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Despite a recent upsurge of research, much remains unknown about the neurobiological mechanisms underlying synaesthesia. By integrating results obtained so far in Magnetic Resonance Imaging (MRI) studies, this contribution sheds light on the role of particular brain regions in synaesthetic experiences. First, in accordance with its sensory nature, it seems that the sensory brain areas corresponding to the type of synaesthetic experience are activated. Synaesthetic colour experiences can activate colour regions in occipito-temporal cortex, but this is not necessarily restricted to V4. Furthermore, sensory and motor brain regions have been obtained that extend beyond the particular type of synaesthesia studied. Second, differences in experimental setup, number and type of synaesthetes tested, and method to delineate regions of interest may help explain inconsistent results obtained in the BOLD-MRI (Blood Oxygen Level Dependent functional MRI) studies. Third, an overview of obtained results shows that a network of brain areas rather than a single brain region underlies synaesthesia. Six brain regions of overlapping results emerge, these regions are in sensory and motor regions as well as 'higher level' regions in parietal and frontal lobe. We propose that these regions are related to three different cognitive processes inherently part of synaesthesia; the sensory processes, the (attentional) 'binding' processes, and cognitive control processes. Finally, we discuss how these functional and structural brain properties might relate to the development of synaesthesia. In particular, we believe this relationship is better understood by separating the question what underlies the presence of synaesthesia ('trait') from what determines particular synaesthetic associations ('type').
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Brain Areas in Synesthesia 1
Running head: Brain Areas in Synesthesia
Brain Areas involved in Synesthesia: A Review
Romke Rouw*, H. Steven Scholte, and Olympia Colizoli
University of Amsterdam, Department of Psychology, the Netherlands
ACCEPTED FOR PUBLICATION IN JOURNAL OF NEUROPSYCHOLOGY, 2011.
* To whom correspondence should be addressed at: R.Rouw@uva.nl
Romke Rouw, Department of Psychology, University of Amsterdam, Roetersstraat 15, 1018WB
Amsterdam, The Netherlands.
Acknowledgments: We thank Michael X Cohen for assistance with the figures and helpful
suggestions on an earlier version of the manuscript. We thank two anonymous reviewers for their
valuable comments.
Brain Areas in Synesthesia 2
Abstract
Despite a recent upsurge of research, much remains unknown about the neurobiological
mechanisms underlying synesthesia. By integrating results obtained so far in MRI studies, this
contribution sheds light on the role of particular brain regions in synesthetic experiences. First, in
accordance with its sensory nature, it seems that the sensory brain areas corresponding to the type
of synesthetic experience are activated. Synesthetic color experiences can activate color regions
in occipitotemporal cortex, but this is not necessarily restricted to V4. Furthermore, sensory and
motor brain regions have been obtained that extend beyond the particular type of synesthesia
studied. Second, differences in experimental setup, number and type of synesthetes tested, and
method to delineate regions of interest may help explain inconsistent results obtained in the
BOLD-MRI studies. Third, an overview of obtained results shows that a network of brain areas
rather than a single brain region underlies synesthesia. Six brain regions of overlapping results
emerge, these regions are in sensory and motor regions as well as ‘higher level’ regions in
parietal and frontal lobe. We propose that these regions are related to three different cognitive
processes inherently part of synesthesia; the sensory processes, the (attentional) ‘binding’
processes, and cognitive control processes. Finally, we discuss how these functional and
structural brain properties might relate to the development of synesthesia. In particular, we
believe this relationship is better understood by separating the question what underlies the
presence of synesthesia (‘trait’) from what determines particular synesthetic associations (‘type’).
Brain Areas in Synesthesia 3
Introduction
“If someone scratches a blackboard with his or her nails, I taste iron. The intro of ‘Time’ by Pink
Floyd is golden yellow and blue. Poems have a color if they are cited, and sometimes when I read
them.” This is an excerpt of a synesthete’s report participating in our research. Synesthesia is a
condition in which a particular sensation (“inducer”) evokes another specific sensation not
commonly associated with it (“concurrent”). Well-known and common examples of synesthesia
are colors evoked by letters or words, and numbers or time units (e.g. days of the week) that
occupy specific locations in space (e.g. Jarick et al., 2009; Smilek et al., 2007; Seymour et al.,
1980; Price & Mentzoni, 2008). Quite different types of synesthesia have also been reported. For
example, synesthetic taste can be elicited by words (e.g. ‘part’ tastes like chicken noodle soup;
Ward et al., 2005). Animate qualities such as personality and gender can be attributed to linguistic
units such as letters, numbers, and days (Simner & Holenstein, 2007). Or certain visual
information, such as flashes or motion, causes the perception of sound (Saenz & Koch, 2008).
The field of synesthesia research has changed over the years from a relatively small group of
researchers targeting a largely unknown phenomenon to a well-accepted research topic that
receives an increasing interest in different fields of cognitive, neurological and developmental
aspects of human functioning. A major influence on this change in perspective is work showing
that synesthesia is a ‘real’ phenomenon (e.g., Baron-Cohen et al., 1987; Baron-Cohen et al., 1993;
Cytowic & Wood, 1982; Cytowic, 1995; Dixon et al., 2000; Palmeri et al., 2002; Smilek et al.,
2001; Ramachandran & Hubbard, 2001a & 2001b; Mattingley et al., 2001). Synesthetes report a
consistent and reliable within-subject experience that is not ‘made up’ and is not evoked by drug
use or mental disease and seems to be present from early childhood.
This phenomenon can therefore now be studied and viewed as a natural variation in healthy
human cognition. Furthermore, the field has taken advantage of new techniques to examine how
certain brain properties relate to synesthesia. Previous papers have provided excellent reviews
aimed in particular at cognitive processes and behavioral experiments, as well as developing
explanatory models for synesthesia (e.g., Grossenbacher & Lovelace, 2001; Rich & Mattingley,
2002; Mattingley, 2009; Hubbard & Ramachandran, 2001b; Hubbard, Brang, Ramachandran, this
issue). As we will discuss below, one interesting recent development is that an increasing number
of studies measure structural as well as functional brain properties in synesthetes. This review
aims to compile what these studies have taught us so far about the neurobiological basis of
Brain Areas in Synesthesia 4
synesthesia. The purpose of this review is to discuss functional and structural localization of
synesthesia rather than timing of network activity; thus, in pursuit of brevity we focus on MRI-
based and not on electrophysiology studies. In particular, four questions are addressed: First, as
color is the most common and most studied synesthetic concurrent, what have we learned about
activation of color areas during synesthesia? Is a particular color area activated during
synesthesia, and is activation limited to that particular area? Second, studies examining the role of
V4 in synesthetic color experiences do not seem completely consistent. What might explain these
inconsistent results? Third, we look at the whole brain rather than specific (color processing)
regions. Which locations in the brain seem particularly relevant in the neurobiological
mechanisms involved in synesthesia? We discuss both activation patterns and structural
differences in the brains of synesthetes versus non-synesthetes. Fourth, differences between
synesthetes and non-synesthetes are found in both structure and functioning of the brain, and this
raises the question what is the role of these differences in the development of synesthesia. We
present a framework to shed light on this issue by separating current findings on what underlies
the presence of synesthesia (‘trait’) from what determines particular synesthetic associations
(‘type’).
Part I: The Synesthetic Brain.
One important way in which synesthesia differs from those simple ‘associations’ between
concepts that are found in the general population (such as between ‘grass’ and ‘green’), is that
standard associations are only made at a conceptual or semantic level. In contrast, the synesthetic
associations also contain a modality-specific or sensory feature. Indeed, perceptual studies
(synesthesia aiding in a crowding task, Hubbard et al., 2005; synesthetic color-opponency,
Nikolić, et al., 2007; synesthetic photisms influencing visual perceptions, Smilek et al., 2001)
have shown the perceptual or percept-like nature of synesthetic experiences. This raises the
intriguing question of what is the relationship between synesthetic experiences and the
corresponding sensory-specific cortices. Theoretical accounts have proposed that activation of
perceptual or sensory areas can take place by ‘cross-activation’ through increased local
connectivity or by ‘disinhibited feedback’ from higher-level cortical areas. The first model
stresses the role of structural brain differences (see Hubbard et al., this issue), possibly due to
genetic predisposition, and a fast cross-over of activation from inducer to concurrent (e.g.,
Ramachandran & Hubbard, 2001b). The second model stresses the role of functional brain
differences only, and disinhibition between brain areas (e.g. from a multisensory nexus as
Brain Areas in Synesthesia 5
superior temporal cortex to sensory areas; Grossenbacher & Lovelace, 2001) or within a brain
area (Cohen Kadosh & Henik, 2007).
The great majority of neuroimaging work on synesthesia examined types of synesthesia in which
color experiences are evoked by hearing or seeing linguistic stimuli. There seems to be confusion
in the literature on the terms used (‘colored-hearing’ and ‘grapheme-color’)1. Most studies
unfortunately did not report whether participants were selectively sensitive to an auditory or a
visual presentation modality, or both. Similarly, a synesthete with colored words might or might
not have colored letters (and vice versa). It is therefore difficult to know the specific
characteristics of the synesthetes in these studies, and we chose to describe the different studies
based on characteristics of the study instead. While ‘grapheme-color’ synesthesia is often tested
by visual presentation of letters and ‘colored-hearing’ synesthesia is often tested by auditory
presentation of words, a more general term is ‘linguistic-color’ synesthesia (Barnett et al., 2008),
(but see Eagleman et al., this issue, showing that these synesthetes might in fact belong to the
category of ‘sequence-color’). In ‘linguistic-color’ synesthetes, a meaningful symbol (e.g. the
letter ‘A’, or the word ‘table’) evokes an additional experience of a particular color (e.g. bright
red). Understanding this type of synesthesia is fundamental, as the majority of synesthetic
inducers are linguistic, and the majority of synesthetic concurrents are color (Barnett et al., 2008;
Rich et al., 2005; Simner et al., 2006). With color as the synesthetic concurrent in these studies, it
follows naturally that a key question (e.g., Paulesu et al., 1995; Nunn et al., 2002; Hubbard et al.,
2005; Rich et al., 2006) is to what degree this synesthetic color experience evokes the same
(brain) mechanisms as a ‘normal’ color experience, i.e. a color experience that is evoked by a
corresponding color stimulus.
1 We thank an anonymous reviewer for pointing out and clarifying this issue.
Brain Areas in Synesthesia 6
Neurobiological basis of Color Processing
V4 is generally regarded as the specialized area processing color. This is mostly based on the
work of Semir Zeki (Zeki, 1990; Zeki et al., 1991). Zeki however writes: “While we refer to
human V4 and V5 as the color and motion centers, respectively, we do not wish to imply that the
processing of color or motion is necessarily their only function, or that these are the only areas
involved with those submodalities of vision. We state only that color and motion are among their
chief functions” (Zeki et al., 1991). Indeed, human V4 is also involved with the processing of
shape (David et al., 2006), deployment of attention (Luck et al., 1997) and retention of shape
information in visual working memory (Sligte et al., 2009). Conversely, V4 is not the only area
involved in normal color vision (e.g. Hadjikhani et al., 1998). While this brain region is certainly
important, color vision is in fact supported by a network of brain areas (Barrett et al., 2001;
Beauchamp et al., 1999; Heywood & Kentridge, 2003; Wandell et al., 2006). Different groups
used BOLD-MRI to show that in humans V1 can be the most responsive area to react to the
difference between color signals and luminance signals (Kleinschmidt et al., 1996; Engel et al.,
1997). Beyond V3, area V4 has been linked with ‘higher-level’ perceptual aspects such as color
constancy (Heywood & Kentridge, 2003). Perceptual color aspects in turn evoke at least partially
different activations from (object) color knowledge (Chao & Martin, 1999; Zeki & Marini, 1998).
Furthermore, which particular ‘color’ brain area is activated is influenced by attentional
modulation (Beauchamp et al., 1999). Moreover, not only V4 seems involved in perceptual color.
Brewer et al. (2005) found, besides V4, additional areas that also respond stronger to color
changes than luminance changes, namely VO1 and VO2. Interestingly, it is possible to decode
which colors were presented to subjects on the basis of V1, V2, V3, hV4 and VO1 (VO2 was not
analyzed) but not based on more parietal areas like LO1, LO2, V3A/B, or MT+ (Brouwer &
Heeger, 2009).
As we will subsequently show, different choices are made in synesthesia research in delineating
the ‘color area’ as a region of interest (ROI), which has implications for the functional properties
and locations of the obtained color regions. Another implication for synesthesia research is that
different cognitive demands (e.g. increased attentional demand) between baseline and
experimental conditions will likely affect brain activation in color regions regardless of the
presence or absence of the synesthetic color. As we will see below, this broader perspective on
color processing areas in the brain aids understanding of some of the contradicting results found
on the role of V4 during synesthetic color experience.
Brain Areas in Synesthesia 7
Activation of V4
In an eminent study, Nunn et al. (2002) measured brain activation in 13 synesthetes while they
listened to words that elicit a synesthetic color. This result was compared with brain regions
activated by colored abstract patterns (‘Mondrians’) in control subjects. The only significant
overlap was found in the left fusiform gyrus, at coordinates similar to those of V4. Hubbard et al.
(2005) found increased activation in V4 in response to seeing grayscale graphemes that evoke
synesthetic color. While studies like these show that synesthetic color experience is related to V4
activation, literature does not present a completely consistent image. For example, Aleman et al.
(2001) and Paulesu et al. (1995) did not find activation in V4 during auditory presentation of
letters numbers. One explanation for not finding V4 activation is lack of power of that particular
study. For example, the use of PET in the study by Paulesu et al., and the fact that Aleman and
colleagues studied only one synesthete could explain the absence of V4 activation.
While these are certainly important factors, they do not explain all null findings. Rich et al.
(2006), and Weiss et al. (2005) examined a similar number of synesthetes (7 and 9, respectively)
as Hubbard et al. (6 synesthetes), but did not obtain increased activation in V4. Remarkably, Rich
et al. did find that mental imagery of color activated right V4 in both synesthetes and non-
synesthetes. Synesthetic color, in contrast, activated the left medial lingual gyrus. As we will
discuss in the next section, whole-brain studies report activation in response to (naming)
synesthetic color in the left posterior ventrolateral region of temporal cortex (Gray et al., 2006), in
middle temporal and fusiform gyrus (Rouw & Scholte, 2007), in right fusiform and inferior
occipital gyrus (Laeng et al., 2009), and in retro-splenial and extrastriate cortex (Weiss et al.,
2001). Taken together, synesthetic color activation is found related to visual cortex, but this is
not restricted to V4. As is reported in ‘real’ color processing (e.g. Schluppeck & Engel, 2002;
Beauchamp et al. 1999), synesthetic color has been found to activate a broader range of areas in
ventral occipitotemporal cortex.
- Please insert Table 1 here -
Another explanation for finding inconsistent results is the heterogeneity in the experiments and
analyses used. As can be seen in Table 1, several characteristics of the studies vary, such as how
color-ROIs were delineated, the experimental manipulation (tasks) used, and the number and
types of synesthetes. The current number of studies is not sufficient to reveal how each of these
Brain Areas in Synesthesia 8
characteristics influences results. One interesting pattern does however catch the eye. Counter to
expectations, relatively many of the studies using auditory stimuli find activation in color
selective regions. A similar pattern emerges when looking at whole-brain studies (Table 2), where
occipital activations are found in studies using auditory presentation. This could be related to the
type of synesthesia tested. Another explanation relates to a different experimental setup. In the
“colored-hearing” studies, the experimental condition of listening to words is contrasted with a
baseline condition of listening to a pure tone. In contrast, several grapheme-color studies have a
visual task in both experimental and baseline conditions. Thus, the baseline condition might
employ brain regions responding to color, as they are expected to respond to other visual
information as well. The additional effect of synesthetic color activation is not necessarily easiest
to obtain in a visual-to-visual contrast.
- Please insert Table 2 here -
The third factor that influences results are individual differences between the subjects. The
relatively small number of subjects in most studies increases the influence of individual
differences. Note that the location of ‘synesthetic color’ activation is subject to both variations in
brain structure and to variations in structure-functioning relationships (Brett et al., 2002). Both
Steven et al. (2006) and Nunn et al. (2002) find V4 activation during synesthetic color, but point
at possible different function-to-structure mappings in synesthetes or synesthetic processes as
compared with ‘normal’ color perception (but see Mattingley, 2009). Individual differences
between synesthetes have also been found to influence synesthetic color activation. Sperling et al.
(2006) studied brain activation during linguistic-color synesthetic experiences and found that two
synesthetes showed bilateral V4 activation while the other two synesthetes did not. Similarly,
Hubbard et al. (2005) found that individual differences in V4 activation correlated with
behavioral effects. As synesthetes are a heterogeneous group (Sperling et al., 2006; Dixon et al.,
2004; Rouw & Scholte, 2010), results are likely influenced by the selection of the synesthetes
tested.
In Table 1, we summarize those studies with specific conclusions about the question whether V4
is activated during synesthetic color experience. These studies examine developmental
synesthetes in whom (auditory or visual) presentation of words, letters or names evoke
synesthetic color. We have also included information, if available, whether V1 is activated during
synesthetic color experience (insufficient information is available on activation in other visual
Brain Areas in Synesthesia 9
areas to include them in the table), and whether V4 was activated in response to normal colors in
the synesthetes. The summary shows how differences between the studies influence results. In
sum, five of the thirteen studies report V4 activation related to the synesthetic color, and four
more studies report activation in response to synesthetic color in other parts of ventral
occipitotemporal cortex. Only two out of nine studies found increased V1 activation related to
synesthetic color experience. Possibly, increased activation in V1 due to synesthesia was
obscured in other studies by activation during both baseline and experimental conditions. It is
also possible that normally striate cortex is not activated sufficiently during synesthetic color
experiences.
The first question addressed here is whether synesthetic color experiences activate ‘normal’ color
regions. It is reasonable to conclude that activity in color areas can be obtained in response to
synesthetic color experiences. However, activation is not limited to V4, and results are not
consistent due to differences in experimental set-up. Three recommendations can be made to
improve sensitivity to synesthetic color activation. The first is using cortical mapping, which both
improves the signal-to-noise ratio and can be used to average regions over subjects. One study
that used retinotopic mapping did indeed obtain a positive relationship between V4 activation and
synesthetic color experiences (Hubbard et al., 2005). The second is using an experimental setup
that takes into account that brain activation in response to general color processing is not limited
to one particular (V4) location, and that ‘color areas’ are likely to respond to other cognitive
functions as well. The third is testing larger groups of synesthetes, and select synesthetes based
on characteristics of their synesthesia (e.g. strong perceptual sensations).
Activation in the whole brain
After addressing the question whether synesthetic color activates V4, and what might explain the
inconsistent results obtained, we now turn to the question which brain regions seem related to
synesthesia. An increase of brain activation obtained in a ROI analysis does not necessarily mean
that this increase is the strongest or most prominent in the whole brain. For example, Aleman et
al. (2001) found increased V1 activation in a ROI analysis but did not obtain increased activation
in any visual area in the whole brain analysis of that same data. Whole brain analyses are
particularly informative about which of all the possible (and perhaps unexpected) brain areas
show the strongest and most consistent activation during synesthesia. These exploratory analyses
are important to understanding the mechanisms involved in synesthesia, considering how little is
known about its neurobiology.
Brain Areas in Synesthesia 10
We compiled the whole-brain studies that measured (with fMRI or PET) brain activation in
response to synesthetic color and displayed these coordinates in an MNI brain. In these studies,
the specific task used, number and type of linguistic-color synesthetes examined, and presentation
of stimulus material differs (see Table 2). We choose the contrasts that seem to most closely
measure the mere presence of synesthetic experience (e.g. grayscale graphemes rather than
contrasting congruent with incongruently colored graphemes). If available, we chose contrasts
that include an interaction with group (synesthete versus control). Only studies reporting
coordinates are included (if needed converted from Talairach to MNI). To increase comparability,
all coordinates provided in the studies are labeled with the Jülich histological atlas, and, if this did
not provide a clear label, with Harvard-Oxford cortical structural atlas. As the study of Sperling et
al. (2006) presents three synesthetes separately, these nine studies provided eleven data points in
total.
On first inspection, these studies show activity at different locations. This could be due to the
differences in experimental and statistical approach. Six brain locations however emerge where
studies (minimally three of the nine) converge in reported locations, despite these differences.
The rather low number of studies allows only for qualitative comment rather than strong
statistical conclusions. Still, we believe it is warranted to discuss the areas of convergence
because they reveal a pattern, which provides insight on what has so far been found in
neuroimaging studies.
The first region is bilateral activation in occipitotemporal cortex. This is an expansion rather than
replications of the studies in Table 1, as they partially include the same studies. The current
analysis shows that activation is found in visual cortex, beyond striate cortex. And that these
findings are strong and consistent enough to appear in whole-brain analyses (left: Laeng et al.,
2009; Steven et al., 2006; Nunn et al., 2002; right: Laeng et al., 2009; Rouw & Scholte, 2007;
Weiss et al., 2001). As can be viewed in Figure 1A, the obtained location of increased activation
is not restricted to coordinates of V4 only. As we discussed in the previous section, this can be
due to differences in measurement methods, but also seems to support a more widespread
network of ventral occipitotemporal areas involved in synesthetic color perception.
- Please insert Figure 1 here -
Brain Areas in Synesthesia 11
The role of visual areas in synesthetic color experiences becomes increasingly clear. One future
direction of research is to develop methods that are more sensitive. Laeng et al. (2009) presented
synesthetes with colored letters, and manipulated color distance between the typeface color of the
letter and of the synesthetic color it evoked. This is an elegant manner to measure a more
(methodologically) sensitive manipulation of the subjective experience itself by manipulating the
nature of the combined (synesthetic and typeface color) experiences rather than merely
contrasting presence versus absence of synesthetic color experience (studies presented in Table
1). The study from Laeng and colleagues showed that increased distance in color space led to
greater recruitment of neural units of V4/V8. This shows that the simultaneous conscious
experience of more than one color is supported by simultaneous activation of the color areas.
Overall, these results show that some of the brain areas in occipitotemporal cortex that are
activated by real color are also activated by synesthetic color. (Although in color brain areas, a
synesthetic color prime does not suppress the BOLD response for subsequently presented real
colors, van Leeuwen et al., 2010). The involvement of corresponding sensory-specific cortex
might explain the perceptual or percept-like nature of the synesthetic experience (Hubbard et al.,
2005; Nikolić et al., 2007; Smilek et al., 2001; Palmeri et al., 2002).
Brain areas specifically tuned to processing graphemes or color, are not sufficient to explain the
activation patterns during linguistic-color synesthesia. The most eye-catching in our analyses are
clusters of activation obtained in parietal cortex, almost exclusively located in posterior parietal
cortex. The posterior parietal cortex consists of the superior parietal lobule and the inferior
parietal lobule. Whole-brain studies report increased activation in both left (Weiss et al., 2005;
Laeng et al., 2009) and right (Paulesu et al., 1995; Weiss et al., 2005; Laeng et al., 2009) superior
parietal lobule in response to synesthetic color experiences. The most compelling area of common
activation across studies was the inferior parietal lobule. With the exception of Laeng et al.
(2009), (and possibly Elias et al., 2003, but the use of different labels complicates comparison
with this study), these studies report activation in the left hemisphere only (Nunn et al., 2002;
Rouw & Scholte, 2010; Steven et al., 2006, Weiss et al., 2005). Inspection of the coordinates of
the obtained clusters showed that some clusters are located more anterior and superior (Laeng et
al., 2009, Nunn et al., 2002, Weiss et al., 2005) and others more posterior and inferior (Laeng et
al., 2009, Rouw et al., 2010, Steven et al., 2006), see Figure 1B. All locations of activation in
inferior parietal lobule, however, are best summarized as either near the intraparietal sulcus, or in
the angular gyrus. The significance of this region was verified in two TMS studies, showing a
decreased effect of synesthetic color in a behavioral task (Esterman et al., 2006; Muggleton et al.,
Brain Areas in Synesthesia 12
2007). It is not yet clear why the TMS studies found only reliable effects on synesthesia after
TMS on right parieto-occipital region, while the neuroimaging studies find mostly left inferior
parietal activation.
The parietal lobule has gained increasing attention in the field of synesthesia research. Its known
role in (attention-based) visual feature binding (Shafritz et al., 2002; Donner et al., 2002) makes
this an important candidate region for binding, or ‘hyperbinding’ the inducer to the concurrent
sensations (Robertson, 2003; Esterman et al., 2006; Hubbard, 2007; Weiss & Fink, 2009). In sum,
brain regions in inferior and superior posterior parietal lobules seem important components of the
network of brain regions involved in synesthesia, possibly related to the ‘binding’ that is an
inherent part of synesthesia.
The fourth region is bilateral insula (Sperling et al., 2006; Nunn et al., 2002; Paulesu, et al., 1995)
and operculum. Insula activation could be related to the conversion process of a particular
external stimulus to a different internal stimulus (Paulesu et al., 1995). Activation in this region
might also be related to the emotional quality that seems to often accompany synesthetic
experiences, as synesthetes often report that a certain ‘feel’ belongs to a synesthetic experience. If
this explanation is correct, increased insula activation can be obtained in different types of
synesthesia.
Five studies found activation in left precentral gyrus (Paulesu et al., 1995; Weiss et al., 2005;
Nunn et al., 2002; Rouw & Scholte, 2010; Laeng et al., 2009), while three found activation in
right precentral gyrus (Paulesu et al., 1995; Laeng et al., 2009; Rouw & Scholte, 2010) (Figure
1C). As it is not directly clear how motor (preparatory) responses could be different between
baseline and experimental task in these studies, it might relate to the synesthetic experience. The
extended activation in brain regions involved in sensing of and acting in the outside world (visual
cortex, activation in and near insula, and precentral activation) suggests a larger network of brain
areas is involved in synesthesia. It possibly also reflects additional aspects of the synesthetic
experience (Eagleman & Goodale, 2009).
The frontal lobe has so far received relatively little attention in synesthesia research, even though
most whole-brain studies (seven out of nine) report activation at some location in frontal cortex
during the synesthetic experience (Table 2). Three studies (Laeng et al., 2009; Paulesu, et al.,
1995; Sperling et al., 2006, the latter study found activation bilaterally) from the nine studies
Brain Areas in Synesthesia 13
found activations very adjacently located (Figure 1D) in right dorsolateral prefrontal cortex.
While this is a small number of studies, activation of this region might reflect an important aspect
of synesthesia, namely increased cognitive control processes (Duncan & Owen, 2000). As the
conflict between internally and externally generated sensations is an inherent part of synesthesia,
certain locations in the synesthetic brain network are expected to be related to cognitive control.
Weiss et al. (2005) found that conflict between physically evoked and synesthetically perceived
colors of letters increased activation in right fusiform gyrus and left dorsolateral prefrontal cortex.
This conflict might also relate to activation in parietal cortex. Cohen Kadosh et al. (2007)
presented a task (slightly different from those used in the studies presented in Table 1), that
showed that a congruency effect modulated activity in the intraparietal sulcus and in the angular
gyrus in the left parietal lobe, as well as the P300 amplitude.
Unfortunately, only a few studies have so far examined brain activation in other types of
synesthesia. These studies do, however, present two similar inferences. The first is activation in
sensory brain areas corresponding to the particular synesthetic experience. An acquired sound-
touch synesthete showed increased activation in secondary somatosensory cortex during
synesthesia (Beauchamp & Ro, 2008). Similarly, the synesthetic experience of touch, evoked by
seeing another person being touched, showed activation patterns that were interpreted as the
brain’s mirror system (somatosensory cortex, left premotor cortex and anterior insula cortex
bilaterally; Blakemore et al., 2005). A patient that reported that certain odors increased his
neuropathic pain (Villemure et al., 2006), showed increased activation during odor-evoked pain
in both pain related areas (including the thalamus, amygdala, insular and anterior cingulate
cortex) as well as trends in primary somatosensory cortex in the hand/arm area, which is where
the man felt the neuropathic pain. Second, in these studies several brain areas rather than only
particular sensory activations were measured. As in linguistic-color synesthesia, a network of
brain areas rather than isolated sensory-specific activation is found related to synesthesia.
A common type of synesthesia, next to colored leters or words, is number-form synesthesia,
where sequences of numbers are experienced on a mental line. Tang et al. (2009) showed that
when demands of the tasks are spatially similar to their number-form representation, the
synesthetes showed increased activation in bilateral precentral gyri, left insula, and several
parietal regions including the left superior parietal lobule and the bilateral posterior intraparietal
sulcus (IPS). The authors related the bilateral posterior IPS to the ordinal representations that are
essential for number-forms. Finding the same activated locations in number-form synesthesia as
Brain Areas in Synesthesia 14
in linguistic-color synesthesia can be due to a similarity in the type of synesthesia (both in
number-form and in linguistic-color synesthesia numbers will induce visual/spatial
representations). It can also reflect that these brain areas are related to synesthesia in general
rather than to a specific type of synesthesia. As in other types of synesthesia, Tang et al. found
more widespread activation than only in corresponding sensory areas, including activation in
frontal, temporal and cingulate gyri. Eagleman (2009) proposes instead a role of temporal cortex
in spatial sequence synesthesia, based on!increased!cross+talk!between!areas!involved!in!
overlearned!sequences!(in!the!middle!temporal!gyrus)!and!an!area!implicated!in!visual!
object!!representation!(in!inferior!temporal!lobe).!
So far, we discussed six regions that have been found to be related to synesthetic experiences.
The current review also shows how certain regions, proposed to play a crucial role in synesthesia,
have not been obtained. Acquired synesthesia studies (Beauchamp & Ro, 2008; Ro et al., 2007)
have suggested a relationship between synesthesia and the thalamus. In these studies, a thalamic
lesion resulted in acquired synesthesia. This was explained as a positive outcome of the neural
plasticity induced by the stroke. No relationship could be established between synesthesia and the
thalamus in the current review. Thalamus (in)activation is seldom reported in neuroimaging
studies. Perhaps the thalamus is not always carefully analyzed in these studies. Alternatively,
inherently different neurobiological mechanisms underlie developmental and acquired
synesthesia. Another prediction that has not received support is the proposed role of the superior
temporal cortex. This polysensory brain area has been proposed to mediate synesthesia via
feedback connections to unisensory cortical areas (Grossenbacher & Lovelace, 2001). The
summary (Table 2) shows that a relationship between synesthetic experiences and this particular
brain area is not supported by current findings.
All findings discussed so far were obtained by measuring brain activity during synesthesia with
BOLD-MRI or PET. We now turn to the question what is the status of research on the structural
properties of brains of synesthetes as compared with non-synesthetes.
Synesthetes have a structurally different brain
Since 2007, three studies have appeared exploring the anatomical differences between synesthetes
and controls in terms of white matter tract coherency as measured with fractional anisotropy (FA)
(Rouw & Scholte, 2007; Hänggi et al., 2008; Jäncke et al., 2009; see Table 3A), and four studies
have appeared exploring these differences in terms of gray matter (Hänggi et al., 2008; Jäncke et
Brain Areas in Synesthesia 15
al., 2009; Weiss & Fink, 2009; Rouw & Scholte, 2010; see Table 3B). An overview of the areas
in which differences were found are given in Table 3. To facilitate the comparison between these
studies in this table, the names of brain areas are derived from the Jülich histological atlas
(Eickhoff et al., 2007), and if this did not provide a clear or strong interpretation, from the
Harvard-Oxford atlas, based on the coordinates provided in these studies.
- Please insert Table 3A and Table 3B here -
Even though the number of publications into the anatomical differences between synesthetes and
controls are limited, we believe that a picture emerges from these studies that converge with the
findings from the functional studies. First, the data support the theory of cross-activation between
these two (inducer and concurrent) areas, mediated by structural (connectivity) differences
(Ramachandran & Hubbard, 2001b). Rouw & Scholte (2007) found increased connectivity
(increased FA values) near the fusiform gyrus in the neighborhood of area V4. This has been
partially replicated by Jäncke et al., 2009, in right fusiform gyrus, at a threshold of p = 0.05.
Furthermore, two of the studies showed that synesthetes have increased gray matter in area V4
(Hänggi et al., 2008; Weiss & Fink, 2009). Interestingly, a case in which either a tone, or a tone
interval induces synesthesia (Hänggi et al., 2008) found increased connectivity (as measured in
increased FA values), as well as increased white and gray matter volume in the primary auditory
cortex. Structural differences in gray and white matter were also found in the concurrent
(gustatory and visual regions) brain areas. Perhaps in less common types of synesthesia, more
distant rather than local cross-activation must be present (Hänggi et al., 2008). Second, in all
three studies dealing with linguistic-color synesthesia, the superior parietal lobe is larger in
synesthetes than controls. Third, synesthesia seems to coincide with an increase in the gray matter
density of sensory areas, even if they are not necessarily related to the synesthetic modality.
Hänggi et al. (2008) and Jäncke et al. (2009) found increased gray matter in V1 and V2, even
though the Hänggi study examined interval-taste and tone-color synesthesia. Jäncke et al. (2009)
found increased gray matter in the secondary somatosensory cortex while this study examined
grapheme-color synesthesia. Perhaps these synesthetes had another type of synesthesia as well,
since different types of synesthesia are likely to co-occur (Simner et al., 2006). It does however
seem unlikely that the researchers did not find or report these additional, visual, types of
synesthesia as a possible explanation to their findings. Another possibility is that this increased
grey matter in sensory cortex is related to individual differences. Rouw & Scholte (2010) found
Brain Areas in Synesthesia 16
increased gray matter in V1, auditory and somatosensory cortex specifically in projector as
compared with associator synesthetes.
Finally, as can be seen in Table 3, it appears that structural differences between synesthetes and
controls can be found in different brain areas, both in terms of white and gray matter. This shows
that synesthesia coincides with large-scale anatomical differences throughout the brain and not
only in the regions involved in the processing of the crossing experiences. As we will discuss
later, these widespread differences indicate that different brain properties might be related to
having the ‘trait’ synesthesia as well as to the particular ‘type’ of synesthesia.
Another implication of these anatomical differences is that it should be taken into account in
interpreting functional differences. Anatomical between-group differences can result in a
difference in BOLD-MRI activation between these groups. For instance, if V4 is in general larger
in synesthetes than in controls, BOLD-MRI activation will appear larger in the synesthetes than
the controls because of different underlying alignment.
Together these studies imply that there are structural differences in synesthetes throughout the
brain. Structural differences are obtained in sensory brain regions that correspond with both
inducer and concurrent information. A similar conclusion can be drawn here as in the previous
section on functional (activation) data. The facts that structural differences are not restricted to
sensory areas, and that differences are obtained in sensory regions that do not correspond with the
particular synesthetic experience, suggest that structural differences are not restricted to the type
of synesthesia. Therefore, these anatomical differences might also be interpreted to suggest that
there is a general disposition to develop synesthesia, irrelevant of the type. This concurs with the
findings on the genetic basis of synesthesia.
Conclusion
The current review shows that V4 is an important, but not sufficient, component of the brain areas
related to synesthetic color experience. Instead, an extended network of areas seems involved in
both linguistic-color and other types of synesthesia. We propose that this network supports three
different cognitive functions that are inherently part of synesthesia. The first are sensory
processes. Current literature indicates that the synesthetic experience activates corresponding
sensory areas. That is, synesthetic experiences activate those brain areas that are normally
involved in a ‘normal’ sensation evoked by an external stimulus. A relationship with sensory
Brain Areas in Synesthesia 17
brain areas that do not correspond with the particular synesthetic associations studied might
reflect the richness of the synesthetic experience (insula activation reflecting the emotional
quality of a synesthetic concurrent). Furthermore, structural brain differences in different sensory
regions might reflect that within a synesthete a predisposition is present to several, not one
particular, type of synesthesia. The second class of cognitive function is related to integrating
(inducer with concurrent) information, such as processes involved in (attentional) feature binding.
The parietal lobe holds the most important candidates for this function. We propose that a third
class of processes involved in synesthesia is cognitive control processes. The simultaneous
presence of different, possibly conflicting, sensations is inherently part of synesthesia. This
‘synesthetic conflict’ has so far been found to be related to frontal cortex (in particular right
dorsolateral prefrontal cortex) and parietal cortex. Finally, the question of whether there are
structural brain differences between synesthetes and non-synesthetes has now been answered
affirmative. What still needs to be determined, however, is the role of these structural and
functional brain differences in the development of synesthesia.
Part II: The Development of the Synesthetic Brain
Genetic differences
Synesthesia tends to run in families. This was observed by Galton (1880) and confirmed in
modern studies, which show that at least 40% of synesthetes have a first-degree relative with
synesthesia (Baron-Cohen et al., 1996; Barnett et al., 2008). Currently, multiple linkage studies
are being conducted which search for polymorphisms related to synesthesia. Recently, the results
from the first genome-wide linkage study of synesthesia were published (Asher et al., 2009),
based on 43 multiplex families. Synesthetes were selected based on their report of ‘auditory-
visual’ synesthesia. This most likely does not constitute a completely homogeneous subject
group, since it is not further specified which particular material (sounds, spoken language, written
language, single phonemes and graphemes) evokes color for each of these subjects. Results
indicate that synesthesia in this subject group is related to multiple, but not unique, gene loci
(2q24, 5q33, 6p12, 12p12). No evidence was found for a relationship with the X-chromosome.
This is relevant because it has been hypothesized that an involvement of genes on the X-
chromosome might drive a predominance of synesthesia in females (Baron-Cohen et al, 1996;
Ward & Simner, 2005). Interestingly, the highest loading marker in this study (D2S142) contains
TBR1, a gene involved in the regulation of reelin (Bulfone et al., 1995), which plays a vital role
Brain Areas in Synesthesia 18
in the development of the cerebral cortex. Knock-out studies targeting this gene have shown that
a deregulation of reelin leads to abnormalities in the laminal organization of the brain (Hevner et
al., 2001) and influences the path-finding of axons (Hevner et al., 2002). Taken together, these
studies suggest that the genetic basis of synesthesia will be found, at least in part, in genes that
influence the development of connectivity in the brain. The synesthetic genotype is a
predisposition, rather than a defined predetermination. One particularly striking discovery is a
case of monozygotic twins where one has synesthesia while the other has not developed it
(Smilek et al., 2002).
Clearly, the starting point in understanding developmental synesthesia is the genetic
predisposition. Both genetic association studies and studies examining familial traits suggest that
synesthetes exhibit particular differences compared to non-synesthetes from birth (Asher et al.,
2009; Barnett et al., 2008). Intermediating between the genetic predisposition and the
extraordinary sensations characteristic to synesthesia are most likely neurobiological settings, in
particular structural brain properties. Bargary and Mitchell (2008) explicate how mutations in
genes directly controlling cortical connectivity can lead to synesthesia. They explain how
differences in axonal guidance, border formation, or pruning, can create direct, feed-forward
connections between adjacent areas that can drive the synesthetic experience. This is an important
contribution in understanding synesthesia, showing how a genetic mutation could lead to
differences in white matter pathways (see Marks, 1975 ; Ramachandran & Hubbard, 2001b;
Spector & Maurer, 2009). Other theories on synesthesia stress a difference in brain functioning
instead (Grossenbacher & Lovelace, 2001; Cohen Kadosh & Walsh, 2008). This is by itself not
contradictory, as differences in brain structure can be expected to lead to differences in brain
functioning, and vice versa (see below). While in the past the question was raised whether
structural differences are present between synesthetic and non-synesthetic brains, this question
has in recent years been answered (Rouw & Scholte, 2007; Hänggi et al., 2008; Jäncke et al.,
2009; Weiss & Fink, 2009; Rouw & Scholte, 2010). What remains to be answered, is the exact
level at which cross-activation occurs, the role of the different brain areas involved, the role of the
structural brain differences, and the role of learning in synesthesia.
Developing synesthesia: trait versus types
Familial studies on synesthesia reveal that having synesthesia, rather than having particular types
of synesthetic associations, runs in families (Barnett et al., 2008; Rich et al., 2005). Thus, your
synesthetically colored letters are a hint that you can probably find synesthetes in your family, but
Brain Areas in Synesthesia 19
it gives no information whether their ‘A’s will also be blue, or even that their synesthesia is
expressed as colored letters. This is in line with the genetic association study, which related
synesthesia to multiple genes, which are expected to relate to general effects rather than effects
limited to a particular brain location. In line with this hypothesis, we found functional and
structural effects not only in those brain areas related to the specific inducer or concurrent, but
also in other sensory areas. Similarly, parietal and frontal mechanisms which we speculate are
involved in the ’binding’ and control mechanisms in synesthesia, are proposedly an inherent part
of the general synesthetic trait, not of a particular type.
Thus, if (genetically based) differences in brain properties shape a general ‘synesthetic
constitution’, this constitution is not specialized to a certain type of synesthesia. In particular,
increased connectivity resulting from a genetic predisposition likely has a widespread rather than
localized effect in the brain. This explains why having a certain type of synesthesia increases the
chance of having other types of synesthesia as well (Sagiv et al., 2006). In addition, if a subject
has several types of synesthesia this does not imply similar properties of these associations (Ward
et al., 2005). The effect of the ‘constitution’ possibly extends beyond synesthesia. Burrack et al.
(2006) found a high prevalence within synesthetes of ‘mitempfindung’, where tactile stimulation
of one part of the body simultaneously produces a sensation at a different location. These authors
note how erratic neural connectivity might underlie both phenomena.
In the development of language (Halliday, 1975) a predisposition is present in the child to learn to
speak a language, but it is the environment determining which particular language a child will
learn. Similarly, a child may be born with a predisposition to develop synesthesia, but will not be
born with a red ‘A’. These highly specific cross-associations are somehow created or picked up in
early childhood (e.g., Rich et al., 2005). Simner et al. (2009) show how the synesthetic
associations are shaped during development, with more associations present in 7.5-year-olds than
in 6.5-year-olds. In special cases, the source of a particular association has been retrieved, such as
finding the refrigerator magnets that shaped a particular synesthetes’ letter-color associations
(Witthoft & Winawer, 2006). More general influences of experience on particular synesthetic
associations have also been found. Grapheme-color synesthetes show biases to certain
associations over others (e.g. higher frequency graphemes are found related to higher frequency
color names, Simner et al., 2005; Simner & Ward, 2007; or more saturated synesthetic colors,
Beeli et al., 2007, or luminance of synesthetic color, Smilek et al., 2007). Importantly, when non-
synesthetes are asked to devise letter-color associations, the same trends (though not necessarily
Brain Areas in Synesthesia 20
as strong) are found as in synesthetes (Marks, 1975; Simner et al., 2005; Rich et al., 2005; Smilek
et al., 2007). Synesthetes share with non-synesthetes the same environment, and therefore the
same environmental influences on specific types of associations over others. This does not relate
to having, or not having, the synesthetic trait. We propose that this notion of how environment
influences synesthetic associations extends to culture; in the current account the number of adults
with synesthesia is expected to be culture-independent, but we hypothesize that the exposure to a
certain type of material in a culture (e.g. the ubiquity of language or music in early childhood)
predicts which particular types of synesthesia develop.
Thus, we see that there are two aspects of synesthesia, with two different answers to the question
‘how does synesthesia develop’. The first question is what underlies having synesthesia in
general. Research has shown a genetic predisposition to synesthesia, which is proposed to bias
general characteristics of brain structure and functioning. These characteristics are idiosyncratic
to synesthetes. One example is a genetic predisposition to develop differences in white matter
pathways. The second question is what underlies having a particular type of synesthetic
association. The specific associations that develop are highly dependent on environment. These
biases can also be found in non-synesthetes as they are under strong influence of the environment
Inducers versus Concurrents
We will now turn to the question what determines which particular material is inducer and which
is concurrent. Synesthetic associations are often (but not always, Cohen Kadosh et al., 2007)
directional. The study from Simner et al. (2009) showed the developmental pattern of learning
synesthetic associations during childhood. As we have argued above, we believe that particular
associations are shaped in interaction with the environment. Rather than a lack of functional
specialization (Cohen Kadosh et al., 2009), we believe that this interaction leads to additional,
highly specialized, cross-connections between inducer and concurrents. We propose that a child
with a predisposition for synesthesia will tend to map newly learned material, onto an already
present, earlier learned category. This can explain why color is the most common concurrent but
rare as an inducer (Barnett et al., 2008), as it is one of the earliest categories learned. Color
categories can be used when learning linguistic material, as pre-linguistic infants have been found
to already perceive color categorically (Franklin & Davies, 2004; Bornstein et al., 1976). While
there are exceptions (such as pain or taste as concurrent) in many types of synesthesia the order in
which material is learned seems to influence inducer-concurrent relationships. A child is likely to
be exposed to taste categories before learning musical tone intervals (Beeli et al., 2005), to taste
Brain Areas in Synesthesia 21
before words (Ward & Simner, 2005), and to animate-like qualities such as personality or gender
before learning linguistic material (Simner & Holenstein, 2007). In terms of biological factors,
Bargary and Mitchell (2008) note how early versus late-maturing brain areas bias the
maintenance of certain cross-activation over others. For example, the brain is ready to store color
information before it is ready to store more complex linguistic information. In line with the
interactive account, the biological and environmental settings are two sides of the same coin.
Functional and structural brain properties are influenced by a child’s learning experiences.
Conversely, a child will tend to show interest to particular material at a moment the brain is ready
to ‘receive’ (process) that type of information.
An important assumption of this interactive account of shaping synesthetic types, is that the
relationship from gene to structural brain properties to behavior, also has a reverse direction: from
behavior back to (structural) brain differences. Recent studies have indeed related expertise or
experience in particular skills to differences measured in white and gray matter properties. The
measured skills are quite diverse: driving a taxi in London, playing an instrument, playing the
game Baduk (A.K.A. Go), meditating, or practicing mathematics (Maguire et al., 2000; Lazar et
al., 2005; Elbert et al., 1995; Habib & Besson, 2009; Han et al., 2009; Lee et al., 2010; Aydin et
al., 2007; Tuch et al., 2005; Johansen-Berg et al., 2007). As in synesthesia research, these studies
are cohort studies, and therefore contrasting groups necessarily precludes conclusions on
causality. Some studies have however obtained longitudinal measurements that allow conclusions
about the direction of the effect. Draganski et al. (2004) examined brain structure with MRI
voxel-based morphometry during the training of a visuo-spatial skill (juggling). The jugglers
showed expansion of gray matter in related brain areas. Furthermore, this expansion was
decreased after three months in which juggling was not practiced. A similar effect of experience-
dependent structural changes was found in white matter (underlying the intraparietal sulcus)
following training of juggling over several weeks (Scholz et al., 2009). A recent study showed
training-induced plasticity of white matter in a purely cognitive skill without motoric component,
namely working memory (Takeuchi et al., 2010).
These studies show that repeated experiences or behavior can in turn affect brain properties. In
principle, it is possible that in synesthesia (as in training a ‘normal’ skill) the particular
synesthetic associations become ‘hardwired’ in the brain. One hypothesis is that particular
synesthetic associations, while they develop, also affect particular brain areas (i.e. corresponding
sensory regions). As argued before, effects obtained in brain imaging studies support the idea of
Brain Areas in Synesthesia 22
both general effect of synesthesia and specifically localized effects based on the particular type of
synesthetic associations. In short, this view would suggest that the synesthetic predisposition
(Asher et al., 2009; Barnett et al., 2008) enables making synesthetic associations, through general
brain properties (e.g. a bias to increased white matter connectivity, Rouw & Scholte 2007; Jäncke
et al., 2009; Hänggi et al., 2008; Bargary & Mitchell, 2008; Ramachandran & Hubbard, 2001a;
Spector & Maurer, 2009). Particular synesthetic associations develop in interaction with the
environment (Simner et al., 2005; Simner & Ward, 2007; Beeli et al., 2007; Smilek et al., 2007;
Rich et al., 2005; Witthoft & Winawer, 2006). These synesthetic associations are ‘hardwired’ in
the brain through changes in structural and functional brain properties. The structural brain
differences that arise through both the ‘trait’ and the ‘type’ of synesthesia (Hänggi et al., 2008;
Jäncke et al., 2009; Rouw & Scholte, 2007; Rouw & Scholte, 2010; Weiss & Fink, 2009) in turn
support the highly persistent, automatic (in the sense that it takes little effort) and consistent
associations in adulthood (Baron Cohen, 1987; Baron-Cohen et al., 1993; Cytowic & Wood,
1982; Dixon et al., 2000; Mattingley et al., 2001).
The role of brain properties in synesthesia raises the interesting question whether the genetic
predisposition is just a ‘stepping stone’ to create synesthetic experiences, or if it is a prerequisite.
A study by Meier & Rothen (2009) has shown that synesthete-like behavior can be obtained in
non-synesthetes after training. The study from Scholz et al. (2009) shows that training a certain
skill may become ‘hard-wired’ as changed properties of white matter tracts. The question whether
learned synesthetes can become ‘real’ synesthetes, both in terms of the perceptual nature of
synesthesia and in terms of their brain structure and functioning, is an interesting topic for future
research.
Brain Areas in Synesthesia 23
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Figure Legends
Figure 1. Brain areas activated during linguistic-color synesthesia, as measured in whole-
brain (BOLD-MRI or PET) studies. Coordinates of obtained activation in nine different studies
are depicted in an MNI brain. For tasks and methods of the studies see Table 1 and 2.
Brain Areas in Synesthesia 33
Table Legends
Table 1. V4 activation (in green) during synesthetic color experience. Studies measuring brain
activation (with BOLD-MRI and PET), during linguistic-color synesthesia, that draw a
conclusion about V4 activation in response to synesthetic color. Indicated are number of
synesthete (Syn) and non-synesthete control (Con) subjects, modality of presentation of stimuli
during fMRI task (Auditory or Visual), the contrast (C) used to measure brain activation and the
fMRI task (T) presented during measurement (C/T means that these two are the same). The
second column presents the analysis method. For each study, three conclusions are presented
(Yes, No, or Not Available): V4 activation during synesthetic color experience; V1 activation
during synesthetic color experience; V4 activation to ‘real’ color in synesthetes.
Table 2. Brain areas activated during linguistic-color synesthesia, as measured in whole-
brain (BOLD-MRI or PET) neuroimaging studies. Presented are Brodmann area (if provided),
left (L) or right (R) hemisphere activation, the label we provided (Jülich histological/Harvard-
Oxford cortical structural atlas), coordinates (if necessary converted to MNI), t or z score of the
effect, modality (visual or auditory) of the presented stimuli, contrast used (S=Synesthete,
C=Control). Below references and threshold of these studies. For tasks see Table 1. We include
only activations and not deactivations in response to synesthetic experience. This is not because
we believe it is less meaningful, but because only a few studies report deactivation, which makes
it difficult to compare between studies.
1 Laeng et al., 2009 (p < .05, 30 voxels).
2 Nunn et al., 2002 (exp1) (voxel-wise p < 0.0005).
3 Paulesu et al., 1995 (p < .01).
4 Rouw & Scholte, 2007 (z > 2.3, p = .05).
5 Rouw & Scholte, 2010 (z > 2.3, p = .05).
6 Sperling et al., 2006 (p < .05).
7 Steven et al., 2006 (z > 2.3, p < .01).
8 Weiss et al., 2001 (p = .001).
9 Weiss et al., 2005 (t = 4.52, p < .05).
Table 3A. Structural brain differences in white matter properties of developmental
synesthetes and non-synesthetes. In columns: hemisphere (left or right), location (derived from
the Jülich histological atlas (Eickhoff et al., 2007) or the Harvard-Oxford atlas, the coordinates,
the t value and extend in mm3 of the effect, method of analyses, number of synesthetes (S) and
controls (C) or musicians (music.) contrasted, and type of synesthesia reported by the authors (IT
= interval-taste & tone-color; GC=grapheme-color).
Table 3B. Structural grey matter differences in developmental synesthetes versus non-
synesthetes. In columns: hemisphere (left or right), location (derived from the Jülich histological
atlas (Eickhoff et al., 2007 or the Harvard-Oxford atlas), coordinates provided in these studies,
the t, p and extent in mm3 of the obtained effect, method (cortical volume, surface areas or
cortical thickness) and subjects contrasted (Synesthetes, Controls, Musicians, Projectors,
Associators). We do not report white matter volume as it was measured in only one study
(Hänggi et al., 2008).
1 Hänggi et al., 2008.
2 Jäncke et al., 2009.
3 Rouw & Scholte, 2007.
4 Rouw & Scholte, 2010.
5 Weiss & Fink, 2009.
Brain Areas in Synesthesia 34
Figure 1.
Brain Areas in Synesthesia 35
Table 1. V4 activation (in green) and/or V1 activation in linguistic-color synesthesia, as well as V4 activation in
these synesthetes during physical color presentation.
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Brain Areas in Synesthesia 36
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Brain Areas in Synesthesia 37
Table 2. Brain areas activated during linguistic-color synesthesia, as measured in whole-brain (BOLD-MRI or
PET) neuroimaging studies.
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Brain Areas in Synesthesia 38
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Brain Areas in Synesthesia 39
Table 3A. Structural brain differences in white matter properties of developmental synesthetes and non-
synesthetes.
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Brain Areas in Synesthesia 40
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... Heritage is carried with a sex-linked genetic mechanism which explains that women lead the sex ratio (6/1) in synesthesia according to some views (Baron-Cohen et al., 1996, Eagleman & Goodale, 2009Ward & Simner, 2005). The studies which focus on synesthesia are mostly bringing neuroscientific explanations of the synesthesia mechanism by using neural measurement techniques and quantitative research methods (Beeli et al., 2008, Brang et al., 2010Grossenbacher & Lovelace, 2001;Hupé et al., 2012;Rouw et al., 2011;Sinke et al., 2012). In other words, neurological studies mostly compare synesthetes and non-synesthetes to focus on the localization areas and communication flow among areas in the brain by using brain tomography, magnetoencephalography, and functional magnetic resonance imaging. ...
... In other words, neurological studies mostly compare synesthetes and non-synesthetes to focus on the localization areas and communication flow among areas in the brain by using brain tomography, magnetoencephalography, and functional magnetic resonance imaging. Finally, the literature might be summarized that grapheme-color synesthesia states an automatic processing that indicates simultaneous activation of both the occipitotemporal cortex (visual functions) and parietal lobe (other sensory functions, such as hearing) (Beeli et al., 2008, Brang et al., 2010Grossenbacher & Lovelace, 2001;Hupé et al., 2012;Rouw et al., 2011;Sinke et al., 2012). ...
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The current research aimed to explore, understand and describe the subjective experiences of synesthesia among six self-reported synesthete siblings. We conducted two studies, one quantitative and one qualitative, for this purpose. The first study aimed to measure whether six siblings actually had synesthesia experiences. Six synesthete siblings and their eighteen non-synesthete peers participated in Study 1. First, participants filled the Eagleman Synesthesia Test Battery - Synesthesia Type Scale. Then, we asked the participants to match some words that we randomly selected from the Turkish dictionary with colors on a color scale. Both cross-sectional and longitudinal comparisons showed that six siblings consistently matched words with specific colors compared to their non-synesthete peers, and these colors hardly change over time. In study 2, we interviewed these siblings and aimed to investigate their synesthetic experiences using an interpretative phenomenological analysis approach. We verbatim transcribed the interviews, and the results showed that three main themes emerged, which were: (1) The nature of the synesthesia experience: Is it really rare?; (2) Details of the synesthesia experience; (3) Time and experience: It can change. The third superordinate theme has a subordinate theme, which is the stability of the associated colors within participants. We discussed the findings in the context of the persistence and changeability of the synesthetic experience and the uniqueness seen among siblings even when raised in a similar environment.
... However, other brain areas, such as the parietal cortex, insula, operculum, precentral gyrus and prefrontal cortex also appear to have a functional role. So far, no single pattern has emerged, but rather a cooperation of different areas seems to be involved (Rouw et al., 2011). ...
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Grapheme-color synesthesia is a normal and healthy variation of human perception. It is characterized by the association of letters or numbers with color perceptions. The etiology of synesthesia is not yet fully understood. Theories include hyperconnectivity in the brain, cross-activation of adjacent or functionally proximate sensory areas of the brain, or various models of lack of inhibitory function in the brain. The growth factor brain-derived neurotrophic (BDNF) plays an important role in the development of neurons, neuronal pathways, and synapses, as well as in the protection of existing neurons in both the central and peripheral nervous systems. ELISA methods were used to compare BDNF serum concentrations between healthy test subjects with and without grapheme-color synesthesia to establish a connection between concentration and the occurrence of synesthesia. The results showed that grapheme-color synesthetes had an increased BDNF serum level compared to the matched control group. Increased levels of BDNF can enhance the brain's ability to adapt to changing environmental conditions, injuries, or experiences, resulting in positive effects. It is discussed whether the integration of sensory information is associated with or results from increased neuroplasticity. The parallels between neurodegeneration and brain regeneration lead to the conclusion that synesthesia, in the sense of an advanced state of consciousness, is in some cases a more differentiated development of the brain rather than a relic of early childhood.
... Indeed, these cortical surface measures can reflect neuroplastic changes associated with aging (Frangou et al., 2019, Lin et al., 2021, cognition (Gautam et al., 2015), intellect and education (Im et al., 2006), and neuropsychiatric conditions (Ha et al., 2005). Importantly, differences in cortical surface measures have been shown in individuals who experience atypical conscious states similar to ASMR, with both mindfulness meditators (Kang et al., 2013) and synesthetes (Rouw et al., 2011) showing increases in cortical thickness compared with matched controls. If ASMR is associated with meditation-like benefits, we would expect to see increased cortical thickness in frontal regions. ...
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We provide a neuroimaging database consisting of 102 synaesthetic brains using state-of-the-art 3 T MRI protocols from the Human Connectome Project (HCP) which is freely available to researchers. This database consists of structural (T1- and T2-weighted) images together with approximately 24 minutes of resting state data per participant. These protocols are designed to be inter-operable and reproducible so that others can add to the dataset or directly compare it against other normative or special samples. In addition, we provide a ‘deep phenotype’ of our sample which includes detailed information about each participant’s synaesthesia together with associated clinical and cognitive measures. This behavioural dataset, which also includes data from (N = 109) non-synaesthetes, is of importance in its own right and is openly available.
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