Painting With all the Colors of the Wind Part Two

PART TWO: WHY DOES SYNESTHESIA HAPPEN?

So, we know a bit about what synesthesia is. But what actually causes these remarkable perceptions?

Well the truth is, as usual, that no one really knows for sure. There is strong evidence for a genetic component to synesthesia, as it tends to run in families. Despite this, however, it isn’t inherited directly- that is,  the type of synesthesia, in terms of what stimuli will produce what sensory responses, doesn’t seem to be inherited at all. If your mother had lexical-gustatory synesthesia, for example, you are statistically more likely to have some form of synesthesia, but there is no  preference towards synesthesia involving vision or taste. This, along with the fact that many people have more than one type of synesthesia, suggests that all forms of developmental synesthesia share some common cause and genetic predisposition (Ward). What this genetic component actually does is still contentiously debated though.

Investigations into synesthesia have been going on for many years. In 1690, John Locke wrote about a blind man who described the color scarlet as “the sound of a trumpet”, and the first well-documented case of synesthesia dates all the way back to 1812, when an Austrian doctor named Georg Sachs included descriptions of his own synesthesia in his medical dissertation (Ward). When the scientist Cornaz reviewed Sach’s paper again in 1848, it generated a lot of interest in the phenomena, and many more cases of synesthesia were discovered and investigated. Cornaz, however, thought that the color-grapheme synesthesia Sachs experienced was related simply to his eyes. He suggested that it was a result of having more color receptors in the eye, and therefore being able to detect additional colors that others couldn’t see (Ward). This explanation has been widely rejected, but it did spark the first significant interest in synesthesia, and people began to suggest other possibilities, such as Lusanna’s 1873 proposal that the “cerebral organs” for music, language and color might be close to each other and might overlap or connect in people with synesthesia (Ward).

Interest in synesthesia seems to have waned during the early 1900s, but it was definitely revitalized in the 1980s, after the neurologist Richard Cytowic published several case studies and a popular book, “The Man Who Tasted Shapes”, about synesthesia. Although his suggestion that synesthesia might be related to the limbic system has also been discredited, he played a huge role in bringing attention back to synesthesia and starting a new era of neuroscientific and psychological research into it.

In terms of the current research into the neural mechanism for what is happening in the sensory systems of synesthetes, there seem to be two major competing schools of thought. One views synesthesia as a result of structural differences in the brain and nervous system, and the other claims that it is due to functional differences in use of the neural circuits we all have. To break down each of these hypotheses, we can look a bit more closely into the arguments of each:

Team Structural Differences
As the researcher Baron-Cohen sees it, synesthesia is best explained by a difference in the number of connections in the brain- more and unusually strong neural pathways could allow for a physical connection between areas of the brain that typically respond to different senses/stimuli. It has also been suggested, by Dr. Daphne Maurer, that everyone is born with these additional connections, but that they are typically lost are we grow. Under this proposal, synesthesia is therefore a result of changes in development that neglect to “prune” these connections (Carpenter).

There is data to support the idea that the brains of people with synesthesia are physically different than those without it. Among the many imaging studies that have been done,  a study by Weiss and Fink 2009 found that the intraparietal sulcus had more gray matter in people with color-grapheme synesthesia, and that it is also activated when those participants were viewing graphemes. In addition, imaging data from Rouw and Scholte 2007 found that people with color-grapheme synesthesia had significantly increased white matter connectivity in brain regions they believe to be implicated with synesthesia.

 

Team Functional Changes
Some scientists think that synesthesia is better explained as the result of using the same brain architecture and connections, but in a different way. Proponents of this hypothesis focus on neural pathways common to everyone, but generally inhibited, or blocked, in one direction. Having that pathway be disinhibited would then allow people with synesthesia to distribute information between these neurons differently (Carpenter, Grossenbacher and Lovelace 2001).

For synesthesia, the major pathways considered are those that function with our sensory systems. A simplified version of these networks goes something like this: Information is carried from receptor cells across the body to different regions of the brain, where it is processed, put into context with the activity of other neurons, and used to form a comprehensive picture of the situation. Then, once the input has been consolidated, and a conscious perception or decision about the course of action has been made, the brain can send feedback and further instructions to the appropriate areas in what are called feed-backward connections.

The idea, then, is that in synesthesia, the inhibitory nature of some feed-backward connections of the sensory systems is deactivated or “disinhibited”, which means that information may be flowing down paths and/or in directions it normally couldn’t.  This would allow a stimulus to interact with the system differently, and potentially “mix” information from multiple sensory inputs or areas, causing synesthesia (Carpenter).

Grossenbacher, a lead advocate for this approach to looking a synesthesia, claims that this explanation is supported by the fact that certain drugs, such as LSD, can produce temporary synesthetic experiences. “I don’t think that new connections are forming in the brains of those individuals for a few hours and then disappearing,” he says. “What’s much more sensible is that existing connections become used in a way that’s neurochemically altered for a few hours.” (Carpenter). What may actually be causing the disinhibition of these pathways, on a molecular level, isn’t known yet.

 

As with all complex scientific concepts, there are no easy answers when it comes to synesthesia, and as always, there are many suggested explanations. The “Teams” above are definitely not divided into black-and-white, entirely separate categories, and many have suggested ideas that combine different aspects of each theory we’ve discussed, along with novel insights.

The most interesting proposals I’ve found are briefly summarized below:

According to scientists, synesthesia could be due to…

  • greater communication in the feed-backward paths (due to either disinhibition or unusual neural connections, both of which could be genetically regulated (Ramachandran).
  • Abnormal connections in the brain (possibly genetic) from resulting from:
    • the way that excess connections are pruned during development (Carpenter, Ramachandran, Ward).
    • the growth of more neural connections than is normal (Ramachandran, Ward).
    • Changed axon-guidance, or pathway formation, that the connections will follow (Ward).
    • Disruption of the formation of border regions in the brain (Ward).
      • Border regions are essentially blockers between adjacent regions, made by inhibition or simply a lack of connections between the areas.

Whatever the true cause of synesthesia is, there is no debating the fact that it is absolutely remarkable. Synesthesia  has also had tremendous impact on culture over time as well, with many influential artists, musicians, and writers purported to have a form of synesthesia. If you want to read about the way that synesthesia has affected a few people who have it, as well as society at large, check out Part Three here: https://chargedmagazine.org/2019/10/painting-with-all-the-colors-of-the-wind-part-three/

References

Carpenter, S. (2001, March). Everyday fantasia: The world of synesthesia. American    Psychological Association, 32(3).

Grossenbacher, P. G., & Lovelace, C. T. (2001). Mechanisms of synesthesia: Cognitive and physiological constraints. Trends in Cognitive Sciences,5(1), 36-41. doi:10.1016/s1364-6613(00)01571-0

Hubbard, E. M., & Ramachandran, V. (2005). Neurocognitive Mechanisms of Synesthesia. Neuron,48(3), 509-520. doi:10.1016/j.neuron.2005.10.012

Ramachandran, V.S., Hubbard, E.M. and Butcher, P.A. (2004). Synesthesia, CrossActivation, and the Foundations of Neuroepistemology. In G. Calvert, C. Spence and B. E. Stein (eds), The Handbook of Multisensory Processes (pp. 867-83). Cambridge, Mass.: The MIT Press.

Rouw, R., & Scholte, S. (2010). Increased structural connectivity in Grapheme-Color Synesthesia. Journal of Vision,7(9), 108-108. doi:10.1167/7.9.108

Ward, J. (2013). Synesthesia. Annual Review of Psychology,64(1), 49-75. doi:10.1146/annurev-psych-113011-143840

 

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  Timothy Durham was convicted of rape when a test showed his DNA genotype matched the DNA recovered from the crime scene. Eye witnesses testified that Durham was in a different state at the time of the incident, but he wasn’t exonerated from his 3000 year sentence until follow up DNA analysis showed that the preliminary forensic analysis used in the trial was misinterpreted (Thomas et al.). DNA testing serves an invaluable part in our criminal justice system, but it comes with complications and bias that can lead to wrongful convictions and misinformed juries.  

Background:

Forensic genetics aims to identify the origin of a biological sample. It can be traced back to Karl Landsteiner who discovered human ABO blood groups. With blood groups, suspects could be eliminated based on their blood type. For example, if a suspect had type A blood and there was type B blood left at the scene by the perpetrator, the investigators could rule out the suspect. Unfortunately, the reverse didn’t work. If the suspect and perpetrator both had the same blood type, it can’t be concluded that the suspect was guilty. Blood identifiers evolved into 8 distinct categories which improved the ability to eliminate suspects, but could only conclude that (if the system matched) it might be the perpetrator or this person might be related to the perpetrator (Jobling and Gill). The field evolved in the 1980s with the discovery of Minisatellites, lines of repetitive DNA that don’t encode proteins. Minisatellite patterns in DNA create what we know today as the DNA fingerprint, and it has a much higher accuracy rate than previous methods (Augustyn et al.). Around the same time, a breakthrough for victims of sexual assault was discovered. In the case of assault, bodily fluids of both the victim and the assaulter can get mixed. A process called differential lysis was created which could selectively increase the concentration of sperm in a fluid sample thereby allowing for accurate DNA testing (Jobling and Gill). Forensics evolved to use single-locus probe testing after several years because of its ease of interpretation. It looked at specific minisatellites that had high variability between subjects. This was the first DNA-based method to be used in a criminal investigation. Two murder homicides from several years apart were connected using DNA evidence. The evidence was then used to exonerate an innocent man, and the guilty party was found when he tried to evade mandatory DNA testing for all men in the small town. His guilt was then reinforced when the DNA profiles matched, and he gave a confession (Jobling and Gill). Finding DNA at a crime scene doesn’t guarantee that you’ll find a murderer. There are issues with non-pure samples and limited samples that make DNA work difficult, and accreditation of facilities and new techniques and take time (Jobling and Gill).  

Subjectivity of DNA Interpretation:

In a 2009 publication, the National Academy of Science discusses the possibility for subjective influence in lab based forensics. The interpretation bias happens in complex cases where, for example, there could be a mixture of DNA. A study published in 2011 looked specifically at this issue. A gang rape happened in Georgia, and the mixture in DNA from the case was used to prosecute one suspect after another suspect took a plea bargain to testify against him. With DNA mixtures, there are three possible conclusions: suspect excluded, suspect cannot be excluded, and inconclusive. If the suspect is excluded, it means that there’s little to no possibility that his DNA is part of the sample. If the suspect cannot be excluded, it means that there’s a possibility that his DNA is part of the sample. In the trial, the DNA examiners who knew the context of the case concluded that the suspect being prosecuted could not be excluded. The 2011 study gave the DNA evidence from this case and the DNA profiles of the suspects to 17 forensic examiners. These examiners had no context of the case, and they all worked independently. Of the 17, only 1 came to the same conclusion (suspect cannot be excluded) as the examiners who knew the context of the case. Twelve of the 17 concluded that the suspect who was prosecuted and convicted had no relation to the DNA found in the sample. Not only does this show that subjectivity occurs due to the context of the case, but the 17 examiners came up with different findings based on their past experiences meaning that not all DNA analysis is objective. Some organizations like the Scientific Working Group on DNA Analysis Methods say that quantitative statistical evidence should be presented with every categorical conclusion, but the US doesn’t require this (Dror and Hampikian).

False Positives:

There are two categories that cause wrongful identification in a DNA report: coincidental matches and false positives. Coincidental matches are DNA matches between two unrelated people. The probability of these matches is about 1 to 500,000 for white individuals and about 1 to 350,000 for black individuals. This small probability of coincidental matches makes people feel confident in DNA evidence. False positives, on the other hand, are matches between DNA and test DNA that result from issues in the forensics lab. There have been multiple cases of forensics labs accidentally switching victim and suspected rapist DNA which lead to convictions that were later overturned when the lab realized the error. There are also cases of misreading or misunderstanding a sample. In a case from 1993, a man was convicted of rape because someone interpreted a mixed sample of victim and perpetrator DNA as an individual sample. The conviction was again overturned. To prevent false convictions, retesting DNA is allowed, but it’s not an efficient solution. Many people are pushing for statistical information on the probability of false positives, so that the jurors can make accurate judgements based on DNA evidence (Thomas et al.).  

Conclusion:

DNA analysis is a useful tool for the criminal justice system, but subjectivity can be an issue in forensic testing. To combat wrongful convictions, there are organizations like The Innocence Project who use DNA testing to free the innocent, but reformed forensic testing standards should be put in place to prevent subjectivity and to ensure juries are correctly informed during trials. https://www.innocenceproject.org/    

Citation:

Augustyn , Adam, et al. “DNA Finerprinting.” Encyclopedia Britannica , 26 Apr. 2018, www.britannica.com/science/DNA-fingerprinting#ref153186. Dror, Itiel E., and Greg Hampikian. “Subjectivity and Bias in Forensic DNA Mixture Interpretation.” Science & Justice, vol. 51, no. 4, 2011, pp. 204–208., doi:10.1016/j.scijus.2011.08.004. Jobling, Mark A., and Peter Gill. “Encoded Evidence: DNA in Forensic Analysis.” Nature Reviews: Genetics, vol. 5, no. 10, Oct. 2004, pp. 739–751., doi:10.1038/nrg1455. Thompson, William C, et al. “How the Probability of a False Positive Affects the Value of DNA Evidence.” Journal of Forensic Sciences, vol. 48, no. 1, Jan. 2003, pp. 1–8., doi:10.1520/jfs2001171.