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Idiopathic inflammatory myopathy (IIM) is a group of autoimmune diseases with clinical features presented with muscle weakness and inflammation in muscle. Compared with EMG and muscle biopsy, imaging examination is more convenient and non - invasive, and is valuable in the assessment of diagnosis, evaluation of disease extent and prognosis. MRI is widely used in clinical practice as its high resolution of soft tissue, which may provides detailed information about muscle. [ABSTRACT FROM AUTHOR]

A correction to the article "Combination of mild hypothermia with neuroprotectants has greater neuroprotective effects during oxygen-glucose deprivation and reoxygenation-mediated neuronal injury" that was published in the previous issue is presented.

Major ozonated autohemotherapy has been shown to promote recovery of upper limb motor function in patients with acute cerebral infarction, but whether major ozonated autohemotherapy affects remote injury remains poorly understood. Here, we assumed that major ozonated autohemotherapy contributes to recovery of clinical function, possibly by reducing remote injury after acute cerebral infarction. Sixty acute cerebral infarction patients aged 30-80 years were equally and randomly allocated to ozone treatment and control groups. Patients in the ozone treatment group received medical treatment and major ozonated autohemotherapy (47 mg/L, 100 mL ozone) for 10 ± 2 days. Patients in the control group received medical treatment only. National Institutes of Health Stroke Scale score, modified Rankin scale score, and reduced degree of fractional anisotropy values of brain magnetic resonance diffusion tensor imaging were remarkably decreased, brain function improved, clinical efficiency significantly increased, and no obvious adverse reactions detected in the ozone treatment group compared with the control group. These findings suggest that major ozonated autohemotherapy promotes recovery of neurological function in acute cerebral infarction patients by reducing remote injury, and additionally, exhibits high safety., Competing Interests: Conflicts of Interest: None declared.

Objective: Mutations in CACNA1A, which encodes the P/Q-type calcium channel subunit, are responsible for at least 3 allelic diseases, namely type 2 episodic ataxia (EA-2), familial hemiplegic migraine?type-1 (FHM1), and spinocerebellar ataxia type-6?(SCA 6). Herein we present a case of ataxia with episodic tremors in a 19-year-old man with a missense mutation of CACNA1A gene and summarize the clinical features, genetic analysis and treatment in this case and in his affected family members., Methods: Physical examinations were conducted for the patient and his affected family members. DNA sample from the proband was analyzed with next-generation sequencing technology to identify the causative mutation. Sanger sequencing was used to confirm the gene mutation in the family members., Results: Physical examinations of the patient revealed signs of ataxia, drunken gait, and tremor of his head and body. Four other members in his family had similar but much milder symptoms. A heterozygous missense mutation in CACNA1A (NM_001127221.1 c.4034G->A, p.R1345Q, exon 25) was identified in the proband, which was confirmed in the affected family members. The proband did not respond to methazolamide treatment, but his tremor symptom was well controlled with flunarizine, a calcium channel blocker., Conclusion: Based on the clinical features, mutation analysis and treatment response, we suggest that this patient with a missense CACNA1A mutation, R1345Q, has a new type of ataxia with episodic tremor other than any of EA2, FHM1, or SCA 6.

Objective: To investigate whether intensive statin therapy during the perioperative period improves outcomes in patients undergoing middle cerebral artery (MCA) stent implantation for ischemic stroke., Methods: Forty patients with ischemic stroke undergoing delayed stent implantation in our department from January, 2010 to November, 2014 were randomized to intensive statin group (atorvastatin, 80 mg/day, 3 days before till 3 days after intervention; n=20) and standard therapy group (atorvastatin, 20 mg/day, n=20). All the patients received long-term atorvastatin treatment thereafter (20 mg/day). Serum levels of C-reactive protein (CRP), vascular cell adhesion molecule-1 (VCAM-1), and soluble extracellular matrix metalloproteinase inducer (EMMPRIN/CD147) were measured at 24 h before and 24 h after the intervention. The primary end point was procedure-related intra-stent thrombosis, 1-month incidence of major adverse cerebrovascular events (stroke, transient ischemic attack, in-stent restenosis, death or unplanned revascularization)., Results: The basic clinical data were similar between the two groups before the intervention (P>0.05). In the intensive therapy group, the levels of CRP, VCAM-1, and sCD147 were significantly lower at 24 h after the intervention than the levels before intervention (P<0.05) and the postoperative levels in the standard therapy group (P<0.05). The levels of CRP, VCAM-1, and sCD147 were all increased after the intervention in the standard therapy group (P>0.05). The incidence of primary end point was lower in intensive therapy group than in standard therapy group (P<0.05)., Conclusion: In patients undergoing MCA intravascular stent implantation for ischemic stroke, perioperative intensive statin therapy improves the patients' outcomes, reduces the levels of CRP, VCAM-1 and sCD147 molecules, and lowers the incidences of cerebrovascular events.

Several studies have demonstrated that mild hypothermia exhibits a neuroprotective role and it can inhibit endothelial cell apoptosis following ischemia/reperfusion injury by decreasing caspase-3 expression. It is hypothesized that mild hypothermia exhibits neuroprotective effects on neurons exposed to ischemia/reperfusion condition produced by oxygen-glucose deprivation. Mild hypothermia significantly reduced the number of apoptotic neurons, decreased the expression of pro-apoptotic protein Bax and increased mitochondrial membrane potential, with the peak of anti-apoptotic effect appearing between 6 and 12 hours after the injury. These findings indicate that mild hypothermia inhibits neuronal apoptosis following ischemia/reperfusion injury by protecting the mitochondria and that the effective time window is 6-12 hours after ischemia/reperfusion injury.

The discrepancy in results regarding neuroprotective agents in animal experiments compared to clinical trials is a major problem. While many neuroprotective agents have been proven effective in a variety of animal ischemic stroke models, none have been shown to work in phase III clinical trials. This review retrospectively summarizes the neuroprotectants selected for human randomized controlled trials (RCT) and explores the reasons behind the clinical translational failure of these agents. Here, we suggest that there are many factors (model selection, anesthetic choice, physiological monitoring, model success criteria, embolus property, reperfusion damage, infarction area, therapeutic time window, drug penetration, blood concentration, gender difference, and outcome evaluation) responsible for this phenomenon. Ultra-early treatment using a "home run" drug and multi-target therapy may be the most promising for future consideration.

Objective: To evaluate the risk factors of prognosis in patients with primary pontine hemorrhage., Methods: A retrospective analysis was conducted using data from 60 patients admitted with a diagnosis of primary pontine hemorrhage to the Department of Neurology of Nanfang Hospital in Guangzhou City. Patients were classified as survivors (n=34) and non-survivors (n=26) according to their outcomes on 30 days from the onset of symptoms. Univariate analysis and multivariate logistic regression analysis were performed on clinical data and imaging features of patients. Receiver operating characteristic curve (ROC curve) analysis was used on continuous parameters verified by multivariate logistic regression analysis to determine their cut-off value., Results: The 30-day mortality was 43.3% for 60 patients with primary pontine hemorrhage. Univariate analysis showed Glasgow coma scale (GCS) at admission, temperature, heart rate, hemorrhage volume, mechanical ventilation, involvement of ventricles and location of hematoma were statistically related to 30-day mortality in patients with primary pontine hemorrhage. Multivariate logistic regression analysis demonstrated that the GCS at admission [odds ratio (OR)=0.745, 95% confidence interval (95%CI) 0.585 to 0.949], hemorrhage volume (OR=1.438, 95%CI 1.077 to 1.919) and location of hematoma (basal-tegmental hemorrhage, OR=0.120, 95%CI 0.016 to 0.904) were independent risk factors of poor prognosis in patients with primary pontine hemorrhage (all P<0.05). ROC curve analysis showed the cut-off value for GCS score at admission and hemorrhage volume was 7.5 and 5.5 ml, respectively., Conclusion: Patients suffering from primary pontine hemorrhage in the basal-tegmental region, GCS<7.5 at admission and hemorrhage volume≥5.5 ml would lead to a poor outcome in 30 days.

Objective: To analyze the risk factors of cerebral microbleeds (CMBs)., Methods: A total of 113 patients with cerebrovascular diseases underwent examinations of magnetic resonance imaging (MRI) of the brain (including T1WI, T2WI, FLAIR, and SWI) and blood biochemical tests, and the brain regions, number and grades of the CMBs were analyzed. The association between CMBs and the cardiovascular risk factors were analyzed., Results: A The occurrence and grade of CMBs were associated with the patients' age, hypertension, diabetes, lacunar infarction, diastolic blood pressure, systolic blood pressure and high-density lipoprotein (HDL) levels (P<0.05). CMB occurrence was significantly associated with diabetes, hypertension, and lacunar infarction (P<0.05), and its incidence varied significantly between different brain regions (P<0.05)., Conclusion: Age, hypertension, diabetes, lacunar infarction, diastolic blood pressure, systolic blood pressure, and HDL are all risk factors for CMBs, among which diabetes, hypertension, and lacunar infarction are significant risk factors. CMBs occurs most frequently in the cortex and subcortical region, followed by the basal ganglia, thalamus, and the cerebellum, and most unlikely in the brainstem.

Objective: To evaluate the clinical application of susceptibility-weighted magnetic resonance imaging (SWAN) in lacunar cerebral infarction imaging., Methods: Forty-two cases of lacunar cerebral infarction, including 18 complicated by high blood pressure, 4 by type 2 diabetes and 12 by both high blood pressure and type 2 diabetes, underwent examinations with SWAN and conventional MRI sequences (including GRE sequence T(1) and T(2), T(2) gradient echo, T(2) FLAIR, DWI). The imaging data were analyzed in comparison with the clinical data of the patients., Results: In 23 patients with lacunar cerebral infarction, intracerebral micro-hemorrhage displayed point-like, round and oval low signal on SWAN. A total of 123 lesions were identified, distributing from the cortical, subcortical, basal ganglia, thalamus, brain stem to the cerebellum. The conventional sequences were more sensitive in detecting the majority of lacunar cerebral infarction than SWAN, while the latter showed better performance in displaying cerebral micro-hemorrhage, tiny blood vessels and small vascular malformations as well as other small vascular diseases. SWAN was superior to other sequences in showing lacunar cerebral infarction complicated by cerebral micro-hemorrhages., Conclusion: MRI SWAN can better display lacunar cerebral infarction associated with cerebral micro-hemorrhages and small veins in the infract region. Identification of the micro-hemorrhages in lacunar cerebral infarction can be critical in determining the proper treatments. Patients with lacunar cerebral infarction are likely to have cerebral micro-hemorrhages in close relation to the number of lacunar infarction sites. The cerebral micro-hemorrhages and lacunar cerebral infraction are both signs of micro-vessel damage of the brain.