close

Вход

Забыли?

вход по аккаунту

?

Diminished auditory mismatch fields in dyslexic adults.

код для вставкиСкачать
ORIGINAL ARTICLES
Diminished Auditory Mismatch Fields
in Dyslexic Adults
Hanna Renvall, MD,1 and Riitta Hari, MD, PhD1,2
Electroencephalographic studies have demonstrated smaller auditory responses to infrequent deviances of speech and
nonspeech sounds in dyslexic than normal-reading subjects. We used a whole-scalp neuromagnetometer to study selectively reactivity of the auditory cortices to sound deviances in 8 dyslexic and 11 normal-reading adults. Within a monotonous sequence of 50-millisecond 1,000Hz binaural tones, tones of 920 and 1,080Hz occurred with 7% probability
each. Magnetic mismatch fields, elicited by the stimulus deviances, were diminished in the left hemisphere of the dyslexic
subjects. The results indicate deficient change detection in the left auditory cortex of right-handed dyslexic adults.
Ann Neurol 2003;53:551–557
Developmental dyslexia, also called specific reading impairment, is a common neurocognitive disorder that
has been associated convincingly with a deficit in phonological processing.1–3 At the same time, growing evidence of mild sensory and motor deficits in many dyslexic subjects has gained increasing interest. For
example, the phonological processing deficit has been
proposed to derive, at least in part, from a more general auditory dysfunction, manifested as impaired temporal processing of sounds.4 Finnish dyslexic adults are
slow in processing successive binaural sounds in an auditory illusion task5 as well as sounds of two different
pitches in a streaming task,6 suggesting that they have
a prolonged short-term “cognitive window”7 or “input
chunk”8 within which the subsequent stimuli may interfere. We have earlier suggested that such prolongation could distort processing of rapid stimulus sequences and the proper development of cortical
representations needed for reading acquisition.8
Abrupt sounds alert the subject and elicit in her auditory cortices transient responses that can be studied
selectively with magnetoencephalography (MEG).9 Recent MEG recordings have shown diminished reactivity in dyslexic adults to rapidly presented auditory
stimuli and to acoustic changes.10,11 Infrequent deviant
sounds, occurring randomly among otherwise monotonous auditory stimulation and differing from them in
various physical parameters, elicit mismatch responses
in electroencephalographic and MEG recordings (for
reviews, see Näätänen12 and Alho13). The mismatch
From the 1Brain Research Unit, Low Temperature Laboratory, Helsinki University of Technology, Espoo; and 2Division of Clinical
Neurophysiology, Helsinki University Central Hospital, Helsinki,
Finland.
Received May 9, 2002, and in revised form Nov 14. Accepted for
publication Dec 5, 2002.
responses are elicited without subject’s attention to the
auditory stimuli. The electric mismatch negativity
(MMN) responses to frequency deviants are smaller in
dysphasic children than in age-matched controls.14
Similarly, impaired behavioral discrimination of /da/
versus /ga/ syllables is associated to diminished MMN
amplitudes in children who suffer from language learning impairment (LLI).15 Although dyslexia is considered a deficit distinct from LLI, these disorders show a
considerable overlap.16 Results from dyslexic subjects
are somewhat contradictory: diminished MMNs have
been found either only to speech sounds,17,18 or to
nonspeech stimuli as well.19,20
The magnetic mismatch fields (MMFs) are generated in the supratemporal auditory cortices.21,22 MEG
can provide accurate information on, for example, interhemispheric differences in cortical reactivity to stimulus changes.9,22 We therefore used a whole-scalp neuromagnetometer to record MMFs to frequency
deviants in a group of Finnish adults with developmental dyslexia. Preliminary results have been presented in
an abstract form.23
Subjects and Methods
We studied, with informed consent, 8 adult dyslexic subjects
(mean ⫾ SEM age 30 ⫾ 2 years; 5 female, 3 male subjects;
all right-handed) and 11 healthy control subjects (29 ⫾ 2
years; 6 female, 5 male subjects; one ambidextrous, 10 righthanded). MEG responses were initially recorded from 10
dyslexic and 13 control subjects but the data of two dyslexic
Address correspondence to Dr Renvall, Brain Research Unit, Low
Temperature Laboratory, Helsinki University of Technology, P.O.
Box 2200, FIN-02015 HUT, Espoo, Finland.
E-mail: hanna@neuro.hut.fi
© 2003 Wiley-Liss, Inc.
551
and two control subjects were discarded due to bad signalto-noise ratio. The dyslexic subjects were selected on the basis of a definite childhood history of difficulties in learning to
read: all subjects had a diagnosis of developmental dyslexia
stated by a psychologist, a speech therapist, or a special educational teacher, and five subjects had participated in special
tutoring at school age. The lowest level of education in the
dyslexic subjects was 11 years; one subject had a university
degree, one was studying toward one, two were studying for
an academic-level professional degree, and the others had
successfully finished vocational education.
All subjects performed five reading-related behavioral tasks
before the MEG recordings. In the oral-reading task, the
subject had to quickly read aloud a Finnish story, and the
reading speed was measured during 1 minute in the middle
of the task. In a computerized word recognition task, the
subject had to decide, as fast as possible, whether a word
presented on a computer screen was a real Finnish word or
an orthographically legal pseudoword. Correctly recognized
words were used for calculating the word recognition speed.
Naming speed was measured with a 5 ⫻ 10 matrix consisting of numbers, letters, and colors. Working memory was
tested with digit spans forward and backward by using the
standard WAIS procedure.24 These tests have been widely
applied previously in our laboratory to clarify the behavioral
differences between subject groups.
During MEG recordings, sounds were led to the subject
binaurally through plastic tubes and earpieces. The oddball
sequence consisted of three tones of 50-msec duration (including 10msec rise and fall times) with interstimulus interval (ISI from onset to onset) of 0.5 seconds. The standard
stimuli, 86% of all, were 1,000Hz in frequency, and the two
deviant stimuli, each with probability of 7%, were of 920
and 1,080Hz. Sound intensity was adjusted to be at a comfortable listening level (65–70dB sound pressure level). The
subject was instructed to ignore the sounds, and all subjects
except one read a self-chosen text during the measurement to
maintain the level of vigilance as stable as possible; the only
(dyslexic) subject who did not read was carefully instructed
to ignore the sounds.
Whole-scalp neuromagnetic signals were measured in a
magnetically shielded room, while the subject was sitting
with the head supported against the helmet-shaped bottom
of the Neuromag-122 magnetometer.25 The device comprises 122 planar first-order SQUID (Superconducting
QUantum Interference Device) gradiometers covering the
whole scalp. Each sensor unit measures two orthogonal tangential derivatives of the magnetic field component Bz normal to the helmet surface. Such gradiometers detect the largest signal just above the activated brain area. Four headposition-indicator coils were attached to the scalp, and their
positions were measured with a three-dimensional digitizer;
the two periauricular points and the nasion specified the
head coordinate frame. The head position with respect to the
sensor array was determined by feeding current to the marker
coils. The recording passband was 0.03 to 100Hz, and the
data were digitized at 300Hz. The averaged signals were digitally low-pass filtered at 40Hz. Vertical electrooculogram
was recorded to discard traces contaminated by eye blinks
and movements. A minimum of 100 responses was averaged
for each deviant.
552
Annals of Neurology
Vol 53
No 5
May 2003
The MMFs were examined by subtracting the responses to
standard sounds from those to deviants. To locate the cerebral sources of the responses, we searched equivalent current
dipoles (ECDs) by a least-squares fit to the data.26 The initial ECDs, one for each hemisphere, were calculated from
subtraction waveforms measured by a subset of 10 to 16
channels over the temporal lobes. An ECD represents the
location, orientation, and strength of current flow in the activated brain area. Only ECDs explaining more than 80% of
the field variance during the MMF peak were accepted for
further analysis. The analysis was extended to the entire time
period, and all channels were taken into account: the previously found ECDs were kept fixed in orientation and location while their strengths were allowed to change. Only dipoles with peak values exceeding at least twice the 50 to 100msec prestimulus root mean square noise (typically 1–
3 nAm) were accepted for further analysis. If no dipole could
be fitted, the prestimulus noise was used as the amplitude
value. The MMF sources were searched separately for both
deviants. In six control and two dyslexic subjects, the best
explanation was obtained by applying the same ECDs for
both deviants.
The sources of the 50msec (P50m) and 100msec
(N100m) deflections were searched for responses elicited by
the standard stimuli; in general, P50m was more prominent
than the N100m response, most likely because of the short
ISI used. All response latencies were measured from the
source waveforms. The hemispheric lateralization of responses was quantified by calculating the lateralization index
(LI) of source strengths between the right (R) and left (L)
hemispheres: LI ⫽ (R ⫺ L)/(R ⫹ L). LI value ranges from
⫺1 (left only) to 1 (right only); the 0 value refers to hemispheric symmetry.
The results were visualized by using the L1 minimum
current estimate method. Minimum current estimate presents the current distribution in which the total sum of
current amplitudes is as small as possible.27 The method
does not require any explicit a priori information about the
number of active brain areas,27 and the results have been
shown to agree with those obtained by multidipole modeling.27,28
The source strengths between the groups were compared
with mixed-model analysis of variance (within-subjects factors hemisphere and deviant frequency). The effect of hemisphere was tested also within each group using repeated measures analysis of variance. Two-tailed Student’s t tests were
used for statistical comparisons of lateralization indices, response latencies, and of the behavioral data. Lateralization
indices were compared between groups with Mann–Whitney
U test.
Results
Behavioral Tasks
The dyslexic subjects were significantly slower than the
control subjects in reading (t test; mean ⫾ SEM 607 ⫾
36msec/word vs 390 ⫾ 12msec/word; p ⬍ 0.001), and
their word recognition times were longer (826 ⫾
62msec vs 516 ⫾ 12msec; p ⬍ 0.002). The dyslexic
subjects were also significantly slower in naming colors,
letters, and numbers (677 ⫾ 56msec/item vs 492 ⫾
26msec/item; p ⬍ 0.02), and they had shorter backward
digit span (4.5 ⫾ 0.5 vs 6.5 ⫾ 0.5; p ⬍ 0.02). Figure 1
depicts the average times to recognize versus read aloud
one Finnish word in our control and dyslexic subjects.
Magnetoencephalographic Responses
Figure 2 depicts auditory evoked fields of the Control
Subject C4 to 920Hz deviant stimuli (top) and the
responses to all stimuli in Control Subjects C4 and
C9 and in Dyslexic Subjects D3 and D4 at channels
showing the largest responses over both hemispheres
(bottom). The MMFs are shown below the response
waveforms. The standard sounds elicited P50m and
N100m responses in these four subjects, with average
peak latencies at 57 and 102msec, respectively, in the
left hemisphere (LH), and at 54 and 96msec in the
right hemisphere (RH). Because of the short ISI, responses were rather small. The deviant stimuli elicited
responses that first followed those to the standard
stimuli but then deviated in both hemispheres, with
peaks on average at 166msec (LH) and at 172msec
(RH).
In both Control Subjects C4 and C9, MMFs were
prominent in both hemispheres, but stronger in the
right than in the left. In the Dyslexic Subject D3,
MMF was prominent to 920Hz and detectable to
1,080Hz stimuli in the RH, but undetectable in the
LH. In Subject D4, MMFs were again clear in the RH,
but very small in the LH.
Figure 3 illustrates the minimum current estimates
of the MMFs for Control Subject C11 and for Dyslexic Subject D3 to 920Hz deviants. In the time win-
Fig 1. The time to recognize versus to read aloud a Finnish
word in dyslexic and control subjects. (filled circles) Dyslexic
subjects; (open circles) control subjects; ms ⫽ millisecond.
dow of 145 to 165 milliseconds, the activation in the
RH is evident in both subjects, whereas LH activation
is visible only in the control subject.
The MMF responses were adequately explained by
two ECDs, one in the left and the other in the right
supratemporal auditory cortex. Figure 4 shows the current dipoles of Control Subject C11, superimposed on
his magnetic resonance images, and the corresponding
MMF source waveforms as a function of time. For
both deviants, the MMFs were prominent in both
hemispheres.
Figure 5 shows the mean (⫾SEM) source strengths
of MMFs in both groups. MMFs were of similar
strength to the two deviants in both hemispheres. In
control subjects, the source strengths did not differ between the hemispheres ( p ⫽ 0.22), but in the dyslexic
group the sources were significantly weaker in the left
than in the right hemisphere ( p ⬍ 0.01). In five dyslexic subjects, the LH responses were so small that no
dipole could be fitted whereas the same was true only
for one control subject. Between groups, MMFs were
significantly smaller in dyslexic subjects than in controls in the LH ( p ⬍ 0.03). The latencies did not differ between groups in either hemisphere (Table).
Figure 6 illustrates the lateralization indices of
MMFs in all subjects. The LIs of control subjects were
symmetrically distributed along the left–right axis
(mean ⫾ SEM, 0.13 ⫾ 0.11; p ⫽ 0.24 compared with
zero), whereas in dyslexic subjects, the LIs were clustered closer to the right end of the axis (0.55 ⫾ 0.12;
p ⬍ 0.004). The distributions of the dyslexic and control subjects differed statistically significantly ( p ⬍
0.02, Mann–Whitney U test).
The P50m latencies and amplitudes did not differ
between the groups or hemispheres.
Discussion
Hemispheric Lateralization
Our MEG recordings showed markedly weaker reactivity of the left auditory cortex of dyslexic than normalreading adults to infrequent changes in tone pitch. Although this type of interhemispheric differences have
not been reported earlier in adult dyslexic subjects, infants with genetically elevated risk for dyslexia have
smaller MMN responses in the left than the right
hemisphere to duration changes within sounds (/atta/
vs /ata/).29
Several studies have shown abnormal hemispheric
balance in the visual and auditory areas of dyslexic
brains.30 –33 For example, symmetry instead of the normal left dominance of planum temporale has been reported frequently (for a recent review, see ref. 34), and
the auditory medial geniculate nucleus is anomalous in
a left-hemisphere–dominant manner in dyslexic subjects.35 In addition, reduction of gray matter within
Renvall and Hari: Mismatch Fields in Dyslexia
553
Fig 2. (top) Auditory evoked fields to
920-Hz deviant stimuli in one control subject. In each channel pair, the upper trace
illustrates the field derivative along the latitude and the lower trace along the longitude. (bottom) Evoked responses to all stimuli and the MMFs, that is, curves obtained
by subtracting the standard waveforms from
those obtained for deviants, at one channel
in the left and right hemisphere for two
control and two dyslexic subjects. AEF ⫽
auditory evoked field; MMF ⫽ magnetic
mismatch field; ms ⫽ millisecond.
the temporal lobe,36 as well as developmental anomalies affecting inferior frontal and superior temporal regions30 are predominant in the left hemisphere. We
cannot rule out possible anatomical abnormalities in
our dyslexic subjects, because magnetic resonance images were available for only one of them.
In our recent MEG study, 100msec auditory cortical
responses were less reactive to acoustical changes in
noise/square-wave sequences in dyslexic than normalreading subjects in both hemispheres.11 In addition,
several other imaging studies37–39 have shown differences between dyslexic subjects and normal readers in
both hemispheres. It remains to be seen whether the
554
Annals of Neurology
Vol 53
No 5
May 2003
MMF responses in dyslexic subjects would diminish
also in the right auditory cortex if smaller frequency
deviances were used.
Reasons for Diminished Mismatch Responses
Typically the 100msec responses increase and MMFs
decrease when the ISI is prolonged.40 Nagarajan and
colleagues10 found smaller 100msec responses to the
second sound of a pair at short intersound intervals in
dyslexic than in normal-reading adults, suggesting prolonged poststimulus suppression and prolongation of
the auditory recovery cycle. Similarly, the smaller
MMFs in dyslexic subjects could be related to a defi-
of dyslexic subjects thus could agree with weakened
bottom-up attentional capture.
Several studies have provided evidence for a magno-
Fig 3. Minimum current estimates for MMFs to 920Hz deviant stimuli in Control Subject C11 and Dyslexic Subject D3
in the time window of 145 to 165 milliseconds.
cient buildup or more rapid fading of the memory
trace. This view is in line with a recent MEG study
demonstrating that whereas 100msec responses to the
second tone of a pair are enhanced at intersound intervals of less than 300msec in normal-reading subjects, the
enhancement effect decreased significantly earlier in dyslexic subjects.41
The mismatch responses, elicited even without attention to the stimuli, are likely to reflect automatic
change detection in the auditory cortex.13 Thereby
they probably depend on neuronal mechanisms that
form the prerequisite for stimulus-driven attentional
capture. Diminished MMFs in the left auditory cortex
Fig 4. (top) Magnetic mismatch field source strengths as a
function of time in Control Subject C11 for 920Hz (continuous line) and 1,080Hz (dotted line) deviant tones. (bottom)
Locations (dots) and the orientations (bar) of the current dipoles used to model the responses superimposed on subject’s
magnetic resonance images. LH ⫽ left hemisphere; RH ⫽
right hemisphere; ms ⫽ millisecond.
‹
Table. Mean (⫾SEM) Latencies and Amplitudes of the P50m Response and of the Magnetic Mismatch Field
Left Hemisphere
Response
P50m
Latencies (msec)
Amplitudes (nAm)
Magnetic mismatch field
Latencies (msec)
920Hz
1,080Hz
Amplitudes (nAm)
920Hz
1,080Hz
Right Hemisphere
Control
Dyslexic
Control
Dyslexic
58 ⫾ 3
8.7 ⫾ 1.2
56 ⫾ 7
7.4 ⫾ 2.0
54 ⫾ 3
7.4 ⫾ 1.3
52 ⫾ 7
8.4 ⫾ 1.5
160 ⫾ 9
170 ⫾ 10
161 ⫾ 15
167 ⫾ 22
167 ⫾ 8
167 ⫾ 9
163 ⫾ 9
179 ⫾ 13
14.3 ⫾ 3.2
12.7 ⫾ 3.2
5.4 ⫾ 1.8
3.4 ⫾ 1.1
18.6 ⫾ 3.4
17.6 ⫾ 3.8
18.1 ⫾ 3.7
13.4 ⫾ 2.1
Renvall and Hari: Mismatch Fields in Dyslexia
555
Fig 5. The magnetic mismatch field source strengths to both
deviant stimuli.
Fig 6. The lateralization indices in both subject groups. The
responses to the two deviants were averaged before lateralization index calculation.
cellular (M) deficit in dyslexic subjects (for reviews, see
Stein and Walsh42 and Habib43). Although debated,
the M-deficit has been attributed to the variable sensory symptoms encountered in dyslexic subjects. In the
visual modality, M-system is crucial for proper attention capturing,44 and dyslexic adults are sluggish in
such tasks.45 One future challenge would be to explore
the relationship between the attentional deficit and the
sensory-specific cortical processing and to clarify their
roles in various sensory and reading-related tasks sensitive to dyslexia.
To conclude, our recordings in dyslexic adults demonstrate weakened reactivity of the left auditory cortex
to infrequent pitch changes, a finding likely to indicate
defective prerequisites for stimus-driven auditory attention.
References
1. Bradley L, Bryant PE. Categorizing sounds and learning to
read—a causal connection. Nature 1983;301:419 – 421.
2. Liberman IY, Shankweiler D. Phonology and the problems of
learning to read and write. Remed Spec Educ 1985;6:8 –17.
3. Frith U, Frith C. Modularity of mind and phonological deficit.
In: von Euler C, Lundberg I, Llinas R, eds. Basic mechanisms
in cognition and language with special reference to phonological problems in dyslexia. Amsterdam: Elsevier, 1998:3–17.
4. Tallal P. Auditory temporal perception, phonics, and reading
disabilities in children. Brain Lang 1980;9:182–198.
556
Annals of Neurology
Vol 53
No 5
May 2003
5. Hari R, Kiesilä P. Deficit of temporal auditory processing in
dyslexic adults. Neurosci Lett 1996;205:138 –140.
6. Helenius P, Uutela K, Hari R. Auditory stream segregation in
dyslexic adults. Brain 1999;122:907–913.
7. Cutting JE, Pisoni DB. An information-processing approach to
speech perception. In: Kavanagh J, Strange W, eds. Speech and
language in the laboratory, school and clinic. Cambridge: MIT
Press, 1978:38 –72.
8. Hari R, Renvall H. Impaired processing of rapid stimulus sequences in dyslexia. Trends Cogn Sci 2001;5:525–532.
9. Hari R. The neuromagnetic method in the study of the human
auditory cortex. In: Grandori F, Hoke M, Romani GL, eds.
Auditory evoked magnetic fields and electric potentials. Advances in Audiology. Vol 6. Basel: Karger, 1990:222–282.
10. Nagarajan S, Mahncke H, Salz T, et al. Cortical auditory signal
processing in poor readers. Proc Natl Acad Sci USA 1999;96:
6483– 6488.
11. Renvall H, Hari R. Auditory cortical responses to speech-like
stimuli in dyslexic adults. J Cogn Neurosci 2002;14:757–768.
12. Näätänen R. Attention and brain function. Hillsdale, NJ: Lawrence Erlbaum Associates, 1992.
13. Alho K. Cerebral generators of mismatch negativity (MMN)
and its magnetic counterpart (MMNm) elicited by sound
changes. Ear Hear 1995;16:38 –51.
14. Korpilahti P, Lang HA. Auditory ERP components and mismatch negativity in dysphasic children. Electroencephalogr Clin
Neurophysiol 1994;91:256 –264.
15. Kraus N, McGee TJ, Carrell TD, et al. Auditory neurophysiologic responses and discrimination deficits in children with
learning problems. Science 1996;273:971–973.
16. Tallal P, Allard L, Miller S, Curtiss S. Academic outcomes of
language impaired children. In: Hulme C, Snowling M, eds.
Dyslexia: biology, cognition and intervention. London: Whurr,
1997:167–181.
17. Schulte-Körne G, Deimel W, Bartling J, Remschmidt H. Auditory processing and dyslexia: evidence for a specific speech
processing deficit. Neuroreport 1998;9:337–340.
18. Schulte-Körne G, Deimel W, Bartling J, Remschmidt H.
Speech perception deficit in dyslexic adults as measured by mismatch negativity (MMN). Int J Psychophysiol 2001;40:77– 87.
19. Baldeweg T, Richardson A, Watkins S, et al. Impaired auditory
frequency discrimination in dyslexia detected with mismatch
evoked potentials. Ann Neurol 1999;45:495–503.
20. Kujala T, Myllyviita K, Tervaniemi M, et al. Basic auditory
dysfunction in dyslexia as demonstrated by brain activity measurements. Psychophysiology 2000;37:262–266.
21. Hari R, Hämäläinen M, Ilmoniemi R, et al. Responses of the
primary auditory cortex to pitch changes in a sequence of tone
pips: neuromagnetic recordings in man. Neurosci Lett 1984;50:
127–132.
22. Levänen S, Ahonen A, Hari R, et al. Deviant auditory stimuli
activate human left and right auditory cortex differently. Cereb
Cortex 1996;6:288 –296.
23. Koivikko (Renvall) H, Hari R. Diminished auditory mismatch
fields in dyslexic adults. Soc Neurosci Abstr 2000;26:1971.
24. Wechsler D. Wechsler adult intelligence scale. Manual. New
York: Psychological Corporation, 1955.
25. Ahonen AI, Hämäläinen MS, Kajola MJ, et al. 122-Channel
SQUID instrument for investigating the magnetic signals from
the human brain. Physica Script 1993;T49:198 –205.
26. Hämäläinen M, Hari R, Ilmoniemi RJ, et al. Magnetoencephalography—theory, instrumentation, and applications to noninvasive studies of the working human brain. Rev Mod Phys
1993;65:413– 497.
27. Uutela K, Hämäläinen MS, Somersalo E. Visualization of magnetoencephalographic data using minimum current estimates.
Neuroimage 1999;10:173–180.
28. Stenbacka L, Vanni S, Uutela K, Hari R. Comparison of minimum current estimate and dipole modeling in the analysis of
simulated activity in the human visual cortices. Neuroimage
2002;16:936 –943.
29. Leppänen PHT, Lyytinen H. Auditory event-related potentials
in the study of developmental language-related disorders. Audiol Neuro-otol 1997;2:308 –340.
30. Galaburda AM, Sherman GF, Rosen GD, et al. Developmental
dyslexia: four consecutive patients with cortical anomalies. Ann
Neurol 1985;18:222–233.
31. Hynd GW, Semrud-Clikeman M, Lorys AR, et al. Brain morphology in developmental dyslexia and attention deficit
disorder/hyperactivity. Arch Neurol 1990;47:919 –926.
32. Jenner AR, Rosen GD, Galaburda AM. Neuronal asymmetries
in primary visual cortex of dyslexic and nondyslexic brains. Ann
Neurol 1999;46:189 –196.
33. Leonard CM, Eckert M, Lombardino LJ, et al. Anatomical risk
factors for phonological dyslexia. Cereb Cortex 2001;11:148–157.
34. Eckert MA, Leonard CM. Structural imaging in dyslexia: the
planum temporale. Ment Retard Dev Disabil Res Rev 2000;6:
198 –206.
35. Galaburda AM, Menard MT, Rosen GD. Evidence for aberrant
auditory anatomy in developmental dyslexia. Proc Natl Acad
Sci USA 1994;91:8010 – 8013.
36. Eliez S, Rumsey JM, Giedd JN, et al. Morphological alteration
of temporal lobe gray matter in dyslexia: an MRI study. J Child
Psychol Psychiatry 2000;41:637– 644.
37. Eden GF, VanMeter JW, Rumsey JM, et al. Abnormal processing of visual motion in dyslexia revealed by functional brain
imaging. Nature 1996;382:66 – 69.
38. Klingberg T, Hedehus M, Temple E, et al. Microstructure of
temporo-parietal white matter as a basis for reading ability: evidence from diffusion tensor magnetic resonance imaging. Neuron 2000;25:493–500.
39. Brown WE, Eliez S, Menon V, et al. Preliminary evidence of
widespread morphological variations of the brain in dyslexia.
Neurology 2001;56:781–783.
40. Sams M, Hari R, Rif J, Knuutila J. The human auditory sensory memory trace persists about 10 sec: neuromagnetic evidence. J Cogn Neurosci 1993;5:363–370.
41. Loveless N, Koivikko H. Sluggish auditory processing in dyslexics is not due to persistence in sensory memory. Neuroreport
2000;11:1903–1906.
42. Stein J, Walsh V. To see but not to read; the magnocellular
theory of dyslexia. Trends Neurosci 1997;20:147–152.
43. Habib M. The neurological basis of developmental dyslexia—an overview and working hypothesis. Brain 2000;123:
2373–2399.
44. Steinman BA, Steinman SB, Lehmkuhle S. Transient visual attention is dominated by the magnocellular stream. Vision Res
1997;37:17–23.
45. Hari R, Renvall H, Tanskanen T. Left minineglect in dyslexic
adults. Brain 2001;124:1373–1380.
Renvall and Hari: Mismatch Fields in Dyslexia
557
Документ
Категория
Без категории
Просмотров
0
Размер файла
462 Кб
Теги
adults, mismatches, diminishes, dyslexia, auditors, field
1/--страниц
Пожаловаться на содержимое документа