Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597530
Title: Haemodynamic-metabolic correlates of cellular pathology after experimental traumatic brain injury
Author: Chen, S. F.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 2003
Availability of Full Text:
Full text unavailable from EThOS. Please contact the current institution’s library for further details.
Abstract:
As a prerequisite for the appropriate design and analysis of later studies in this thesis, the initial aim of the thesis was to characterise the spatio-temporal changes in cellular pathology after moderate controlled cortical impact (CCI) injury. Damage to the cortex and hippocampus was characterised by early neuronal loss together with a transient reactive astrocytosis, microglial/macrophage response and an increase in both immature oligodendrocytes and putative neural precursor cells. The pattern of damage to the dorsal regions of the thalamus was markedly different with less severe reductions in neuronal staining, a persistent astrocytic and microglial/ macrophage response, a transient increase in immature oligodendrocytes cells and an absence of any increase in neural precursor cells. The spatial pattern of axonal injury was unilateral and centred around the contusion site and adjacent structures. The mean density and diameter of cortical microvessels was significantly reduced and increased, respectively, but only at the initial time-points. These data indicate that TBI is highly complex involving a number of pathologies, each with a specific regional and temporal response. In order to investigate the role of acute haemodynamic and metabolic dysfunction - major factors involved in the pathogenesis of axonal injury, the topographical inter-relationship between local cerebral blood flow (LCBF) and metabolic rate for glucose (LCMRglu) was determined at 3 hrs after CCI injury and assessed for the degree of correspondence with the evolving axonal injury. The increase in axonal damage between 3 and 24 hrs was negatively correlated to LCBF and positively correlated to the ratio of metabolism/blood flow. CBF augmentation by acetazolamide in the first 3 hrs normalised the metabolism/blood flow ratio and reduced significantly further axonal injury at 24 hrs indicating the critical dependence of axonal outcome on flow-metabolism in the acute injury stage.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.597530  DOI: Not available
Share: