Synesthesia part 2: how we think it might occur in the brain

To recap: Synesthesia = pretty cool. Things that most of us experience in a single modality (e.g. aurally), synesthetes (people who have synesthesia) experience in one or more additional modality. For example, on hearing a particular tone, a synesthete might also see a color. There are many different types of synesthesia. Awesome, right?

Note that synesthesia is automatic and involuntary, and it strongly runs in families. However, the genes implicated in synesthesia have not yet been isolated.

There seem to be two main hypotheses right now on how synesthesia might arise in the brain. Both have their proponents and naysayers. I’m going to briefly walk you through the two hypotheses and the evidence for each.

The first is the cross-activation hypothesis, which was proposed by Hubbard and colleagues (2005). Hubbard et al. were studying grapheme-color synesthesia—in which letters and numbers (graphemes) are perceived to have particular colors—using functional magnetic resonance imaging (fMRI). fMRI monitors changes in blood flow in different areas of the brain. More blood flow to an area = more activity in that area of the brain. Hubbard and colleagues found that when grapheme-color syesthetes were presented with a grapheme, V4, a part of their brains involved in color processing, was active as well as the adjacent visual word form area (VWFA). Non-synesthete control subjects did not have activity in their V4 areas when shown graphemes—they only had activity in their VFWAs.

See? The VWFA is in green, and V4 is red.

Hubbard et al. thought that this difference in activity in the brains of synesthetes could be due to cross-activation. In other words, activation of one sensory pathway directly causes activation in another sensory pathway. This could occur due a lack of normal neural pruning between the pathways in early development. If there was a mutation that caused neural pruning to occur abnormally, this could also account for the heritability of synesthesia. Hubbard and Ramachandran (2005) cite a study in macaque monkeys showing that in the V4 brain region and the region of the VWFA were neurally connected in prenatal macaques but not in adult macaques. A connection study like this one would be the best way to test the cross-activation hypothesis, but such a study cannot be done on humans because it is…um…invasive, to say the least.

Another fMRI study on word-color synesthesia found activation of the V4 and V8 (another color processing region) only in the synesthetes in response to a hearing a spoken word (Nunn et al. 2002). The authors felt their results supported the cross-activation hypothesis.

The second hypothesis is known as disinhibition feedback, and it was proposed by Grossenbacher and Lovelace (2001). This hypothesis suggests that synesthesia is caused by disinhibited feedback from a so-called multisensory nexus in the brain, where signals from multiple pathways are fed forward to other brain areas. In most people, these signals are sufficiently inhibited such that they do not experience synesthesia.

Grossenbacher and Lovelace thought that since synesthesia could be induced by drugs such as LSD, synesthesia should not require any abnormal brain architecture to occur, since non-synesthetes who experience synesthesia under the influence of LSD presumably lack the atypical brain architecture.

Another piece of evidence that may support disinhibition feedback is the case of a man who his vision at the age of forty (cited in Hubbard and Ramachandran 2005). After two years, he reported that tactile stimuli elicited for him the impression of seeing movement. A more intense tactile stimulus was needed to give the impression of seeing movement when the man held his hands in front of his face, suggesting that his synesthesia was related to a kind of top-down sensory processing. The two-year delay between the man’s loss of his vision and the development of his synesthesia, however, does suggest some kind of neural rewiring.

When considering these hypotheses, it’s important to keep in mind that we don’t know that congenital synesthesia and drug-induced synesthesia arise through the same mechanisms. Congenital and drug-induced synesthesia have very different characters, and it does not necessarily make sense to claim they have similar origins in the brain. We also don’t know that the many different types of congenital synesthesias have the same neural mechanisms.

I personally think that the cross-activation hypothesis seems stronger, more logical, has more evidence in its favor. But you know, I’m just an undergrad, and not particularly (or at all) qualified to spout an opinion on the topic.

But you never know. Maybe in fifty years we’ll have learned that neither cross-activation nor disinhibited feedback are responsible for synesthesia, and neurobiologists will look back on these hypotheses and giggle in the same way we now giggle about Freud and his theories on penis envy.

Grossenbacher, P. G.; Lovelace, C. T., Mechanisms of synesthesia: cognitive and physiological constraints. Trends in Cognitive Sciences 2001, 5 (1), 36-41.

Hubbard, E. M.; Ramachandran, V. S., Neurocognitive Mechanisms of Synesthesia. Neuron 2005, 48 (3), 509-520.

Hubbard, E. M.; Arman, A. C.; Ramachandran, V. S.; Boynton, G. M., Individual Differences among Grapheme-Color Synesthetes: Brain-Behavior Correlations. Neuron 2005, 45 (6), 975-985.

Nunn, J. A.; Gregory, L. J.; Brammer, M.; Williams, S. C. R.; Parslow, D. M.; Morgan, M. J.; Morris, R. G.; Bullmore, E. T.; Baron-Cohen, S.; Gray, J. A., Functional magnetic resonance imaging of synesthesia: activation of V4/V8 by spoken words. Nat Neurosci 2002, 5 (4), 371-375.

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