tt.ll, 



HANDBOOK OF PHYSIOLOGY 



NEl'ROl'IIYSIOLOCY III 



rved at certain stages of intoxication by mescaline 

 262). 



I In- common factor underlying the changes in 

 motion and flicker perception might be an abnormal 

 interaction of stimuli successively applied to the in- 

 jured neural substrate. This interpretation is suggested 

 bv results of two-flash experiments with patients who 

 (on standard perimetric tests) appeared to have 

 normal vision in their foveal region but homonymous 

 defects in the periphery of their visual fields (24). If 

 a conditioning flash is presented to the fovea, and 

 followed within critical time by a test flash to the 

 same area, the threshold for the first flash may be 

 normal, but that for the second flash greatly raised. 

 These observations suggest an abnormal recovery 

 cycle; the injured visual system takes longer than the 

 intact one to recover from the effects of the first flash. 

 The abnormality is found even when the first flash 

 is presented to one eye and the second to the other. 

 There may be analogous abnormalities in the 

 temporal interaction of tactile stimuli following 

 lesions of central somatosensory pathways (238, 444, 

 445). As Weinstein has shown (525), parietal lobe 

 lesions in man produce exaggerated time errors for 

 weights. In normal subjects, successive application of 

 two weights, e.g. to the supported hands, leads rather 

 regularly to an overestimation of the second weight 

 (so-called negative time error). This normal per- 

 ceptual error is markedly enhanced after parietal 

 lobe lesions. Apparently, unilateral lesions of either 

 parietal lobe suffice to produce this exaggerated time 

 error which is found, curiously, in both hands (ipsi- 

 lateral and contralateral to the parietal lesion). 



It has been argued that these and similar dis- 

 turbances of interaction (between simultaneous and 

 successive stimuli 1 might be at the root ol what is 

 commonly interpreted as visual or tactile agnosia 

 (25, 417, 466). Disorders ol serial patterning of im- 

 pulses, if sullieieniK severe, could easily prevent 

 recognition ol objects through the affected sense 

 modality. Such an interpretation of disorders in 

 object recognition, after cerebral lesions, would thus 

 be an alternative to the more traditional notion of a 

 selective loss of higher ('apperceptive' or 'associative') 

 function in the presence oi seemingly intact sensor) 

 performance. 



|s, ii \iin\ sii DIES, Disturbances in motion perception 



.in- outstanding among aftereffects of sensor) dep- 

 rivation Patients 'born blind' (due 10 conui-nil.il 

 cataracts] reputedly complain of continual illusory 

 movements of objects in their environment after their 



cataracts have been removed by surgery 15111 Un- 

 fortunately, evaluation of these reports is rendered 

 difficult by the absence of adequate analyses of per- 

 ception in the cases thus far reported, e.g. in the 

 accounts compiled by von Senden (511). Clearly, 

 visual performance after cataract extraction requires 

 experimental study rather than casual description 

 (538). The reports might mean, as Hebb (188) has 

 suggested, that pattern vision after early and pro- 

 longed visual deprivation has to be learned, and that 

 illusory motions result from an inability, on the part 

 of the patient, to discriminate motions of his own 

 (\es from those of the environment as long as pattern 

 perception is imperfect. It must be noted, however, 

 that the eyes of such patients are engaged in continual 

 irregular and dissociated movements (an "ataxia of 

 gaze'); the data are insufficient to decide whether 

 these oculomotor disturbances merely reflect the 

 perceptual difficulties or are in some way their cause. 

 The same peculiar ataxia of gaze, together with 

 marked perceptual disturbances, has been noted by 

 Ricsen in chimpanzees reared in darkness or under 

 uniform (patternless) visual stimulation (401). 



In man, even temporary deprivation can lead to 

 disordered motion perception during the first tew 

 minutes or hours following return to a normal visual 

 environment. Thus, in the ingenious isolation studies 

 sponsored by Hebb at McGill University in Montreal 

 (40, 205), volunteer adult subjects were deprived of 

 pattern vision for several hours or days. The subject 

 was lying on a cot with translucent goggles covering 

 his eyes; he wore earphones which delivered a mask- 

 ing noise and had cardboard gauntlets on his arms 

 and hands. During the deprivation period, many 

 subjects experienced hallucinations, upon release 

 from confinement, they complained of illusor) mo- 

 tion of objects seen; they also misjudged the apparent 

 speed of real (visually apprehended) movements. 



It is possible that analogous visual effects might be 

 obtained after short-term exposure to a 'noisy' (maxi- 

 mally unstable) visual field, rather than a uniform 

 stable field. Following exposures of as little as 30 

 min. to the "snow' on a television picture screen, 

 normal subjects markcdlv underestimate the actual 

 speed of a moving test object IK)-,). Conversely, pro- 

 longed exposure to .1 stable visu.il pattern leads to 

 overestimates of visu.il speed, Areas of a normal 

 visual field 'satiated' in such fashion show diminished 

 flicker fusion, and apparent motion effects are also 

 altered in the same wa-j .is in patients with defects 

 resulting from cerebral lesions, the targets have to 



