Neurovascular Coupling in Seizures

Teskey, G. Campbell; Tran, Cam Ha T.

doi:10.3390/neuroglia2010005

Cited by 5 publications

(2 citation statements)

References 85 publications

(112 reference statements)

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“…Figure 2), of the order of 10 mL/100 g/min, which suggests that other processes are also involved. A candidate mechanism is increased activity of glia, to clear excessive extracellular potassium, which is known to be associated with regional CBF increases 54–57 . The relative strength of these counteracting mechanisms and their temporal relation may then define the net effect.…”

Section: Discussionmentioning

confidence: 99%

Changes in postictal cerebral perfusion are related to the duration of electroconvulsive therapy‐induced seizures

Pottkämper,

Verdijk,

Aalbregt

et al. 2023

Epilepsia

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ObjectivePostictal symptoms may result from cerebral hypoperfusion which is possibly a consequence of seizure‐induced vasoconstriction. Longer seizures have previously been shown to cause more severe postictal hypoperfusion in rats and epilepsy patients. We studied cerebral perfusion after generalized seizures elicited by electroconvulsive therapy (ECT) and its relation to seizure duration.MethodsPatients with a major depressive episode who underwent ECT were included. During treatment, 21‐channel continuous electroencephalogram (EEG) was recorded. Arterial spin labeling magnetic resonance imaging (ASL‐MRI) scans were acquired before the ECT‐course (baseline) and approximately one hour after an ECT‐induced seizure (postictal) to quantify global and regional gray matter cerebral blood flow (CBF). Seizure duration was assessed from the period of epileptiform discharges on the EEG. Healthy controls were scanned twice to assess test‐retest variability. We performed hypothesis‐driven Bayesian analyses to study the relation between global and regional perfusion changes and seizure duration.ResultsTwenty‐four patients and twenty‐seven healthy controls were included. Changes in postictal global and regional CBF were correlated with seizure duration. In patients with longer seizure durations, global decrease in CBF reached values up to 28 ml/100g/min. Regional reductions in CBF were most prominent in the inferior frontal gyrus, cingulate gyrus, and insula (up to ~35 ml/100g/min). In patients with shorter seizures global and regional perfusion increased (up to ~20 ml/100g/min). These perfusion changes were larger than changes observed in healthy controls, with a maximum median global CBF increase of 12 ml/100g/min and a maximum median global CBF decrease of 20 ml/100g/min.SignificanceSeizure duration is a key factor determining postictal perfusion changes. In future studies, seizure duration needs to be considered as confounding factor due to its opposite effect on postictal perfusion. .

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Section: Discussionmentioning

confidence: 99%

Changes in postictal cerebral perfusion are related to the duration of electroconvulsive therapy‐induced seizures

Pottkämper,

Verdijk,

Aalbregt

et al. 2023

Epilepsia

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“…The interaction between neurovascular and neurometabolic coupling is critical to supply the high energy demands of the brain during both normal physiology and pathological conditions as seen in seizures and could possibly contribute to our neurovascular hypothesis of SUDEP (Teskey and Tran, 2021). Increased neural activity raises the metabolic rate and subsequent oxygen utilization by mitochondria which in turn reduces the availability of free oxygen in a system.…”

Section: Chronic Cox-2 Inhibitors and Ltcc Antagonists Extend Life In...mentioning

confidence: 99%

Sudden unexpected death in epilepsy is prevented by blocking postictal hypoxia

et al. 2023

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Sudden unexpected death in epilepsy is prevented by blocking postictal hypoxia

George

Farrell

Colangeli

et al. 2022

Preprint

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Epilepsy is at times a fatal disease. Sudden unexpected death in epilepsy (SUDEP) is the leading cause of mortality in people with intractable epilepsy and is defined by exclusion; non-accidental, non-toxicologic, and non-anatomic causes of death. While SUDEP often follows a bilateral tonic-clonic seizure, the mechanisms that ultimately lead to terminal apnea and then asystole remain elusive and there is a lack preventative treatments. Based on the observation that discrete seizures lead to local vasoconstriction, resulting in hypoperfusion, hypoxia and behavioural disturbances in the forebrain (Farrell et al., 2016 eLife), we reasoned that similar mechanisms may play a role in SUDEP when seizures invade the brainstem. Here we tested this neurovascular-based hypothesis of SUDEP in awake non-anesthetized mice by pharmacologically preventing seizure-induced vasoconstriction, with cyclooxygenase-2 or L-type calcium channel antagonists. In both acute and chronic mouse models of SUDEP, ibuprofen and nicardipine extended life. We also examined the potential role of spreading depolarization in the acute model of SUDEP. These data provide a proof of principle for the neurovascular hypothesis of SUDEP and the use of currently available treatments to prevent it.

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Neurovascular Coupling in Seizures

Cited by 5 publications

References 85 publications

Changes in postictal cerebral perfusion are related to the duration of electroconvulsive therapy‐induced seizures

Changes in postictal cerebral perfusion are related to the duration of electroconvulsive therapy‐induced seizures

Sudden unexpected death in epilepsy is prevented by blocking postictal hypoxia

Sudden unexpected death in epilepsy is prevented by blocking postictal hypoxia

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