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Malondialdehyde, Glutathione Peroxidase, and Superoxide Dismutase in Cerebrospinal Fluid During Cerebral Vasospasm in Monkeys
- R. Loch Macdonald, Bryce K.A. Weir, Tim D. Runzer, Michael G.A. Grace
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- Journal:
- Canadian Journal of Neurological Sciences / Volume 19 / Issue 3 / August 1992
- Published online by Cambridge University Press:
- 18 September 2015, pp. 326-332
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- Article
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Cerebral vasospasm may result from lipid peroxidation induced by oxyhemoglobin in the subarachnoid space after subarachnoid hemorrhage. To test this theory, vasospasm was induced in monkeys by intrathecal injections of oxyhemoglobin or supernatant fluid from autologous blood incubated in vitro. Concentration of malondialdehyde (MDA), a product of lipid peroxidation, was elevated in cerebrospinal fluid (CSF) in association with vasospasm caused by oxyhemoglobin and supernatant fluid. Intrathecal injections of methemoglobin or bilirubin did not cause vasospasm or increased CSF MDA. Activity of glutathione peroxidase in CSF increased significantly after injection of oxyhemoglobin and methemoglobin. There were no significant changes in CSF superoxide dismutase activity although there was a trend towards higher activities in animals treated with oxyhemoglobin, methemoglobin, bilirubin, and supernatant fluid. These results show oxyhemoglobin-induced vasospasm is associated with MDA and lipid peroxidation in the subarachnoid space. Furthermore, detection of peroxidation products after injection of oxyhemoglobin in the absence of erythrocyte membranes indicates that oxyhemoglobin may directly damage cerebral arteries and brain by inducing lipid peroxidation in these structures. Depletion of free-radical scavenging enzymes in CSF did not seem necessary for development of vasospasm. In fact, there was a tendency for vasospasm to elevate enzyme activities, as if production of scavengers was induced by excess free radicals in the subarachnoid space.
84 - Aneurysms and arteriovenous malformations
- from PART X - CEREBROVASCULAR DISORDERS
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- By Marcus A. Stoodley, University of New South Wales, Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, NSW, Australia, Bryce K.A. Weir, Pritzker School of Medicine, University of Chicago, Chief, Section of Neurosurgery, University of Chicago Medical Center, Chicago, IL, USA
- Edited by Arthur K. Asbury, University of Pennsylvania School of Medicine, Guy M. McKhann, The Johns Hopkins University School of Medicine, W. Ian McDonald, University College London, Peter J. Goadsby, University College London, Justin C. McArthur, The Johns Hopkins University School of Medicine
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- Book:
- Diseases of the Nervous System
- Published online:
- 05 August 2016
- Print publication:
- 11 November 2002, pp 1392-1404
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Summary
Intracranial aneurysms and arteriovenous malformations (AVMs) are structural vascular lesions that are life threatening by virtue of their propensity to cause intracranial hemorrhage. The Greek word ‘aneurysma’ is derived from a combination of ‘ana-’ (up, through) and ‘eurynein’ (to widen) (Haubrich, 1984). Peripheral aneurysms were well recognized by Hippocratic times, when physicians were familiar with superficial traumatic vascular lesions (Weir, 1987). The first description of an intracranial aneurysm was probably by Biumi, in 1765 (Biumi, 1778) and the first clinical description differentiating subarachnoid hemorrhage (SAH) from other types of apoplexy was in 1813 (Blackall, 1825). Various surgical attempts were made to treat intracranial aneurysms in the late nineteenth and early twentieth centuries, including proximal ligation by Horsley and others and packing with muscle by Dott (1933), before the first definitive cure by clip application, which was performed by Dandy in 1937 (Dandy, 1938).
Cerebral arteriovenous malformations (AVMs) are some of the more challenging lesions to come under the ambit of neurological surgery. Regarding surgery for AVMs, Cushing considered any attempt at excision ‘foolhardy’ (Cushing & Bailey, 1928) and Northfield stated, ‘The dangers of fatal hemorrhage and the extensive damage to brain forbid any attempt’ (Northfield, 1940). It was not until the mid-twentieth century that these lesions were recognized as malformations rather than neoplasms. With the advent of arteriography and its widespread use by the 1940s and 1950s, an understanding of the configuration of feeding arteries and draining veins of AVMs emerged, along with more favourable surgical results (Bergstrand et al., 1936; Olivecrona & Riives, 1948; Pilcher, 1946).
Clinical presentation
Spontaneous disruption of the abnormal walls of AVMs and aneurysms results in intracranial hemorrhage with obvious catastrophic consequences. Most aneurysms and AVMs are not detected until such a rupture occurs. A minority of lesions will come to clinical attention because they cause mass effect on cranial nerves or the brain, obstruction of cerebrospinal fluid pathways, or epilepsy. Aneurysms occasionally present with ischemic deficits caused by thromboemboli originating from the aneurysm sac. Investigation of neurological symptoms with high resolution CT or MRI is leading to an increase in the incidental detection of vascular abnormalities.