15 research outputs found
Cardiovascular Pathophysiology in Chronic Kidney Disease: Opportunities to Transition from Disease to Health
Background: Chronic kidney disease (CKD) is common, and is associated with a high burden of cardiovascular disease. This cardiovascular risk is incompletely explained by traditional risk factors, calling attention to a need to better understand the pathways in CKD contributing to adverse cardiovascular outcomes. Findings: Pathophysiological derangements associated with CKD, including disordered sodium, potassium, and water homeostasis, renin-angiotensin-aldosterone and sympathetic activity, anemia, bone and mineral metabolism, uremia, and toxin accumulation may contribute directly to progression of cardiovascular disease and adverse outcomes. Conclusion: Improving cardiovascular health in patients with CKD requires improved understanding of renocardiac pathophysiology. Ultimately, the most successful strategy may be prevention of incident CKD itself
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Herophilus, Erasistratus, Aretaeus, and Galen: ancient roots of the Bell-Magendie Law
Since the early 19th century, significant controversy has persisted over the competing claims of two men, Charles Bell and François Magendie, to a pivotal discovery: that the dorsal spinal roots subserve sensation, whereas the ventral spinal roots subserve motion. However, the foundations of neuroanatomy on which Bell and Magendie built their research was formed two millennia in advance. Exploration of the work of four ancient scholars--Herophilus, Erasistratus, Aretaeus, and Galen--reveals a remarkable early appreciation of the separate neural pathways (if not the correct physiology) responsible for sensory and motor control
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Ventriculoperitoneal shunting of idiopathic normal pressure hydrocephalus increases midbrain size: a potential mechanism for gait improvement
Idiopathic normal pressure hydrocephalus (INPH) is characterized by a classic clinical triad of symptoms, including dementia, urinary incontinence, and gait disturbance. Recent work has demonstrated that the maximal midbrain anteroposterior (AP) diameter is significantly smaller in patients with INPH than in healthy, age-matched controls. The current study was undertaken to determine the effect of ventriculoperitoneal shunt placement on midbrain dimensions in INPH patients.
Twelve consecutive INPH patients undergoing ventriculoperitoneal shunt placement with pre- and postoperative computed tomographic scans at the Columbia University Medical Center were enrolled. Each patient's pre- and postoperative maximum AP and left-to-right diameters of the midbrain at the pontomesencephalic junction were independently measured in a blinded fashion by two of the authors. The average value of each dimension was computed by calculating the mean values of the measurements of the two observers.
Both the mean AP diameter (preoperative mean, 2.06 +/- 0.04 cm; postoperative mean, 2.27 +/- 0.05; P = 0.0007) and left-to-right diameter (preoperative mean, 2.80 +/- 0.07; postoperative mean, 3.03 +/- 0.08; P = 0.0029) increased from pre- to postoperative imaging. The approximate cross-sectional area determined as the product of AP and left-to-right diameters also increased from pre- to postoperative images (preoperative mean, 5.79 +/- 0.22 cm; postoperative mean, 6.90 +/- 0.25 cm; P = 0.00049).
This study provides supportive evidence that midbrain cytoarchitecture may play a role in the pathophysiology and post-ventriculoperitoneal shunt gait improvement of INPH patients