Seeing Sounds, On and Off Drugs
What does a sound look like?
The question may seem bogus, but it’s meaningful to a handful of individuals, including myself. Around 4% of the population has synesthesia, a neurological phenomenon in which senses are “crossed”; one sense automatically triggers the experience of another. Some people really can see the ding of a bell or the honk of a horn.
Individuals with genuine synesthesia are usually born with it, but some may acquire it through brain damage. Every individual synesthete is different, and synesthesia appears in many forms. Personally, I experience:
- Color-grapheme synesthesia, in which numbers and letters seem innately linked to specific colors
2. Ordinal linguistic personification, in which ordered sequences (like numbers or months) are linked to personalities
3. Auditory-visual synesthesia, in which shapes or colors appear with sounds
While these are my personal synesthetic experiences, there are many more. Some people may taste words, touch sounds, or see ordered sequences spiraling in their mind. These experiences are consistent and predictable; for example, “N” has always been green, and will be green every time I think of it.
It’s possible to temporarily induce synesthetic experiences with drugs, particularly psychedelics. Most drug-induced synesthesia occurs with classic psychedelics: LSD, psilocybin, DMT, and mescaline. Other drugs such as MDMA, ketamine, and cannabis have reportedly triggered these experiences as well.
Psychedelics are known to produce visual effects, namely geometric patterns that appear on external surfaces and within the mind. These hallucinations are not necessarily synesthetic in nature; however, some users report these visuals morphing with other senses to create a synesthetic experience.
For instance, some may see patterns moving to the beat of music, or the appearance of sound waves exiting a speaker. According to a 2013 review of several studies, most drug-induced synesthetic effects are auditory-visual in nature. Currently, there is no consensus regarding the degree of similarity between these experiences and the experiences of genuine synesthetes. However, drug-induced synesthesia tends to be random and sporadic, as opposed to the consistency of genuine synesthesia.
So how does synesthesia work in the brain? Right now, there are two main models that explain it:
- Bottom-Up Hypothesis: In synesthetes, connections between sensory areas of the brain are either abnormally sensitive or overabundant. This could be due to issues in brain development; normally, unused neural connections are removed, and failure to do so may lead to abnormal brain connections between sensory areas.
- Top-Down Hypothesis: Some areas of the brain deal with multiple senses, and constantly give off random feedback. Normally, this feedback is inhibited by the brain, and we don’t experience it. In synesthetes, the brain may have trouble blocking this random feedback, and will try to make sense of it by perceiving two senses as linked. This may also account for drug-induced synesthesia.
These models are not mutually exclusive and are not the only logical explanations for synesthesia. The mechanisms behind the complex experiences of individual synesthetes have yet to be agreed upon.
One complex hypothesis for synesthesia involves serotonin, a chemical involved in mood regulation. Psychedelics act by mimicking the shape of serotonin and binding to its receptors. However, because psychedelics and serotonin are very different chemicals, different effects occur. Psychedelic hallucinations are generally attributed to the drug’s action at specific serotonin receptors.
This concept is central to Brang and Ramachandran’s 2007 serotonin hypothesis, which states that synesthesia may arise from excess serotonin in the brain. Fluoxetine, a drug that blocks serotonin receptors, has been reported to stop synesthesia in two instances.
Additionally, there have been several instances of people actually acquiring synesthesia after brain injury. Following tissue damage, neurotransmitters such as serotonin flood the brain, which may serve to increase brain connectivity. Brain injuries that induce synesthesia also often induce autistic behaviors and savant abilities. Interestingly, synesthesia is remarkably prevalent in individuals with autism, which has also been linked with an imbalance of serotonin.
While the serotonin hypothesis is interesting and notable, it is not specific enough to completely address the mystery of synesthesia. There are issues that have not been addressed; for instance, synesthetic effects have also been linked to drugs that do not act on serotonin receptors, like ketamine.
Overall, more research is required to make conclusions about the mechanisms behind synesthesia, the neural connections involved, and the serotonin hypothesis. However, there has been progressively more doubt regarding whether genuine and drug-induced synesthesia share a common mechanism.
Because the synesthetic experience is hard to describe, the topic can be difficult to discuss. It may be possible that drug-induced synesthesia is actually a completely different experience than genuine synesthesia, but our words aren’t precise enough to explain them. Hopefully, technological advancement can overcome this barrier and allow researchers to more accurately study the mechanisms behind synesthesia.
