(Stroke. 2001;32:817.)
© 2001 American Heart Association, Inc.
Letters to the Editor |
Department of Neurosurgery, University Medical School of Pécs, Pécs, Hungary
To the Editor:
I read with interest the recent article by Ohkuma et al.1 The authors observed microcirculatory changes in addition to the marked marked luminal narrowing of large arteries detected as severe angiographic vasospasm. Cerebral vasospasm associated with aneurysmal subarachnoid hemorrhage (SAH), which is angiographically characterized as persistent luminal narrowing of the major extraparenchymal cerebral arteries, affects cerebral microcirculation and causes decreased cerebral blood flow and delayed ischemic neurological deficits.
These observations are strongly supported by studies on the function of the blood-brain barrier (BBB) in the acute stage of SAH.2 Disturbances in microcirculation were found to be accompanied by barrier disruption of the intraparenchymal microvessels located proximal or distal to experimental cisternal SAH.3 A significant increase in the permeability of the BBB after SAH has been described in humans and in different experimental settings.4 It was found in nearly two fifths of patients within 5 days of SAH, and the majority of these patients developed vasospasm and ischemic complications in the late phase of SAH and had a poor prognosis.5
It can be speculated that the circulatory and permeability changes of intraparenchymal microvessels are possibly involved in the pathogenesis of the post-SAH cerebral dysfunction visible in humans.6 There is still a need for precise understanding of basic mechanisms underlying the post-SAH global brain dysfunction, and pathophysiological and experimental data may provide significant clinical implications for the management of patients with SAH and for assessing the rationale of new pharmacological approaches.4
References
1.
Ohkuma H,
Manabe H, Tanaka M, Suzuki S. Impact of cerebral microcirculatory
changes on cerebral blood flow during cerebral vasospasm after
aneurysmal subarachnoid haemorrhage.
Stroke. 2000;31:16211627.
2. Dóczi T. The pathogenetic and prognostic significance of blood-brain barrier damage at the acute stage of aneurysmal subarachnoid haemorrhage: clinical and experimental studies. Acta Neurochir (Wien). 1985;77:110132.[Medline] [Order article via Infotrieve]
3.
Joshita H, Kassel
NF, Sasaki T. Blood-brain barrier disturbance following
subarachnoid hemorrhage in rabbits.
Stroke. 1990;21:10511058.
4. Germano A, dAvella D, Imperatore C, Caruso G, Tomasello F. Time-course of blood brain barrier permeability changes after experimental subarachnoid hemorrhage. Acta Neurochir (Wien). 2000;142:575581.[Medline] [Order article via Infotrieve]
5. Dóczi T, Ambrose J, OLaoire SA. The significance of contrast enhancement in cranial computed tomography following subarachnoid hemorrhage. J Neurosurg. 1984;60:335342.[Medline] [Order article via Infotrieve]
6.
Dóczi T, Joó F,
Sonkodi S, Ådám G. Increased vulnerability of the blood-brain
barrier to experimental subarachnoid hemorrhage in
spontaneously hypertensive rats.
Stroke. 1986;17:498501.
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