Your browser doesn't support javascript.
loading
Idiopathic intracranial hypertension pathogenesis: The jugular hypothesis.
Fargen, Kyle M; Midtlien, Jackson P; Margraf, Connor R; Hui, Ferdinand K.
Afiliación
  • Fargen KM; Departments of Neurological Surgery and Radiology, Wake Forest University, Winston-Salem, NC, USA.
  • Midtlien JP; Departments of Neurological Surgery and Radiology, Wake Forest University, Winston-Salem, NC, USA.
  • Margraf CR; Departments of Neurological Surgery and Radiology, Wake Forest University, Winston-Salem, NC, USA.
  • Hui FK; Neuroscience Institute, Division of Neurointerventional Surgery, Queen's Medical Center, Honolulu, HI, USA.
Interv Neuroradiol ; : 15910199241270660, 2024 Aug 08.
Article en En | MEDLINE | ID: mdl-39113487
ABSTRACT
In spite of expanding research, idiopathic intracranial hypertension (IIH) and its spectrum conditions remain challenging to treat. The failure to develop effective treatment strategies is largely due to poor agreement on a coherent disease pathogenesis model. Herein we provide a hypothesis of a unifying model centered around the internal jugular veins (IJV) to explain the development of IIH, which contends the following (1) the IJV are prone to both physiological and pathological compression throughout their course, including compression near C1 and the styloid process, dynamic muscular/carotid compression from C3 to C6, and lymphatic compression; (2) severe dynamic IJV stenosis with developments of large cervical gradients is common in IIH-spectrum patients and significantly impacts intracranial venous and cerebrospinal fluid (CSF) pressures; (3) pre-existing IJV stenosis may be exacerbated by infectious/inflammatory etiologies that induce retromandibular cervical lymphatic hypertrophy; (4) extra-jugular venous collaterals dilate with chronic use but are insufficient resulting in impaired aggregate cerebral venous outflow; (5) poor IJV outflow initiates, or in conjunction with other factors, contributes to intracranial venous hypertension and congestion leading to higher CSF pressures and intracranial pressure (ICP); (6) glymphatic congestion occurs but is insufficient to compensate and this pathway becomes overwhelmed; and (7) elevated intracranial CSF pressures triggers extramural venous sinus stenosis in susceptible individuals that amplifies ICP elevation producing severe clinical manifestations. Future studies must focus on establishing norms for dynamic cerebral venous outflow and IJV physiology in the absence of disease so that we may better understand and define the diseased state.
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Interv Neuroradiol Asunto de la revista: NEUROLOGIA / RADIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Interv Neuroradiol Asunto de la revista: NEUROLOGIA / RADIOLOGIA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos