Articles: function.
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Randomized Controlled Trial
How does treadmill training contribute to botulinum toxin application plus routine physical therapy in ambulatory children with spastic bilateral cerebral palsy? A randomized controlled trial.
In spite of treadmill training and multilevel botulinum toxin (BoNT-A) injection being the two most commonly used treatment methods in pediatric rehabilitation management, there was no study investigating the effect of treadmill training after BoNT-A injection in children with cerebral palsy (CP). ⋯ Treadmill training in addition to routine physical therapy after BoNT-A injection is beneficial for hip muscle strength, ankle selective motor control, walking quality, and functional mobility in the short term.
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Moderate to severe tricuspid regurgitation (TR) is known to cause right ventricular (RV) failure and death. Although TR is traditionally classified as primary or secondary, recently, a new class of TR called idiopathic TR has been proposed, with varying definitions among different studies. ⋯ Idiopathic TR was associated with better RV function than the other secondary TRs. Thus, idiopathic TR should be strictly defined and regarded as a distinct type of TR.
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Haematoma expansion affects a fifth of patients within 24 h of the onset of acute intracerebral haemorrhage and is associated with death and disability, which makes it an appealing therapeutic target. The time in which active intervention can be done is short as expansion occurs mostly within the first 3 h after onset. ⋯ Blood pressure lowering and haemostatic treatment minimise haematoma expansion but have not led to improved functional outcomes in randomised clinical trials. Ultra-early enrolment and selection of participants on the basis of non-contrast CT imaging markers could focus future clinical trials to show clinical benefit in people at high risk of expansion or investigate heterogeneity of treatment effects in clinical trials with broad inclusion criteria.
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Hereditary optic neuropathies result from defects in the human genome, both nuclear and mitochondrial. The two main and most recognised phenotypes are dominant optic atrophy and Leber hereditary optic neuropathy. ⋯ A unifying feature in the pathophysiology of these disorders appears to involve mitochondrial dysfunction, suggesting that the retinal ganglion cells and their axons are especially susceptible to perturbations in mitochondrial homoeostasis. As we better understand the pathogenesis behind these genetic diseases, aetiologically targeted therapies are emerging and entering into clinical trials, including treatments aimed at halting the cascade of neurodegeneration, replacing or editing the defective genes or their protein products, and potentially regenerating damaged optic nerves, as well as preventing generational disease transmission.