Foleybager4934
To report the results of adjustable graded augmentation of superior rectus transposition, a novel modification of superior rectus transposition (SRT) designed to reduce postoperative vertical or torsional diplopia.
The medical records of patients who underwent adjustable graded augmentation of SRT with or without adjustable medial rectus recession (MRc) from February 2017 to December 2019 were reviewed retrospectively. A Mendez ring was used to monitor torsional change after transposition of the superior rectus muscle to the lateral rectus muscle and after sequential placement of 2 or 3 augmentation sutures by superior rectus-lateral rectus loop myopexy. If excessive mechanical intorsion was induced, the responsible augmentation suture was severed intraoperatively. If torsional or vertical diplopia was noted after recovery, the distal-most augmentation suture was cut. https://www.selleckchem.com/products/dorsomorphin-2hcl.html Exotropia was managed by severing the distal-most augmentation suture or by medial rectus adjustment.
A total of 8 patients who underwent adjustable graded augmentation of SRT were included (6 using the 3-suture technique) 3 for esotropic Duane syndrome, 2 for abducens nerve palsy, 1 for Moebius syndrome, and 2 for combined trochlear and abducens nerve palsies. Of the 8 patients, 4 had prior strabismus surgery, and 1 patient had previously undergone treatment with botulinum toxin. Severing one augmentation suture in 3 cases resolved vertical (n=2) or torsional (n=1) diplopia and consecutive exotropia (n=2), resulting in excellent alignment and reduction of torticollis to ≤4° in 7 cases. The technique proved insufficient in 1 patient, who had undergone 3 prior strabismus procedures.
In this study cohort, adjustable graded augmentation of SRT effectively managed the risk of postoperative vertical or torsional diplopia.
In this study cohort, adjustable graded augmentation of SRT effectively managed the risk of postoperative vertical or torsional diplopia.Glia cells are often viewed as support cells in the central nervous system, but recent discoveries highlight their importance in physiological functions and in neurological diseases. Central to this are leukodystrophies, a group of progressive, neurogenetic disease affecting white matter pathology. In this review, we take a closer look at multiple leukodystrophies, classified based on the primary glial cell type that is affected. While white matter diseases involve oligodendrocyte and myelin loss, we discuss how astrocytes and microglia are affected and impinge on oligodendrocyte, myelin and axonal pathology. We provide an overview of the leukodystrophies covering their hallmark features, clinical phenotypes, diverse molecular pathways, and potential therapeutics for clinical trials. Glial cells are gaining momentum as cellular therapeutic targets for treatment of demyelinating diseases such as leukodystrophies, currently with no treatment options. Here, we bring the much needed attention to role of glia in leukodystrophies, an integral step towards furthering disease comprehension, understanding mechanisms and developing future therapeutics.
In Parkinson's disease (PD) patients, the subthalamic nucleus (STN) has prominent oscillatory activity in the beta band, which may be related to the motor symptoms severity. Local field potential (LFP) studies using standard four-contact deep brain stimulation (DBS) leads indicate that the source of beta activity in the STN region is the dorsolateral segment of the nucleus. However, these leads have few contacts outside of the STN, making the source localization of beta activity around the STN region uncertain.
This study aimed to investigate the electrophysiological characteristics of the STN and the surrounding area in PD to better locate the source of these oscillations and their clinical relevance.
Eight PD patients were bilaterally implanted in the STN with the eight ring-contact DBS lead (Boston Scientific Corporation). LFPs were recorded intra-operatively from each DBS contact in the off medication state at rest. Each contact location was normalized relative to the STN borders based on microelective hypothesis that beta activity in the STN region arises from volume conduction from other sources. We demonstrate intrinsic STN beta-HFA PAC as an independent marker of DBS effect.
Our findings support the hypothesis that the primary source of beta oscillations is located in dorsal STN, and argue against the alternative hypothesis that beta activity in the STN region arises from volume conduction from other sources. We demonstrate intrinsic STN beta-HFA PAC as an independent marker of DBS effect.Human genetics provides unbiased insights into the causes of human disease, which can be used to create a foundation for effective ways to more accurately diagnose patients, stratify patients for more successful clinical trials, discover and develop new therapies, and ultimately help patients choose the safest and most promising therapeutic option based on their risk profile. But the process for translating basic observations from human genetics studies into pathogenic disease mechanisms and treatments is laborious and complex, and this challenge has particularly slowed the development of interventions for neurodegenerative disease. In this review, we discuss the many steps in the process, the important considerations at each stage, and some of the latest tools and technologies that are available to help investigators translate insights from human genetics into diagnostic and therapeutic strategies that will lead to the sort of advances in clinical care that make a difference for patients.Many jurisdictions implemented intensive social distancing to suppress SARS-CoV-2 transmission. The challenge now is to mitigate the ongoing COVID-19 epidemic without overburdening economic and social activities. An agent-based model simulated the population of King County, Washington. SARS-CoV-2 transmission probabilities were estimated by fitting simulated to observed hospital admissions. Interventions considered included encouraging telecommuting, reducing contacts to high-risk persons, and reductions to contacts outside of the home, among others. Removing all existing interventions would result in nearly 42,000 COVID-19 hospitalizations between June 2020 and January 2021, with peak hospital occupancy exceeding available beds 6-fold. Combining interventions is predicted to reduce total hospitalizations by 48% (95% CI, 47-49%), with peak COVID-19 hospital occupancy of 70% of total beds. Targeted school closures can further reduce the peak occupancy. Combining low-impact interventions may mitigate the course of the COVID-19 epidemic, keeping hospital burden within the capacity of the healthcare system.