Conceived and designed the experiments: TO JP JMS. Performed the experiments: TO CR AMM LO-T. Analyzed the data: TO JP JMS AT JB AP-L. Contributed reagents/materials/analysis tools: JP RN. Wrote the paper: TO JMS AMM AT AP-L. Provided engineering support and ad-hoc software development for the experiment: RN AC JMM JLC.
The authors have declared that no competing interests exist.
Over three months of intensive training with a tactile stimulation device, 18 blind and 10 blindfolded seeing subjects improved in their ability to identify geometric figures by touch. Seven blind subjects spontaneously reported ‘visual qualia’, the subjective sensation of seeing flashes of light congruent with tactile stimuli. In the latter subjects tactile stimulation evoked activation of occipital cortex on electroencephalography (EEG). None of the blind subjects who failed to experience visual qualia, despite identical tactile stimulation training, showed EEG recruitment of occipital cortex. None of the blindfolded seeing humans reported visual-like sensations during tactile stimulation. These findings support the notion that the conscious experience of seeing is linked to the activation of occipital brain regions in people with blindness. Moreover, the findings indicate that provision of visual information can be achieved through non-visual sensory modalities which may help to minimize the disability of blind individuals, affording them some degree of object recognition and navigation aid.
Cross-modality sensory stimulation may offer a good opportunity to improve recognition, localization and navigation in blind people. A coherent and unified perceptual experience is created by the brain with multisensorial input
In the blind the high demand required by object recognition appears to also recruit ventral and dorsal occipital areas
Evoked potentials are useful to study brain activity triggered by external stimuli using surface recordings. Around 50 msec after stimulation, and even earlier, primary somatosensory cortical activation is normally found. In the case of tactile stimuli, this happens in parietal areas contralateral to the stimulated hand. Circa 100 msec shape and object automatic recognition takes place as well in somatosensory areas. After 300 msec some activity related to objects with poor-defined identity happens, as well as some matching between perception and stored representations in cognitive processing in prefrontal areas
However, there are no published studies aimed at understanding the relationship between activation of lateral occipital cortex and the ability to recognize objects presented to the hand along time. Thus, we tested if repetitive passive tactile stimulation leads to activation of visual areas and recognition of spatial patterns in people with blindness.
We used passive repetitive tactile stimulation over a period of 3 months, one hour a day for five days a week, with vertical, horizontal and oblique lines generated randomly by a tactile stimulator. Our aims were (a) to study if repetitive tactile stimulation can create cross-modality and improve recognition and localization of patterns in blind people, and (b) to evaluate the impact of this training on brain activity. We performed EEG recording during the initial stimulation session and in the last session.
After a call for volunteers was made, we studied 18 blind subjects (13 men, 5 women) that were recruited consecutively from the National Organization of Spanish Blind to participate in the study, plus10 controls (blindfolded seeing normal individuals, 4 men and 6 women) of similar ages to the blind group, who had no visual deficit at all and had no previous history of synesthesias. All participants were informed of the nature and purpose of the experiment and all gave their written informed consent. Whenever minors were consented, both the minor and his/her legal representative were informed, minors' assented and their legal representatives consented in written form acknowledging the minors assent as well. The study was approved by the Hospital Clínico San Carlos Clinical Research Bioethical Committee (Universidad Complutense, Madrid, Spain) committee/institutional review board and consent adhered to the Declaration of Helsinki. Participants had no history of neurological, psychiatric, cognitive or sensorimotor deficits, other than blindness. They all had normal EEGs at baseline.
Nine subjects had early onset blindness (loss of vision before 5 years of age) while the rest, but one, were late blind, having lost their sight after age 15. Four subjects had absolute congenital blindness (from birth), ten had no residual vision at all at the time of our study, while eight had minimal residual vision. Causes of blindness were diverse: congenital nystagmus, glaucoma, retinopathy, congenital cataracts, lenticular fibroplasia, macular degeneration, optic atrophy, Peter's anomaly with microphtalmia, retinal detachment, retina necrosis, retinitis pigmentosa and uveitis (
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1 | 16 | F | R | Congenital nystagmus | 1 | Yes; light perception <5% | Yes: “I can see a white line … Honestly, I can see it but I do not feel it” |
2 | 14 | M | L | Retinitis pigmentosa | 4 | Yes; light perception <7% | Yes: “I can see white lines … I can see lights oriented either vertically, horizontally or obliquely … I see it but I do no longer feel it in my hand” |
3 | 15 | F | R | Bilateral uveitis | 4 | Yes; light perception <7% | Yes: “There are lines in grey tones, steel-like” |
4 | 32 | M | R | Retinal detachment | 12 | No | Yes: “I see phosphenes always oriented in the direction of the line … I see phosphenes, but can hardly feel it on the hand” |
5 | 51 | M | L | Microphtalmia and Peter's syndrome | 3 | Yes; light perception <3% | Yes: “I can see a luminous line on the dark screen … A major change happened when I suddenly completely forgot the tactile sensations and started seeing in my mind the lights transmitted by the stimuli” |
6 | 69 | M | R | Bilateral uveitis | 35 | No | Yes: “I can see light with greater and greater clarity and intensity” |
7 | 72 | F | R | Optic pathway bilateral atrophy | 9 | No | Yes: “It is like if I see aligned lights” |
8 | 22 | M | R | Retrolental fibroplasia | from birth | No | No |
9 | 40 | M | L | Retinal necrosis | 30 | No | No |
10 | 43 | M | R | Glaucoma and retinopathy | 32 | No | No |
11 | 50 | M | R | Optic pathway bilateral lesion | 22 | No | No |
12 | 56 | F | R | Macular degeneration and retinosis | 29 | No | No |
13 | 57 | M | R | Macular degeneration and spot degeneration | 45 | No | No |
14 | 59 | M | R | Congenital cataracts | From birth | Yes; light perception <7% | No |
15 | 42 | M | R | Congenital glaucoma | From birth | No | No |
16 | 31 | M | R | Retinitis pigmentosa | 16 | Yes; light perception <3% | No |
17 | 64 | M | R | Congenital cataracts | From birth | Yes; left eye: light perception <2% (right eye: no) | No |
18 | 54 | F | R | Optic pathway bilateral atrophy | 1,5 | Yes; light perception left eye <2%, light perception right eye <7% | No |
M = male, F = female. R = right, L = left. L/P = light perception.
All of the blind subjects were initially considered as a single category, but they were later classified into two groups according to the subjective report, or its absence, of visual-like perception. Group 1 (G1, seven blind participants who reported visual sensations, mean age = 32.83, SD = 15.78); Group 2 (G2, eleven blind who did not and even denied visual sensations when explicitly asked, mean age = 46.99, SD = 13.03); and Group 3 (G3, ten blindfolded subjects with no visual deficit, mean age = 39.12, SD = 11.17).
All but three subjects were right-handed and were stimulated on the palm of their right hand. The left-handed individuals underwent the procedure on their left hands (
All subjects underwent intensive training in the use of a tactile sensory device. The stimulation program was completed over a period of three months and involved daily sessions five days a week (Monday to Friday). The control group (G3) underwent exactly the same protocol but they were blindfolded just before each training session until the session ended.
Training consisted of repetitive tactile stimulation with lines oriented vertically, horizontally or obliquely in a random fashion, using a tactile piezoelectric device. Each line was presented for 300 msec at 40 Hz, and followed by a blank pause of 700 msec; hence each direction repeated during one second. The frequency of 40 Hz was chosen based upon the findings that thalamo-cortical connections fire at 40 Hz
Each stimulation session lasted 60 minutes and included the presentation of approximately 3600 stimuli per session. The generation of repetitive passive tactile stimuli was achieved using a single tactile piezoelectric device with 1536 stimulation points (i.e., a tactile matrix with 32×48 pixels). Each nylon point had a 1.3 mm diameter and they were spaced every 2.4 mm, equally in both dimensions. The device generated a 5 cms double line made up 30 dots each (60 dots in total). The dots of each line were stimulated simultaneously, not directionally. Each point was individually controlled both in height (.0 or 0.7 mm) and frequency (40 Hz) by a custom developed software program.
EEG was recorded with a 32 channel Neuronic Medicid Equipment using a standard 10–20 electrocap. We used 32 channels (Fz, pFz, Cz, pCZ, Pz, Oz, Fp1, Fp2, F3, F4, F7, F8, PF3, PF4, pC3, C4, PC4, T1, T2, T3, T4, T3A, T4A, T5, T6, P3, P4, O1 and O2) from the standard 10–20 electrocap. Impedance of all electrodes was kept below 5 kΩ. The electrooculogram (EOG) was recorded with two pairs of leads in order to register horizontal and vertical eye movement. Data were recorded using a mastoid electrode as reference. Sampling rate was 1000 Hz. Amplifier frequency bands were set between 0.05–30.0 Hz.
Low-resolution electromagnetic tomography (LORETA) was applied to each individual event-related potential (ERP) recording to identify underlying brain electric sources of the scalp potentials. LORETA is a reverse solution method that computes the three-dimensional distribution of neural generators in the brain as a current density value (A/m2), for a total of 2394 voxels, with the constraint that neighbouring voxels show maximal similarity. This analysis was realized for a time window of 20 msc (between −10 and +10 msc starting from the high amplitude peak measured from the Pz electrode) (
(A) A tactile piezoelectric device with 1536 stimulation points of stimulation is used (B) on the dominant hand, being applied on the palm. (C) EEG is then recorded with a 32 channel-cap. (D) The electrophysiological response of the evoked potential N100 component was measured in each task. Only frequent stimuli responses were analyzed. The time frame to analyze the N100 component was 80–140 ms and it was determined by searching for the maximal amplitude in the respective time window at the Pz electrode. The LORETA analysis was made opening a time window of −10 to +10 ms starting from the high amplitude pick measured in Pz electrode.
Source analysis under model (anatomic construction) was obtained using the traditional LORETA method
Subjects were instructed to simply experience the stimulation and try to identify the line orientation. Subjects were not allowed to move their hand during the stimulation (
Both at baseline and the end of the tactile training program, all subjects were tested using a two-alternative forced-choice response task and underwent an ERP study.
For the behavioural assessment, subjects were asked to discriminate pairs of tactile stimuli: horizontal (80% of the stimuli, frequent) or oblique lines (20%, infrequent). The latter task required blind subjects to first detect each stimulus; they were then asked to exclusively respond to the oblique lines by pressing a button. Subjects' responses, errors and response times were collected for further analysis.
For the ERP study, EEG recording was performed in a soundproof room with dim lighting. Subjects were comfortably seated and were instructed to stay awake, keep their eyes open and avoid abrupt movements. Only non-target trials (horizontal lines) were considered for ERP N100 latency (N100) analysis in order to avoid contamination with motor neural activation during response production. Epochs were 1000 msec in duration with a 200 msec pre-stimulus interval and a post-stimulus length of 800 msec. Baseline was defined as the average voltage over the period from 200 msec prior to stimulus onset.
In order to establish if there were significant differences in reaction time (RT) and N100, before and after training (pre-test and post-test) in each group, paired t-tests were used. Linear regression analyses and Pearson correlation coefficients were carried out to examine the relationships between pre-test and post-test values of the variables RT and N100 in each group. Evaluation of differences between groups due to the training was done using a repeated-measures mixed-effects model. The between-subjects factor was the group (G1, G2 and G3) and the within-subjects factor was the time while the repeated measures were the RT and N100. Statistical analyses were conducted using SPSS and Statgraphics Plus software.
Source analysis for each participant was carried out (
The behavioural results demonstrate that over three months of tactile stimulation training, blind participants (G1 and G2), as well as the blindfolded seeing controls (G3), demonstrated an increase in tactile discriminative ability. Before training, G1 and G2 subjects made an average 15% of omission errors (failures to recognize the tactile stimuli) and reported incorrect line orientations in an additional 7% of stimuli (identification errors). At the end of the experiment, there were on average less than 1% omission errors and less than 1% identification errors in G1 and G2. Average omission errors before training in G3 (blindfolded control group) were 17% while at the end of the experiment errors were reduced to 2%.
During the last three weeks of the experiment seven individuals (G1) reported that they were seeing lights or brief flashes of light (phosphenes) while undergoing the tactile stimulation. These phosphenes appeared to become elongated into lines and eventually appeared vertical, horizontal or oblique, consistent with the tactile stimuli presented. In almost all cases, the perceived visual sensations matched the presented tactile stimuli (<1% mistakes within G1) and appeared to become more and more vivid with time. At this stage an open narrative account was taken from this group who experienced visual qualia. Moreover, the vividness of the visual percepts eventually was spontaneously reported as much greater than the tactile sensations, which appeared to lose saliency in four of these seven subjects (
As it can be inferred from
N100 and RT means and standard deviations, pre-test and post-test, for each group are shown in
Pre-test mean (SD) | Post-test mean (SD) | t-statistic | p value | |
N100 | ||||
G1 | 120.3 (6.8) | 91.9 (7.3) | 3.012 | 0.024* |
G2 | 105.1 (5.4) | 98.3 (5.9) | 0.686 | 0.508 |
G3 | 98.8 (5.7) | 101.7 (6.1) | −0.413 | 0.689 |
RT | ||||
G1 | 645.5 (29.5) | 616.5 (27.7) | 1.492 | 0.186 |
G2 | 606.3 (23.5) | 559.9 (22.1) | 1.716 | 0.117 |
G3 | 643.5 (24.7) | 620.5 (23.2) | 2.167 | 0.058 |
Paired t-tests results and p-values are shown. (*) statistically significant.
Paired t-tests shows statistically significant differences only for N100 in G1 (p = 0.024), that is to say, N100 latency in G1 decreased significantly because of training.
The relationship between pre-test and post-test values for N100 and RT was investigated using linear regression analyses in the three groups.
The results for the variable RT are more homogeneous in all groups as the correlation is positive in all of them, but not statistically significant in G1 and G2 (both p>0.16) with correlation coefficients r = 0.47 and r = 0.45 respectively. However this effect is statistically significant in G3 where a strong linear relationship is observed between the pre-test and post-test RT values (p<0.0001) with a correlation coefficient r = 0.98.
To evaluate the effects of training, a repeated-measures mixed-effects model was used.
Error bars indicate SE.
Statistical analysis shows differences close to statistical significance amongst N100 means along time (F = 4.12, p = 0.053). The interaction N100*group is also close to being statistically significant (F = 2.70, p = 0.087). Finally, the group effect is not significant (F = 0.45, p = 0.641).
Training effect upon N100 was previously studied in every group separately (
Error bars indicate SE.
As illustrated in
Maximal intensity projection areas are displayed in red.
Using SM significant differences between pre-test and post-test for each group are found in G1 in BA 17, 18, 19, 9 and 46, in G2 in BA 4, 9 and 39, and in G3 in BA 21, 22, 7, 17, 18 and 48 (
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AAL | BA | x | y | z | T2 Hotelling | Pretest | Postest |
G1 | |||||||
Left Calcarine | 18 | 108 | 76 | 152 | 166,6682** | 1,9642 | 5,3346 |
Left Calcarine | 17 | 109 | 76 | 151 | 150,82 87 * | 1,7493 | 4,6792 |
Left Lingual | 19 | 110 | 75 | 152 | 134,9632 * | 1,7117 | 4,5672 |
Left Lingual | 18 | 107 | 72 | 150 | 130,4462 * | 1,7647 | 4,7350 |
Left Occipital Superior | 19 | 115 | 99 | 176 | 72,6548 * | 1,7124 | 5,0543 |
Right Middle Frontal | 9 | 48 | 125 | 80 | 61,7910 * | 0,7742 | 0,7643 |
Left Frontal Middle | 9 | 128 | 120 | 70 | 59,0519 * | 1,4497 | 0,4701 |
Right Lingual | 17 | 85 | 65 | 176 | 50,7121 * | 2,4206 | 11,8244 |
G2 | |||||||
Right Frontal Middle | 9 | 44 | 128 | 80 | 29,0635** | 0,5201 | 1,6203 |
Right Angular | 39 | 44 | 97 | 144 | 21,8607 * | 1,2949 | 2,5158 |
Left Superior Occipital | 17 | 100 | 90 | 192 | 20,4368 * | 0,9870 | 0,6192 |
Left Calcarine | 16 | 96 | 69 | 196 | 18,9137 * | 0,8518 | 0,8928 |
Right Post-central | 3 | 46 | 108 | 107 | 17,1995* | 0,8363 | 1,1732 |
G3 | |||||||
Left Middle temporal | 37 | 114 | 72 | 160 | 124,7300*** | 7,7973 | 1,7731 |
Left Middle occipital | 19 | 136 | 79 | 161 | 112,1210*** | 90,6255 | 2,3392 |
Left Inferior Occipital | 37 | 140 | 61 | 154 | 100,2741*** | 211,7078 | 2,4962 |
Left Inferior Temporal | 37 | 144 | 63 | 155 | 105,7695*** | 201,8498 | 2,7039 |
Left Fusiform | 37 | 131 | 57 | 145 | 67,1131** | 103,5997 | 1,6238 |
Right Opercular Rolandic | 48 | 31 | 87 | 107 | 59,3316** | 118,1168 | 2,2864 |
Right Postcentral | 43 | 24 | 95 | 105 | 57.8739** | 72,0106 | 1,1750 |
Right Superior Temporal | 48 | 35 | 79 | 107 | 56,8068* | 143,7001 | 2,5432 |
Right Middle Cingulum | 23 | 73 | 115 | 127 | 50,2679** | 3,3344 | 1,2536 |
Left Angular | 39 | 131 | 102 | 150 | 46,4443** | 5,4738 | 0,8514 |
Right Middle Cingulum | 23 | 70 | 116 | 128 | 45,7150* | 1,4218 | 0,5232 |
Right Supramarginal | 40 | 26 | 110 | 110 | 43,6336** | 26,9931 | 1,2630 |
Left Superior occipital | 18 | 108 | 104 | 159 | 36,3355** | 6,1381 | 4,9371 |
Left Cuneus | 18 | 108 | 106 | 164 | 33,9557** | 7,7053 | 5,3461 |
Right Middle Temporal | 20 | 35 | 59 | 102 | 22,7929* | 127,5687 | 1,7227 |
Right Sup Parietal | 5 | 72 | 143 | 142 | 22,8391* | 17,9683 | 2,0495 |
Right Inferior Parietal | 40 | 35 | 116 | 140 | 21,8265* | 9,9151 | 1,7221 |
Right Post-central | 3 | 46 | 108 | 107 | 17,1995* | 0,8363 | 1,1732 |
Right Inferior Temporal | 20 | 36 | 32 | 92 | 17,5265* | 15,0795 | 0,3774 |
G1 T2 (3–5) = 147.284 for α = .01, = 46.383 for α = .05. G2 T2 (3–10) = 28.466 for α = .01, = 15.248 for α = .05. G3 T2 (3–9) = 72.40764 for α = .001, = 32.59783 for α = .01, = 16.76635 for α = .05. AAL = Anatomical label corresponding to Probabilistic Brain Atlas. BA = Brodmann areas. x, y, z = co-ordinates from PBA in three spatial axes. L = Left; R = Right. * p<.05; ** p<.01 ** and p<.001***.
LORETA mean maps obtained with independent Hotelling T2.
AAL | BA | x | y | z | T2 Hotelling | Mean | |
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Left Precuneus | 7 | 104 | 120 | 148 | 14,1740* | 1,4213 | 5,6151 |
Left occipital middle | 19 | 136 | 79 | 171 | 12,4028* | 1,4846 | 50,0659 |
Left Precuneus | 5 | 105 | 130 | 156 | 12,2543* | 1,9200 | 7,1426 |
Left Occipital Inferior | 19 | 131 | 60 | 160 | 11,1081* | 1,7229 | 22,5433 |
Left Fusiform | 37 | 124 | 63 | 153 | 11,0257* | 1,0918 | 39,8153 |
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Left Occipital Middle | 17 | 120 | 76 | 188 | 11,5080* | 2,8626 | 1,779 |
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Left Angular | 39 | 131 | 108 | 139 | 19,3610* | 1.0899 | 1,0510 |
Left Frontal Superior | 10 | 104 | 95 | 22 | 18,1697* | 0,6452 | 0,4443 |
Left Inferior parietal | 39 | 132 | 112 | 144 | 17,0643* | 2,9607 | 2,7202 |
Right Middle Superior | 10 | 87 | 101 | 33 | 16,8351* | 1,8370 | 2,0047 |
Left Middle Superior Frontal | 10 | 104 | 81 | 36 | 15,4223* | 0,7925 | 0,6370 |
Left Anterior Cingulum | 32 | 88 | 87 | 48 | 14,0570* | 3,5205 | 3,2940 |
Left Frontal Sup Orbital | 11 | 104 | 63 | 29 | 13,8279* | 2,1197 | 1,3116 |
Right Orbital Middle Frontal | 11 | 87 | 63 | 32 | 13,1320* | 3,8556 | 3,2801 |
Right Anterior Cingulum | 32 | 87 | 77 | 48 | 13,0165* | 3,3313 | 2,9261 |
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Right Suparmarginal | 40 | 24 | 112 | 132 | 15.8530* | 0,4546 | 0,8095 |
Left Middle Frontal | 8 | 116 | 131 | 72 | 12,5649* | 6,3213 | 0,9366 |
Left Fusiform | 36 | 114 | 35 | 97 | 12,2738* | 0,3167 | 1,6700 |
Right Parahippocampo | 35 | 72 | 45 | 90 | 12,1686* | 0,7467 | 1,0636 |
Left Middle Occipital | 18 | 120 | 76 | 174 | 12,1421* | 1,3117 | 0,7835 |
Right Angular | 39 | 29 | 101 | 141 | 12,0550* | 3,8171 | 2,4069 |
Rigt Fusiform | 18 | 64 | 60 | 167 | 11,9019* | 1,8244 | 1,6919 |
Right Middle Tempo Pole | 36 | 64 | 37 | 86 | 11,8748* | 0,6551 | 0,8717 |
Rigt Lingual | 18 | 68 | 62 | 167 | 11,2649* | 1,9821 | 1,9651 |
Left Hippocampo | 35 | 112 | 53 | 99 | 11,1020* | 0,3501 | 1,5751 |
Rigt Fusiform | 36 | 66 | 29 | 91 | 11,0176* | 0,5722 | 0,7780 |
Righ Inferior Occipital | 19 | 56 | 59 | 168 | 11,0393* | 2,2506 | 1,5684 |
Pre-test G2 vs G3 T2 (3–19) = 10.7186 for α = .05 . Post-test G1 vs G2 T2 (3–15) = 11.4105 for α = .05. Post-test G1 vs G3 T2 (3–14) = 12.21604 for α = .05. Post-test G2 vs G3 T2 (3–19) = 10.7186 for α = .05. AAL = Anatomical label corresponding to Probabilistic Brain Atlas. BA = Brodmann areas. x, y, z = co-ordinates from PBA in three spatial axes. L = Left; R = Right. * p<.05; ** p<.01 ** and p<.001***.
After tactile passive repetitive training during an extended (3 months) intensive period people with blindness who spontaneously report visual sensations (G1) exhibited a much shorter RT, considerably decrease in N100 latency and, in parallel with their visual sensations, an activation of the occipital lobe. However no activation of the occipital cortex was found in those blind subjects who did not report any visual qualia (G2), the subjective experience of seeing. We postulate that activation of the occipital cortex, by tactile stimuli results in visual qualia in some blind subjects. Functional activation of the visual cortex by non-visual tactile stimulation has been reported in people with blindness
It seems as if subjects in G1 ‘learned’ a synesthetic perception with repeated stimulation. It is rather interesting that in G1 subjects tactile sensation decreased when the visual qualia became prominent (
There was a frontal activity in G2, both in pre-test and post-test, which did not happen in the other two groups. An increased attentional process may have played a role and, in fact, the four blinds from birth within G2 had a very marked frontal activity (
In two groups (G2 and G3) the training program did not elicit changes in the pattern of EEG activation or the subjective experience of the stimulation. One possible explanation for this finding that would account for the disparity between the group memberships (i.e., blind subjects vs. normal seeing controls), takes into account the stability of brain networks including the primary visual cortex. Indeed, whenever there has likely been a well established neuronal network, such as in subjects with late blindness, or complete lack of visual input because of congenital blindness, cross-modal connectivity failed to occur. The issue of congenitally blind still remains controversial, as our findings (blind subjects from birth did not experience visual qualia and their occipital areas were not activated) are not fully concordant with previous research
In normal subjects (G3) at baseline many areas were greatly activated and they were widely distributed, but the pattern of activation (and the number of significantly activated brain regions) was reduced after the training protocol. Though habituation may have played a role in this shift in controls, the initial novelty of line orientation information provided in a non-visual fashion to otherwise normally sighted people may be another explanation for the initial high activation. G3 post-test results may indicate a more efficient way of dealing with tactile stimulation through learning. In sighted subjects, early recruitment of primary visual cortex for tactile processing has been found over a few days of blindfolding and intensive tactile training, or auditory training
In all groups we found that the pre-test activation of the temporal middle complex was significantly reduced after extended training (post-test). Temporal areas are linked to auditive perception, highly enhanced in people with blindness. Moreover, blind subjects display a higher activation of multiple sensory cortical areas than sighted people
In contrast to previous literature
Our findings in blind subjects who experienced cross-modal induction of visual percepts (G1) also replicate the “visual” matching of the shape of the stimulus
Other authors
Taking into account evidence from human electrophysiology, neuropsychology and animal studies, some authors have suggested that the brain integrates congruent different sensory modalities and that this integration starts as early as 100 ms after stimulus presentation
A few caveats are in order. First, we used a limited set of EEG channels because this was the only one available for us at the time. Second, it remains to be established whether the nature of tactile stimuli or the intensity and repetitive training fashion are critical for obtaining the observed effect. Third, other neuroimaging techniques, such as resting fMRI, default state or coherence analysis, for example, could throw more conclusive data on the newer neuroplasticity. Another limitation is the restriction to a 3-month training period. We do not know if further changes may occur should the passive tactile training continue for a longer duration. Importantly, the most relevant findings are derived from post-hoc analysis. Therefore, no predictive analysis of regression or otherwise could be run. Finally, we studied a limited sample. This is particularly critical in the case of the four subjects included in our study who suffer from congenital blindness as the previous organization of visual cortical columns may be a limiting factor in this domain. Future studies should address, with a larger sample, which blind individuals are more likely to experience visual qualia and to what extent these qualia may affect spatial-processing.
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The authors want to thank Professor Gabriel A. de Erausquin (University of Southern Florida, USA) and Ms. Donna van Meer (Washington University, St Louis, USA) for their invaluable help in the preparation and correction of this manuscript.