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Cerebral blood flow and autoregulation in normal pressure hydrocephalus.
Neurosurgery 1997 June
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.
CONCLUSION: 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.
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.
CONCLUSION: 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.
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