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http://projects.csail.mit.edu/courseware/?term=how-to-make-a-good-argument-essay how to make a good argument essay Infants with the two major complications of ivh, namely pvhi and pvd, are at much higher risk of neurologic impairments than those with ivh alone viagra over the counter uk 2013. Infants with pvd/phh requiring significant intervention often manifest spastic diparesis and cognitive impairments due to bilateral periventricular wmi. Infants with a localized, unilateral pvhi usually develop a spastic hemiparesis affecting the arm and leg with minimal or mild cognitive impairments (55). Quadriparesis and significant cognitive deficits (including mental retardation) are more likely if the pvhi is extensive or bilateral, or if there is also coexisting pvl, which is common (58). In addition to cognitive and motor impairments, infants with severe phh and/or pvhi are at risk for developing cerebral visual impairment and epilepsy (58). Outcome in term newborns with ivh relates to factors other than ivh alone, as uncomplicated small ivh in this population has a favorable prognosis. Infants with a history of trauma or perinatal asphyxia, or with neuroimaging evidence of thalamic hemorrhagic infarction, hypoxic-ischemic brain injury, or other parenchymal lesions, are at high risk for significant cognitive and/or motor deficits and epilepsy. Neurologic disorders v. I 703 periventricular leukomalacia a. Etiology and pathogenesis. Pvl is a lesion found predominantly in the preterm infant and is the neuropathologic lesion underlying much of the cognitive, motor and sensory impairments and disabilities in children born prematurely. The true incidence of this lesion is not known, largely because detection of the mild form of this lesion is difficult using conventional neuroimaging and because the threshold for determining signal abnormality in the cerebral white matter has not been rigorously defined. White matter injury is a term used increasingly in place of the traditional term periventricular kukomalacia or periventricular leukoencephalopathy, although the term pvl is still commonly used. Wmi is a somewhat broader term than pvl in that it denotes the diffuse lesion of the cerebral white matter that extends beyond the periventricular regions defined in initial neuropathologic and ultrasonographic studies and is often a noncystic lesion. An even more encompassing term, "encephalopathy of prematurity," was proposed by volpe to include the findings of neuronal abnormalities in gray matter structures demonstrated by neuropathology and neuroimaging studies in addition to the wmi (59). This term is not yet in widespread use in the literature but is a term that reflects increasing evidence that premature newborns suffer a brain injury that affects many gray matter structures in addition to the cerebral white matter. Note that wmi with a similar imaging pattern to pvl in the preterm infant has also been reported in infants hom at term (60), particularly in those who underwent surgical repair of congenital heart disease (61). The characteristic neuropathology of pvl was first described in detail by banker and larroche in their classic 1962 report of the histologic findings in 51 autopsy specimens (62). They described the classic features of pvl to include bilateral areas of focal necrosis, gliosis, and disruption of axons, with the so-called "retraction clubs and balls." the topographical distribution of the lesions was noted to be in the periventricular white matter dorsolateral to the lateral ventricles, primarily anterior to the frontal horn (at the level of the foramen of monro) and lateral to the occipital horns. They noted that a severe "anoxic" episode occurred in 50 of 51 infants, that the lesions were consistently observed in the location of the border zone of the vascular supply, and that 75% of the group had been born prematurely. They thus suggested two key features of the pathogenesis of pvl, namely, (i) hypoxia-ischemia affecting the watershed regions of the white matter, and (ii) a particular vulnerability of the periventricular white matter of the premature brain. Further neuropathologic studies have extended these initial observations, demonstrating that in many cases pvl consists of areas of both focal necrosis (which become cystic) and a diffuse white matter lesion.

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essay about homework There are viagra over the counter uk 2013 several risk assessment models available for estimating vte risk specific to hospitalized medical and surgical patients. 5–7,12 while none of these models have been 168  section 1  |  cardiovascular disorders clinical presentation and diagnosis of pe general •• most commonly develops in patients with risk factors for vte (table 10–1) during or following a hospitalization. Although many patients will have symptoms of dvt prior to developing a pe, many do not and some patients can be asymtomatic. Patients may die suddenly before effective treatment can be initiated. Symptoms •• may complain of cough, pleuritic chest pain, chest tightness, shortness of breath with or without exertion, wheezing, or palpitations. •• may present with hemoptysis (spit or cough up blood). •• may complain of dizziness or lightheadedness. •• may be confused for a myocardial infarction (mi) or pneumonia, and objective testing must be performed to establish the diagnosis. Signs •• may have tachypnea (increased respiratory rate) and tachycardia (increased heart rate).

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