28 BRAIN MECHANISMS AND LEARNING 



or peduncle is cut a few hours prior to a high spinal section, an enduring 

 postural asymmetry remains in the hind quarters (de Giorgio, 1943). This 

 is reminiscent of the continued unidirectional circling by a decorticate 

 dog, the direction depending upon which hemisphere was first removed. 

 A comparable postural asymmetry in the spinal cat is seen long after a 

 severe inflammatory lesion is produced in one paw; the previously 

 damaged leg is pulled into sharp flexion, with crossed extension of the 

 other, when a spinal section is made (Sperensky, 1944)- Clinical experience 

 with trigger points, and the demonstration that anginal and other pains 

 can develop a permanent referral to another bociy region which has been 

 irritated at the time the pain occurs, points in the same direction (see 

 Gerard, 1951). 



The growing evidence of a relation of deep forebrain structures to 

 learning and recall has not yet crystallized. The amygdala seems to exert 

 an adverse influence on fixation, and the reticular formation and hypo- 

 thalamus have also been found to be involved. Conversely, recent memory 

 fails with damage to the mammilary body, the fornix, and the amygdala 

 (Morrell, 1956; Bickford ct ah, i9.vS; Jasper and Rasmussen, 1958; 

 Samuels, 1959; Doty, 1960; Gerard, 1960a). Recently, the stimulation of 

 the midbrain tegmentum has been reported (Thompson, 1958; Glickman, 

 1958) to cause forgetting; while stimulation of the caudate impairs fixa- 

 tion. The whole situation is confused by difliculties in distinguishing 

 between fixation on the one hand and retention and recall on the other. 

 The use of hypnosis as a tool to maximize recall has long given unexpected 

 results; and recent reports by responsible workers — such as the hypnotic 

 recall of a conversation which occurred during surgical anaesthesia of the 

 individual doing the recalling; or recall of experiences during a given year 

 of childhood but only when an hypnotic suggestion had brought the 

 individual back to that age (Sheerer and Reift, 1959) — demonstrates our 

 small understanding of the complex phenomena of fixation and recall. 



The mechanism of fixation of experience is not known, but two sets of 

 data give strong clues concerning its nature. First, is a group of well- 

 known changes that attend continued activity of neurones: thresholds go 

 through increased and decreased phases; after-potentials are increased 

 enormously in magnitude and duration; post-tetantic potentiation is 

 associated with greatly increased reflex responses ; and the like. The other 

 phenomena relate to the existence c^f a considerable period, of minutes to 

 hours, between having an experience and fixing it. If neural activity is 

 interfered with during this fixation period, by electroshock, by cold, 

 by heat-block, and the like, fixation is interfered with and permanent 



