging, including head CT and routine MRI for parenchymal lesions and signs of dural venous sinus thrombosis, as well as the MRV/ DSA findings. The Clinical and laboratory data were reviewed and recorded for further analysis. results: 117 patients were included in this study, 68 (58.1%) were females. Parenchymal lesions were identified in 56.4% (66/117) of the patients on structural imaging, including focal edema in 30.8%, hemorrhage in 19.7%, and brain swelling in 4.3% of the patients. Patients with parenchymal lesions presented with more often seizures (P < 0.001) and less often headache (P = 0.049). Intraluminal thrombus within the sinuses or veins on structural imaging was found in 28.2% (33/117) of the patients. Patients with both intraluminal thrombus and parenchymal lesions on structural imaging had more acute onset (P = 0.01) and present more consciousness disturbance (P = 0.007). conclusion: Intracranial lesions on structural imaging are frequently found in patients with CVT. Patients with parenchymal lesions on structural imaging, especially with intraluminal thrombus simultaneously, tend to have a severe clinical picture and might lead to a devastating or fatal outcome. Structural imaging may help on early diagnosis and predict the poor outcome of CVT. [ABSTRACT FROM AUTHOR]

Objective: It is critical to identify factors that significantly impede the correct action of calling emergency medical service (EMS) in the high-risk population with a previous history of transient ischemic attack (TIA) and further explore the urban–rural difference in China.Methods: Participants with previous TIA from the China National Stroke Screening Survey and its branch study (FAST-RIGHT) were interviewed cross-sectionally (n = 2,036). The associations between the outcome measure of not calling EMS and multiple potential risk factors were examined, including demographic information, live (or not) with families, medical insurance type, urban or rural residence, awareness of stroke symptoms, annual personal income, presence of cardiovascular disease or risk factors, and stroke history in family members or friends. The sample was further stratified to explore the urban–rural difference by their residency.Results: The proportion of not calling EMS was 36.8% among all participants with previous TIA, and these were 21.7 and 48.4% among urban and rural participants, respectively. Among rural participants, risk factors that were significantly associated with not calling EMS included primary school education [odds ratio (OR) 2.50, 95% confidence interval (CI) 1.89–3.33], living with family (OR 2.09, 95% CI 1.33–3.36), unaware stroke symptoms (OR 2.60, 95% CI 1.81–3.78), and low income (OR 1.57, 95% CI 1.19–2.07). Among urban participants, only low income was significantly associated with an increased risk of not calling EMS (OR 1.74, 95% CI 1.10–2.72).Conclusions: Rural residents with previous TIA in China had a higher percentage of not calling EMS. Multiple risk factors have been identified that call for targeted intervention strategies.

Cases of autoimmune glial fibrillary acidic protein (GFAP) astrocytopathy who were initially diagnosed with chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) were rarely reported. Herein, we reported a 31-year-old woman who presented with 7 years of recurrent headache. Her clinical history, symptoms, brain MRI enhancement features, and response to treatment during each attack were reviewed. Her brain MRI 7 years ago demonstrated characteristic pepper-like enhancement of pontine and cerebellum and her symptoms resolved completely after taking a high-dose of steroids. She was suspected with the diagnosis of CLIPPERS, and she experienced five relapses once the oral steroid was tapered below 20 mg/day. During her last relapse, she experienced fever and psychosis, and GFAPα-antibodies were detected in her serum and cerebrospinal fluid by antigen-transfected HEK293 cell-based assay (indirect immunofluorescence assay). She obtained relief again after steroid therapy, and her diagnosis converted to autoimmune GFAP astrocytopathy. Autoimmune GFAP astrocytopathy may mimic CLIPPERS, both clinically and radiologically. Long-term follow-up is essential for necessary diagnosis revision at each new attack in patients with a diagnosis of CLIPPERS.

Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) are X-linked recessive neuromuscular disorders caused by mutations in DMD. A high-quality database of DMD/BMD is essential not only for clinical practice but also for fundamental research. Here, we aimed to build the largest Chinese national dystrophinopathy database using the National Rare Diseases Registry System of China. Peking Union Medical College Hospital (PUMCH) was the National Rare Diseases Center of China. This research involved 2013 patients with dystrophinopathies, whose diagnoses were confirmed; they were registered and followed up at PUMCH from March 2011 to December 2018. Family history, clinical signs, and treatment data were reported for patients with DMD and BMD at different rates. All six serum biochemical indexes could accurately distinguish between DMD and BMD patients. Copy number variations were the most frequent mutation type (79.2% in DMD and 84.3% in BMD), of which large deletions accounted for 88.4 and 88.6%, large duplications accounted for 11.6 and 11.4% in DMD and BMD, respectively. An exon deletion hotspot, located in exons 45–54, was observed in DMD, and intron 44 was the most frequent deletion starting point (26.5%). Duplication and single nucleotide variations appeared to be uniformly distributed among all exons. Eleven patients were identified to have ultrarare mutation types. Eleven other patients suffered from two separate mutations simultaneously, some of which may have taken place via dependent mechanisms. Thus, we have established the largest hospital-based Chinese dystrophinopathy database via the National Rare Diseases Registry System. This study provides valuable information for further diagnostic and therapeutic studies of dystrophinopathy.