An experimental study of acute subarachnoid haemorrhage in baboons: changes in cerebral blood volume, blood flow, electrical activity and water content.

Kuyama, Hideyuki; Ladds, A.; Branston, Neil M.; Nitta, Masahiro; Symon, Lindsay

doi:10.1136/jnnp.47.4.354

Cited by 41 publications

(22 citation statements)

References 33 publications

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“…Several studies demonstrate a significant reduction of cerebral blood flow minutes after SAH, thereby implicating a role for acute cerebral ischemia in the pathophysiology of acute SAH (6,7,21,33,34). Our results indirectly support these observations of reduced CBF after SAH and imply that changes in CBF occur prior to the cellular changes.…”

Section: Discussionsupporting

confidence: 84%

“…4). One can postulate that the variability of the evolution of the T 2 -weighted image intensities between the two hemispheres may reflect the hemispheric asymmetry known to occur in the timecourse of rCBF or rCBV reductions after SAH (7,21). It is interesting to note the ϳ1.5 min delay between the onset of T 2 -weighted signal reductions and the subsequent onset of marked reductions in ADC, reflecting cellular depolarization (Fig.…”

Section: Discussionmentioning

confidence: 95%

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Spreading waves of transient and prolonged decreases in water diffusion after subarachnoid hemorrhage in rats

Beaulieu¹,

Busch²,

Crespigny³

et al. 2000

Magn. Reson. Med.

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Diffusion-weighted MRI (DWI), which can detect cortical spreading depressions (SDs) as propagating waves of reduced apparent diffusion coefficient (ADC) of water, was used to investigate whether spreading depression occurs after subarachnoid hemorrhage (SAH) induced by endovascular perforation in the rat. Eleven rats underwent SAH while positioned in the magnet. The ADC measurements had a temporal resolution of 12 sec. Transient decreases in ADC to 74 ؎ 5% of pre-SAH values were observed in three rats after SAH, which propagated over the cortex with an average speed of 4.2 ؎ 0.6 mm/min, consistent with an SD wave. Furthermore, in all 11 rats, a wavefront of reduced ADC, which did not resolve within the 12 min observation period, spread at a speed of 3.2 ؎ 1.7 mm/min in the ipsilateral cortex, and again is consistent with the speed of SD propagation. Therefore, spreading depression-like cellular depolarization is a consequence of acute subarachnoid hemorrhage in rats. Subarachnoid hemorrhage (SAH) is a devastating disease, yet little is known about how SAH impacts the brain acutely. Recent interest in the acute phase of SAH is stimulated by the anticipation of a variety of neuroprotective treatments. Therefore, it is important to understand the mechanisms of brain injury during SAH and efforts have been made to elucidate the immediate hemodynamic and cellular responses. There is a transient decrease in cerebral blood flow and a reduction in cerebral oxygen metabolism during the first minutes of SAH (1). Induction of hsp70, a heat-shock protein that is a sensitive marker of neuronal injury and expression of immediate early genes such as c-fos and c-jun is stimulated in rat brain within hours after SAH (2,3). Interestingly, the noncompetitive N-methyl-Daspartate (NMDA) receptor antagonist MK-801 blocked expression of c-fos and c-jun mRNA in the cerebral cortex after SAH (3). Furthermore, decreases in the electroencephalogram (EEG) activity (4 -6) and delays in sensory conduction, measured using somatosensory-evoked potentials (7), have been observed within minutes of SAH.The aforementioned results demonstrate that there are marked deleterious effects on the brain immediately after SAH. Some of the results, notably the blockage of gene expression by MK-801, which is known to suppress spreading depressions (SDs), and the periodic reduction of the EEG amplitude, indicate that spreading depression may play a role in the pathophysiology of acute SAH. Spreading depression refers to a wave of cell depolarization that propagates through the brain tissue at speeds of ϳ3-4 mm/min (8), participating in the cortical response to other noxious stimuli to the brain such as focal cerebral ischemia or trauma (9) in animal models. To the best of our knowledge, however, its occurrence after SAH has not been reported.Magnetic resonance imaging (MRI) is able to noninvasively detect spreading depressions with good spatial and temporal resolution (10,11). In particular, diffusionweighted MRI (DWI) detects spreading depression as propagat...

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Section: Discussionsupporting

confidence: 84%

Section: Discussionmentioning

confidence: 95%

Spreading waves of transient and prolonged decreases in water diffusion after subarachnoid hemorrhage in rats

Beaulieu¹,

Busch²,

Crespigny³

et al. 2000

Magn. Reson. Med.

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show abstract

“…17,19 Experimental models indicate that microcirculatory dysfunction after SAH may result from an initial period of global ischemia, 20,21 followed by subsequent recovery of cerebral circulation and "rebound" hyperemia in the setting of abnormal autoregulation. 20 In punctured artery models of experimental SAH, global edema develops 1 to 6 hours after ictus, 20,22 confirming that this type of edema can develop very early after the insult.…”

Section: Discussionmentioning

confidence: 92%

Global Cerebral Edema After Subarachnoid Hemorrhage

Claassen

Carhuapoma

Kreiter

et al. 2002

Stroke

467

169

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Background and Purpose-Cerebral edema visualized by CT is often seen after subarachnoid hemorrhage (SAH).Inflammatory or circulatory mechanisms have been postulated to explain this radiographic observation after SAH. We sought to determine the frequency, causes, and impact on outcome of early and delayed global cerebral edema after SAH. Methods-We evaluated the presence of global edema on admission and follow-up CT scans in 374 SAH patients admitted within 5 days of onset to our Neurological Intensive Care Unit between July 1996 and February 2001. Using multivariate analysis, we identified predictors of global cerebral edema and evaluated the impact of global edema on outcome 3 months after onset with the modified Rankin Scale. Results-Global edema was present on admission CT scans in 8% (nϭ29) and developed secondarily in 12% (nϭ44) of the patients. Global edema on admission was predicted by loss of consciousness at ictus and increasing Hunt-Hess grade. Delayed global edema was predicted by aneurysm size Ͼ10 mm, loss of consciousness at ictus, use of vasopressors, and increased SAH sum scores. Thirty-seven percent (nϭ137) of the patients were dead or severely disabled (modified Rankin Scale 4 to 6) at 3 months. Death or severe disability was predicted by any global edema, aneurysm size Ͼ10 mm, loss of consciousness at ictus, increased National Institutes of Health Stroke Scale scores, and older age. Conclusions-Global edema is an independent risk factor for mortality and poor outcome after SAH. Loss of consciousness, which may reflect ictal cerebral circulatory arrest, is a risk factor for admission global edema, and vasopressor-induced hypertension is associated with the development of delayed global edema. Critical care management strategies that minimize edema formation after SAH may improve outcome.

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“…In patients 5,7,8,9,12,14 imaging was performed in 1 or more days after aneurysm repair recognized as a general cerebral reflex phenomenon following severe traumatic brain injury and SAH [26,28]. Microcirculatory dysfunction, loss of blood-brain barrier integrity, induction of cytokines and other inflammatory mediators, endothelial and glial cell activation, intravascular aggregation of erythrocytes and platelets, and shifting of water into the intracellular compartment have all been implicated in the pathogenesis of global brain edema after severe brain injury, but their relative importance after SAH is not known [4,[29][30][31][32][33]. Based on the initial peripheral oxygen saturation and arterial partial pressure of oxygen, none of the patients was hypoxemic upon arrival.…”

Section: Discussionmentioning

confidence: 99%

Acute Ischemic Injury on Diffusion-Weighted Magnetic Resonance Imaging after Poor Grade Subarachnoid Hemorrhage

et al. 2010

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Admission DWI demonstrates multifocal areas of acute ischemic injury in poor grade SAH patients. These ischemic lesions may be related to transient intracranial circulatory arrest, acute vasoconstriction, microcirculatory disturbances, or decreased cerebral perfusion from neurogenic cardiac dysfunction. Ischemic brain injury in poor grade SAH may be a feasible target for acute resuscitation strategies.

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An experimental study of acute subarachnoid haemorrhage in baboons: changes in cerebral blood volume, blood flow, electrical activity and water content.

Cited by 41 publications

References 33 publications

Spreading waves of transient and prolonged decreases in water diffusion after subarachnoid hemorrhage in rats

Spreading waves of transient and prolonged decreases in water diffusion after subarachnoid hemorrhage in rats

Global Cerebral Edema After Subarachnoid Hemorrhage

Acute Ischemic Injury on Diffusion-Weighted Magnetic Resonance Imaging after Poor Grade Subarachnoid Hemorrhage

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