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The science of synesthesia: How some can hear colors or taste words
Article

The science of synesthesia: How some can hear colors or taste words

The science of synesthesia: How some can hear colors or taste words
Article

The science of synesthesia: How some can hear colors or taste words

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For most people, the plain, black letters on this page are rather unremarkable. For less than four percent of the population however, these words are a little more colorful, tactile, or might even ‘taste sweet’ when read.  


Since the 1980s, scientists have been attempting to understand the neurocognitive mechanisms of synesthesia, the rare neurological phenomenon in which a stimulus produces a second concurrent, involuntary experience. While any two or more combinations of experiences are possible, some types are more common than others. When achromatic letters (like the words here) and numerals (known as graphemes) elicit experiences of color, this is known as ‘grapheme-colour synesthesia.’


Early studies suggested that synesthesia varies greatly from person to person. Genetic mechanisms underlying the phenomenon are still not well understood, with recent studies indicating that synesthesia is more complex than the x-linked dominance put forth by early researchers.


In the early 2000s, discussions in this field were dominated by whether synesthesia was the result of a failure in neural pruning or if it was a type of disinhibition. To date, three different broad architectural mechanisms for synesthesia have been proposed, including local cross-activation, long-range disinhibited feedback, and re-entrant processing.


Local cross-activation

In 2005, neuroscientists Edward Hubbard and Vilayanur Ramachandran proposed that due to the fact that the visual word form area (VWFA) and the color processing region hV4 in the brain are adjacent to one another, grapheme-colour synesthesia may be the result of direct cross-activation between these two areas.


This mechanism could potentially be explained by a lack of neural pruning. Prenatal connections between inferior temporal regions and V4 have been previously observed. Findings from a 1997 study indicated that 70 to 90 percent of connections between these regions are from higher areas (especially the temporal area, TEO) in fetal macaques, while that falls to only 20 to 30 percent in adults. Hubbard and Ramachandran argued that if a genetic mutation led to a failure in prenatal pathway pruning, the connections between VWFA and hV4 in the brain could remain intact well into adulthood. This could potentially explain those who see colors while viewing graphemes.


Cross-activation accounts for contextual differences by assuming that the feedback mechanisms are already present in synesthetes, which also explains top-down modulations in non-synesthetes. When anterior inferior temporal regions (AIT) activate in the brain, neurons firing from posterior inferior temporal regions (PIT) are directly biased, which alters neuron responses. The different pattern in PIT (VWFA) neuronal firing will result in a different cross-activation of V4 neurons. Ultimately, this would lead to a difference in grapheme perception experienced by each individual.


Long-range disinhibited feedback

Other studies in recent years have focused on synesthesia as a possible result of disinhibited feedback from a multisensory nexus like the temporo-parietal-occipital junction. This hypothesis is supported by case studies, such as one conducted in 1999 on a subject who became blind when he was 40-years-old. After two years of blindness, the subject reported that tactile stimuli produced the perception of visual movement. The intensity of his synesthetic experience was found to be greater when the subject had his hand in front of him rather than behind. Scientists conducting the study suggested this could be due to top-down multisensory activation in his brain, mediated by parietal structures.


Re-entrant processing

The last model proposed for synesthesia is a hybrid mechanism, suggesting that synesthesia is the result of aberrant re-entrant processing. The main differences between this model and cross-activation, is how feedback modulates the colors experienced by a person in grapheme-color synesthesia. In 2001, a group at the University of Waterloo in Ontario, Canada led by Daniel Smilek, proposed that grapheme-colour synesthesia could be the result of aberrant neural activity from anterior (AIT) feeding back to posterior inferior temporal regions (PIT) and V4 after an initial sweep of activity from V1-V4 to PIT and AIT. Neural activity feeding back to PIT results in recognition of the grapheme and possibly influences the synesthetic colors as a result.


Several studies conducted between 2001 and 2005 provide evidence that visual context and meaning affect the colors perceived in grapheme-colour synesthesia. This evidence appears to favor the re-entrant processing model over cross-activation, while more recent follow-up studies appear consistent with both cross-activation and re-entrant processing.


A 2014 study by the Department of Psychology at Kobe University in Japan attempted to understand the neural mechanism for the coloring of words in grapheme-color synesthesia. Subjects exhibited one or a combination of three types of effects: words taking on the color of their constituent letters; words taking on the color of the first letter, or word colour being influenced by its semantic meaning. The scientists found that semantically-induced synesthesia appears consistent with a type of re-entrant processing while the other effects are consistent with the cross-activation model.


Multiple mechanisms? None of the above?

Conflicting data from different research groups suggest it is possible that the three mechanisms described here are not mutually exclusive, or simply, that different synesthetes exhibit different mechanisms of action. Due to the fact that synesthesia is a broad term incorporating many types of stimuli (ie. graphemes, music, colours, etc.), and that these stimuli are processed in various brain regions, a collection of distinct architectural mechanisms may be required to account for these differences.


References
  1. Hubbard E. et al. (2005) Neurocognitive Mechanisms of Synesthesia. Neuron 48:509–520.
  2. Hubbard E. (2007) Neurophysiology of Synesthesia. Current Psychiatry Reports 9:193–199.
  3. Mroczko-Wasowicz A. et al. (2014) Semantic mechanisms may be responsible for developing synesthesia. Front. Hum. Neurosci. 8:509.
  4. Takemasa Y. et al. (2014) Multiple neural mechanisms for coloring words in synesthesia. NeuroImage 94:360–371.
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