Some studies demonstrated that the damages regarding ventricular enlargement and regional grey matter deficits, the brain structural correlates of specific symptoms, may cause auditory hallucinations. (O'Daly OG, et al., 2007). If you look to the schizophrenia spectrum, regarding to the severity of symptoms, auditory hallucinations are seen at pacients with paranoid symptoms. Catatonic pacients are experiencing more visual halluciantions.

Is a intriguing and interesting question. When Esquirol defined hallucinations, he adhered closely to the visual perception as model. His cases they presented visual hallucinations, although in you definition of hallucinations, he postulated that this symptom might observed in all sensorial modalities. Baillarger in 1846, presented multiple cases examples of auditory hallucinations (acoasm and auditory verbal hallucinations). Maybe this question is a example of historical driven problem. However, they are theories that found an intimate relation between auditory verbal hallucinations and internal speech and thought. Likewise, they are some empirical studies that find relations between auditory verbal hallucinations and dissciative phenomena (e.g., depersonalization experiencies). Arguably, auditory verbal hallucinations they not are perceptual phenomena. Is curious likewise that, save in toxic states, the visual hallucinations are in tow of insight, but this is not the case in auditory verbal hallucinations. Maybe the key for answer the question of Suni, is in the notions as self, self-consciousness, and thought as internal dialogue.

Thought as internal dialogue is common in dissociative identity disorder and related conditions. Some researchers believe that auditory hallucinations are also of dissociative nature even in schizophrenia. However the latter thesis is controversial.

Actually, dissociative voices usually respond to the questions of the interviewer as well whereas schizophrenic ones not. Thus, research on dissociation may illuminate some aspect of this question. At least, research on auditory and visual hallucinations should tak into account that dissociation and psychosis are distinct (they may coexist sometimes though) phenomena which may end up in hallucinations anyway. However, their mechanism may be different.

Well, theories of hallucinations that invoke misidentified internal speech or thoughts as causes of auditory hallucinations explain why AH are commoner, but on the whole have a harder time explaining visual hallucinations, particularly fantastical scenes. These might require misidentified imagery (fantasies) to be the origin of visual hallucinations, in which case one could argue that these types of fantasy are less common or more easily identified than internal speech.

The question is then which of the range of available theories one prefers; and incidentally, why is the reverse true for delirium? It all depends on your wider theory of schizophrenia etc.

Well, it si beyond argument that the auditory verbal hallucinations have concentrated a high mount of research in the two precedent decades. Visual hallucinations are in this context a relatively neglected phenomena. Likewise, the relation between hallucinations and dissociation is a vexing issue. The dissociative phenomena, nowaday, in terms of empirical data, is a mediator, not a causal variable. The theory of discrimination of reality, to my knowledge, was applied to all hallucinations (R.P. Bentall applied this theory in the nineties of past century). In any case, the original question of Suni is why there are more auditory hallucinations than visual hallucinations in functional psychiatric disorders?

Agreeing to @Francisco Cerrascoso Lopez sir. The question is why there are more auditory hallucinations than visual hallucinations in functional psychiatric disorders even though human relay more on visual system? it may be associated with the thought process or rather origin of hallucination.

Some elements are to be carry considerable weight in a response to the question of Suni:

- The descriptive traits of VH are poorly understand, but recent models about this symptom ( e.g. Collerton et al, 2012; DOI 10.1007/978-1-4614-0959-5_6) stress the role of attention and the top-down and bottom-up information processing. The models of complex cognition take in count that the information processing is driven conceptually.

- In this sense, in the humans is predominant the verbal behavior for your power to modify the non-verbal aspects of behavior (e.g., the research about rule-governed behavior, or the works of Vygotsky about thought). In other words, the human behavior is mediate symbolically. So, the verbal and symbolic behavior is dominant about visual and other perception modalities. E.g., we see a table, not dots, light, lines, etc.

- Indirect evidence lines for my argument here are that in simple VH , the neurobiological sites activated they are the brain sites activated in visual perception. In VH descriptively more complex, the pattern of brain activation is more complex. Likewise , the CONCEPTS of schizophrenia in Bleuler, and discordance (in french, in the original) of Chaslin, they point to a peculiar consciousness state akin to a dissociative state. Likewise, in complex auditory verbal hallucinations, your descriptive characters point to a dialogical relation between the AVH and the hallucinator ( see McCarthy-Jones et al, in press, DOI: 10.1093/schbul/sbs156), missing in complex VH (although the descriptive properties of VH they are less understands nowadays that AVH). Likewise, the historical research in hallucinations (see Berrios and Markova, 2012; DOI 10.1007/978-1-4614-0959-5_5) dispute the perceptual model underlying the hallucinations.

- So, notions as self and self-conciousness they are relevants here. In fact, the works of authors as Sass, Stanghellini or Moskowitz, point to Self as a key matter in the descriptive psychopathology of schizophrenia and functional psychosis.

What about the possibility that one of the key components of functional psychosis is a dysfunction in the stimulus filtering mechanism of auditory pathways, possibly related to white matter connectivity? [Rotarska-Jagiela, A, et al (2009). Anatomical brain connectivity and positive symptoms of schizophrenia: A diffusion tensor imaging study. Psychiatry Research: Neuroimaging, 174 (1): 9-16.]. I have had patients who heard white noise and other common sounds (eg, scraping of chairs on the floor) and interpreted these stimuli as voices directed at them, ie, auditory hallucinations. Perhaps the same neurological filtering structures do not exist, or are not as easily compromised, in the visual pathways.

https://www.researchgate.net/profile/Neil_Krohn/ i was also thinking in these terms of white matter connectivity.

Neil writes;

>

I've had many patients report hearing voices 'hidden' within the sound of airconditioners, background traffic noise, and similar background white noise.

In psychotic disorders this is very common symptom.

If the positive (acute) symptoms of schizophrenia are in part due to overactive dopaminergic systemns, then it's quite possible that these misperceptions are symptoms of the brain desperately trying to find pattern where there is none. Our nervous systemns are designed to filter input from the senses to find signals in all the noise around us. A little dopamine increases the responsivity of the systemn, (hence the fight-or-flight response) but too much dopamine increases the chance of detecting things that aren't actually there.

Hearing murmuring voices in the sound of a stream flowing, or the wind through leaves, is quite a common event for people who spend much time in natural environments. The difference is whether the person has insight into what is happening, or whether they begin to listen to the voices and build delusions upon them.

When people use methamphetamine in high doses they may experience a psychotic episode due to elevated dopamine levels. Again, level of insight varies from individual to individual. Two kinds of hallucination are commonly reported in amphetamine-induced-psychosis;

Auditory hallucinations which are (at least initially) misperceptions;

Otherwise healthy people suffering amphetamine induced psychosis often experience delusions of persecution. These typically manifest initially as the sufferer "mishearing" other people's conversation- for example strangers walking down the opposite side of the street are talking, and the person believes they overheard their own name being spoken. Surely your own name is one of the sounds your brain is most strongly conditioned/trained to recognise and respond to? If your brain is overstimulated/over-reactive you may think any similar sound is someone referring to you...

Visual hallucinations which are disturbances in the periphery of the visual field. These are things like shadows or reflections, (especially moving ones, eg caused by traffic driving by). These manifest as briefly glimpsed objects moving past- I had a client who described them as "ghost dogs". Again, this would appear to be an over-responsive nervous systemn "jumping to conclusions". The shadow of a passing car is percieved as a movement at knee height. Your brain doesn't pay that much attention to data from this part of your eye- (what you see in your peripheral

visual field owes as much to memory filling in the blanks as it does to photons hitting your retina)- and so when overstimulated your brain "fills in the gaps" and

(in my clients case) interprets the sensory information as a shadowy dog running beside the road.

I'd suggest that in the case of hallucinations in psychotic disorders, methamphetamine can model very similar symptoms, and it's quite likely there are similar neurochemical substrates.

Paul.

A very pertinent question, one which most schizophrenia researchers conveniently ignore. Benjamin Rush wondered about this, and supplied what I think is the correct answer -- that ear disease is commoner than eye disease in psychiatric patients. As noted above, I think all auditory hallucinations are triggered by sounds, external environmental ones or internal ones (tinnitus). All cognitive theories fall at the first fence, as they cannot give a simple unitary explanation for verbal, musical and visual hallucinations. The brain dopamine and tinnitus systems are identical.

In addition to the eyes, the vestibular system is an overlooked source of visual hallucinations, in migraine, for example. It is exquisitely sensitive to toxins, foods and drugs, and serves as the body's poison monitor, hence the vomiting reflex. So I would guess that when body metabolism is deranged with fevers or infections, harmful substances first disrupt the vestibular rather than auditory part of the inner ear, hence visual hallucinations predominate here, unlike in psychoses.

Is it not true that of both the visible and auditory spectrum humans only perceive a tiny sliver of what is actually there. For example we knew about infra red and ultra violet by their effect well before we confirmed their presence via modern technology yet some animals have this ability present in their senses. Also we know many animals hear, and even smell a vast world compared to the dull witted human species. Just the other week in New Zealand a small tsunami wave of under half a meter was due on our shores from an earthquake in the Pacific yet all the sea birds headed inland for a couple of hours.

To continue this stream of thought... we know some substances such as LSD and other amphetamines or more traditional Shamanic drugs seem to 'widen' the perception range of sensory information. My personal experience of this state was during a time of high stress combined with mercury poisoning and sleep deprivation. I feel it is a survival mechanism causing hyper vigilance via the stress hormones and when chronic leads to a state of information overload.

Paranoia comes from fear and not understanding the 'expanded state'. After all we are constantly surrounded by quantum information, natural patterns, sacred geometry etc but we don't normally notice it. Our human brains are meaning making machines and when no logical explanation is available to explain why you can suddenly 'hear' the thoughts of others, know what is about to happen just moments before it does, have an internal voice direct you to finding a lost love one or save a stranger from suicide then we enter a scary world of the unknown.

When life keeps showing you its not madness but real events, usually fairly subtle, there is a barrage of possibilities, insights and information. Many people are happy to know that life is not random and if the danger has passed will return to a less sensitive state, others become religious but for some this state becomes terrifying. They then look for an outside influence, in the past it was curses, spirits, demons and now its CIA, aliens and Truman show like trickery. I personally sat quietly for 30 minutes being 3 seconds ahead of time... by saying 'this is interesting' over and over to myself I did not 'freak out' but instead realized my electromagnetic field had become conscious allowing me to 'intuit' quantum information, much like the communication every cell int the body has with all the other cells.... well this is my theory from lived experience anyway.

What psychologist (he may have been a psychiatrist) Stanlov Groff did in the 1950's was very courageous, he took LSD and experienced altered states of consciousness rather than sit in his safe chair behind a safe desk and judge the unusual experiences of others as pathological. I was told that the mix of endorphins, adrenaline, noradrenaline and cortisol was in its effect similar to cocaine. Add in physical exhaustion causing a dehydrated and acidic state plus sleep deprivation and nutritional depletion the question becomes who would not experience 'madness' in that state, yourself included.

...Sure, paranoid people, like the rest of us, do occasionally have enemies. But if these imaging studies are replicated, the results will mean that the real enemies of paranoid people are their own brains. >>>

http://www.nytimes.com/2003/04/01/health/behavior-self-protection-or-delusion-the-many-varieties-of-paranoia.html?pagewanted=2

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I would add to this discussion the work of Paul Lewicki and the role that nonconscious information processing might play in the phenomena of illusions, hallucinations, cognitive biases, and to some extent delusions. Lewicki and colleagues found that a process of self-perpetuation exists, in which all individuals make judgments based on a heuristic that includes previous data input and "beliefs." These judgments are frequently biased and factually inaccurate, but also account for nonconscious phenomena such as the inability of experts to articulate the basis of their expertise. [Lewicki, Paul, Hill, Thomas, & Czyzewska, Maria (1992). Nonconscious acquisition of information. American Psychologist, 47, 796-801]. How does nonconscious processing impact the frequency or quality of hallucinations, especially comparing normal vs. psychiatric populations?

I have recently stumbled on 'Dimethyltryptamine. (DMT)' where it is generated naturally (in many plants including lawn grass) and how we produce it in our own brains/body. As a hallucinogen could it be that the 'mental health' experience of psychosis is simply this neurotransmitter reaching levels high enough to produce a noticeable effect?

I see that the better known search engines carefully separate the experience of people ingesting DMT and mental health experiences. Why? so as to not step on the delicate toes of the DSM created culture of illness and disease? I would love to know more on this topic as my personal experience of never taking any 'recreational' drugs but having been psychotic for a short but fascinating time sound very similar in visual hallucination, from other peoples accounts. Interesting the visions I did have 20 years ago have all come true over the years but in more metaphoric terms rather than literal.

I recommend Broome et al - sorry I can't find a link to the full text;

http://www.schres-journal.com/article/S0920-9964%2805%2900072-1/abstract

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Paul.

This is a fascinating topic. I would suggest future research along the lines of finding the correlates of visual vs . auditory hallucinations. In other words, what background factors might predispose to one or the other. It would also be valuable to see which medications might be more effective on certain specific types of hallucinations.

Hi Heather,

Dimethyltryptamine is an extremely fascinating chemical. There's about 150 acacia species here in Australia that contain it, and dozens of species in which it is relatively easily extracted from the bark. In my work we occasionally encounter people making DMT and smoking it for the hallucinogenic effect, which is very intense but short lived.

It (and it's close cousins 5-MeO-DMT and 5-OH-DMT (bufotenin) ) are found in many plants, some of which have been used as ritual hallucinogens by various cultures around the world.

Bufotenin is also the psychedelic substance found in the secretions of some poisonous toads, and 4-phosphoryloxy-N,N-dimethyltryptamine is psilocybin, the active principle in many "magic mushroom" species.

DMT occurs naturally in humans and other mammals, and this endogenous DMT has indeed been conjectured to play a role in all sorts of unusual psychological or neuro-chemical states, although the general consensus of scientific opinion appears to be that "the jury is still out" as to what role it does play.

Endogenous DMT is present in your brain right now, but while various theories have been advanced that fluctuating levels of DMT are responsible for not only for symptoms of schizophrenia, but also for dreams, near death experiences, ecstatic religious visions etc, there is no strong scientific evidence in favour of these conjectures (or against them. Yet?).

While studies show that some people suffering acute symptoms of schizophrenia have higher levels of DMT in their cerebro-spinal fluid than controls, this difference is not statistically significant;

http://bjp.rcpsych.org/content/132/2/139.short

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This, and similar studies, make it very unlikely that fluctuations in endogenous DMT can be a "one size fits all" explanation symptoms of psychotic disorders.

Much of the hype around DMT can be attributed to this guy:

http://rickstrassman.com/index.php?option=com_content&view=article&id=61&Itemid=60 but unfortunately there isn't any published scientific research at all to back these claims

DMT and it's cousins may actually be useful substances for treating some psychiatric problems, or as adjuncts to psychological counseling.

https://mycotopia.net/forums/attachments/lifestyles/187583d1284163814-pilot-study-psilocybine-treatment-anxiety-patients-advanced-stage-cancer.pdf

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More detailed info on DMT here;

http://www.lycaeum.org/leda/Chemicals/DMT.11.shtml

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A very similar hypothesis is that adrenochrome (the oxidation by-product of adrenaline) plays a causal role in schizophrenia. (Adrenochrome was made famous by Hunter S Thompson in "Fear and Loathing in Las Vegas").

Abram Hoffer and Humphry Osmond claim that adrenochrome is a neurotoxic psychotomimetic substance and may be responsible for schizophrenia.

They speculate that megadoses of vitamin C and niacin could be used to treat symptoms of schizophrenia by reducing adrenochrome levels.

http://www.orthomolecular.org/library/jom/1999/articles/1999-v14n01-p049.shtml

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The only real problem with this hypothesis is that adrenochrome is not actually a halllucinogenic substance...

http://www.erowid.org/experiences/exp.php?ID=51847

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http://www.erowid.org/experiences/exp.php?ID=65371

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Alexander Shulgin (who is basically God to most research organic chemists) described adrenochrome as a "fascinating red herring."

The original paper, in which Hoffer obtained "profound psychomimetic symptoms"

from as little as 0.5 mg S.C. or I.V is in J. Mental Sci. 100, 29, '54

However it appears that the original, positive reports were based on experiments with a single, mentally unstable patient.

http://www.erowid.org/library/books_online/hallucinogens_hoffer_osmond.pdf

.

However later research found negative results or no significant effects with doses of up to 25mg:

Am. J. Psychiat. 111, 603, '55

Am. J. Psychiat. 115, 162, '58

Am. J. Psychiat. 116, 454, '59

Lancet ii, 308, '58

These studies led to the conclusion that, while forms of adrenochrome have haemostatic and other physiological properties, adrenochrome is not hallucinogenic, psychotomimetic, or even psychoactive;

Lancet, I 1287, 1960

Sorry I don't have any links to hand for these old articles. There is a good discussion (er- yes- it's wiki) here;

http://en.wikipedia.org/wiki/Abram_Hoffer#Research

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So, just to point out the obvious, don't build elaborate hypothesis upon a sample where n = 1.

I should also point out that mega-doses of Niacin are extremely dangerous, and that liver failure is a particularly unpleasant way to die.

Paul.

Here's a few pieces of the puzzle:

We spend more of our days in silence than in darkness. Thus, when we are awake and not dreaming and have eyes and ears open, Hallucinations intrude more easily in audiation (imagined sounds, including a song stuck in our head) than in imagination (images pictured in the mind) We also have more material available in audiation, partly in the form of thoughts which tend to be imagined as words, but more importantly in our sensory memory: Our brains are designed accordingly to have only a 10th of a second of sensory memory for visual stimuli, but a 3-4 second "echo" of auditory stimuli. In schizophrenia, our internally produced and echoed and images and sounds are hard to distinguish from external stimuli.*

Putting the puzzle together: When we produce internal/imagined auditory perceptions, we are more likely to mistake them for external stimuli than for visual images, we are more likely to hold them in memory long enough to perceive them, and going back to my first statement about silence (even the gaps between spoken words), we are less likely to have those perceptions over-ridden by external stimuli.

*When someone without schizophrenia has a song stuck in his or her head or has ringing in the ears or has an imagined thought in words, we know that it's produced inside the head; a mental glitch in schizophrenia, involving the temporal lobe where auditory signals are processed (another piece of the puzzle I left out earlier) makes it more difficult to tell whether the voices are imagined or sensed. A frustrating problem, triggering some delusions about words being broadcast into the mind.

I have thoroughly reviewed the literature on musical hallucinations in normals, psychotics, mystics, etc. These are not produced in the head, but always start off in a hypersensitive inner ear. Of the millions of patients with tinnitus I have tested myself or seen reported in the literature, I do not know of a single example where the tinnitus has started in the brain, as a result of primary brain disorder. A normal brain is quite capable of coming to odd conclusions when having to construct reality from unusual auditory input.

Anthony Gordon that is perfectly fine regarding "musical Hallucination". But in Psychiatry as it is , people hear more than music.... like second person and third person hallucination. How can Tinnitus explain these phenomenon. How can the odd conclusions from normal brain be that much complex enough to explain these phenomenons.

Perhaps some people pick up radio stations with all the metal in their teeth and its not a hallucination at all.... Certainly plenty of m/h patients say this but who are we to say this cant be real?

Suni, hearing voices clearly involves speech and language areas of the brain. But the question is, how did these develop in the first place? In many conditions a continuum has been shown, from hearing noises to music to voices, then back down again as the patient recovers (eg alcoholic hallucinosis). Occam tell me that the causes of hearing music and voices are likely to be similar, and in fact I cannot find any known cause or risk factor for voices that is not also one for music. If anyone knows of one, I would like to know, as it would invalidate my theory. Even tinnitus from a damaged ear can induce profound psychological and psychiatric changes, no doubt by rewiring the brain.

Because the visual halucination are distorisons of perception in toxic, metabolic and infectious deliriums (visual predominant, , but is possible all other type of halucinations, too). On other side auditive haluccinations are predominant by Sch-like symptomatic and so called functional psychotic state with very prominent discomunication/acommunication (autistic) state. (many of this psychosis are symptomatic, too).

Googling ' Functional Hallucination' shows there is general acceptance of this term. Patients may not be aware of some external ot internal sound that is triggering their auditory hallucinations, and psychiatrists do not usually bother to ask, though if they did, it would not necessarily be easy to find the trigger stimulus. So functional hallucinations are liable to be far commoner than realised, in fact I do not think there is such a thing as a pure auditory "hallucination", they are all misperceptions, ie FHs.

In both cases is obligatory the functional and morfological examination of visual or/and auditory systems!

As research clinician, I fully agree with the argument that auditory hallucinations are more frequently observed than visual hallucinations. I would like to point out that the visual and auditory system occupy different "roles" regarding schizophrenia. While the visual perceptual channel is associated with the causes and the development of schizophrenia, the auditory perception channel is rather associated with symptom expression. Here are some arguments that support this view.

First, it has been argued that the actual rate of visual hallucinations might be underestimated by clinicians (Bracha, Wolkowitz, Lorh, Karson, & Bigelow, 1989). Auditory hallucinations might be more often than not accompanied by visual hallucinations. However, patients are able to report on visual hallucinations only after their state has been ameliorated with antipsychotic treatment. This means that auditory hallucinations are routinely recorded during diagnostic interviews, whereas visual hallucinations, being reportable long after patients have first been seen by the medical staff, are not (Bracha et al., 1989).

Second, according to a recent meta-analysis, auditory hallucinations are proposed to be internally generated speech perceptions (Hugdahl et al., 2007) and self-reported inner speech characteristics appear similar in patients and healthy controls (Langdon, Jones, Connaughton, & Fernyhough, 2009). Thus, auditory hallucinations might not directly depend on sensory input, that is, they may not be a result of a malfunctioning auditory sensory system. Instead, it could be anomalies in the visual system that underlie the expression and progression of schizophrenia. This hypothesis is in line with Frith (1996) who argues that it is the distinction of the inner voice from outside stimuli and the prediction of sensory events that is deficient in patients. This corroborates the assumption that cognitive processes that are NOT specific to the auditory domain underlie auditory hallucinations.

Third, if malfunctioning of the auditory system was the decisive contributing factor to the development, expression, and progression of schizophrenia, absence of auditory input (deafness) should be a protecting factor for developing psychosis. Malfunctioning of the auditory perceptual system has, however, not been identified as a protecting factor against schizophrenia. In fact, multiple examples for (even prelingually) deaf individuals that develop schizophrenia are readily available in the literature (e.g., du Feu & McKenna, 1999; Schonauer, Achtergarde, Gotthardt, & Folkerts, 1998) questioning further a causal influence between auditory sensory input and development of psychosis. On the other hand, the absence of visual input (blindness) has been proposed as protection marker against psychosis (Landgraf et. al. 2012; Landgraf & Osterheider 2013; Silverstein et al.; 2013). Until today, no single case of an innately blind person that has developed psychosis has been reported (personal literature search). Hence, the visual system significantly contributes to a coherent subjective experience in the majority of human beings, thus probably contributing more significantly to an aberration of self-experience in schizophrenia than does the auditory system. The auditory system might be a symptom channel in already manifested schizophrenia, that is, this system is prone to sensory perceptions in the absence of externally generated stimuli.

Fourth, while up to 52% of patients with schizophrenia suffer from visual and up to 98% from auditory hallucinations (Bracha et al., 1989), visual and visuo-spatial performance does not only appear to be compromised in patients but has been proposed a genetic marker for the disease (Braff, Freedman, Schork, & Gottesman, 2007; Hallmayer et al., 2003). A wealth of studies shows that the visual system is impaired in relatives of schizophrenia patients, whereas auditory abnormalities appear to be constrained to the symptomatology of the patient and not to their family members.

While I acknowledge the important role of the auditory system for the expression of specific symptoms of the disease, I would like to point out that 1) these symptoms might be routinely over-represented due to timing of diagnostic assessments, 2) cognitive processes NOT specific to the auditory domain have been proposed to account for hallucinatory symptoms, 3) the auditory system might be more of a channel of symptom expression since it is the visual, not auditory, input that has been proposed as a protection marker against psychosis, and 4) genetic studies show the implication of the visual system in prediction and progression measures of the disease.

References

Bracha, H.S., Wolkowitz, O.M., Lorh, J.B., Karson, C.N., & Bigelow, L.B. (1989). High prevalence of visual hallucinations in research subjects with chronic schizophrenia. American Journal of Psychiatry, 146(4), 526-528.

Braff, D. L., Freedman, R., Schork, N. J., & Gottesman, II. (2007). Deconstructing schizophrenia: an overview of the use of endophenotypes in order to understand a complex disorder. Schizophrenia Bulletin, 33(1), 21-32.

Carvill, S. (2001). Sensory impairments, intellectual disability and psychiatry. Journal of Intellectual Disability Research, 45(6), 467-483.

du Feu, M., & McKenna, P. J. (1999). Prelingually profoundly deaf schizophrenic patients who hear voices: a phenomenological analysis. Acta Psychiatrica Scandinavica, 99(6), 453-459.

Frith, C. D. (1996). The role of the prefrontal cortex in self-consciousness: the case of auditory hallucinations. Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences, 351(1346), 1505-1512.

Hallmayer, J. F., Jablensky, A., Michie, P., Woodbury, M., Salmon, B., Combrinck, J., . . . Kent, A. (2003). Linkage analysis of candidate regions using a composite neurocognitive phenotype correlated with schizophrenia. Molecular Psychiatry, 8(5), 511-523.

Hugdahl, K., Loberg, E. M., Specht, K., Steen, V. M., van Wageningen, H., & Jorgensen, H. A. (2007). Auditory hallucinations in schizophrenia: the role of cognitive, brain structural and genetic disturbances in the left temporal lobe. Front Hum Neurosci, 1, 6.

Landgraf, S., Amado, I., Berthoz, A., Krebs, M. O., & van der Meer, E. (2012). Cognitive Identity in Schizophrenia: Vision, Space, and Body Perception from Prodrome to Syndrome. Current Psychiatry Reviews, 2(8), 1-20.

Landgraf, S., & Osterheider, M. (2013). "To see or not to see: that is the question." The "Protection-Against-Schizophrenia" (PaSZ) model: evidence from congenital blindness and visuo-cognitive aberrations. Front Psychol, 4, 352. doi: 10.3389/fpsyg.2013.00352

Langdon, R., Jones, S. R., Connaughton, E., & Fernyhough, C. (2009). The phenomenology of inner speech: comparison of schizophrenia patients with auditory verbal hallucinations and healthy controls. Psychological Medicine, 39(4), 655-663.

Riscalla, L.M. (1980). Blindness and schizophrenia. Medical Hypotheses, 6(12), 1327-1328.

Schonauer, K., Achtergarde, D., Gotthardt, U., & Folkerts, H. W. (1998). Hallucinatory modalities in prelingually deaf schizophrenic patients: a retrospective analysis of 67 cases. Acta Psychiatrica Scandinavica, 98(5), 377-383.

Silverstein, S. M., Wang, Y., & Roche, M. W. (2013). Base rates, blindness, and schizophrenia. Frontiers in psychology, 4, 157. doi: 10.3389/fpsyg.2013.00157

"Frith (1996) .. argues that it is the distinction of the inner voice from outside stimuli and the prediction of sensory events that is deficient in patients. This corroborates the assumption that cognitive processes that are NOT specific to the auditory domain underlie auditory hallucinations." After hearing him talk about his theory, I once asked him if it had anything to say about non-verbal auditory hallucinations eg musical ones. His reply was succinct: "No". This immediately places the general explanatory value of his theory however elegant below that of the theory that hallucinations are due to spirit possession.

"if malfunctioning of the auditory system was the decisive contributing factor to the development, expression, and progression of schizophrenia, absence of auditory input (deafness) should be a protecting factor for developing psychosis". Not according to my theory. It is hypersensitive not hyposensitive hearing that is relevant.

"multiple examples for (even prelingually) deaf individuals that develop schizophrenia are readily available". True in general, but I wonder if total congenital deafness, which is quite rare, protects. Absence of the vestibular part protects against motion sickness as shown by William James.

"auditory abnormalities appear to be constrained to the symptomatology of the patient and not to their family members". So are more related than visual ones to the disease than to the underlying predisposition?

"The auditory system might be a symptom channel in already manifested schizophrenia". This study below finds massive odds ratios for early deafness. I think this is mediated by periods or auditory distortion and hyperactivity, and not sensory deprivation:-

Psychol Med. 2012 Nov 30:1-10. [Epub ahead of print]

Hearing and speech impairment at age 4 and risk of later non-affective psychosis.

Fors A, Abel KM, Wicks S, Magnusson C, Dalman C.

BACKGROUND: Schizophrenia often becomes manifest in late adolescence and young adulthood but deviations in physical and behavioural development may already be present in childhood. We investigated the relationship between hearing impairment (measured with audiometry) and speech impairment (broadly defined) at age 4 years and adult risk of non-affective psychosis. Method We performed a population-based, case-control study in Sweden with 105 cases of schizophrenia or other non-affective psychoses and 213 controls matched for sex, date and place of birth. Information on hearing and speech impairment at age 4, along with potential confounding factors, was retrieved from Well Baby Clinic records.

RESULTS: Hearing impairment [odds ratio 6.0] and speech impairment (OR 2.6) at age 4 were associated with an increased risk of non-affective psychotic illness. These associations were mutually independent and not explained by parental psychiatric history, occupational class or obstetric complications.

CONCLUSIONS: These results support the hypothesis that psychosis has a developmental aspect with presentation of antecedent markers early in childhood, long before the disease becomes manifest. Our findings add to the growing evidence that early hearing impairment and speech impairment are risk indicators for later non-affective psychosis and possibly represent aetiological clues and potentially modifiable risk factors. Notably, speech impairment and language impairment are both detectable with inexpensive, easily accessible screening.

Thanks Steffen for those references, and your excellent discussion of the implications.

Regards,

Paul.

....Hearing impairment [odds ratio 6.0] and speech impairment (OR 2.6) at. age 4 were associated with an increased risk of non-affective psychotic illness. These associations were mutually independent and not explained by parental psychiatric history, occupational class or obstetric complications1 EUREKA! The hallucination are consequences of deteriration, dysfunction and/or distortion in system /perception!

The psychiatrist must make the full examination of auditory system!

I dont support the distinction to affective and nonaffective psychosis.... The shizoprenic patients have very deep affective reactions! The paranoid schyophrenia is more affective, than schiyophrenic psychosis / it are many articles about this topic.

"fear" is the prime" emotion" in Depression. Thats why is affecting is connecting with hallucinations (visual)

"fear" is the prime" emotion"

Long ago the scariest place to be was the middle of the jungle. Vision was of limited use in the day, of no use at night. Even today if you go out at night in the country you get very strong orientation reflexes, startle reactions and fear respones to even the quietest sounds.

"affecting is connecting with hallucinations (visual)"

Auditory hallucinations are commoner than visual in psychoses. For example, see Brit J Psychiatry 2003;182:543. Of 96 with bipolar affective disorder, 30 had auditory halls and 25 visual halls. Chidhood trauma correlated with the auditory but not the visual halls.

right, childhood trauma and from the first beginning of mother-chield connection. and then according to Z.Freud, "children is father of human" (free translation), trauma as "Primary Emotion" is reflected during all human life. That is some kind of rigide emotion..

Maybe Vigotski Theory can help in combination with cognitive - behavioral approach:)

"the verbal and symbolic behavior is dominant about visual and other perception modalitie"- there is cognitive behavior. Motor functions are producing "symbolic behavior" if they are associated with an emotion. Then they get "rigide" function-