Dural sinus collapsibility, idiopathic intracranial hypertension, and the pathogenesis of chronic migraine

Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial...

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Vydané v:Neurological sciences Ročník 40; číslo Suppl 1; s. 59 - 70
Hlavní autori: De Simone, Roberto, Ranieri, Angelo, Sansone, Mattia, Marano, Enrico, Russo, Cinzia Valeria, Saccà, Francesco, Bonavita, Vincenzo
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: Cham Springer International Publishing 01.05.2019
Springer Nature B.V
Predmet:
Calcitonin gene-related peptide
Cortex
Headache
Hypertension
Innervation
Medicine
Medicine & Public Health
Migraine
Neurology
Neuroradiology
Neurosciences
Neurosurgery
Optic nerve
Psychiatry
Review Article
Swelling
Therapeutic applications
Sinus stenosis
Chronic migraine
Bridge vein
Idiopathic intracranial hypertension
Self-limiting venous collapse
Starling resistor
ISSN:1590-1874, 1590-3478, 1590-3478
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Abstract Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as “intracranial pressure sensor” played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.
AbstractList Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as “intracranial pressure sensor” played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.
Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as "intracranial pressure sensor" played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.
Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as "intracranial pressure sensor" played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.Available evidences suggest that a number of known assumption on idiopathic intracranial hypertension (IIH) with or without papilledema might be discussed. These include (1) the primary pathogenetic role of an excessive dural sinus collapsibility in IIH, allowing a new relatively stable intracranial fluids pressure balance at higher values; (2) the non-mandatory role of papilledema for a definite diagnosis; (3) the possibly much higher prevalence of IIH without papilledema than currently considered; (4) the crucial role of the cerebral compliance exhaustion that precede the raise in intracranial pressure and that may already be pathologic in cases showing a moderately elevated opening pressure; (5) the role as "intracranial pressure sensor" played by the trigeminovascular innervation of dural sinuses and cortical bridge veins, which could represent a major source of CGRP and may explain the high comorbidity and the emerging causative link between IIHWOP and chronic migraine (CM). Accordingly, the control of intracranial pressure is to be considered a promising new therapeutic target in CM.
Author Bonavita, Vincenzo
Marano, Enrico
Saccà, Francesco
Ranieri, Angelo
De Simone, Roberto
Russo, Cinzia Valeria
Sansone, Mattia
Author_xml – sequence: 1
  givenname: Roberto
  surname: De Simone
  fullname: De Simone, Roberto
  email: rodesimo@unina.it
  organization: Department of Neuroscience, Reproductive Sciences and Odontostomatology, Headache Centre, University Federico II of Naples
– sequence: 2
  givenname: Angelo
  surname: Ranieri
  fullname: Ranieri, Angelo
  organization: Division of Neurology and Stroke Unit, Hospital A. Cardarelli
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  givenname: Mattia
  surname: Sansone
  fullname: Sansone, Mattia
  organization: Department of Neuroscience, Reproductive Sciences and Odontostomatology, Headache Centre, University Federico II of Naples
– sequence: 4
  givenname: Enrico
  surname: Marano
  fullname: Marano, Enrico
  organization: Department of Neuroscience, Reproductive Sciences and Odontostomatology, Headache Centre, University Federico II of Naples
– sequence: 5
  givenname: Cinzia Valeria
  surname: Russo
  fullname: Russo, Cinzia Valeria
  organization: Department of Neuroscience, Reproductive Sciences and Odontostomatology, Headache Centre, University Federico II of Naples
– sequence: 6
  givenname: Francesco
  surname: Saccà
  fullname: Saccà, Francesco
  organization: Department of Neuroscience, Reproductive Sciences and Odontostomatology, Headache Centre, University Federico II of Naples
– sequence: 7
  givenname: Vincenzo
  surname: Bonavita
  fullname: Bonavita, Vincenzo
  organization: Istituto di Diagnosi e Cura Hermitage Capodimonte
BackLink https://www.ncbi.nlm.nih.gov/pubmed/30838545$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright Fondazione Società Italiana di Neurologia 2019
Neurological Sciences is a copyright of Springer, (2019). All Rights Reserved.
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IngestDate Thu Sep 04 19:19:34 EDT 2025
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Wed Feb 19 02:36:12 EST 2025
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Issue Suppl 1
Keywords Sinus stenosis
Chronic migraine
Bridge vein
Idiopathic intracranial hypertension
Self-limiting venous collapse
Starling resistor
Language English
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Springer Nature B.V
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SubjectTerms Calcitonin gene-related peptide
Cortex
Headache
Hypertension
Innervation
Medicine
Medicine & Public Health
Migraine
Neurology
Neuroradiology
Neurosciences
Neurosurgery
Optic nerve
Psychiatry
Review Article
Swelling
Therapeutic applications
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Title Dural sinus collapsibility, idiopathic intracranial hypertension, and the pathogenesis of chronic migraine
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