neurological correlates of synaesthesia

Ishmael Beckford Tongs MCT 2 Sound Cognition & Perception

SynaesthesiaWhich neural mechanism is responsible for all the forms of Synaesthetic experience?

Synaesthesia results from sensory stimulation in one modality or stream which in turn induces stimulation in a second1. Empirically this is experienced as the inductive sense producing a concurrent sense impression (sound – colour for instance). These inducers thus systematically 2 trigger the synaesthetic concurrents to which they are correspondingly mapped 3

The field of synaesthesia research is currently experiencing much renewed interest and interdisciplinary research into genetics, autism, induced synaesthesia and even the relationship between cross-modal experience and mental illness is being pursued. Unfortunately, the low resolutions of FMRI (Functional Magnetic Resolution Imaging) and MRI (Magnetic Resolution Imaging) scans mean that our understanding of the neural correlates behind synaesthesia is far from comprehensive. The disinhibited feedback hyperbinding and cross activation theories are pre eminent among theories. The former suggests that synaesthesia arises out the disinhibition of feedback travelling up toward a multi-modal "sensory nexus"4 resulting in the transfer of information down the concurrent pathways. The cross activation hypothesis claims that synaesthesia arises out of crosstalk/activation/wiring between adjacent brain regions as a result of a genetic mutation causing defective pruning. This is most evident in grapheme-colour synaesthesia where the Left Hemisphere (colour) and Gyrus (grapheme) of the Fusiform region are cross linked5. The hyperbinding hypothesis combines the two aforementioned theories stating that the failure of the neonatal synaesthete's brain to prune the over-proliferation of synaptic connections results in a lack of specialisation which in turn leads to atypical neural binding patterns. These binding patterns create multi-modal and unimodal connections (across and within sensory processing regions) which account for the inducer - concurrent relationships seen in synaesthesia.6

Current synaesthetic research is primed toward decoding the neural patterns governing cross-modal sensory experience. The sheer diversity and complexity of human neural architecture complicates this assay however. There can be no single mechanism responsible for all synaesthetic experience.

Auditory Synaesthesia II

Auditory Synaesthesia consistently produces multi-modal sensory experience in 1 J. Neufeld, C. Sinke, M. Zedler, W. Dillo, H.M. Emrich, S. Bleich, G.R. Szycik (2012) Disinhibited feedback as a cause of synaesthesia: Evidence from a functional connectivity study on auditory-visual synaesthetes Neuropsychologia, Vol. 50 no. 7, June 2012, Pages pp. 1471–1477 2 S Marks, L.E. (1975) On colored-hearing synaesthesia: cross-modal translations of sensory dimension Psychology Bull. 82 pp. 303–331 3 P. Grossenbacher, C. Lovelace (2001) Mechanisms of synaesthesia: cognitive and physiological constraints Trends in Cognitive Sciences Vol.5 No.1 pp.36–414 P. Grossenbacher, C. Lovelace (2001) Mechanisms of synesthesia: cognitive and physiological constraints Trends in Cognitive Sciences, Vol.5 No.1 pp. 36–41 5 V.S. Ramachandran and E.M. Hubbard (2001) Synaesthesia—A Window Into Perception, Thought and LanguageJournal of Consciousness Studies Vol. 8, No. 12, 2001, pp. 3–346 R.C Kadosh, A. Henik and Vincent Walsh (2009) Synaesthesia: learned or lost? Developmental Science pp. 484–491


response to an auditory stimulus or vice versa (grapheme – sound for example). Thus a “sharp rap on a table [may arouse] a faint but distinct narrow flash of brightness”.7 One case study reported a diversity of auditory - synaesthetic manifestations including the presentation of “vivid complex shapes in response to tones...upon which colour was superimposed"8

Another case documented by Zigler presented two US college students who responded to timbral stimuli with "tridimensional" shapes: "Every instrument excites a specific form, which maintains roughly the same features at all pitches, intensities, and durations".9 In addition colours can be spatially oriented in the visual field as evidenced by one participant for whom Sirens induced "a thin bright line moving across his visual field". It is therefore clear that Auditory Synaesthesia is not limited to pitch - colour mapping. Most auditory - synaesthetes tend to experience several colours when exposed to chords. These are discrete colours implying that the neural mechanisms operate on a reductive as opposed to a gestalt level with the tone as fundamental unit. Experiments moreover illustrated that synaesthetes demonstrated a tendency to use finegrain controls to reproduce colours to a higher degree of accuracy than controls. "80.7%, SD = 22 vs 61.6%, SD = 19.2". There was also far more associative consistency over time. Additionally it has been observed that a pure sine wave (consisting of a single partial) is less "colourful" than a tone with higher levels of spectral content i.e. a violin. This could be due to pitch being determined by the wider overall "Periodicity" of a tone as opposed to theidentity of the fundamental.10

Zigler's experiment furthermore showed that controls and synaesthetes map timbral content in much the same way with very little variance. This he claimed was evidence for functional cerebral similarities between the auditory - synaesthetic and "neurotypical" brain. Indeed it was explained that they employ "identical strategies"11 for correlating pitch lightness mappings to sound. With this he challenged the Cross - activation al hypothesis claiming instead that Auditory Synaesthesia merely involves a higher degree of neural activity or neuronal density in the corresponding cerebral centres. It is not clear whether this is being applied to all auditory - synaesthetic experience or to pitch lightness mappingshowever. Calvert's experiment found that synaesthetes all exhibited increased IPC activity (FMRIimaging used). The (left hemispheric) IPC has been implicated in the " cross modal synthesis" of dynamic spatio-orientation - that is velocity determination and general audiovisual motion discrimination. It has been further implicated in "multi-modal associations... multi-modal integratory attention and multi-modal integratory associations". 12

Robertson identified it as being integral to attention and visual motor control and coordination. Robertson's research indicates that its role in "crossmodal integration" and "feature binding" makes it the central axis or "Nexus" about which the coupled inducer andconcurrent regions can interact. 13

The IPC has been labelled the synaesthetic "Powerhouse" processing colour dimensional and textural information - qualitative phenomena directly involved in much of synaesthetic experience. It has been suggested in fact that the IPC may well process the 7 J. Ward, Huckstep, E. Tsakanikos (2006) Sound-Colour Synaesthesia: to What Extent Does it Use Cross-Modal Mechanisms Common to us All? Cortex Vol.42 No.2 pp. 264–280

8 J. Ward, Huckstep, E. Tsakanikos (2006) Sound-Colour Synaesthesia: to What Extent Does it Use Cross-Modal Mechanisms Common to us All? Cortex Vol.42 No.2 pp. 264–2809 M.J Zigler (1930) Tone shapes: a novel type of synaesthesia Journal of General Psychology Vol. 3 277-28710 R. Plomp Pitch of Complex Tones (1967) The Journal of the Acoustical Society of America Vol.1 pp.11J. Ward, Huckstep, E. Tsakanikos (2006) Sound-Colour Synaesthesia: to What Extent Does it Use Cross-Modal Mechanisms Common to us All? Cortex Vol.42 No.2 pp. 264–28012 R. Rouwe, H.S.Stolte (2010) Neural Basis of Individual Differences in Synaesthetic Experiences The Journal of Neuroscience Vol. 30No.18 pp. 6205-6213

13 J. Neufeld, C. Sinke, W. Dillo, H. M. Emrich, G. R. Szycik, D. Dima, S. Bleich, and M. Zedler (2012) The neural correlates of coloured music: A functional MRI investigation of auditory–visual synaesthesia Neuropsychologia Vol.50 No.1 pp.85-89.


synaesthetically generated photisms experienced by synaesthetes. Of course this approach is based on an understanding of the IPC produced by low resolution brain scanners which cannot for example examine microtubular structures. Thus we are limited to a generalised picture.

Fig.1 Graph indicating that Synaesthetes and Controls assign similar Munsell Chroma values(Hue Lightness and Colour) to instrumental timbres 14

III Cross activation

The cross activation hypothesis grew out of Ramachandran and Hubbard's desire to provide "concrete testable proposals regarding the exact anatomical locus (or loci) and theextent of ‘cross-wiring’" 15

in the synaesthetic brain. The aim then was to correlate synaesthetic experience to specific neural location(s). Though this assay /was limited to Grapheme-colour synesthesia there is a common neurological thread running through all the varieties of multi-modal sensation as acknowledged by Ramachandran: " the argument may be valid for other kinds as well" Referring to neuroanatomical studies he identified that the colour processing and visual grapheme cerebral centres are located in the fusiform gyrus with thelatter located adjacent to V4 (inferior temporal cortex) which had been previously

14 J Ward, Huckstep, E. Tsakanikos (2006) Sound-Colour Synaesthesia: to What Extent Does it Use Cross-Modal Mechanisms Common to us All? Cortex Vol.42 No.2 pp. 264–280

15 E.M Hubbard, D. Brang, V.S Ramachandran (2011) Cross activation theory at 10 Journal of Neuropsychology Vol. 5 No. 2, pp. 152–177


implicated in automatic colour constancy operations. Ramachandran hypothesised that these two areas become cross wired in synaesthetes and drew the analogy of "cross-activation of the hand area by the face in amputees with phantom arms"16. J. Neufield and his team provided an example of a subject who experienced timbre induced geometric photisms. The geometric complexity of the photisms was directly linked to the complexity of the tone or chord heard. In order to process these photisms. The superior temporal sulcus (separating inferior temporal and sub temporal gyri) has been identified by Ryan A. Stevenson and Thomas W. James as one of the primary multi-modal brain regions involved in audiovisual processing.17 The inferior parietal cortex is moreover involved in multi-modal sensory processing. The two brain regions may well be cross wired, (given their adjacency) producing a synaesthetic experience in which the perception of timbre produces photistic phenomena. Alternatively Pantey and her team discovered that specific timbres produced auditory cortical activation18. Different timbres were apportioned enhanced representations which were in turn dependent on musical experience. The auditory processing cortex (Brodmannareas 41 and 42) may process timbral information in this instance. The current scientific "conceit" is to apply a single mechanism across an entire population, which explains why the two models proposed have been presumed to be representative of all synaesthetes. Rouwe and Stolte discovered that associator and projector synaesthetes employ distinct neural mechanisms when responding synaesthetically.19 Hupe and his team moreover found that “In 10 [grapheme-colour] synaesthetes... color areas and retinotopic areas were not activated by synaesthetic colors”20. That is to say they discovered that the colour processing cerebral regions were not responsible for their synaesthetic experience. Projectors project their experience onto the world and consequently the critical brain regions are those related to processing and acting in the outside world (Visual Auditory and Motor cortices). In the associator subtype experience is located within the mind itself and the neural response pattern shows reliance on the Hippocampus and Parahippocampal Gyrus which have been identified as being crucial in memory formation and retrieval. K.J Barnett et al noted in fact that “even within types there are vast individualdifferences in the way that stimuli induce synaesthesia and in the subjective synaesthetic experience”21Thus it is evident that even within the synaesthetic population there is much neurodiversity and so an extrapolative approach is not warranted.

16 E.M Hubbard, D Brang, V.S Ramachandran (2011) Cross activation theory at 10 Journal of Neuropsychology Vol. 5 No. 2, pp. 152–17717R.A Stevenson, T.W James (2009) Audiovisual integration in human superior temporal sulcus: Inverse effectiveness and the neural processing of speech and object recognition Neuroimage pp. 1210-122318 C. Pantev, C.A Larry, E. Roberts, M. Schulz, A. Engelien and B. Ross (2001) Timbre-specific enhancement of auditorycortical representations in musicians Neuroreport Vol. 12 pp. 164-17919 R. Rouwe, H.S.Stolte (2010) Neural Basis of Individual Differences in Synaesthetic Experiences The Journal of Neuroscience Vol. 30No. 18 pp. 6205-621320 J.M Hupe, C. Bordier and M. Dojat (2011) The Neural Bases of Grapheme-Color Synaesthesia Are Not Localized in Real Color-Sensitive Areas Cerebral Cortex pp. 1622-163321 K.J Barnett, C. Finucane, J.E Asher, G. Bargary, A.P Corvin, M.J Mitchell (2001) Familial patterns and the origins of individual differences in synaesthesia Cognition pp. 871-93


Fig. 2 Lateral neuroanatomical diagram illustrating proximity of cerebral regions22

IV Genetics

Ramachandran speculated that a genetic mutation might in fact result in defective pruning leading to an overabundance of connections or a hyperconnective state. Bennett

22 S.J Dearmond M.M Fusco M.M Dewey (1989) Structure of the human brain: A photographic atlas Oxford University Press pp.


et al conducted one of the first well documented studies into the heredity of synesthesia discovering that 42% of the test subjects reported a first degree relative with the condition23. They stated that “[Their] findings strongly indicate that various types of synaesthesia are fundamentally related at the genetic level, but that the explicit associations and the individual differences between synaesthetes are influenced by other factors”24. They found that multiple inducer concurrent associations were to be found withinthe same family indicating that across the many manifestations of synesthesia there is a global genetic link. It has furthermore been suggested that the mutation is x linked, evidenced by the slight preponderance of females over males (2:1) and the rarity of male to male inheritance25. The high ratio of females to males in synaesthetic families also supports these claims

VDisinhibited feedback

The Disinhibited Feedback model first proposed in 1997 by Grossenbacher posits that synesthesia occurs through the disinhibition of neural feedback from a multi-modal sensory nexus such as the IPC26. It is characterised by reciprocal feedforward27 (unidirectional neural transmissions unreliant on top down information transference) and feedback mechanisms (top down transmission of information). This process can be observed in the visual and auditory systems where neural feedbackfrom higher level processing regions exert change at the earliest phase of cortical processing. In short the inductive neural transmissions converge with activity from the multisensory nexus (inter/intra stimulus domains). In the synaesthetic brain the inductive signal feeds back along other sensory pathways. This causes activation of the concurrent which in turn results in synaesthetic experience. This disinhibition has been theorised to occur due to an imbalance in the ratio of excitatory to inhibitory neurotransmitters28

The fundamental difference between the disinhibited model and cross activated model is that the latter proposes architectural abnormalities which then give rise to synaesthetic experience while the former proposes mechanisms common to all individuals both Neurotypical and otherwise. One might assume that the ability of altered states (psychedelics, hypnotism, meditation) to induce synesthesia implies that the mechanisms of synesthesia may in fact be common to all. In actuality drug induced synaesthetic experience tends to rely on bottom up neural processes while the higher order disinhibited feedback is absolutely essential in innate synesthesia due to conceptualisation. It was in fact found that synesthesia is in some cases driven by “late perceptual processing”29.23 K.J Barnett, C. Finucane, J.E Asher, G. Bargary, A.P Corvin, M.J Mitchell (2001) Familial patterns and the origins of individual differences in synaesthesia Cognition pp. 871-93

24 K.J Barnett, C. Finucane, J.E Asher, G. Bargary, A.P Corvin, M.J Mitchell (2001) Familial patterns and the origins of individual differences in synaesthesia Cognition pp. 871-9325 J. Ward, J. Simner (2004) Is synesthesia an x linked dominant trait with lethality in males? Perception vol. 34 no.4 pp. 611-62326P. Grossenbacher, C. Lovelace (2001) Mechanisms of synesthesia: cognitive and physiological constraints Trends in Cognitive Sciences, Vol.5 No.1 pp. 36–41 27 A.N Rich, J.B Mattingley (2002) Anomalous perception in synesthesia: A cognitive neuroscience perspective pp.43-5028J. Simner, E.M Hubbard (2006) Variants of synesthesia interact in cognitive tasks: Evidence for implicit associations and late connectivity in crosstalk theories pp.805-81529 G. Bargary, K.V Barnett, K.J Mitchell, F.N Newell Coloured speech synesthesia is triggered by multisensory not unisensory perception (2009) Psychological Science pp. 529-533


Synaesthesia is directly linked to information processing as opposed to bottom up sensory signal transmission. Thus a synaesthete will need to conceptualise the musical phenomena and process this before the synaesthetic experience can be induced. It was also discovered by Dixon et al30 that presenting a subject with incongruent and congruent graphemes which could be interpreted as either letters or digits resulted in different photisms. The photisms themselves were reliant upon the digit-letter interpretation as opposed to the incongruent colours. The subject had to process the meaning of the graphemes in her higher cognitive centres before a synaesthetic experience could be invoked. In brief synesthesia is “concept driven”31

Fig.3 schematic representation of disinhibited feedback32

In Fig.3. A stimulus sends a signal up through the different representational stages (each box is a representation at a different phase along the pathway). The inducer and concurrent pathways are separated to prevent sensory inputs triggering the “wrong” response. The inhibition of feedback normally inhibits the inductive signals propagating through other pathways (signals are forward feeding black arrows). In the synaesthetic brain this process is disinhibited. Thus the inductive signal can activate a concurrent pathway either through pathway convergence or horizontal activation. The grey arrows indicate these two possible mechanisms

VIIAutistic Spectrum Disorder

Autism spectrum disorders are a continuum of disorders characterised by pervasive developmental conditions. Multiple areas are affected including social communication, language, sensory processing, executive functioning and social intelligence. While it has been classed as a behavioural condition33 there are neural characteristics which tend to

30 M.J Dixon, D. Smilek, P.L Duffy, M.P Zanna, P.M Merikle (2006) The role of meaning in grapheme-colour synaesthesia Cortex pp. 243-52. 31 Mike J. Dixon, Daniel Smilek, Cera Cudahy,Philip M. Merikle (2006) Five plus Two equals Yellow Nature Vol. 3 pp.36532 P.G Grossenbacher, C.T Lovelace (2001) Mechanisms of synesthesia:Cognitive and Neurophysiological constraints pp.36-4333 K.Dillenburger, J.A Jordan, L. McKerr, P. Devine, M. Keenan (2013) Autism Spectrum Disorder: Public awareness and attitudes Research in Autism Spectrum Disorders pp.1558–1567


propagate across a large proportion of the autist population. One such characteristic is hyperconnectivity. Hyperconnectivity is defined as the proliferation of short distance connections between different brain regions A neurotypical brain will tend to have many long distance connections as illustrated in fig.4The primary conclusion drawn from the above graphic is that the mean system-wide connectivity for ASD (Autistic Spectrum Disorder) children is higher than that of TD (typically developing) children. In fact autistic children had higher levels of connectivity both within and between subsystems. Corchesne et al discovered that there is a synaptic overabundance in the prefrontal cortex of autistic children34. This has been surmised to be a result of hyperplasic growth in cerebral grey matter and cerebral and cerebellar white matter35. Similar White matter proliferation was observed in the brains of grapheme – colour synaesthetes in Bargarie's study.36 Higher levels of diffusion anisotropy at various locationswere attributed to greater myelin or axonal density. That is to say there is greater “coherence” and “density” at the microstructural level. The occurrence of synesthesia in Simon Baron Cohen's autistic sample37 was determined to be 18.9% in contrast to 7.22% observed among the neurotypical controls. Another study moreover identified genetic correspondence between synesthesia and autism. Gene GRIN2B (MIM 138252) (responsible for the enhancement of learning and memory and implicated in savantism autism and synesthesia).

Fig.4 System representation displaying difference between typical and autistic neuralconnectivity 38

34 E. Courchesne, R. Carper, N. Akshoomoff (2011) Evidence of Brain Overgrowth in the First Year of Life in Autism JAMA Vol. 290 No. 3 pp. 337-34535 Courchesne E, Karns C, Davis HR, (2001) Unusual brain growth patterns in early life in patients with autistic disorder: an MRI study Neurology Vol.57 No.2 pp. 245-254.36 G. Bargary, K.J Mitchell (2008) Synaesthesia and Cortical connectivity Trends in Neurosciences Vol.31 No.7 pp.335-34237 S. Baron-Cohen, D. Johnson, J. Asher, S. Wheelwright, S.E Fisher, P.K Gregersen, C. Allison (2013) Is synaesthesia more common in autism? Molecular autism Vol. 57 No. 2 pp. 245-54. 38 K. Supekar L.Q Uddin, A. Khouzam, J. Phillips, W.D. Gaillard,L.E Kenworthy, B.E Yerys, C.J. Vaidya and V. Menon (2013) Brain hyperconnectivity in children with autism and its links to social deficits Cell Rep. Vol.5 No. 3 pp.738-747


VIHyperbinding

Perceptual experience consists of a “sensory mosaic”39 comprised of different sensory modalities. These are fragmented and parcelled out to the cortex for processing. They are then recombined into a gestalt sensory experience. Both sensory recognition and object integration are requisite for veridical processing for instance. It is moreover worth noting that neuroimaging studies in humans have revealed that the visual system is made up of two general information processing streams (temporal and parietal) with ten visual cortical regions.40 The auditory system is similarly fragmented to facilitate acoustic scene analysis and spectral analysis. Esterman found moreover that TMS (Transcranial Magnetic Stimulation) can in fact induce “Illusory conjunctions” - a perceptual illusion in which the characteristics of one object are transposed onto another in the visual field41. This form of binding problem in which multi-modal integration fails to form the correct sensory conjunctions has been implicated in synaesthessia. Auditory feature binding consists of acoustical scene analysis (identifying specific sounds amongst several acoustic streams) and feature analysis (spectral content rhythm pitch)

Fig.4 Audio-Optical Synergic Integration Schematic42

Auditory processing consists of segmentation (deconstructing a signal into segments)

39 L.C Robertson (2001) Binding, spatial attention and perceptual awareness Nat Rev Neurosci. Vol. 4 No. 2 pp.93-10240 R.B.H. Tootell, A.M. Dale, M.I Sereno and R. Malach (1996) New images from the human visual cortex Trends in Neuroscience

Vol.19 pp.481-48941 M. Esterman, T. Verstynen, L.C Robertson (2006) Attenuating illusory binding with TMS of the right parietal cortex Neuroimage Vol.

35 pp.1247-125542 G. Zhuo, X.Yu (2010) Real world auditory perception related to auditory feature binding IEEE Computer Society


and grouping in which a multi-modal stream is formed. Fig.4 provides a useful schematic diagram of this process . Segmentation occurs in step one while the cross modal synergic mechanism refers to the formation of the multi-modal stream which in this case is a synaesthetic experience. In the example of timbre (inducer) photism (concurrent) synaesthesia a sound signal is analysed; spectral information segmented and decoded and these features are bound to an optical signal in synergic integration. These processes are accounted for by two forms of hyperbinding. The first relates to associative memory and the second is an adaptation of the hyperconnectivity theory. The former is a neural phenomenon in which associative memory is significantly enhanced. It has been succinctly defined as the “obligatory formation of overly broad associations between events occurring in close temporal and spatial contiguity”. This is said to be a product of poor sensory inhibition. Logan's obligatory retrieval theory states that directing one's attention to an object will invoke one's associative memory – meaning that associated objects will be retrieved from memory.43 This is an important factor in the development of automaticity – the transfer fromconscious to automatic processing. . Cohen proposed that grapheme colour synaesthetes in fact learn synesthesia through associating graphemic magnitude (spatial,size and temporal values) with luminance (colour value)44. His argument was derived from Beeli's proposition that experience with graphemes “shapes synaesthetic experience”45. There are also parallels with Smilek's similar proposal that a neonates early exposure to graphemes affects the development of synesthesia46

Cohen furthermore hybridised the cross activation and disinhibition theories in a novel concept derived from Johnson's”Interactive specialisation approach to cognitive development”47. The theory states that neural specialisation (different brain regions acquiring specificity of function) occurs during post natal cognitive development. This is said to occur as a result of competition between cortical regions as well as bias (neurotransmitter type and synaptic density) Cohen goes on to quote Knudsen's “sensitive period”48 theory.(there is a critical window where the brain's patterns of neuroplasticity are being determined) ( He theorised that defective pruning mechanisms could result in synaptic super-density and a proliferation of non functional sensory inputs. This overabundance of inputs results in hyperbinding patterns both within and between sensory modalities. Hyperbinding in this instance refers to cross-modal connectivity as opposed to general architectural connectivity as described in the hyperconnectivtiy model.

VIIIConclusion

It is clear then that no one hypothesis can provide a comprehensive account of the neural correlates behind synaesthesia. These models are also not mutually exclusive 49.

43 G.D Logan (1998) What is learned during automization? Human Perception and Performance Vol. 24 No. 6 pp.1720-173644R.C Kadosh, A. Henik and V. Walsh (2009) Synaesthesia: learned or lost? Developmental Science Vol.12 No.3 pp. 484-49145 G. Beeli ,M. Esslen, L. Jäncke (2007) Frequency Colour correlates in grapheme-color synesthesia Psychological Science Vol. 18

No. 9 pp. 788-79246 D. Smilek, J.S.A Carriere, M.J Dixon, P.A Merikle (2007) Grapheme frequency and luminance in grapheme-colour synaesthesia

Psychological Science pp. 793-795 47 M.H Johnson (2011) Interactive Specialization: A domain-general framework for human functional brain development? Developmental Cognitive Neuroscience, Vol. 1 No. 1 pp. 7–21

48 E. Knudsen (2004) Sensitive periods in the development of the brain and behavior J Cogn Neurosci. Vol. 6 No. 8 pp.412-2

49 E.M Hubbard Neurophysiology of synaesthesia (2007) Current psychiatry reports Vol.9 No. 3: pp. 93-199


The hyperbinding account in particular is dependent on cross activation and defective pruning and the disinhibited feedback model emerges out of the theory of cross activated brain regions. The patterns of inheritance within families (different forms of synaesthesia occurring within the one family) would imply that each model is responsible for a variety of synaesthetic conditions.50

Current synaesthetic research is attempting to continue to make lateral connections between known neural abnormalities (i.e. autism) and synaesthetic experience; deepen our understanding of the base mechanisms already identified and examine the range of variation within the synaesthetic populations. Additionally scientists aim to challenge long held assumptions51. Future expansions of neuroimaging technology aim to enhance pulse sequencing (radio frequency pulses directed at cerebral tissue), field strengths and spatial/temporal specificity (resolution in the temporal and spatial domains) This will facilitate the refinement of our concepts. The goal then is to use past and future discoveries to advance neurocognitive science. Kadosh states that ”the study of synaesthesia could advance our understanding of the normal and abnormal human brain and cognition”52. Advancing synaesthesia as a science will have interdisciplinary implications for linguistics, emotion53, sensory perception neuroanatomy and ultimately consciousness and perception research

50 E.M Hubbard Neurophysiology of synaesthesia (2007) Current psychiatry reports Vol.9 No. 3: pp. 93-19951 D. Ophelia, C. Spence (2013) Are we all born synaesthetic? Examining the neonatal synaesthesia hypothesis Neuroscience and Biobehavioral Reviews Vol.37 No.7 pp. 1240-125352 R.C Kadosh A. Henik (2008) Can synaesthesia research inform cognitive science? TRENDS in Cognitive Sciences Vol.11 No.4 pp.177-

185

53 R.C Kadosh A. Henik (2008) Can synaesthesia research inform cognitive science? TRENDS in Cognitive Sciences Vol.11 No.4 pp.177-185

neurological correlates of synaesthesia

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auditory synaesthesia

synaesthesia results

mechanisms of synaesthesia

induced synaesthesia

cause of synaesthesia

graphemecolour synaesthesia

field of synaesthesia

coloredhearing synaesthesia