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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5253_Библиотеки_им_академика_М_И_Перельмана.pdf
Qian & Bi
(2014)
66
26 dyslexic & 27 control
children
Age & IQ
CDM
Yes
Yes
Gori et al.
(2016)
67
Study 1
15 dyslexic, 18 age-matched,
13 reading-matched children
Age or RA only
CDM
Yes
Gori et al.
(2016)
67
Study 2 (pre-
readers)
12 RD & 60 control children
Age & IQ
CDM
Yes
Yes, from
additional studies
on treatment
Joo et al.
(2017)
68
48 children, 20 of whom
received reading intervention
CDM
Yes
No
Rodrigues et al.
(2017)
69
33 dyslexic & 34 control
children
Age & IQ,
excluded ADHD
Speed discrimination, CS
(3.5 cpd)
Yes
Flint & Pammer
(2019)
70
10 dyslexic, 10 semi-literate,
10 illiterate, 10 control adults
Age
CDM, CFM, FDT
Yes, M-D
deficit in
dyslexia, not
in illiterate
Piotrowska &
Willis (2019)
71
Cross-sectional, 132
unselected children
Controlled for
age & IQ
CDM, CFM
Yes, for
CDM not
CFM
No; best predictor
of reading is
phonological
awareness
Contemori et
al. (2019)
72
19 dyslexic &19 control
children
Age
Flicker detection
No; argue
for problem
in
magno/parv
o balance
Chapter 5 The magnocellular-dorsal (M-D) deficit and associated theories
119
Ciavarelli et al.
(2021)
73
27 dyslexic & 23 control
children
Age
Motion discrimination
No; argue
for
inefficient
magno-
parvo
coactivation
Vilhena et al.
(2021)
74
62 dyslexic & 62 control
children/adults
Age, sex, VA
FDT
Yes
Manning et al.
(2021)
75
50 dyslexic & 50 control
children
Age
CDM, direction
integration, EEG
Yes (at later
processing
stages)
Stein (2021)
76
68 dyslexic & 88 control
adults
Age,
socioeconomic
status
VEP
Yes
Lazaro et al.
(2021)
77
10 dyslexic children &
adolescents
Within-subjects
design
CDM
Yes
Mascheretti et
al. (2021)
78
25 dyslexic & 24 control
children
Age (groups
differed in sex
ratio & IQ)
CDM & gratings
fMRI with multiple kernel
learning
Yes
Suggestive;
correlational
association
Ebrahimi et al.
(2022)
79
30 dyslexic children
randomly allocated to M-D
based visual motion training
or computer games
Age, IQ,
educational
level, reading,
CDM
CDM
Yes
Yes
Liu et al
(2022)
80
14 dyslexic & 22 control
children
Age (groups
differed in IQ)
CDM, fMRI
Yes
Yes
Vision, Reading Difficulties and Visual Stress
120
Manning et al.
(2022)
81
48 dyslexic & 48 control
children
Age
CDM
Yes
Meng et al.
(2022)
82
13 dyslexic & 13 control
children
Age (groups
differed in IQ)
VEP
Yes
Santoni et al.
(2023)
83
26 dyslexic & 31 control
adults
Age, IQ (groups
differed in sex
ratio)
VEP
Yes
Turri et al.
(2023)
84
26 dyslexic & 31 control
adults
Age, IQ (groups
differed in sex
ratio)
EEG
Yes
*ADHD, attention deficit/hyperactivity disorder; CDM, coherent dot motion; CFM, coherent form motion; CPD, cycles per
degree; CS, contrast sensitivity; CSF, contrast sensitivity function; EEG, electroencephalogram; FDT, frequency doubling
(illusion) technology; fMRI, functional magnetic resonance imaging; IQ, intelligence quotient; RA, reading age; RD, reading
difficulty; VA, visual acuity; VEP, visual evoked potentials. Studies are case control studies, unless otherwise stated. The
final two columns only include an entry when the study addressed the issue in the column heading.
Chapter 5 The magnocellular-dorsal (M-D) deficit and associated theories
121
Is a M-D deficit associated with reading difficulty?
A review in 2001 summarised a large body of research indicating
that up to two thirds of people with dyslexia have a deficit of the M-D
subsystem.85 Many more recent publications have supported this
association (not all finding such a high prevalence),
11 32 39 44-46 48 49 51 53-55
61-71 74-76 86
although others have not supported the M-D deficit
hypothesis.
33 34 42 43 47 50 52 56-58 60 72 73 87-89
There is some evidence, in both
dyslexia and autism,90 that the M-D visual deficit is associated with
timing or temporal functions in modalities other than vision (e.g.
auditory),
41 91
although some data do not support this.53 In contrast,
Heim and colleagues indicated that there is a temporal processing
deficit in the auditory but not in the visual modality.43 One study that
did find impaired cross-modal temporal processing in dyslexia noted
that the deficit was so subtle that it was unlikely to be causally related
to the dyslexia.48
Stein recently further developed the M-D deficit hypothesis, linking
temporal processing by M-type neurons not only in the visual and
auditory systems, but also in somatosensory, proprioceptive, and
motor systems.92 Another research group argues, dyslexia is
associated with a limitation in the balance between magno and parvo
processing,72 reframed as the magnocellular-parvocellular coactivation
hypothesis.73 Most recent reviews support the M-D deficit hypothesis
in dyslexia.
2 93
One study found the M-D deficit only in the dysphoneidectic
subtype of dyslexia,39 but another study found the M-D deficit appears
to have a similar prevalence in the three main subtypes of dyslexia
(dysphonetic, dyseidectic, mixed; see Chapter 1).44
Visual stress is a separate disorder that sometimes coexists with
dyslexia (Chapter 1) and visual stress is often alleviated by coloured
Vision, Reading Difficulties and Visual Stress
122
filters (Chapters 6-9). Stein and colleagues have hypothesised that
yellow filters ‘boost the M-D system’ by reducing inhibition from short-
wavelength cones,
94 95
although this has been disputed96 and is not
supported by data from Kuba and colleagues.97 When Stein and
colleagues attempted to test the effect of yellow filters using blue filters
as a control, they found that some participants benefitted more from
the blue.98 Their findings may be explained by visual stress, and greater
beneficial effects may have been found if they had coloured the lenses
according to individual needs (Chapter 7). Visual stress itself is not
explained by the M-D deficit: several studies have shown M-D function
to be normal in most people with visual stress.
60 99-102
The one study
that has found a correlation between visual stress and M-D function
studied an unselected sample (not selected, for example, for reading
difficulties). The authors considered their findings could be explained
by the M-D test (coherent motion) causing symptoms of visual stress.
103
Putative mechanisms for the benefit from coloured filters in visual
stress are discussed in Chapter 8.
Evans and colleagues in 1994 compared the results of two tests that
had been used to measure M-D function in dyslexia and found only a
modest correlation between the results of the two tests.9 More recent
studies support this finding,
11 55 62
which has been attributed to the
possibility that different tests detect different types of the so-called M-
D deficit, which may contribute to different aspects of reading skills.
55
62 82
For example, Wilmer and colleagues found that a deficit in
coherent motion is associated with low accuracy at reading tests, and
a deficit in discriminating velocities is linked with slow performance at
reading tests.55 Tests of motion perception are often used to
investigate the M-D deficit, and one study indicates that a deficit in
performance with this test is associated with a particular gene deletion
which occurs in a subset of dyslexics.
104
More recently, dyslexic
populations have been found to have deficits in speed discrimination
Chapter 5 The magnocellular-dorsal (M-D) deficit and associated theories
123
and achromatic contrast sensitivity, both attributed to the M-D
system.69
Sperling and colleagues noted that studies identifying a M-D deficit
often use stimuli on computer displays (e.g., coherent motion tasks)
involving a considerable amount of “visual noise” (like television
static).56 They hypothesised that the underlying problem these
experiments detect is not a M-D deficit, but a deficit in noise exclusion.
They presented experimental evidence supporting this hypothesis.
56 57
However, some of the early research that found evidence for a M-D
deficit used stimuli that were free of visual noise (Table 5.2),
9 105 106
and
more recent research has not supported Sperling’s hypothesis.
67 75
Nonetheless, it is interesting to note that some evidence indicating
elevated background visual noise is associated with symptoms of
inattention in attention deficit disorder.
107
It has been hypothesised by
Hancock and colleagues that increased neuronal noise may be a
biological mechanism for dyslexia.
108
Hancock et al.
108
attribute
increased noise to cortical hyperexcitability, which has been found to
be associated with the benefit from coloured filters experienced by
some people with dyslexia (Chapter 8) and with neurological disorders
(Chapter 11). Recent research has provided further support for the
increased neuronal noise hypothesis.81
Does a M-D deficit cause reading difficulty?
A multiple case-study of dyslexic children concluded that the M-D
deficit may actually be quite rare in dyslexia, be unrelated to visual
stress, and be unlikely to be causally related to the poor reading.60
However this study only included 23 dyslexic and 22 control children.
It was at one time argued that a M-D deficit might impair reading
because the M-D system was failing to inhibit the parvo system during
saccades,
109 110
but this hypothesis has since been disconfirmed.
111
Vision, Reading Difficulties and Visual Stress
124
Another hypothesis, that the M-D deficit might contribute causally to
poor reading by causing saccadic dysfunction,
112
has also not been
supported by more recent research.58 The M-D deficit appears to co-
occur with a phonological deficit in dyslexia.26
Evans and colleagues found the M-D deficit in dyslexia (assessed
with a flicker detection task) was not associated with impaired
performance at a visual search task.9 Iles and colleagues showed that
dyslexic participants with a M-D deficit performed more poorly at serial
but not parallel search.
113
The M-D deficit has been associated with
reading and spelling errors that might be expected to result from visual
confusions.
36 37 41 53
The M-D deficit is correlated with binocular
instability (Figure 5.2),
114 115
and it is therefore possible that it is the
binocular instability that accounts for these visual confusions rather
than the M-D deficit per se.
116
Stein has argued that the M-D system
plays a key role in the first stage of control of convergence eye
movement.92
Figure 5.2. Graph showing the relationship, in a group of dyslexic children,
whereby worse flicker perception (taken as a sign of a M-D deficit) is
associated with low vergence amplitude (a sign of binocular instability).
-2.4
-2.5
-2.6
-2.7
-2.8
0
10
20
30
40
50
Log Flicker Threshold
Vergence Amplitude
Chapter 5 The magnocellular-dorsal (M-D) deficit and associated theories
125
Reproduced with permission from Evans et al. (1993, 1996).
115 116
Kevan and Pammer measured M-D function, using coherent motion
and the frequency doubling technique, in children at familial risk of
dyslexia before they commence reading instruction.63 The M-D deficit
was present before learning to read, indicating the deficit is unlikely to
result from lack of reading experience.63 Other research supports the
view that the M-D deficit is not a direct cause of reading disability, but
could be a contributory factor in some cases.
61 64
Ben-Yehudah and
colleagues found that some tasks which have been used to
demonstrate an M-D deficit in dyslexia only detect an abnormality
when they require sequential comparisons and suggest this may result
from deficits in visual perception or in visual memory.
45 117
Olulade and colleagues, in a sophisticated study involving fMRI, a
test of motion perception and an evaluation of changes following
reading training (tutoring), concluded the M-D visual deficit is a
consequence and not a cause of poor reading in dyslexia.65 This
conflicts with some of the earlier work cited above. Stein interpreted
the findings of Olulade et al. as showing that motion sensitivity is a
likely cause of poor reading and considers the cerebellum as “almost
part of the M-D system”.
92 98
Joo and colleagues reject both viewpoints
(see below).68
Evidence of the M-D deficit (see Table 5.2) has been found in
Chinese dyslexic children,66 and associated with impaired recognition
of orthographic Chinese characters.
66 118
This is consistent with a causal
role, and a fMRI study has linked orthographic awareness in Chinese
children with the M-D pathway.
119
Flint and Pammer, sought evidence of a M-D deficit in dyslexic
adults compared with normal, illiterate, and semi-literate readers.70
Only the dyslexic readers showed a M-D deficit, and it was therefore
Vision, Reading Difficulties and Visual Stress
126
concluded that the M-D deficit was not a consequence of failing to learn
to read. This study supports a causal role for the M-D deficit.70
Piotrowska and Willis evaluated M-D function alongside several
other functions that have been implicated as possible causes of
dyslexia (e.g., phonological awareness, processing speed, and working
memory) in a large sample of dyslexic children.71 Although there was
evidence of a M-D deficit (a lower sensitivity to global motion), this only
accounted for 3% of the variance in reading scores. The best predictors
of reading performance were phonological awareness, non-verbal
intelligence, and socio-economic status. The authors stressed the
importance of controlling for confounding variables and concluded,
dyslexia encompasses a range of profiles related to a range of possible
risk factors, symptoms, and underlying brain mechanisms.71
Ebrahimi and colleagues selected small groups of poor readers with
a M-D deficit and compared a treatment designed to train M-D function
with a control treatment.
120
Although the conclusions were interpreted
as supporting a causal role for an M-D deficit, the control treatment
seemed to be a poor match for the experimental treatment, and the
researchers were not masked.
In normal readers, Bellocchi and Leclercq found evidence of an
association between reading skills and M-D function in early readers
but not in older children.
121
The researchers suggested that efficient
visual magnocellular functioning is important in order to develop good
decoding skills in the early stages of learning to read, possibly because
early reading places high demands on visuo-attentional processing.
Although the above evidence is generally convergent in showing
that a proportion of dyslexic people have a deficit of the M-D visual
system, there is little evidence that the deficit is specific to dyslexia. An
M-D deficit also occurs in several diseases, including glaucoma,
8 122
diabetes,
123
retinitis pigmentosa,
124
and migraine.
125
However, in these
Chapter 5 The magnocellular-dorsal (M-D) deficit and associated theories
127
conditions the M-D deficit is probably not present when the child is
learning to read: in contrast, a M-D deficit has been found in pre-
readers at familial risk of dyslexia.63 In a longitudinal study, Gori and
colleagues found that in pre-readers impaired motion perception,
believed to indicate a M-D deficit, predicts future reading
development.67 This is suggestive of a causal relationship.
A study designed to address causality supported the view that the
M-D deficit, as assessed by motion sensitivity, is not a main cause of
dyslexia, or caused by dyslexia, but the two correlates may be indirectly
related through another common mechanism (e.g., genetic).68
Alternatively, poor motion processing is just one of many factors that
contribute to reading difficulties.68 Ciavarelli and colleagues suggested
that, rather than a causal relationship between vision and reading,
both tasks rely on similar neuro-modulatory resources that are
abnormal in dyslexia (an excitatory-inhibitory imbalance).73
A functional MRI study by Liu and colleagues in 2022 found that
activation of the left area V5/MT+ and right posterior parietal cortex
was weaker in dyslexic children than in a control group.80 M-D activity
in good readers (but not the dyslexic group) was linked to orthographic
awareness.
There is little evidence for a double dissociation: some patients with
parvo deficits and some with M-D deficits, each having different
profiles of disability. Without such a double dissociation it remains
possible that M-D deficits reflect damage to a relatively fragile part of
the visual system (larger magno cells have greater metabolic demand),
and that such damage can occur in a variety of retinal and neurological
conditions.
Some authors have assumed that symptoms such as eyestrain,
headaches,
126
and words and letters appearing to move92 result from
the M-D deficit, but there appears to be no strong evidence to support
Vision, Reading Difficulties and Visual Stress
128
this notion.