Cross-sectional analysis of CBF values was carried out among 668 volunteers and patients. Subjects were subdivided according to age, gender, and degree of cerebrovascular disease, ranging from healthy volunteers with or without risk factors for stroke to patients with multi-infarct dementia. Four-year longitudinal analysis was also carried out on 230 individuals from the original sample. Decrements in CBF values were evidenced by both cross-sectional and longitudinal analysis in relation to advancing age, progressive cerebrovascular disease, and dementia. Regional, age-related CBF declines in healthy volunteers were heterogeneous, possibly related to changes in levels of functional activity within different brain regions.

SYNOPSIS Measurements of noninvasive regional cerebral blood flow (rCBF) were made by the 133Xe inhalation method in 71 patients with different types of headache and 32 age matched normal controls. Flow gray (Fg) was calculated by two compartmental analysis from the x‐ray subtracted gamma curves, and extracerebral flow indices (EFI) were calculated as an estimate of the percentage contribution by extracerebral tissues.During the headache phase, mean Fg in a group (N = 13) with classic and common migraine was significantly higher compared to a comparable group (N = 12) measured in the headache‐free interval. Serial measurement made during progression in the severity of the migraine headaches showed accompanying increases in the mean Fg as the headache worsened. In 24 patients with severe migraine studied 2‐48 hours after the headache subsided, the mean Fg values remained significantly increased during this immediate post‐headache interval compared with patients who were headache‐free for six days or longer. Serial measurements made during and after the headache showed progressive reduction of mean Fg values to normal within six days after the headache subsided. Marked cerebral dysauto‐regulation was present during the migraine headache and showed progressive recovery as the headache subsided. Reduction of the head pain by administration of codeine decreased hemispheric Fg values but did not change the high flows in the basilar artery territory. Conversely, administration of ergotamine did not change hemispheric Fg values but reduced rCBF in brain stem‐cerebellar regions. Significant regional reductions of Fg correlating with the neurological deficit was measured during the prodrome of classic migraine and during the headache and post‐headache intervals of complicated migraine. During cluster headaches, mean Fg values were also significantly increased and the extracerebral flow indices showed marked increases with highest values recorded at the site of the headache. It was concluded that cerebral hyperperfusion during migraine headaches is mainly due to post‐ischemic reactive hyperemia but may be compounded by functional hyperemia due to the head pain itself.

Background and Purpose-Individuals with mild cognitive impairment (MCI) are at increased risk of Alzheimer's disease (AD) and probably other forms of dementia. Some subtypes of vascular dementia (VaD) may possess minor neuropathological changes of AD that may contribute to cognitive impairments. It was posited that MCI, identified by criteria described here, might present as a prodrome for VaD and AD. Methods-Serial Mini-Mental State Examination was administered at 3-to 6-month intervals, and neuroimaging was performed annually. Subtle cognitive dysfunctions were weighted and measured according to MCI criteria defined here. Subjects identified with MCI were then followed up for an additional 3.88Ϯ3.01 years. Diagnoses of VaD and AD were made according to established criteria. Results-During 3.72Ϯ2.94 years of follow-up of the original normative subjects, 73 of 291 (25.1%) developed MCI. Of the 27 subjects who developed VaD, 15 (55.6%) had prodromal MCI. Of these, two thirds were subclassified as having small-vessel dementia. The remaining 12 patients with VaD (44.4%) were diagnosed directly from a cognitively normal status without preceding MCI. These were predominantly multi-infarct or strategic-infarct dementia (66.7%). An additional 35 MCI subjects (47.9%) developed AD. Both VaD and AD diagnosed after MCI prodromes manifested similar spectral domains of cognitive impairments, which included memory, during their MCI stages. Conclusions-In some VaD subtypes, particularly those caused by subcortical microvascular disease, dementia may be preceded by MCI, which has similar domains of cognitive impairment and a similar progressive course that may mimic AD.

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Combining the CCSE and MMSE screening tests resulted in higher sensitivity than was achieved by MMSE alone and maintained specificity at comparable levels for identifying MCI. The results confirmed that CMC has optimal correctness and utility as a brief cognitive test for screening MCI as a prodrome for dementia among non-demented elderly populations.

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