Spreading Depolarization

Leng, Lewis Z.; Fink, Matthew E.; Iadecola, Costantino

doi:10.1001/archneurol.2010.226

Cited by 43 publications

(12 citation statements)

References 57 publications

(52 reference statements)

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“…Clinically, clusters of PIDs have been associated with neurological deterioration in patients (Dreier et al, 2006). Therefore, PIDs may be a therapeutic target in stroke and other brain injury states (Lauritzen et al, 2010; Leng et al, 2011). …”

Section: Introductionmentioning

confidence: 99%

Supply-Demand Mismatch Transients in Susceptible Peri-infarct Hot Zones Explain the Origins of Spreading Injury Depolarizations

Bornstädt

Houben

Seidel

et al. 2015

Neuron

162

180

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SUMMARY Peri-infarct depolarizations (PIDs) are seemingly spontaneous spreading depression-like waves that negatively impact tissue outcome in both experimental and human stroke. Factors triggering PIDs are unknown. Here, we show that somatosensory activation of peri-infarct cortex triggers PIDs when the activated cortex is within a critical range of ischemia. We show that the mechanism involves increased oxygen utilization within the activated cortex, worsening the supply-demand mismatch. We support the concept by clinical data showing that mismatch predisposes to PIDs in human stroke as well. Conversely, transient worsening of mismatch by episodic hypoxemia or hypotension also reproducibly triggers PIDs. Therefore, PIDs are triggered upon supply-demand mismatch transients in metastable peri-infarct hot zones due to increased demand or reduced supply. Based on the data, we propose that minimizing sensory stimulation and hypoxic or hypotensive transients in stroke and brain injury would reduce PID incidence and their adverse impact on outcome.

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Section: Introductionmentioning

confidence: 99%

Supply-Demand Mismatch Transients in Susceptible Peri-infarct Hot Zones Explain the Origins of Spreading Injury Depolarizations

Bornstädt

Houben

Seidel

et al. 2015

Neuron

162

180

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“…When cerebral parenchymal damage occurs in SAH, either due to early brain lesion (cortical spreading depolarization, blood-brain barrier dysfunction and ultimately neuronal cell death) [9,10] or to DCI [11], these changes affect water diffusion and anisotropy and may lead to abnormal DWI parameters. It is known, for instance, that ADC values are affected in white matter not only in the acute [12] but also in the subacute phase of SAH [13].…”

Section: Background and Purposementioning

confidence: 99%

Evolution of diffusion tensor imaging parameters after acute subarachnoid haemorrhage: a prospective cohort study

et al. 2016

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Introduction Few studies assessed diffusion tensor imaging (DTI) changes in the acute phase of subarachnoid haemorrhage (SAH). We prospectively evaluated DTI parameters in the acute phase of SAH and 8-10 days after and analysed whether changes could be related to SAH severity or to the development of delayed cerebral ischemia (DCI). Methods Apparent diffusion coefficient (ADC) and fractional anisotropy (FA) changes over time were assessed in a prospective cohort of patients with acute SAH. Two MRI studies were performed at <72 h (MRI-1) and 8-10 days (MRI-2). DTI parameters were recorded in 15 ROIs. Linear mixed regression models were used.

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“…Their contributions to the pathophysiology of brain injury are increasingly appreciated (Hossmann, 1996; Lauritzen et al, 2011; Leng et al, 2011). Manipulating PID incidence impacts infarct size in many models (Mies et al, 1993; Back et al, 1996; Takano et al, 1996), and cumulative depolarization duration predicts local pathology (Dijkhuizen et al, 1999; Higuchi et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Peri-infarct depolarizations during focal ischemia in the awake Spontaneously Hypertensive Rat. Minimizing anesthesia confounds in experimental stroke

2016

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Anesthesia profoundly impacts peri-infarct depolarizations (PIDs), but only one prior report has described their monitoring during experimental stroke in awake animals. Since temporal patterns of PID occurrence are model specific, the current study examined PID incidence during focal ischemia in the awake Spontaneously Hypertensive Rat (SHR), and documented the impact of both prior and concurrent isoflurane anesthesia. For awake recordings, electrodes were implanted under isoflurane anesthesia 1 day to 5 weeks prior to occlusion surgery. Rats were then subjected to permanent or transient (2 hour) tandem occlusion of the middle cerebral and ipsilateral common carotid arteries, followed by PID monitoring for up to 3 days. Comparison perfusion imaging studies evaluated PID-associated hyperemic transients during permanent ischemia under anesthesia at varied intervals following prior isoflurane exposure. Prior anesthesia attenuated PID number at intervals up to 1 week, establishing 2 weeks as a practical recovery duration following surgical preparation to avoid isoflurane preconditioning effects. PIDs in awake SHR were limited to the first 4 hours after permanent occlusions. Maintaining anesthesia during this interval reduced PID number, and prolonged their occurrence through several hours following anesthesia termination. Although PID number otherwise correlated with infarct size, PID suppression by anesthesia was not protective in the absence of reperfusion. PIDs persisted up to 36 hours after transient occlusions. These results differ markedly from the one previous report of such monitoring in awake Sprague-Dawley rats, which found an extended biphasic PID time course during 24 hours after both permanent and transient filament occlusions. PID occurrence closely reflects the time course of infarct progression in the respective models, and may be more useful than absolute PID number as an index of ongoing pathology.

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Spreading Depolarization

Cited by 43 publications

References 57 publications

Supply-Demand Mismatch Transients in Susceptible Peri-infarct Hot Zones Explain the Origins of Spreading Injury Depolarizations

Supply-Demand Mismatch Transients in Susceptible Peri-infarct Hot Zones Explain the Origins of Spreading Injury Depolarizations

Evolution of diffusion tensor imaging parameters after acute subarachnoid haemorrhage: a prospective cohort study

Peri-infarct depolarizations during focal ischemia in the awake Spontaneously Hypertensive Rat. Minimizing anesthesia confounds in experimental stroke

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