EEG Studies of Normal and Encephalomalacia Chicks. ∗

Abstract

Although review of the literature fails to show the use of EEG in the study of function or abnormalities of the chicken brain, we have used this technic for studying nutritional encephalomalacia, one of the vitamin E deficiency syndromes. This condition, as described by Pappenheimer, involves primarily the cerebellum and to some extent the medulla and cerebrum, sparing the optic lobes (1–3). We have compared EEG records of standard tracings, photostimulation and pentylenetetrazol-induced convulsions, using normal birds, and chicks with various stages of nutritional encephalomalacia.

Administration of diets deficient in Vit. E induces in chicks certain well known syndromes, i.e., encephalomalacia, exudative diathesis and muscular degeneration. In former studies of vitamin deficiencies, each bird usually showed more than one of these syndromes. Recent experiments have made it possible to differentiate nutritional factors pertinent to each syndrome by modifying the diets and producing single syndromes in individual experimental chickens. For example, selenium protects against exudative diathesis(4). Linoleic or arachidonic acid is necessary for development of encephalomalacia(5). Selenium and antioxidant protect chicks from muscle degeneration when they are fed a low sulfur containing diet(6). Diets deficient in arginine protect chickens from myopathy when they are on myopathy-producing diets(7).

Chickens fed for 2 or 3 weeks on diets which produce encephalomalacia exhibit various clinical signs which include ataxia, uncontrollable bicycling movements, coma and death. At the time our tracings were made a variety of these signs were evident.

Material and methods. Nichol 108 cockerels were placed on encephalomalacia producing diets, with controls kept on basal diets. EEG tracings were made from birds of each group selected at random from ages 4 to 20 days. Suitable restraining containers eliminated the use of any sedating drugs during the procedure.