Hypoxic adaptation during development: Relation to pattern of neurological presentation and cognitive disability
Hypoxic adaptation during development: Relation to pattern of neurological presentation and cognitive disability
Children with acute hypoxic-ischaemic events (e.g. stroke) and chronic neurological conditions associated with hypoxia frequently present to paediatric neurologists. Failure to adapt to hypoxia may be a common pathophysiological pathway linking a number of other conditions of childhood with cognitive deficit. There is evidence that congenital cardiac disease, asthma and sleep disordered breathing, for example, are associated with cognitive deficit, but little is known about the mechanism and whether there is any structural change. This review describes what is known about how the brain reacts and adapts to hypoxia, focusing on epilepsy and sickle cell disease (SCD). We prospectively recorded overnight oxyhaemoglobin saturation (SpO 2) in 18 children with intractable epilepsy, six of whom were currently or recently in minor status (MS). Children with MS were more likely to have an abnormal sleep study defined as either mean baseline SpO2 <94 or >4 dips of >4 in SpO2/hour (p = .04). In our series of prospectively followed patients with SCD who subsequently developed acute neurological symptoms and signs, mean overnight SpO2 was lower in those with cerebrovascular disease on magnetic resonance angiography (Mann-Whitney, p = .01). Acute, intermittent and chronic hypoxia may have detrimental effects on the brain, the clinical manifestations perhaps depending on rapidity of presentation and prior exposure.
411-427
Kirkham, Fenella J.
1dfbc0d5-aebe-4439-9fb2-dac6503bcd58
Datta, Avijit K.
bfb3ae05-e720-41ed-8dd9-acd47e754245
July 2006
Kirkham, Fenella J.
1dfbc0d5-aebe-4439-9fb2-dac6503bcd58
Datta, Avijit K.
bfb3ae05-e720-41ed-8dd9-acd47e754245
Kirkham, Fenella J. and Datta, Avijit K.
(2006)
Hypoxic adaptation during development: Relation to pattern of neurological presentation and cognitive disability.
Developmental Science, 9 (4), .
(doi:10.1111/j.1467-7687.2006.00507.x).
Abstract
Children with acute hypoxic-ischaemic events (e.g. stroke) and chronic neurological conditions associated with hypoxia frequently present to paediatric neurologists. Failure to adapt to hypoxia may be a common pathophysiological pathway linking a number of other conditions of childhood with cognitive deficit. There is evidence that congenital cardiac disease, asthma and sleep disordered breathing, for example, are associated with cognitive deficit, but little is known about the mechanism and whether there is any structural change. This review describes what is known about how the brain reacts and adapts to hypoxia, focusing on epilepsy and sickle cell disease (SCD). We prospectively recorded overnight oxyhaemoglobin saturation (SpO 2) in 18 children with intractable epilepsy, six of whom were currently or recently in minor status (MS). Children with MS were more likely to have an abnormal sleep study defined as either mean baseline SpO2 <94 or >4 dips of >4 in SpO2/hour (p = .04). In our series of prospectively followed patients with SCD who subsequently developed acute neurological symptoms and signs, mean overnight SpO2 was lower in those with cerebrovascular disease on magnetic resonance angiography (Mann-Whitney, p = .01). Acute, intermittent and chronic hypoxia may have detrimental effects on the brain, the clinical manifestations perhaps depending on rapidity of presentation and prior exposure.
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Published date: July 2006
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Local EPrints ID: 428345
URI: http://eprints.soton.ac.uk/id/eprint/428345
ISSN: 1363-755X
PURE UUID: 5893d416-872d-4054-8912-7eef73666d44
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Date deposited: 21 Feb 2019 17:30
Last modified: 06 Jun 2024 01:39
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Avijit K. Datta
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