Acquired synesthesia in retinitis pigmentosa

Armel, K. Carrie; Ramachandran, Vilayanur S.

doi:10.1080/13554799908411982

Cited by 76 publications

(14 citation statements)

References 11 publications

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“…It has been reported following stroke (Ro et al, 2007; Beauchamp and Ro, 2008; Thomas-Anterion et al, 2010; Schott, 2012), traumatic brain injury (Brogaard et al, 2012; Brogaard and Marlow, 2013), neuropathology involving the optic nerve and/or chiasm (Jacobs et al, 1981; Armel and Ramachandran, 1999; Afra et al, 2009), seizures (Jacome and Gumnit, 1979), migraine (Alstadhaug and Benjaminsen, 2010), post-hypnotic suggestion (Cohen Kadosh et al, 2009) and sensory substitution (Ward and Wright, 2012). Audio-visual synesthesia has been reported to be the most common acquired type (Afra et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Serotonergic Hyperactivity as a Potential Factor in Developmental, Acquired and Drug-Induced Synesthesia

Brogaard

2013

Front. Hum. Neurosci.

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Though synesthesia research has seen a huge growth in recent decades, and tremendous progress has been made in terms of understanding the mechanism and cause of synesthesia, we are still left mostly in the dark when it comes to the mechanistic commonalities (if any) among developmental, acquired and drug-induced synesthesia. We know that many forms of synesthesia involve aberrant structural or functional brain connectivity. Proposed mechanisms include direct projection and disinhibited feedback mechanisms, in which information from two otherwise structurally or functionally separate brain regions mix. We also know that synesthesia sometimes runs in families. However, it is unclear what causes its onset. Studies of psychedelic drugs, such as psilocybin, LSD and mescaline, reveal that exposure to these drugs can induce synesthesia. One neurotransmitter suspected to be central to the perceptual changes is serotonin. Excessive serotonin in the brain may cause many of the characteristics of psychedelic intoxication. Excessive serotonin levels may also play a role in synesthesia acquired after brain injury. In brain injury sudden cell death floods local brain regions with serotonin and glutamate. This neurotransmitter flooding could perhaps result in unusual feature binding. Finally, developmental synesthesia that occurs in individuals with autism may be a result of alterations in the serotonergic system, leading to a blockage of regular gating mechanisms. I conclude on these grounds that one commonality among at least some cases of acquired, developmental and drug-induced synesthesia may be the presence of excessive levels of serotonin, which increases the excitability and connectedness of sensory brain regions.

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Section: Introductionmentioning

confidence: 99%

Serotonergic Hyperactivity as a Potential Factor in Developmental, Acquired and Drug-Induced Synesthesia

Brogaard

2013

Front. Hum. Neurosci.

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“…This is why here we consider that the real question is that of artificially induced synaesthesia—a label which maintains the contrast with the spontaneous forms of synaesthesia that have been documented to develop in children, and encompass cases of training, including following the use of certain conversion devices, as well as drugs or hypnosis. Possible artificially induced synaesthesia, in turn, can be distinguished from what might be better called late emerging synaesthesia that is supposed to occur spontaneously after certain kinds of brain damage or sensory deprivation (e.g., Lessel and Cohen, 1979; Jacobs et al, 1981; Bender et al, 1982; Vike et al, 1984; Rizzo and Eslinger, 1989; Harrison and Baron-Cohen, 1996; Armel and Ramachandran, 1999; Ro et al, 2007; see also Ward, 2007; Afra et al, 2009). The current article will focus on the possibility of an artificial induction of synaesthesia through associative learning.…”

Section: Introductionmentioning

confidence: 99%

Training, hypnosis, and drugs: artificial synaesthesia, or artificial paradises?

Deroy

Spence

2013

Front. Psychol.

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The last few years have seen the publication of a number of studies by researchers claiming to have induced “synaesthesia,” “pseudo-synaesthesia,” or “synaesthesia-like” phenomena in non-synaesthetic participants. Although the intention of these studies has been to try and shed light on the way in which synaesthesia might have been acquired in developmental synaesthestes, we argue that they may only have documented a phenomenon that has elsewhere been accounted for in terms of the acquisition of sensory associations and is not evidently linked to synaesthesia. As synaesthesia remains largely defined in terms of the involuntary elicitation of conscious concurrents, we suggest that the theoretical rapprochement with synaesthesia (in any of its guises) is unnecessary, and potentially distracting. It might therefore, be less confusing if researchers were to avoid referring to synaesthesia when characterizing cases that lack robust evidence of a conscious manifestation. Even in the case of those other conditions for which conscious experiences are better evidenced, when training has been occurred during hypnotic suggestion, or when it has been combined with drugs, we argue that not every conscious manifestation should necessarily be counted as synaesthetic. Finally, we stress that cases of associative learning are unlikely to shed light on two highly specific characteristic of the majority of cases of developmental synaesthesia in terms of learning patterns: First, their resistance to change through exposure once the synaesthetic repertoire has been fixed; Second, the transfer of conditioned responses between concurrents and inducers after training. We conclude by questioning whether, in adulthood, it is ever possible to acquire the kind of synaesthesia that is typically documented in the developmental form of the condition. The available evidence instead seems to point to there being a critical period for the development of synaesthesia, probably only in those with a genetic predisposition to develop the condition.

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“…Armel and colleagues reported a case of acquired tactile-visual synesthesia17 in a patient with retinitis pigmentosa and progressive visual decline, until complete blindness at age 40. Synesthesia in from of tactile stimuli evoking vivid visual sensations started at age 42.…”

Section: Other Acquired Synesthesiasmentioning

confidence: 99%

Acquired auditory-visual synesthesia: A window to early cross-modal sensory interactions

Afra

Funke

Matsuo

2009

PRBM

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Synesthesia is experienced when sensory stimulation of one sensory modality elicits an involuntary sensation in another sensory modality. Auditory-visual synesthesia occurs when auditory stimuli elicit visual sensations. It has developmental, induced and acquired varieties. The acquired variety has been reported in association with deafferentation of the visual system as well as temporal lobe pathology with intact visual pathways. The induced variety has been reported in experimental and post-surgical blindfolding, as well as intake of hallucinogenic or psychedelics. Although in humans there is no known anatomical pathway connecting auditory areas to primary and/or early visual association areas, there is imaging and neurophysiologic evidence to the presence of early cross modal interactions between the auditory and visual sensory pathways. Synesthesia may be a window of opportunity to study these cross modal interactions. Here we review the existing literature in the acquired and induced auditory-visual synesthesias and discuss the possible neural mechanisms.

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Acquired synesthesia in retinitis pigmentosa

Cited by 76 publications

References 11 publications

Serotonergic Hyperactivity as a Potential Factor in Developmental, Acquired and Drug-Induced Synesthesia

Serotonergic Hyperactivity as a Potential Factor in Developmental, Acquired and Drug-Induced Synesthesia

Training, hypnosis, and drugs: artificial synaesthesia, or artificial paradises?

Acquired auditory-visual synesthesia: A window to early cross-modal sensory interactions

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