Synaesthesia: Sensing the World with a Super-charged Brain
By: Jonathon Chio
“Men ought to know that from nothing else but the brain come joys, delights, laughter and sports, and sorrows, griefs, despondency, and lamentations. And by this, in an especial manner, we acquire wisdom, and knowledge, and see and hear and know what are foul and what are fair, what are bad and what are good, and what are sweet and what are unsavory… In these ways I am of the opinion that the brain exercises the greatest power in the man.” – Hippocrates, On the Sacred Disease (Fourth century B.C.)
Hippocrates’ pronouncement calls us to use our curiosity as fuel to explore how the 86 billion neurons in the human brain contribute towards human sensation.1 One model for sensation depicts sensory nerves (bundles of neurons) transmitting electrical impulses to sensory regions in the brain. Processing of afferent signals by the sensory brain regions determines subsequent efferent response. However, this mechanism is inadequate at explaining higher-order sensory processes. Studying synaesthetes, individuals with extraordinary sensory capabilities who can smell sounds, taste words and view numbers in color, may help to elucidate a more accurate mechanism.
Background of synaesthesia and its different types
Gustav Fechner made the first recorded description of synaesthesia.2 Currently with an estimated prevalence of 1/2000 individuals, synaesthesia is thought to be a consequence of aberrant cross-wiring among the brain’s neurons.3 Neuroimaging studies have revealed that altered neural connections exist in the white matter. The increased connectivity allows stimuli to activate atypical brain regions and trigger unexpected sensations. Although the possibility of synaesthesia in non-human animals can’t be completely discounted, research has suggested that synaesthesia is a human-specific phenomenon.4
Different types of synaesthesia have been named according to “X → Y” nomenclature. “X” is the inducer stimuli and “Y” is the atypical, concurrent and involuntarily elicited experience.5 Although not exhaustive, Table 1 describes the majority of known synaesthesia types.
|Grapheme-color (most common)||Visual perception of numbers and letters in associated colors|
|Chromesthesia||Auditory stimuli evoke colors|
|Spatial sequence||Visual perception of numerical sequences in different spatial organizations / levels|
|Auditory-visual||Auditory stimuli lead to visual perceptions|
|Mirror-touch||Observing another person being touched and feeling the same sensation in self|
|Lexical-gustatory||Spoken and written language elicit tastes and smells|
Table 1: Majority of known synaesthesia types, where left column is the inducer stimuli and the right column is the elicited experience.
Synaesthetes can be identified by testing for unique sensations. For instance, to test for grapheme-color synaesthesia, individuals are presented with a screen consisting of 2’s and 5’s as below; those without grapheme-color synaesthesia will see Panel (a), while grapheme-color synaesthetes will see Panel (b) in Figure 1. Neuroimaging studies have also indicated that grapheme-color synaesthetes have abundant connections between the occipital lobe and temporal lobe’s fusiform gyrus (which processes color information).
Probable causes of synaesthesia: immunology and genetics
As synaesthetes’ brains have aberrant white matter connections, synaesthesia may be caused by abnormal brain development. A young (immature) brain contains an excessive number of synaptic connections.6 These links are selectively eliminated in a maturation process known as synaptic pruning, which occurs when an immature brain goes through “critical periods” of development.7 During the critical periods, neuronal networks are shaped by sensory stimuli; 6 more active synapses and networks are kept and strengthened in favor of those less activated.7 This “survival of the fittest scenario” popularized the adages “Use it or lose it” and “Cells that fire together, wire together”.
Microglia, which are the resident immune cells of the central nervous system (CNS), are responsible for synaptic pruning.7,8 They represent 10-12% of all cells in the adult CNS. Although primarily known for their response towards CNS injury, research has revealed that microglia also perform synaptic pruning during critical periods. Microglial-dependent pruning is based on 2 main factors; directions from innate immune molecules to direct phagocytosis, and neuronal activation. If microglia were to perform irregular synaptic pruning, excess amounts of white matter could remain between different brain regions, creating an environment potentially primed for greater communication.
Altered amounts of protein (white matter) are partially responsible for synaesthesia. As genes control protein production, researchers began to investigate possible genetic origins of synaesthesia. In 2009, Asher and colleagues performed the first-ever whole-genome scan; albeit in only auditory-visual synaesthetes. As there are more female than male synaesthetes, synaesthesia was originally hypothesized to follow Mendelian genetics, have X-linked dominant mode of inheritance, and be controlled by a single loci.3 Contrary to X-linked gene expression, Asher and colleagues found chromosomes 2q24, 5q33, 6p12, and 12p12 were linked to auditory-visual synaesthetes. The genes in Table 2 showed the strongest correlations with neuronal communication.
|TBRI||Development of the cerebral cortex|
|SCN1A, SCN2A||Excitability threshold for neuronal networks (sodium channels)|
|GALNT13||Myelination of central nervous system through expression of neuronal sugar groups|
|GRIN2B||Long-term potentiation/ learning/ memory|
|DPYSL3||Axonal growth, guidance, neuronal differentiation|
Table 2: Genes that showed the strongest correlations with neuronal communication in Asher et al and their known function.
Side effects of synaethesia: Greater memory and empathy
Synaesthetes have stronger memory and associated networks.9 For example, grapheme-color synaesthetes have more robust memory for words. However, the improvements occurred on a local level. Relative to non-synaesthetes, only visual long term memory and the parvo-cellular system (responsible for color and object input) were significantly better.9,10 Anatomically, this has been reflected to having less gray matter in the motion-specialized region of the orbital lobe.11
Given the great plasticity of synaesthetic brains, another phenomenon related to synaesthesia is phantom limb pain; which is the sensation of mild to extreme pain in the area where a limb had been amputated.12 Despite the limb not existing, nerve endings at the site of amputation continue transmission of pain signals to the brain. The presence of pain is explained by neuroanatomical reorganization; brain regions that continue to receive sensory input incorporate those regions deprived of sensory innervation. The extent of the incorporation correlates positively with the pain felt by the individual. Thus, given the plasticity that can occur after limb amputation, perhaps it is not surprising that one of three amputees develop mirror-touch synaesthesia.13 Mirror synaesthetic sensations generated were more intense when observing real (as opposed to inanimate) bodies being touched. Further, highly empathic individuals are predisposed to strengthening of existing neuronal pathways responsible for communication after observed and felt touch. Thus, while research on synaesthesia is still in its infancy, the findings have far-reaching implications.
In the human endeavour to understand the brain, studying synaesthetes offers great insight. As their brain circuitry is quite different from those without synaesthesia, synaesthetes can help advance our understanding of how the brain navigates through a world that constantly assaults our senses. By revealing how the brain segregates and integrates different sensations to construct our perception of consciousness, studying synaesthesia will facilitate our journey as we probe the organ that exercises the greatest power in man.
- Azevedo F, Carvalho L, Grinberg L, et al. Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. The Journal of Comparative Neurology. 2009;513(5):532-541.
- Swain F. Can synaesthesia be learnt? [Internet]. BBC. 2016 [cited 4 February 2016]. Available from: http://www.bbc.com/future/story/20140611-can-synaesthesia-be-learnt)
- Asher J, Lamb J, Brocklebank D, et al. A Whole-Genome Scan and Fine-Mapping Linkage Study of Auditory-Visual Synesthesia Reveals Evidence of Linkage to Chromosomes 2q24, 5q33, 6p12, and 12p12. The American Journal of Human Genetics. 2009;84(2):279-285.
- Terhune D, Rothen N, Cohen Kadosh R. Correcting misconceptions about synaesthesia. Neurobiology of Learning and Memory. 2013;103:1-2.
- Ward J. Synesthesia. Annual Review of Psychology. 2013;64(1):49-75.
- Hensch T. The Power of the Infant Brain. Sci Am. 2016;314(2):64-69.
- Schafer D, Lehrman E, Kautzman A, et al. Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner. Neuron. 2012;74(4):691-705.
- Witcher K, Eiferman D, Godbout J. Priming the Inflammatory Pump of the CNS after Traumatic Brain Injury. Trends in Neurosciences. 2015;38(10):609-620.
- Ward J, Hovard P, Jones A, et al. Enhanced recognition memory in grapheme-color synaesthesia for different categories of visual stimuli. Frontiers in Psychology. 2013;4.
- Rothen N, Meier B. Grapheme–colour synaesthesia yields an ordinary rather than extraordinary memory advantage: Evidence from a group study. Memory. 2010;18(3):258-264.
- Banissy M, Stewart L, Muggleton N, et al. Grapheme-color and tone-color synesthesia is associated with structural brain changes in visual regions implicated in color, form, and motion. Cognitive Neuroscience. 2011;3(1):29-35.
- Jutzeler C, Curt A, Kramer J. Relationship between chronic pain and brain reorganization after deafferentation: A systematic review of functional MRI findings. NeuroImage: Clinical. 2015;9:599-606.
- Goller A, Richards K, Novak S et al. Mirror-touch synaesthesia in the phantom limbs of amputees. Cortex. 2013;49(1):243-251.