Axonal pathology in subarachnoid and intracerebral haemorrhage
Axonal pathology in subarachnoid and intracerebral haemorrhage
Electrically active axons degenerate in the presence of nitric oxide (NO) in vitro. High CSF NO concentrations have been observed in patients with hemorrhagic brain injury such as subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
This study investigated the evidence for axonal injury in SAH and ICH and related this to CSF NO levels. In this study, neurofilament phosphoforms (NfH(SMI34), NfH(SMI35), NfH(SMI38), NfH(SMI310)), surrogate markers for axonal injury, and NO metabolites (nitrate, nitrite = NOx) were measured by ELISA in cerebrospinal fluid (CSF) from patients with SAH and ICH and from a group of controls. Injury severity was classified using the Glasgow Coma Scale, and survival was used as the outcome measure. Compared to the control group, a higher proportion of patients with SAH and ICH had elevated NfH(SMI34) levels from day 0 to day 6 (p < 0.001), elevated NfH(SMI35) levels from day 1 to 6 (p < 0.001), and elevated NfH(SMI310) levels at day 0, 1, 4, and 6 (p < 0.001). The NOx levels were higher in the SAH and ICH patients than in the controls (p < 0.05) and distinguished the non-survivors from the survivors (p < 0.05). No direct correlation was found for NOx with any of the NfH phosphoforms. This study provides evidence for primary and secondary axonal injury in patients with SAH and ICH, with non-survivors also having higher NOx levels. CSF NfH phosphoforms might emerge as a putative surrogate marker for monitoring the development for secondary axonal degeneration in neurocritical care and guiding targeted neuroprotective strategies.
acute brain injury, haemorrhagic stroke, hypocretin-1
407-414
Petzold, A.
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Rejdak, K.
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Lim, D.
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Belli, A.
173116e3-a9e8-4ed2-afc4-932f7001eeb0
Sen, J.
afcde186-d116-4538-bd4e-6d8ba01746b3
Keir, G.
fbca9e6b-cb9c-4c91-a2f7-0fbebc44308b
Kitchen, N.
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Smith, M.
558e1c6b-5c57-444a-9508-509c50128f91
Thompson, E.J.
e12914d3-902a-4423-9b9a-e53c0f6085b5
2005
Petzold, A.
3142ddf4-b2e1-4f9f-bfad-ba869e3b190f
Rejdak, K.
5010abc6-e96f-4f49-a175-a66c23f275a9
Lim, D.
70e6df14-2641-4ea0-9484-2b0008f37c8e
Belli, A.
173116e3-a9e8-4ed2-afc4-932f7001eeb0
Sen, J.
afcde186-d116-4538-bd4e-6d8ba01746b3
Keir, G.
fbca9e6b-cb9c-4c91-a2f7-0fbebc44308b
Kitchen, N.
28d7232f-fd11-4ae3-9eb6-05845dcf9200
Smith, M.
558e1c6b-5c57-444a-9508-509c50128f91
Thompson, E.J.
e12914d3-902a-4423-9b9a-e53c0f6085b5
Petzold, A., Rejdak, K., Lim, D., Belli, A., Sen, J., Keir, G., Kitchen, N., Smith, M. and Thompson, E.J.
(2005)
Axonal pathology in subarachnoid and intracerebral haemorrhage.
Journal of Neurotrauma, 22 (3), .
(doi:10.1089/neu.2005.22.407).
Abstract
Electrically active axons degenerate in the presence of nitric oxide (NO) in vitro. High CSF NO concentrations have been observed in patients with hemorrhagic brain injury such as subarachnoid hemorrhage (SAH) and intracerebral hemorrhage (ICH).
This study investigated the evidence for axonal injury in SAH and ICH and related this to CSF NO levels. In this study, neurofilament phosphoforms (NfH(SMI34), NfH(SMI35), NfH(SMI38), NfH(SMI310)), surrogate markers for axonal injury, and NO metabolites (nitrate, nitrite = NOx) were measured by ELISA in cerebrospinal fluid (CSF) from patients with SAH and ICH and from a group of controls. Injury severity was classified using the Glasgow Coma Scale, and survival was used as the outcome measure. Compared to the control group, a higher proportion of patients with SAH and ICH had elevated NfH(SMI34) levels from day 0 to day 6 (p < 0.001), elevated NfH(SMI35) levels from day 1 to 6 (p < 0.001), and elevated NfH(SMI310) levels at day 0, 1, 4, and 6 (p < 0.001). The NOx levels were higher in the SAH and ICH patients than in the controls (p < 0.05) and distinguished the non-survivors from the survivors (p < 0.05). No direct correlation was found for NOx with any of the NfH phosphoforms. This study provides evidence for primary and secondary axonal injury in patients with SAH and ICH, with non-survivors also having higher NOx levels. CSF NfH phosphoforms might emerge as a putative surrogate marker for monitoring the development for secondary axonal degeneration in neurocritical care and guiding targeted neuroprotective strategies.
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Published date: 2005
Keywords:
acute brain injury, haemorrhagic stroke, hypocretin-1
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Local EPrints ID: 27684
URI: http://eprints.soton.ac.uk/id/eprint/27684
ISSN: 0897-7151
PURE UUID: 39b57ac8-6dc4-4d27-98ca-71397520974f
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Date deposited: 25 Apr 2006
Last modified: 15 Mar 2024 07:20
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Author:
A. Petzold
Author:
K. Rejdak
Author:
D. Lim
Author:
A. Belli
Author:
J. Sen
Author:
G. Keir
Author:
N. Kitchen
Author:
M. Smith
Author:
E.J. Thompson
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