**4. Crossmodal plasticity**

As sensory organs are highly specialized, the cooperative interplay of sensory systems improves perception through multimodal integration enhancing reliability of the information conveyed by each sensory channel, all the more so when individuals are engaged in a perceptually complex behavioral context. Hence, it has been assumed for decades that multimodal integration favors crossmodal plasticity and promotes functional compensation following partial or total deprivation of a sensory modality. Accordingly, a cortical area deprived of its dominant sensory input exhibits an increased responsiveness to stimulation of other modalities, thereby changing its functional tuning. There are a wealth of electrophysiological, neuroimaging and behavioral studies carried out in deaf and blind subjects that have provided convincing evidence for intersensory substitution in deprived cortical areas and experience-dependent reorganization in the areas taking over the defective sensory modality [59–63]. The plasticity mechanisms mediating these changes have also been extensively investigated, with a focus on the ingrowth of novel heteromodal projections or the unmasking of already existing heteromodal inputs. In this chapter, we focus the discussion on crossmodal plasticity occurring within primary areas.

### **4.1 Heteromodal recruitment of deprived visual cortex**

### *4.1.1 Visual to somatosensory substitution*

Capacity for tactile perception to substitute, at least partly, for the loss of vision has long been established [64]. Neuroimaging studies have provided evidence that the occipital visual cortex can be recruited by tactile tasks in blind subjects. For example, a PET study revealed that blind subjects display activation of primary and secondary visual cortical areas during tactile discrimination tasks, in contrast to sighted subjects who exhibited deactivation (i.e., decreased regional cerebral blood flow) in these areas [65]. In addition, this study showed that tactile recruitment of the visual cortex may be task-specific, since a non-discrimination tactile task did not activate V1 in either the blind or sighted subjects. This finding was corroborated in a fMRI study which also showed that electrical stimulation of the hand reading Braille dots did not evoke activation in the visual cortex, suggesting that the tactile recruitment in the visual cortex may result from high-order supramodal processing [66]. Interestingly, transcranial magnetic stimulation (TMS) of the occipital

**149**

*Interplay between Primary Cortical Areas and Crossmodal Plasticity*

visual cortex overlying Brodmann areas 17, 18 and 19 in early-onset blind subjects, while they were identifying Braille or embossed Roman letters, was found to distort tactile perception [67]. By contrast, no such impairment of tactile performance was observed in sighted subjects. Furthermore, V1 was not only strongly activated during Braille reading, but also during Braille writing from memory in the most foveal part of V1 [68]. However, activation of occipital areas during Braille reading was not found in late-onset blind subjects, and their stimulation by TMS did not disrupt braille reading [69]. This report is at variance with other studies showing V1 activation in late onset blind subjects during braille reading [70, 71]. Individuals who lost sight as adults, and subsequently learned Braille, still exhibit activity in V1, although the spatial extent of the activation in the visual cortex is greater for those who became blind early in life [71]. Moreover, the early-onset blind subjects were found to display stronger activation in the occipital cortex contralateral to the hand

In late-blind patients with retinitis pigmentosa, vision deprivation leads to an elevated activation of the visual cortex in response to tactile stimuli during a discriminative task, with higher activation as the degree of vision loss was greater [72]. It is worth mentioning that even in normally sighted adults, five days of complete visual deprivation combined with intensive tactile training result in increased BOLD signal within the occipital cortex in response to tactile stimulation, hence reflecting visual areas engagement in the processing of non-visual information [73]. This crossmodal activation was reversed within 24 hours of removing the blindfold. Surprisingly, even after a short period of blindfolding (40-60 min), V1 activation was observed while the subjects performed a fine spatial tactile discrimination task [74]. Along the same lines, a one-week visual deprivation in juvenile mice was found to improve whisker function. This short period deprivation was sufficient to

Considering both the improvement in Braille character tactile discrimination after the five-day blindfolding period [73] and the impairment of Braille character recognition after disruption of the occipital cortex by TMS [67], it is reasonable to infer that crossmodal changes taking place in the visually deprived occipital cortex are behaviorally adaptive. A further argument stems from an interesting study showing that, when systematically stimulating the occipital cortex with single pulse TMS, early- and late -onset blind subjects have reported tactile sensations in the Braille-reading fingers, that were somatotopically mapped onto the visual cortex, whereas blindfolded sighted controls reported only phosphenes [76]. Further evidence for the adaptive function of tactile information processing in the visual cortex of early blind subjects comes from a study reporting the case of a proficient Braille reader blind from birth who was no longer able to read Braille (Braille alexia) after bilateral ischemic stroke to the occipital cortex, while somatosensory perception was otherwise unchanged [77]. The core evidence reported herein supports the view that the recruitment of V1 by somatosensory inputs in the context of compensatory behavioral strategy (Braille reading) accounts, at least in part, for the

Numerous studies have documented the fact that occipital cortical areas can be activated by auditory inputs in blind subjects (for reviews, see [60, 78]). For example, in the early-blind macaque, the occipital visual cortical areas were shown to respond to auditory stimulation [79]; Likewise, auditory responses in the visual cortex of neonatally enucleated rats have been recorded in a third of the V1 neurons recorded [80]. Contrary to a prevailing view, recent studies in late blind subjects

sharpen the tuning of layer 2/3 neurons in the barrel field of S1 [75].

superior tactile perceptual abilities of blind people [67].

*4.1.2 Visual to auditory substitution*

*DOI: http://dx.doi.org/10.5772/intechopen.95450*

used for reading Braille.

#### *Interplay between Primary Cortical Areas and Crossmodal Plasticity DOI: http://dx.doi.org/10.5772/intechopen.95450*

*Connectivity and Functional Specialization in the Brain*

**4. Crossmodal plasticity**

within primary areas.

The set of studies reviewed highlights the broad panoply of connectivity patterns and functional interactions between primary areas that underpin a flexible cooperation at an early stage of sensory processing. Tentatively, we propose that early crossmodal interactions in primary areas contribute to refining and sharpening neural response tuning adapted to improving "immediate" perception and eliminating perceptual ambiguity. This perceptual optimization could occur through rapid neurophysiological mechanisms operating in the corticocortical circuitry (e. g., local suppressive inhibition, sub-additive or supra-additive integration, oscillatory entrainment of neuronal networks) and serve automated behavioral responses. According to this view, cognitive influences exerted onto higher-order cortical integration areas, operating through relatively slower mechanisms, would adaptively modulate the early multimodal integration to fulfill a more complex integration processing influenced by attention and motivation so as

As sensory organs are highly specialized, the cooperative interplay of sensory systems improves perception through multimodal integration enhancing reliability of the information conveyed by each sensory channel, all the more so when individuals are engaged in a perceptually complex behavioral context. Hence, it has been assumed for decades that multimodal integration favors crossmodal plasticity and promotes functional compensation following partial or total deprivation of a sensory modality. Accordingly, a cortical area deprived of its dominant sensory input exhibits an increased responsiveness to stimulation of other modalities, thereby changing its functional tuning. There are a wealth of electrophysiological, neuroimaging and behavioral studies carried out in deaf and blind subjects that have provided convincing evidence for intersensory substitution in deprived cortical areas and experience-dependent reorganization in the areas taking over the defective sensory modality [59–63]. The plasticity mechanisms mediating these changes have also been extensively investigated, with a focus on the ingrowth of novel heteromodal projections or the unmasking of already existing heteromodal inputs. In this chapter, we focus the discussion on crossmodal plasticity occurring

Capacity for tactile perception to substitute, at least partly, for the loss of vision has long been established [64]. Neuroimaging studies have provided evidence that the occipital visual cortex can be recruited by tactile tasks in blind subjects. For example, a PET study revealed that blind subjects display activation of primary and secondary visual cortical areas during tactile discrimination tasks, in contrast to sighted subjects who exhibited deactivation (i.e., decreased regional cerebral blood flow) in these areas [65]. In addition, this study showed that tactile recruitment of the visual cortex may be task-specific, since a non-discrimination tactile task did not activate V1 in either the blind or sighted subjects. This finding was corroborated in a fMRI study which also showed that electrical stimulation of the hand reading Braille dots did not evoke activation in the visual cortex, suggesting that the tactile recruitment in the visual cortex may result from high-order supramodal processing [66]. Interestingly, transcranial magnetic stimulation (TMS) of the occipital

to adjust perception to a continuously changing behavioral context.

**4.1 Heteromodal recruitment of deprived visual cortex**

*4.1.1 Visual to somatosensory substitution*

**148**

visual cortex overlying Brodmann areas 17, 18 and 19 in early-onset blind subjects, while they were identifying Braille or embossed Roman letters, was found to distort tactile perception [67]. By contrast, no such impairment of tactile performance was observed in sighted subjects. Furthermore, V1 was not only strongly activated during Braille reading, but also during Braille writing from memory in the most foveal part of V1 [68]. However, activation of occipital areas during Braille reading was not found in late-onset blind subjects, and their stimulation by TMS did not disrupt braille reading [69]. This report is at variance with other studies showing V1 activation in late onset blind subjects during braille reading [70, 71]. Individuals who lost sight as adults, and subsequently learned Braille, still exhibit activity in V1, although the spatial extent of the activation in the visual cortex is greater for those who became blind early in life [71]. Moreover, the early-onset blind subjects were found to display stronger activation in the occipital cortex contralateral to the hand used for reading Braille.

In late-blind patients with retinitis pigmentosa, vision deprivation leads to an elevated activation of the visual cortex in response to tactile stimuli during a discriminative task, with higher activation as the degree of vision loss was greater [72]. It is worth mentioning that even in normally sighted adults, five days of complete visual deprivation combined with intensive tactile training result in increased BOLD signal within the occipital cortex in response to tactile stimulation, hence reflecting visual areas engagement in the processing of non-visual information [73]. This crossmodal activation was reversed within 24 hours of removing the blindfold. Surprisingly, even after a short period of blindfolding (40-60 min), V1 activation was observed while the subjects performed a fine spatial tactile discrimination task [74]. Along the same lines, a one-week visual deprivation in juvenile mice was found to improve whisker function. This short period deprivation was sufficient to sharpen the tuning of layer 2/3 neurons in the barrel field of S1 [75].

Considering both the improvement in Braille character tactile discrimination after the five-day blindfolding period [73] and the impairment of Braille character recognition after disruption of the occipital cortex by TMS [67], it is reasonable to infer that crossmodal changes taking place in the visually deprived occipital cortex are behaviorally adaptive. A further argument stems from an interesting study showing that, when systematically stimulating the occipital cortex with single pulse TMS, early- and late -onset blind subjects have reported tactile sensations in the Braille-reading fingers, that were somatotopically mapped onto the visual cortex, whereas blindfolded sighted controls reported only phosphenes [76]. Further evidence for the adaptive function of tactile information processing in the visual cortex of early blind subjects comes from a study reporting the case of a proficient Braille reader blind from birth who was no longer able to read Braille (Braille alexia) after bilateral ischemic stroke to the occipital cortex, while somatosensory perception was otherwise unchanged [77]. The core evidence reported herein supports the view that the recruitment of V1 by somatosensory inputs in the context of compensatory behavioral strategy (Braille reading) accounts, at least in part, for the superior tactile perceptual abilities of blind people [67].

### *4.1.2 Visual to auditory substitution*

Numerous studies have documented the fact that occipital cortical areas can be activated by auditory inputs in blind subjects (for reviews, see [60, 78]). For example, in the early-blind macaque, the occipital visual cortical areas were shown to respond to auditory stimulation [79]; Likewise, auditory responses in the visual cortex of neonatally enucleated rats have been recorded in a third of the V1 neurons recorded [80]. Contrary to a prevailing view, recent studies in late blind subjects

have demonstrated that crossmodal plastic changes also occur in the adult. Sound change detection was found to recruit occipital cortical areas in individuals with both early- and late-onset blindness [81]. Further evidence was provided by a positron emission tomography (PET) study showing that visual cortical areas, including V1, were activated during auditory word processing in the congenitally blind and in subjects who had become blind after puberty [70].

There has been longstanding controversy about whether auditory signal processing can compensate for impaired accuracy of spatial representation in blind subjects. For example, fMRI studies have shown that, in early-blind people, V1 is activated during auditory detection and recognition [82] as well as during auditory localization tasks [83]. Early blind subjects are found to localize sound sources with a better accuracy than sighted subjects, in particular in monaural condition [84]. In this study, it was reported that subjects displaying a residual peripheral vision localized sound less precisely than sighted or totally blind subjects. Moreover, in blind individuals, experts at perceiving space through sound echoes using clicks (echolocators), evidence was found for a retinotopic-like mapping of sounds in V1 [85]. This finding indicates that the early visual area can be adapted to precisely remap spatial locations after visual loss. It is worth mentioning that the degree of retinotopic-like mapping of sound echoes was positively associated with echo localization ability [85]. Overall, the findings reported above strongly suggest that crossmodal substitution leading to a functional remapping of sensory and cognitive functions in the deprived cortex depends upon the extent of sensory loss and the nature of the task to be compensated for. It turns out that the crossmodal substitution is limited by the degree of functional overlap or cooperativity between sensory systems. It is worth mentioning a fMRI investigation using auditory discrimination in the congenitally blind with a focus on the effective connectivity between different cortical and thalamic regions via dynamic causal modeling [86]. The data showed a clear enhancement of BOLD responses in bilateral V1 during the auditory task, hence corroborating a previous study [87], and provided evidence for stronger corticocortical effective connectivity from A1 to V1 in blind than in sighted subjects. Furthermore, a combination of dynamic causal modeling with Bayesian selection has demonstrated that auditory-driven activity in the occipital cortex of the congenitally blind is best explained by direct feed-forward connections from A1 to V1, whereas it relies more on indirect feedback inputs from parietal regions in the late-onset blind subjects [88]. This study suggests that visual deprivation during an early critical period induces a crossmodal plasticity under the form of a transfer of spatial processing competency to a non-visual modality in the deprived cortex.

#### **4.2 Heteromodal recruitment of deprived auditory cortex**

In this section, we will not distinguish data related to the recruitment of the deprived auditory cortex by somatosensory or visual modalities. As found in blind subjects, animal and human studies have provided ample evidence of crossmodal plasticity after hearing loss. Recruitment of the deprived auditory cortical areas during somatosensory and visual stimulation in deaf individuals was repeatedly observed in higher-order auditory cortex (for review: [60, 89]). By contrast, it remains controversial whether the deafferented primary auditory cortex may be activated by spared sensory modalities. An electrophysiological investigation in congenitally deaf cats failed to detect crossmodal responses to visual or somatosensory stimuli in A1 [90]. Moreover, inactivation of A1 by cooling had no obvious effect on behaviorally-tested visual functions in the congenitally deaf cats [91]. Yet, after early destruction of cochlear receptors, photic stimulation was found to elicit neural activation in A1 of mature cats [92]. However, this crossmodal modification

**151**

*Interplay between Primary Cortical Areas and Crossmodal Plasticity*

was observed after early-onset deprivation (one week), a period in which primary cortical areas are not yet well defined, but not after late-onset (2 month-old cats) auditory deprivation. Nevertheless, there is evidence in deaf cats for alteration in the pattern of heteromodal thalamocortical and corticocortical projections from somatosensory and visual areas to A1 [93]. Somatosensory projections were more prominent in early- and late-onset deaf animals, whereas projections originating from the visual areas were less apparent in the late-onset than early-onset deaf animals. These findings suggest that crossmodal anatomical plasticity in the deprived auditory cortex differs depending on the age of deafness onset and sensory modality. Furthermore, in early-deaf cats, increased projections from neighboring visual and somatosensory areas to the core auditory cortex including A1 and the surrounding anterior auditory field (AAF) have been described [94]. Interestingly, a study combining electrophysiological recording with cortical myelo-architecture description in congenitally deaf mice showed that the visual and somatosensory spatial domains had taken over auditory domains within A1 and AAF [95]. This finding demonstrates extensive re-specification of cortical fields following auditory loss. In addition, in early deafened ferrets, recordings from single-units in the core auditory cortex showed that 72% were activated by somatosensory stimulation, compared to 1% in hearing controls [96]. In adult-deafened ferrets, extensive crossmodal reorganization of core auditory cortex was also described, which was characterized by a consistent somatosensory conversion in neuron responsiveness within 16 days after deafening [97], thus demonstrating that crossmodal plasticity can also occur after the period of sensory system maturation. These data suggest that subthreshold tactile inputs found in hearing animals can transform into suprathreshold responses in adult deafened animals. In this regard, it is worth mentioning that somatosensory inputs to the core auditory cortex represent the majority of non-auditory effects in hearing ferrets [96]. This specificity may be due to the greater functional similarities between somatosensory and auditory modalities regarding temporal precision underlying frequency percept (e.g. vibrotactile stimulations), compared to that

The recruitment of A1 for the processing of visual stimuli was also revealed by fMRI investigations in congenitally or early deaf subjects [98–100]. Moreover, in adult-onset single-sided deafness (SSD), seeded functional connectivity of visual cortices revealed enhancement in visual areas and reduction in auditory regions, suggesting adaptive functional modifications of the visual network [101]. Furthermore, V1 seeds demonstrated increased connectivity in multiple regions, including those dedicated to speech (inferior parietal lobule) or somatosensory processing (postcentral gyrus). It is also noticeable that activation of A1 was observed in deaf subjects with total hearing loss during sign language tasks, but not in subjects with residual hearing ability [102], suggesting that this crossmodal plasticity depends on the extent of hearing loss. Additional evidence of compensatory functional changes comes from the observation that congenitally deaf cats, compared with hearing cats, have superior localization abilities in the peripheral visual field and lower visual movement detection thresholds [91]. In this study, reversible deactivation of posterior auditory cortex was found to selectively eliminate superior visual localization abilities, whereas deactivation of the dorsal auditory cortex eliminated superior visual motion detection. It is of interest that measuring the fMRI signal changes in response to spatially co-registered visual, somatosensory and bimodal stimuli, the visual responses which were stronger in congenitally deaf than hearing adults, appeared to be weaker than those elicited by somatosensory stimulation [103]. This is consistent with the above-mentioned finding on the prevalence of somatosensory over visual inputs in the core auditory cortex [96]. Congenital deafness was also found to enhance the accuracy of suprathreshold

*DOI: http://dx.doi.org/10.5772/intechopen.95450*

between audition and vision.

#### *Interplay between Primary Cortical Areas and Crossmodal Plasticity DOI: http://dx.doi.org/10.5772/intechopen.95450*

*Connectivity and Functional Specialization in the Brain*

subjects who had become blind after puberty [70].

**4.2 Heteromodal recruitment of deprived auditory cortex**

In this section, we will not distinguish data related to the recruitment of the deprived auditory cortex by somatosensory or visual modalities. As found in blind subjects, animal and human studies have provided ample evidence of crossmodal plasticity after hearing loss. Recruitment of the deprived auditory cortical areas during somatosensory and visual stimulation in deaf individuals was repeatedly observed in higher-order auditory cortex (for review: [60, 89]). By contrast, it remains controversial whether the deafferented primary auditory cortex may be activated by spared sensory modalities. An electrophysiological investigation in congenitally deaf cats failed to detect crossmodal responses to visual or somatosensory stimuli in A1 [90]. Moreover, inactivation of A1 by cooling had no obvious effect on behaviorally-tested visual functions in the congenitally deaf cats [91]. Yet, after early destruction of cochlear receptors, photic stimulation was found to elicit neural activation in A1 of mature cats [92]. However, this crossmodal modification

have demonstrated that crossmodal plastic changes also occur in the adult. Sound change detection was found to recruit occipital cortical areas in individuals with both early- and late-onset blindness [81]. Further evidence was provided by a positron emission tomography (PET) study showing that visual cortical areas, including V1, were activated during auditory word processing in the congenitally blind and in

There has been longstanding controversy about whether auditory signal processing can compensate for impaired accuracy of spatial representation in blind subjects. For example, fMRI studies have shown that, in early-blind people, V1 is activated during auditory detection and recognition [82] as well as during auditory localization tasks [83]. Early blind subjects are found to localize sound sources with a better accuracy than sighted subjects, in particular in monaural condition [84]. In this study, it was reported that subjects displaying a residual peripheral vision localized sound less precisely than sighted or totally blind subjects. Moreover, in blind individuals, experts at perceiving space through sound echoes using clicks (echolocators), evidence was found for a retinotopic-like mapping of sounds in V1 [85]. This finding indicates that the early visual area can be adapted to precisely remap spatial locations after visual loss. It is worth mentioning that the degree of retinotopic-like mapping of sound echoes was positively associated with echo localization ability [85]. Overall, the findings reported above strongly suggest that crossmodal substitution leading to a functional remapping of sensory and cognitive functions in the deprived cortex depends upon the extent of sensory loss and the nature of the task to be compensated for. It turns out that the crossmodal substitution is limited by the degree of functional overlap or cooperativity between sensory systems. It is worth mentioning a fMRI investigation using auditory discrimination in the congenitally blind with a focus on the effective connectivity between different cortical and thalamic regions via dynamic causal modeling [86]. The data showed a clear enhancement of BOLD responses in bilateral V1 during the auditory task, hence corroborating a previous study [87], and provided evidence for stronger corticocortical effective connectivity from A1 to V1 in blind than in sighted subjects. Furthermore, a combination of dynamic causal modeling with Bayesian selection has demonstrated that auditory-driven activity in the occipital cortex of the congenitally blind is best explained by direct feed-forward connections from A1 to V1, whereas it relies more on indirect feedback inputs from parietal regions in the late-onset blind subjects [88]. This study suggests that visual deprivation during an early critical period induces a crossmodal plasticity under the form of a transfer of spatial processing competency to a non-visual modality in the deprived cortex.

**150**

was observed after early-onset deprivation (one week), a period in which primary cortical areas are not yet well defined, but not after late-onset (2 month-old cats) auditory deprivation. Nevertheless, there is evidence in deaf cats for alteration in the pattern of heteromodal thalamocortical and corticocortical projections from somatosensory and visual areas to A1 [93]. Somatosensory projections were more prominent in early- and late-onset deaf animals, whereas projections originating from the visual areas were less apparent in the late-onset than early-onset deaf animals. These findings suggest that crossmodal anatomical plasticity in the deprived auditory cortex differs depending on the age of deafness onset and sensory modality. Furthermore, in early-deaf cats, increased projections from neighboring visual and somatosensory areas to the core auditory cortex including A1 and the surrounding anterior auditory field (AAF) have been described [94]. Interestingly, a study combining electrophysiological recording with cortical myelo-architecture description in congenitally deaf mice showed that the visual and somatosensory spatial domains had taken over auditory domains within A1 and AAF [95]. This finding demonstrates extensive re-specification of cortical fields following auditory loss. In addition, in early deafened ferrets, recordings from single-units in the core auditory cortex showed that 72% were activated by somatosensory stimulation, compared to 1% in hearing controls [96]. In adult-deafened ferrets, extensive crossmodal reorganization of core auditory cortex was also described, which was characterized by a consistent somatosensory conversion in neuron responsiveness within 16 days after deafening [97], thus demonstrating that crossmodal plasticity can also occur after the period of sensory system maturation. These data suggest that subthreshold tactile inputs found in hearing animals can transform into suprathreshold responses in adult deafened animals. In this regard, it is worth mentioning that somatosensory inputs to the core auditory cortex represent the majority of non-auditory effects in hearing ferrets [96]. This specificity may be due to the greater functional similarities between somatosensory and auditory modalities regarding temporal precision underlying frequency percept (e.g. vibrotactile stimulations), compared to that between audition and vision.

The recruitment of A1 for the processing of visual stimuli was also revealed by fMRI investigations in congenitally or early deaf subjects [98–100]. Moreover, in adult-onset single-sided deafness (SSD), seeded functional connectivity of visual cortices revealed enhancement in visual areas and reduction in auditory regions, suggesting adaptive functional modifications of the visual network [101]. Furthermore, V1 seeds demonstrated increased connectivity in multiple regions, including those dedicated to speech (inferior parietal lobule) or somatosensory processing (postcentral gyrus). It is also noticeable that activation of A1 was observed in deaf subjects with total hearing loss during sign language tasks, but not in subjects with residual hearing ability [102], suggesting that this crossmodal plasticity depends on the extent of hearing loss. Additional evidence of compensatory functional changes comes from the observation that congenitally deaf cats, compared with hearing cats, have superior localization abilities in the peripheral visual field and lower visual movement detection thresholds [91]. In this study, reversible deactivation of posterior auditory cortex was found to selectively eliminate superior visual localization abilities, whereas deactivation of the dorsal auditory cortex eliminated superior visual motion detection. It is of interest that measuring the fMRI signal changes in response to spatially co-registered visual, somatosensory and bimodal stimuli, the visual responses which were stronger in congenitally deaf than hearing adults, appeared to be weaker than those elicited by somatosensory stimulation [103]. This is consistent with the above-mentioned finding on the prevalence of somatosensory over visual inputs in the core auditory cortex [96]. Congenital deafness was also found to enhance the accuracy of suprathreshold

tactile change detection, while tactile frequency discrimination thresholds tended to be reduced [104]. Beyond noticeable interspecies differences in the potential of crossmodal reorganization [61], the aforementioned studies highlight that deprived auditory sensory cortical areas become re-engaged in the processing of remaining sensory modalities.
