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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied electrophysiologically by single cell recording in the visual cortex, whether modification of the visual system in developing and in adult cats by hydrocephalus has an effect on processing of visual information. One of our cats (H1) had developed a complete hydrocephalus and the others partial, as proved by either complete or partial dilation of the lateral ventricles, respectively and by the thinning of the cortex. Despite this, the horizontal lamination and the vertical organization of the cortex were fully preserved. Except for the optic radiation and the corpus callosum which was remarkably modified, the optic tract, chiasm, nerve and retina were morphologically and histologically normal. The visual behavior of the hydrocephalic cats was normal. This was also reflected, by and large, in the physiological properties of the visual cortex. However, in cat H1 there were many more visually unresponsive cortical cells in comparison to its matched controls (C1) and the normal cats. A reduced responsiveness was also found in cat H2 with partial hydrocephalus but not in the other partial hydrocephalic cats. Similarly, the ocular dominance distribution of the cells was affected in cat H1 in comparison to the control cats as indicated by the changes found in the relative proportions of contralaterally and ipsilaterally driven cells in the two hemispheres. No change was, however, found in the partially hydrocephalic cats. Most of the cells in the hydrocephalic cats were orientation specific, similarly to the result of their matched controls. Direction specific cells were much smaller in proportion in cat H1 but not in the other cats, in comparison with their matched controls. In keeping with this, a large increase was found in the receptive field area of cat H1, a smaller one in cat H2 and none in the other hydrocephalic cats in comparison to the matched controls. The eccentricity distribution of the receptive fields in the hydrocephalic cats was the same as expected under normal conditions. It was concluded that in the way hydrocephalus had modified the brain of several of our cats, a quantitative effect was induced in visual cortex cells leading to some degradation of function; this change, however, did not interfere with their basic visual properties.
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PMID:Hydrocephalus in developing cats: physiological properties of visual cortex cells. 228 52

The effect of hydrocephalus on cerebral glucose utilization as reflected by deoxyglucose uptake has been examined in rats with inherited hydrocephalus at 10, 20, and 28 days after birth using a semiquantitative method. Injection of [14C]deoxyglucose intraperitoneally was followed by freezing the brain, sectioning, and quantitative autoradiography of 10 brain regions. Brain [14C] concentration, cortical thickness, and plasma glucose concentrations were measured. Maximal thinning of the cerebral cortex had already occurred by 10 days after birth, although obvious symptoms such as gait disturbance developed after 20 days. In control rats, the cerebral isotope concentration was lower and more homogeneous at 10 days than at 20 or 28 days, which may be a reflection of the use of metabolic substrates other than glucose in younger animals. In order to make comparisons between control and hydrocephalic groups, tissue isotope concentrations were normalized to cerebellar cortex which was not affected by the hydrocephalus at any age. In hydrocephalic rats at 10 and 20 days, the concentration of [14C] was lower in all areas except the inferior colliculi and pons but the reduction was only significant in the sensory-motor cortex at 10 days and in the caudate nuclei at 20 days. By 28 days after birth, all areas except the cerebellum (six cortical regions, inferior colliculi, pons, and caudate) had significantly lower isotope concentrations in the hydrocephalic group. It is concluded that cerebral glucose metabolism is significantly reduced by 28 days after birth in H-Tx rats with congenital hydrocephalus and that less marked reductions occur prior to 28 days.
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PMID:The uptake of [14C]deoxyglucose into brain of young rats with inherited hydrocephalus. 291 63

Five neonates with perinatally lethal osteogenesis imperfecta (OI) have come to necropsy at Women & Infants' Hospital of Rhode Island in the past eight years. Four had true hydrocephalus, defined as enlargement of the lateral ventricles with thinning of the cortical mantle. In all 4 hydrocephalus was diagnosed by sonography before birth. All 4 died almost immediately after birth, whereas the neonate without hydrocephalus lived for 22 days. Significant necropsy findings in the 4 with hydrocephalus included healing occipital-bone fractures with stenosis of the foramen magnum, remote and recent cerebral parenchymal and intraventricular hemorrhage, and remote and recent subarachnoid hemorrhage. True hydrocephalus of intrauterine onset has rarely been described in perinatally lethal OI, but its high incidence (80%) in this population suggests that it may be a common phenomenon. Hydrocephalus of intrauterine onset in perinatally lethal OI may indicate relatively more severe disease.
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PMID:Hydrocephalus of intrauterine onset in perinatally lethal osteogenesis imperfecta: clinical, sonographic, and pathologic correlations. 306 1

The neuropathology of congenital hydrocephalus in SUMS/NP mice was investigated in this study. Hydrocephalus occurred with an incidence of 16.5% and was evident in the form of an enlarged head soon after birth. The condition was progressive; affected mice gradually became noticeably smaller than normals, acquired functional disturbances and died before ever breeding. Hydrocephalic mice exhibited enormous dilatation of the lateral ventricles, thinning of the cortex and compression and distortion of the diencephalon and striatum. Examination of the midbrain in these animals revealed that the proximal cerebral aqueduct was diminished in size, occluded or absent. Evidence of its anomalous development was seen as early as day 15 of foetal development. This is in substantial agreement with previous reports on this strain. Although the mechanism by which this occurs is still unknown, abnormal development of the adjoining diencephalon and/or rostral midbrain is likely to be involved.
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PMID:Neuropathology of congenital hydrocephalus in the SUMS/NP mouse. 340 65

This study was undertaken to identify findings on magnetic resonance (MR) imaging that might possibly differentiate among several dementia states in the elderly or predict response to shunt therapy in patients with normal-pressure hydrocephalus (NPH). The MR findings were retrospectively reviewed in 54 patients who were divided into four clinical categories: NPH (17 patients), obstructive hydrocephalus (eight patients), Alzheimer disease (eight patients), and non-Alzheimer dementia (21 patients). Three MR findings were evaluated in each case: increased periventricular (PVS) and white matter (WMS) signal on T2-weighted images, CSF flow void sign (CFVS) in the aqueduct, and corpus callosum thinning. Neither the PVS/WMS nor corpus callosum thinning patterns were useful for distinguishing among the four clinical groups. At low field strength, the absence of a marked or moderate CFVS, however, may militate against a diagnosis of NPH. All 17 patients with NPH underwent a shunt procedure after the MR study. A better response to shunt therapy occurred in patients without WMS and with more severe PVS.
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PMID:MR findings in normal-pressure hydrocephalus: significance and comparison with other forms of dementia. 368 Jul 6

Two cases of pneumocephalus after ventriculoperitoneal shunt placement in patients with posterior fossa tumors were reported. In each instance, air entered the ventricles through a porencephalic cavity in the temporal lobe that communicated with the mastoid air cells. Thinning of the petrous bone may occur secondary to chronic hydrocephalus or congenital factors. The decrease of intracranial pressure after a shunt might play a role in causing pneumocephalus. The early discovery of the site of air entrance by computed tomographic scan and the direct repair of the bone and dural defect should be mandatory.
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PMID:Spontaneous intracerebral pneumocephalus after ventriculoperitoneal shunting in patients with posterior fossa tumors: report of two cases. 370 28

Sixty-four infants were selected for evaluation of hydrocephalus and associated cerebral anomalies on CT scan; initial findings are compared with follow-up results after shunt therapy and correlated with psychomotor development. Analysis indicates that initial high-grade cortical thinning, the capability of the brain to recover after CSF diversion, and size and number of associated cerebral anomalies can all be considered decisive factors in estimating prognosis in infantile hydrocephalus.
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PMID:The significance of morphological details for developmental outcome in infantile hydrocephalus. 383 35

Brain tissue damage in congenital hydrocephalic rat (LEW/Jms) was studied in the aspects of the hydrocephalic brain edema and the changes of the vascular apparatus. The characteristic findings in this study were the changes of the small blood vessels and the intracerebral cavity formation. In the acute stage of hydrocephalus (2 to 5 days after birth), spongy appearance and necrosis of the brain edema were observed in the periventricular white matter. The stenotic or obstructive vascular changes were located in connection with the hydrocephalic brain tissue. In this stage, the intracerebral cavity was formed particularly in the periventricular edematous white matter resulting in a thinning of the occipital lobes. In the late stage of hydrocephalus (9 to 15 days after birth), the lateral ventricles were severely dilated, and a markedly dilatated intracerebral cavity was observed in the periventricular white matter. The edematous area was observed adjacent to the dilated lateral ventricles or the intracerebral cavity. In the late stage, the number of small vessels filled with carbon black decreased in the area of the CSF edema when compared to the acute stage, and many obstructive blood vessels were observed in the same area. Moreover, dilatated blood vessels without carbon black were observed in the border zone between the normal and the edematous area adjacent to the intracerebral cavity. These vascular changes may occur by the accumulation of the CSF as well as the mechanical compression, and consequently lead to the microcirculatory disturbance. These microcirculatory disturbances may contribute to the intracerebral cavity formation with the accumulation of the CSF in the extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain tissue damage in congenital hydrocephalus of the inbred rat, LEW/Jms--intracerebral cavity formation]. 387 51

Experimental hydrocephalus was induced by an intracisternal injection of 4% or 40% kaolin suspension in 2 days old Wistar rats. They were examined histologically and microangiographically 2 weeks after the injection of kaolin. Hydrocephalic rats were classified into 2 groups, severe hydrocephalic group A and mild hydrocephalic group B. In group A, a marked enlargement of the entire ventricular system with a thinning of the cerebral mantle was observed. On the other hand, the dilatation of the fourth ventricle was more pronounced compared with the other ventricles in group B. In group A, a spongy appearance of brain tissue was observed in the periventricular white matter accompanied with an intracerebral cavity. In these edematous areas, the lack of carbon black perfusion was apparent indicating an occurrence of microcirculatory disturbances. These microcirculatory disturbances and mechanical compression to the cerebral parenchyma may produce defective brain tissue (intracerebral cavity formation). The ependymal cell walls and subependymal glial cell layers were well preserved in spite of the damaged periventricular white matter. In group A, kaolin was present in the fourth ventricle and Sylvian aqueduct. Subependymal gliosis containing macrophages and newly produced blood vessels were observed in the region between the periventricular brain tissue and kaolin granules. These findings indicate that kaolin may produce changes in the ependymal cell and cerebral parenchyma as well as fibrosis and meningitis in the subarachnoid space.
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PMID:[Characteristics of brain tissue damage in kaolin-induced infantile rat hydrocephalus]. 396 87

To determine the effects of increased cerebrospinal 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.
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PMID:Neuronal effects of experimentally induced hydrocephalus in newborn rats. 405 81


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