Metabolic assessment of a migraine model using relaxation‐enhanced <sup>1</sup><scp>H</scp> spectroscopy at ultrahigh field

Abad, Nastaren; Rosenberg, Jens T.; Roussel, Tangi; Grice, Dillon C.; Harrington, Michael G.; Grant, Samuel C.

doi:10.1002/mrm.26811

Cited by 11 publications

(9 citation statements)

References 63 publications

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“…Examples of the mitochondrial effects of nitric oxide in animals include inhibition of the mitochondrial respiratory chain in cultured astro cytes 242 . By contrast, use of 1 H MRS in rats has shown that cortical lactate increases as early as 10 min after intraperitoneal injection of nitroglycerin, suggesting that the widely used nitroglycerin model of migraine involves metabolic, in addition to vascular, changes 243 .…”

Section: Trigeminovascular Systemmentioning

confidence: 90%

The metabolic face of migraine — from pathophysiology to treatment

et al. 2019

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Migraine can be regarded as a conserved, adaptive response that occurs in genetically predisposed individuals with a mismatch between the brain's energy reserve and workload. Given the high prevalence of migraine, genotypes associated with the condition seem likely to have conferred an evolutionary advantage. Technological advances have enabled the examination of different aspects of cerebral metabolism in patients with migraine, and complementary animal research has highlighted possible metabolic mechanisms in migraine pathophysiology. An increasing amount of evidence-much of it clinical-suggests that migraine is a response to cerebral energy deficiency or oxidative stress levels that exceed antioxidant capacity and that the attack itself helps to restore brain energy homeostasis and reduces harmful oxidative stress levels. Greater understanding of metabolism in migraine offers novel therapeutic opportunities. In this Review , we describe the evidence for abnormalities in energy metabolism and mitochondrial function in migraine, with a focus on clinical data (including neuroimaging, biochemical, genetic and therapeutic studies), and consider the relationship of these abnormalities with the abnormal sensory processing and cerebral hyper-responsivity observed in migraine. We discuss experimental data to consider potential mechanisms by which metabolic abnormalities could generate attacks. Finally , we highlight potential treatments that target cerebral metabolism, such as nutraceuticals, ketone bodies and dietary interventions.

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Section: Trigeminovascular Systemmentioning

confidence: 90%

The metabolic face of migraine — from pathophysiology to treatment

et al. 2019

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“…This excitation yielded maximum signal for a repetition time (TR) of 180 ms and effective dwell time (time between the end of excitation and start of acquisition) less than 660 μs. Six averages yielded a total of 3000 repetitions for the complete data acquisition of a single slice, which permitted the complete dataset for four slices to be acquired in nine minutes and corresponds to the time course of a previous study that assessed metabolic changes in NTG-triggered rats [1] while still yielding a sodium SNR in excess of 30:1.…”

Section: Methodsmentioning

confidence: 99%

Dynamic sodium imaging at ultra-high field reveals progression in a preclinical migraine model

Abad

Rosenberg

Hike

et al. 2018

PAIN

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Under the hypothesis that increased extracellular sodium induces sustained neuronal excitability with the onset and progression of migraine, this study evaluates dynamic in vivo Na fluxes in the brain of a preclinical rodent analogue of migraine. Ultra-high field Na magnetic resonance imaging (MRI) at 21.1 T has demonstrated potential to quantify sodium concentrations with good spatial and temporal resolution after the onset of central sensitization. Sprague-Dawley male rats with implanted intraperitoneal lines were studied by MRI before and after an in situ injection of 10 mg/kg of nitroglycerin (NTG) vs vehicle and saline controls. Slice-selective Na images were acquired using a multislice free induction decay-based chemical shift imaging sequence with resolution of 1.1 × 1.1 × 3 mm for a 9-minute acquisition. A total of 27 repeated scans were acquired over 1 hour of baseline scanning and longitudinally up to 3 hours after injection. Increases of Na MRI signal in the brainstem, extracerebral cerebrospinal fluid, and cisterna magna were evident almost immediately after NTG injection, gaining significance from controls in 36 minutes. The cerebellum and third ventricle also showed sustained trends of increased Na, with the former gaining significance at over 2 hours after NTG injection. The data provide evidence of an early change in sodium concentration, markedly in posterior fossa cerebrospinal fluid and brainstem regions. Further study of fluctuations of sodium concentration and their modulation with treatments could help understand the dynamic features of migraine, locate a putative migraine generator, and guide development of therapeutic measures to correct the disturbance of sodium homeostasis.

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“…Migraine is accompanied with a complex chain of biochemical changes in the CSF and brain which may contribute, together with sodium, to regulation of water movement across the BCSFB. For instance, it has been shown that CSF (and plasma) content of organic osmolytes, such as taurine and glutamate, which can significantly regulate brain cell volume homeostasis (Schousboe and Pasantes-Morales, 1992;Fisher et al, 2008), changes during migraine (Martinez et al, 1993;Cananzi et al, 1995;van Dongen et al, 2017;Abad et al, 2018b). However, it is yet to be determined how the variations in organic osmolyte levels can influence the osmotically driven water transport across the BCSFB.…”

Section: Discussionmentioning

confidence: 99%

Regulation of CSF and Brain Tissue Sodium Levels by the Blood-CSF and Blood-Brain Barriers During Migraine

Ghaffari

Grant

Petzold

et al. 2020

Front. Comput. Neurosci.

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Cerebrospinal fluid (CSF) and brain tissue sodium levels increase during migraine. However, little is known regarding the underlying mechanisms of sodium homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of sodium dysregulation in the brain is important, since correction of the altered sodium homeostasis could potentially treat migraine. Under the hypothesis that disturbances in sodium transport mechanisms at the blood-CSF barrier (BCSFB) and/or the blood-brain barrier (BBB) are the underlying cause of the elevated CSF and brain tissue sodium levels during migraines, we developed a mechanistic, differential equation model of a rat's brain to compare the significance of the BCSFB and the BBB in controlling CSF and brain tissue sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue and blood. Sodium transport from blood to CSF across the BCSFB, and from blood to brain tissue across the BBB were modeled by influx permeability coefficients P BCSFB and P BBB , respectively, while sodium movement from CSF into blood across the BCSFB, and from brain tissue to blood across the BBB were modeled by efflux permeability coefficients P ′ BCSFB and P ′ BBB , respectively. We then performed a global sensitivity analysis to investigate the sensitivity of the ventricular CSF, subarachnoid CSF and brain tissue sodium concentrations to pathophysiological variations in P BCSFB , P BBB , P ′ BCSFB and P ′ BBB . Our results show that the ventricular CSF sodium concentration is highly influenced by perturbations of P BCSFB , and to a much lesser extent by perturbations of P ′ BCSFB . Brain tissue and subarachnoid CSF sodium concentrations are more sensitive to pathophysiological variations of P BBB and P ′ BBB than variations of P BCSFB and P ′ BCSFB within 30 min of the onset of the perturbations. However, P BCSFB is the most sensitive model parameter, followed by P BBB and P ′ BBB , in controlling brain tissue and subarachnoid CSF sodium levels within 3 h of the perturbation onset.

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Metabolic assessment of a migraine model using relaxation‐enhanced ¹H spectroscopy at ultrahigh field

Cited by 11 publications

References 63 publications

The metabolic face of migraine — from pathophysiology to treatment

The metabolic face of migraine — from pathophysiology to treatment

Dynamic sodium imaging at ultra-high field reveals progression in a preclinical migraine model

Regulation of CSF and Brain Tissue Sodium Levels by the Blood-CSF and Blood-Brain Barriers During Migraine

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Metabolic assessment of a migraine model using relaxation‐enhanced 1H spectroscopy at ultrahigh field

Cited by 11 publications

References 63 publications

The metabolic face of migraine — from pathophysiology to treatment

The metabolic face of migraine — from pathophysiology to treatment

Dynamic sodium imaging at ultra-high field reveals progression in a preclinical migraine model

Regulation of CSF and Brain Tissue Sodium Levels by the Blood-CSF and Blood-Brain Barriers During Migraine

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Metabolic assessment of a migraine model using relaxation‐enhanced ¹H spectroscopy at ultrahigh field