(1) The induced colours led to perceptual grouping and pop-out, (2) a grapheme rendered invisible through ‘crowding’ or lateral masking induced synaesthetic colours — a form of blindsight — and (3) peripherally presented graphemes did not induce colours even when they were clearly visible. Taken collectively, these and other experiments prove conclusively that synaesthesia is a genuine percep- tual phenomenon, not an effect based on memory associations from childhood or on vague metaphorical speech. We identify different subtypes of number–colour synaesthesia (...) and propose that they are caused by hyperconnectivity between col- our and number areas at different stages in processing; lower synaesthetes may have cross-wiring (or cross-activation) within the fusiform gyrus, whereas higher synaesthetes may have cross-activation in the angular gyrus. This hyperconnec- tivity might be caused by a genetic mutation that causes defective pruning of con- nections between brain maps. The mutation may further be expressed selectively (due to transcription factors) in the fusiform or angular gyri, and this may explain the existence of different forms of synaesthesia. If expressed very diffusely, there may be extensive cross-wiring between brain regions that represent abstract concepts, which would explain the link between creativity, metaphor and synaesthesia (and the higher incidence of synaesthesia among artists and poets). Also, hyperconnectivity between the sensory cortex and amygdala would explain the heightened aversion synaesthetes experience when seeing numbers printed in the ‘wrong’ colour. Lastly, kindling (induced hyperconnectivity in the temporal lobes of temporal lobe epilepsy [TLE] patients) may explain the purported higher incidence of synaesthesia in these patients. We conclude with a synaesthesia-based theory. (shrink)
The mechanism by which humans perceive others differs greatly from how humans perceive inanimate objects. Unlike inanimate objects, humans have the distinct property of being “like me” in the eyes of the observer. This allows us to use the same systems that process knowledge about self-performed actions, self-conceived thoughts, and self-experienced emotions to understand actions, thoughts, and emotions in others. The authors propose that internal simulation mechanisms, such as the mirror neuron system, are necessary for normal development of recognition, imitation, (...) theory of mind, empathy, and language. Additionally, the authors suggest that dysfunctional simulation mechanisms may underlie the social and communicative deficits seen in individuals with autism spectrum disorders. (shrink)
We studied two otherwise normal, synaesthetic subjects who `saw' a speci¢c colour every time they saw a speci¢c number or letter. We conducted four experiments in order to show that this was a genuine perceptual experience rather than merely a memory association. (i)The synaesthetically induced colours could lead to perceptual grouping, even though the inducing numerals or letters did not. (ii)Synaesthetically induced colours were not experienced if the graphemes were presented peripherally. (iii)Roman numerals were ine¡ective: the actual number grapheme was (...) required. (iv)If two graphemes were alternated the induced colours were also seen in alternation. However, colours were no longer experienced if the graphemes were alternated at more than 4 Hz. We propose that grapheme colour synaesthesia arises from `cross-wiring' between the `colour centre' (area V4 or V8)and the `number area', both of which lie in the fusiform gyrus. We also suggest a similar explanation for the representation of metaphors in the brain: hence, the higher incidence of synaesthesia among artists and poets. (shrink)
Neurological syndromes in which consciousness seems to malfunction, such as temporal lobe epilepsy, visual scotomas, Charles Bonnet syndrome, and synesthesia offer valuable clues about the normal functions of consciousness and ‘qualia’. An investigation into these syndromes reveals, we argue, that qualia are different from other brain states in that they possess three functional characteristics, which we state in the form of ‘three laws of qualia’. First, they are irrevocable: I cannot simply decide to start seeing the sunset as green, or (...) feel pain as if it were an itch; second, qualia do not always produce the same behaviour: given a set of qualia, we can choose from a potentially infinite set of possible behaviours to execute; and third, qualia endure in short-term memory, as opposed to non-conscious brain states involved in the on-line guidance of behaviour in real time. We suggest that qualia have evolved these and other attributes because of their role in facilitating non-automatic, decision-based action. We also suggest that the apparent epistemic barrier to knowing what qualia another person is experiencing can be overcome by using a ‘bridge’ of neurons; and we offer a hypothesis about the relation between qualia and one's sense of self. (shrink)
Patients with right parietal lesions often deny their paralysis , but do they have "tacit" knowledge of their paralysis? I devised three novel tests to explore this. First, the patients were given a choice between a bimanual task vs a unimanual one . They chose the former on 17 of 18 trials and, surprisingly, showed no frustration or learning despite repeated failed attempts. I conclude that they have no tacit knowledge of paralysis . Second, I used a "virtual reality box" (...) to convey the optical illusion to the patient that she was moving her paralyzed left hand up and down to the rhythm of a metronome, and yet she showed no sign of surprise. Third, I irrigated patient BM′s left ear canal with cold water, a procedure that is known to shift that patient′s spatial frame of reference by stimulating the vestibular system. Surprisingly, this allowed her "repressed" memory of paralysis to come to the surface; she said she had been paralyzed continuously for several days. I suggest that the vestibular stimulation produces these remarkable effects by mimicking REM sleep. These patients also emply a whole arsenal of grossly exaggerated Freudian "defense mechanisms" to account for their paralysis. To explain this, I propose that in normal individuals the left hemisphere ordinarily deals with small, local anomalies by trying to impose consistency but, when the anomaly exceeds threshold, an interaction with the right hemisphere forces a "paradigm shift". A failure of this process, in patients with right hemisphere damage, might partially account for anosognosia. Finally, I present a new conceptual framework that may help link several psychological and neurological phenomena such as Freudian defense mechanisms, vestibular stimulation, anosognosia, memory repression, visual illusions, anterograde amnesia, REM sleep, dreaming, and humor. (shrink)
This article supplements our earlier paper on synaesthesia published in JCS (Ramachandran & Hubbard, 2001a). We discuss the phenomenology of synaesthesia in greater detail, raise several new questions that have emerged from recent studies, and suggest some tentative answers to these questions.
Jones and Coleman are among a handful of otherwise normal as a child and the number 5 was red and 6 was green. This the- people who have synesthesia. They experience the ordinary ory does not answer why only some people retain such vivid world in extraordinary ways and seem to inhabit a mysterious sensory memories, however. You might _think _of cold when you no-man’s-land between fantasy and reality. For them the sens- look at a picture of an ice cube, (...) but you probably do not feel es—touch, taste, hearing, vision and smell—get mixed up in- cold, no matter how many encounters you may have had with stead of remaining separate. ice and snow during your youth. Modern scientists have known about synesthesia since Another prevalent idea is that synesthetes are merely being 1880, when Francis Galton, a cousin of Charles Darwin, pub- metaphorical when they describe the note C flat as “red” or say lished a paper in _Nature _on the phenomenon. But most have that chicken tastes “pointy”—just as you and I might speak of brushed it aside as fakery, an artifact of drug use (LSD and a “loud” shirt or “sharp” cheddar cheese. Our ordinary lan- mescaline can produce similar effects) or a mere curiosity. guage is replete with such sense-related metaphors, and perhaps About four years ago, however, we and others began to un- synesthetes are just especially gifted in this regard. cover brain processes that could account for synesthesia. Along We began trying to find out whether synesthesia is a gen- the way, we also found new clues to some of the most mysteri- uine sensory experience in 1999. This deceptively simple ques- ous aspects of the human mind, such as the emergence of ab- tion had plagued researchers in this field for decades. One nat- stract thought, metaphor and perhaps even language. ural approach is to start by asking the subjects outright: “Is this A common explanation of synesthesia is that the affected just a memory, or do you actually see the color as if it were right people are simply experiencing childhood memories and asso- in front of you?” When we tried asking this question, we did ciations.. (shrink)
Apotemnophilia, a disorder that blurs the distinction between neurology and psychiatry, is characterized by the intense and longstanding desire for amputation of a speci¢c limb. Here we present evidence from two individuals suggestive that this condition, long thought to be entirely psychological in origin, actually has a neurological basis. We found heightened skin conductance response..
There are currently two main philosophical theories of perception - Direct Realism and the Representative Theory. The former is supported by most contemporary philosophers, whereas the latter forms the groundwork for most scientific theories in this area. The paper describes a recent experiment involving retinal and cortical rivalry that provides strong empirical evidence that the Direct Realist theory is incorrect. There are of course a large number of related experiments on visual perception that would tend to lead us to the (...) same conclusion, but the experiment described in this paper does so in a singularly direct and straightforward manner. Often the most telling experiments are the simplest. (shrink)
The target article discusses a model of how brain circuits mediate social behaviors such as imitation and mindreading. Hurley suggests potential mechanisms for development of shared circuits. We propose that empirical studies can be designed to differentiate the influence of genetic and learning-based factors on the development of shared circuits. We use the mirror neuron system as a model system.
In this commentary we discuss a predictive sensorimotor illusion, the size-weight illusion, in which the smaller of two objects of equal weight is perceived as heavier. We suggest that Grush's emulation theory can explain this illusion as a mismatch between predicted and actual sensorimotor feedback, and present preliminary data suggesting that the cerebellum may be critical for implementing the emulator.