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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.

The authors report the unusual case of an aneurysm arising from the extracranial portion of the left posterior inferior cerebellar artery (PICA). The patient was a 39-year-old woman who developed a subarachnoid hemorrhage. The hemorrhage was in the basal, ambient, and Sylvian cisterns, but not in the ventricles. There were no focal neurological deficits, and the clinical grading was 1. On cerebral angiograms, the PICA was found to originate from the vertebral artery as low as 17.9 mm below the foramen magnum and to enter into the spinal canal through the intervertebral foramina of C1-C2. The artery went up to the posterior fossa and had only the cranial loop with an absence of the caudal loop. The saccular aneurysm hung on the initial segment of the PICA and was located at the C1 level. The patient developed motor aphasia and hemiparesis on the right side 15 days after onset, and an infarction was disclosed in the boundary zones of the left parietal lobe on a computed tomographic scan. The aneurysm was successfully obliterated by a neck clipping 2 months later, and the patient was discharged in good condition. The literature discussing PICA aneurysms in the extracranial, as well as distal, portion is reviewed.

To delineate the pathophysiology of periventricular hemodynamics in normal pressure hydrocephalus, we performed quantitative and three-dimensional measurements of cerebral blood flow (CBF) by using xenon-enhanced computed tomographic scans. Measurements were made on 7 patients in whom normal pressure hydrocephalus after subarachnoid hemorrhage had been confirmed by clinical improvement after shunting. We compared mean CBF values in the white matter and cortex of the frontal, temporal, parietal, and occipital lobes and in the thalamus before and after shunting, with an evaluation of dementia and the extent of ventricular dilation and periventricular lucency on computed tomographic scans. CBF returned to within normal limits in the white matter of the frontal and temporoparieto-occipital lobes. CBF restoration closely correlated with clinical improvement and reduction in ventricular dilation and periventricular lucency. We speculate that ischemia occurs initially in the periventricular white matter as a result of diffused cerebrospinal fluid and then extends of the cortex and to the thalamus, causing a "misery perfusion" state with neuronal dysfunction. Incomplete improvement of dementia and CBF in the cortex and thalamus may be explained by preexisting arteriosclerosis in aged patients, coexisting brain damage caused by subarachnoid hemorrhage and subsequent surgical insult in aneurysm patients, and delayed recovery of cortical function that has been secondarily impaired by the periventricular lesions.

To elucidate the pathophysiology of mental disturbances associated with chronic subdural hematoma, we performed quantitative and three-dimensional measurements of cerebral blood flow (CBF) on xenon-enhanced computed tomographic scans in 12 patients who had chronic subdural hematomas and manifested mental disturbances. In 2 patients who had no headache or hemiparesis, minimal mass effect, and severe multiple infarctions on computed tomographic scan, mentation did not improve after surgery. The CBF reduction was severe, and it further deteriorated after surgery. On the other hand, mentation improved to a varied extent in the other 10 patients, who had headache and/or hemiparesis and minimal, moderate, or severe mass effect and minimal or moderate multiple infarctions on computed tomographic scan. The CBF reduction was diffuse on both sides, but was more marked in the thalamus and putamen than it was in the cortex and subcortex. It was restored after surgery, but insufficiently. The restoration rate was statistically significant only in the thalamus, on both sides (with and without hematoma) (P less than 0.05). Dementia scores and CBF values after surgery were correlated on the side with the hematoma in the frontal cortex and thalamus (P less than 0.01) and in the hemisphere and temporoparietal cortex (P less than 0.05). There was no correlation on the side with the hematoma in the occipital cortex, putamen, and frontal and temporoparieto-occipital subcortices or on the side without the hematoma. The thalamus undergoes displacement and distortion by the hematoma, which in turn leads to changes in consciousness. Postoperative residual mental deficits consist primarily of dementia related to preexisting multiple infarctions.(ABSTRACT TRUNCATED AT 250 WORDS)