title: Compensatory mechanisms in patients with benign intracranial hypertension syndrome.
abstract: 135 patients from 16 to 59 years old with benign intracranial hypertension syndrome (BIH) due to postinflammatory processes (A), venous outflow disorders (V), and endocrinological disorders (G) were investigated by CT, MRI, MRI-Ag, carotid-Ag and constant pressure infusion test. All the obtained data were analyzed and possible relationships between the parameters of CSF dynamics and the clinical data were evaluated. Correlative analysis of the obtained data was performed and the main mechanisms of compensation of BIH syndrome were established. In patients of group A disturbances of CSF absorption system with high level of CSF outflow resistance (R) and secondary elevation of brain elastance (EL) were common. In patients of this group venous disorders were of secondary nature and appeared in a later period of the disease. The patients of group V showed increased intrasinus pressure, which correlated to high R and EL. In patients of group G we found the signs of CSF hyper-production with high level of EL. Increased R in patients of this group seemed to be a secondary reaction. The investigation identified the main stages of evolution and compensation of hypertension in the patients with BIH syndrome. The obtained data may be used in optimizing the conservative therapy and indications for lumboperitoneal shunting.
authors.affiliation: Burdenko Neurosurgical Institute, Moscow, Russia.
authors.forename: S S
authors.initials: SS
authors.lastname: Gasparian
authors.forename: N K
authors.initials: NK
authors.lastname: Serova
authors.forename: E Ya
authors.initials: EY
authors.lastname: Sherbakova
authors.forename: T N
authors.initials: TN
authors.lastname: Belova
mesh_terms: D000293:Adolescent; D000328:Adult; D002555:Cerebrospinal Fluid / Q000502:physiology; D005260:Female; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology; D008297:Male; D008875:Middle Aged; D011559:Pseudotumor Cerebri / Q000209:etiology / Q000503:physiopathology*