Clusters of Spreading Depolarizations Are Associated With Disturbed Cerebral Metabolism in Patients With Aneurysmal Subarachnoid Hemorrhage

Sakowitz, Oliver W.; Santos, Edgar; Nagel, Angela; Krajewski, Kara; Hertle, Daniel N.; Vajkoczy, Peter; Dreier, Jens P.; Unterberg, Andreas; Sarrafzadeh, Asita

doi:10.1161/strokeaha.112.672352

Cited by 69 publications

(70 citation statements)

References 9 publications

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“…It should be noted though that the term ''SD cluster'' is not yet well-defined in patients (Dreier et al, 2006). Current working definition for a clustered SD is that it occurs within 2 hr from the previous one (Sakowitz et al, 2013).…”

Section: Facilitation Of Cell Death By Sd In Metabolically Compromisementioning

confidence: 99%

The Stroke-Migraine Depolarization Continuum

Dreier

Reiffurth

2015

Neuron

271

349

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The term spreading depolarization (SD) refers to waves of abrupt, sustained mass depolarization in gray matter of the CNS. SD, which spreads from neuron to neuron in affected tissue, is characterized by a rapid near-breakdown of the neuronal transmembrane ion gradients. SD can be induced by hypoxic conditions--such as from ischemia--and facilitates neuronal death in energy-compromised tissue. SD has also been implicated in migraine aura, where SD is assumed to ascend in well-nourished tissue and is typically benign. In addition to these two ends of the "SD continuum," an SD wave can propagate from an energy-depleted tissue into surrounding, well-nourished tissue, as is often the case in stroke and brain trauma. This review presents the neurobiology of SD--its triggers and propagation mechanisms--as well as clinical manifestations of SD, including overlaps and differences between migraine aura and stroke, and recent developments in neuromonitoring aimed at better diagnosis and more targeted treatments.

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Section: Facilitation Of Cell Death By Sd In Metabolically Compromisementioning

confidence: 99%

The Stroke-Migraine Depolarization Continuum

Dreier

Reiffurth

2015

Neuron

271

349

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“…In patients with aSAH, there is growing evidence that CSDs occur abundantly [33]. Investigators in a recent clinical study demonstrated that clustered CSDs are associated with a transient decrease in CMD glucose and an increase in CMD lactate and CMD LPR, which they measured by cerebral microdialysis [34] (Figure 4). …”

Section: Discussionmentioning

confidence: 99%

Higher brain extracellular potassium is associated with brain metabolic distress and poor outcome after aneurysmal subarachnoid hemorrhage

et al. 2014

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IntroductionElevated brain potassium levels ([K+]) are associated with neuronal damage in experimental models. The role of brain extracellular [K+] in patients with poor-grade aneurysmal subarachnoid hemorrhage (aSAH) and its association with hemorrhage load, metabolic dysfunction and outcome has not been studied so far.MethodsCerebral microdialysis (CMD) samples from 28 poor grade aSAH patients were analyzed for CMD [K+] for 12 consecutive days after ictus, and time-matched to brain metabolic and hemodynamic parameters as well as corresponding plasma [K+]. Statistical analysis was performed using a generalized estimating equation with an autoregressive function to handle repeated observations of an individual patient.ResultsCMD [K+] did not correlate with plasma [K+] (Spearman’s ρ = 0.114, P = 0.109). Higher CMD [K+] was associated with the presence of intracerebral hematoma on admission head computed tomography, CMD lactate/pyruvate ratio >40 and CMD lactate >4 mmol/L (P < 0.05). In vitro retrodialysis data suggest that high CMD [K+] was of brain cellular origin. Higher CMD [K+] was significantly associated with poor 3-month outcome, even after adjusting for age and disease severity (P < 0.01).ConclusionsThe results of this pilot study suggest that brain extracellular [K+] may serve as a biomarker for brain tissue injury in poor-grade aSAH patients. Further studies are needed to elucidate the relevance of brain interstitial K+ levels in the pathophysiology of secondary brain injury after aSAH.

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“…The combination of decreased CBF and increased energy requirements imposed by CSD may worsen neuronal injury [79]. Clustered spreading depolarisations are related to metabolic changes suggestive of ongoing secondary damage primarily in nonischemic brain tissue [80]. Experimentally, spreading depolarization leads to massive increase in glutamate, decrease in glucose, and increase in lactate levels [81].…”

Section: Early Brain Injurymentioning

confidence: 99%

To Look Beyond Vasospasm in Aneurysmal Subarachnoid Haemorrhage

Cossu

Messerer

Oddo

et al. 2014

BioMed Research International

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Delayed cerebral vasospasm has classically been considered the most important and treatable cause of mortality and morbidity in patients with aneurysmal subarachnoid hemorrhage (aSAH). Secondary ischemia (or delayed ischemic neurological deficit, DIND) has been shown to be the leading determinant of poor clinical outcome in patients with aSAH surviving the early phase and cerebral vasospasm has been attributed to being primarily responsible. Recently, various clinical trials aimed at treating vasospasm have produced disappointing results. DIND seems to have a multifactorial etiology and vasospasm may simply represent one contributing factor and not the major determinant. Increasing evidence shows that a series of early secondary cerebral insults may occur following aneurysm rupture (the so-called early brain injury). This further aggravates the initial insult and actually determines the functional outcome. A better understanding of these mechanisms and their prevention in the very early phase is needed to improve the prognosis. The aim of this review is to summarize the existing literature on this topic and so to illustrate how the presence of cerebral vasospasm may not necessarily be a prerequisite for DIND development. The various factors determining DIND that worsen functional outcome and prognosis are then discussed.

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Clusters of Spreading Depolarizations Are Associated With Disturbed Cerebral Metabolism in Patients With Aneurysmal Subarachnoid Hemorrhage

Cited by 69 publications

References 9 publications

The Stroke-Migraine Depolarization Continuum

The Stroke-Migraine Depolarization Continuum

Higher brain extracellular potassium is associated with brain metabolic distress and poor outcome after aneurysmal subarachnoid hemorrhage

To Look Beyond Vasospasm in Aneurysmal Subarachnoid Haemorrhage

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