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A previous generation was taught that the neuronal effects of concussion might be described by "a neurometabolic cascade." That hypothesis was an important historical advance. But an acceleration in basic research during the last two decades has revealed the limitations of that model. First, rather than a cascade -- implying a one-way progression from health to harm --concussion instead seems to trigger a battle royale for the well-being of neurons, glia, vasculature, and the blood--brain barrier. Each potentially deleterious biological phenomenon is answered by a potentially neuroprotective defense. Second, although metabolic stress is part of neuronal jeopardy, concussive brain injury involves a combination of energy crisis with profound alterations of gene expression, multiple molecular toxicities, inflammatory assaults, neurovascular compromise, and other harmful processes. Third, contrary to the twentieth-century theory of biological restoration in roughly 3--14 days, recent evidence admonishes that the spectrum and duration of common concussive effects has yet to be determined.
Structural and functional brain imaging have helped to elucidate the neural pathways involved in hydrocephalic cognitive impairment. In addition, studies of brain metabolism and blood flow, molecular imaging, and cerebrospinal fluid (CSF) physiology have provided novel windows into the pathogenesis of dementia in idiopathic normal pressure hydrocephalus (iNPH). A number of pathophysiologic mechanisms have been identified that are potentially relevant to the pathogenesis of the cognitive symptoms of iNPH, namely, mechanical distortion, pressure effects, and cerebrovascular compromise. A possible synthesis of these mechanisms would be that an imbalance of CSF production and clearance leads to progressive ventricular enlargement. The profile of cognitive impairments in iNPH is recognizably that of a subcortical pathological process. Deficiencies in attention, working memory, set shifting, response inhibition and other aspects of executive functioning are commonly observed in iNPH and can be seen early in the disease course.
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