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✓确定cerebrospi增加的影响nal fluid (CSF) pressure on neuronal morphology, obstructive hydrocephalus was induced by injecting kaolin into the fourth ventricle and cisterna magna of 1-day-old rats. The animals were sacrificed 10 to 12 days later, at which time severe ventriculomegaly and cortical thinning were apparent in the parieto-occipital region. Tissue from this area was processed by rapid Golgi methods. Well impregnated pyramidal neurons were examined by light microscopy, and their somatic and dendritic features compared to those of age-matched littermate controls. The somata of medium pyramidal neurons were unaffected, but their basilar dendrites had fewer branches and those that remained were shorter. A variable reduction in dendritic spines occurred, such that some branches were totally denuded while others exhibited spine densities similar to those seen in control animals. The most striking alteration was the occurrence of frequent dendritic varicosities. These enlargements of the dendritic shaft separated by extremely thin constrictions gave the affected segment a beaded appearance. Both dendritic spine loss and varicosity formation were most notable on distal portions of individual branches and within regions of the dendritic tree closest to the ventricular and meningeal surfaces. These alterations are consistent with other reports of dendritic changes associated with aging, mental retardation, and alcohol exposure. These observations suggest that hydrocephalus causes dendritic deterioration or retardation of dendritic maturation. The fact that neuronal morphology was not more severely affected may indicate that these effects are reversible.

Object.The authors of previous studies have suggested that connectivity within the cerebral cortex may be irreversibly altered by hydrocephalus. To examine connectivity-related changes directly, the authors conducted a study in which they used an axonal tracer in an animal model of infantile hydrocephalus.

Methods.In five hydrocephalic kittens low-pressure ventriculoperitoneal (VP) shunts were placed 10 to 14 days after induction of hydrocephalus by intracisternal kaolin injections. Wheat germ agglutinin-conjugated horseradish peroxidase was injected laterally into the motor cortex in hydrocephalic animals 9 to 15 days after kaolin injection, and 1, 2, and 4 weeks after VP shunt insertion in shunt-treated animals, and in age-matched controls.

减少antero,逆行标记是most profound within the contralateral cortex and portions of the midbrain. Thalamic nuclei exhibited reductions in anterograde and retrograde labeling. Labeling within cell bodies of the ventral tegmental area decreased greatly in animals with untreated hydrocephalus, in which retrograde labeling was reduced in the locus coeruleus but did not affect the raphe nucleus. Shunt treatment increased both antero- and retrograde labeling of contralateral motor cortex to near-normal levels. Thalamic relay nuclei recovered antero- and retrograde labeling, although not to levels exhibited in controls. Shunt therapy restored cellular labeling within the ventral tegmental area and locus coeruleus. Recovery of labeling occurred as early as 7 days after shunt insertion.

Conclusions.Collectively, analysis of these data indicates the following. 1) Cortical connectivity involving both afferent and efferent pathways was impaired in untreated hydrocephalic animals. 2) Shunt therapy improved both cortical afferent and efferent connectivity. 3) Complete reestablishment of the cortical efferent pathways, however, did not occur. Cortical pathway dysfunction, if permanent, could cause many of the motor and cognitive deficits seen clinically in children with hydrocephalus.

✓为了识别关键缺口prevailing knowledge of hydrocephalus, the authors formulated 10 key questions. 1) How do we define hydrocephalus? 2) How is cerebrosinal fluid (CSF) absorbed normally and what are the causes of CSF malabsorption in hydrocephalus? 3) Why do the ventricles dilate in communicating hydrocephalus? 4) What happens to the structure and function of the brain when it is compressed and stretched by the expanding ventricles? 5) What is the role of cerebrovenous pressure in hydrocephalus? 6) What causes normal-pressure hydrocephalus? 7) What causes low-pressure hydrocephalus? 8) What is the pathophysiology of slit ventricle syndrome? 9) What is the pathophysiological basis for neurological impairment in hydrocephalus, and to what extent is it reversible? 10) How is the brain of a child with hydrocephalus different from that of a young or elderly adult? Rigorous answers to these questions should lead to more effective and reliable treatments for this disorder.