title: Cerebral blood flow and autoregulation in normal pressure hydrocephalus.
abstract: OBJECTIVE
  We tried to identify indications for cerebrospinal fluid shunting in patients with normal pressure hydrocephalus.
  
  
  METHODS
  We studied the cerebral blood flow (CBF) and vascular response to acetazolamide in the white matter, cortex, and thalamus of 21 patients with normal pressure hydrocephalus, comparing patients who improved clinically after shunting with those who did not. We used xenon-enhanced computed tomography for the CBF measurements.
  
  
  RESULTS
  Preoperatively, both groups had globally reduced CBF, but the reduction was more pronounced in the unimproved patients. The vascular response was impaired only in the white matter of the patients who improved later. After shunting, restoration of CBF, more marked in the white matter, and recovery of vascular response in the white matter paralleled clinical improvement and a reduction in ventricular dilation and periventricular lucency on computed tomographic scans in nine patients. The CBF reduction, however, deteriorated in the 12 patients who did not improve clinically.
  
  
  CONCLUSIONS
  We conclude that the underlying disease in the improved patients was ischemia, with a loss of autoregulatory capacity in the periventricular white matter caused by cerebrospinal fluid diffusion. Those who did not improve had irreversible brain damage in which the CBF reduction was secondary to metabolic depression and autoregulation was preserved. We also conclude that patients suspected of having normal pressure hydrocephalus will improve clinically after shunting if preoperative hemispheric CBF is greater than 20 ml/100 g per minute and the vascular response to acetazolamide is impaired only in the periventricular white matter. They will not improve, however, if the preoperative CBF is less than 20 ml/100 g per minute and the vascular response to acetazolamide is intact.
authors.affiliation: Department of Neurosurgery, Fukuoka University, Chikushi Hospital, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Tanaka
authors.forename: M
authors.initials: M
authors.lastname: Kimura
authors.forename: Y
authors.initials: Y
authors.lastname: Nakayama
authors.forename: S
authors.initials: S
authors.lastname: Yoshinaga
authors.forename: M
authors.initials: M
authors.lastname: Tomonaga
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001921:Brain / Q000098:blood supply*; D001925:Brain Damage, Chronic / Q000503:physiopathology; D002545:Brain Ischemia / Q000503:physiopathology / Q000601:surgery; D015170:Cerebrospinal Fluid Pressure / Q000502:physiology; D002557:Cerebrospinal Fluid Shunts; D005260:Female; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D006850:Hydrocephalus, Normal Pressure / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery; D008297:Male; D008875:Middle Aged; D009460:Neurologic Examination; D011183:Postoperative Complications / Q000503:physiopathology; D012039:Regional Blood Flow / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology / Q000601:surgery; D014057:Tomography, X-Ray Computed / Q000379:methods; D014978:Xenon
chemical_list: D014978:Xenon