Clinical observations of acute onset of myopic optic neuropathy in a real-world setting

AIM: To describe the clinical features of acute myopic onset of optic neuropathy and observe the effects of retrobulbar and systemic glucocorticoid therapy in a realworld setting.METHODS: A retrospective observational case series included 18 patients with a clinical diagnosis of acute onset of myopic optic neuropathy in a real-world setting. While the patients were using retrobulbar and systemic glucocorticoid therapy, various imaging examination data were analysed, and the clinical features of myopic optic neuropathy were summarized for 6 mo to 2 y. RESULTS: The included group of patients with acute onset of myopic optic neuropathy consisted mostly of females(n=11). The visual field(VF) showed abnormalities in bilateral eyes, including the spread of physiological blind spots, central and paracentral dark spots, and centripetal peripheral VF reduction;but central vision with no subjective changes. The visual evoked potential(VEP) was abnormal in all eyes with vision loss. The best corrected visual acuity(BCVA) was improved from 1.04±0.63 to 0.47±0.57(log MAR) af ter glucocor ticoid treatment(P<0.05). In patients with a short course(within 1 wk), recovery was fast and achieved the same BCVA as recorded before the onset within 6 d. However, in patients with the long course(1 to 2 wk), recovery was slow and did not achieve the BCVA recorded before the onset within 10 d. The changes of intraocular pressure(IOP) were not obvious before and after treatment(18.68±5.30 vs 19.55±5.34 mm Hg, P>0.05). There was no recurrence during long-term followup observation.CONCLUSION: The acute onset of myopic optic neuropathy is characterized by BCVA and VF abnormalities in bilateral eyes. Retrobulbar and systemic glucocorticoid therapy is effective.

Prognostic value of C-reactive protein levels within 6 hours after the onset of acute anterior myocardial infarction with primary PCI

Background Increased levels of inflammatory markers have been documented in various settings of coronary artery disease. The vulnerability of coronary lesions in acute myocardial infarction(AMI) at the time of onset may be related to serum levels of C reactive protein(CRP) on admission, before CRP levels are affected by myocardial damage.Objective This study assessed the predictive value of CRP levels within six hours after the onset of acute anterior myocardial infarction with primary percutaneous coronary intervention(PCI).Methods The plasma CRP of 76 patients with first acute anterior myocardial infarction was measured within 6 hours after onset. They were divided into 2 groups: group 1( n =20) with elevated CRP( ≥0.3mg/dl ) on admission within 6 hours after onset and group 2( n =56) with normal CRP( <0.3mg/dl ) within 6 hours after onset. All patients were treated by primary PCI. The primary combined end points, including death due to cardiac causes, re MI related to the infarction artery(RIA) and repeat intervention of the RIA, and the restenosis rate were assessed in relation to CRP levels within 6 hours after onset. Left ventricular end diastolic volume index(EDVI),end systolic volume index(ESVI),and ejection fraction(EF) on admission and 6 month after the onset were assessed by left ventriculography. Changes in EDVI(ΔEDVI),ESVI(ΔESVI), and EF(ΔEF) were obtained by subtracting respective on admission values from corresponding 6 month follow up values. Results There were no significant differences in baseline characteristics between the two groups. The primary combined end points were significantly more frequent in group 1(20%) than those in group 2( 1.79% , P <0.01 ).In addition, restenosis rates were significantly higher in group 1 than in group 2(41.18% vs 16.07%, P<0.05). Group 1 showed greater increases in left ventricular volume and less improvement in EF compared with group 2(ΔEDVI 6.31 ±2.17 vs 3.29 ±9.46ml/m 2 , ΔESVI 5.92 ±2.31 vs 3.86 ±1.08ml/m 2 , ΔEF 1.92 ±0.47 vs 4.79 ±1.73% , P <0.05 , respectively).Conclusions CRP levels within 6 hours after the onset of AMI might predict adverse outcome after primary PCI and progressive ventricular remodeling within 6 month of AMI.

Late onset acute Vogt-Koyanagi-Harada syndromechallenges on the way

Dear Editor,We would like to share some clinical cases of late onset acute Vogt-Koyanagi-Harada syndrome （VKH）, a rare diagnosis in this age range.

Effect of long-term low dose of aspirin on severity of disease following onset of acute cerebral infarction

BACKGROUND： Aspirin can decrease the incidence risk of high-risk crowdgroup of cerebral infarction, but there are still controversy if it might decrease the degree of disease in degree of patients with acute cerebral infarction. OBJECTIVE： To observe the effect of lower dose of aspirin during taking for a long time on disease degree of disease following onset of acute cerebral infarction. DESIGN： Grouping according to the admission time and 1：1 paired observation.SETTING ： Department of Neurology, Qilu Hospital of Shandong University.PARTICIPANTS ： The participants in present study were 321 patients with acute cerebral infarction who received treatments in the Department of Neurology, Qilu Hospital of Shandong University from January 1999 to June 2000. There were 190 male and 131 female ,with mean （65±11 ）years of age. Inclusive criteria： ① A focal neurological disturbance occurred suddenly and had lasted for more than 24 hours, patients were admitted within 3 days after onset of disease; ② A computed tomography of the brain was performed and excluded hemorrhage in all patients; ③ The patients were proved internal carotid occlusions by clinical features and image findings; ④ The functions of limbs were normal （before the first stroke） or almost normal （before the second stroke）. Exclusive criteria：①The patients who had have cardiogenic cerebral embolism; ②The patients who had taken warfarin orally and other platelet agglutination drugs. METHODS ：①All the patients were divided into 2 groups according to whether they had taken aspirin before： aspirin-treated group （n=110） and blank control group （n=211）. there were 70 male and 40 female in aspirin-treated group, with average（65±10） years of age.All patients had taken 50-100 mg/d aspirin for 6 months to 10 years before onset. There were 120 male and 91 female in blank control group, with average （65±13） years of age. Patients received a clinical scoring within 3 days and similar therapeutic measures （such as anti-platelet agglutination, improving cerebral circulation and metabolism-promoting reagent）. Two groups of patients had the same basic conditions except for taking aspirin or not before. ②The matched pairs were made between 50 cases selected from aspirin-treated group and 50 cases from non-aspirin-treated groups according to age, gender, and other stroke risk factors. ③ Evaluation： Degree of disease after onset was evaluated by means of Acute Cerebral Infarction Clinical Neurologic Impairment Degree Scoring Standard of Carotid Artery System. MAIN OUTCOME MEASURES： Acute Cerebral Infarction Clinical Neurologic Impairment Degree Scoring Standard of Carotid Artery System. RESULTS ： All 321 patients entered the stage of analysis with no loss in the midway. ① The symptom following onset of acute cerebral infarction was evaluated with clinical neurologic impairment scoring criteria, there were no significant differences between aspirin group and blank control group [（17.39±9.90） vs （16.22 ± 9.98） （t=1.025, P〉 0.05）]. ② No significant differences were found in 1：1 matched pairs of 100 cases from aspirin group and blank control group （t=1.74, P 〉 0.05）. CONCLUSION ： Taking a lower dose of aspirin during long time may not decrease the degree of disease following onset of acute cerebral infarction.

Significance of neuroglobin in serum of acute atherosclerotic cerebral infarction patients

This study sought to examine neuroglobin （NGB） in the serum of acute cerebral infarction patients with double-antibody sandwich enzyme-linked immunosorbent assay to identify all risk factors, calculate infarct size, assess neurological impairment, and analyze the relation between NGB and each of these factors. The double-antibody sandwich assay indicated that levels of NGB in serum were unaltered within 6 hours following acute cerebral infarction compared with normal levels. NGB levels then underwent a distinct change, peaking at 24 hours then returning to normal levels in 72 hours. The results suggest that the level of NGB might be related to infarct size and low-density lipoprotein at 24 hours after acute cerebral infarction. There were no significant differences in neurological impairment scores and infarct size at different periods following infarction. The findings indicated that the level of NGB in serum of acute cerebral infarction patients was correlated with infarct time.