Visual modularity

The way in which the primate visual system operates is currently under intense scientific scrutiny. One dominant thesis is that different properties of the visual world (colour, motion, form and so forth) require different computational solutions which are implemented in anatomically/functionally distinct regions that operate independently – that is, in a modular fashion (Calabretta & Parisi, 2005).

Modularity for Motion Processing
Akinetopsia is an intriguing condition brought about by damage to the extra-striate area hMT+ that renders humans and monkeys unable to perceive motion (Zihl et al., 1983, 1991) and indicates that there might be a “motion centre” in the brain. Of course, such data can only indicate that this area is at least necessary to motion perception, not that it is sufficient; however, other evidence has shown the importance of this area to primate motion perception. Specifically, physiological, neuroimaging, perceptual, electrical- and transcranial magnetic stimulation evidence (Table 1) all come together on the area V5/hMT+. Converging evidence of this type is supportive of a module for motion processing. However, this view is likely to be incomplete: other areas are involved with motion perception, including V1 (Orban et al., 1986; Movshon & Newsome, 1996, Born and Bradley, 2005), V2 and V3a (see Grill-Spector and Malach, 2004) and areas surrounding V5/hMT+ (Table 2). A recent fMRI study put the number of motion areas at twenty-one (Stiers et al., 2006:83). Clearly a stream of diverse anatomical areas subserves motion perception. However, the extent to which this is ‘pure’ is in question: with Akinetopsia come severe difficulties in obtaining structure from motion (Rizzo, Nawrot, Zihl, 1995). V5/hMT+ has since been implicated in this function (Grunewald, Bradley & Andersen, 2002) as well as determining depth (DeAngelis, Cumming and Newsome, 1998). Thus the current evidence suggests that motion processing occurs in a modular stream, although with a role in form and depth perception at higher levels.

Table 1 | Evidence for a “motion centre” in the primate brain

Table 2 | Evidence for a motion processing surrounding V5

Modularity for Color Processing
Similar converging evidence suggests modularity for color. Beginning with Gowers’ (1888) finding that damage to the fusiform/lingual gyri in occipitotemporal cortex correlates with a loss in color perception (achromatopsia) the notion of a “color centre” in the primate brain has had growing support (e.g. Meadows, 1974; Sacks and Wasserman, 1987; Zeki, 1990; Grüsser and Landis, 1991). Again, such clinical evidence only implicates that this region is critical to color perception and nothing more. Other evidence, however, including neuroimaging (Bartels and Zeki, 2005; Bartels and Zeki, 2000; Stiers et al., 2006) and physiology (Wachtler et al. 2003; Kusunoki, Moutoussis & Zeki, 2006) converges on V4 as necessary to color perception. A recent meta-analysis has also shown a specific lesion common to achromats corresponding to V4 (Bouvier and Engel, 2006). From another direction altogether it has been found that when synathetes experience color by a non-visual stimulus V4 is active (Rich et al., 2006; Sperling et al., 2006). On the basis of this evidence it would seem that color processing is modular. However, as with motion processing it is likely that this conclusion is inaccurate. Other evidence shown in Table 3 implicates different areas’ involvement with color. It may thus be more instructive to consider a multistage color processing stream from the retina through to cortical areas including at least V1, V2, V4, PITd and TEO. Consonant with motion perception there appear to be a constellation of areas drawn upon for color perception. In addition, V4 may have a special but not exclusive role. For example, single cell recording has shown only V4 cells respond to the color of a stimuli rather than its waveband, whereas others areas involved with color do not (Wachtler et al. 2003; Kusunoki, Moutoussis & Zeki, 2006).

Table 3 | Evidence against a “color centre” in the primate brain 

Modularity for Form Processing
Another clinical case that would a priori suggest a module for modularity in visual processing is visual agnosia. The well studied patient DF is unable to recognize or discriminate objects (Mishkin, Ungerleider and Macko, 1983) owing to damage in areas of the lateral occipital cortex (James et al., 2003) although she can see scenes without problem – she can literally see the forest but not the trees (Steeves et al. 2006). Neuroimaging of intact individuals reveals strong occipito-temporal activation during object presentation and greater activation still for object recognition (see Grill-Spector, 2003). Of course, such activation could be due to other processes, such as visual attention. However, other evidence that shows a tight coupling of perceptual and physiological changes (Sheinberg and Logothetis, 2001) suggests activation in this area does underpin object recognition. Within these regions are more specialized areas for face or fine grained analysis (Gauthier, Skudlarski, Gore and Anderson, 2000), place perception (Epstein & Kanwisher, 1998) and human body perception (Downing, Jiang, Shuman and Kanwisher, 2001). Perhaps some of the strongest evidence for the modular nature of these processing systems is the double dissociation between object- and face (prosop-) agnosia (e.g. Moscowitch, Winocur and Behrmann, 1997). However, as with color and motion, early areas (see Pasupathy, 2006 for a comprehensive review) are implicated too lending support to the idea of a multistage stream terminating in the inferotemporal cortex rather than an isolated module.

Functional modularity
Much of the confusion concerning modularity exists because there is evidence for specific areas (e.g. V4 or V5/hMT+) and the concomitant behavioral deficits following brain insult (thus taken as evidence for modularity). In addition, evidence shows other areas are involved and that these areas subserve processing of multiple properties (e.g. V1: see Leventhal et al, 1995) (thus taken as evidence against modularity). That these streams have the same implementation in early visual areas, like V1 is not inconsistent with a modular viewpoint: to adopt the canonical analogy in cognition, it is possible for different software to run on the same hardware. A consideration of psychophysics and neuropsychological data would suggest support this. For example, psychophysics has shown that percepts for different properties are realized asynchronously (Moutoussis & Zeki 1997, Viviani & Aymoz, 2001). In addition, although achromats experience other cognitive defects (Gegenfurtner, 2003) they do not have motion or form deficits when their lesion is restricted to V4 (Zeki, 2005). Relatedly, Zihl and colleagues’ (1983) Akinetopsia patient shows no deficit to color or object perception (although deriving depth and structure from motion is problematic, see above) and object agnostics do not have damaged motion or color perception, making the three disorders triply dissociable. Taken together this evidence suggests that even though distinct properties may employ the same early visual areas they are functionally independent. Furthermore, that the intensity of subjective perceptual experience (e.g. color) correlates with activity in these specific areas (e.g. V4) (Bartels and Zeki, 2005), the recent evidence that synathetes show V4 activation during the perceptual experience of color, as well as the fact that damage to these areas results in concomitant behavioral deficits (the processing may be occurring but perceivers do not have access to the information) are all evidence for visual modularity.