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Pattern recognition suppression: Difference between revisions

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'''Pattern recognition suppression''' can be described as a partial to complete inability to mentally process visual information regardless of its clarity. For example, although one may be able to see what is in front of them in perfect detail, they will have a reduced ability to understand what they are looking at. This can render even the most common of everyday objects as unrecognizable.
'''Pattern recognition suppression''' can be described as a partial to complete inability to mentally process visual information regardless of its clarity. For example, although one may be able to see what is in front of them in perfect detail, they will have a reduced ability to understand what they are looking at. This can render even the most common of everyday objects as unrecognizable.
Loss of contact with the external world is due to the blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a central role in the transmission of incoming signals from all sensory modalities.<ref>Cline, H. T., Debski, E. A., and Constantine-Paton, M. (1987). N-methyl-D-aspartate receptor antagonist desegregates eye-specific stripes. Proceedings of the National Academy of Sciences, 84, 4342-4345. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC305081/</ref><ref>Cotman, C. W., Monaghan, D. T., Ottersen, O. P., and Storm-Mathisen, J. (1987). Anatomical organization of excitatory amino acid receptors and their pathways. Trends in Neurosciences, 107, 273-279. https://doi.org/10.1016/0166-2236(87)90172-X</ref><ref>Davies, J., and Watkins, J. C. (1983). Role of excitatory amino acid receptors in mono- and polysynaptic excitation in the cat spinal cord. Experimental Brain Research, 49, 280-290. https://doi.org/10.1007/BF00238587</ref><ref>Greenamyre, J. T., Young, A. B., and Penney, J. B. (1984). Quantitative autoradiographic distribution of l-[3H]glutamate binding sites in rat central nervous system. Journal of Neuroscience, 4, 2133-2144. http://www.jneurosci.org/content/4/8/2133</ref><ref>Headley, P. M., West, D. C., and Roe, C. (1985). Actions of ketamine and the role of N-methyl-aspartate receptors in the spinal cord: Studies on nociceptive and other neuronal responses. Neurological Neurobiology, 14, 325-335.</ref><ref>Kisvardy, Z. F., Cowey, A., Smith, A. D., and Somogyi, P. (1989). Interlaminar and lateral excitatory amino acid connections in the striate cortex of monkey. Journal of Neuroscience, 9, 667-682. http://www.jneurosci.org/content/9/2/667.long</ref><ref name="Monaghan1989">Monaghan, D. T., Bridges, R. J., and Cotman, C. W. (1989). The excitatory amino acid receptors: Their classes, pharmacology and distinct properties in the function of the nervous system. Annual Review of Pharmacology and Toxicology, 29, 365-402. https://doi.org/10.1146/annurev.pa.29.040189.002053</ref><ref>Oye, N., Paulsen, O., and Maurset, A. (1992). Effects of ketamine on sensory perception: Evidence for a role of N-methyl-D-aspartate receptors. Journal of Pharmacology and Experimental Therapeutics, 260, 1209-1213. http://jpet.aspetjournals.org/content/260/3/1209.long</ref> NMDA receptors form the molecular substrate of a gate and have their highest concentration in the hippocampus, a part of the medial temporal lobe where data from the external world is integrated with internal programs. NMDA antagonists close this gated channel to incoming data.<ref name="Monaghan1989"/><ref>Collingridge, G. L. (1987). The role of NMDA receptors in learning and memory. Nature, 330, 604-605. https://doi.org/10.1038/330604a0</ref><ref>Cotman, C. W., Monaghan, D. T., and Ganong, A. H. (1988). Excitatory amino acid neurotransmission: NMDA receptors and Hebb-type synaptic plasticity. Annual Review of Neuroscience, 11, 61-80. https://doi.org/10.1146/annurev.ne.11.030188.000425</ref><ref>McNaughton, B. C., and Morris, R. G. M. (1987). Hippocampal synaptic enhancement and information storage within a distributed system. Trends in Neurosciences, 10, 408-415. https://doi.org/10.1016/0166-2236(87)90011-7</ref><ref>Morris, R. G. M., Anderson, E., Lynch, G. S., and Baudry, M. (1986). Selective impairment of learning and blockade of EPT by NMDA antagonist APS. Nature, 319, 744-776.</ref><ref>Jansen, K. L. (1997). The ketamine model of the near-death experience: A central role for the N-methyl-D-aspartate receptor. Journal of Near-Death Studies, 16(1), 14-15. https://doi.org/10.1023/A:1025055109480</ref>
From a theoretical, neurophysiological point of view, NMDA antagonists do not suppress the perception and processing of sensory stimuli. Sensory stimuli without any nociceptive character are transmitted up to primary sensory cortices under anaesthesia. There is, however, a dissociation between the primary sensory cortices and the secondary ''evaluation'' of sensory stimuli. This allows for the clinical observation of dreams and hallucinations during general anaesthesia.<ref>Schwender, D., Klasing, S., Madler, C., Pöppel, E., & Peter, K. (1993). Mid-latency auditory evoked potentials during ketamine anaesthesia in humans. British Journal of Anaesthesia, 71(5), 632. https://doi.org/10.1093/bja/71.5.629</ref>


Pattern recognition suppression is often accompanied by other coinciding effects such as [[analysis suppression]] and [[thought deceleration]]. It is most commonly induced under the influence of [[dosage#heavy|heavy]] [[dosage|dosages]] of [[dissociative]] or [[antipsychotic]] compounds, such as [[ketamine]], [[quetiapine]], [[PCP]], and [[DXM]]. However, it can also occur to a lesser extent under the influence of extremely heavy dosages of [[psychedelic]] compounds such as [[LSD]], [[psilocybin]], and [[mescaline]].
Pattern recognition suppression is often accompanied by other coinciding effects such as [[analysis suppression]] and [[thought deceleration]]. It is most commonly induced under the influence of [[dosage#heavy|heavy]] [[dosage|dosages]] of [[dissociative]] or [[antipsychotic]] compounds, such as [[ketamine]], [[quetiapine]], [[PCP]], and [[DXM]]. However, it can also occur to a lesser extent under the influence of extremely heavy dosages of [[psychedelic]] compounds such as [[LSD]], [[psilocybin]], and [[mescaline]].

Revision as of 14:26, 21 February 2018

Pattern recognition suppression can be described as a partial to complete inability to mentally process visual information regardless of its clarity. For example, although one may be able to see what is in front of them in perfect detail, they will have a reduced ability to understand what they are looking at. This can render even the most common of everyday objects as unrecognizable.

Loss of contact with the external world is due to the blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a central role in the transmission of incoming signals from all sensory modalities.[1][2][3][4][5][6][7][8] NMDA receptors form the molecular substrate of a gate and have their highest concentration in the hippocampus, a part of the medial temporal lobe where data from the external world is integrated with internal programs. NMDA antagonists close this gated channel to incoming data.[7][9][10][11][12][13]

From a theoretical, neurophysiological point of view, NMDA antagonists do not suppress the perception and processing of sensory stimuli. Sensory stimuli without any nociceptive character are transmitted up to primary sensory cortices under anaesthesia. There is, however, a dissociation between the primary sensory cortices and the secondary evaluation of sensory stimuli. This allows for the clinical observation of dreams and hallucinations during general anaesthesia.[14]

Pattern recognition suppression is often accompanied by other coinciding effects such as analysis suppression and thought deceleration. It is most commonly induced under the influence of heavy dosages of dissociative or antipsychotic compounds, such as ketamine, quetiapine, PCP, and DXM. However, it can also occur to a lesser extent under the influence of extremely heavy dosages of psychedelic compounds such as LSD, psilocybin, and mescaline.

Psychoactive substances

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

See also

  1. ↑ Cline, H. T., Debski, E. A., and Constantine-Paton, M. (1987). N-methyl-D-aspartate receptor antagonist desegregates eye-specific stripes. Proceedings of the National Academy of Sciences, 84, 4342-4345. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC305081/
  2. ↑ Cotman, C. W., Monaghan, D. T., Ottersen, O. P., and Storm-Mathisen, J. (1987). Anatomical organization of excitatory amino acid receptors and their pathways. Trends in Neurosciences, 107, 273-279. https://doi.org/10.1016/0166-2236(87)90172-X
  3. ↑ Davies, J., and Watkins, J. C. (1983). Role of excitatory amino acid receptors in mono- and polysynaptic excitation in the cat spinal cord. Experimental Brain Research, 49, 280-290. https://doi.org/10.1007/BF00238587
  4. ↑ Greenamyre, J. T., Young, A. B., and Penney, J. B. (1984). Quantitative autoradiographic distribution of l-[3H]glutamate binding sites in rat central nervous system. Journal of Neuroscience, 4, 2133-2144. http://www.jneurosci.org/content/4/8/2133
  5. ↑ Headley, P. M., West, D. C., and Roe, C. (1985). Actions of ketamine and the role of N-methyl-aspartate receptors in the spinal cord: Studies on nociceptive and other neuronal responses. Neurological Neurobiology, 14, 325-335.
  6. ↑ Kisvardy, Z. F., Cowey, A., Smith, A. D., and Somogyi, P. (1989). Interlaminar and lateral excitatory amino acid connections in the striate cortex of monkey. Journal of Neuroscience, 9, 667-682. http://www.jneurosci.org/content/9/2/667.long
  7. ↑ 7.0 7.1 Monaghan, D. T., Bridges, R. J., and Cotman, C. W. (1989). The excitatory amino acid receptors: Their classes, pharmacology and distinct properties in the function of the nervous system. Annual Review of Pharmacology and Toxicology, 29, 365-402. https://doi.org/10.1146/annurev.pa.29.040189.002053
  8. ↑ Oye, N., Paulsen, O., and Maurset, A. (1992). Effects of ketamine on sensory perception: Evidence for a role of N-methyl-D-aspartate receptors. Journal of Pharmacology and Experimental Therapeutics, 260, 1209-1213. http://jpet.aspetjournals.org/content/260/3/1209.long
  9. ↑ Collingridge, G. L. (1987). The role of NMDA receptors in learning and memory. Nature, 330, 604-605. https://doi.org/10.1038/330604a0
  10. ↑ Cotman, C. W., Monaghan, D. T., and Ganong, A. H. (1988). Excitatory amino acid neurotransmission: NMDA receptors and Hebb-type synaptic plasticity. Annual Review of Neuroscience, 11, 61-80. https://doi.org/10.1146/annurev.ne.11.030188.000425
  11. ↑ McNaughton, B. C., and Morris, R. G. M. (1987). Hippocampal synaptic enhancement and information storage within a distributed system. Trends in Neurosciences, 10, 408-415. https://doi.org/10.1016/0166-2236(87)90011-7
  12. ↑ Morris, R. G. M., Anderson, E., Lynch, G. S., and Baudry, M. (1986). Selective impairment of learning and blockade of EPT by NMDA antagonist APS. Nature, 319, 744-776.
  13. ↑ Jansen, K. L. (1997). The ketamine model of the near-death experience: A central role for the N-methyl-D-aspartate receptor. Journal of Near-Death Studies, 16(1), 14-15. https://doi.org/10.1023/A:1025055109480
  14. ↑ Schwender, D., Klasing, S., Madler, C., Pöppel, E., & Peter, K. (1993). Mid-latency auditory evoked potentials during ketamine anaesthesia in humans. British Journal of Anaesthesia, 71(5), 632. https://doi.org/10.1093/bja/71.5.629
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