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Visual acuity enhancement: Difference between revisions

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Acuity enhancement is often accompanied by other coinciding effects such as [[color enhancement]] and [[pattern recognition enhancement]]. It is most commonly induced under the influence of [[dosage#mild|mild]] [[dosage|dosages]] of [[psychedelic]] compounds, such as [[LSD]], [[psilocybin]], and [[mescaline]]. However, it can also occur to a lesser extent under the influence of certain [[stimulants]] and [[dissociatives]] such as [[MDMA]] or [[3-MeO-PCP]].
Acuity enhancement is often accompanied by other coinciding effects such as [[color enhancement]] and [[pattern recognition enhancement]].<ref>Papoutsis, I., Nikolaou, P., Stefanidou, M., Spiliopoulou, C., & Athanaselis, S. (2015). 25B-NBOMe and its precursor 2C-B: modern trends and hidden dangers. Forensic Toxicology, 33(1), 4. https://doi.org/10.1007/s11419-014-0242-9</ref><ref>Bersani, F. S., Corazza, O., Albano, G., Valeriani, G., Santacroce, R., Bolzan Mariotti Posocco, F., ... & Schifano, F. (2014). 25C-NBOMe: preliminary data on pharmacology, psychoactive effects, and toxicity of a new potent and dangerous hallucinogenic drug. BioMed Research International, 2014. https://dx.doi.org/10.1155/2014/734749</ref> It is most commonly induced under the influence of [[dosage#mild|mild]] [[dosage|dosages]] of [[psychedelic]] compounds, such as [[LSD]], [[psilocybin]], and [[mescaline]]. However, it can also occur to a lesser extent under the influence of certain [[stimulants]] and [[dissociatives]] such as [[MDMA]] or [[3-MeO-PCP]].
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Revision as of 06:51, 21 February 2018

{{#ev:gfycat|https://giant.gfycat.com/IndolentDeliriousGiantschnauzer.webm%7C400x225%7Cright%7CVisual acuity enhancement by StingrayZ - This animation serves as a replication of visual acuity enhancement, which is a common psychedelic effect. It demonstrates the general differences between normal vision and acuity enhancement by shifting between the two states. There is also a subtle amount of visual drifting within this replication.|frame}} Acuity enhancement can be described as an enhancement of the clearness and clarity of vision. This results in the visual details of the external environment becoming sharpened to the point where the edges of objects become perceived as extremely focused, clear and defined. The experience of acuity enhancement can be likened to bringing a camera or projector lens that was slightly blurry into focus. At its highest level, one may experience the perception that they can now observe and comprehend their entire visual field simultaneously, including their peripheral vision. This is in contrast to a sober person, who is typically only able to perceive the small area of central vision in detail. [1] [2]

While under the influence of this effect, it is very common for people to suddenly notice patterns and details in the environment they may have never previously noticed or appreciated.[3] For example, when looking at sceneries, nature, and everyday textures the complexity and perceived beauty of the visual input often becomes suddenly obvious.

In particular, it is thought that a fundamental feature of information-processing dysfunction in both hallucinogen-induced states and schizophrenia-spectrum disorders is the inability of these subjects to screen out, inhibit, filter, or gate extraneous stimuli and to attend selectively to salient features of the environment.[4][5][6][7][8][9] The CSTC model posits that the thalamus, with its various nuclei, plays a key role in controlling or gating extero- and interoceptive information to the cortex and is thereby fundamentally involved in the regulation of the level of awareness and attention.[10][11][12][13] Psychedelic interruption of cortico-striato-thalamo-cortical loops that inhibit the lower brain structures' sensory gating systems[14][15] results in enhanced availability of information normally repressed by these systems. Vollenweider[14] attributed the mechanisms of action of psychedelics to effects on the frontal-subcortical circuits, principal organizational networks involving neuronal linkages and feedback loops of the frontal cortical areas with the thalamus. Psychedelic interruption of serotonergic inhibition of thalamic screening results in a flood of information that can overwhelm the frontal brain with a variety of normally repressed sensations that enhance the availability of information managed by these ancient levels of the brain.[16]


Acuity enhancement is often accompanied by other coinciding effects such as color enhancement and pattern recognition enhancement.[17][18] It is most commonly induced under the influence of mild dosages of psychedelic compounds, such as LSD, psilocybin, and mescaline. However, it can also occur to a lesser extent under the influence of certain stimulants and dissociatives such as MDMA or 3-MeO-PCP.

Image examples


Psychoactive substances

Compounds within our psychoactive substance index which may cause this effect include:

... further results

Experience reports

Anecdotal reports which describe this effect within our experience index include:

See also

References

  1. ↑ Fischer, R., Hill, R., Thatcher, K., & Scheib, J. (1970). Psilocybin-induced contraction of nearby visual space. Agents and actions, 1(4), 195. https://doi.org/10.1007/BF01965761
  2. ↑ Sardegna, Jill; Shelly, Susan; Rutzen, Allan Richard; Scott M Steidl (2002). The Encyclopedia of Blindness and Vision Impairment. Infobase Publishing. p. 253. ISBN 978-0-8160-6623-0. Retrieved 30 November 2014.
  3. ↑ Hill, R. M., & Fischer, R. (1971). Interpretation of visual space under drug-induced ergotropic and trophotropic arousal. Agents and actions, 2(3), 128. https://doi.org/10.1007/BF01966750
  4. ↑ Bleuler, E. Dementia praecox oder die Gruppe der Schizophrenien, 1st ed. Vienna: Deutike; 1911. https://doi.org/10.1192/bjp.149.5.661
  5. ↑ Karper, L. P.; Freeman, G. K.; Grillon, C.; Morgan, C. A.; Charney, D. S.; Krystal, J. H. Preliminary evidence of an association between sensorimotor gating and distractibility in psychosis. J. Neuropsychiatry Clin. Neurosci. 8:60–66; 1996. https://doi.org/10.1176/jnp.8.1.60
  6. ↑ Karper, L. P.; Grillon, C.; Charney, D. S.; Krystal, J. H. The effect of ketamine on pre-pulse inhibition and attention. Neuropsychopharmacology 124; 1994. https://doi.org/10.1016/0920-9964(95)95554-M
  7. ↑ McGhie, A.; Chapman, J. Disorders of attention and perception in early schizophrenia. Br. J. Med. Psychol. 34:103–116; 1961. https://dx.doi.org/10.1111/j.2044-8341.1961.tb00936.x
  8. ↑ Scharfetter, C. Ego-pychopathology: The concept and its empirical evaluation. Psychol. Med. 11:273–280; 1981. https://doi.org/10.1017/S0033291700052090
  9. ↑ Vollenweider, F. X. Advances and pathophysiological models of hallucinogen drug actions in humans: A preamble to schizophrenia research. Pharmacopsychiatry 31:92–103; 1998. https://doi.org/10.1055/s-2007-979353
  10. ↑ Goddard, A. W.; Charney, D. S. Toward an integrated neurobiology of panic disorder. J. Clin. Psychiatry 58(suppl. 2):4–11; 1997. https://psycnet.apa.org/record/1997-03330-001
  11. ↑ Steriade, M.; Descheˆnes, M. Cellular thalamic mechanisms. In: Bentivoglio, M.; Spreafico, R., eds. Intrathalamic and brainstem-thalamic networks involved in resting and alert state. Amsterdam: Elsevier; 1988:37–62. https://ci.nii.ac.jp/naid/10017402609/en/
  12. ↑ Steriade, M.; McCormick, D. A.; Sejnowski, T. J. Thalamocortical oscillations in the sleeping and aroused brain. Science 262:697–685; 1993. https://www.ncbi.nlm.nih.gov/pubmed/8235588
  13. ↑ Vollenweider, F. X., & Geyer, M. A. (2001). A systems model of altered consciousness: integrating natural and drug-induced psychoses. Brain research bulletin, 56(5), 497-8. https://doi.org/10.1016/S0361-9230(01)00646-3
  14. ↑ 14.0 14.1 Vollenweider F. (1998). Recent advances and concepts in the search for biological correlates of hallucinogen-induced altered states of consciousness. Heffter Rev. Psychedel. Res. 1, 21–32. https://ci.nii.ac.jp/naid/10019112167/
  15. ↑ Vollenweider F., Geyer M. (2001). A systems model of altered consciousness: integrating natural and drug psychoses. Brain Res. Bull. 56, 495–507. https://doi.org/10.1016/S0361-9230(01)00646-3
  16. ↑ Winkelman, M. J. (2017). The Mechanisms of Psychedelic Visionary Experiences: Hypotheses from Evolutionary Psychology. Frontiers in Neuroscience, 11, 539. https://dx.doi.org/10.3389%2Ffnins.2017.00539
  17. ↑ Papoutsis, I., Nikolaou, P., Stefanidou, M., Spiliopoulou, C., & Athanaselis, S. (2015). 25B-NBOMe and its precursor 2C-B: modern trends and hidden dangers. Forensic Toxicology, 33(1), 4. https://doi.org/10.1007/s11419-014-0242-9
  18. ↑ Bersani, F. S., Corazza, O., Albano, G., Valeriani, G., Santacroce, R., Bolzan Mariotti Posocco, F., ... & Schifano, F. (2014). 25C-NBOMe: preliminary data on pharmacology, psychoactive effects, and toxicity of a new potent and dangerous hallucinogenic drug. BioMed Research International, 2014. https://dx.doi.org/10.1155/2014/734749
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