Biomedical subjects
Publications and source records attributed to D L Rail.
Understanding of cognitive function and dysfunction depends on a knowledge of the neural substrate for symbol formation. Despite a vast literature on the nature of symbolism, fundamental neurophysiological mechanisms underlying the ontogeny of symbol formation have been neglected. This paper develops a theory outlining the formation and evolution of a symbol couched in terms of the neural substrate.
Symbols integrate cortical modular activity into constantly meaningful yet dissolving patterns. Symbolism is posited as one of the keys to an understanding of neurophysiological processes underlying these patterns. A theory of symbol production is proposed based on a consideration of constraints in neural space. The theory is related to inner speech and thought.
UNLABELLED: The rupture of advanced atheromatous plaques initiates a significant number of cases of coronary artery thrombosis and subsequent myocardial infarction. HYPOTHESIS: The range of outcomes following plaque rupture is determined to a large extent by the interaction between the turbulent arterial stream and the visco-elastic properties of the extruded atheromatous material. Thrombosis is a secondary event. Research into the visco-elastic behaviour of atheromatous material may predict predisposition to myocardial infarction.
The computerized tomographic scan in a case of hypertensive encephalopathy showed widespread areas of diminished density in the white matter, mainly in the upper and posterior parts of the hemispheres. The abnormalities resolved within three months of the institution of treatment. We suggest that the low-density areas are focal collections of edema fluid extravasated through ischemic segments of the vessel wall.
Acute and delayed effects of embolizing cerebral surface vessels with cholesterol crystals were studied by direct observation in anesthetized rats and rabbits, using an open-skull technique, and by histological examination of brains at intervals of one day and one week following embolization. The number and size spectrum of crystals, which were infused into the ipsilateral internal carotid artery, were believed to approximate those released by a rupturing large atheromatous plaque in man, but the other lipid materials contained in such plaques were intentionally excluded. It was found that cholesterol crystals had only limited ability to impede blood flow in the 20--80 mu diameter arteries in view. They were also inert within the lumen, causing no vessel wall reaction even after a week; nor was any evidence seen of a thrombogenic effect. Local caliber changes in the containing artery were reproducibly seen, with dilatation of the arterial segment proximal to the embolus and narrowing of the segment in front. These changes appeared to represent an active response of the vessel wall, rather than a passive response to alterations in intraluminal pressure. The difficulty in subsequently locating cholesterol emboli histologically was confirmed. Possible therapeutic implications for atheroembolic cerebral infarction in man were discussed.
Cerebral atheroembolism, in which mainly lipid emboli are released from rupturing atheromatous plaques, may occur without apparent effect, or result in cerebral ischemia and infarction. The reasons behind these unpredictable consequences were sought in the interaction, in vitro and in an animal model, between the main lipid components of advanced plaques. Pure preparations of representative lipids were each harmless when embolized into the cerebral circulation. In contrast, combinations in proportions similar to those in advanced human plaques caused infarction, whether these were synthetic mixtures or extracts from plaques of the entire lipid fraction. The most important physical interaction between the lipids was aggregation of crystals by oils. Between cholesterol and the mainly liquid esters, this created in vitro a range of glutinous aggregates. Triglyceride lowered the melting point of esters, increasing their oiliness, and reduced the cohesiveness of aggregates in the face of operative mechanical forces through a fall in viscosity. Phospholipid, acting principally as an emulsifying agent, promoted dispersion of the oil, secondarily freeing the crystals from its aggregating effect. In the plaque, the balance of these factors will determine the size and number of particles likely to embolize, and, therefore, the clinical outcome should the plaque rupture.