The neurological basis of synesthesia

There are two major classes of theories concerning the neural basis of synesthesia.

Both theories start from the observation that there are dedicated regions of the brain that are specialized for certain functions. For example, the part of the human brain involved in processing visual input, called the visual cortex can be further subdivided into regions that are preferentially involved in color processing (the fourth visual area, V4) or with motion processing, called V5 or MT. Based on this notion of specialized regions, some researchers have suggested that increased cross-talk between different regions specialized for different functions may account for different types of synesthesia.

For example, Ramachandran and Hubbard (2001) have noted that regions involved in the identification of letters and numbers lie adjacent to V4, which is involved in color processing. They have therefore suggested that the additional experience of seeing colors when looking at graphemes might be due to "cross-activation" of V4. This cross-activation may arise due to a failure of the normal developmental process of pruning, which is one of the key mechanisms of synaptic plasticity, in which connections between brain regions are partially eliminated with development (note this need not be all or none). Similarly, tastes evoked by hearing words (lexical -> gustatory synesthesia) may be due to increased connectivity between adject regions of the insula in the depths of the lateral sulcus involved in taste processing that lie adjacent to temporal lobe regions involved in auditory processing. Similarly, taste -> touch synesthesia may arise from connections between gustatory regions and regions of the somatosensory system involved in processing touch. Note, however, that not all forms of synesthesia are easily explained by adjacency.

Alternatively, synesthesia may arise though "disinhibited feedback" or a reduction in the amount inhibition along feedback pathways (Grossenbacher and Lovelace, 2001). It is well established that information not only travels from the primary sensory areas to association areas such as the parietal lobe or the limbic system, but also travels back in the opposite diretion, from "higher order" cortical regions to early sensory areas. Normally, the balance of excitation and inhibition are maintained. However, if this feedback were not adequately inhibited, then signals coming from later stages of processing might influence earlier stages of processing, such that tones would activation visual cortical areas in synesthetes more than in non-synesthtes. In this case, it might be possible to temporarily have synesthetic experiences after taking drugs like LSD or mescaline. Indeed, some psychedelic drug users report synesthesia like experiences, although the exact degree of similarity between these drug induced experiences and congenital synesthesia is still unclear. Given that synesthesia is known to run in families, it has been suggested that a genetic difference, or single nucleotide polymorphisms (SNPs, pronounced "SNiPs") might be responsible for either decreased pruning or decreased inhibition in the synesthete brain, leading to increased activation. Note, too, that these theories are not mutually exclusive. It may be that both mechanisms are possible causes of synesthesia, but that one or the other is present in differing degrees between different synesthetes, or for different sub-types of synesthesia.

Neuroimaging studies using positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) have demonstrated significant differences between the brains of synesthetes and non-synesthetes. In the first such study, Paulesu and colleagues (1995) used PET to demonstrate that some regions of the visual cortex (but not V4) were more active when auditory word -> color synesthetes listened to words compared to tones. More recent studies using fMRI have demonstrated that V4 is more active in both word -> color and grapheme -> color synesthetes (Nunn et al., 2002; Hubbard et al., 2005; Sperling et al., 2006). However, these neuroimaging studies do not have the spatial and temporal resolution to distinguish between the pruning and disinhibited feedback theories. Future research will continue to examine these questions using not only fMRI but also diffusion tensor imaging (DTI), which allows researchers to directly investigate neural connectivity in the human brain and magnetic resonance spectroscopy (MRS) which allows researchers to measure the amounts of different neurotransmitters in the brain.

Papers

 * Cytowic, Richard E. 1996.  "Synesthesia: Phenomenology And Neuropsychology" Fulltext
 * Cytowic, Richard E. 1997.  "Synaesthesia: phenomenology and neuropsychology - a review of     current knowledge."  In S. Baron-Cohen and J. Harrison (Eds.); Synaesthesia: Classic and   Contemporary Readings; Oxford, England: Blackwell.  Pp. 17-39.
 * Frith, C. D., and E. Paulesu. 1997.  "The physiological basis of synaesthesia."  In S. Baron-Cohen and J. Harrison (Eds.); Synaesthesia: Classic and Contemporary Readings; Oxford, England:Blackwell.  Pp. 123-147.
 * Grossenbacher, Peter G., and Christopher T. Lovelace. 2001.  "Mechanisms of synesthesia: cognitive and physiological constraints."  Trends in Cognitive Sciences; volume 5:1: 36-41.
 * Kennedy, H., A. Batardiere, C. Dehay, and P. Barone. 1997. "Synaesthesia: implications for developmental neurobiology."  In S. Baron-Cohen and J. Harrison (Eds.); Synaesthesia: Classic and conntemporary Readings; Oxford, England: Blackwell.  Pp. 243-256.
 * Paulesu, E., J. Harrison, S. Baron-Cohen, J.D.G. Watson, L. Goldstein, J. Heather, R.S.J. Frackowiak, and C.D. Frith. 1995.  The physiology of coloured hearing: A PET activation study of colour-word synaesthesia.  Brain; volume 118: 661-676.

Papers

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