Observations on the pathogenesis of Thiamine-Deficiency Encephalopathy in the Cat (Felis Domesticus).
The cerebral lesions of thiamine deficiency have been studied in a variety of species. Experimentally, thiamine-deficiency encephalopathy has been reproduced In the eat, dog, fox, monkey, pigeon and fish and published accounts of its natural occurrence in the fox, cat and man are available. In spite of this difference in species the lesions within the brain show a high degree of consistency in both character and distribution. Essentially, the cerebral lesions consist of focal haemorrhage and oedema restricted to the nuclear masses of the periventricular grey matter, and associated with a variable degree of neuronal degeneration. Few attempts have been made to ascertain the mechanism of development of these lesions although many theories have been proposed. It is established that phosphorylated thiamine acts as a co-enzyme in pyruvate oxidation, and that in a deficiency of the vitamin normal carbohydrate metabolism is disrupted and pyruvate accumulates in the blood and tissues. The oxidation of pyruvate provides an almost exclusive source of energy for cerebral activities. The abnormal accumulation of pyruvic acid which occurs in thiamine deficiency were thought to be directly noxious to endothelia, or to be capable of causing nervous tissue damage, the results of which upset the ionic balance on the cerebral side of the blood-brain- barrier, resulting in the production of oedema and haemorrhage. A direct anti-angiodegenerative effect has been attributed to vitamin B1. In an attempt to throw more light on this problem, it was decided to investigate the development of the characteristic cerebral lesions of thiamine deficiency in cats, and to study in particular the role of the vascular elements and their supporting glia. These elements are presumed to form the anatomical basis of the functional blood-brain-barrier which is responsible for the selective transport between blood and brain. Because of this, experiments were conducted to determine if an altered cerebro-vascular permeability occurred in thiamine deficiency and led to the production of the focal oedema and haemorrhage.