Altered brain energy metabolism in demented patients with multiple subcortical ischemic lesions. Working hypotheses.

We report the results of brain metabolic studies (using magnetic resonance spectroscopy) in three groups of individuals: (1) demented patients with multiple subcortical ischemic lesions (n = 18); (2) nondemented, age-matched controls (n = 21); and (3) demented patients with neurodegenerative disease, probably of the Alzheimer type (n = 19). Patients with dementia with subcortical vascular lesions, as demonstrated by appropriate imaging studies, had an increase of phosphate energy charge in areas of the cerebral cortex (especially prominent in the frontal regions) superficial to and excluded from the subcortical lesions. We hypothesize that this increased energy charge might be caused by reduced metabolic activity of disconnected brain tissue or by astrocytic hypertrophy and hyperplasia that accompanies subtle ischemic, cortical alterations.

In vivo 31P NMR profiles of Alzheimer's disease and multiple subcortical infarct dementia.

We used in vivo phosphorus 31 nuclear magnetic resonance (31P NMR) spectroscopy to study regional high-energy phosphate and phospholipid metabolism in brains of patients with dementia associated with probable Alzheimer's disease (AD) and multiple subcortical cerebral infarctions (MSID). The MSID patients demonstrated elevations of the phosphocreatine (PCr)/inorganic orthophosphate (Pi) ratio in both the temporoparietal and frontal regions. Phosphomonoesters (PME) and the ratio of PME to phosphodiesters were elevated in the temporoparietal region of AD.

Stroke risk and age do not predict behavioral activation of brain blood flow.

Twenty-four neurologically normal subjects, 12 in their twenties and 12 in their sixties, were included in a protocol that studied the relationship of resting cerebral blood flow and cerebral blood flow activation by neuropsychological testing to age and stroke risk factors. Both age and a stroke risk index were predictive of a reduced resting cerebral blood flow. Despite this, cerebral blood flow activation relative to resting flow was preserved.