Does cataract surgery in patients with concurrent lower lid malposition increase the risk of postoperative endophthalmitis?

OBJECTIVE: To evaluate the safety of performing cataract surgery prior to eyelid (entropion/ectropion) surgery in patients with concurrent cataract and lower eyelid malposition. DESIGN: Retrospective case series. PARTICIPANTS AND METHODS: Patients with concurrent lower eyelid malposition and cataract undergoing cataract surgery before lower eyelid repair from 2013 to 2020 were identified from two ophthalmologists (M.L.W., G.R.). Both surgeries were performed by the same ophthalmologist, with eyelid repair completed at least 1 month following cataract extraction. Data analysis was performed with two-parameter estimations. The primary outcome was the postoperative endophthalmitis rate in this cohort. RESULTS: 129 cases in 90 patients were found (86 involutional entropion and 43 involutional ectropion). No cases of endophthalmitis were encountered. Statistical analysis using the 95% Jeffreys interval for one-sample binomial proportion revealed an upper limit of 1.9%. The Agresti-Caffo interval of the proportional difference between the study procedure and historical incidence data of postoperative endophthalmitis following cataract surgery alone yielded an estimate of 0.8% with an upper confidence limit of 2.2%. CONCLUSION: We present preliminary evidence on the endophthalmitis risk in patients with concurrent lower eyelid malposition and cataract who undergo cataract surgery prior to eyelid repair. We propose that this strategy may be a viable option to expedite vision restoration and reduce the risk of recurrent lower eyelid malposition in select patients. More data are required to reach statistically significant noninferiority and show that a malpositioned lower eyelid is not a risk factor for postoperative endophthalmitis following cataract surgery.

Dissociations of cognitive inhibition, response inhibition, and emotional interference: Voxelwise ALE meta-analyses of fMRI studies.

Inhibitory control is the stopping of a mental process with or without intention, conceptualized as mental suppression of competing information because of limited cognitive capacity. Inhibitory control dysfunction is a core characteristic of many major psychiatric disorders. Inhibition is generally thought to involve the prefrontal cortex; however, a single inhibitory mechanism is insufficient for interpreting the heterogeneous nature of human cognition. It remains unclear whether different dimensions of inhibitory processes-specifically cognitive inhibition, response inhibition, and emotional interference-rely on dissociated neural systems. We conducted systematic meta-analyses of fMRI studies in the BrainMap database supplemented by PubMed using whole-brain activation likelihood estimation. A total of 66 study experiments including 1,447 participants and 987 foci revealed that while the left anterior insula was concordant in all inhibitory dimensions, cognitive inhibition reliably activated specific dorsal frontal inhibitory system, engaging dorsal anterior cingulate, dorsolateral prefrontal cortex, and parietal areas, whereas emotional interference reliably implicated a ventral inhibitory system, involving the ventral surface of the inferior frontal gyrus and the amygdala. Response inhibition showed concordant clusters in the fronto-striatal system, including the dorsal anterior cingulate region and extended supplementary motor areas, the dorsal and ventral lateral prefrontal cortex, basal ganglia, midbrain regions, and parietal regions. We provide an empirically derived dimensional model of inhibition characterizing neural systems underlying different aspects of inhibitory mechanisms. This study offers a fundamental framework to advance current understanding of inhibition and provides new insights for future clinical research into disorders with different types of inhibition-related dysfunctions.

Impaired Frontal-Limbic White Matter Maturation in Children at Risk for Major Depression.

Depression is among the most common neuropsychiatric disorders. It remains unclear whether brain abnormalities associated with depression reflect the pathological state of the disease or neurobiological traits predisposing individuals to depression. Parental history of depression is a risk factor that more than triples the risk of depression. We compared white matter (WM) microstructure cross-sectionally in 40 children ages 8-14 with versus without parental history of depression (At-Risk vs. Control). There were significant differences in age-related changes of fractional anisotropy (FA) between the groups, localized in the anterior fronto-limbic WM pathways, including the anterior cingulum and the genu of the corpus callosum. Control children exhibited typical increasing FA with age, whereas At-Risk children exhibited atypical decreasing FA with age in these fronto-limbic regions. Furthermore, dorsal cingulate FA significantly correlated with depressive symptoms for At-Risk children. The results suggest maturational WM microstructure differences in mood-regulatory neurocircuitry that may contribute to neurodevelopmental risk for depression. The study provides new insights into neurodevelopmental susceptibility to depression and related disabilities that may promote early preventive intervention approaches.

Neurorehabilitation for Multiple Sclerosis Patients with Emotional Dysfunctions.

Depression frequently develops in multiple sclerosis (MS) patients, exacerbating the manifestations of the disease and making its management challenging. To date, no consensus has been reached regarding effective treatments for these sufferers due to limited understanding regarding the underlying mechanisms responsible for emotional disorders that are highly comorbid with this disease. There is an urgent need to rethink current treatment options for these patients. This article aims to optimize the treatment outcomes and improve the quality of life for MS patients. Based on an in-depth and critical review of the current literature, we provide a neurorehabilitative framework that explains possible regulatory mechanisms underlying the emotional symptoms highly developed in MS. This article offers practical knowledge and therapeutic strategies to optimize the treatment options in the current care system for MS, as well as for other disabling diseases.