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1.
The impact of vaccination and new SARS-CoV-2 variants on peri-operative outcomes is unclear. We aimed to update previously published consensus recommendations on timing of elective surgery after SARS-CoV-2 infection to assist policymakers, administrative staff, clinicians and patients. The guidance remains that patients should avoid elective surgery within 7 weeks of infection, unless the benefits of doing so exceed the risk of waiting. We recommend individualised multidisciplinary risk assessment for patients requiring elective surgery within 7 weeks of SARS-CoV-2 infection. This should include baseline mortality risk calculation and assessment of risk modifiers (patient factors; SARS-CoV-2 infection; surgical factors). Asymptomatic SARS-CoV-2 infection with previous variants increased peri-operative mortality risk three-fold throughout the 6 weeks after infection, and assumptions that asymptomatic or mildly symptomatic omicron SARS-CoV-2 infection does not add risk are currently unfounded. Patients with persistent symptoms and those with moderate-to-severe COVID-19 may require a longer delay than 7 weeks. Elective surgery should not take place within 10 days of diagnosis of SARS-CoV-2 infection, predominantly because the patient may be infectious, which is a risk to surgical pathways, staff and other patients. We now emphasise that timing of surgery should include the assessment of baseline and increased risk, optimising vaccination and functional status, and shared decision-making. While these recommendations focus on the omicron variant and current evidence, the principles may also be of relevance to future variants. As further data emerge, these recommendations may be revised.  相似文献   
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Chronic orofacial pain of neuropathic origin can present diagnostic and management dilemmas to dental practitioners and also affects the patient's quality of life. Intracranial aneurysms are a potential cause of stroke (e.g. sub‐arachnoid haemorrhage) that is usually associated with, high rates of mortality and morbidity. A patient who had been previously managed for symptoms of temporomandibular joint disorder (TMD) presented with sharp, shooting pain of moderate intensity. It was precipitated by swallowing, and radiated to the right throat, posterior border of the mandible, ear and temporomandibular joint. Clinical and radiological investigations ruled out odontogenic pain, TMD and other more common types of facial pain. Magnetic resonance imaging revealed a 7 × 6 mm aneurysm in the right middle cerebral artery (MCA) which was subsequently surgically clipped. Interestingly, the facial pain resolved after this procedure. Compression of the insular region of the brain innervated by the trigeminal, glossopharyngeal and vagus nerves provides a plausible explanation for the pain reported. To our knowledge, this is the first case of facial neuralgia associated with an aneurysm in the MCA which emphasizes the importance of a multidisciplinary approach in the diagnosis and management of unusual cases of chronic orofacial pain.  相似文献   
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BACKGROUND AND PURPOSE:Carotid intraplaque hemorrhage is associated with stroke, plaque thickness, stenosis, ulceration, and adventitial inflammation. Conflicting data exist on whether calcification is a marker of plaque instability, and no data exist on adventitial calcification. Our goal was to determine whether adventitial calcification and soft plaque (a rim sign) help predict carotid intraplaque hemorrhage.MATERIALS AND METHODS:This was a retrospective cohort study of 96 patients who underwent carotid MRA and CTA within 1 month, from 2009 to 2016. We excluded occlusions (n = 4) and near occlusions (n = 0), leaving 188 carotid arteries. Intraplaque hemorrhage was detected by using MPRAGE. Calcification, adventitial pattern, stenosis, maximum plaque thickness (total, soft, and hard), ulceration, and intraluminal thrombus on CTA were recorded. Atherosclerosis risk factors and medications were recorded. We used mixed-effects multivariable Poisson regression, accounting for 2 vessels per patient. For the final model, backward elimination was used with a threshold of P < .10. Receiver operating characteristic analysis determined intraplaque hemorrhage by using the area under the curve.RESULTS:Our final model included the rim sign (prevalence ratio = 11.9, P < .001) and maximum soft-plaque thickness (prevalence ratio = 1.2, P = .06). This model had excellent intraplaque hemorrhage prediction (area under the curve = 0.94), outperforming the rim sign, maximum soft-plaque thickness, NASCET stenosis, and ulceration (area under the curve = 0.88, 0.86, 0.77, and 0.63, respectively; P < .001). Addition of the rim sign performed better than each marker alone, including maximum soft-plaque thickness (area under the curve = 0.94 versus 0.86, P < .001), NASCET stenosis (area under the curve = 0.90 versus 0.77, P < .001), and ulceration (area under the curve = 0.90 versus 0.63, P < .001).CONCLUSIONS:The CTA rim sign of adventitial calcification with internal soft plaque is highly predictive of carotid intraplaque hemorrhage.

Carotid atherosclerotic plaque contributes to 10%–15% of ischemic strokes in the United States.1 MR imaging–detected carotid intraplaque hemorrhage (IPH) is an accepted marker of plaque instability and stroke risk independent of stenosis, with an annual stroke rate as high as 45% in patients with >50% stenosis and IPH.25 Carotid IPH can be detected with heavily T1-weighted sequences, including the MPRAGE sequence, which can discriminate between IPH and lipid/necrotic core.6 MPRAGE is superior in detecting IPH compared with conventional MR imaging sequences, with higher sensitivity, specificity, and interrater reliability compared with 3D TOF or FSE T1WI sequences.7Lumen markers have been linked to IPH, including stenosis, plaque thickness, and ulceration. These markers can be detected by CTA. IPH is known to increase in prevalence with increasing lumen stenosis.8 Additional studies have suggested that CTA-detected ulceration can be used as a surrogate marker for IPH.9 Plaque thickness has also recently been associated with high plaque signal on 3D TOF imaging, attributed to IPH.10,11 Recently, we found that these markers in combination (plaque thickness, millimeter stenosis, and ulceration) allow optimal discrimination of IPH in a model including the clinical factors of age and male sex.12 Together these factors may provide clues to the pathogenesis of IPH.Most recently, studies have linked IPH with adventitial inflammation and microvessel permeability detectable by using dynamic contrast-enhanced MR imaging.8,13 Adventitial inflammation and oxidative stress have also been linked to endothelial bone-morphogenic proteins,14 suggesting that adventitial calcification may also represent a marker of adventitial inflammation15; however, this has not yet been investigated in the setting of IPH. Vascular calcification is often seen with carotid plaque, though conflicting data exist in relation to plaque vulnerability. One study of 30 patients found that fibrous cap inflammation more often occurs in noncalcified than in calcified plaques, suggesting that calcification indicates plaque stability.16 An additional study of patients with symptomatic plaques (recent TIA, stroke, or amaurosis fugax) versus asymptomatic patients with critical stenosis found that the percentage of plaque calcification area was 2-fold greater in asymptomatic-versus-symptomatic plaques, and there was an inverse relationship between calcification and macrophage infiltration.17 A different study investigating 611 carotid plaques by CT and MR imaging found that larger calcification volume was associated with higher IPH prevalence and a lower lipid core prevalence, suggesting that calcification may not be a stabilizing factor.18 However, these studies evaluated total calcification volume or its binary presence or absence, and adventitial calcification coupled with soft plaque has not yet been addressed, to our knowledge.Because IPH is becoming more clinically relevant in identifying cryptogenic stroke sources19 and IPH indicates a medically refractory population with high future stroke risk,4 prediction models are greatly needed in patients undergoing alternate imaging such as CTA. Of clinical relevance, a CTA-IPH prediction model would be especially useful in patients with contraindications to MR imaging (eg, with pacemakers) or as a cost-saving measure to prevent unneeded MR imaging in patients with very high or very low likelihood of IPH. Current prediction models discussed above based on plaque thickness, stenosis, and ulceration leave room for improvement. Because adventitial inflammation is highly associated with IPH and chronic inflammation is associated with calcification, this study was undertaken to determine whether adventitial calcification with internal soft plaque (a rim sign) could aid in carotid IPH prediction. Our hypothesis was that the rim sign may help predict carotid IPH compared with standard markers, including soft-plaque thickness, stenosis, or ulceration alone.  相似文献   
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We present two cases of recurrent progressive multifocal leukoencephalopathy (PML) in patients with long standing virally suppressed human immunodeficiency virus (HIV) and normal CD4+ T cell count who were taking stable regimens of highly active antiretroviral therapy (HAART). This has significant implications for other patients with a past history of PML, not just those with HIV but also those on medications such as natalizumab or fumarates.  相似文献   
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ObjectiveTo quantify changes in segmented brain volumes over 12 months in children with mucopolysaccharidosis types IIIA and IIIB (MPS IIIA and IIIB).MethodsIn order to establish suitable outcome measures for clinical trials, twenty-five children greater than 2 years of age were enrolled in a prospective natural history study of MPS IIIA and IIIB at Nationwide Children's Hospital. Data from sedated non-contrast brain 3 T MRIs and neuropsychological measures were reviewed from the baseline visit and at 12-month follow-up. No intervention beyond standard clinical care was provided. Age- and sex-matched controls were gathered from the National Institute of Mental Health Data Archive. Automated brain volume segmentation with longitudinal processing was performed using FreeSurfer.ResultsOf the 25 subjects enrolled with MPS III, 17 children (4 females, 13 males) completed at least one MRI with interpretable volumetric data. The ages ranged from 2.8 to 13.7 years old (average 7.2 years old) at enrollment, including 8 with MPS IIIA and 9 with MPS IIIB. At baseline, individuals with MPS III demonstrated reduced cerebral white matter and corpus callosum volumes, but greater volumes of the lateral ventricles, cerebellar cortex, and cerebellar white matter compared to controls. Among the 13 individuals with MPS III with two interpretable MRIs, there were annualized losses or plateaus in supratentorial brain tissue volumes (cerebral cortex ?42.10 ± 18.52 cm3/year [mean ± SD], cerebral white matter ?4.37 ± 11.82 cm3/year, subcortical gray matter ?6.54 ± 3.63 cm3/year, corpus callosum ?0.18 ± 0.62 cm3/yr) and in cerebellar cortex (?0.49 ± 12.57 cm3/year), with a compensatory increase in lateral ventricular volume (7.17 ± 6.79 cm3/year). Reductions in the cerebral cortex and subcortical gray matter were more striking in individuals younger than 8 years of age. Greater cerebral cortex volume was associated with higher fine and gross motor functioning on the Mullen Scales of Early Learning, while greater subcortical gray matter volume was associated with higher nonverbal functioning on the Leiter International Performance Scale. Larger cerebellar cortex was associated with higher receptive language performance on the Mullen, but greater cerebellar white matter correlated with worse adaptive functioning on the Vineland Adaptive Behavioral Scales and visual problem-solving on the Mullen.ConclusionsLoss or plateauing of supratentorial brain tissue volumes may serve as longitudinal biomarkers of MPS III age-related disease progression compared to age-related growth in typically developing controls. Abnormally increased cerebellar white matter in MPS III, and its association with worse performance on neuropsychological measures, suggest the possibility of pathophysiological mechanisms distinct from neurodegeneration-associated atrophy that warrant further investigation.  相似文献   
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