Eidetic Memory

Eidetic memory is the ability to recall extremely detailed and vivid images. It is also refered to as “photographic” memory because it is just like taking a photograph and retrieving it from your memory ‘album’ from which you can see every details of it. However, there is still a debate on whether a true eidetic memory exists.

Sheldon Couoer, a main character in the TV series The Big Bang Theory

1 Visual Memory

1.1 Introduction

Visual memory is the ability to process visual stimuli and to encode, store and retrieve the resulting neural representations. It involves the ability to judge whether a visual stimulus has been encountered previously.[1] Although it has been reported that the capacity of storing declarative information is remarkably high, there is a limit to how much visual information can be stored in a short period of time. [2] Visual information lasts about half a second and may be stored in the short term memory storage (STM) for up to 30 seconds. In the early 1960s, George Sperling conducted experiments that involved the flashing of a grid of letters for 50 milliseconds and it was found that the information in a brief visual stimulus remains available for encoding even after the stimulus is no longer present.[3],[4] However, without rehearsal, this information will be lost and not be consolidated into the long term memory storage (LTM).

In the past decade, there have been reports of individuals who claim to possess the ability to process and recall enormous amounts of visual information, so called photographic memory or eidetic memory. For example, in 1920s, a Russian psychologist Alexander Luria reported that a man named Solomon Shereshevskii was an individual who seemed to have eidetic memory.[5] He possessed unusual sensory response to stimuli and he could retain vivid images of things he briefly saw 15 years ago.

"Had a memory so perfect that he could recall every minute of his life in graphic detail" -Luria, A.-

This, of course, deviates from the generally accepted view of the visual system having a limited capacity to process and recall information. Recent research has implicated some brain structures and rate-limiting molecules involved in memory formation and that modifications of their mechanisms and expression, respectively, may contribute to exceptional enhancement of visual working memory found in some individuals.

2 The Visual System

The Visual Pathway [17]
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2.1 Parvocellular pathway bias

Image processing starts with the retina where different populations of ganglion cells generate signals in response to a visual stimuli. These signals are then sent to the the lateral geniculate nucleus (LGN) in the thalamus through the optic nerve. LGN s is divided into the parvocellular layer and the magnocellular layer, and these layers project visual signals to the primary visual cortex (V1) for further analysis. An EEG study revealed grapheme-colour synaesthetes are more responsive to parvocellular pathways and less responsive to magnocellular pathways compared to non-synaesthetes.[6] Synaesthesia is a condition where stimulation of a single sensory modality leads to experiences in a second sensory modality, and it has been suggested that synaesthetes have superior memory for recognizing or recollecting abstract figures and patterns over non-synaesthete and in fact, Solomon Shereshevskii was also a synaesthete. The parvocellular pathway is related to processes that involve high spatial frequency, high contrast, colour, and visual recognition whereas the magnocellular pathway is associated with processes that involve low spatial frequency, low contrast, achromatic stimuli, and motion perception.[1],[7] The fact that this pathway is favoured by the brain regions upstream in the visual processing pathway in individuals with enhanced visual memory, could be a possibly explain the neural mechanism(s) underlying eidetic memory.

2.2 Primary visual cortex activation during mental imagery task

Complex information such as orientation, direction and colour sensitivity is extracted from the visual signals within the cortical neurons of V1.[1] Interestingly, a experiment using positron emission tomography (PET) has shown that V1 is activated more in imagery task than in perception task.[8] In visual mental imagery, objects are visualized in their absence while visual perception requires their physical presence. Eidetic memory could be considered as a complete mental imagery since it is the ability to recall images when they are no longer present, mental imagery. The fact that V1 is activated more when images are mentally visualized, may suggest that this area is involved in the retrieval process of visual information . Further experiments should be done to test if there is any significant difference in the level activation of V1 between subjects with superior visual memory and controls.

3 Hippocampus

The extracts of visual signals processed by the cortical neurons of V1 are further analyzed and distributed to various other cortical areas. The hippocampus (HC) is a part of the medial temporal lobe that receives visual information the inferior temporal cortex through parahippocampal cortex (PRh) and entorhinal cortex (EC).[1] HC has been long recognized for its importance in memory formation and lesions studies have shown that damage to the HC impairs all three “what”, “where”, and “when” components of recognition memory.

3.1 Complete removal of hippocampus

The case study of H.M. gives a clinical evidence that HC is important for formation of new memories.[9] Although HM lost the ability to form new memories and his long-term declarative memory was largely affected, he retained memories that formed before the removal of HC. Because he could retrieve old memory without the presence of his entire HC, it suggests that memories are stored in various parts of the brain and structures other than HC are (also) responsible for the process of retrieval.

3.2 Partial hippocampal damage

A study done on rats showed that hippocampus damage causes severe loss of visual memories formed prior to damage.[Bibliography item 10 not found.] This demonstrates that damage to hippocampus may lead to loss of stored information – retrograde amnesia.

3.3 Removal of entire partially damaged hippocampus

A clinical study done on epileptic patients with right hippocampal damage showed that the right hippocampus has special involvement in visual memory.[10] In this study, the patients exhibited impaired visual memory prior to surgical removal of their right hippocampi but interestingly, they partially improved on visual memory tasks after the surgery. These may lead to conclusion that HC is only involved in memory consolidation but not in memory retrieval.

3.4 hippocampus and visual memory

There are two possible ways to interpret the results discussed in sections 3.1,3.2 and 3.3. First, it could be that hippocampus is indeed involved in both memory consolidation and retrieval. Or, it could be that when the entire hippocampus is removed, the ability to retrieve already existing visual information is intact but when hippocampus is partially damaged, retrograde amnesia is induced.

4 Molecular basis of memory

Although there is no memory molecule to date that has scientifically shown to be responsible for exceptional memory, some molecules have been implicated in enhanced visual memory in animal models.

4.1 NR2B subunit

The N-methyl-D-aspartate (NMDA) receptor is the molecular switch for controlling synaptic plasticity and learning and memory.[11] The NR2A and NR2B subunits that make up the NMDA receptor are predominant in excitatory cortical and hippocampal pyramidal cells. It has been postulated that the shortening of NMDA currents and increased threshold for synaptic plasticity induction is due to the drastic decrease in the proportion of NR2B-containing NMDA receptors. [((bibcite13))] This led to an experiment where transgenic rats were generated that overexpressed the NR2B subunit in the HC and cortex. The transgenic rats showed enhanced recognition memory when they were tested on three tests: novel object recognition test, hidden platform water maze, T-maze spatial working memory testwhen synaptic properties were measured in the Schaffer collateral-CA1 path, single titanic stimulus was able to evoke significantly larger long-term potentiation (LTP) in transgenic hippocampal slices. This enhanced LTP was found to be NMDA receptor dependent because LTP was blocked with application of selective NMDA receptor blocker, AP-5. NR2B-selective antagonist Ro-25-6981was then used to block NR2B-containing NMDA receptors and it was found that NR2B subunits are required for LTP.

4.2 CREB

The biochemical responses produced by activation of NMDA receptors include changes in gene expression in the cell nucleus by activating the transcription factor called cAMP-response-element-binding protein (CREB).[13] CREB regulates a transcription factor cascade that ultimately leads to growth and synapse-specific structural changes. It is also a key control point for long-term memory (LTM) formation; loss of CREB impairs LTM while leaving learning and short-term memory (STM) intact.

The importance of CREB in terms of visual memory comes from an experiment that used a transgenic mouse line with a brain-specific inducible CREB repressor.[14] This experiment showed that CREB malfunction greatly impairs memory for objects and spatial location of objects.

In a gain of function experiment with Drosophila, maximal level of memory was produced just in one day of training for transgenic flies expressing an activator isoform of CREB while wild type flies took ten days to achieve the same level; in CREB-activated flies, LTM was induced with less training.

4.3 Estrogen receptors

In a study that examined the effect of estrogen replacement therapy (ERT) in postmenopausal women, those who were receiving ERT exhibited better performances on the Benton Visual Retention Test (BVRT) which was used to measure short-term visual memory and visual perception. [15] It was then postulated that ERT may protect against visual memory decline in aging women. Furthermore, in another study when estrogen was given to rats, their visual and spatial memory were rapidly enhanced. [16]

Bibliography
1. Khan, Z., Martín-Montañez, E. & Baxter, M. Visual perception and memory systems: from cortex to medial temporal lobe. Cellular and Molecular Life Sciences 68, 1737-1754, doi:10.1007/s00018-011-0641-6 (2011).
2. Bear, M., Connors, B. & Paradiso, M. Neuroscience : Exploring the Brain. 3rd. Ed. edn, (2007).
3. Sperling, G. THE INFORMATION AVAILABLE IN BRIEF VISUAL PRESENTATIONS. Psychological Monographs 74, 1-29 (1960).
4. Erwin, D. E. EXTRACTION OF INFORMATION FROM VISUAL PERSISTENCE. American Journal of Psychology 89, 659-667, doi:10.2307/1421464 (1976).
5. Luria, A. R. The mind of a mnemonist; a little book about a vast memory. (Basic Books, 1968).
6. Barnett, K. J. et al. Differences in early sensory-perceptual processing in synesthesia: A visual evoked potential study. Neuroimage 43, 605-613, doi:10.1016/j.neuroimage.2008.07.028 (2008).
7. Rothen, N., Meier, B. & Ward, J. Enhanced memory ability: Insights from synaesthesia. Neuroscience and Biobehavioral Reviews 36, 1952-1963, doi:10.1016/j.neubiorev.2012.05.004 (2012).
8. Kosslyn, S. M. et al. VISUAL MENTAL-IMAGERY ACTIVATES TOPOGRAPHICALLY ORGANIZED VISUAL-CORTEX - PET INVESTIGATIONS. Journal of Cognitive Neuroscience 5, 263-287, doi:10.1162/jocn.1993.5.3.263 (1993).
9. Scoville, W. B. & Milner, B. Loss of recent memory after bilateral hippocampal lesions. Journal of Neurology, Neurosurgery & Psychiatry 20, 11-21, doi:http://dx.doi.org/10.1136/jnnp.20.1.11 (1957).
: 10 :Epp, J., Keith, J. & Spanswick, S. Retrograde amnesia for visual memories after hippocampal damage in rats. Learning & Memory 15, 214-221, doi:http://dx.doi.org/10.1101/lm.788008 (2008).
10. Gleissner, U., Helmstaedter, C. & Elger, C. E. Right hippocampal contribution to visual memory: a presurgical and postsurgical study in patients with temporal lobe epilepsy. Journal of Neurology Neurosurgery and Psychiatry 65, 665-669, doi:10.1136/jnnp.65.5.665 (1998).
11. Li, F. & Tsien, J. Z. Memory and the NMDA Receptors. New England Journal of Medicine 361, 302-303 (2009).
12. Wang, D. et al. Genetic Enhancement of Memory and Long-Term Potentiation but Not CA1 Long-Term Depression in NR2B Transgenic Rats. Plos One 4 (2009).
13. Tully, T., Bourtchouladze, R., Scott, R. & Tallman, J. Targeting the CREB pathway for memory enhancers. Nature Reviews Drug :covery 2, 267-277 (2003).
14. Bozon, B. et al. MAPK, CREB and zif268 are all required for the consolidation of recognition memory. Philosophical Transactions of the Royal Society of London Series B-Biological Sciences 358, 805-814 (2003).
15. Resnick, S. M., Metter, E. J. & Zonderman, A. B. Estrogen replacement therapy and longitudinal decline in visual memory - A possible protective effect? Neurology 49, 1491-1497 (1997).
16. Luine, V. N. Rapid Enhancement of Visual and Place Memory by Estrogens in Rats. Endocrinology (Philadelphia) 144, 2836-2844 (2003).
17. "Visual Pathways." Web log post. Visual Pathways. Web. 25 Mar. 2014. <http://www.cog.brown.edu/courses/cg0001/lectures/visualpaths.html>.

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