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The distribution of occlusive atherosclerotic lesions in the aortocranial circulation as determined by arteriography was correlated with results of plasma lipid and lipoprotein determinations of patients with symptoms and signs of cerebrovascular disease. The incidence of hyperlipoproteinemia in the total study population was 31.8%. The frequency of hyperlipoproteinemia was signigicantly higher in patients with atherosclerotic lesions limited to extracranial (51%) and intracranial major vessels (44.2%) when compared to the total number of patients and patients with only intracranial small-vessel disease (P less than .05). Type IV hyperlipoproteinemia was the most common abnormality (extracranial group, 42% type IV, 9% type II; intracranial major-vessel group, 35.8% type IV, 8.4% type II). Patients with intracranial small-vessel disease had the lowest frequency of hyperlipoproteinemia (14.2%). The frequency of hypertension with or without hyperlipoproteinemia was higher in patients with intracranial small-vessel disease (P less than .01).

A prominent feature in dementia is intellectual deterioration. Review of the clinical literature indicates a lack of suitably quantitated studies of specific intellectual defects in dementia. The present study investigated the performance of patients with multi-infarct dementia (MID), dementia due to Alzheimer's disease (AD), and vertebrobasilar insufficiency (VBI) with dementia using the Wechsler Adult Intelligence Scale (WAIS). Forty-two patients ranging in age from 45 to 85 years (x 66) were included. Significant differences in cognitive and intellectual performance were found between patients with dementia due to VBI and MID versus neuronal atrophy of the Alzheimer's type. The group with AD performed significantly and consistently lower on all measures. There were no significant differences between the two cerebrovascular disease groups, even though the MID group performed consistently more poorly than the VBI group. A discriminant function analysis classified 74% of the patients correctly based on the individual WAIS scores. The diagnosis was more easily made when tasks measuring visual motor coordination and abstract reasoning were included in the analysis.

Regional cerebral blood flow (rCBF) was measured after intracarotid injection of 133Xe concurrently with measurements of local cerebral blood flow (LCBF) after injection of 133Xe directly into the distal stump of the occluded middle cerebral artery (MCA) by the use of the gamma camera after producing experimental ischemia in baboons by occluding the MCA. Regional MCA stump pressure (rMCAP) was also measured. Regions of ischemia assessed by intracarotid injection of 133Xe correlated well with the territory of infarct defined by injection of 133Xe into the distal MCA stump. Flow values in ischemic regions obtained by direct injection of 133Xe into the MCA were 15% to 20% lower than those obtained by intracarotid injection of 133Xe. Possible explanations for these differences are discussed. During induced hypertension autoregulation in ischemic areas was abolished and paradoxical responses of LCBF and rMCAP to changes in arterial carbon dioxide tension (PaCO2) were confirmed.

The effect of intravenous infusion of 10 per cent glycerol on regional cerebral blood flow (using hydrogen bolus and Xenon-133 (133Xe) clearance methods) and metabolism was investigated in 57 patients with recent cerebral infarction. Hemispheric blood flow (HBF) increased, together with increase in regional cerebral blood flow (rCBF) and cerebral blood volume (rCBV), in foci of brain ischemia. Hemispheric oxygen consumption (HMIO2) decreased together with hemispheric respiratory quotient. Systemic blood levels of glucose, lactate, pyruvate, and triglycerides also increased after glycerol while free fatty acids (FFA) and inorganic phosphate (Pi) decreased. Hemispheric glucose consumption was unaltered after glycerol so that hemispheric glucose to oxygen ratio tended to rise. Pyruvate and lactate production by brain was unchanged. Glycerol moved across the blood brain barrier into brain and cerebrospinal fluid (CSF). Release of FFA and Pi from infarcted brain was reversed by glycerol. Total phosphate balance was maintained actoss brain both before and after glycerol infusion. Triglycerides increased in CSF after glycerol, originating either from cerebral blood or as a result of lipogenesis in cerebral tissue. The EEG Recording and neurological status of the patients improved despite decreased brain oxygen consumption. Results of this study suggest that after intravenous infusion of 10 per cent glycerol in patients with recent cerebral infarction, glycerol rapidly enters the CSF and brain compartments and favorably affects the stroke process in two ways: first, by redistribution of cerebral blood flow with increase in rCBF and rCBV in ischemic brain secondary to reduction in focal cerebral edema; and second glycerol may become an alternative source of energy either by being directly metabolized by the brain, or indirectly, by enhancing lipogenesis, or by both processes. Involvement of glycerol in lipogenesis with esterification to accumulated FFA might lead to improved coupling of oxidative phosphorylation, a hypothesis that fits the finding of improved neuronal function despite further decrease in cerebral hemispheric oxygen consumption.

Cerebral hemispheric blood flow (HBF) and metabolism were measured before and after withdrawal of 20 to 30 ml of cerebrospinal fluid (CSF) over a 10-minute interval in eight patients with recent cerebral infarction and in four patients with Alzheimer's disease (AD). Immediately after CSF removal HBF decreased significantly in the AD group (-14%) but showed no significant change in the stroke group (-5%). There was rapid reduction in cerebral venous O2 content and some increase in cerebral venous PCO2 appearing within 60 seconds of CSF withdrawal, interpreted as a rapid reduction of cerebral blood flow (CBF) as judged by cerebral A-VO2 differences. The reduction in CBF was confirmed by the hydrogen clearance method. Reduction of CBF in response to lowering CSF pressure is presumably of neurogenic origin since it was rapid and occurred without changes in PaCO2 or MABP. Furthermore, measurement of HBF demonstrated that cerebral metabolism constant after CSF removal. It is postulated that in AD, reduction of HBF following CSF withdrawal is mediated by a disordered neurogenic veno-arterial vasoconstriction reflex which is stimulated by rapid reduction in CSF pressure (CSFP). In patients with stroke, when cerebral perfusion pressure is increased by lowering CSFP, CBF is maintained constant most likely by a physiological cerebral veno-arterial vasoconstrictive reflex. Apparently, this vasocontrictive reflex becomes excessive in Alzheimer's disease, possibly due to cerebral neurogenic imbalance.