PubMed · 14144587
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P A TAPELLA. 1964-04-27. [COMA].. https://pubmed.ncbi.nlm.nih.gov/14144587/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
CASE REPORT: A 10-month-old boy, with congenital deafness and blindness associated with chromosomal deletion [46XY, del(13)(q32)], presented with intractable ascites 9 months after ventriculo-peritoneal shunting for congenital hydrocephalus. Revision of the ventriculo-atrial shunt resulted in shunt failure 1 month later. External ventricular drainage revealed cerebrospinal fluid (CSF) overproduction (2,000 ml/day). Magnetic resonance imaging showed marked lobular enlargement of the bilateral choroid plexuses extending from the trigone to the body and inferior horn of the lateral ventricle. Multi-staged resection was performed via bilateral temporo-occipital transcortical approaches, and CSF production significantly decreased to 100 ml/day postoperatively. Histological assessment of the villous surface suggested villous hyperplasia of the choroid plexus and thorough evaluation including the proximal portion of the lobular lesion near the attachment revealed choroid plexus papilloma. He was discharged after ventriculo-peritoneal shunting without additional neurological deficits except for hyperreflexia of the left extremities. CONCLUSION: CSF overproduction caused by bilateral choroid plexus papillomas can result in hydrocephalus. Radical resection of the bilateral ventricular lesions should be considered for this entity. Thorough evaluation of the surgical specimen is recommended because histological examination of only the lobular surface of the choroid plexus lesion may fail to identify choroid plexus neoplasm.
INTRODUCTION: Treatment of obstructive hydrocephalus in children with tuberculous meningitis (TBM) depends on the level of the cerebrospinal fluid (CSF) block. Air-encephalography is regarded as the gold standard for differentiating communicating and non-communicating hydrocephalus. Since air-encephalography involves a lumbar puncture, it carries the risk of cerebral herniation. AIM. The aim of this study was to determine whether communicating and non-communicating hydrocephalus in TBM can be differentiated by means of cranial computerised tomography (CT). METHODS: A number of CT indices were measured in 50 children with communicating and 34 children with non-communicating hydrocephalus according to air-encephalographic findings. RESULTS: The only CT finding that correlated with the type of hydrocephalus was the shape of the third ventricle. Significantly more children with non-communicating hydrocephalus had a rounded third ventricle than those with communicating hydrocephalus. CONCLUSION: CT is therefore not useful in determining the level of CSF block in TBM. Air-encephalography remains the most reliable way of determining the level of CSF obstruction.
The ketogenic diet (KD), established to treat intractable childhood epilepsy, has emerged as the principal treatment of GLUT1 deficiency syndrome (OMIM 606777). This defect of glucose transport into the brain results in hypoglycorrhachia causing epilepsy, developmental delay, and a complex motor disorder in early childhood. Ketones provided by a high-fat, low-carbohydrate diet serve as an alternative fuel to the brain. Glucose, lactate, lipids, and ketones in blood and cerebrospinal fluid were investigated in five GLUT1-deficient patients before and on the KD. Hypoglycorrhachia was detected in the non-ketotic and ketotic state. In ketosis, lactate concentrations in the cerebrospinal fluid increased moderately. The CSF/blood ratio for acetoacetate was higher compared to beta-hydroxybutyrate. Free fatty acids did not enter the brain in significant amounts. Blood concentrations of essential fatty acids determined in 18 GLUT1-deficient patients on the KD were sufficient in all age groups. The effects of the KD in GLUT1 deficiency syndrome, particularly the course of blood lipids, are discussed in an illustrative case. In this syndrome, the KD effectively restores brain energy metabolism. Ketosis does not influence impaired GLUT1-mediated glucose transport into brain: hypoglycorrhachia, the biochemical hallmark of the disease, can be identified in GLUT1-deficient patients on a KD. The effects of ketosis on the concentrations of glucose, lactate, ketones, and fatty acids in blood and cerebrospinal fluid in this entity are discussed in view of previous data on ketosis in man.