Background: Cardiopulmonary resuscitation (CPR) can lead to various neurologic outcomes in patients with hypoxicischemic encephalopathy (HIE). This study investigated the usefulness of clinical markers and electroencephalography (EEG) in predicting the neurologic prognosis of HIE after CPR. Methods: We reviewed the clinical findings of 51 patients with HIE, including the medical history, the duration from the onset of symptoms to the recovery of spontaneous circulation, Glasgow Coma Scale (GCS) and Full Outline of Unresponsiveness (FOUR) scores, and presence of seizure or status epilepticus. Patients were divided into three outcomes groups: death, persistent vegetative state, and recovering alertness and awareness. Digital EEG and visual and quantitative analyses were performed in each patient. For quantitative EEG (qEEG) analysis, we defined and compared the distance in the spatial band-power patterns and phase coherence patterns between healthy normal subjects and each patient. Results: Patients with HIE showed a high mortality rate (54.9%, 28/51), and their neurologic prognosis was significantly related to the initial GCS and FOUR scores. In the qEEG analysis, patients' groups showed a prominent delta frequency band, and the healthy normal group presented a marked alpha predominance. As the severity decreased, the similarity in the spatial band-power pattern and functional connectivity pattern between normal subjects and patients increased. Conclusions: Low initial GCS and FOUR scores could be predictive of a poor neurologic prognosis in patients with HIE, and qEEG analysis might be a useful predictor of their neurologic outcomes.
Recent advances in resting-state functional MRI have revealed altered functional networks in Alzheimer's disease (AD), especially those of the default mode network (DMN) and central executive network (CEN). However, few studies have evaluated whether small vessel disease (SVD) or combined amyloid and SVD burdens affect the DMN or CEN.The aim of this study was to evaluate whether SVD or combined amyloid and SVD burdens affect the DMN or CEN.In this cross-sectional study, we investigated the resting-state functional connectivity within DMN and CEN in 37 Pittsburgh compound-B (PiB)(+) AD, 37 PiB(-) subcortical vascular dementia (SVaD), 13 mixed dementia patients, and 65 normal controls.When the resting-state DMN of PiB(+) AD and PiB(-) SVaD patients were compared, the PiB(+) AD patients displayed lower functional connectivity in the inferior parietal lobule while the PiB(-) SVaD patients displayed lower functional connectivity in the medial frontal and superior frontal gyri. Compared to the PiB(-) SVaD or PiB(+) AD, the mixed dementia patients displayed lower functional connectivity within the DMN in the posterior cingulate gyrus. When the resting-state CEN connectivity of PiB(+) AD and PiB(-) SVaD patients were compared, the PiB(-) SVaD patients displayed lower functional connectivity in the anterior insular region. Compared to the PiB(-) SVaD or PiB(+) AD, the mixed dementia patients displayed lower functional connectivity within the CEN in the inferior frontal gyrus.Our findings suggest that in PiB(+) AD and PiB(-) SVaD, there is divergent disruptions in resting-state DMN and CEN. Furthermore, patients with combined amyloid and SVD burdens exhibited more disrupted resting-state DMN and CEN than patients with only amyloid or SVD burden.
Background and PurposeaaThe most important treatment for subcortical vascular dementia (SVaD) is controlling the blood pressure (BP).However, the few studies that have investigated the relationships between diurnal BP rhythm and subcortical ischemic vascular cognitive impairment have produced inconclusive results.In the study presented here, the 24-hour BP values of three groups of subjects-patients with subcortical vascular mild cognitive impairment (SvMCI), patients with SVaD, and normal controls-were compared using working criteria and 24-hour ambulatory BP (ABP) monitoring.MethodsaaThe subjects (42 patients with SVaD, 37 patients with SvMCI, and 30 controls) were selected according to the study's inclusion/exclusion criteria.All subjects underwent brain magnetic resonance (MR) imaging and MR angiography, detailed neuropsychological testing, and 24-hour ABP monitoring.ResultsaaThe prevalence of nondippers differed markedly between the control group and both the SVaD and SvMCI groups.Loss of nocturnal dipping was significantly associated with SVaD [odds ratio (OR), 4.827; 95% confidence interval (CI), 1.07-12.05].ConclusionsaaIt was found that SVaD is associated with loss of nocturnal BP dipping combined with increased pulse pressure and systolic BP (SBP) variability.Correction of these factors could therefore be important in the prevention of SVaD, independent of measures used to reduce BP.
Amnestic mild cognitive impairment (aMCI) represents a pre-dementia stage of Alzheimer's disease (AD). According to the severity of objective memory impairment, aMCI patients can be classified into subjects with milder degree of impairment and those with more severe impairment. Although previous studies showed that aMCI subjects with milder memory impairment have slower rates of AD progression than those with more severe memory impairment, there has been no study comparing regional cortical thickness according to this classification of aMCI. Cortical thickness across the entire brain and neuropsychological performance were measured in 271 patients with aMCI and 234 subjects with normal cognition (NC). According to the performances in delayed recall items of memory tests, aMCI patients were divided into early-stage aMCI (EMCI, N = 91) with milder degree of memory impairment (scores between -1.5 SD and -1.0 SD compared to age-, sex-, and education-matched norms) and late-stage MCI (LMCI, N = 180) with more severe memory impairment (lower than -1.5 SD). We performed ANCOVAs to compare neuropsychological performances and vertex-wise cortical thinning in EMCI, LMCI, and NC. Compared to NC subjects, EMCI patients showed cortical thinning in the left medial temporal lobe, and LMCI patients showed cortical thinning in bilateral medial temporal lobes, bilateral medial and lateral parietal cortices, bilateral dorsolateral prefrontal cortices, right posterior cingulate cortex, and bilateral anterior temporal cortices. When the two aMCI groups were directly compared, LMCI patients showed more cortical thinning in the right medial temporal lobe, right posterior cingulate cortex, right lateral parietal cortex, and right dorsolateral prefrontal cortex. Both EMCI and LMCI patients showed lower performances in all neuropsychological tests compared to NC. When directly compared with EMCI, LMCI subjects had poorer performance in all memory tests and COWAT supermarket test, while having comparable scores in other tests.
Objective: Angiotensin (Ang) II by activating cytosolic phospholipase A2a (cPLA2a) releases arachidonic acid (AA), and the pro-hypertensive AA metabolites mediate Ang II-induced hypertension and associated pathogenesis. These findings and the demonstration that Ang II increases blood pressure via generation of oxidative stress in subfornical organ (SFO) in the brain, led us to hypothesize that these effects of Ang II are dependent on cPLA2a activation in SFO. Design and method: To test this hypothesis, we investigated the effect of Ang II infusion (700ng/kg/min, s.c.) for 14 days in wild type (cPLA2a+/+) and cPLA2a-/- mice transduced in SFO with enhanced cyan-fluorescence protein (Ad-ECFP)-cPLA2a DNA. Results: Ang II increased mean arterial pressure (MAP) measured by radio-telemetry in cPLA2a+/+ but not cPLA2a-/- mice (100 ± 2 to 161 ± 6 mmHg vs. 104 ± 3 to 112 ± 3 mmHg, respectively, P < 0.05). Ang II increased cPLA2 activity, measured by immunohistochemistry using anti-phospho-Ser505, in SFO of cPLA2a+/+ but not cPLA2a-/- mice. Ang II increased reactive oxygen species (ROS) production measured by dihydroethidium staining (5.09 ± 0.31 to 8.99 ± 0.33 AU, P < 0.05), in SFO of cPLA2a+/+ but not in cPLA2a-/- mice. Ad-ECFP-cPLA2a DNA (1x1012 pfu/0.5 μL) but not Ad-GFP DNA transduced in SFO of cPLA2a-/- mice, restored Ang II effect on MAP and ROS production (115 ± 4 to 149 ± 2 mmHg and 4.40 ± 0.31 to 7.66 ± 0.47 AU with Ad-ECFP-cPLA2a DNA vs. 109 ± 5 to 116 ± 4 mmHg, and 4.04 ± 0.35 to 4.56 ± 0.19 AU with Ad-GFP, respectively, P < 0.05). In contrast, Ad-cPLA2a shRNA, but not Ad-shRNA transduced in SFO of cPLA2a+/+ mice, inhibited cPLA2 expression and its activity, and abolished Ang II-induced increase in blood pressure. Conclusions: These observations suggest that AA released by cPLA2a via one or more of its metabolites increase oxidative stress in SFO that promotes development of hypertension.
Recent advances in resting state functional MRI have revealed altered functional networks in Alzheimer's disease (AD), especially that of the default mode network (DMN) and central executive network (CEN). However, few studies have evaluated whether small vessel disease (SVD) or combined amyloid and SVD burdens affect the DMN or CEN. We investigated the resting state DMN and CEN connectivities in 39 Pittsburg compound-B (PiB)+AD (pure AD), 33 PiB− subcortical vascular dementia (pure SVaD), 17 PiB+SVaD (mixed dementia) patients, and 64 normal controls. Compared to pure SVaD, pure AD patients showed decreased DMN connectivity in the left inferior parietal lobule and increased connectivity in the right medial frontal and left syperior frontal gyri. Compared to pure SVaD or pure AD, mixed dementia patients showed decreased DMN connectivity in the right posterior cingulate gyrus, and in the left posterior cingulate and left superior frontal gyri, respectively. Compared to pure AD, pure SVaD patients showed decreased CEN connectivity in the left insula regions. Compared to pure SVaD or pure AD, mixed dementia patients showed decreased CEN connectivity in the left inferior frontal gyrus. Our findings suggest that in pure AD and pure SVaD, there is divergent disruptions in resting state DMN and CEN connectivity. Furthermore, patients with combined amyloid and SVD burdens had more disrupted resting state DMN and CEN connectivity than patients with only amyloid or SVD burden.
Purpose: To report a case of noninfectious endophthalmitis after intravitreal injection of aflibercept.Case summary: A 67-year-old male patient presented with sudden vision loss 2 days after intravitreal aflibercept injection for neovascular age-related macular degeneration.Mild conjunctival injection and moderate inflammation in the anterior chamber were noted, but he had no ocular pain or hypopyon.The patient was diagnosed with noninfectious endophthalmitis and successfully treated with topical antibiotics and topical steroid eye drops.The infection was apparently cleared at 3 days.At 10 days after the initial presentation, his vision loss resolved completely.Conclusions: Noninfectious endophthalmitis after intravitreal injection of aflibercept can be treated with topical steroids.
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