Cerebral akinetopsia

Cerebral akinetopsia is a selective impairment in motion perception. Only two cases of akinetopsia from bilateral lesions have been well described, LM and AF. LM has been the subject of many reports (Zihl et al., 1983, 1991; Hess et al., 1989; McLeod et al., 1989; Baker et al., 1991; Shipp et al., 1994; Rizzo et al., 1995; Campbell et al., 1997; Marcar et al., 1997). Symptomatically, LM had no impression of motion in depth or of rapid motion (Zihl et al., 1983). Fast targets appeared to jump rather than move (Zihl et al., 1991). Subjects with motion deficits from unilateral lesions are either asymptomatic or have more subtle complaints, such as “feeling disturbed by visually cluttered moving scenes” and trouble judging the speed and direction of cars (Vaina and Cowey, 1996; Vaina et al., 1998).

Tests for motion perception require computer-animated displays that are not available in most clinics. It is not possible to infer perceptual deficits solely from impaired motor responses to moving stimuli, such as pursuit eye movements. Although LM and AF had impaired smooth pursuit (Zihl et al., 1983), subjects with unilateral lesions impairing motion perception may have normal smooth pursuit, and conversely subjects with abnormal pursuit may have normal motion perception (Barton et al., 1996a).

Many different aspects of motion perception can be tested. Even with extensive bilateral lesions, not all motion perception is lost. Distinguishing moving from stationary stimuli is still possible (Zihl et al., 1983) and the contrast sensitivity for moving striped patterns is almost normal (Hess et al., 1989). LM could discriminate the direction of small spots (Zihl et al., 1991) and random dot patterns in which all dots were moving in the same direction (Baker et al., 1991; Rizzo et al., 1995). However, LM and AF had trouble perceiving differences in speed, and their perception of direction was severely affected when even small amounts of random motion or stationary noise were added (Baker et al., 1991; Vaina, 1994; Rizzo et al., 1995).

These deficits are reflected in a number of perceptual tasks involving motion cues. When searching among multiple objects for a target, LM could not restrict her attention to moving objects (McLeod et al., 1989). LM and AF could not identify two-dimensional shapes defined by differences in motion between the object and its background. LM was also impaired for three-dimensional shapes defined by motion (Vaina, 1994; Rizzo et al., 1995). When lip-reading, LM had trouble with polysyllables uttered rapidly, and her judgment of sound was biased by auditory rather than visual cues (Campbell et al., 1997). On the other hand, LM could easily see biological motion (e.g., identifying the movements of a human body).

LM suffered sagittal sinus thrombosis with bilateral cerebral infarction of lateral occipitotemporal cortex (Zihl et al., 1991). AF had acute hypertensive hemorrhage with similar bilateral lateral occipitotemporal lesions (Vaina, 1994). In monkeys, motion-specific responses are found in areas V5 (middle temporal area) and V5a (medial superior temporal area), in the superior temporal sulcal region (Zeki, 1991). The lateral occipitotemporal area has been identified from histological markers and functional imaging as homologous to monkey area V5 (Clarke and Miklossy, 1990; Watson et al., 1993; Tootell and Taylor, 1995; Barton et al., 1996b). The correspondence of this region to monkey V5 is strengthened by a study showing similar patterns of deficit and spared abilities in LM and monkeys with V5 ablations (Marcar et al., 1997). Stimulation of the putative location of V5 in humans causes impairments in motion perception (Blanke et al., 2002; Cowey et al., 2006).

Unilateral lesions of the human V5 area (Fig. 9.7) cause more subtle abnormalities of motion perception. Some small series report contralateral hemifield defects for speed discrimination (Plant et al., 1993; Greenlee et al., 1995), detecting boundaries between regions with different motion, and discriminating direction amidst motion noise (Barton et al., 1995). As in LM and AF, motion detection and contrast thresholds for motion direction are normal (Plant et al., 1993; Greenlee et al., 1995). At present, there are few data on hemispheric differences. While an earlier study found a predominance of right-sided lesions (Vaina, 1989), similar defects have been identified subsequently with damage to either side (Regan et al., 1992; Barton et al., 1995). Fig. 9.7. Hemiakinetopsia. Magnetic resonance axial image from a 23-year-old man 1 year after he suffered a hemorrhagic infarction of the right lateral occipitotemporal lobe (small arrow). He had impaired ipsilateral pursuit and abnormal motion perception. (Reproduced from Barton et al. (1996a), by permission of Oxford University Press.)

Are different types of motion perception affected by different lesions? Studies show that subjects can differ considerably in the pattern of preserved versus affected motion processes (Vaina et al., 2005). First-order motion refers to stimuli in which motion can be computed by correlating the spatial distribution of luminance in the visual scene over time. However, we can discern motion from other information besides luminance, such as contrast, texture, stereopsis, and flicker. These are known as second-order motion. Initial case studies suggested that first- and second-order motion may have separate loci, with second-order motion affected by a lesion near the V5 region (Vaina and Cowey, 1996; Vaina et al., 1999) and first-order motion by a medial occipital lesion affecting V2 and V3 (Vaina et al., 1998), but recent studies have found that deficits of first- and second-order motion perception co-localize to the V5 region (Greenlee and Smith, 1997; Braun et al., 1998). Some segregation of first- and second-order processing is still possible, though, as impaired first-order and preserved second-order motion perception were occasionally seen in subjects with smaller peri-V5 lesions (Greenlee and Smith, 1997). An fMRI study (Smith et al., 1998) suggested that signals from second-order motion first emerge in V3 and VP, and may be later integrated with first-order motion signals in V5.

Other studies contrasting individual cases have suggested that lesions in the V5 region may selectively impair the integration of motion signals over larger areas, as suggested before (Barton et al., 1995), while medial lesions affecting the V3 region may impair judgment of speed or the detection of boundaries between regions of different movement (motion segregation) (Vaina et al., 2005). Another potential distinction is between these short-range processes and the more long-range integration of position data that gives rise to apparent or “high-level” motion perception. Defects in high-level motion perception arise from parietal rather than occipitotemporal lesions, and may be related more to defects in transient visual attention than the processing of motion signals (Batelli et al., 2001, 2003). Likewise, the perception of biological motion, as when one derives the percept of a walking motion from point sources of light attached to a body, is impaired primarily by lesions not of V5 but of the more anterior superior temporal polysensory area (Vaina and Gross, 2004).

The relation of pursuit eye movements to motion perception is of interest. During pursuit, the fMRI signal related to motion perception is enhanced in V5 and in a more dorsal parieto-occipital location (Barton et al., 1996b; Freitag et al., 1998). Some of the neural activity in area V5a during pursuit may be information about the eye movement itself (efference copy). Since movement of images on the retina can be generated either by moving objects while the eye remains still, or by eye movement while the world remains still, efference copy may serve to disambiguate the two. A subject with vertigo induced by moving objects could not take his own eye movements into account when estimating object motion (Haarmeier et al., 1997). He had bilateral occipitoparietal lesions, possibly of a homolog of V5a.

Other defects can be associated with akinetopsia. The proximity of the optic radiations means that hemianopic defects are frequent. The two akinetopsic subjects had large lesions and, not surprisingly, defects on other perceptual tasks. AF was poor at recognizing objects seen from unusual angles and in incomplete line drawings, and on spatial tests such as hyperacuity, line orientation, line bisection, spatial location, and stereopsis. LM had poor perception of forms constructed from cues of texture, stereopsis, or density (Rizzo et al., 1995).

The prognosis of motion perceptual deficits is still unclear. Two cases showed significant improvement over 6–12 months (Barton and Sharpe, 1998; Braun et al., 1998). In monkeys the pace and degree of recovery are correlated with the size of the lesion and the extent of damage to both V5 and V5a (Yamasaki and Wurtz, 1991). Recovery with larger lesions presumably reflects adaptation involving other surviving motion-responsive regions of cortex.