ObjectivesTo investigate the association between degeneration of retinal structure and shrinkage of the optic tract in patients after thalamic stroke.Materials and methodsPatients with unilateral thalamic stroke were included. Structural magnetic resonance imaging (MRI) and optical coherence tomography (OCT) were performed to obtain parameters of optic tract shrinkage (lateral index) and retina structural thickness (retinal nerve fiber layer, RNFL; peripapillary retinal nerve fiber layer, pRNFL; ganglion cell-inner plexiform layer, GCIP), respectively. Visual acuity (VA) examination under illumination was conducted using Snellen charts and then converted to the logarithm of the minimum angle of resolution (LogMAR). We investigated the association between LI and OCT parameters and their relationships with VA.ResultsA total of 33 patients and 23 age-sex matched stroke-free healthy controls were enrolled. Patients with thalamic stroke showed altered LI compared with control participants (P = 0.011) and a significantly increased value of LI in the subgroup of disease duration more than 6 months (P = 0.004). In these patients, LI were significantly associated with pRNFL thickness (β = 0.349, 95% confidence interval [CI]: 0.134–0.564, P = 0.002) after adjusting for confounders (age, sex, hypertension, diabetes, dyslipidemia, and lesion volume). LI and pRNFL were both significantly associated with VA in all patients (LI: β = −0.275, 95% CI: −0.539 to −0.011, P = 0.041; pRNFL: β = −0.023, 95% CI: −0.046 to −0.001, P = 0.040) and in subgroup of disease duration more than 6 months (LI: β = −0.290, 95% CI: −0.469 to −0.111, P = 0.002; pRNFL: β = −0.041, 95% CI: −0.065 to −0.017, P = 0.003).ConclusionShrinkage of the optic tract can be detected in patients with thalamic stroke, especially after 6 months of stroke onset. In these patients, the extent of optic tract atrophy is associated with pRNFL thickness, and they are both related to visual acuity changes.
Background: The retina and brain share similar neuronal and microvascular features. We aimed to investigate the retinal thickness and microvasculature in patients with thalamic infarcts compared with control participants. Material and methods: Swept-source optical coherence tomography (SS-OCT) was used to image the macular thickness (retinal nerve fiber layer, RNFL; ganglion cell-inner plexiform layer, GCIP), while OCT angiography was used to image the microvasculature (superficial vascular plexus, SVP; intermediate capillary plexus, ICP; deep capillary plexus, DCP). Inbuilt software was used to measure the macular thickness (µm) and microvascular density (%). Lesion volumes were quantitively assessed based on structural magnetic resonance images. Results: A total of 35 patients with unilateral thalamic infarction and 31 age–sex-matched controls were enrolled. Compared with control participants, thalamic infarction patients showed a significantly thinner thickness of RNFL (p < 0.01) and GCIP (p = 0.02), and a lower density of SVP (p = 0.001) and ICP (p = 0.022). In the group of patients, ipsilateral eyes showed significant reductions in SVP (p = 0.033), RNFL (p = 0.01) and GCIP (p = 0.043). When divided into three groups based on disease duration (<1 month, 1–6 months, and >6 months), no significant differences were found among these groups. After adjusting for confounders, SVP, ICP, DCP, RNFL, and GCIP were significantly correlated with lesion volume in patients. Conclusions: Thalamic infarction patients showed significant macular structure and microvasculature changes. Lesion size was significantly correlated with these alterations. These findings may be useful for further research into the clinical utility of retinal imaging in stroke patients, especially those with damage to the visual pathway.
Background It is unclear whether non-high-density lipoprotein cholesterol (Non-HDL-C) is associated with haemorrhagic transformation (HT) after acute ischaemic stroke (AIS). We aimed to explore the association between Non-HDL-C and HT, as well as compare the predictive values of Non-HDL-C and low-density lipoprotein cholesterol (LDL-C) for HT. Methods We consecutively enrolled AIS patients within 7 days of stroke onset. Participants were divided into four categories according to quartiles of Non-HDL-C. HT was assessed by follow-up brain imaging. We assessed the association between Non-HDL-C, LDL-C and HT in multivariate logistic regression analysis. Results A total of 2043 patients were included, among whom 232 were identified as HT. Compared with the highest quartiles, the first, second and third quartiles of Non-HDL-C were associated with increased risk of HT (adjusted odds ratios [ORs] 1.74 [95% confidence interval [CI] 1.09–2.78], 2.01[95% CI 1.26–3.20], and 1.76 [95% CI 1.10–2.83], respectively, P for trend = 0.024). Similar results were found for LDL-C. There was significant interaction between Non-HDL-C and age (P for interaction = 0.021). The addition of Non-HDL-C and LDL-C to conventional factors significantly improved predictive values [Non-HDL-C, net reclassification index (NRI) 0.24, 95%CI 0.17–0.31, P < 0.001; LDL-C, NRI 0.15, 95%CI 0.08–0.22, P = 0.03]. Conclusions Low Non-HDL-C was associated with increased risks of HT. In addition, Non-HDL-C has similar effects as LDL-C for predicting HT.
Background: We aimed to assess the retinal structural and choroidal changes in carotid artery stenosis (CAS) patients and their association with cerebral hemodynamic changes. Asymptomatic and symptomatic patients with unilateral CAS were enrolled in our study. Material and methods: Swept-source optical coherence tomography (SS-OCT) was used to image the retinal nerve fiber layer (RNFL), ganglion cell-inner plexiform layer (GCIPL), while SS-OCT angiography (SS-OCTA) was used to image and measure the choroidal vascular volume (CVV) and choroidal vascular index (CVI). Computed Tomography Perfusion (CTP) was used to assess the cerebral perfusion parameters; relative perfusion (r) was calculated as the ratio of the value on the contralateral side to that on the ipsilateral side. Results: Compared with contralateral eyes, ipsilateral eyes showed significantly thinner RNFL (p < 0.001), GCIPL (p = 0.013) and CVV (p = 0.001). Relative cerebral blood volume (rCBV) showed a significant correlation with RNFL (p < 0.001), GCIPL (p < 0.001) and CVI (p = 0.027), while the relative permeability surface (rPS) correlated with RNFL (p < 0.001) and GCIPL (p < 0.001). Conclusions: Our report suggests that retinal and choroidal changes have the potential to detect hemodynamic changes in CAS patients and could predict the risk of stroke.
Background and purpose: Hemorrhagic transformation (HT) has an adverse effect on the prognosis of patients with acute ischemic stroke, and it is currently known associated with coagulation system. But the conclusion is not consistent and remains to be identified. The aim of this study was to investigate the association between coagulation function and spontaneous hemorrhagic transformation. Methods: Patients within 7 days from onset of ischemic stroke who did not receive reperfusion therapy (thrombolysis or endovascular treatment) were included between January 2016 and October 2017. Coagulation function indicators, including prothrombin time (PT), activated partial thromboplastin time (APTT), international normalized ratio (INR), thrombin time (TT) and fibrinogen (FIB), were tested within 24 hours after admission. HT was defined as hemorrhage presented on follow-up magnetic resonance imaging (MRI) or computed tomography (CT) but not on baseline CT. We performed binary logistic regression to examine the association between coagulation function and HT. The coagulation indicators were entered into logistic regression analysis as continuous variables (per 1- unit/L increase) and four-categorized variables (with data collapsed into quartiles), respectively. Results: A total of 1141 patients were included (mean age, 64 ± 15 years; 63.7% males). 102 patients experienced HT (8.9%), of whom 14 patients experienced symptomatic HT (sHT, 1.2%). After adjustment for confounders, TT in the highest quartile is inversely associated with risk of HT (as continuous variable, odds ratio [OR] 0.85; 95% confidence level [CI] 0.73 – 0.99, P = 0.042; as fourcategorized variable, OR 0.36, 95% CI 0.18 – 0.7, P = 0.003). Whether as continuous variables or four-categorized variables, PT, INR, APTT and FIB had no association with HT. Conclusion: Not the whole process of coagulation function is associated with spontaneous HT. Prolonged TT, which may indicate an extension of the last step of the coagulation process, is independently and inversely associated with spontaneous HT in patients with acute ischemic stroke.
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