Susan Weathers

Leukoaraiosis correlates with cerebral hypoperfusion in vascular dementia.

Leukoaraiosis quantified by computerized densitometric measurements of reduced Hounsfield numbers was correlated with local cerebral blood flow on the same computed tomographic images of 35 patients with multi-infarct dementia and 16 age-matched elderly normal volunteers. The ratio for area of frontal leukoaraiosis to total area of parenchyma among the patients was significantly greater than that among the normal volunteers (5.8 +/- 2.3% compared with 3.1 +/- 1.3%, p less than 0.001). Severity of leukoaraiosis around the frontal horns of the lateral ventricles correlated significantly with severity of leukoaraiosis of the centrum semiovale adjacent to the bodies of the lateral ventricles. Cerebral blood flow values for all representative cerebral regions except the parietal white matter were reduced among the patients compared with the normal volunteers. Multivariate regression analysis revealed that reduced cerebral perfusion in the putamen and thalamus correlated significantly with the severity of leukoaraiosis. Cerebral hypoperfusion in territories supplied by deep penetrating arteries may contribute to the pathogenesis of leukoaraiosis.

CT changes associated with normal aging of the human brain

CT was used to measure changes in cerebral gray and white matter tissue densities associated with normal aging, using a cross-sectional design, in order to provide normative data for comparisons with abnormal aging such as dementias of Alzheimers and vascular types. Cerebral compartmental densities were measured using plain CT, and their perfusion values were recorded during stable xenon inhalation (CT-CBF), among 81 neurologically and cognitively normal volunteers of different ages. Results led to the conclusion that cortical gray matter tissue densities progressively decline (polio-araiosis) after age 60. Cortical polio-araiosis is coupled with regional hypoperfusion but not with cortical atrophy. It is speculated that the cortical hypodensity identified by CT imaging parallels declines in cortical synaptic density, as reported from autopsy studies using anti-synaptophysin staining of cerebral cortex obtained from normal people above and below age 60. The coupling of cortical hypoperfusion with polio-araiosis is believed to reflect age-related reductions of cortical metabolic demands as reported by PET. During normal aging leuko-araiosis correlates directly with cortical atrophy, suggesting that anterograde axonal degeneration resulting from cortical neuronal dearborization play a role in its causation.

Patterns of cerebral hypoperfusion compared among demented and nondemented patients with stroke.

Background and Purpose No reports are available that compare local cerebral perfusion among groups of patients suffering from multiple cerebral infarctions with and without cognitive impairments. The present study was designed to correlate changes in regional cerebral perfusion that may lead to dementia among patients with multiple cerebral infarctions by comparing measurements of local cerebral blood flow. Methods Local perfusion was measured using xenon-contrasted computed tomographic scanning among two groups of patients who had suffered from multiple cerebral infarctions: Group D (n=12) were demented and had severe cognitive impairments, and group I (n11) were cognitively intact Results were compared with similar measurements among neurologically and cognitively normal, age-matched volunteers (group N, n=16). Results Mean local perfusion values were reduced among both groups with cerebral infarctions but to a more marked degree in group D (p<0.05). Perfusion of cerebral white matter was diffusely and severely reduced in group D (p<0.05) but was mildly reduced only in frontal and capsular white matter in group I (p<0.05). Perfusion of cerebral cortex was reduced in frontal (p<0.01) and temporal (p<0.01) regions among both groups but to a significantly greater degree in group D subjects (frontal, p<0.05; temporal, p<0.01), who also showed hypoperfiision of the occipital cortex (p<0.05), apparently because of underlying leukoaraiosis and cortical disconnections. Perfusion of the basal ganglia was reduced to the same degree among both groups of stroke patients (p<0.01). Conclusions: Leukoaraiosis with white matter hypoperfusion appears to be an important determinant for cognitive impairments among patients with multiple cerebral infarctions.

Leukb‐Araiosis and Cerebral Hypoperfusion Compared in Elderly Normals and Alzheimer's Dementia

To elucidate the pathogenesis of leuko‐araiosis in patients with Alzheimers disease by utilizing CT densitometry of the brain and measurements of local perfusion in order to quantify the extent of leuko‐araiosis and local hypoperfusion compared with similar measurements made among age‐matched normal volunteers.

Cerebral hypoperfusion correlates with mild and parenchymal loss with severe multi-infarct dementia

Relative contributions of two potential pathogenetic factors for cognitive impairments among patients with multi-infarct dementia (MID) are reported. Cognitive test scores were correlated with measures of cerebral hypoperfusion and loss of brain parenchyma. Local cerebral blood flow values were determined utilizing stable xenon contrasted computed tomography and volumes for brain parenchyma were estimated from ratios of volumes of infarcted brain plus cerebrospinal fluid/total intracranial volume measured on the same CT slices among two groups of patients, one with mild and the other with severe MID. A total of 26 demented patients with multiple cerebral infarcts were divided into 2 index groups, one with mild and the other with severe MID (mild MID, CCSE greater than or equal to 15, n = 16; severe MID, CCSE less than 15, n = 10). Results were compared with similar measures among age-matched neurologically normal volunteers (n = 14). Ratios for volumes of lost brain parenchyma were significantly higher among severe MID patients than among age-matched normal volunteers, whereas estimates of brain loss among patients with mild MID did not differ from elderly normal volunteers. In patients with mild MID, LCBF values for cortical gray matter were decreased compared with age-matched normal volunteers. Results suggest that chronic cerebral hypoperfusion is an important determinant for mild dementia among patients in the early stages of MID, but volumes of lost cerebral parenchyma due to cerebral infarctions is an important determinant for advanced stages of MID.

Cerebral Hyperemia During Spontaneous Cluster Headaches With Excessive Cerebral Vasoconstriction to Hyperoxia

SYNOPSIS

Role of Thalamus and White Matter in Cognitive Outcome After Head Injury

Local CBF (LCBF) and local partition coefficients (LΛ) were measured by xenon-enhanced computed tomography among 15 patients with remote cerebral trauma resulting from severe head injury. Results were compared with similar measures among age-matched normal volunteers (N = 20). The patients were divided into two groups according to different outcomes based on serial cognitive testing: Group I (N = 10) improved but Group D (N = 5) deteriorated throughout a mean interval of 10 years of follow-up. Initial LCBF measurements were performed at mean intervals of 6.8 years after injury. Cortical LCBF values were decreased in frontal (p < 0.01) and temporal (p < 0.05) regions among both groups, but only in Group D were flow values decreased in putamen and thalamus (p < 0.05). LΛ values were reduced in frontotemporal cortex among both groups but in the thalamus only among Group D (p < 0.05). Mean white matter flow values were normal in Group I but were reduced in Group D (p < 0.05). Mean partition coefficients for white matter were reduced in both groups (p < 0.01) but were lower in Group D (p < 0.05). Reduced perfusion of frontotemporal gray matter is consonant with neuropathological reports following severe brain trauma of neuronal atrophy, gliosis, and infarction affecting these regions. Group comparisons between patients who cognitively improved versus those that deteriorated demonstrate an association between reductions of CBF in putamen, thalamus and subcortical white matter and impaired cognition after severe head injury.

Cognitive recovery correlates with white-matter restitution after head injury

Longitudinal measurements of local cerebral perfusion (LCBF) and local partition coefficients (L lambda) using xenon-enhanced computed tomography were examined in six patients who had suffered from head injury at a mean age of 30 +/- 9.3 years. They were selected from a larger group with head injury because all were observed longitudinally to make excellent cognitive recovery some years after acute cerebral trauma. Results were compared with similar longitudinal measurements made in six age-matched neurologically normal volunteers. In the index group, cognitive test scores were reduced at the time of the first LCBP measurement but significantly improved to normal at the time of the second. The mean interval between measurements was 2.7 +/- 0.7 years. At the time of the first measurement, all six patients exhibited abnormal volumes of white matter with reduced Hounsfield numbers and LCBF and L lambda values. Abnormalities in volume of white matter and LCBF and L lambda values improved to normal at the time of the second measurement. Perfusion values for frontal cortex, putamen, and thalamus were still slightly reduced but also improved toward normal between measurements. Cognitive recovery correlated best with restoration of white matter integrity, suggesting that following head injury, cognitive impairments may be associated with temporary disconnections of corticothalamic projection systems.

Cerebral white matter perfusion in dementia of Alzheimer type.

Summary:Local cerebral blood flow was measured in 19 patients with probable dementia of Alzheimer type (DAT) by using xenon-enhanced computerized tomography (CT) and CT densitometry to accurately differentiate white from gray matter. Patients met standard diagnostic criteria for probable DAT and results were compared with similar measures in 26 age-matched, neurologically and cognitively normal volunteers. Perfusions of frontal and occipital white matter as well as frontal, parietal, temporal, and occipital cortex were reduced in DAT compared with age-matched normals. White matter perfusion differences were not observed among DAT patients with and without risk factors for stroke. Reduced perfusion of frontal white matter correlated significantly with reduced perfusion of thalamus and putamen in patients with DAT. Results confirm the frequent association of white matter abnormalities in patients with DAT that are possibly caused by amyloid angiopathy and may contribute to cognitive impairments.

Longitudinal measurement of cerebral perfusion in patients with multi-infarct dementia

Longitudinal measurements of local cerebral blood flow (LCBF) were performed in 13 patients with multi-infarct dementia (MID) utilizing the xenon-enhanced computed tomography-CBF method. Subjects were divided into two groups: a group consisting of five patients with MID who deteriorated (aged 60.6 ± 5.3 years) and whose CCSE scores decreased and a stable group comprised of eight patients (aged 64.5 ± 4.5 years) whose CCSE scores did not change. Mean intervals between first and second LCBF measurements were 663 ± 182 days for the deteriorated group and 795 ± 495 days for the stable group. In the deteriorated group, LCBF values for frontal cortex, thalamus, and frontal white matter had declined further at the second measurement. In the stable group, LCBF values were not uniformly stable, but there were no overall mean decreases. The annual rate of decline among patients who deteriorated for frontal cortex, thalamus, and frontal white matter exceeded annual declines measured in elderly normal volunteers. Results suggest that progressive cerebral hypoperfusion contributes to cognitive declines in mild MID, but, if cerebral perfusion of frontal lobes and basal ganglia can become stabilized, further cognitive deterioration can be prevented.