title: Pathomechanisms of symptomatic developmental venous anomalies.
abstract: OBJECTIVE
  Although it is generally accepted that developmental venous anomalies (DVAs) are benign vascular malformations, over the past years, we have seen patients with symptomatic DVAs. Therefore, we performed a retrospective study and a literature study to review how, when, and why DVAs can become clinically significant.
  
  
  METHODS
  Charts and angiographic films of 17 patients with DVAs whose 18 vascular symptoms could be attributed to a DVA were selected from a neurovascular databank of our hospital. MRI had to be available to rule out any other associated disease. In the literature, 51 cases of well-documented symptomatic DVAs were found. Pathomechanisms were divided into mechanical and flow-related causes.
  
  
  RESULTS
  Mechanical (obstructive or compressive) pathomechanisms accounted for 14 of 69 symptomatic patients resulting in hydrocephalus or nerve compression syndromes. Flow-related pathomechanisms (49 of 69 patients) could be subdivided into complications resulting from an increase of flow into the DVA (owing to an arteriovenous shunt using the DVA as the drainage route; n=19) or a decrease of outflow (n=26) or a remote shunt with increased venous pressure (n=4) leading to symptoms of venous congestion. In 6 cases, no specific pathomechanisms were detected.
  
  
  CONCLUSIONS
  Although DVAs should be considered benign, under rare circumstances, they can be symptomatic. DVAs, as extreme variations of normal venous drainage, may represent a more fragile venous drainage system that can be more easily affected by in- and outflow alterations. The integrity of the DVA needs to be preserved irrespective of the treatment that should be tailored to the specific pathomechanism.
authors.affiliation: Service de Neuroradiologie Diagnostique et Thérapeutique, Hôpital de Bicêtre, Le Kremlin-Bicêtre, Paris, France.
authors.forename: Vitor M
authors.initials: VM
authors.lastname: Pereira
authors.forename: Sasikhan
authors.initials: S
authors.lastname: Geibprasert
authors.forename: Timo
authors.initials: T
authors.lastname: Krings
authors.forename: Thaweesak
authors.initials: T
authors.lastname: Aurboonyawat
authors.forename: Augustin
authors.initials: A
authors.lastname: Ozanne
authors.forename: Frederique
authors.initials: F
authors.lastname: Toulgoat
authors.forename: Sirintara
authors.initials: S
authors.lastname: Pongpech
authors.forename: Pierre L
authors.initials: PL
authors.lastname: Lasjaunias
mesh_terms: D000293:Adolescent; D000328:Adult; D001164:Arteriovenous Fistula / Q000209:etiology; D001794:Blood Pressure; D020787:Central Nervous System Venous Angioma / Q000150:complications / Q000503:physiopathology* / Q000628:therapy; D002648:Child; D002675:Child, Preschool; D004621:Embolization, Therapeutic; D005260:Female; D018056:Hemorheology; D006801:Humans; D006849:Hydrocephalus / Q000209:etiology; D007223:Infant; D007231:Infant, Newborn; D002538:Intracranial Arteriovenous Malformations / Q000150:complications / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D009408:Nerve Compression Syndromes / Q000209:etiology; D010291:Paresis / Q000209:etiology; D016634:Radiosurgery; D012640:Seizures / Q000209:etiology; D013314:Stress, Mechanical; D020521:Stroke / Q000209:etiology