Our findings indicate that synaesthesia is significantly more common in adults with autism than in typical adults, based on self-report. The rate of synaesthesia in autism (18.9%) was almost three times greater than in the typical sample (7.22%), whose rate overlaps with the 4% reported previously (given confidence intervals) [1]. We predicted that synaesthesia would be more prevalent in autism than in controls if these conditions were interdependent, perhaps because they share some underlying biological causal factor, such as local neural hyper-connectivity. Four mechanisms have been proposed to account for neural hyper-connectivity: faulty axonal pruning, differences in axon guidance, disinhibition, and atypical border formation [37]. Interestingly, a recent study has revealed a significant phenotypic and genetic overlap between synaesthesia and absolute pitch [38], a trait that has also been reported to occur at increased frequency in people with autism [39, 40]. This strengthens the case that autism and synaesthesia are linked at multiple levels.

It is possible that the elevated rate of synaesthesia in autism might be explained by people with autism being more likely to report abnormal sensory perceptual experiences than people without the condition. Although it is true that adults with autism score highly on sensory sensitivity questionnaires [41], we doubt this can explain the current results, because our sample included some individuals with autism (n = 3) who claimed they did not have synaesthesia, but were judged by the experimenters to have synaesthesia on the basis of their questionnaire responses. Because they reported not having synaesthesia, we conservatively considered them to be non-synaesthetes. These participants with autism declared that they did not have synaesthesia because they said they were uncertain whether their experiences counted. Thus, the high rate of synaesthesia in autism is unlikely to be an over-estimate, and could even be an under-estimate. A related possible explanation of the comorbid association might be failure in inhibition/greater cortical excitation [42]. This is in line with the high scores on sensory sensitivity questionnaires [43], and is compatible with the finding that synaesthesia occurs more frequently in autism than in the general population.

There are several limitations of this study. First, we were unable to collect complete consistency tests to validate the prevalence estimates, which will be important to explore in future work. It may be the case that traditional ToGs are not suitable for people with autism and that these will require modification. If the ToG-R is used in future studies, it should be completed in person, so that the experimenter can ensure that there is no missing data. Future studies could also consider using computerized immediate retests [44] as alternative ways for validation. It will also be interesting to test if the current results extend to children with autism, or to more impaired individuals with autism, since our sample only included high-functioning adults. Second, response rates to the initial invitations were low, which is not unusual in survey research [45], therefore, other studies must become available to confirm the observed synaesthesia prevalence rates observed, and extrapolation from the current study should be done with caution until other such surveys have been conducted. Third, this question has not yet been tested in different clinical groups to assess if this link is specific to autism. Fourth, it would be interesting to test how people with autism and synaesthesia differ from those with autism alone. As far as we know, there has not yet been a study investigating autism vs. synaesthesia vs. comorbidity between these two conditions using MRI or fMRI, which should now become a research priority in this area. Fifth, we recognize that the Synaesthesia Questionnaire is a self-report instrument that in future studies needs to be evaluated in terms of its reliability and validity. Most importantly, the next step in future research must be to explore the biological mechanisms causing the elevated rate of synaesthesia in autism.