The field of neuropsychology
examines the relationship between central nervous system function and behavior,
often in cases of pathology. Scientists have long speculated on the links between cortical
function and impaired behavior, and in the past have relied on studies of gross
brain abnormality (e.g., the case of Phineas Gage) in order to gain insight into
this relationship. Studies of specific visual and auditory processes now
contribute considerably to our understanding of diseases and disorders that
involve central nervous system pathology. These
disorders include dyslexia, mental retardation, schizophrenia, and autism, as
well as progressive neurodegenerative disorders such as AlzheimerÝs disease,
ParkinsonÝs disease, and multiple sclerosis.
One challenge confronting
researchers in these areas is that many disorders show multiple behavioral
impairments. Most neurological
disorders have a characteristic profile of spared and impaired behavioral
abilities: some behaviors are relatively unaffected; others may be profoundly
affected. For many syndromes,
scientists still seek to identify the range of different behaviors that show
impairments, the relative magnitude of these impairments, and the cortical and
subcortical areas of the brain that may be affected.
Without the answers to the
questions above science cannot begin to understand and explain these
disabilities. Obviously there is a
great interest to society, as well. If
we know how and to what extent different behaviors are affected there may be
ways to help compensate or reduce the impact of an impairment. Perhaps much the
same way large-print books help the visually impaired.
Also, we may discover that specialized training may be able to reduce or
eliminate some perceptual impairments. There
is evidence that suggests that this may be true with dyslexia (Merzenich et al.,
Sensory psychologists have
contributed greatly to our understanding of these disorders. Because such a
large proportion of cerebral cortex is devoted to processing sensory
information, studies of sensation and perception offer a ýwindowţ into the
brain. The information gathered from these studies helps identify specific
sensory or perceptual impairments, helps infer the cortical locations of the
impairments, and helps move us towards thorough causal explanations.
As examples, we consider the cases of developmental dyslexia and
Dyslexia refers to a broad family of impairments.
Generally speaking, dyslexia is a term used to define a severe learning
problem that is unrelated to intellectual ability, emotional disturbance, gross
sensory or physical handicaps, sociocultural status, or insufficient schooling.
The most common type of dyslexa, specific reading disability (SRD)
involves difficulties in learning to read and write.
At present we lack clear agreement about the nature of dyslexia,
including its causes and symptomology. In
fact, a minority of investigators even propose that dyslexia simply represents
the lowest portion of the normal distribution of these abilities in the general
population, rather than a distinctive disorder (Shaywitz, Escobar,
Fletcher, & Makuch, 1992).
However, most researchers agree
that dyslexia probably results from abnormal neurodevelopment.
Psychophysical studies suggest problems that are neural in origin as do
anatomical studies of brain structure and physiological studies of neural
activity. Stein and Walsh (1997) provide a succinct and recent review.
SRD is a reading impairment and
children diagnosed with SRD are impaired in their abilities to auditorially
distinguish the small differences among phonemes, the smallest units of speech (Brunswick &
Rippon, 1994; Merzenich et al.,
Other verbal skills such as the rapid naming of objects and the ability
to break words down into smaller segments (i.e., cowboy to ýcowţ and
ýboyţ) are also impaired (Eden, Stein, Wood, & Wood;
A recent, systematic study of
the nature of phonological processing in dyslexia was conducted by Shaywitz et
al. (1998). Shaywitz et al.
(1998) required dyslexic readers and control
participants to perform a series of tasks, some of which required extensive
phonological processing and others that required very little.
While the participants engaged in these tasks, Shaywitz et al. used a
brain imaging technique called fMRI (functional magnetic resonance imaging) to
measure and map the pattern of neural activity in cerebral cortex.
Shaywitz et al. observed what they refer to as a ýneural signatureţ
of dyslexia: A pattern of neural overactivation in some areas of cortex and
underactivation in others. Some of
the affected areas include traditional language areas and traditional visual
ones. The authors interpret their
findings as evidence that dyslexia is primarily a phonological impairment, and
one that may involve a functional disruption of the mapping of the visual image
(the printed words) to phonology during reading.
These findings and this theory of dyslexia explain a large set of the
research findings in this area and may describe the most proximal cause of SRD.
There is considerable evidence
that children with SRD exhibit a set of visual perceptual problems that precede
this stage, however, and researchers are working to characterize their
relationship to SRD. Lovegrove, Garzia, & Nicholson (1990) provide a good
discussion of the early work in this area. A large literature now documents impairments in motion
perception (Cornelissen, Richardson, Mason, Fowler, & Stein,
1995; Eden et
al., 1996) contrast sensitivity (Borsting et al.,
1996; Cornelissen et al.,
Drasdo, & Richards, 1994), flicker sensitivity (Evans et al.,
1994), as well as other tasks that preferentially involve the magnocellular
Hogben, Clark, & Pratt, 1996).
Further support for visual perceptual correlates of SRD comes from a
recent study revealing a correlation between motion detection thresholds and
word reading performance in children without SRD (Cornelissen, Hansen,
Hutton, Evangelinou, & Stein, 1998).
Anatomical and physiological
abnormalities in the brain are associated with these behavioral abnormalities.
In individuals with dyslexia the magnocellular layers of the LGN have
been reported to be disordered and the cells themselves much smaller than normal
Drislane, & Galaburda, 1991).
Eden et al. (1996) used fMRI to reveal abnormal neural activity during
visual motion processing in adults with dyslexia.
In an attempt to explain the
range of perceptual and anatomical impairments that are associated with SRD,
investigators have recently suggested that dyslexia may be linked to a general
sensory temporal processing impairment (Farmer & Klein,
1995; Stein &
Walsh, 1997). That is, individuals
with SRD have difficulty in processing sensory information that is brief or that
changes rapidly over time. Studies
of visual perceptual abilities of children with SRD would be consistent with
this explanation, as well as studies that show that children with SRD have
difficulties with some non-verbal auditory perceptual tasks as well as verbal
Again, the role that
psychological research will play in understanding SRD will be large.
Psychological research will help identify the cause(s) of SRD by helping
to detail all the behaviors that are affected.
A thorough description of SRD is very helpful because it permits
researchers to eliminate alternative explanations of dyslexia that cannot
explain the profile of impairments. Psychological
research may also help find ways to compensate of help minimize the affect of
the impairment, for example, with specialized training.
Merzenich et al. (1996) report that children with learning disability can
improve their abilities to perceive speech and nonspeech auditory stimuli with
relatively little (8 to 16 hours) training.
Sensory psychologists have
typically investigated these impairments in contrast sensitivity using specialized stimuli
(e.g. sine wave gratings). Several undergraduate students working in one of our
laboratories decided to investigate how well children with SRD would perform
with more real-world stimuli, for example a visual acuity chart made up of high
and low contrast letters. These
students used a computer program designed in-house to test a group of children
with and without dyslexia on their abilities to read low and high contrast
Tumbling-E's. The Figures below show
of the stimuli used.
The Figures below show representations of the stimuli used.
Figure 19. The panel on the left shows E's that are black on a white background-they have high luminance contrast. The panel on the right shows E's that are gray on a white background-they have low luminance contrast.
The student's hypothesis, based on reports in the literature, was that
children with SRD would perform no differently than the children without SRD on
the high-contrast E's but have difficulty in correctly identifying the
The data collected are shown in
The data collected are shown in the Figures below.
Figure 20. Each graph shows proportion correct for the different size E's, shown as the Snellen acuity equivalent (the way your optometrist describes the size of the letters). The panel on the left shows the data for both groups of children when the E's were high contrast; the right panel for the low contrast stimuli.
Notice that there was no
difference in performance between groups when the letter contrast was high.
Both groups of children could see the large to small E's equally well.
In the right panel, however, you can see that when the contrast between
the letters and the background was reduced the performance for the children with
dyslexia was affected to a much larger extent. Our students had demonstrated
that the effects of reduced contrast apply to the critical stimuli present in
reading: individual letters (Ballew, Brooks, &
More importantly, special stimuli and conditions were not required to
observe the effects (see also Woods &
Studies of sensation and
perception have also contributed to our understanding of progressive
neurodegenerative disorders, such as AlzheimerÝs disease.
AlzheimerÝs disease is characterized by neuropathology (neurofibrillary
tangles and amyloid plaques in cerebral cortex) and behavioral impairment,
primarily progressive cognitive decline. To
the general public, AlzheimerÝs disease is a ýmemory disorder.ţ
AlzheimerÝs disease involves memory impairments, but it involves other
behavioral deficits as well. In
fact, according to the Diagnostic and Statistical Manual of Mental Disorders
(American Psychiatric Association DSM-IV, 1994) a diagnosis of AlzheimerÝs
disease (Dementia of the AlzheimerÝs type) requires the presence of
other non-memory related symptoms.
Early work suggested that the
sensory systems and general perceptual abilities were spared in AlzheimerÝs
disease. The initial observation
that primary visual cortex was relatively free of the plaques and tangles that
are characteristic of the disease and because visual acuity in AlzheimerÝs
patients was not significantly different from that typically observed in normal
aging supported this conclusion. Science,
in its thoroughness, continued to investigate and assess other cognitive and
noncognitive behaviors. As research
in the area continued and specific perceptual skills were assessed, however,
several visual and perceptual changes associated with AlzheimerÝs disease were
In addition to visual changes
that are a consequence of normal aging, AlzheimerÝs disease is now associated
with ganglion cell death in the retina (Blanks, Hinton,
Sadun, & Miller; 1989), a substantial degeneration of optic nerve fibers
& Miller, 1986), and cell loss in primary visual cortex (Hof & Morrison,
The association of visual
perceptual problems with AlzheimerÝs disease is now well documented.
Relative to age-matched controls, individuals with AlzheimerÝs disease
have been reported to have impairments in contrast sensitivity (Bassi, Solomon,
& Young, 1993; Gilmore & Whitehouse,
1995), blue-yellow color
Suguira, Corkin, & Growdon, 1993), depth
perception (Mittenburg, Malloy,
Petrick, & Knee, 1993) and motion perception (Gilmore,
Wenk, Naylor, & Koss, 1994). The
extent of the visual problems in AlzheimerÝs disease has led many
investigators to consider the visual sequelae one of the hallmarks of the
disease. In fact, some investigators have reported that AlzheimerÝs
disease may have its origin in the visual sensory pathways (Gilmore &
Importantly, research in visual
perception may have helped identify a set of new diagnostic tools. There is
evidence that in AlzheimerÝs disease the perceptual impairments may present before
many of the cognitive impairments. Some individuals with AlzheimerÝs disease
report consulting their optometrist or ophthalmologist concerning a vision
problem before memory or cognitive impairments became evident (Kiyosawa et al.,
1989). Researchers are currently investigating the extent to which visual
perceptual tests may be used clinically to help identify AlzheimerÝs disease
and other progressive neuropathologies in their earliest stages.