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Pulmonary vascular disease resulting from CHDs may be the most preventable cause of pulmonary artery hypertension worldwide. Many children in developing countries still do not have access to early closure of clinically significant defects, and the long-term outcomes after corrective surgery remain unclear. Focused on long-term results after isolated ventricular septal defect repair, our review sought to determine the most effective medical therapy for the pre-operative management of elevated left-to-right shunts in patients with an isolated ventricular septal defect.
We identified articles specific to the surgical repair of isolated ventricular septal defects. Specific parameters included the pathophysiology and pre-operative medical management of pulmonary over-circulation and outcomes.
Studies most commonly focused on histologic changes to the pulmonary vasculature and levels of thromboxanes, prostaglandins, nitric oxide, endothelin, and matrix metalloproteinases. Only 2/44 studies mentioned targeted pharmacologic management to any of these systems related to ventricular septal defect repair; no study offered evidence-based guidelines to manage pulmonary over-circulation with ventricular septal defects. Most studies with long-term data indicated a measurable frequency of pulmonary artery hypertension or diminished exercise capacity late after ventricular septal defect repair.
Long-term pulmonary vascular and respiratory changes can occur in children after ventricular septal defect repair. Research should be directed at providing an evidenced-based approach to the medical management of infants and children with ventricular septal defects (and naturally all CHDs) to minimise consequences of pulmonary artery hypertension, particularly as defect repair may occur late in underprivileged societies.
Dissociative seizures (DS) are brief episodes of disrupted awareness and behavioural control that may resemble epileptic seizures. They are thought to arise in the context of impaired emotion processing and disinhibition. In a multi-perspective neuropsychological study, we aim to assess specific metacognitive traits and behavioural features involved in the affective and cognitive underpinnings of DS (emotion recognition and regulation, inhibition, interoception and sense of agency).
Twenty prospectively recruited patients with video-EEG-confirmed DS and 20 healthy controls underwent comprehensive neuropsychological and psychiatric testing using validated questionnaires and structured interviews. Behavioural experimental data was obtained using a custom-made emotional go/no-go task, a digital Libet clock setup and a heartbeat counting paradigm.
Emotion recognition, as quantified in the emotional go/no-go task, was impaired in the DS group, and correlated with alexithymic traits. Behavioural inhibition, especially under conditions that would require emotion regulation, was also reduced in the emotional go/no-go task compared to controls and was correlated with neuropsychometric measures of emotion regulation. Data from the Libet clock experiment suggested impaired behavioural awareness in DS patients. No evidence of impaired interoceptive awareness was found in the heartbeat counting task.
These results represent comprehensive experimental evidence for alterations in emotional and behavioural awareness and control in patients with DS that yield empirical evidence for current psychopathological models. Our findings offer a more detailed understanding of key pathogenic factors in DS and provide theoretical support for recently developed cognitive-behavioural therapies for DS.
Wake-up stroke (WUS) or ischemic stroke occurring during sleep accounts for 14%–29.6% of all ischemic strokes. Management of WUS is complicated by its narrow therapeutic time window and attributable risk factors, which can affect the safety and efficacy of administering intravenous (IV) tissue plasminogen activator (t-PA). This manuscript will review risk factors of WUS, with a focus on obstructive sleep apnea, potential mechanisms of WUS, and evaluate studies assessing safety and efficacy of IV t-PA treatment in WUS patients guided by neuroimaging to estimate time of symptom onset. The authors used PubMed (1966 to March 2018) to search for the term “Wake-Up Stroke” cross-referenced with “pathophysiology,” ‘‘pathogenesis,” “pathology,” “magnetic resonance imaging,” “obstructive sleep apnea,” or “treatment.” English language Papers were reviewed. Also reviewed were pertinent papers from the reference list of the above-matched manuscripts. Studies that focused only on acute Strokes with known-onset of symptoms were not reviewed. Literature showed several potential risk factors associated with increased risk of WUS. Although the onset of WUS is unknown, a few studies investigated the potential benefit of magnetic resonance imaging (MRI) in estimating the age of onset which encouraged conducting clinical trials assessing the efficacy of MRI-guided thrombolytic therapy in WUS.
Previous morphology and diffusion-imaging studies have suggested that structural changes in white matter is an important part of the pathophysiology of obsessive–compulsive disorder (OCD). However, different methodological approaches and the heterogeneity of patient samples question the validity of the findings.
Materials and methods
In total, 30 patients were matched for age and sex with 30 healthy controls. All participants underwent T1-weighted magnetic resonance imaging, diffusion tensor imaging and T2 fluid-attenuated inversion recovery. Voxel-based morphometry and tract-based spatial statistics were used to compare white matter volumes and diffusion tensor imaging between groups. These data were analysed correcting for the effects of multiple comparisons, age, sex, severity and duration of illness as nuisance covariates. White matter hyperintensities were manually identified.
Increase in fractional anisotropy in cerebellum was the most prominent result. A decrease in fractional anisotrophy in patients comparable with previous studies was located in forceps minor. There were no differences in the white matter morphology or in the white matter hyperintensities between patients and healthy controls.
Decrease in fractional anisotrophy in forceps minor and increase in cerebellum were found, and they were not due to neither white matter hyperintensities nor morphology of the white matter. Cerebellar hyperconnectivity could be an important part of OCD pathophysiology.
The aetiology of depression is not fully understood, which allows many different perspectives on aetiology to be adopted. Researchers and clinicians may be attracted to concepts of aetiology that parallel other diagnoses with which they are familiar. Such parallels may assume the role of informal models or metaphors for depressive disorders. They may even function as informal scientific theories of aetiology, energising research activities by guiding hypothesis generation and organising new knowledge. Parallels between different types of disease may ultimately prove valuable as frameworks supporting the emergence and maturation of new knowledge. However, such models may be counterproductive if their basis, which is likely to lay at least partially in analogy, is unacknowledged or overlooked. This could cause such models to appear more compelling than they really are. Listing examples of situations in which models of depression may arise from, or be strengthened by, parallels to other familiar conditions may increase the accessibility of such models either to criticism or support. However, such a list has not yet appeared in the literature. The present paper was written with the modest goal of stating several examples of models or metaphors for depression.
This paper adopted narrative review methods. The intention was not to produce a comprehensive list of such ideas, but rather to identify prominent examples of ways of thinking about depression that may have been invigorated as a result parallels with other types of disease.
Eight possible models are identified: depressive disorders as chemical imbalances (e.g., a presumed or theoretical imbalance of normally balanced neurotransmission in the brain), degenerative conditions (e.g., a brain disease characterised by atrophy of specified brain structures), toxicological syndromes (a result of exposure to a noxious psychological environment), injuries (e.g., externally induced brain damage related to stress), deficiency states (e.g., a serotonin deficiency), an obsolete category (e.g., similar to obsolete terms such as ‘consumption’ or ‘dropsy’), medical mysteries (e.g., a condition poised for a paradigm-shifting breakthrough) or evolutionary vestiges (residual components of once adaptive mechanisms have become maladaptive in modern environments).
Conceptualisation of depressive disorders may be partially shaped by familiar disease concepts. Analogies of this sort may ultimately be productive (e.g., through generating hypotheses by analogy) or destructive (e.g., by structuring knowledge in incorrect, but intellectually seductive, ways).
The association between eustachian tube dysfunction and middle-ear effusion is well established. Studies have also demonstrated pathological changes affecting the middle-ear mucosa associated with chronic sinonasal inflammation. No previous studies have evaluated symptoms related to sinonasal inflammatory disease in different ear diseases.
To assess the presence of sinonasal symptoms in ear diseases using the Dundee Rhinogram.
Data were collected prospectively in the period February–October 2011. Sinonasal symptoms were graded using the Dundee Rhinogram. Student's t-test analyses were performed to identify any statistically significant associations.
In total, 164 patients were assessed. There was a statistically significant association between sinonasal symptoms and mucosal middle-ear diseases (p < 0.005). The mean sinonasal symptoms score for mucosal middle-ear disease patients was 5.94 (range, 0–32).
Assessment of sinonasal symptoms is paramount in patients presenting with an ear symptom; inflammatory sinonasal disease treatment may become necessary in the management of middle-ear mucosal disease for better patient outcome.
We aimed to evaluate the relationship between swimming pool pollutants and allergic rhinitis in swimming pool workers.
Materials and methods:
Twenty-seven indoor pool workers (group 1) and 49 control subjects (group 2) were enrolled in the study. A skin prick test was performed and a nasal smear was obtained from each subject to evaluate rhinitis.
When the groups were compared in terms of epithelial cells, group 1 had significantly more epithelial cells than group 2. When the groups were compared with regard to eosinophils, group 1 had significantly more eosinophils than group 2. The skin prick test results for both groups were not significantly different.
Indoor pool workers showed severe symptoms of rhinitis and eosinophilic nasal cytology, likely due to chlorine. Nasal cytology is an easy-to-administer diagnostic test and can be used to follow up rhinitis in indoor pool workers, along with nasal endoscopy, a detailed clinical history and a skin prick test.
Several theories have been proposed to explain the pathophysiology of gait dysfunction in normal pressure hydrocephalus (NPH). The variety of potential targets includes midbrain compression or atrophy, cortical dysfunction, cortical-subcortical or intracortical circuit abnormalities, postural disturbance, dopamine signaling abnormalities, and regional cerebral blood flow (rCBF) depression. This chapter presents objective measures of gait dysfunction that have been used clinically, and highlights some of the major theories postulated to explain gait dysfunction in NPH. Gait dysfunction in NPH has characteristic features that include a slow pace, short stride length, wide stance, and low foot-floor elevation. Objective measures of gait can be used to quantify the pattern of walking and step-taking, focusing on walking speed, stride length, cadence, equilibrium, and posture. Recognition of cortical involvement in locomotion stems from multiple research efforts evaluating gait in healthy individuals and those with cognitive disturbances.