I 102 



HANDBOOK OF PHYSIOLOGY 



NEUROPHYSIOLOGY II 



to the superior coUiculus and from there are dis- 

 tributed to the oculomotor nuclei. 



In support of such a scheme one can cite the 

 rather rare patients witli bilateral damage to the 

 peristriate region who have a spasm of fixation 

 whereby they have great difficulty in transferring 

 their point of fixation once they have visually grasped 

 a particular object. Such a patient was described by 

 Holmes (83) and the symptom may form part of 

 Balint's syndrome (77). Here the mechanism just 

 described is presumably intact but cannot be in- 

 hibited readily in order to transfer gaze to other 

 targets. Even more rare are patients in whom the 

 occipital visual centers are intact, and there is no 

 visual defect, but who find it impossible to maintain 

 fixation steadily even though the eyes can be moved 

 to command. It is suggested that the lesion inter- 

 rupts the occipitocollicular fibers as they run through 

 the pulvinar (83). 



It is also temptino to think of the frontal eye field 

 as an area concerned with 'voluntary" eye move- 

 ments, i.e. with movements of the eyes on command 

 and the initiation of large scale scanning movements. 

 In a very clear analysis Graham Brown (25) divided 

 this area into two, an upper in which stimulation 

 gives rise to movement of the head without move- 

 ment of the eyeballs relative to the head. If, however, 

 the head is restrained, the eyes then move in their 

 sockets. Stimulation of the lower area gives move- 

 ment of the eyes to the opposite side and little or no 

 movement of the head. 



Carmichael et at. (27) believe that lesions of the 

 angular and supramarginal gyri impair optokinetic 

 nystagmus, and Henderson & Crosby (78) find an 

 inhibitory eflfect on optokinetic nystagmus exerted by 

 the frontal eyefield. They agree that areas 18 and 19 

 must be intact for optokinetic nystagmus to appear. 

 The frontal area has been reinvestigated recently by 

 Crosby et al. (47) in the inacaque. These authors 

 have obtained an orderly series of eye movements on 

 stimulating sites in the frontal lobe regularly lo- 

 cated along two loci at right angles to each other. 

 Apart from providing yet more evidence of topo- 

 logical organization in the central nervous system, 

 this observation is unusually difficult to interpret. 



It is, however, rather surprising that the frontal 

 lobe is included with the occipital by Fox & Holmes 

 (66) as areas in which lesions can impair optokinetic 

 nystagmus. 



SUBSIDI.ARY CENTERS OF G.\ZE 



It has been claimed that there are two subsidiary 

 centers for eye movement, one the lateral center for 

 gaze in the pons located in or near the para-abducens 

 nucleus (82), the other for vertical movements in or 

 below the superior coUiculus. The strongest evidence 

 for the center for lateral movements is that lesions 

 in this part of the pons have caused bilateral supra- 

 nuclear palsy of adversi\e movements l30th of the 

 lateral and of the medial recti. Adversive movements 

 of medial recti are impaired but convergence move- 

 ments are unaffected. It has therefore been assumed 

 that cortical fibers descend to this nucleus and that 

 fibers from it run to both abducens nuclei and to 

 the medial rectus via the posterior longitudinal 

 bundle. There are others who consider the sugges- 

 tion of a pontine center for gaze an unprofitable 

 hvpothesis (3, 32), and it is doubtful if any center for 

 vertical movement need be postulated other than 

 the layers of the superior coUiculus. 



EYE MOVEMENT IN M.\N 



Fixation Mnvements 



Eye movement has been intensively studied by 

 photographic methods for the last 50 years (57, 58, 

 96). Recently the movements during fixation have 

 been examined by means of reflection from a drop of 

 mercury on the cornea (7), from a contact lens (53, 

 56, 119, 120), and most recently from a mirror 

 carried on a stalk from a contact lens (55) and a 

 light cup (88). All authors agree that during fixation 

 there is a) a continuous tremor with amplitude of 4 

 to 6 ' at 30 to 50 cps, h) irregular flicks of 5 to 60' at 

 irregular intervals and c) a slow drift of about i ' per 

 sec. The tremor seems to be due to irregularity of 

 excitation of the extraocular muscles which receive 

 a heavy tonic discharge at rates in each unit well 

 below fusion frequency (13). During attempted 

 fixation, flicks and drift seem to be random so that 

 the image travels around the central area of the fovea 

 100 ju diameter. As the image approaches the edge 

 of this area (see fig. 9), it is found that the likelihood 

 increases that the next flick will move the image 

 back to the center of the fovea (53). 



The efifect of these mo\ ements is to move the edge 

 of the vi.sual image across the cones of the fovea. 

 This constant movement opposes the adaptation of 



