User:Jamy Jung/sandbox

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These edits were made on text that was sourced and copied from the Wikipedia article on Sensory Overload.


*important: I removed echolalia and sensory processing disorder from the list of "As component of other disorders and conditions" since they are not independent conditions and are almost always a symptom associated with other conditions such as autism, stroke, or schizophrenia. Another reason I did this was because they fall under an umbrella of other conditions which makes it almost impossible to make meaningful edits or contribution to them since finding research on them is limited to them being components of other conditions. I would have decide what parts of echolalia or SPD are independent of autism or other conditions when in reality they are a part of a heterogeneous phenotype of other conditions.


Sensory overload[edit]

From Wikipedia, the free encyclopedia Jump to navigationJump to search Sensory overload occurs when one or more of the body's senses experiences over-stimulation from the environment. There are many environmental elements that affect an individual. Examples of these elements are urbanization, crowding, noise, mass media, technology, and the explosive growth of information.




As component of other disorders and conditions[edit]

Sensory overload has been found to be associated with other disorders and conditions such as:

  • Attention deficit hyperactivity disorder (ADHD)
    • People with ADHD display hypersensitivity to sensory stimuli from a young age; this hypersensitivity often persists into adulthood.[1][2] People with ADHD do not seem to differ in sensory processing in regard to most event-related potentials; however, they do display significant differences in event related potential responses involved with late cognitive processing such as P300, CNV, Pe which may indicate that hypersensitivity in ADHD is caused by abnormalities in the expectation of and allocation of attention to sensory stimuli.[2] Abnormalities in later cognitive processing may contribute to hypersensitivity and the sensation of sensory overload in people with ADHD.
  • Posttraumatic stress disorder (PTSD)
    • People with PTSD are prone to sensory overload due to a general hypersensitivity to sensory stimuli partially caused by sensory gating issues; this is supported by the fact that people with PTSD suffer from impaired P50 gating and an inability to filter redundant auditory stimuli.[3][4] Irregularities in the production of and response to neurotransmitters is one possible etiology for sensory overload in people with PTSD; specifically, people with PTSD may display hypersensitivity to stimuli due to chronic homeostatic imbalances in dopamine and norepinephrine.[3] The hypersensitivity of people with PTSD to sensory stimuli is supported by an augmented P300 event-related potential response compared to healthy controls which indicates a semi-permanent heightened attention to deviant and salient stimuli.[4]
  • Obsessive-compulsive disorder (OCD)[5]
    • People with OCD display a cognitive inflexibility to changing environments.[6] It seems that people with OCD are hypersensitive to stimuli that are indicative of negative situations,[7] and this hypersensitivity may contribute to sensory overload. It is theorized that people with OCD have compulsions to carry out repetitive actions due to self-doubt and a desire to achieve perfection.[8] A common trigger for compulsions in people with OCD is the perception of contamination; people with OCD commonly deal with the perception of contamination with repetitive hand washing.[8] In a situation where a person with OCD is subjected to an environmental stimuli that elicits compulsion, such as getting dirt on their hands, they may feel overwhelmed by sensory stimuli and deal with this sensory overload through mitigating the stress with compulsions such as repetitive hand washing.
  • Dissociative Identity Disorder (DID)
  • Schizophrenia (see also sensory gating) [9]
    • People with schizophrenia are prone to sensory overload since people with the condition cannot divert their attention from repetitive and unimportant sensory stimuli.[10] The inability to focus on relevant stimuli and filter out unnecessary and excessive sensory stimuli displayed in schizophrenics is due to physiological sensory gating issues, and the paired click P50 test can be used to determine if an individual has abnormalities in sensory gating and is therefore prone to sensory overload.[11] A proposed theory that explains sensory overload in schizophrenic patients is that abnormalities in alpha-7 [10] and low affinity nicotinic acetylcholine receptors prevent normal transduction pathways between the cortex and hippocampus that facilitate sensory gating.[11]
  • Misophonia, a pathological 'hatred of sound'
    • People with misophonia display hypersensitivity to certain pattern-based noises such as the sound of chewing, slurping, finger tapping, foot shuffling, throat clearing, pen clicking, and keyboard tapping; people with misophonia respond to triggering sounds with emotional distress and increased hormonal activity of the sympathetic system.[12] When people with misophonia are subjected to noises that trigger misophonic responses, they feel as if they are being overloaded by auditory stimuli and seek to escape from or block out the triggering noise.[12] Compared to healthy controls, people with misophonia display a lower N100 peak in response to mismatch negative (MMN), but this is not a reliable biomarker for the condition and sensory overload.[12] A more reliable indicator that hints at proneness to sensory overload is heightened activation of the anterior insular cortex which is evoked by trigger noises and can be measured by fMRI; the anterior insular cortex may be involved with the pathway that gives rise to the sensation of sensory overload in people with misophonia.[12]
  • Synesthesia
    • There is evidence that the visual cortex of people with grapheme-color synesthesia is more excitable than that of typical people; additionally, people with grapheme-color synesthesia respond more strongly to visual stimuli compared to people without the condition.[13] People with grapheme-color synesthesia report feeling visual stress and discomfort in response to gratings of mid and high spatial frequencies,[13] correlating to a sensory overload response evoked by intense visual stimuli.
  • Generalized anxiety disorder (GAD)
    • People with general anxiety disorder are highly sensitive to external anxiety triggering stimuli and deal with exposure to these triggers through neurotic thoughts.[14] People with GAD are biased to perceive sensory stimuli as negative or threatening and this bias feeds into negative thought processes which further exacerbate feelings of worry, stress, and anxiety.[14] People with GAD are hypersensitive and hypervigilant to ambiguous, neutral, and emotional stimuli and often compartmentalize such stimuli as negative.[14] People with GAD are prone to sensory overload when in novel settings or interacting with new people since ambiguous and neutral stimuli in these instances are usually processed as threatening or negative; adolescents and children with GAD are especially avoidant of and distressed by novel stimuli which is theorized to be elicited by either a hyperactive sympathetic nervous system or an under-active parasympathetic nervous system.[14]
  • Autism spectrum disorders[15][16]
    • People with autism suffer from auditory hypersensitivity which can lead to sensory overload.[17] Although people with autism do not suffer from abnormalities in P50 sensory gating, they have anomalies in sensory gating related to the N100 test which indicates an irregularity in attention-related direction and top-down mental pathways.[17] It is speculated that disturbances and issues with directing attention towards relevant or salient stimuli, evinced by deviations from standard P200 and N100 responses, is partially responsible for the sensation of being overwhelmed by sensory stimuli in people with autism.[17]
  • Tourette syndrome (TS)
    • It has been suggested that people with Tourette syndrome have a hypersensitivity to bodily sensation that originates in higher order processing partially the result of distorted and higher than average amplitude of afferent somatic signals.[18] People with Tourette syndrome sense urges to do tics that are often localized to regions of the body that carry out the tic response.[18] It is theorized that tics might be caused by sensory processing issues where sensations trigger movements which manifest as tics.[19] Additionally, people with Tourette syndrome display a moderate inability to inhibit distracting stimuli[20] which might lead to sensory overload. People with Tourette syndrome may be prone to carry out tics in an environment of overwhelming sensory stimuli.
  • Fibromyalgia (FM)
    • People with fibromyalgia are hypersensitive to intense stimuli such as bright lights, loud noises, perfumes, and cold temperatures; people with the condition also have hyper-excitable nociceptors.[21] When people with fibromyalgia are subjected to intense stimuli, they experience sensory overload in the form of pain. It is theorized that abnormal activity of the left dorsolateral prefrontal cortex and reduced production of or reception to serotonin are partially responsible for the sensation of pain in response to intense stimuli.[21]
  • Chronic fatigue syndrome (ME/CFS)
    • People with chronic fatigue syndrome display a hypersensitivity to noxious stimuli, stress, and pain.[22] These sensitivities are partially explained by abnormal neurotransmitter pathways involving serotonin and acetylcholine.[22] When people with the condition are exposed to intense stimuli, they report pain, fatigue, nausea, and reduced cognitive abilities; chronic sensory overload causes the sensation of brain fog.[22]


  1. ^ Panagiotidi, Maria; Overton, Paul G.; Stafford, Tom (01 2018). "The relationship between ADHD traits and sensory sensitivity in the general population". Comprehensive Psychiatry. 80: 179–185. doi:10.1016/j.comppsych.2017.10.008. ISSN 1532-8384. PMID 29121555. {{cite journal}}: Check date values in: |date= (help)
  2. ^ a b Kaiser, Anna; Aggensteiner, Pascal-M.; Baumeister, Sarah; Holz, Nathalie E.; Banaschewski, Tobias; Brandeis, Daniel (2020-05-01). "Earlier versus later cognitive event-related potentials (ERPs) in attention-deficit/hyperactivity disorder (ADHD): A meta-analysis". Neuroscience & Biobehavioral Reviews. 112: 117–134. doi:10.1016/j.neubiorev.2020.01.019. ISSN 0149-7634.
  3. ^ a b Clancy, Kevin; Ding, Mingzhou; Bernat, Edward; Schmidt, Norman B.; Li, Wen (2017-07-01). "Restless 'rest': intrinsic sensory hyperactivity and disinhibition in post-traumatic stress disorder". Brain: A Journal of Neurology. 140 (7): 2041–2050. doi:10.1093/brain/awx116. ISSN 1460-2156. PMC 6059177. PMID 28582479.
  4. ^ a b Javanbakht, Arash; Liberzon, Israel; Amirsadri, Alireza; Gjini, Klevest; Boutros, Nash N (2011-10-12). "Event-related potential studies of post-traumatic stress disorder: a critical review and synthesis". Biology of Mood & Anxiety Disorders. 1: 5. doi:10.1186/2045-5380-1-5. ISSN 2045-5380. PMC 3377169. PMID 22738160.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  5. ^ https://oxfordmedicine.com/view/10.1093/med/9780190228163.001.0001/med-9780190228163-chapter-11
  6. ^ Gruner, Patricia; Pittenger, Christopher (03 14, 2017). "Cognitive inflexibility in Obsessive-Compulsive Disorder". Neuroscience. 345: 243–255. doi:10.1016/j.neuroscience.2016.07.030. ISSN 1873-7544. PMC 5288350. PMID 27491478. {{cite journal}}: Check date values in: |date= (help)
  7. ^ Kumari, Veena; Kaviani, Hossein; Raven, Peter W.; Gray, Jeffrey A.; Checkley, Stuart A. (2001-01-01). "Enhanced Startle Reactions to Acoustic Stimuli in Patients With Obsessive-Compulsive Disorder". American Journal of Psychiatry. 158 (1): 134–136. doi:10.1176/appi.ajp.158.1.134. ISSN 0002-953X.
  8. ^ a b Greisberg, Scott; McKay, Dean (2003-02-01). "Neuropsychology of obsessive-compulsive disorder: a review and treatment implications". Clinical Psychology Review. 23 (1): 95–117. doi:10.1016/S0272-7358(02)00232-5. ISSN 0272-7358.
  9. ^ Ghadirian, A.M. (1976). "Sensory Perceptual Limitation in Schizophrenia". Psychotherapy and Psychosomatics. 27: 115–119 – via JSTOR.
  10. ^ a b Vlcek, Premysl; Bob, Petr; Raboch, Jiri (2014). "Sensory disturbances, inhibitory deficits, and the P50 wave in schizophrenia". Neuropsychiatric Disease and Treatment. 10: 1309–1315. doi:10.2147/NDT.S64219. ISSN 1176-6328. PMC 4106969. PMID 25075189.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  11. ^ a b Potter, David; Summerfelt, Ann; Gold, James; Buchanan, Robert W. (2006-10). "Review of clinical correlates of P50 sensory gating abnormalities in patients with schizophrenia". Schizophrenia Bulletin. 32 (4): 692–700. doi:10.1093/schbul/sbj050. ISSN 0586-7614. PMC 2632276. PMID 16469942. {{cite journal}}: Check date values in: |date= (help)
  12. ^ a b c d Brout, Jennifer J.; Edelstein, Miren; Erfanian, Mercede; Mannino, Michael; Miller, Lucy J.; Rouw, Romke; Kumar, Sukhbinder; Rosenthal, M. Zachary (2018). "Investigating Misophonia: A Review of the Empirical Literature, Clinical Implications, and a Research Agenda". Frontiers in Neuroscience. 12. doi:10.3389/fnins.2018.00036. ISSN 1662-453X. PMC 5808324. PMID 29467604.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  13. ^ a b Ward, Jamie; Hoadley, Claire; Hughes, James E. A.; Smith, Paula; Allison, Carrie; Baron-Cohen, Simon; Simner, Julia (2017-03). "Atypical sensory sensitivity as a shared feature between synaesthesia and autism". Scientific Reports. 7 (1): 41155. doi:10.1038/srep41155. ISSN 2045-2322. PMC 5339734. PMID 28266503. {{cite journal}}: Check date values in: |date= (help)CS1 maint: PMC format (link)
  14. ^ a b c d Newman, Michelle G.; Llera, Sandra J.; Erickson, Thane M.; Przeworski, Amy; Castonguay, Louis G. (2013-03-28). "Worry and Generalized Anxiety Disorder: A Review and Theoretical Synthesis of Evidence on Nature, Etiology, Mechanisms, and Treatment". Annual Review of Clinical Psychology. 9 (1): 275–297. doi:10.1146/annurev-clinpsy-050212-185544. ISSN 1548-5943. PMC 4964851. PMID 23537486.{{cite journal}}: CS1 maint: PMC format (link)
  15. ^ O'Neill M; Jones RS (June 1997). "Sensory-perceptual abnormalities in autism: a case for more research?". J Autism Dev Disord. 27 (3): 283–93. doi:10.1023/A:1025850431170. PMID 9229259.
  16. ^ Marco EJ; Hinkley LB; Hill SS; Nagarajan SS (May 2011). "Sensory processing in autism: a review of neurophysiologic findings". Pediatr. Res. 69 (5 Pt 2): 48R–54R. doi:10.1203/PDR.0b013e3182130c54. PMC 3086654. PMID 21289533.
  17. ^ a b c Chien, Yi-Ling; Hsieh, Ming H.; Gau, Susan Shur-Fen (2019-12). "P50-N100-P200 sensory gating deficits in adolescents and young adults with autism spectrum disorders". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 95: 109683. doi:10.1016/j.pnpbp.2019.109683. {{cite journal}}: Check date values in: |date= (help)
  18. ^ a b Rose, Olivia; Hartmann, Andreas; Worbe, Yulia; Scharf, Jeremiah M.; Black, Kevin J. (2019). "Tourette syndrome research highlights from 2018". F1000Research. 8: 988. doi:10.12688/f1000research.19542.1. ISSN 2046-1402. PMC 6719747. PMID 31508215.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  19. ^ Hartmann, Andreas; Worbe, Yulia; Black, Kevin J. (2018). "Tourette syndrome research highlights from 2017". F1000Research. 7: 1122. doi:10.12688/f1000research.15558.1. ISSN 2046-1402. PMC 6107994. PMID 30210792.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  20. ^ Morand-Beaulieu, Simon; Leclerc, Julie B.; Valois, Philippe; Lavoie, Marc E.; O’Connor, Kieron P.; Gauthier, Bruno (2017-08-18). "A Review of the Neuropsychological Dimensions of Tourette Syndrome". Brain Sciences. 7 (8). doi:10.3390/brainsci7080106. ISSN 2076-3425. PMC 5575626. PMID 28820427.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  21. ^ a b Atzeni, Fabiola; Talotta, Rossella; Masala, Ignazio Francesco; Giacomelli, Camillo; Conversano, Ciro; Nucera, Valeria; Lucchino, Bruno; Iannuccelli, Cristina; Di Franco, Manuela; Bazzichi, Laura (2019-01). "One year in review 2019: fibromyalgia". Clinical and Experimental Rheumatology. 37 Suppl 116 (1): 3–10. ISSN 0392-856X. PMID 30747097. {{cite journal}}: Check date values in: |date= (help)
  22. ^ a b c Cortes Rivera, Mateo; Mastronardi, Claudio; Silva-Aldana, Claudia T.; Arcos-Burgos, Mauricio; Lidbury, Brett A. (2019-08-07). "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Comprehensive Review". Diagnostics. 9 (3). doi:10.3390/diagnostics9030091. ISSN 2075-4418. PMC 6787585. PMID 31394725.{{cite journal}}: CS1 maint: unflagged free DOI (link)


These edits were made on text copied from the Selective auditory attention page.

-I removed some ambiguities and redundancies from the introduction but did not change any of the ideas or research cited in it. I also added some information from the "history" section of the article on the various models of selective auditory attention.

-I clarified some of the text from "disorder status," added how selective auditory attention could be affected in people with sensory disorders and provided citations for this claim.

-Fixed some grammatical and ambiguous pronoun issues in Frank's contribution to "History".

Selective auditory attention[edit]

Selective auditory attention or selective hearing is a type of selective attention that involves the auditory system. Selective hearing is the action in which people focus their attention intentionally on a specific source of a sound or spoken words. When people use selective hearing, noise from the surrounding environment is heard by the auditory system but only certain parts of the auditory information are chosen to be processed by the brain. Auditory attention is usually directed at things people are most interested in hearing. In an article by Krans, Isbell, Giuliano, and Neville (2013), selective auditory attention is defined as the ability to acknowledge some stimuli while ignoring other stimuli that is occurring at the same time. An example of this is a student focusing on a teacher giving a lesson while ignoring the sounds of classmates in a rowdy classroom (p. 53). This is an example of bottlenecking where all information cannot be processed simultaneously so only some sensory information gets through the "bottleneck" and is processed. The human brain cannot process all the sensory information that occurs in an environment so only the most relevant and important information is thoroughly processed by the brain. There have been many models that theorize the pathway of selective auditory attention, notably the early selection model, late selection model, and attenuation model. Selective hearing is not a physiological disorder but is rather a human capability to block out sounds and noise. It is the notion of ignoring certain auditory stimuli in the surrounding environment to select other auditory stimuli to direct attention at.

History[edit]

Early researches on selective auditory attention can be traced back to 1953, when Colin Cherry introduced the "cocktail party problem". At the time, air traffic controllers at the control tower received messages from pilots through loudspeakers. Hearing mixed voices through a single loudspeaker made the task very difficult. In Cherry's experiment, mimicking the problem faced by air traffic controllers, participants had to listen to two messages played simultaneously from one loudspeaker and repeat what they heard. This was later termed the dichotic listening task.

Though introduced by Colin Cherry, Donald Broadbent is often regarded as the first to systematically apply dichotic listening tests in research on selective auditory attention. Broadbent used the method of dichotic listening to test how participants selectively attend to stimuli when overloaded with auditory stimuli. Broadbent used his findings to develop the filter model of attention in 1958. Broadbent theorized that the human information processing system has a "bottleneck" due to limited capacity and that the brain performs an "early selection" before processing auditory information. Broadbent proposed that auditory information enters an unlimited sensory buffer and that one stream of information is filtered out and passes through to be cohesive, while all others that are not selected quickly decay in salience and are not processed. Broadbent's model contradicts the cocktail party phenomenon because Broadbent's model predicts that people would never respond to their name from unattended sources since unattended information is discarded before being processed.

Deutsch & Deutsch's late selection model proposed in 1963 is a competing model to Broadbent's early selection model. Deutsch & Deutsch's model theorizes that all information and sensory input are attended to and processed for meaning. Later in the processing routine, just before information enters the short-term memory, a filter analyzes the semantic characteristics of the information, letting stimuli containing relevant information pass through to short-term memory and removing unimportant information. Deutsch & Deutsch's model for selective auditory attention suggests that weak response to unattended stimuli comes from an internal decision on informational relevance, where more important stimuli are prioritized to enter the working memory first.

In 1964, Anne Treisman, a graduate student of Broadbent, improved Broadbent's theory and proposed her own attenuation model. In Treisman's model, unattended information is attenuated, tuned down compared to attended information, but still processed. For example, imagine that you are exposed to three extraneous sources of sound in a coffee shop while ordering a drink (chatter, coffee brewer, music), Treisman's model indicates that you would still pick up on the latter three sounds while attending to the cashier and that these extraneous sources of noise would be muffled as if their "volumes" were turned down. Treisman also suggests that a threshold mechanism exists in selective auditory attention in which words from unattended streams of information can grab one's attention. Words of low threshold, higher level of meaning, and importance, such as one's name and "watch out", redirect one's attention to where it is urgent to do so.

Recent research[edit]

Recently, researchers have attempted to explain mechanisms implicated in selective auditory attention. In 2012, an assistant professor in residence of the Neurological Surgery and Physiology in the University of California San Francisco examined the selective cortical representation of attended speaker in multiple-talker speech perception. Edward Chang and his colleague, Nima Mesgarani undertook a study that recruited three patients affected by severe epilepsy, who were undergoing treatment surgery. All patients were recorded to have normal hearing. The procedure of this study required the surgeons to place a thin sheet of electrodes under the skull on the outer surface of the cortex. The activity of electrodes was recorded in the auditory cortex. The patients were given two speech samples to listen to and they were told to distinguish the words spoken by the speakers. The speech samples were simultaneously played and different speech phrases were spoken by different speakers. Chang and Mesgarani found an increase in neural responses in the auditory cortex when the patients heard words from the target speaker. Chang went on to explain that the method of this experiment was well-conducted as it was able to observe the neural patterns that tells when the patient's auditory attention shifted to the other speaker. This clearly shows the selectivity of auditory attention in humans.

The development of selective attention has also been examined. Jones and Moore for instance, studied how well children across various age groups could hear and respond to a target sound when it was masked by other auditory stimuli. They discovered that 9– to 11-year-old children became as adept as adults at paying attention only to the target sound and filtering out the masking sound (2015, p. 366). This shows that research on selective auditory information is important to continue as it allows us to better understand our world.

Prevalence[edit]

The prevalence of selective hearing has not been clearly researched yet. However, there are some that have argued that the proportion of selective hearing is particularly higher in males than females. Ida Zündorf, Hans-Otto Karnath and Jörg Lewald carried out a study in 2010 which investigated the advantages and abilities males have in the localization of auditory information. A sound localization task centered on the cocktail party effect was utilized in their study. The male and female participants had to try to pick out sounds from a specific source, on top of other competing sounds from other sources. The results showed that the males had a better performance overall. Female participants found it more difficult to locate target sounds in a multiple-source environment. Zündorf et al. suggested that there may be sex differences in the attention processes that helped locate the target sound from a multiple-source auditory field. While men and women do have some differences when it comes to selective auditory hearing, they both struggle when presented with the challenge of multitasking, especially when tasks that are to be attempted concurrently are very similar in nature (Dittrich, and Stahl, 2012, p. 626).

Disorder status[edit]

Selective hearing is not known to be a disorder of the physiological or psychological aspect. According to the World Health Organization (WHO), a hearing disorder happens when there is a complete loss of hearing in the ears. It means the loss of the ability to hear. Technically speaking, selective hearing is not "deafness" to a certain sound message. Rather, it is the selectivity of an individual to attend audibly to a sound message. The whole sound message is physically heard by the ear but the brain systematically filters out unwanted information to focus on relevant or important portions of the message. Selective auditory attention is a normal sensory process of the brain, and there can be abnormalities related to this process in people with sensory processing disorders such as attention deficit hyperactive disorder[1], post traumatic stress disorder[2], and Schizophrenia[3].

  1. ^ Vlcek, Premysl; Bob, Petr; Raboch, Jiri (2014). "Sensory disturbances, inhibitory deficits, and the P50 wave in schizophrenia". Neuropsychiatric Disease and Treatment. 10: 1309–1315. doi:10.2147/NDT.S64219. ISSN 1176-6328. PMC 4106969. PMID 25075189.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  2. ^ Javanbakht, Arash; Liberzon, Israel; Amirsadri, Alireza; Gjini, Klevest; Boutros, Nash N. (2011-10-12). "Event-related potential studies of post-traumatic stress disorder: a critical review and synthesis". Biology of Mood & Anxiety Disorders. 1 (1): 5. doi:10.1186/2045-5380-1-5. ISSN 2045-5380. PMC 3377169. PMID 22738160.{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)
  3. ^ Vlcek, Premysl; Bob, Petr; Raboch, Jiri (2014). "Sensory disturbances, inhibitory deficits, and the P50 wave in schizophrenia". Neuropsychiatric Disease and Treatment. 10: 1309–1315. doi:10.2147/NDT.S64219. ISSN 1176-6328. PMC 4106969. PMID 25075189.{{cite journal}}: CS1 maint: unflagged free DOI (link)