Migraine Associated with Patent Foramen Ovale May Be Caused by Reactivation of Cerebral Toxoplasmosis Triggered by Arterial Blood Oxygen Desaturation.
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| Title: | Migraine Associated with Patent Foramen Ovale May Be Caused by Reactivation of Cerebral Toxoplasmosis Triggered by Arterial Blood Oxygen Desaturation. |
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| Authors: | Prandota, Joseph (AUTHOR) |
| Source: | International Journal of Neuroscience. Feb2010, Vol. 120 Issue 2, p81-87. 7p. 1 Chart. |
| Subjects: | Migraine, Cerebral toxoplasmosis, Gene expression, Cytokines, Genetic regulation |
| Abstract: | Approximately two billion people worldwide are chronically infected with T. gondii and yet with largely unknown consequences. On the other hand, several authors reported an association between migraine and patent foramen ovale (PFO), and different types of headaches, including migraine, may be precipitated by various diseased states or medications associated with marked immune irregularities, which sometimes cause reactivation of latent cerebral toxoplasmosis (CT). Recently, in a group of 104 subjects with migraine, 46 individuals (44.2%) were found to be seropositive for T. gondii. PFO, atrial septal defects, as well as pulmonary right-to-left shunts are usually associated with a various degree of arterial blood oxygen desaturation. Hypoxia is associated with an increase in the generation of several proinflammatory cytokines and other inflammation mediators, such as TNF-α, IL-1-β, IL-6, IL-8, chemokines (monocyte chemoattractant protein-1, CC-chemokine receptor 2, macrophage inflammatory protein-1α, intercellular adhesion molecule-1), acute-phase protein gene expressions, COX-2 gene transcription, induction of iNOS, and reactive oxygen species. Moreover, hypoxia markedly decreased T-lymphocyte IL-2 mRNA, a key cytokine responsible for B-cell proliferation and immunoglobulin secretion, and ischemic tissues demonstrated intravascular neutrophil accumulation, vascular damage, and increased vascular wall permeability. Interestingly, T. gondii activates hypoxia-inducible factor 1 already at physiologically relevant oxygen levels and requires HIF1 for growth and survival. These abnormalities may cause imbalance in the host/T. gondii immune system, which finally results in the reactivation of CT. In addition, hypoxia may participate in paradoxical microembolism because arterial oxygen desaturation enhances expression of plasminogen activator inhibitor-1, an important factor which suppresses fibrinolysis, and this effect may be further amplified by a decreased expression of plasminogen activators, finally causing blood hypercoagulability and paradoxical microembolism. In summary, further studies are required to verify the above-presented pathomechanisms probably responsible for the association between PFO and the development of migraine. It is possible that some migraineurs with PFO may benefit from evaluation and treatment of toxoplasmosis in the future once more information is known. [ABSTRACT FROM AUTHOR] |
| Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 51420281 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Migraine Associated with Patent Foramen Ovale May Be Caused by Reactivation of Cerebral Toxoplasmosis Triggered by Arterial Blood Oxygen Desaturation. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Prandota%2C+Joseph%22">Prandota, Joseph</searchLink> (AUTHOR) – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22International+Journal+of+Neuroscience%22">International Journal of Neuroscience</searchLink>. Feb2010, Vol. 120 Issue 2, p81-87. 7p. 1 Chart. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Migraine%22">Migraine</searchLink><br /><searchLink fieldCode="DE" term="%22Cerebral+toxoplasmosis%22">Cerebral toxoplasmosis</searchLink><br /><searchLink fieldCode="DE" term="%22Gene+expression%22">Gene expression</searchLink><br /><searchLink fieldCode="DE" term="%22Cytokines%22">Cytokines</searchLink><br /><searchLink fieldCode="DE" term="%22Genetic+regulation%22">Genetic regulation</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Approximately two billion people worldwide are chronically infected with T. gondii and yet with largely unknown consequences. On the other hand, several authors reported an association between migraine and patent foramen ovale (PFO), and different types of headaches, including migraine, may be precipitated by various diseased states or medications associated with marked immune irregularities, which sometimes cause reactivation of latent cerebral toxoplasmosis (CT). Recently, in a group of 104 subjects with migraine, 46 individuals (44.2%) were found to be seropositive for T. gondii. PFO, atrial septal defects, as well as pulmonary right-to-left shunts are usually associated with a various degree of arterial blood oxygen desaturation. Hypoxia is associated with an increase in the generation of several proinflammatory cytokines and other inflammation mediators, such as TNF-α, IL-1-β, IL-6, IL-8, chemokines (monocyte chemoattractant protein-1, CC-chemokine receptor 2, macrophage inflammatory protein-1α, intercellular adhesion molecule-1), acute-phase protein gene expressions, COX-2 gene transcription, induction of iNOS, and reactive oxygen species. Moreover, hypoxia markedly decreased T-lymphocyte IL-2 mRNA, a key cytokine responsible for B-cell proliferation and immunoglobulin secretion, and ischemic tissues demonstrated intravascular neutrophil accumulation, vascular damage, and increased vascular wall permeability. Interestingly, T. gondii activates hypoxia-inducible factor 1 already at physiologically relevant oxygen levels and requires HIF1 for growth and survival. These abnormalities may cause imbalance in the host/T. gondii immune system, which finally results in the reactivation of CT. In addition, hypoxia may participate in paradoxical microembolism because arterial oxygen desaturation enhances expression of plasminogen activator inhibitor-1, an important factor which suppresses fibrinolysis, and this effect may be further amplified by a decreased expression of plasminogen activators, finally causing blood hypercoagulability and paradoxical microembolism. In summary, further studies are required to verify the above-presented pathomechanisms probably responsible for the association between PFO and the development of migraine. It is possible that some migraineurs with PFO may benefit from evaluation and treatment of toxoplasmosis in the future once more information is known. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of International Journal of Neuroscience is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.3109/00207450903458647 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 7 StartPage: 81 Subjects: – SubjectFull: Migraine Type: general – SubjectFull: Cerebral toxoplasmosis Type: general – SubjectFull: Gene expression Type: general – SubjectFull: Cytokines Type: general – SubjectFull: Genetic regulation Type: general Titles: – TitleFull: Migraine Associated with Patent Foramen Ovale May Be Caused by Reactivation of Cerebral Toxoplasmosis Triggered by Arterial Blood Oxygen Desaturation. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Prandota, Joseph IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 02 Text: Feb2010 Type: published Y: 2010 Identifiers: – Type: issn-print Value: 00207454 Numbering: – Type: volume Value: 120 – Type: issue Value: 2 Titles: – TitleFull: International Journal of Neuroscience Type: main |
| ResultId | 1 |
