The Relationship between Visual Interpolation Ability and Leukoaraiosis in Healthy Subjects

The Relationship between Visual Interpolation Ability and Leukoaraiosis in Healthy Subjects

Kaechang Park, Yinlai Jiang, Shuoyu Wang
DOI: 10.4018/978-1-60960-559-9.ch001
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Abstract

This chapter examines the relationship between leukoaraiosis (LA) and visual interpolation ability (VIA) in healthy subjects using a novel method that involves the quantitative measurement of VIA. LA has been found through neuroimaging studies and is caused by demyelinization and degenerative changes in arterioles that are related to atherosclerosis (Breteler et al., 1994). Moderate and severe LA have been regarded as surrogate markers for stroke and cognitive impairment. In the present study, the bilateral extent of LA was significantly associated with a decline in VIA. This result demonstrates the clinical importance of mild LA in addition to moderate and severe LA. It also indicates a useful possible application of this method for the early detection of cognitive impairment.
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Introduction

In both natural and artificial environments, because of factors such as occlusion and darkness, it is impossible to visualize the complete details of objects. Thus, the recognition of an object from its separate visible fragments, defined as visual interpolation, is a fundamental ability of the visual system.

Psychological studies have divided visual interpolation into two types, according to their differences in phenomenology. These two types are modal interpolation and amodal interpolation (Michotte, Thines & Crabbe, 1964/1991). In modal interpolation, objects that are interpolated have a sensory presence in areas that lack local specification. Modal interpolation occurs when portions of an object are camouflaged by an underlying surface that happens to project the same luminance and color as a nearer object, as shown in Figure 1A. In amodal interpolation, one perceives or registers unspecified parts of objects even though the relationships among the parts are hidden. The most ordinary amodal interpolation occurs when portions of an object are occluded by another object (Figure 1B). No matter which type of interpolation occurs in the early processing of visual cognition, images are recognized in late visual processing based on scattered and incomplete information. For example, as shown in Figure 1C, a letter “A” that is partially erased can be perceived using the precondition that it is an alphabetical image. However, it is unclear whether modal or amodal interpolation occurs in this case.

Figure 1.

Illustrations of visual interpolation. (A) Modal interpolation (Kanizsa triangle). A white triangle is perceived even though it is not drawn. (B) Amodal interpolation. A triangle is perceived despite partial occlusion by a disk. (C) Common incomplete object. The letter A is perceived from its fragments despite partial erasure.

978-1-60960-559-9.ch001.f01

We previously found that cortical activation in the frontal cortex and occipital cortex during incomplete-letter recognition was compared with complete-letter recognition using fNIRS (functional near-infrared spectroscopy). The findings demonstrated that the oxygenated hemoglobin concentration during the incomplete-letter recognition task was larger than the concentration during the complete-letter recognition task. Furthermore, significant differences in the oxygenated hemoglobin concentration were observed in the lateral prefrontal and occipital areas. These findings indicate that the lateral frontal cortex plays an important role in the recognition of incomplete objects.

We had previously used a quantitative method to measure visual interpolation ability (VIA) with partially erased letters (Jiang & Wang, 2007; 2008). This method may be used to evaluate the subtle decline in visual function of healthy subjects who show no cognitive impairment in conventional examinations. Leukoaraiosis (LA) has been found through neuroimaging and is caused by pathological changes such as demyelinization, gliosis, vessel lipohyalinosis, and disturbed blood-brain exchange (Breteler et al., 1994). Postmortem studies have indicated that LA is associated with degenerative changes in arterioles that are related to atherosclerosis (Hachinski, Potter & Merskey, 1987). This finding suggests that cerebral arteriosclerosis of the penetrating vessels is the main factor responsible for LA pathogenesis. However, a small extent of LA is frequently can be diagnosed in young people, although the pathogenic implications of these diagnoses remain unclear (Moody, Thore, Anstrom, Challa & Langefeld et al., 2004; Park, Yasuda, Toyonaga, Yamada & Nakabayashi et al., 2007). On the other hand, a large extent of LA diagnosed in elderly patients is well known to be caused by near infarcts that result in recurrent stroke and cognitive impairment, especially of the frontal lobe (Moody et al., 2004). In the present study, we used a novel VIA measurement method to determine whether the small extent of LA diagnosed in healthy middle-aged individuals affects visual cognitive function.

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