ReviewHeadache2010
Capillary endothelial Na(+), K(+), ATPase transporter homeostasis and a new theory for migraine pathophysiology.
Review in Headache, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Association between Migraines and Prior Proton Pump Inhibitor Use: A Nested Case-Control Study Using a National Health Screening Cohort.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Article
- Regulation of CSF and Brain Tissue Sodium Levels by the Blood-CSF and Blood-Brain Barriers During Migraine.Frontiers in computational neuroscience · 2020Article
- Article
- Dynamic sodium imaging at ultra-high field reveals progression in a preclinical migraine model.Pain · 2018Article
- Metabolic assessment of a migraine model using relaxation-enhancedMagnetic resonance in medicine · 2018Article
- Severe Headache or Migraine History is Inversely Correlated With Dietary Sodium Intake: NHANES 1999-2004.Headache · 2016Article
- Genetics of vestibular disorders: pathophysiological insights.Journal of neurology · 2016Review
- Roads Less Traveled: Sexual Dimorphism and Mast Cell Contributions to Migraine Pathology.Frontiers in immunology · 2016Review
- Spreading Depression, Spreading Depolarizations, and the Cerebral Vasculature.Physiological reviews · 2015Review
- Sodium 3D COncentration MApping (COMA 3D) using (23)Na and proton MRI.Journal of magnetic resonance (San Diego, Calif. : 1997) · 2014Article
- Altered brainstem auditory evoked potentials in a rat central sensitization model are similar to those in migraine.Brain research · 2014Article
- Phospholipase C activity increases in cerebrospinal fluid from migraineurs in proportion to the number of comorbid conditions: a case-control study.The journal of headache and pain · 2013Article
- Na,K-ATPase alpha isoforms at the blood-cerebrospinal fluid-trigeminal nerve and blood-retina interfaces in the rat.Fluids and barriers of the CNS · 2013Article
- Sodium MRI in a rat migraine model and a NEURON simulation study support a role for sodium in migraine.Cephalalgia : an international journal of headache · 2011Article
- Na, K-ATPase: Ubiquitous Multifunctional Transmembrane Protein and its Relevance to Various Pathophysiological Conditions.Journal of clinical medicine research · 2010Article
- Cerebrospinal fluid sodium rhythms.Cerebrospinal fluid research · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundCerebrospinal fluid sodium concentration ([Na(+)](csf)) increases during migraine, but the cause of the increase is not known.
objectiveAnalyze biochemical pathways that influence [Na(+)](csf) to identify mechanisms that are consistent with migraine.
methodWe reviewed sodium physiology and biochemistry publications for links to migraine and pain.
resultsIncreased capillary endothelial cell (CEC) Na(+), K(+), -ATPase transporter (NKAT) activity is probably the primary cause of increased [Na(+)](csf). Physiological fluctuations of all NKAT regulators in blood, many known to be involved in migraine, are monitored by receptors on the luminal wall of brain CECs; signals are then transduced to their abluminal NKATs that alter brain extracellular sodium ([Na(+)](e)) and potassium ([K(+)](e)).
conclusionsWe propose a theoretical mechanism for aura and migraine when NKAT activity shifts outside normal limits: (1) CEC NKAT activity below a lower limit increases [K(+)](e), facilitates cortical spreading depression, and causes aura; (2) CEC NKAT activity above an upper limit elevates [Na(+)](e), increases neuronal excitability, and causes migraine; (3) migraine-without-aura may arise from CEC NKAT over-activity without requiring a prior decrease in activity and its consequent spreading depression; (4) migraine triggers disturb, and treatments improve, CEC NKAT homeostasis; (5) CEC NKAT-induced regulation of neural and vasomotor excitability coordinates vascular and neuronal activities, and includes occasional pathology from CEC NKAT-induced apoptosis or cerebral infarction.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.