Cellular damage and prevention in childhood hydrocephalus
- PMID: 15446588
- PMCID: PMC8095857
- DOI: 10.1111/j.1750-3639.2004.tb00071.x
Cellular damage and prevention in childhood hydrocephalus
Abstract
The literature concerning brain damage due to hydrocephalus, especially in children and animal models, is reviewed. The following conclusions are reached: 1. Hydrocephalus has a deleterious effect on brain that is dependent on magnitude and duration of ventriculomegaly and modified by the age of onset. 2. Animal models have many histopathological similarities to humans and can be used to understand the pathogenesis of brain damage. 3. Periventricular axons and myelin are the primary targets of injury. The pathogenesis has similarities to traumatic and ischemic white matter injury. Secondary changes in neurons reflect compensation to the stress or ultimately the disconnection. 4. Altered efflux of extracellular fluid could result in accumulation of waste products that might interfere with neuron function. Further research is needed in this as well as the blood-brain barrier in hydrocephalus. 5. Some, but not all, of the changes are preventable by shunting CSF. However, axon loss cannot be reversed, therefore shunting in a given case must be considered carefully. 6. Experimental work has so far failed to show any benefit in reducing CSF production. Pharmacologic protection of the brain, at least as a temporary measure, holds some promise but more pre-clinical research is required.
References
-
- Abdolvahabi RM, Mitchell JA, Diaz FG, McAllister JP, II (2000) A brief review of the effects of chronic hydrocephalus on the gonadotropin releasing hormone system: Implications for amenorrhea and precocious puberty. Neurol Res 22:123–126. - PubMed
-
- Acikgoz B, Akpinar G, Bingol N, Usseli I (1999) Angiotensin II receptor content within the circumventricular organs increases after experimental hydrocephalus in rats. Acta Neurochir 141: 1095–1099. - PubMed
-
- Arteel GE, Thurman RG, Raleigh JA (1998) Reductive metabolism of the hypoxia marker pimonidazole is regulated by oxygen tension independent of the pyridine nucleotide redox state. Eur J Biochem 253:743–750. - PubMed
-
- Balasubramaniam J, Del Bigio MR (2002) Analysis of age‐dependant alteration in the brain gene expression profile following induction of hydrocephalus in rats. Exp Neurol 173:105–113. - PubMed
-
- Becker B, Kolker AE, Krupin T (1967) Isosorbide. An oral hyperosmotic agent. Arch Ophthalmol 78: 147–150. - PubMed
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