CSF ascites: a rare complication of ventriculoperitoneal shunt surgery.
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CSF ascites is a very rare complication of ventriculoperitoneal (VP) shunt procedure. No definite explanation has been offered for the inability of the peritoneum to absorb the CSF. Two children who underwent VP shunting for hydrocephalus, presented with ascites 3 (1/2) years and 4 months respectively, after the shunt was placed. The treatment of choice is conversion of the VP shunt to a ventriculoatrial shunt. (+info)
Infection of central nervous system by motile Enterococcus: first case report.
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A 66-year-old man with four indwelling ventriculoperitoneal shunts for multiloculated hydrocephalus from a complicated case of meningitis a year before developed shunt infection based on a syndrome of fever, drowsiness, and cerebrospinal fluid neutrophil pleocytosis in the background of repeated surgical manipulation to relieve successive shunt blockages. The cerebrospinal fluid culture, which yielded a motile Enterococcus species, was believed to originate from the gut. This isolate was lost in storage and could not be characterized further. The patient improved with vancomycin and high-dose ampicillin therapy. He relapsed a month later with Enterococcus gallinarum shunt infection, which responded to high-dose ampicillin and gentamicin therapy. This is probably the first case report of motile Enterococcus infection of the central nervous system. (+info)
Corpus callosal signal changes in patients with obstructive hydrocephalus after ventriculoperitoneal shunting.
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BACKGROUND AND PURPOSE: Few reports have documented signal abnormalities within the corpus callosum on MR studies obtained after ventricular decompression in patients with hydrocephalus. Our purpose was to establish the frequency of this finding in shunted patients and attempt to elucidate its cause and clinical significance. METHODS: All patients with hydrocephalus shunted between 1989 and 1999 with postoperative MR studies available for review were included in the study group. Imaging analysis consisted of documenting hypointense signal on T1-weighted sagittal images and hyperintense signal on double-echo T2-weighted axial images within the corpus callosum. RESULTS: Characteristic signal abnormalities in the corpus callosum were noted in nine of 161 patients with shunted hydrocephalus studied with MR imaging. All nine patients were asymptomatic in regard to these MR findings. Comparison with preoperative scans and surgical records revealed that all patients with signal changes on postshunt scans had chronic obstructive hydrocephalus at presentation. Preshunt MR images were notable for marked elevation of the corpus callosum, which subsequently descended after ventricular decompression, suggesting that the cause of the signal changes was related to compression of the corpus callosum against the rigid falx. CONCLUSION: Signal abnormalities within the corpus callosum after ventricular shunting for obstructive hydrocephalus are not uncommon and are probably produced by compression of the corpus callosum against the falx before ventricular decompression. This distinctive appearance should not be mistaken for significant disease. Recognition of this pattern of signal abnormality will help avoid unnecessary intervention. (+info)
Transforming growth factor-beta1 in the cerebrospinal fluid of patients with subarachnoid hemorrhage: titers derived from exogenous and endogenous sources.
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Transforming growth factor-beta1 (TGF-beta1) is a fibrogenic cytokine that is involved in postinjury repair and is implicated in the etiology of postsubarachnoid hemorrhage (SAH) chronic communicating hydrocephalus. TGF-beta1 was measured by enzyme-linked immunosorbant assay (ELISA) in sequential samples of cerebrospinal fluid (CSF) in 11 patients with hydrocephalus after SAH; levels were seen to be biphasically elevated and sources were investigated. TGF-beta1 levels were compared with albumin levels that estimated CSF blood content. Control samples from nonhemorrhagic hydrocephalics were tested similarly. Mean total TGF-beta1 levels were elevated to 4400+/-3435 (+/-SD) pg/mL greater than control levels of 97+/-42 at 1 to 2 days posthemorrhage. Thereafter, levels fell to 714+/-401 by 5 to 6 days posthemorrhage, then rose to a second peak of 1667+/-774 at 9 to 10 days posthemorrhage, remaining significantly increased until 19 days posthemorrhage (P = 0.007). The first peak probably derived from extravasated platelets and correlated with increased albumin levels in the CSF. The second TGF-beta1 peak rose greater than CSF albumin levels that had stabilized at this time, and thus was attributed to a tissue-specific response rather than a re-bleed. TGF-beta1 was detected in the choroid secretory epithelium from controls, but levels were greater in SAH patients at 10 to 12 days posthemorrhage. The authors conclude that the elevated levels of TGF-beta1 in CSF after SAH are derived initially from blood and later from endogenous sources such as the choroid plexus. (+info)
Periventricular changes associated with spontaneous canine hydrocephalus.
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Causes of canine juvenile hydrocephalus have been well documented. However, the effects of hydrocephalus on periventricular white matter have been only partially described. The present report shows that hydrocephalus-associated lesions of the periventricular white matter, i.e., formation of diverticula, clefts, and tears, are prevalent. Marked hydrocephalus was identified at necropsy in 20 juvenile dogs between 1990 and 1999. The severity grade was based upon a ratio of lateral ventricular dimensions to cortical thickness. All animals exhibited ependymal lesions consisting of attenuation, with or without abortive attempts of ependymal regeneration, and ulceration. In 10 dogs (50%), unilateral or bilateral periventricular diverticula and cleft formation in the region of the caudate nucleus were observed. The diverticula were formed at the caudal pole of the caudate nucleus, communicated with the ventricular lumen, and were associated with ependymal denudation. Loss of the ependymal lining probably contributes to a bulk shift of cerebrospinal fluid from the ventricular lumen to the periventricular white matter, leading to diverticulum formation. Clefts were observed within the parenchyma at the border of the internal capsule and putamen, consistent with an ischemic insult. Occasionally tearing with separation of the caudate nucleus from the subcortical white matter was found, representing unification of expanding clefts and diverticula. In one of the few clinically well-documented cases, tearing was correlated with a sudden decline in neurologic function, culminating in euthanasia. However, tears and clefts may exhibit a chronicity of several days, as indicated by the presence of astroglial scars along the lesion margins. (+info)
Hydrocephalus in mice following X-irradiation at early gestational stage: possibly due to persistent deceleration of cell proliferation.
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The pathogenesis of X-ray-induced congenital hydrocephalus was studied. Pregnant mice were irradiated at 1.4 Gy on gestational day 7 (G7). Four hours after irradiation, extensive cell death was evident in the neuroepithelium and underlying mesoderm of the head region, and proliferating cell nuclear antigen (PCNA)-immunoreactive cells almost disappeared. Embryos with thinner lamina terminalis of the telencephalon, when compared with that of the control, were found in the irradiated group on G9. As early as G11 in some irradiated embryos the telencephalic wall was thinner and lateral ventricles were larger than those of the control. The choroid invagination from the lamina terminalis began on G11 in the control brain, but not in the affected brain. During the following development, fetuses with readily apparent hydrocephalus were consistently found among irradiated fetuses. In these brains the brain mantle was thinner, the corpus striatum and thalamic regions were smaller, and lateral ventricles were larger than those of the control. Even on G11 and G13 the frequencies of PCNA-positive cells in the brain mantle and other brain regions were lower in the hydrocephalic brain than those of the control, suggesting a decelerated proliferation of successive cell generations following exposure to X-rays. The cerebral aqueduct was open in the hydrocephalic brain during the fetal period when the lateral ventricles were dilated. The head was vaulted after birth but the cerebral aqueduct was not completely occluded even in these animals. These findings suggested that cell death in the neuroepithelium followed by a persistent deceleration of neural cell proliferation, resulting in the hypoplasia of brain parenchyma with compensatory ventricular dilatation, is important for the establishment of hydrocephalus. (+info)
Ocular significance of intraventricular haemorrhage in premature infants.
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AIM: To document ocular outcome in premature infants with intraventricular haemorrhages (IVH). METHODS: 68 preterm infants with IVH were examined. RESULTS: Mean gestational age was 28.1 weeks (range 24-35). Mean birth weight was 1045.9 g (630-2240). Mean follow up was 54.6 months (6-150). IVH is graded from 1 to 4 based on the severity of haemorrhages. The incidence of ocular abnormalities was compared between low grade IVH (grade 1 and 2) and high grade IVH (grade 3 and 4). Of the 68 infants with IVH, ROP occurred in 33 infants (48.5%); 13 (43.3%) had low grade IVH; 20 (52.6%) had high grade IVH. Strabismus developed in 30 infants (44.1%); 14 (46.6%) had low grade IVH; 16 (42.1%) had high grade IVH. Infants with high grade IVH were at significant greater risk than infants with low grade IVH for the development of optic atrophy (31.5% v 16.6%), hydrocephalus (57.8% v 10%). CONCLUSION: This study highlights the serious significance of all grades of IVH with the higher incidence of optic atrophy and hydrocephalus with high grade IVH. (+info)
Children with macrocrania: clinical and imaging predictors of disorders requiring surgery.
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BACKGROUND AND PURPOSE: Macrocrania is a common pediatric clinical condition affecting up to 5% of the population. The purpose of this study was to determine clinical and imaging predictors that are useful in the differentiation of disorders requiring surgical treatment from those that can be treated medically in children with macrocrania. METHODS: In a 3-year 7-month retrospective study, 88 patients (median age, 8 months; interquartile range, 5--13 months) with macrocrania and no known underlying neurologic disorder underwent imaging of the brain (sonography, n = 36; CT, n = 31; MR imaging = 21). The study was conducted in a pediatric tertiary care referral center. Clinical and imaging data were correlated to final diagnosis by means of logistic regression and receiver operating characteristic curves. RESULTS: Sixteen (18%) of the patients had disorders requiring surgery: communicating hydrocephalus, n = 7; noncommunicating hydrocephalus, n = 3; hemorrhagic subdural collections, n = 3; neoplasm, n = 1; encysted cavum septi pellucidi, n = 1; and vein of Galen malformation, n = 1. Clinical predictors of disorders requiring surgery included vomiting (P =.007), labor instrumentation (P =.026), developmental delay (P =.008), and abnormal neurologic findings (P =.028). Imaging predictors of disorders requiring surgery included a focal space-occupying lesion (P <.0001) and moderate-to-severe ventriculomegaly (P <.0001). The diagnostic sensitivity of the combination of independent clinical and imaging predictors was higher than that of independent clinical predictors alone, being 100% (95% confidence interval = 96.9%, 100%) and 93.8% (95% confidence interval = 88.7%, 98.8%), respectively. A trend indicated that the area under the receiver operating characteristic curve for clinical plus imaging findings (0.95) was greater than that for clinical findings alone (0.85) (P =.09). An increase in the number of clinical and imaging predictors was highly correlated with an increased risk of a disorder requiring surgery (P <.0001). CONCLUSION: Baseline neuroimaging is indicated for children with macrocrania because the combination of clinical and imaging predictors has the best diagnostic performance in determining the need for surgical versus nonsurgical management. (+info)