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Brain metabolism in adult chronic hydrocephalus.

Artikel i vetenskaplig tidskrift
Författare Daniel Kondziella
Ursula Sonnewald
Mats Tullberg
Carsten Wikkelsö
Publicerad i Journal of neurochemistry
Volym 106
Nummer/häfte 4
Sidor 1515-24
ISSN 1471-4159
Publiceringsår 2008
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 1515-24
Språk en
Länkar dx.doi.org/10.1111/j.1471-4159.2008...
Ämnesord Adult, Aging, pathology, physiology, Animals, Brain, metabolism, physiopathology, Chronic Disease, Humans, Hydrocephalus, Normal Pressure, metabolism, physiopathology
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

Normal pressure hydrocephalus (NPH) is the most frequent form of chronic hydrocephalus in adults. NPH remains underdiagnosed although between 5% and 10% of all demented patients may suffer from this disorder. As dementia is an increasing demographic problem, treatable forms such as in NPH have become a central issue in neurology. Despite the traditional perception of hydrocephalus being a disorder of disturbed CSF dynamics, in NPH metabolic impairment seems at least as important. So far, the only valid animal model of NPH is chronic adult kaolin hydrocephalus. In this model, opening of alternative CSF outflow pathways leads to normal or near-normal intracranial pressure and CSF outflow resistance. Yet, various metabolic disturbances cause ongoing ventricular enlargement and characteristic symptoms including cognitive decline and gait ataxia. Delayed hippocampal neuronal death, accumulation of beta-amyloid and disturbed cholinergic neurotransmission may contribute to memory dysfunction. Compromised periventricular blood flow, decreased dopamine levels in the substantia nigra and damaged striatal GABAergic interneurons may reflect basal ganglia symptoms. At least in human hydrocephalus cerebrovascular co-morbidity of the white matter plays an important role as well. It seems that in hydrocephalus from a certain 'point of no return' metabolic impairment becomes decoupled from CSF dynamics and, at least partly, self-sustained. This is probably the reason why despite restored CSF circulation by shunting many patients with chronic hydrocephalus still suffer from severe neurological deficits. The present paper offers a comprehensive review of the experimental and clinical data suggesting metabolic disturbances in chronic hydrocephalus.

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