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HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



ous occupation sucli as walking or lictcing ceases; the 

 facial expression changes to one of 'attention" or 

 'arousal,' perhaps associated with some surprise, 

 bewUderment or anxiety; the animal raises its head, 

 the eyes open and the pupils dilate; there are slight 

 pricking movements of the ears and quick anxious 

 glancing movements of the eyes and head, usually to 

 the contralateral side. This searching may result in 

 circling movements to the side opposite that stimu- 

 lated. The animals appear to be alert during the 

 stimulation and respond adequately to various types 

 of external stimuli. However, the reaction to such 

 stimuli frequently seems to be decreased, the animal's 

 attention apparently being fixed on 'something else.' 

 It seems likely that the contraversive movements of 

 the head and deviation of the eyes, both with a sur- 

 prisingly long latency, observed by Hess (103) on 

 excitation of the anterior part of the cingulate and of 

 the medial orbitofrontal cortex, represent part of the 

 same phenomenon. Similar behavioral arousal has 

 recently been obtained in the monkey on stimulation 

 of points in the anterior cingulate and temporal polar 

 cortex (223). Responsive sites were also located in the 

 superior gyrus of the temporal lobe, the orbital sur- 

 face, the intermediate frontal cortex (frontal eye-field), 

 parts of the sensorimotor cortex and the paraoccipital 

 region. 



It is of considerable interest that all these points 

 from which behavioral 'arousal' has been induced in 

 the awake cat and monkey appear to be situated 

 within the regions shown in the anesthetized animal 

 to exert an inhibitorv influence on spontaneous move- 

 ments (cf. above). The initial arrest of prestimulatory 

 somatic activities with cessation of all movements in 

 execution without any loss of muscular tone consti- 

 tutes a most conspicuous feature of the 'searching' or 

 'arousal' response. Also, other isolated phenomena 

 which have been recorded in the anesthetized animals, 

 such as the pupillodilatation, the arterial pressure 

 rise and the facilitation of cortically induced move- 

 ments, possibly represent fragments of the total com- 

 plex 'arousal' response seen in the freely mo\ing 

 animal. 



At subcortical levels apparently similar behavioral 

 arousal has been produced from part of the amygdala 

 (86, 87, 128, 129, 166), the hippocampus (12, 130, 

 131, 166), the perifornical and posterior hypothalamic 

 regions (104, 105), the dorsomedial and anterior 

 thalamic nuclei, the intralaminar nuclei of the thal- 

 amus (5) and from other parts of the brain-stem 

 reticular system (223). The behavioral arousal evoked 

 from the inedial orbitofrontal and cingulate cortex 



persists after bilateral destruction of the cingulum 

 bundle, hippocampus, habenulae, striae medullaris 

 thalami, amygdala and a number of the other brain- 

 stem nuclei. It is abolished following lesions of the 

 anterior basal part of the internal capsule and of por- 

 tions of the intralaminar nuclei, suggesting the in- 

 volvement of the thalamic reticular system in the 

 cortically induced arousal (119). Physiological and 

 anatomical evidence for an intimate relationship 

 between the cingulate, subcallosal and orbitoinsulo- 

 temporal polar cortex and the thalamic reticular and 

 the brain-stem activating system has been given in 

 several studies (70, 95; 126, pp. 156 and 238; 200, 

 210, 231). 



Reactions of fear have been produced in man on 

 stimulating the anterior temporal cortex, particu- 

 larly along the anteromedial portion of the first 

 temporal convolution and periamygdaloid region 

 (187). In animals fear and rage reactions, not un- 

 common manifestations of temporal lobe seizures (65, 

 84, 187, 188, 271), have been elicited from the amyg- 

 dala (86, 129, 134, 166). According to Gastaut et at. 

 (83, 86) fear reactions merge into rage on increasing 

 the stimulus strength. However, the recent study by 

 Ursin and Kaada (257a) indicates that the two 

 phenomena in cats may be induced independently 

 of each other from two separate, partly overlapping 

 zones within the amygdala and not from the peri- 

 amygdaloid cortex itself. It seeins likely that in 

 epileptics a discharging lesion in the anterior temporal 

 cortex may cause these symptoms by spread to the 

 amygdala through the rich connections known to exist 

 between the two structures. Also, the behavior autont- 

 atism (with unresponsiveness, confusion, masticatory 

 movements, and inappropriate but often elaborate 

 behavior and amnesia) which has been reproduced in 

 epileptics on stimulating points centering in the peri- 

 amygdaloid region (65, 66, 123, 169, 187) is possibly 

 caused by spread of the abnormal discharges through 

 the amygdala or the hippocampus to the brain stem. 

 (This matter is considered in the succeeding chapters 

 on the hippocampus and amygdala in this Handbook.) 



Effects on Etcctrocortical Activity 



The spontaneous electrical activity recorded from 

 the cingulate and orbitoinsulotemporal polar cortex 

 in the awake or anesthetized animal does not differ 

 essentially from that recorded from neocortical areas, 

 except that no intermittent 'barbiturate spindles' at 

 a frequency of 6 to 12 per sec. are present in the pyri- 

 form cortex (99, 126). 



