Chronic Cerebral Hypoperfusion Protects Against Acute Focal Ischemia,Improves Motor Function, and Results in Vascular Remodeling

Heo, Ji Hoe; Kim, Seo Hyun; Kim, Eun Hee; Lee, Ki Young

doi:10.2174/156720208783565627

Cited by 15 publications

(7 citation statements)

References 21 publications

(27 reference statements)

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“…Whereas this may seem an insurmountable requirement, there is some evidence that long-term preconditioning is feasible. For example, long-term hypo-perfusion protects against acute focal ischemia, improves motor function, and elicits structural changes in the brain, such as a rise in blood vessel density (Kim et al , 2008). Moreover, dietary phytochemicals that can also precondition, such as resveratrol from grapes, can be ingested over the long term.…”

Section: 0 Caveats: Have We Been Doing the Right Experiments?mentioning

confidence: 99%

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Stetler

Leak

Gan

et al. 2014

Progress in Neurobiology

167

140

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Preconditioning is a phenomenon in which brief episodes of a sublethal insult induce robust protection against subsequent lethal injuries. Preconditioning has been observed in multiple organisms and can occur in the brain as well as other tissues. Extensive animal studies suggest that the brain can be preconditioned to resist acute injuries, such as ischemic stroke, neonatal hypoxia/ischemia, trauma, and agents that are used in models of neurodegenerative diseases, such as Parkinson’s disease and Alzheimer’s disease. Effective preconditioning stimuli are numerous and diverse, ranging from transient ischemia, hypoxia, hyperbaric oxygen, hypothermia and hyperthermia, to exposure to neurotoxins and pharmacological agents. The phenomenon of “cross-tolerance,” in which a sublethal stress protects against a different type of injury, suggests that different preconditioning stimuli may confer protection against a wide range of injuries. Research conducted over the past few decades indicates that brain preconditioning is complex, involving multiple effectors such as metabolic inhibition, activation of extra- and intracellular defense mechanisms, a shift in the neuronal excitatory/inhibitory balance, and reduction in inflammatory sequelae. An improved understanding of brain preconditioning should help us identify innovative therapeutic strategies that prevent or at least reduce neuronal damage in susceptible patients. In this review, we focus on the experimental evidence of preconditioning in the brain and systematically survey the models used to develop paradigms for neuroprotection, and then discuss the clinical potential of brain preconditioning. In a subsequent components of this two-part series, we will discuss the cellular and molecular events that are likely to underlie these phenomena.

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Section: 0 Caveats: Have We Been Doing the Right Experiments?mentioning

confidence: 99%

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Stetler

Leak

Gan

et al. 2014

Progress in Neurobiology

167

140

View full text Add to dashboard Cite

show abstract

“…Furthermore, the nervous tissue may have been to some degree metabolically adapted increasing its tolerance to acute ischemia [11, 12]. It seems possible that such factors may have contributed to the patient's atypically mild focal signs when the hypoperfusion was acutely aggravated by the PCoA occlusion [8, 10, 11, 12]. While this explanation is somewhat speculative, there are two important points supporting our hypothesis of chronic ICA occlusion.…”

Section: Discussionmentioning

confidence: 87%

“…If the patient's ICA was chronically occluded, the left anterior circulation would be dependent entirely on blood supply from the vertebrobasilar vessels through the prominent PCoA, likely leading to chronic hypoperfusion [8, 9]. In rats, chronic cerebral hypoperfusion induces compensatory changes in brain tissue such as vascular remodeling and metabolic adaptation [10, 11]. Therefore, in previously hypoperfused brains, tissue damage after acute ischemia is less severe and is reflected by milder motor disability compared to healthy brains [10].…”

Section: Discussionmentioning

confidence: 99%

“…In rats, chronic cerebral hypoperfusion induces compensatory changes in brain tissue such as vascular remodeling and metabolic adaptation [10, 11]. Therefore, in previously hypoperfused brains, tissue damage after acute ischemia is less severe and is reflected by milder motor disability compared to healthy brains [10]. It may be that in our patient, a chronic hypoperfusion of the left hemisphere had induced vascular remodeling and an increase of the vascular reserve possibly involving leptomeningeal collaterals [8, 10].…”

Section: Discussionmentioning

confidence: 99%

“…Therefore, in previously hypoperfused brains, tissue damage after acute ischemia is less severe and is reflected by milder motor disability compared to healthy brains [10]. It may be that in our patient, a chronic hypoperfusion of the left hemisphere had induced vascular remodeling and an increase of the vascular reserve possibly involving leptomeningeal collaterals [8, 10]. Furthermore, the nervous tissue may have been to some degree metabolically adapted increasing its tolerance to acute ischemia [11, 12].…”

Section: Discussionmentioning

confidence: 99%

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Hypoperfusion of an Entire Cerebral Hemisphere – Stroke or Postictal Deficit?

et al. 2011

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The clinical differential diagnosis between ischemic stroke and postictal deficit is sometimes challenging. If the clinical presentation is inconclusive, perfusion imaging can help to identify stroke patients for thrombolysis therapy. However, also epileptic phenomena may alter cerebral perfusion. Hypoperfusion spreading beyond the borders of cerebrovascular territories is usually considered suggestive of an etiology other than stroke. We present a patient whose clinical symptoms suggested a postictal deficit rather than an acute stroke. CT perfusion imaging showed hypoperfusion of the entire left cerebral hemisphere covering all vascular territories. CT angiography revealed occlusions in the ipsilateral internal carotid artery and in the circle of Willis as the cause of the global hypoperfusion. The patient was treated with i.v. thrombolysis and recovered with moderate disability. This is the first description of hyperacute ischemia of an entire cerebral hemisphere and its treatment with thrombolysis. It demonstrates the potential of modern neuroimaging in identifying atypically presenting strokes and shows that i.v. thrombolysis can be effectively and safely used to treat such potentially fatal insults.

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Beyond BOLD: Optimizing functional imaging in stroke populations

Veldsman

Cumming

Brodtmann

2014

Human Brain Mapping

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Blood oxygenation level-dependent (BOLD) signal changes are often assumed to directly reflect neural activity changes. Yet the real relationship is indirect, reliant on numerous assumptions, and subject to several sources of noise. Deviations from the core assumptions of BOLD contrast functional magnetic resonance imaging (fMRI), and their implications, have been well characterized in healthy populations, but are frequently neglected in stroke populations. In addition to conspicuous local structural and vascular changes after stroke, there are many less obvious challenges in the imaging of stroke populations. Perilesional ischemic changes, remodeling in regions distant to lesion sites, and diffuse perfusion changes all complicate interpretation of BOLD signal changes in standard fMRI protocols. Most stroke patients are also older than the young populations on which assumptions of neurovascular coupling and the typical analysis pipelines are based. We present a review of the evidence to show that the basic assumption of neurovascular coupling on which BOLD-fMRI relies does not capture the complex changes arising from stroke, both pathological and recovery related. As a result, estimating neural activity using the canonical hemodynamic response function is inappropriate in a number of contexts. We review methods designed to better estimate neural activity in stroke populations. One promising alternative to event-related fMRI is a resting-state-derived functional connectivity approach. Resting-state fMRI is well suited to stroke populations because it makes no performance demands on patients and is capable of revealing network-based pathology beyond the lesion site.

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Chronic Cerebral Hypoperfusion Protects Against Acute Focal Ischemia,Improves Motor Function, and Results in Vascular Remodeling

Cited by 15 publications

References 21 publications

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Preconditioning provides neuroprotection in models of CNS disease: Paradigms and clinical significance

Hypoperfusion of an Entire Cerebral Hemisphere – Stroke or Postictal Deficit?

Beyond BOLD: Optimizing functional imaging in stroke populations

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