Synaesthesia and the Brain


Synaesthesia is a complex experience and, being rare, it is difficult to study. Nevertheless, several interesting theories have been proposed and tested. The idea that synaesthesia is a mental illness is long gone, but that doesn't mean it's not "all in the head"! Positron Emission Tomography (PET) scans have shown that different areas of the brain are active for synaesthetes experiencing a cross-modal association than for non-synesthetes engaged in the same task. The synaesthetic experience depends exclusively on the left brain and is associated with a decreased blood supply to the neocortex. This results in enhanced limbic expression. Therefore, we can assume that the system responsible for synaesthesia is located or influenced by the limbic system more than the neocortex, which is not what most people would predict without the evidence from the PET scans. Additional support for this is that there is an emotional aspect associated with a synesthetic experience. In fact, in order to fulfill the diagnostic criteria for synaesthesia an emotional response must be present.

Cases of synaesthesia may be idiopathic (developmental), with the person having experienced synaesthesia as long as they can remember, or non-idiopathic, resulting from a known etiology or mechanism which is acquired and produced synaesthesia.

Non-Idiopathic Synesthesia

Seizure Induced

One type of non-idiopathic synaesthesia is epileptic synaesthesia. This type of synaesthesia is experienced during electrical discharge (seizure) in the limbic region of the brain and is found in less than 7 percent of all temporal lobe - limbic seizures. Seizures which remain confined to the hippocampus in the limbic area of the brain produce elementary sensations, such as a simple taste like bitter. Those which spread to the cortex of the temporal lobe produce more specific and elaborated perceptions, such as the taste of a chocolate chip cookie. Indeed, it has been found that electrical stimulation of the temporal cortex alone evokes synaesthesia.

Drug Induced

Synaesthesia may also be induced by drugs, especially hallucinogenic compounds such as mescalin, peyote or LSD. This, however, is relatively infrequent.

Neuron Degeneration Induced

Another cause may be deafferation, the loss of certain neurons which make up nerves, or sensory deprivation. An example is that a sound evoking simple visions, such as a flash of light, may be seen in the portion of the visual field in which a person is blind.

Brain Damage Induced

Acquired synaesthesia tends to arise from damage to anterior portions of the brain, often the optic nerve. Frazinno, Yap, and Gross (1994), in accordance with this observation, found that 27-31% of neurons in the ventral portion of the premotor cortex are bimodal. This means that some neurons in all people respond to both vision and touch stimuli. These sensory systems are often found in parallel in the brain. There have been a few cases in which synaesthesia was brought on by gross brain stem lesions. The removal of one patient's brain stem tumor put an end to his experience of synaesthesia.

Spinal Cord Damage Induced

A unique experience that is technically synaesthesia may occur in about 12% of people with spinal cord injuries. In some people, a touch above a lesion causes a local sensation as well as a sensation in other parts of the body not normally related to the stimulated area. These phantom sensations appear to come from an artificial synapse located near the lesion.

Concussion Induced

In two percent of concussions, photo- or audio-algesic synaesthesia occurs. This is a temporary condition where sudden noises or bright light cause momentary pain extending into the trunk of the body or an extremity.

Idiopathic Synesthesia

Most cases of synaesthesia, however, are idiopathic; it is their normal mode of perception. There have been a number of theories put forward to explain this phenomenon. Those which follow are not necessarily mutually exclusive, for no single theory is likely to account successfully for all the various forms of developmental synaesthesia.

Uninhibited Natural State

One view, held by Richard Cytowic, is that everyone is synaesthetic in reality; most of us are just not consciously aware of it. Under this theory, it is posited that a stimulus causes a rebalancing of regional metabolism. This is the way a migraine is produced. Only, with synaesthesia, the stimulus causes parts of the brain to become electrically disconnected from one another so that the normal processes of the limbic system of the brain are released and can be sensed in our conscious state. As yet, there is little evidence for this point of view.

Neonatal Synaesthesia Hypothesis

Another school of thought is that there is a normal phase of synaesthesia in development, that all babies experience sensory input in an undifferentiated way in early infancy, probably up to about 4 months in age. This intermodal unity has been the focus of many studies. It has been found, for example, that neonates are able to detect tactile (touch)-visual correspondences. At a critical period, the senses may become increasingly modular, presumably because modularity leads to more rapid and efficient information processing and is therefore highly adaptive. In adults with synaesthesia the process of modularization of the senses may not have been completed. Connections between different sensory modalities in synaesthetes may have either grown or not died off. Although no conclusive findings have been produced for humans, it is known that such connections exist between auditory and visual areas in the early developing brain of many species. In the macaque monkey and domestic cat, transient connections exist up to three months after birth. There exists the possibility that the normal human brain also contains these connections but that there is an inhibitory mechanism, like a kind of gate, which prevents their activation. This inhibitory mechanism may be dysfunctional in synaesthetes.

Certain studies have led researchers to believe that, in late infancy, there is a change in the aspects of stimulation attended to. Infants respond only to differences in amount of stimulation whereas adults, while retaining this ability, respond to differences between modalities of stimulation instead. In this sense, we all have synaesthetic capabilities.

Influence of Genetics

There is evidence that some people may be more prone to developing synaesthesia due to their genetic makeup. This would involve the expression of genes that regulate the migration and maturation of neurons in the developing brain, or 'neuronal pruning' of the sort mentioned earlier. It is speculated that women are at least six times as likely to exhibit this condition than men. This shows that the condition is sex-linked and dominant. It has been found by others, that synaesthesia can be transmitted by any sex combination, leading to the belief that the trait is not sex-linked but, rather, autosomal.

Colored Hearing Theories

For colored hearing synaesthesia in particular, three psychological theories have been put forward. The doctrine of the unity of the senses or linkage theory, proposes that the perpetuation of a primitive perceptual experience in the limbic system is the root cause of color synaesthesia. As this system evolved, the perception was differentiated into two separate senses, hearing and vision.
A similar theory, the crosstalk theory, holds that auditory and visual information pathways may cross in synaesthetes. These cross-modal neural connections may be numerically greater than usual or simply used in different ways.
Some believe higher cognitive/cortical level processing (the limbic system is thought to be lower level) to be involved. According to this view, colored hearing synaesthesia is the result of a chain of mental associations, some of the intermediate links having dropped out of awareness. For instance, a person may see red every time they hear a trumpet because of the red uniforms of a brass band.

Feedback connections aid us in imagery, memory, sensory attention and other cognitive functions, but could they also result in synaesthesia? Auditory and visual information must meet somewhere in the brain or we could not process them in conjunction as they occur. These systems may contain feedback pathways normally but, in synaesthetes, they may be altered to include information from the other senses!

As you can see, synaesthesia is an extremely complex phenomenon. As methods for exploring the way the brain works improve, the mechanisms of synaesthesia may be revealed.


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