Purpose: To document the presentation and management of congenital III nerve palsy and monocular elevation deficiency to single ophthalmologist over a 14-year period. Surgical management was reviewed and visual outcome was analysed.
Methods: A retrospective study was conducted of all patients presenting during a period between 1992 and 2006 to the private practice of a paediatric ophthalmologist, with either congenital III or monocular elevation deficiency. For patients requiring surgical intervention pre- and post-surgical data were documented and analysed.
Results: A total of 19 congenital III and 13 monocular elevation deficiency patients were identified. There were eight surgical patients in each congenital III nerve palsy group and in the monocular elevation deficiency group. The congenital III group had a preoperative mean exotropia for near of -36 prism dioptres (PD) compared with postoperative mean exotropia for near -16 PD. Preoperative mean hypotropia for near of -19 PD was improved to postoperative mean hypotropia of -5 PD. The monocular elevation deficiency group had preoperative mean esotropia for near of +6 PD compared with postoperative mean exotropia for near -5 PD. Preoperative mean hypotropia for near of -15 PD was improved to postoperative mean hypotropia of -7 PD. At last follow up both groups had a majority of mild or no amblyopia noted.
Conclusion: Superficially, congenital III and monocular elevation deficiency may appear similar, both frequently having ptosis and hypotropia as features. Careful clinical assessment of the horizontal alignment and the result of forced duction testing will usually allow them to be distinguished. Congenital III more frequently requires surgery for exotropia as well as surgery for hypotropia and monocular elevation deficiency more often requires surgery just for hypotropia. The ptosis surgery is similar for either diagnosis in this study. Significant cosmetic improvement, as well as excellent visual acuity outcomes can be achieved.
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http://dx.doi.org/10.1111/j.1442-9071.2007.01613.x | DOI Listing |
Front Cardiovasc Med
January 2025
Instituto de Investigación de Enfermedades Tropicales, Universidad Nacional Toribio Rodríguez de Mendoza de Amazonas (UNTRM), Amazonas, Peru.
Introduction: Attaining what the American Heart Association terms Ideal Cardiovascular Health (ICVH) is viewed as an essential objective for preventing cardiovascular diseases (CVD).
Objective: To determine the prevalence of ICVH, stratified by sex and region and its associated factors in the adult population of Peru.
Materials And Methods: Analytical cross-sectional study.
Cancer Pathog Ther
January 2025
Department of Pharmaceutical Sciences, College of Pharmacy, University of Illinois, Chicago, IL 60607, USA.
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View Article and Find Full Text PDFFree Radic Biol Med
January 2025
BRIC-National Institute of Animal Biotechnology, Hyderabad, Telangana 500032, India. Electronic address:
Follicular ovarian cysts (FOCs) are prevalent reproductive disorders in both humans and animals, especially in livestock, where they cause economic losses by reducing fertility and productivity. FOCs are marked by a dominant follicle that fails to ovulate, disrupting the estrous cycle and reproductive efficiency. Previous studies indicate that the follicular fluid (FF) in cystic ovaries shows oxidative imbalance, affecting oocyte quality by altering glutathione peroxidase (GPX1) and selenium pathways.
View Article and Find Full Text PDFBiochimie
January 2025
Jagiellonian University Medical College, Faculty of Health Sciences, Department of Medical Physiology, Chair of Biomedical Sciences, 12 Michalowskiego st., 33-332 Cracow, Poland.
Obesity treatment requires an individualized approach, emphasizing the need to identify metabolic pathways of diagnostic relevance. Toll-like receptors (TLRs), particularly TLR2 and TLR4, play a crucial role in metabolic disorders, as receptor deficiencies improves insulin sensitivity and reduces obesity-related inflammation. Additionally, hydrogen sulfide (HS) influences lipolysis, adipogenesis, and adipose tissue browning through persulfidation.
View Article and Find Full Text PDFUnlabelled: SYNGAP1 is a key Ras-GAP protein enriched at excitatory synapses, with mutations causing intellectual disability and epilepsy in humans. Recent studies have revealed that in addition to its role as a negative regulator of G-protein signaling through its GAP enzymatic activity, SYNGAP1 plays an important structural role through its interaction with post-synaptic density proteins. Here, we reveal that intrinsic excitability deficits and seizure phenotypes in heterozygous Syngap1 knockout (KO) mice are differentially dependent on Syngap1 GAP activity.
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