2020-02-12 19:12:18 (edited by daigonite 2020-02-12 19:26:44)

Hello everyone,

So I was reading today and apparently, schizophrenia does not appear in people who are totally blind:

https://www.sciencedirect.com/science/a … via%3Dihub
https://www.frontiersin.org/articles/10 … 00624/full
https://www.cambridge.org/core/journals … F103817378

So I'm just going to be upfront and honest, I think looking for biological determinations here is pretty stupid and the biological changes are more effects than causes. There's clearly something up going on with this. I was wondering what you guys thought.

I think we all know that being blind doesn't protect you from delusional thinking. We all know some blind people who have some crazy weird beliefs - although this in of itself isn't schizophrenia. Delusional thinking is a consequence of unregulated thinking patterns, and that can happen to anyone. In my experience in some cases blind people are more susceptible because they are limited with what information they have access to due to accessibility issues. I was thinking there is probably an element regarding rate of diagnoses and how blindness interferes with schizophrenic presentation.

Have any of you had any minor auditory hallucinations before? Totally blind people specifically. For example, thinking you hear something that you don't. I would imagine its less common in blind people just because how much blind people depend on it but I find it hard to believe that it never happens. It happens a lot for me, sometimes I feel like someone is calling my name because of abuse I dealt with as a kid. I think its possible for a similar mechanism to emerge in blind people. If this is the case this provides a clear way for schizophrenia to develop in blind people; but it may just not "present" like schizophrenia because blind people interact differently than sighted people with these issues.

This is really serious in terms of implications because it is hard evidence that analyzing schizophrenia as an individualized condition is simply wrong and is a consequence of complex social factors.

you like those kinds of gays because they're gays made for straights

2020-02-12 20:47:10

i don't thing they are wrong.

Ladies and gentlemen, this is your captain speaking. We have a small problem. All four engines have stopped. We are doing our damnedest to get them going again. I trust you are not in too much distress.

2020-02-12 22:22:59

I'm gonna have to hard disagree, if what you're saying is that blind people can't get schizophrenia. I think at the very least this approach is irresponsible without actually investigating possible social causes.

They're literally saying that being born blind makes you somehow immune to schizophrenia. This is an extremely bold claim, because it implies a lot about how we should treat schizophrenic people. They're literally blaming this on the fact that blind people don't get admitted into mental hospitals for it. This is such piss poor evidence I dont' even know where to begin.

Now, I don't think that this is a commonly held belief in the field, but it indicates the direction science tries to solve the problem instead of seeing the obvious - that a lack of blind diagnoses of schizophrenia likely indicates a problem with how we see schizophrenia.

But this contrasts everything I understand about blind people and delusion. People born totally blind absolutely are vulnerable to delusion, in fact I would say moreso because they are generally socially isolated so they have less people to fight back problems. If like many blind people they're forced to live by themselves and have little social interaction there's nothing stopping them from getting delusional thought patterns. So many blind people believe in a ton of weird conspiracies that I just don't see how its possible to assume delusion is impossible in the blind. They definitely are more vulnerable to other mental health issues. There's also the fact that blind people already have enough trouble getting access to mental health treatments.

I think what's really happening is that blind people, for some reason, are not diagnosed as schizophrenic. This is because whatever schizophrenia actually is presents differently in blind people due to their blindness. If schizophrenia is a consequence of social condition rather than some individual affect, this would be explained because the social conditions surrounding schizophrenia shape differently in blind people due to the material consequences of being blind. In this model schizophrenic people are people who lose touch with reality because reality is a shared experience between many people, and is a result of extreme social isolation caused by a variety of physical and mental factors.

This is huge because it means potentially a lot of blind people are actually schizophrenic but they never present as such. A possible explanation is that its well known that many borderline schizophrenic eccentric individuals are able to manage their symptoms well enough that they don't present, because the risk of admitting schizophrenia is too high (you lose your rights, you open yourself up to a lot of abuse ect).

This is why I ask for other people's personal experiences. Auditory hallucinations are extremely common for example and I swear I've heard my blind friends say they have experienced them before. It's just when you think you hear something that you didn't, like an external voice. This is an early disruptive sign which usually is minor and means nothing but is basically how it starts. Schizophrenic behavior likely has a different pathway in blind people - not that it doesn't exist at all.

The fact that these "Scientists" aren't looking into this is mind numbing. We are going to be looking into it further. If we are right about this, it really shatters the view that schizophrenia is some sort of individualized condition, but it also demonstrates how we are essentially cutting off entire populations from treatment.

you like those kinds of gays because they're gays made for straights

2020-02-12 22:23:27

I dunno... Blind people have quirks sighted people don't ever deal with, such as the whole rocking bak and forth thing and digging one's fingers into their eyes or the corners of their eyes or whatever.  I've heard people say that it's lack of sensory stimulation.  Where sighted people can constantly look around they are spending more energy sensory wise than blind people are.  I've never personally bought it as it doesn't happen to all blind people; I'm totaly blind and don't rock and don't screw my knuckles into my eyes.
My thing, however, is sound.  I always want sound... I must make sound if there is no sound!  I cannot comfortably live without sound in some sense or another!  I hate silence so much so that it actually frightens me.  This may have something to do with the fact that I'm slowly but surely losing hearing and don't know where it'll end.
Still, I wonder if a lot of blindisms, for better lack of word choice, are associated with underlying causes we aren't recognizing for what they are and or simply ignoring them.

When life gives you oranges, demand lemons since everyone else is obviously getting them.

2020-02-12 22:33:30 (edited by daigonite 2020-02-12 22:35:44)

See this is what I don't get.

Think about this Noc; you've heard about those sensory deprivation tanks, right? Those legit cause people to go crazy because they lose contact with the outside world. People have delusions within 48 hours and often beg to be released because its that bad. So when you lose you're hearing, this is part of what you're losing - your connection to the world.

So what makes people think that going BLIND would fix that? Being blind causes an immediate physical disconnect from experiencing light. But far more importantly, it causes a disconnect socially. I think all of you guys know how bad the isolation can get. And really, this disconnect from the outside world is what causes these issues to emerge - you can't filter out the crazy thoughts when you aren't getting people to say, "yo, that's silly and here's why".

This is a problem in general cuz people can't talk about their crazy thoughts so they just get crazier and crazier until they develop traditional schizophrenia signs.

But yeah, I definitely agree that blind people do function differently than sighted people - and what I'm trying to say is because of this, it causes us to not understand the actual mental health experience of the blind. We can understand some things but other things like schizophrenia maybe present completely differently because of the different input models. This is a huge oversight because it means that not only are blind people just being neglected in general, it means that psychiatry has no model for actually understanding these "blindisms". This is a problem emerging in other disability circles but I think this example is probably the most strong example I've seen thus far.

Sorry for being so tight on this subject, this is probably a really difficult thing to think about. Hell, neglect of mental health issues when being blind would be a strong indicator of evidence of this problem as well.

you like those kinds of gays because they're gays made for straights

2020-02-12 22:37:24

Hi.

At 4 yeah I agree, I also don't have the problem of rocking around or screweing up my eye sockets, I don't get blind people who are doing this, but hey, to each their own, they have to get a job some day as well.
I also think that this is quite the bold statement, you gotta wonder how much research went into that.

Greetings moritz.

Hail the unholy church of Satan, go share it's greatness.

2020-02-13 01:23:53

So an update on looking into this.

The second article linked is actually really helpful and it helps provide an outline for why people seem to believe that somehow blindness "prevents" schizophrenia (spoiler, it might help a little but not much).

So lets get out of the way the really dumb talking points.  BTW when I say "blind people" its a shorthand for people born blind.

1. They talk about how audio hallucinations are rarer in blind people because they have more acute hearing. Now, I'm still not convinced that auditory hallucinations don't occur in blind people, but doesn't it make sense that the sense that's very much used for navigating the world, especially far away things? People born blind can mostly only sense far away things with their sense of sound. So, since its so heavily in tune with the outside world, its of course going to be less likely to develop hallucinations.

This is seen in traditional schizophrenia as well - visual hallucinations are actually very rare and an indication of severe illness. If there are blind schizophrenic people, they are probably extremely severely schizophrenic by the time that we actually can observe it

2. They suggested blind people have superior language processing. This may be true but their methods completely fail to take into account how blindness impacts language development. The "object" in the person's head that comes from hearing a word is actually different in a blind person than a sighted person - something that's most obvious when talking about things that blind people dont experience, such as color or light.

3. There's this really funny part where they basically suggest blind people have stronger sense of smell (which may be true i guess) and that not smelling your mom growing up can trigger schizophrenia (lol rip gay dads)

There was interesting grain of protection blindness does actually seem to offer against schizophrenia development though. People born blind are forced to gain relativistic understanding as opposed to a combined world view, as what vision presents. This has subtle ways on how we process information in general. Sighted people actually use relativistic thinking too, just not as frequently. Anyways, this prevents ideas from getting as "firmly locked in place" because blind people build larger navigational understanding from smaller pieces.

Now to me, this suggests to me something incredible - that blind people present schizophrenia in a way that is literally invisible to psychiatric understanding. That is to say, schizophrenia is really "sighted schizophrenia". Furthermore, this suggests that blind people have a unique mental topology that has been completely neglected up to this point. AKA, blind people have unique forms of mental suffering that really can't be shoved into sighted models.

It's unbelievably stupid honestly its like these people have never talked to an actual blind person while doing all this research. Literally losing my mind right now. I need to stress that the solution isn't "to accommodate blind people", it's to recognize that the psychiatric system is broken because it doesn't recognize that blind people are literally different from sighted people.

you like those kinds of gays because they're gays made for straights

2020-02-13 03:29:19 (edited by SirBadger 2020-02-13 03:34:18)

well I can blow this out of the water pretty mutch strait away because I have a blind friend who has schizophrenia. she does have a little sight so maybe the totally blind thing is different but i'm not buying it.
I also have 2 blind friends that are Dyslexic witch I like the majority of the world was always told is word blindness. so when they look at a word it gets scrambled up. turns out, not the case. you can be a Dyslexic braille reader too and have trouble typing or brailing words.

Who's that trip trapping over My bridge? Come find out.

2020-02-13 04:19:43

Here's the thing I have trouble with.

At its base, schizophrenia is chemical or mechanical, something amiss in the brain. This is why, for instance, there is a definitive, if fairly weak, link between teenage marijuana abuse and increased susceptibility to schizophrenia.
So where does that translate into "blind people don't get schizophrenia"? I just...don't understand that one.
I would want/need hard physical evidence that the brain of a blind-from-birth individual is wired such that schizophrenia is impossible. If that can be provided, at least beyond reasonable doubt, then okay, I'd bite. Until then though? Not so much.

You're quite right about perception and the progress of the disease, however (language processing, relativistic thinking, increased sense of smell, etc). Those things are apt to give some small protection from the deeper ravages of the disorder. So I'm willing to accept that it might be more difficult for a blind person to develop schizophrenia, or to deteriorate/develop greater symptoms, at least where the delusions are concerned.

Check out my Manamon text walkthrough at the following link:
https://www.dropbox.com/s/z8ls3rc3f4mkb … n.txt?dl=1

2020-02-13 04:36:44 (edited by daigonite 2020-02-13 04:38:28)

SirBadger wrote:

well I can blow this out of the water pretty mutch strait away because I have a blind friend who has schizophrenia. she does have a little sight so maybe the totally blind thing is different but i'm not buying it.
I also have 2 blind friends that are Dyslexic witch I like the majority of the world was always told is word blindness. so when they look at a word it gets scrambled up. turns out, not the case. you can be a Dyslexic braille reader too and have trouble typing or brailing words.

Is she born blind? Its about being born blind, not going blind. Partial vision changes things cuz when you're born blind you never get exposed to light/color/ect.

Jayde wrote:

Here's the thing I have trouble with.

At its base, schizophrenia is chemical or mechanical, something amiss in the brain. This is why, for instance, there is a definitive, if fairly weak, link between teenage marijuana abuse and increased susceptibility to schizophrenia.
So where does that translate into "blind people don't get schizophrenia"? I just...don't understand that one.
I would want/need hard physical evidence that the brain of a blind-from-birth individual is wired such that schizophrenia is impossible. If that can be provided, at least beyond reasonable doubt, then okay, I'd bite. Until then though? Not so much.

You're quite right about perception and the progress of the disease, however (language processing, relativistic thinking, increased sense of smell, etc). Those things are apt to give some small protection from the deeper ravages of the disorder. So I'm willing to accept that it might be more difficult for a blind person to develop schizophrenia, or to deteriorate/develop greater symptoms, at least where the delusions are concerned.

See, this is the thing - you can't just dissolve shit into brain chemicals. Brain chemicals are a result of repeated changes to the brain from stress. For example, something that studies can't actually research very well, is how drugs change people's thought patterns. If brains become schizophrenic from illogical thought patterns, then the chemicals will eventually adapt to show that and make it appear as if the chemicals changed. This is the problem with identifying so called "risk factors" - the risk factors are more like a different shape that makes something more vulnerable to certain conditions rather than being inferior. (I should point out thought that seratonin is heavily criticized as a vector for mental illness in literature, a gross oversimplification of the situation). This is why thinking critically is important.

But think about how even when accepting the chemical paradigm that it doesn't line up with what we observe with "schizophrenic" behavior. Something is up here and it's not the mental illness - its the diagnosis itself. The diagnosis is limited by what we *expect* to see in people. And because those expectations are based around sighted people...

And while I do think there is some minor protection from developing schizophrenia for people born blind, I think this depends greatly on social conditions. Consider that blind people are usually isolated and alone. This makes blind people already vulnerable to potential psychoses. The fact that it doesn't present like "schizophrenia" doesn't mean its not happening, it means its not visible.

I should really stress here too that there is a lot of people who don't "present" as schizophrenic either who have serious delusions, who are able to regulate them to prevent requiring a diagnosis. So even in sighted people the diagnosis is already extremely shaky. A lot of the intersections between diagnoses have more to do with the criteria than the actual disorders themselves.

The problem is that I think that what we are starting to realize is that "schizophrenia" is based on sighted understanding of psychology - when we say "greater symptoms" we are assuming that the symptoms don't just manifest themselves in other ways - but we literally cannot know that, and psychiatry as it stands is not armed to solve the question, nor will it be able to properly adapt. As we analyze the differences between the different physical disabilities we will only fractionally divide how many different ways the mind can work. I should also point out that the benefit from the relational thinking that blind people employ is pretty situational and requires social support - if you're isolated and in a vacuum you're going to still spin out no matter how well you can adapt your reasoning, because you have no frame of reference.

This is the whole problem with the sensory deprivation tanks - not so much the loss of senses as the loss of connection with the outside world.

Reality is a social condition. When you disconnect from that social condition, you develop psychosis.

you like those kinds of gays because they're gays made for straights

2020-02-13 05:04:27

@10 she was born blind. or at least legally blind. also delusions, like hearing voices etc aren't all of the condition. it also involves paranoya and other symptoms depending on the person.

Who's that trip trapping over My bridge? Come find out.

2020-02-13 05:42:24

SirBadger, the issue is that we're talking about the totally blind here, people who have never experienced visual processing.

Daigonite, I hear what you're saying, but I'm not 100% convinced. You seem to be tending toward nurture over nature (i.e., bad thoughts and bad social situations make the brain screw with chemical makeup and so the disease is diagnosed inside out). I'm not saying you're flat wrong, but I don't think you're dead right either. I think there are still very good arguments on both sides. I mean, people who seem relatively well-adjusted can suddenly and almost inextricably end up in psychosis, so why would that be? I've no doubt that what you say regarding socialization and isolation has a lot of truth to it though. This sort of thing absolutely can and does make mental health worse. I am not, and never was, trying to reduce schizophrenia to something to be medicated and forgotten about, or to be hand-waved. But I think we turn it into a purely social disease at our peril. I think, in truth, that the social and chemical aspects work hand in hand, and can feed off of each other (i.e., if you start having symptoms, you may self-isolate and make things worse).

Check out my Manamon text walkthrough at the following link:
https://www.dropbox.com/s/z8ls3rc3f4mkb … n.txt?dl=1

2020-02-13 05:54:21

@11 - if she was able to see color then it probably doesn't count. Light perception maybe. And yes, schizophrenia is a range of symptoms. I think the other subtypes may just be underdiagnosed in blind people, I don't understand for example how paranoid schizophrenia has no pathway.

Daigonite, I hear what you're saying, but I'm not 100% convinced. You seem to be tending toward nurture over nature (i.e., bad thoughts and bad social situations make the brain screw with chemical makeup and so the disease is diagnosed inside out). I'm not saying you're flat wrong, but I don't think you're dead right either.

Not really. In fact, I acknowledge readily the material conditions (nature) of where these issues arise. However, I interpret what these material conditions mean. I don't believe in the essentialist idea that your brain starts out as a sort of "road map that develops". Your brain is a dynamic piece of hardware that is unpredictable - and this interpretation of "nature" is what I take objection to.

I think there are still very good arguments on both sides.

haha no. sorry but no

I mean, people who seem relatively well-adjusted can suddenly and almost inextricably end up in psychosis, so why would that be?

no offense but do you talk to people who have psychosis? The reason why this happens is because people are not going to tell people that they have serious psychosis unless they literally can't help themselves. Some people are naive and don't realize how they sound psychotic so people give them help earlier.

Many very creative people struggle with delusional thinking, they're just able to manage it. The idea of "function" hides disability like this.

I've no doubt that what you say regarding socialization and isolation has a lot of truth to it though. This sort of thing absolutely can and does make mental health worse. I am not, and never was, trying to reduce schizophrenia to something to be medicated and forgotten about, or to be hand-waved. But I think we turn it into a purely social disease at our peril. I think, in truth, that the social and chemical aspects work hand in hand, and can feed off of each other (i.e., if you start having symptoms, you may self-isolate and make things worse).

This doesn't actually address my criticism of chemicals though, that the observation of chemicals is post-hoc. I think you're reducing my argument somewhat - individuals are unique and predispose individuals to various types of interactions, making some people more vulnerable to schizophrenia than others - however, the vulnerability is caused by social effects which are what really should be addressed. Medications are simply a patch for these individual problems caused by this social issues. Like I have friends who are maxed out on drugs and are so vulnerable they have to very carefully take anything new or else they will literally start seeing demons - those drugs are gonna stop working one day. Yeah, real great fix. Read about felix guattari and schizo-analysis, while he never achieved his extremely ambitious goal, i think his work was in the right direction and has provided substantial work for disability related theory in general.

you like those kinds of gays because they're gays made for straights

2020-02-13 12:37:15

Greetings all.

Although I wasn't born blind, I did lose my sight when I was a few hours old because I was born premature. As for being a schizophrenic, I do believe that I am the psychiatric definition of a schizophrenic. I heard voices as though they were external ever since I could remember and when I was a child, they kept me up most nights. Sometimes the voices say words repeatedly and other times bits of music and frightening noises kept playing in my mind. No I was never diagnosed and my performance in both primary and secondary school was heavily affected. I know how it feels to hear multiple voices in your mind telling you not only how useless and worthless you are but to also cause harm to others. These voices cannot and will not be silenced by conventional means and medication is only a temporary solution. I also know how it feels when the demons watch you so they can pounce on you when you eventually do fall asleep and enter their realms.

You may therefor ask what solution did I find that works for me 100% of the time and I did find a solution with the help of Jehovah; the website on my profile is what has aided me from April 2017. If you look at my facebook page, I've written many posts attached to news articles regarding this and other topics. While I'd be foolish to deny science in the role of mental health, I won't restrict myself to it either because I definitely believe that schizophrenia is a spiritual affliction that can and does affect the brain chemically rather than it being only chemical in nature. Many of you would say that I hold to irrational beliefs but are they truly irrational when the end result of me having said beliefs is that I've been able to improve myself and to be at peace at long last?

Finally, I definitely believe that being totally blind or otherwise does not protect you from any kind of mental/emotional/spiritual disorder. I must admit to not liking reading those articles mentioned in post 1 and besides, I've never heard of anyone who believes in spirituality entering the mental health profession/field, nor have I ever heard of a blind or otherwise disabled individual go into said field either. Maybe they should and for once we can have someone who will be loving, kind, compassionate, merciful and forgiving to fellow sufferers. The mental health carer's manual, the paper on mental disorders related to but are not schizophrenia, the paper on how to cope with all mental disorders and how to ensure that life doesn't get so bad that you'd contemplate suicide, the DSM diagnostic statistics manual and what happens when love and compassion is taken out of the profession/field; the above articles will help in this endeavour. To sum up, I don't believe that whether or not you're blind from birth truly matters when it comes to any mental disorder, nor do I believe that any other disability affects whether or not you suffer from aforesaid mental disorders for that matter. I do however believe that the articles you referenced were written in ignorance and there wasn't anyone who were spiritualists that contributed to any of those articles. If there were then we could have a productive discussion. I did say earlier that I've never heard of any blind/disabled individual going into the mental health profession but I do know of at least one individual, counsellor Trina not her real name but the name she used on vorail who went into the profession as a Christian counsellor. She was the one who told me that there are some in the profession that do actually care about their patients and who do treat them with respect and dignity. Speaking of which, never under estimate the power of prayer or of true counselling.

Kind regards, Amin Abdullah.

2020-02-13 14:31:33

I coppied this from https://www.frontiersin.org/articles/10 … 00624/full and I've divided this into 2 posts.

THIS ARTICLE IS PART OF THE RESEARCH TOPIC
Visual Dysfunction in Schizophrenia: A View into the Mechanisms of Madness? View all 31  Articles





Suggest a Research Topic >
   
24,794
TOTAL VIEWS
HYPOTHESIS AND THEORY ARTICLE
Front. Psychol., 21 January 2013 | https://doi.org/10.3389/fpsyg.2012.00624
Cognitive and neuroplasticity mechanisms by which congenital or early blindness may confer a protective effect against schizophrenia
Steven M. Silverstein1,2*, Yushi Wang1 and Brian P. Keane1,2,3
1University Behavioral HealthCare, University of Medicine and Dentistry of New Jersey, Piscataway, NJ, USA
2Department of Psychiatry, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ, USA
3Rutgers University Center for Cognitive Science, Piscataway, NJ, USA
Several authors have noted that there are no reported cases of people with schizophrenia who were born blind or who developed blindness shortly after birth, suggesting that congenital or early (C/E) blindness may serve as a protective factor against schizophrenia. By what mechanisms might this effect operate? Here, we hypothesize that C/E blindness offers protection by strengthening cognitive functions whose impairment characterizes schizophrenia, and by constraining cognitive processes that exhibit excessive flexibility in schizophrenia. After briefly summarizing evidence that schizophrenia is fundamentally a cognitive disorder, we review areas of perceptual and cognitive function that are both impaired in the illness and augmented in C/E blindness, as compared to healthy sighted individuals. We next discuss: (1) the role of neuroplasticity in driving these cognitive changes in C/E blindness; (2) evidence that C/E blindness does not confer protective effects against other mental disorders; and (3) evidence that other forms of C/E sensory loss (e.g., deafness) do not reduce the risk of schizophrenia. We conclude by discussing implications of these data for designing cognitive training interventions to reduce schizophrenia-related cognitive impairment, and perhaps to reduce the likelihood of the development of the disorder itself.
Introduction
Over the past 60 years, several authors (Chevigny and Braverman, 1950; Abely and Carton, 1967; Horrobin, 1979; Riscalla, 1980; Feierman, 1982; Sanders et al., 2003) have postulated that congenital or early (C/E) blindness may serve as a protective factor against the development of schizophrenia. Supporting data derive from several sources, including literature reviews, examination of cohorts of blind patients in psychiatric hospitals, and surveys of agencies that treat large numbers of blind people. The most recent of these Sanders et al. (2003) noted that across all past papers, there has not been even one reported case of a congenitally blind person who developed schizophrenia. While we identified one reported case of a blind “schizophrenic” child (Stewart and Sardo, 1965), the 6-year-old described in that paper had many symptoms of autism and no symptoms of psychosis, and would almost certainly be diagnosed with an autism-spectrum disorder using DSM-III (American Psychiatric Association, 1980) or later criteria. In contrast to the lack of cases of people with C/E blindness who meet modern criteria for schizophrenia, reports do exist of people who develop both blindness and schizophrenia later in life (Checkley and Slade, 1979). We therefore hypothesize that it is the brain changes that occur secondary to C/E blindness – rather than blindness per se – that protect against schizophrenia. However, the mechanisms that confer this apparent protection have not yet been identified. In this paper, we advance the hypothesis that protection occurs by (1) strengthening the perceptual and cognitive functions whose impairment forms the essential nature of schizophrenia; and (2) constraining cognitive processes that are excessively neuroplastic in the illness.
In the discussion below, after briefly summarizing the position that schizophrenia is fundamentally a cognitive (i.e., information-processing) disorder, we review evidence that a cluster of perceptual and cognitive functions is at once markedly impaired in schizophrenia and significantly augmented in C/E blindness, compared to healthy sighted individuals (see Table 1). In subsequent sections, we explicate the role of neuroplasticity in driving these perceptual and cognitive differences, we provide evidence that C/E blindness does not confer protection against other mental disorders (e.g., depression, anorexia nervosa) and finally we argue that other forms of C/E sensory loss (e.g., deafness) do not reduce the risk of schizophrenia. We conclude by noting the implications of these data for designing cognitive training interventions for patients and people at high risk for the disorder, and for developing interventions to prevent schizophrenia.
TABLE 1
www.frontiersin.org
Table 1. Summary of cognitive and brain function enhancements (+) and impairments (−), compared to healthy sighted individuals, in C/E blindness and schizophrenia.
Schizophrenia as a Cognitive Disorder: Kraepelin and Dementia Praecox Revisited
Although the most obvious clinical features of schizophrenia include psychotic symptoms such as hallucinations, delusions, and bizarre behavior, it has long been thought that such symptoms are secondary, compensatory, features of the disorder. In contrast, much evidence suggests that the core features of schizophrenia are cognitive in nature, involving disturbances in perception, attention, memory, learning, language, and context-based modulation of these processes as a function of expectations and action plans (Kraepelin, 1903; Bleuler, 1950; Weiss, 1989; Phillips and Silverstein, 2003; Nuechterlein et al., 2012; Tamminga, 2013; Khan, in press). In this way, schizophrenia can be viewed as similar to brain disorders such as Parkinson’s disease dementia and dementia with Lewy bodies, in which psychotic symptoms can occur, but are often late-developing phenomena, and are not considered the defining features of the disorder (Ballard et al., 2001; Williams-Gray et al., 2006; Ffytche, 2007). A large body of research evidence now indicates that perceptual and cognitive impairments are found in nearly all people with schizophrenia, and occur with greater frequency than psychotic symptoms (Palmer et al., 2009). Significant cognitive impairment is also easily detectable in most schizophrenia patients even when psychotic symptoms are in remission (Altshuler et al., 2004). In addition: (1) low intelligence is a risk factor for schizophrenia; (2) cognitive decline and intellectual underperformance precede the onset of psychotic symptoms (and therefore the diagnosis) by many years; (3) decline in cognitive functioning continues after psychosis onset; and (4) this pattern of changes is not found in other major mental illnesses, even those that can include psychotic symptoms, such as bipolar disorder (Neumann et al., 1995; Schenkel and Silverstein, 2004; Khan, in press). Cognitive impairments in schizophrenia are also significantly correlated with level of functional disability (Green, 1996; Silverstein et al., 1998), and are therefore important treatment targets.
Domains of Perceptual and Cognitive Functioning that are Strengthened by C/E Blindness and Impaired in Schizophrenia
Auditory Perception
Compared to sighted people (and in some cases to late-blind people), C/E blind individuals are characterized by enhanced auditory acuity for pitch, better pitch discrimination, better pitch-timbre categorization (Wan et al., 2010), better speech discrimination (Hertrich et al., 2009), better sound localization, better temporal auditory resolution, better noise-embedded speech discrimination (Niemeyer and Starlinger, 1981; Muchnik et al., 1991), lower sound threshold for identification of pseudo-words (Rokem and Ahissar, 2009), shorter latencies for auditory event-related potentials (ERPs; Roder et al., 1996, 1999), and greater tolerance for short stimulus-onset asynchronies in an auditory backward masking task (Stevens and Weaver, 2005). C/E blindness is also associated with comprehension of ultra-fast synthetic speech at a rate of ∼25 syllables per second, which is close to three times the rate at which non-blind individuals can comprehend such speech (Hertrich et al., 2009). In addition, C/E blind subjects have shown larger mismatch negativity (MMN) components of the ERP, suggesting a compensatory improvement in pre-attentional processes (Kujala et al., 1995). It has been demonstrated that these sensory and perceptual processing differences are due to enhanced basic perceptual skills, not to “higher order” functions such as attention, memory, language, or executive functions (reviewed in Cattaneo and Vecchi, 2011).
The above findings are in contrast to what has been observed in schizophrenia, in which, for example, patients are typically characterized by poor auditory acuity, precision, and discrimination (including in tone matching) (Javitt et al., 1997; Rabinowicz et al., 2000; Li et al., 2002; Rojas et al., 2007; Turetsky et al., 2009; Perrin et al., 2010; Kantrowitz et al., 2013), impairments in sound localization (Perrin et al., 2010), temporal resolution of sound (Foucher et al., 2007), auditory backward masking (Kallstrand et al., 2002), pre-attentional processing as indicated by the (smaller) MMN ERP component (Umbricht et al., 2003), and longer latency of post-attentional auditory ERPs (Ward et al., 1991; Sevik et al., 2011; Iyer et al., 2012). Individuals with schizophrenia also have abnormal processing of speech sounds (Ngan et al., 2003; Hirano et al., 2008), are worse than other groups at detecting speech embedded in noise, and are more likely than controls to identify non-speech sounds as speech (Vercammen et al., 2008). Importantly, it has been shown that these impairments in pitch processing in schizophrenia are not secondary to symptoms, medication, or poor attentional functioning (Rabinowicz et al., 2000).
The impaired auditory functions noted above are not mere laboratory curiosities; they have important clinical and functional implications. For example, poor sound localization is thought to be associated with an externalization bias in which there is a reduced ability to recognize that the sound of one’s own voice is coming from the self, as opposed to an external cause, which may contribute to delusional thinking (Johns et al., 2001; Ilankovic et al., 2011). At a more general level, perception has been conceptualized as an active, hypothesis-generating function that involves generating a model of the world, and then updating this model via coding of prediction error (i.e., the degree to which continued incoming sensory input does not conform to the current perceptual model of the world; Corlett et al., 2009; Clark, in press). It has been postulated that symptoms of schizophrenia, such as hallucinations and delusions may result from an impaired ability to detect inconsistencies between what would normally be expected (based on past experience) and incoming sensory information (Corlett et al., 2007, 2009; Clark, in press). Both faulty bottom-up processing and poor quality top-down feedback, as have been demonstrated in schizophrenia (Silverstein and Keane, 2009, 2011a,b), would degrade the quality of perceptual representations and the extent to which they are modified by context to most accurately reflect the nature of reality (Corlett et al., 2007, 2009; Clark, in press; Silverstein, in press). The result can be abnormal perceptions, hypersalience of normally ignored stimuli, and new and unusual beliefs to account for these changes in subjective experience – in short, an internal representation of the world that can deviate markedly from reality, and increasingly so over time (Clark, in press). In contrast, as C/E blindness is associated with enhanced sensory and perceptual processing, it can be seen how this would reduce the likelihood of the sort of prediction coding failures, and their sequelae, associated with schizophrenia. The auditory impairments in schizophrenia described above have also been shown to have other important consequences, which would not occur in people with C/E blindness, such as problems decoding cues to emotion in speech (Leitman et al., 2011; Gold et al., 2012) and impaired semantic analysis (Leitman et al., 2007).
Auditory Attention
Blindness has been associated with enhancements in several components of attention that are impaired in schizophrenia. For example, on reaction time tasks, blind subjects are superior to sighted individuals in responding to auditory and tactile cues (Collignon and De Volder, 2009). On tactile and auditory selective attention tasks involving spatial discrimination, blind people are more efficient than sighted subjects (Roder et al., 1996, 1999; Hotting and Roder, 2004; Collignon et al., 2006). Since these studies demonstrated that blind and sighted participants did not differ in sensory sensitivity on these tasks, these findings appear to reflect superior attentional capabilities (Cattaneo and Vecchi, 2011), although teasing apart attentional and perceptual deficits is often difficult. Blindness is also associated with superior performance on tasks of divided attention, such as dichotic listening (Hugdahl et al., 2004), and tasks requiring dividing attention across more than one sensory modality (Kujala et al., 1995). Again, such a pattern of performance contrasts sharply with what has been long been observed in schizophrenia, namely, severely impaired selective and divided auditory attention (Bleuler, 1950; Green et al., 1994; Heinrichs and Zakzanis, 1998; Bruder et al., 1999; Light and Braff, 2005a,b; Scholes and Martin-Iverson, 2010). In short, the improvements in sensory, perceptual, and attentional auditory functioning in C/E blindness represent changes that appear to essentially eliminate the possibility of the development of the set of auditory impairments and their consequences that form an important component of schizophrenia.
Working and Long-Term Memory
Compared to healthy, sighted individuals, C/E blind individuals have superior working memory capacity, in terms of both the amount that can be processed, and the ability to recall the sequence in which information was presented (Hull and Mason, 1995; Amedi et al., 2003; Roder and Neville, 2003; Raz et al., 2007). The authors of a recent study that matched perceptual threshold of blind and sighted subjects concluded that superior short-term memory in C/E blind people was due to enhancement of stimulus encoding (related to the processes reviewed above), rather than to differences in storage or recall processes (Rokem and Ahissar, 2009). In addition, it is thought that, in C/E blindness, primary reliance on controlled, sequential processes (i.e., via haptic and auditory perception) during navigation – as opposed to the more automatic and parallel processing normally afforded by vision – leads to superior working memory abilities (Raz et al., 2007; Salillas et al., 2009; Cattaneo and Vecchi, 2011). C/E blind people have also demonstrated superior long-term memory compared to sighted controls (Bull et al., 1983; Roder et al., 2001). All of this is in stark contrast to schizophrenia, in which working memory (Silver et al., 2003; Conklin et al., 2005; Brahmbhatt et al., 2006; Horan et al., 2008; Silverstein et al., 2010) and long-term memory (Van Snellenberg, 2009) impairments are typically observed, along with problems in stimulus organization during encoding (Harvey et al., 1986; Brebion et al., 1997, 2004; Landgraf et al., 2011).
These data have important clinical implications. A critical function of WM is to integrate perceptual information with information stored in long-term memory, to allow for efficient learning, memory, and reasoning (Cattaneo and Vecchi, 2011). Enhanced WM abilities would thus facilitate these other processes, as is the case in C/E blindness (Cattaneo and Vecchi, 2011), whereas impairment would have the opposite effect, as is the case in schizophrenia (Tek et al., 2002). Thus, it can again be seen how C/E blindness could protect against development of the cognitive impairments that comprise the syndrome of schizophrenia.
Language
Congenital or early blind children often experience language delays and abnormalities related to semantic, syntactic, and phonological processing (Perez-Pereira and Conti-Ramsden, 1999). One possible consequence of these is a reduction in the risk of developing disordered thought, which is commonly seen in schizophrenia. For example, many thought-disordered patients with schizophrenia have a tendency toward overabstraction and overinclusion in their thinking, as well as overly elaborated (and more easily primed) semantic networks (Siekmeier and Hoffman, 2002; Lerner et al., 2012). In addition, compared to healthy controls, individuals with schizophrenia more often use language in odd ways, including generating neologisms (i.e., novel words; Solovay et al., 1987; Kreher et al., 2008). In contrast, it has been shown that compared to sighted children, blind children are characterized by a lack of overgeneralization of concepts and categories, and a reduced number of word inventions (Andersen et al., 1984, 1993). It has also been shown that semantic networks in blind children are more dependent on language, and less dependent on sensory experience, than sighted children (Pring, 1988). This could be a protective factor against delusion formation secondary to altered sensory experience, as has been hypothesized to exist in schizophrenia (Maher, 1974; Uhlhaas and Mishara, 2007).
Olfaction
Cuevas et al. (2009) demonstrated that congenitally blind males were better at discriminating odors, and at naming familiar odors, compared to sighted subjects. Other studies have reported mixed results, for example, demonstrating superior odor identification but not odor sensitivity (Wakefield et al., 2004). However, studies with mixed findings have grouped early blind and late-blind subjects together, and did not match groups on gender (women are typically better than men at olfaction tasks; Cattaneo and Vecchi, 2011). While more research is needed on this issue, evidence does suggest that people born blind may develop increased olfactory abilities (Kupers et al., 2011). This is in contrast to people with schizophrenia, in which olfactory impairments have been reported (Nguyen et al., 2010; Kamath et al., 2011). Although the functional consequences of olfactory impairment in schizophrenia are not well understood, such deficits could impair self-regulation, learning, attachment, and interpersonal functioning (see Sullivan, 2003). For example, the detection of maternal odor can promote attachment to the mother, reduce stress, and help normalize the sleep-wake cycle in infants (Goodin-Jones et al., 1997; Sullivan and Toubas, 1998). In addition, odor perception is important in forming bonds with peers in childhood (Sullivan, 2000). It is therefore interesting that risk for schizophrenia is associated with problems in maternal attachment (demonstrated at 3 days, 1, and 6 years of age; Naslund et al., 1984; Persson-Blennow et al., 1984; McNeil and Kaij, 1987), increased stress reactivity (Myin-Germeys and van Os, 2007), and fewer peer relationships (Schenkel and Silverstein, 2004), as well as olfactory processing deficits (Brewer et al., 2003).
Construction of Subjective Experience
In this section, we discuss: (1) differences between people who are C/E blind and people with schizophrenia with regard to the relative importance of parallel versus serial data acquisition in the generation and quality of subjective experience; and (2) the role that preservation of a form of visual imagery in C/E blindness may play in the integration of experience. As noted above, C/E blind people rely to a much greater extent than sighted people on serial processing due to primary reliance on haptic and auditory processing, and lack of visual input. That is, due to the temporal-sequential nature of data acquisition about objects in auditory and haptic perception, the relatively smaller amounts of information available at any one time in haptic perception compared to vision (Barber and Lederman, 1988; Amadeo and Speicher, 1995; Herssens, 2010), and the more rapidly changing nature of information flow in audition relative to vision (Shamma et al., 2011), formation of coherent mental representations in haptics and audition requires that information must be “built up” over time to a greater extent than in vision (Geenens, 1999). One result of this imposed learning style is that C/E blind individuals develop abilities in sequential and controlled processing that may be superior to those of sighted people (Vecchi et al., 2004; Raz et al., 2007). In addition, as we argue below, compensatory processes involving working memory capacity, perceptual organization via controlled processing, multisensory integration, learning, and a preserved form of visual imagery lead to a rich, seemingly automatic, and non-fragmented flow of experience (see Cattaneo et al., 2008; Salillas et al., 2009 and above; Cattaneo and Vecchi, 2011). In contrast, in schizophrenia, impairments in working memory capacity, perceptual organization, and multisensory integration, which develop long after birth and for which there appear to be no compensation, contribute to an over-reliance on serial processing that is often inefficient, and that can lead to fragmented subjective experience (Chapman, 1966; Knight, 1984; Carr and Wale, 1986; Knight and Silverstein, 1998; Silverstein and Keane, 2011a). This is illustrated in the following quote from a person with schizophrenia: “Everything I see is split up. It’s like a photograph that’s torn in bits and put together again. If somebody moves or speaks, everything I see disappears quickly and I have to put it together again” (Chapman, 1966, p. 229).
Interesting examples of how blind individuals construct mental representations incrementally via haptic perception come from Helen Keller’s (1908) book The World I Live In; her descriptions also illustrate how this process can be facilitated by prior knowledge and augmented with imagery. For example, she noted: “My fingers cannot, of course, get the impression of a large whole at a glance; but I feel the parts, and my mind puts them together” (p. 7). Similarly: “My hand has its share in this multiple knowledge, but it must never be forgotten that with the fingers I see only a very small portion of a surface, and that I must pass my hand continually over it before my touch grasps the whole. It is still more important, however, to remember that my imagination is not tethered to certain points, locations, and distances. It puts all the parts together simultaneously as if it saw or knew instead of feeling them.” (pp. 28–29). It is true of course that vision also incrementally builds distal representations, viz, through saccades or shifts in attention (Ullman, 1984), but because this process is not limited by the speed of grasping and reaching, it plausibly occurs over a much shorter time scale, lessening the load on working memory. In short, while C/E blindness is characterized by a greater than normal reliance on serial processing, compensatory processes lead to superior serial processing abilities and to integrated subjective experience.
In addition, we speculate that a preserved form of visual imagery is involved in the spatial integration abilities of C/E blind people. A reasonable amount of evidence supports the presence of imagery in C/E blindness, including: (1) visual cortex areas are activated by input from other senses in blind and non-blind people (Amedi et al., 2001, 2002; Ortiz et al., 2011); (2) the occipital lobe helps generate mental representations even when there has been no prior visual input (Amedi et al., 2008); (3) after training with tactile stimulation, blind people reported visual qualia, and the extent of these reports were related to ERP activity in the lateral occipital complex (Ortiz et al., 2011); (4) C/E blind people have visual content in their dreams, and can draw it, and the extent of their dream imagery is negatively correlated with EEG alpha band power, just as it is in sighted individuals (Bertolo et al., 2003); (5) C/E blind people report visual imagery (Cornoldi et al., 1979; Zimler and Keenan, 1983), although this is reduced, and more verbally mediated, compared to sighted people (Cornoldi et al., 1979); (6) however, spatial representation is not completely verbally mediated in blind people; during the encoding and working memory maintenance phases of a haptic mental rotation task, both sighted and blind subjects demonstrated increased parietal activation (as demonstrated in ERP data; Roder et al., 1997); (7) spatial images are supramodal, in that they are not simply the sum of modality-specific inputs; (8) there are several characteristics of visual experience, such as size, contour, and edge information, shape and texture that can be perceived through touch, and blind people can generate visual representations of haptically explored objects (reviewed in Cattaneo et al., 2008; Cattaneo and Vecchi, 2011); (9) vision and haptics may share common representations (Aleman et al., 2001); and (10) both the dorsal and ventral pathways are thought to contain supramodal regions to code shape and location of objects, respectively, regardless of the nature of the sensory input (Pietrini et al., 2009). We suggest, based on the quotes cited above, and others in the literature, that these “visual” experiences and supramodal representations aid in integrating subjective experience in C/E blindness. However, direct evidence for this claim has not yet been reported.
C/E Blindness is Protected from Negative Developmental Effects of Visual Processing Impairments
Vision allows for the simultaneous perception of a great deal of information, and therefore for attention to be spread over many stimuli, or to be switched between stimuli. In schizophrenia, with its related sensory gating deficits, this can lead to the experience of being flooded with stimuli, and of stimuli being more intense than usual (Carr and Wale, 1986). In contrast, blindness is associated with touch as the primary method of exploring the environment. The nature of haptic perception is such that the person can only attend to the object currently being touched, and in this way attention cannot be involuntarily drawn to other objects (unless there are auditory or olfactory cues to other objects; Cattaneo and Vecchi, 2011).
Of course, we are not saying that vision is, by itself, a risk factor for schizophrenia. However, in combination with sensory gating, perceptual organization, and working memory impairments, visual processing, with its parallel inputs, may contribute to sensory flooding and subsequent disorganized cognition and behavior in schizophrenia. That is, visual impairment may be a risk factor for schizophrenia, not only in being reflective of abnormal neural development but also by being a cause of it. Conversely, C/E blindness may exert its protective effects against schizophrenia, in part, by preventing the possibility of abnormal visual input. Evidence consistent with this comes from several sources, including: (1) visual dysfunction in children of mothers with schizophrenia predicts the later development of schizophrenia (Schubert et al., 2005); (2) children (regardless of parental history) who later developed schizophrenia-spectrum disorders had significantly higher eye exam scale and strabismus scale scores compared to children who developed other non-psychotic psychopathology and children who did not develop a mental illness, while functioning in other sensory domains was far less impaired (Schiffman et al., 2006); and (3) the high specificity of visual abnormalities for predicting transition to schizophrenia among at-risk youth (Klosterkotter, 1992). In all of these cases, even if the presence of visual dysfunction is a reflection of the diathesis for schizophrenia rather than a primary cause of it, the continued state of abnormal visual input may lead to further perceptual and cognitive problems throughout development that increase the risk of developing the full-blown disorder.
Impaired visual functioning may also compromise multisensory integration, which, in turn, may lead to other cognitive deficits in schizophrenia. Efficient integration of different sensory inputs requires remapping these into an external spatial reference frame (Roder et al., 2007), which requires normal vision to properly develop (Collignon et al., 2009). However, in schizophrenia, there are multiple visual processing impairments (e.g., in gain control, perceptual organization, motion perception, etc.; Butler et al., 2008). Multisensory integration is also impaired in schizophrenia (Williams et al., 2010), and it is thought that deficits in visual processing contribute to this (Landgraf et al., 2012). In contrast, blind people appear to rely on somatotopic spatial coordinates as opposed to external, visual, coordinates (Roder et al., 2004). Therefore, in contrast to schizophrenia, in C/E blindness, the primary sense used to create a reference frame for multisensory integration (i.e., touch) is associated with superior perceptual abilities compared to sighted people.
Blind people rely primarily on vestibular and somatosensory feedback for motor control. This leads to enhanced voluntary motor control and motor-kinesthetic processing (Deutschlander et al., 2009). In contrast, schizophrenia is associated with impaired motor control (Cortese et al., 2005; Putzhammer and Klein, 2006; Velasques et al., 2011), and it has been hypothesized that this could be related to passivity phenomena and the development of delusions of control (e.g., the belief that one is not the agent of one’s own actions, and/or that an external entity is controlling one’s thoughts and/or actions; Danckert et al., 2004). Abnormalities in movement have also been observed in people at high risk for schizophrenia (Mittal et al., 2008). Therefore, the enhanced development of motor control and kinesthetic processing in C/E blindness can be viewed as protective against these schizophrenia-related symptom formation processes.
Finally, it has been recently proposed that visual processing disturbances in individuals at-risk for schizophrenia may contribute to the later development of the disorder by causing impairments in body perception, involving the senses of “ego boundaries,” body ownership, body agency, and sense of self in space. These phenomena may then lead to problems in sense of identity, and in awareness of symptoms and insight into illness (Landgraf et al., 2012). Body ownership and agency can be measured experimentally with the “rubber hand illusion” (Ehrsson et al., 2004). In this paradigm, subjects have the experience that they are touching their own right hand with their left index finger, when in reality they are touching a rubber hand with their left index finger while the experimenter touches their right hand in a synchronized manner. This effect is enhanced in schizophrenia and is thought to reflect abnormal body perception including a reduction in sense of body ownership (Thakkar et al., 2011). In contrast, in people with C/E blindness, the illusion is not experienced (Petkova et al., 2012). These results have been interpreted as indicating that C/E blind people have a more veridical perception of self-touch, along with a less flexible and dynamic representation of their own body in space compared to sighted individuals (Petkova et al., 2012). We believe that this reduced flexibility in dynamic representation of the body, secondary to loss of vision, is a protective factor against the body perception abnormalities associated with schizophrenia that were noted above.
Neuroplasticity
In this section we review evidence on how and where in the brain changes occur in response to C/E blindness, and how these subserve the changes in cognitive functioning discussed above. There is a large literature on brain plasticity in blind people, including evidence for developmental crossmodal plasticity (see below) – where areas of the occipital lobe are recruited for auditory and haptic perception (see Cattaneo and Vecchi, 2011 for a review), and also for olfaction (Kupers et al., 2011). Beyond this, however, other changes in developmental intramodal plasticity can occur which appear to result in perceptual and cognitive abilities that are opposite to those found in schizophrenia. For example, a magnetic source localization study (Elbert et al., 2002) indicated that dipoles associated with processing low- and high-frequency tones were more distant in blind people than in sighted subjects, suggesting an expansion of regions in the auditory cortex, supporting the superior pitch discrimination abilities noted above. Further evidence for intramodal plasticity in blind individuals is reduced hemodynamic responses to auditory stimulation in comparison to sighted subjects, which is thought to reflect increased efficiency in auditory signal processing within the temporal lobe, in light of the generally superior auditory processing abilities in this population (Stevens and Weaver, 2009). Evidence for changes regarding haptic perception comes from findings of reduced accuracy in identifying which finger is touched during a sensory threshold task (Sterr et al., 1998, 2003), within the context of overall superior tactile perception (Wong et al., 2011). These data suggested altered cortical representations for touch in the sense that the cortical representations of individual fingers are “fused” together due to their simultaneous use during Braille reading. Moreover, these data are strongest for the hand used to read Braille, and do not generalize to other body parts that are not used for reading, such as lips. Of note, the “holistic” processing of Braille letter patterns and reduced precision of individual finger-level input is in contrast to what is often observed in the visual processing of people with schizophrenia, where processing of holistic visual patterns is impaired, sometimes with enhanced processing of individual visual details (reviewed in Uhlhaas and Silverstein, 2005; Silverstein and Keane, 2011a).
Developmental crossmodal plasticity can lead to superior performance compared to sighted subjects, and there are several interesting instances of this relevant to schizophrenia. For example, somatosensory and auditory ERP data from oddball and MMN tasks (which involve detection of a deviation from a sequential pattern in an attended or unattended sequence of stimuli, respectively), indicate normal ERP amplitude, with more activity over the occipital cortex in blind subjects, and enhanced pre-attentional processing in blind compared to sighted subjects (Kujala et al., 1995; Roder et al., 1996). This is in marked contrast to abnormal ERP amplitudes during oddball and MMN tasks in people with schizophrenia (e.g., Kayser et al., 2001) as noted above. Aside from developmental neuroplasticity, other ERP data from oddball tasks in people with schizophrenia suggested reduced short-term neuroplasticity. For example, when people with schizophrenia are presented with a high-frequency sequence of individual auditory stimulations, their ERP signatures reveal abnormally reduced long-term potentiation (Mears and Spencer, 2012). In contrast, short-term neuroplasticity, at least involving the occipital cortex, may be greater in people with C/E blindness (De Volder et al., 1999).
A major focus of research on visual processing in schizophrenia is impaired functioning in the dorsal and ventral visual streams. Therefore, we briefly summarize evidence that, in contrast to what is observed in schizophrenia, functioning in these pathways is intact in C/E blindness, despite the absence of visual input. Much evidence suggests that the dorsal stream is specialized for determining where an object is and for guiding action, whereas the ventral stream is specialized for analyzing form and color for determining what an object is (Goodale, 1993; Goodale et al., 2005). Many studies indicate impaired functioning of both of these streams in schizophrenia (e.g., King et al., 2008; Silverstein et al., 2009; Sehatpour et al., 2010; Lalor et al., 2012; Plomp et al., 2012). Surprisingly, these pathways appear to subserve similar functions in blind people as they do in psychiatrically healthy sighted people, suggesting that they can develop even in the absence of visual experience, and therefore that their representations are supramodal (Cattaneo and Vecchi, 2011; Ptito et al., 2012). For example, during spatial imagery tasks using auditory or tactile stimuli, early blind and sighted individuals demonstrated similar dorsal stream and frontal eye field activation, as assessed via PET or fMRI (Vanlierde et al., 2003; Garg et al., 2007; Bonino et al., 2008). In addition, dorsal areas devoted to processing motion information in sighted people (e.g., V5/MT) are employed in blind people in response to tactile and auditory motion cues (e.g., Ptito et al., 2009; Bedny et al., 2010; Matteau et al., 2010). These areas are notably underactivated during perception of visual motion in schizophrenia, in the context of impaired motion perception (Chen, 2011). In the ventral stream, blind subjects demonstrated similar activation during tactile object perception to that shown by sighted subjects during visual and haptic exploration of the same objects (Pietrini et al., 2004; Ptito et al., 2012).
It should be noted that while occipital lobe activity can occur in sighted subjects during tactile and auditory processing tasks, this has been found to be due to visual imagery (Sathian, 2005), which activates early visual cortex areas in a retinotopic fashion (Slotnick et al., 2005), and to calibration of head-centered sound localization (Zimmer et al., 2004). In contrast, occipital cortex activity in C/E blind subjects appears to support actual non-visual stimulus processing, and to represent a true crossmodal reorganization (see Roder et al., 1997; Cattaneo and Vecchi, 2011 for a review). Consistent with this, transcranial magnetic stimulation (TMS), applied to the occipital cortex, disrupts Braille reading ability in blind individuals, but not in sighted individuals, whereas the reverse is true when TMS is applied over the somatosensory cortex in the parietal lobe (Cohen et al., 1997). Similarly, TMS over the occipital cortex induces tactile sensations in blind readers’ fingers, but only phosphene perception for sighted subjects (Ptito et al., 2008).
As noted above, schizophrenia patients have demonstrated olfactory deficits in several studies, while C/E blind individuals have demonstrated superior olfactory abilities. A recent study, comparing congenitally blind subjects to blindfolded sighted controls, demonstrated that this is due to enhanced processing in areas normally dedicated to olfaction (e.g., amygdala, hippocampus) and in multiple regions of the occipital cortex (Kupers et al., 2011). This is further evidence of both the supramodal nature of representations in the C/E visually deprived occipital lobe, and also of crossmodal plasticity in C/E blindness.
In addition to subserving enhanced non-visual sensory processing, fMRI data indicate that the occipital lobe in C/E blind individuals also supports syntactic and semantic (more so than phonological) aspects of language processing (Roder et al., 2002; Burton et al., 2003), as well as verbal memory, episodic memory, and verbal fluency (Amedi et al., 2003; Raz et al., 2005), all of these being processes that are impaired in schizophrenia (Tendolkar et al., 2002; Fisher et al., 2009; Costafreda et al., 2011). For example, in addition to occipital lobe activation during memory retrieval, and a correlation between occipital activation and episodic memory in blind but not sighted subjects (Raz et al., 2005), repetitive transcranial magnetic stimulation (rTMS) over the occipital lobe impaired performance in a verb generation task for blind but not sighted subjects (Amedi et al., 2004).
Another consequence of blindness may be increased communication between brain regions. Several studies have demonstrated increased effective connectivity between the occipital lobe and temporal and prefrontal regions in early blind individuals (e.g., Noppeney et al., 2003; Leclerc et al., 2005). This is in contrast to schizophrenia, where reduced connectivity is typically found (e.g., Kim et al., 2008; Dima et al., 2009, 2010), including between occipital and temporal and frontal regions (Rigucci et al., 2012).
Finally, Sanders et al. (2003), based on evidence of visual cortex plasticity in dark-reared animals (Chen and Bear, 2007; Chen et al., 2007), proposed that an effect of early blindness is increased NMDA-receptor activity (although accompanied by reduced numbers of receptors) in visual cortex, and in regions with which this has many connections, primarily the anterior cingulate cortex (ACC), which is involved in resolving response competition and context sensitivity, two cognitive domains that are impaired in schizophrenia (Cohen and Servan-Schreiber, 1992; Dolan et al., 1995; Phillips and Silverstein, 2003). Moreover, schizophrenia has been characterized by NMDA-receptor hypofunction (Phillips and Silverstein, 2003), and, in numerous studies, by ACC hypoactivation (Dolan et al., 1995). The consequences of NMDA-receptor hypofunction in schizophrenia have been hypothesized to include impairments in sensory gating, perception, working memory, learning, and the full range of positive and negative symptoms (Phillips and Silverstein, 2003; Coyle, 2012). Therefore, an increase in NMDA-receptor activity in C/E blindness could have widespread positive effects on cognition, and protective effects against symptoms.
In short, there are several ways in which the neuroplasticity that results from C/E blindness results in changes that are opposite to those observed in schizophrenia, and that may represent protective effects. Specifically, the evidence reviewed above suggests that, in C/E blindness: (1) despite the loss of visual input, cortical reorganization during early development leads to accurate form and space perception (via auditory and tactile processing) which is supported by brain areas that function abnormally in schizophrenia (e.g., dorsal and ventral visual streams); (2) this developmental plasticity also leads to use of occipital areas for functions such as preattentive processing (e.g., as reflected in the MMN), language, memory, and olfaction – all of which are impaired in schizophrenia – which may underlie the superior functioning in those areas in C/E blindness reviewed above; and (3) in addition to these sequelae of developmental plasticity in C/E blindness, there is also evidence of normal later-onset plasticity, which may in part reflect prolonged plasticity of the occipital cortex in C/E blindness (De Volder et al., 1999), and which is the basis for the success of sensory substitution devices (Ward and Meijer, 2010). In contrast, later-onset plasticity has been shown to be reduced in schizophrenia in several domains (Fitzgerald et al., 2004; Oxley et al., 2004; Daskalakis et al., 2008; Hasan et al., 2011, 2012; Mears and Spencer, 2012).
Congenital or Early Blindness is Not Protective Against Mental Disorders in General
While C/E blindness may protect against schizophrenia, they do not protect against mental illness in general. A range of mental and behavioral disorders has been reported in blind people. For example, anxiety levels have been reported to be higher in congenitally blind than sighted adolescents (Bolat et al., 2011), and autistic symptoms and autism are common in blind children (Keeler, 1958; Wing, 1969; Chess, 1971; Chase, 1972; Fraiberg, 1977; Rogers and Newhart-Larson, 1989; Brown et al., 1997; Ek et al., 1998; Carvill, 2001). Sharp (1993) reported a case of anorexia nervosa and depression in a woman blind since the age of 9 months. A recent case study (Kocourkova et al., 2011) described a case of an adolescent patient, blind from early childhood, who showed symptoms of anorexia, depression, suicidal behavior, and self-harming. A conclusion in this report was that body image is a mental construct that is not dependent on sensory perception. Finally, Musial et al. (2007) reported a case of arachnophobia in a congenitally blind person, suggesting that visual cues are not necessary for the development of phobic disorders.
Congenital Deafblindness is Not Protective Against Schizophrenia
Protective effects of blindness may not exist if other forms of severe sensory loss are present. For example, congenital deafblindness is associated with elevated rates of psychosis, as well as mental retardation (Dammeyer, 2011). Also, children with Usher syndrome, in which people are typically deaf from birth and then develop retinitis pigmentosa leading to blindness in childhood, has been associated with psychotic symptoms and schizophrenia (Dammeyer, 2012). The reason why adding deafness to blindness removes the apparent effect of the latter against schizophrenia is not clear at present. One possibility is that blindness by itself presents a surmountable challenge to cope with the environment and thereby fosters compensatory sensory, perceptual, and cognitive changes that lead to a surprisingly high level of functioning. Deafblindness, on the other hand, may so seriously restrict the opportunity for environmental interaction that it also stunts the development of cognitively based coping strategies. For example, congenital deafblindness typically leads to significant delays in achieving several cognitive milestones, and to profound impairments in speed of processing, the ability to integrate disparate items of information, attention, communication, and the capacity for symbolic understanding and expression (Geenens, 1999; Bruce, 2005; Shamma et al., 2011). It is worth noting here that although C/E blindness and C/E deafblindness are both relatively rare, there are no published cases of the former being comorbid with schizophrenia, whereas there are many reported cases of this comorbidity with the latter.
Sensory Loss in General Does Not Protect Against Schizophrenia
Another important consideration is that sensory loss per se does not protect against schizophrenia. For example, deafness occurs in schizophrenia at as high a rate as in the general population (Kitson and Fry, 1990), and congenital deafness is a risk factor for the development of psychotic symptoms (Thewissen et al., 2005; Atkinson, 2006), including, interestingly, higher rates of visual and somatic hallucinations than are found in the non-deaf people with schizophrenia (Cutting, 1985), which often co-occur with reports of hearing voices (Du Feu and McKenna, 1999). And, while deafness may be associated with compensatory cognitive changes (see Bross, 1979; Dye and Bavelier, 2010; e.g., heightened attention to visual peripheral cues in people who use sign language; Proksch and Bavelier, 2002), these appear to not protect against schizophrenia, although they may lead to subtle differences in profiles of cognitive impairment between deaf and hearing people with schizophrenia (Horton and Silverstein, 2007, 2011). Moreover, in some cases, compensatory changes may not develop until adulthood (Rettenbach et al., 1999).
Mediating Biological Variables
The hypothesized protective effects of blindness on schizophrenia may be mediated by other factors. For example, Horrobin (1979) proposed that abnormal pineal gland function and resulting prostaglandin activity are etiological factors in schizophrenia. This is supported by evidence of increased inflammation and reduced melatonin levels in schizophrenia patients (Anderson and Maes, 2012; Muller et al., 2012). Conversely, blind individuals have elevated melatonin levels (Bellastella et al., 1995), which has been shown to attenuate cognitive impairments (Peck et al., 2004) and reduce inflammation (Cuzzocrea et al., 1999; Sharma et al., 2012). Another potential mechanism involves cortical thickness and pruning. Schizophrenia is typically characterized by cortical thinning (Cobia et al., 2012), and it has been hypothesized that excessive neuronal pruning takes place during adolescence (Boksa, 2012). In contrast, the visual cortex of C/E blind people – which as noted above is involved in multiple perceptual and cognitive processes – is thicker than in sighted people, and is thought to be characterized by a less than normal amount of pruning, due to deprivation of visual experience (Jiang et al., 2009). A consequence of this thickening is that, even if genes related to schizophrenia cause excessive pruning in someone with C/E blindness, the remaining number of neurons may still be greater than normal in some areas. This, in combination with the cortical reorganization noted above, leading to occipital regions being used for non-visual cognitive processes, may protect blind people against crossing the threshold needed for psychotic symptoms to emerge (i.e., an adequate number of neurons devoted to specific types of processing may be present even if pruning is excessive).
Conclusion
This paper builds on previous reports of a lack of schizophrenia in people with C/E blindness by advancing the hypothesis that the latter alters cognition and fosters neuroplasticity in ways that confer protective effects against schizophrenia. The reviewed evidence indicates that: (1) schizophrenia is primarily a cognitive disorder; (2) many of the cognitive functions that are impaired in schizophrenia are enhanced among the C/E blind; (3) C/E blindness involves reduced flexibility in language and in dynamic representation of the body, and these reductions may protect against thought disorder and alterations in experience of the self, respectively; (4) the mechanisms noted in 2 and 3 above are significantly less affected if the onset of blindness is after the first few months of life; (5) other forms of C/E sensory loss do not protect against schizophrenia; and (6) C/E blindness does not protect against other disorders, suggesting that there is a special link between schizophrenia and visual processing.
Of course, schizophrenia is characterized by cognitive impairments in addition to those described here, such as in executive functioning, that are thought to rely heavily on functioning of the dorsolateral prefrontal cortex (DLPFC). There appears to be almost no research comparing blind (congenital or acquired) and sighted people on these functions, however, and so whether blindness confers any protective effects on them remains an open question. Note, however, that the DLPFC does not fully develop until late adolescence or early adulthood. In contrast, cognitive and academic decline, and interpersonal dysfunction, typically begin in late childhood or early adolescence in people who go on to develop schizophrenia, and this age range corresponds to the time frame in which the visual system in humans is most plastic (i.e., until ∼14–16 years of age; Cohen et al., 1999). This suggests that the protective sequelae of C/E blindness involve changes in more basic sensory, perceptual, and cognitive (i.e., non-executive) functions.
While the idea of one abnormal condition having a protective effect against another condition may seem unusual, it is not unknown. For example, several studies have now replicated the finding that schizophrenia appears to have an inverse relationship with rheumatoid arthritis (RA), with some estimates putting the risk for RA among schizophrenia patients at 30% that of control counterparts (Eaton et al., 1992; Mors et al., 1999; Oken and Schulzer, 1999). Conversely, there may also be a reduced risk for developing schizophrenia among individuals with RA (Gorwood et al., 2004). This is especially low considering smoking is a risk factor for developing RA (Stolt et al., 2003) and that a disproportionally large percentage (60–90%) of individuals with schizophrenia smoke (Dervaux and Laqueille, 2008). As noted, we hypothesize that the cognitive benefits conferred by C/E blindness act as a prophylactic for schizophrenia but not other mental disorders. This hypothesis, if confirmed, has implications for determining when cognitive training should occur for people with, or at-risk for, schizophrenia, and for the nature of such training. It also has implications for whether insights from C/E blindness can be used to design interventions to prevent schizophrenia. Each of these issues will be addressed in turn below.
Evidence from animal studies indicates that prevention of schizophrenia-related cognitive impairment can be achieved by early cognitive training. For example, in one study, rats received a ventral hippocampus lesion that induces a spatial working memory deficit similar to that found among schizophrenia patients. It was found that among animals that had been provided with pre-lesioning cognitive training, the typical post-lesion working memory deficit did not arise (Lee et al., 2012). While similar preventive data do not exist in humans, a recent study of cognitive remediation in first-episode schizophrenia demonstrated that it significantly slowed the typical gray matter loss associated with the first years after an initial psychotic episode (Eack et al., 2010). Therefore, it is reasonable to study whether the long-term effects of cognitive training in people at high risk for the disorder could be at least as strong, if not stronger, than effects of cognitive training introduced after a diagnosis of schizophrenia is made, given that the effects are occurring in the context of a healthier and younger brain.
But when should training occur? Evidence indicates that intervening when people first begin to show psychotic symptoms or functional decline (i.e., in the “ultra high-risk” state) can delay, but does not prevent, schizophrenia (Yung and Nelson, 2011). Therefore, it has recently been proposed that intervening at a “pluripotent risk stage” – the time of the earliest emergence of behavioral and cognitive difficulties (typically 9–13 years of age) that are non-specific as to final diagnosis – would be more effective (Agius et al., 2010; McGorry, 2010; McGorry et al., 2010; Morgan et al., in press). Whether or not such a strategy can prevent schizophrenia, it may be an ideal time for intensive cognitive training, in terms of affording protection against later and severe schizophrenia-related cognitive impairment. Of course, even earlier training could be effective, but the feasibility of identifying people at high risk for mental illness at younger than 9-years old has not been well-established, except in cases where an identical twin or first-degree relative has the disorder.
What sort of training would be effective? Based on the evidence reviewed above, we suggest that cognitive training in young people at-risk for schizophrenia should be comprehensive in nature, and should focus to a greater degree than it has in the past on sensory and perceptual functioning. For example, in addition to a focus on improving aspects of attention, it should focus on improving sensory tuning and the accuracy of sensory representations, perceptual organization, multisensory integration, and controlled processing including integration of bottom-up sensory data with stored information (see Heller quotes above, and Hemsley, 1996). Some interventions have already demonstrated success in improving functioning in these specific areas in humans (Temple et al., 2003; Mahncke et al., 2006; Genevsky et al., 2010) and animals (Polley et al., 2006; Zhou et al., 2011). In addition, although schizophrenia patients often demonstrate reduced plasticity, it is not absent, and capacity for perceptual and cognitive change has been demonstrated (Fisher et al., 2009, 2010; Silverstein and Keane, 2009) both in and outside the context of specific interventions. Therefore, it is possible that even greater plasticity can be harnessed earlier in the developmental course of the illness, before psychotic symptoms emerge and near the onset of, or prior to, cognitive and functional decline. In addition, it has already been demonstrated in schizophrenia that improving auditory precision by repeated practicing of tone discrimination leads to improvements in auditory and (more interestingly) higher level cognitive functions (e.g., verbal learning and memory; Adcock et al., 2009; Fisher et al., 2009). Therefore, broader improvements (beyond the trained task) may occur in at-risk youth with similar practice.
An additional strategy for people at-risk for schizophrenia involves increasing reliance on non-visual sensory modalities to enhance their functioning. Already it has been shown in people with established schizophrenia, for example, that steady-state auditory responses, which are typically abnormally reduced and associated with an increase in broadband noise, can be significantly improved, and to a greater degree than occurs in healthy people, by closing the eyes during task performance (Griskova-Bulanova et al., 2012). Fostering cognitive reserve, and trying to prevent schizophrenia, or at least minimize later illness-related cognitive impairment, by strengthening capacity and efficiency in non-visual domains is an as yet untested strategy. However, the goal of creating a schizophrenia-specific, acquired cognitive reserve, in a manner guided by compensatory changes observed in C/E blindness, would appear to be a reasonable and promising direction to pursue, given that premorbid cognitive reserve predicts later cognitive functioning in normal aging (Steffener and Stern, 2012), neurodegenerative disorders (Koerts et al., 2012; Stern, 2012), and schizophrenia (de La Serna et al., 2013).
Can an understanding of cognition and neuroplasticity in C/E blindness be used to reduce the likelihood of schizophrenia? At first glance, the answer seems to be “no” since: (1) only C/E blindness (but not blindness acquired after the first few months of life) is associated with a protective effect; (2) it is difficult to identify most people who will develop schizophrenia during the first year of life; (3) it is not clear what type of training could be given to people less than 1-year old, given limited attention span and undeveloped verbal abilities; and (4) the presence of vision is likely to reduce the extent of developmental neuroplasticity. However, the ultimate answer to this question may not be this simple. For example, much remains to be learned about biological and computational changes associated with C/E, and later-developing, blindness, and so further investigation into these issues may reveal clues for intervention development. Also, it is not known beyond what age fostering neuroplasticity and cognitive enhancement might no longer be able to prevent schizophrenia, but only reduce schizophrenia-related cognitive impairment. Third, since it is not C/E blindness per se, but rather, the corresponding brain and cognitive changes that are protective against schizophrenia, it is possible that methods other than naturally occurring C/E blindness can confer protective effects. For example, an open question is the extent to which particularly intensive sensory-perceptual-cognitive interventions delivered to at-risk youth past the first year of life can create some of the protective changes associated with naturally occurring C/E blindness.
Conflict of Interest Statement
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

2020-02-13 14:32:26

Acknowledgments
We thank Thomas Papathomas, Matt Roche, Keith Feigenson, James Gold, and Judy Thompson for their helpful comments on earlier drafts of this manuscript. We also thank Ms. Arwen Lockley for her helpful insights on blindness and schizophrenia, and the two reviewers for their helpful suggestions. This work was supported by a National Research Service Award (F32MH094102) to Brian P. Keane, and R01MH093439 to Steven M. Silverstein.
References
Abely, P., and Carton, C. (1967). [The man of night and the man of silence. Prologue to an attempted comparative psychopathologic and psychiatric study of the blind and deaf]. Ann. Med. Psychol. (Paris) 125, 111–125.
Pubmed Abstract | Pubmed Full Text
Adcock, R. A., Dale, C., Fisher, M., Aldebot, S., Genevsky, A., Simpson, G. V., et al. (2009). When top-down meets bottom-up: auditory training enhances verbal memory in schizophrenia. Schizophr. Bull. 35, 1132–1141.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Agius, M., Goh, C., Ulhaq, S., and McGorry, P. (2010). The staging model in schizophrenia, and its clinical implications. Psychiatr. Danub. 22, 211–220.
Pubmed Abstract | Pubmed Full Text
Aleman, A., Van Lee, L., Mantione, M. H., Verkoijen, I. G., and De Haan, E. H. (2001). Visual imagery without visual experience: evidence from congenitally totally blind people. Neuroreport 12, 2601–2604.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Altshuler, L. L., Ventura, J., Van Gorp, W. G., Green, M. F., Theberge, D. C., and Mintz, J. (2004). Neurocognitive function in clinically stable men with bipolar I disorder or schizophrenia and normal control subjects. Biol. Psychiatry 56, 560–569.
Pubmed Abstract | Pubmed Full Text
Amadeo, D., and Speicher, K. (1995). Essential environmental and spatial concerns for the congenitally visually impaired. J. Plan. Educ. Res. 14, 113–122.
Amedi, A., Floel, A., Knecht, S., Zohary, E., and Cohen, L. G. (2004). Transcranial magnetic stimulation of the occipital pole interferes with verbal processing in blind subjects. Nat. Neurosci. 7, 1266–1270.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Amedi, A., Jacobson, G., Hendler, T., Malach, R., and Zohary, E. (2002). Convergence of visual and tactile shape processing in the human lateral occipital complex. Cereb. Cortex 12, 1202–1212.
Pubmed Abstract | Pubmed Full Text
Amedi, A., Malach, R., Hendler, T., Peled, S., and Zohary, E. (2001). Visuo-haptic object-related activation in the ventral visual pathway. Nat. Neurosci. 4, 324–330.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Amedi, A., Merabet, L. B., Camprodon, J., Bermpohl, F., Fox, S., Ronen, I., et al. (2008). Neural and behavioral correlates of drawing in an early blind painter: a case study. Brain Res. 1242, 252–262.
Pubmed Abstract | Pubmed Full Text
Amedi, A., Raz, N., Pianka, P., Malach, R., and Zohary, E. (2003). Early ‘visual’ cortex activation correlates with superior verbal memory performance in the blind. Nat. Neurosci. 6, 758–766.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
American Psychiatric Association. (1980). Diagnostic and Statistical Manual of Mental Disorders, 3rd Edn. Washington: American Psychiatric Association.
Andersen, E. S., Dunlea, A., and Kekelis, L. S. (1984). Blind children’s language: resolving some differences. J. Child Lang. 11, 645–664.
Pubmed Abstract | Pubmed Full Text
Andersen, E. S., Dunlea, A., and Kekelis, L. S. (1993). The impact of input: language acquisition in the visually impaired. First Lang. 13, 23–49.
CrossRef Full Text
Anderson, G., and Maes, M. (2012). Melatonin: an overlooked factor in schizophrenia and in the inhibition of anti-psychotic side effects. Metab. Brain Dis. 27, 113–119.
Pubmed Abstract | Pubmed Full Text
Atkinson, J. R. (2006). The perceptual characteristics of voice-hallucinations in deaf people: insights into the nature of subvocal thought and sensory feedback loops. Schizophr. Bull. 32, 701–708.
Pubmed Abstract | Pubmed Full Text
Ballard, C. G., O’Brien, J. T., Swann, A. G., Thompson, P., Neill, D., and McKeith, I. G. (2001). The natural history of psychosis and depression in dementia with Lewy bodies and Alzheimer’s disease: persistence and new cases over 1 year of follow-up. J. Clin. Psychiatry 62, 46–49.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Barber, P. O., and Lederman, S. J. (1988). Encoding direction in manipulatory space. J. Vis. Impair. Blind. 82, 99–106.
Bedny, M., Konkle, T., Pelphrey, K., Saxe, R., and Pascual-Leone, A. (2010). Sensitive period for a multimodal response in human visual motion area MT/MST. Curr. Biol. 20, 1900–1906.
Pubmed Abstract | Pubmed Full Text
Bellastella, A., Sinisi, A. A., Criscuolo, T., De Bellis, A., Carella, C., Iorio, S., et al. (1995). Melatonin and the pituitary-thyroid axis status in blind adults: a possible resetting after puberty. Clin. Endocrinol. (Oxf.) 43, 707–711.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Bertolo, H., Paiva, T., Pessoa, L., Mestre, T., Marques, R., and Santos, R. (2003). Visual dream content, graphical representation and EEG alpha activity in congenitally blind subjects. Brain Res. Cogn. Brain Res. 15, 277–284.
Pubmed Abstract | Pubmed Full Text
Bleuler, E. (1950). Dementia Praecox or the Group of Schizophrenias. New York: International Universities Press.
Boksa, P. (2012). Abnormal synaptic pruning in schizophrenia: urban myth or reality? J. Psychiatry Neurosci. 37, 75–77.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Bolat, N., Dogangun, B., Yavuz, M., Demir, T., and Kayaalp, L. (2011). Depression and anxiety levels and self-concept characteristics of adolescents with congenital complete visual impairment. Turk. Psikiyatri. Derg. 22, 77–82.
Pubmed Abstract | Pubmed Full Text
Bonino, D., Ricciardi, E., Sani, L., Gentili, C., Vanello, N., Guazzelli, M., et al. (2008). Tactile spatial working memory activates the dorsal extrastriate cortical pathway in congenitally blind individuals. Arch. Ital. Biol. 146, 133–146.
Pubmed Abstract | Pubmed Full Text
Brahmbhatt, S. B., Haut, K., Csernansky, J. G., and Barch, D. M. (2006). Neural correlates of verbal and nonverbal working memory deficits in individuals with schizophrenia and their high-risk siblings. Schizophr. Res. 87, 191–204.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Brebion, G., Amador, X., Smith, M. J., and Gorman, J. M. (1997). Mechanisms underlying memory impairment in schizophrenia. Psychol. Med. 27, 383–393.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Brebion, G., David, A. S., Jones, H., and Pilowsky, L. S. (2004). Semantic organization and verbal memory efficiency in patients with schizophrenia. Neuropsychology 18, 378–383.
Pubmed Abstract | Pubmed Full Text
Brewer, W. J., Wood, S. J., McGorry, P. D., Francey, S. M., Phillips, L. J., Yung, A. R., et al. (2003). Impairment of olfactory identification ability in individuals at ultra-high risk for psychosis who later develop schizophrenia. Am. J. Psychiatry 160, 1790–1794.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Bross, M. (1979). Residual sensory capacities of the deaf: a signal detection analysis of a visual discrimination task. Percept. Mot. Skills 48, 187–194.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Brown, R., Hobson, R. P., Lee, A., and Stevenson, J. (1997). Are there “autistic-like” features in congenitally blind children? J. Child Psychol. Psychiatry 38, 693–703.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Bruce, S. M. (2005). The impact of congenital deafblindness on the struggle to symbolism. Int. J. Disabil. Dev. Educ. 52, 223–251.
CrossRef Full Text
Bruder, G., Kayser, J., Tenke, C., Amador, X., Friedman, M., Sharif, Z., et al. (1999). Left temporal lobe dysfunction in schizophrenia: event-related potential and behavioral evidence from phonetic and tonal dichotic listening tasks. Arch. Gen. Psychiatry 56, 267–276.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Bull, R., Rathborn, H., and Clifford, B. R. (1983). The voice-recognition accuracy of blind listeners. Perception 12, 223–226.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Burton, H., Diamond, J. B., and McDermott, K. B. (2003). Dissociating cortical regions activated by semantic and phonological tasks: a FMRI study in blind and sighted people. J. Neurophysiol. 90, 1965–1982.
Pubmed Abstract | Pubmed Full Text
Butler, P. D., Silverstein, S. M., and Dakin, S. C. (2008). Visual perception and its impairment in schizophrenia. Biol. Psychiatry 64, 40–47.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Carr, V., and Wale, J. (1986). Schizophrenia: an information processing model. Aust. N. Z. J. Psychiatry 20, 136–155.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Carvill, S. (2001). Sensory impairments, intellectual disability and psychiatry. J. Intellect. Disabil. Res. 45, 467–483.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cattaneo, Z., and Vecchi, T. (2011). Blind Vision. Cambridge: MIT Press.
Cattaneo, Z., Vecchi, T., Cornoldi, C., Mammarella, I., Bonino, D., Ricciardi, E., et al. (2008). Imagery and spatial processes in blindness and visual impairment. Neurosci. Biobehav. Rev. 32, 1346–1360.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Chapman, J. (1966). The early symptoms of schizophrenia. Br. J. Psychiatry 112, 225–251.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Chase, J. B. (1972). Retrolental Fibroplasia and Autistic Symptomatology. New York, NY: New York America Foundation for the Blind.
Checkley, S. A., and Slade, A. P. (1979). Blindness and schizophrenia. Lancet 313, 730–731.
CrossRef Full Text
Chen, Q., He, S., Hu, X. L., Yu, J., Zhou, Y., Zheng, J., et al. (2007). Differential roles of NR2A- and NR2B-containing NMDA receptors in activity-dependent brain-derived neurotrophic factor gene regulation and limbic epileptogenesis. J. Neurosci. 27, 542–552.
Pubmed Abstract | Pubmed Full Text
Chen, W. S., and Bear, M. F. (2007). Activity-dependent regulation of NR2B translation contributes to metaplasticity in mouse visual cortex. Neuropharmacology 52, 200–214.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Chen, Y. (2011). Abnormal visual motion processing in schizophrenia: a review of research progress. Schizophr. Bull. 37, 709–715.
Pubmed Abstract | Pubmed Full Text
Chess, S. (1971). Autism in children with congenital rubella. J. Autism Child. Schizophr. 1, 33–47.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Chevigny, H., and Braverman, S. (1950). The Adjustment of the Blind. New Haven: Yale University Press.
Clark, A. (in press). Whatever (next)? Predictive brains, situated agents, and the future of cognitive science. Behav. Brain Sci.
Cobia, D. J., Smith, M. J., Wang, L., and Csernansky, J. G. (2012). Longitudinal progression of frontal and temporal lobe changes in schizophrenia. Schizophr. Res. 139, 1–6.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cohen, J. D., and Servan-Schreiber, D. (1992). Context, cortex, and dopamine: a connectionist approach to behavior and biology in schizophrenia. Psychol. Rev. 99, 45–77.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cohen, L. G., Celnik, P., Pascual-Leone, A., Corwell, B., Falz, L., Dambrosia, J., et al. (1997). Functional relevance of cross-modal plasticity in blind humans. Nature 389, 180–183.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cohen, L. G., Weeks, R. A., Sadato, N., Celnik, P., Ishii, K., and Hallett, M. (1999). Period of susceptibility for cross-modal plasticity in the blind. Ann. Neurol. 45, 451–460.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Collignon, O., and De Volder, A. G. (2009). Further evidence that congenitally blind participants react faster to auditory and tactile spatial targets. Can. J. Exp. Psychol. 63, 287–293.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Collignon, O., Renier, L., Bruyer, R., Tranduy, D., and Veraart, C. (2006). Improved selective and divided spatial attention in early blind subjects. Brain Res. 1075, 175–182.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Collignon, O., Voss, P., Lassonde, M., and Lepore, F. (2009). Cross-modal plasticity for the spatial processing of sounds in visually deprived subjects. Exp. Brain Res. 192, 343–358.
Pubmed Abstract | Pubmed Full Text
Conklin, H. M., Curtis, C. E., Calkins, M. E., and Iacono, W. G. (2005). Working memory functioning in schizophrenia patients and their first-degree relatives: cognitive functioning shedding light on etiology. Neuropsychologia 43, 930–942.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Corlett, P. R., Frith, C. D., and Fletcher, P. C. (2009). From drugs to deprivation: a Bayesian framework for understanding models of psychosis. Psychopharmacology (Berl.) 206, 515–530.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Corlett, P. R., Honey, G. D., and Fletcher, P. C. (2007). From prediction error to psychosis: ketamine as a pharmacological model of delusions. J. Psychopharmacol. (Oxford) 21, 238–252.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cornoldi, C., Calore, D., and Pra-Baldi, A. (1979). Imagery rating and recall in congenitally blind subjects. Percept. Mot. Skills 48, 627–639.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cortese, L., Caligiuri, M. P., Malla, A. K., Manchanda, R., Takhar, J., and Haricharan, R. (2005). Relationship of neuromotor disturbances to psychosis symptoms in first-episode neuroleptic-naive schizophrenia patients. Schizophr. Res. 75, 65–75.
Pubmed Abstract | Pubmed Full Text
Costafreda, S. G., Fu, C. H., Picchioni, M., Toulopoulou, T., McDonald, C., Kravariti, E., et al. (2011). Pattern of neural responses to verbal fluency shows diagnostic specificity for schizophrenia and bipolar disorder. BMC Psychiatry 11:18. doi:10.1186/1471-244X-11-18
CrossRef Full Text
Coyle, J. T. (2012). NMDA receptor and schizophrenia: a brief history. Schizophr. Bull. 38, 920–926.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Cuevas, I., Plaza, P., Rombaux, P., De Volder, A. G., and Renier, L. (2009). Odour discrimination and identification are improved in early blindness. Neuropsychologia 47, 3079–3083.
Pubmed Abstract | Pubmed Full Text
Cutting, J. (1985). The Psychology of Schizophrenia. Edinburgh: Livingstone.
Cuzzocrea, S., Costantino, G., Mazzon, E., and Caputi, A. P. (1999). Regulation of prostaglandin production in carrageenan-induced pleurisy by melatonin. J. Pineal Res. 27, 9–14.
Pubmed Abstract | Pubmed Full Text
Dammeyer, J. (2011). Mental and behavioral disorders among people with congenital deafblindness. Res. Dev. Disabil. 32, 571–575.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Dammeyer, J. (2012). Children with Usher syndrome: mental and behavioral disorders. Behav. Brain Funct. 8, 16.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Danckert, J., Saoud, M., and Maruff, P. (2004). Attention, motor control and motor imagery in schizophrenia: implications for the role of the parietal cortex. Schizophr. Res. 70, 241–261.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Daskalakis, Z. J., Christensen, B. K., Fitzgerald, P. B., and Chen, R. (2008). Dysfunctional neural plasticity in patients with schizophrenia. Arch. Gen. Psychiatry 65, 378–385.
Pubmed Abstract | Pubmed Full Text
de La Serna, E., Andres-Perpina, S., Puig, O., Baeza, I., Bombin, I., Bartres-Faz, D., et al. (2013). Cognitive reserve as a predictor of two year neuropsychological performance in early onset first-episode schizophrenia. Schizophr. Res. 143, 125–131.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
De Volder, A. G., Catalan-Ahumada, M., Robert, A., Bol, A., Labar, D., Coppens, A., et al. (1999). Changes in occipital cortex activity in early blind humans using a sensory substitution device. Brain Res. 826, 128–134.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Dervaux, A., and Laqueille, X. (2008). [Smoking and schizophrenia: epidemiological and clinical features]. Encephale 34, 299–305.
Pubmed Abstract | Pubmed Full Text
Deutschlander, A., Stephan, T., Hufner, K., Wagner, J., Wiesmann, M., Strupp, M., et al. (2009). Imagined locomotion in the blind: an fMRI study. Neuroimage 45, 122–128.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Dima, D., Dietrich, D. E., Dillo, W., and Emrich, H. M. (2010). Impaired top-down processes in schizophrenia: a DCM study of ERPs. Neuroimage 52, 824–832.
Pubmed Abstract | Pubmed Full Text
Dima, D., Roiser, J. P., Dietrich, D. E., Bonnemann, C., Lanfermann, H., Emrich, H. M., et al. (2009). Understanding why patients with schizophrenia do not perceive the hollow-mask illusion using dynamic causal modelling. Neuroimage 46, 1180–1186.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Dolan, R. J., Fletcher, P., Frith, C. D., Friston, K. J., Frackowiak, R. S., and Grasby, P. M. (1995). Dopaminergic modulation of impaired cognitive activation in the anterior cingulate cortex in schizophrenia. Nature 378, 180–182.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Du Feu, M., and McKenna, P. J. (1999). Prelingually profoundly deaf schizophrenic patients who hear voices: a phenomenological analysis. Acta Psychiatr. Scand. 99, 453–459.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Dye, M. W., and Bavelier, D. (2010). Attentional enhancements and deficits in deaf populations: an integrative review. Restor. Neurol. Neurosci. 28, 181–192.
Pubmed Abstract | Pubmed Full Text
Eack, S. M., Hogarty, G. E., Cho, R. Y., Prasad, K. M., Greenwald, D. P., Hogarty, S. S., et al. (2010). Neuroprotective effects of cognitive enhancement therapy against gray matter loss in early schizophrenia: results from a 2-year randomized controlled trial. Arch. Gen. Psychiatry 67, 674–682.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Eaton, W. W., Hayward, C., and Ram, R. (1992). Schizophrenia and rheumatoid arthritis: a review. Schizophr. Res. 6, 181–192.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ehrsson, H. H., Spence, C., and Passingham, R. E. (2004). That’s my hand! Activity in premotor cortex reflects feeling of ownership of a limb. Science 305, 875–877.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ek, U., Fernell, E., Jacobson, L., and Gillberg, C. (1998). Relation between blindness due to retinopathy of prematurity and autistic spectrum disorders: a population based study. Dev. Med. Child Neurol. 40, 297–301.
Pubmed Abstract | Pubmed Full Text
Elbert, T., Sterr, A., Rockstroh, B., Pantev, C., Muller, M. M., and Taub, E. (2002). Expansion of the tonotopic area in the auditory cortex of the blind. J. Neurosci. 22, 9941–9944.
Pubmed Abstract | Pubmed Full Text
Feierman, J. R. (1982). Nocturnalism: an ethological theory of schizophrenia. Med. Hypotheses 9, 455–479.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ffytche, D. H. (2007). Visual hallucinatory syndromes: past, present, and future. Dialogues Clin. Neurosci. 9, 173–189.
Pubmed Abstract | Pubmed Full Text
Fisher, M., Holland, C., Merzenich, M. M., and Vinogradov, S. (2009). Using neuroplasticity-based auditory training to improve verbal memory in schizophrenia. Am. J. Psychiatry 166, 805–811.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Fisher, M., Holland, C., Subramaniam, K., and Vinogradov, S. (2010). Neuroplasticity-based cognitive training in schizophrenia: an interim report on the effects 6 months later. Schizophr. Bull. 36, 869–879.
Pubmed Abstract | Pubmed Full Text
Fitzgerald, P. B., Brown, T. L., Marston, N. A., Oxley, T., De Castella, A., Daskalakis, Z. J., et al. (2004). Reduced plastic brain responses in schizophrenia: a transcranial magnetic stimulation study. Schizophr. Res. 71, 17–26.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Foucher, J. R., Lacambre, M., Pham, B. T., Giersch, A., and Elliott, M. A. (2007). Low time resolution in schizophrenia Lengthened windows of simultaneity for visual, auditory and bimodal stimuli. Schizophr. Res. 97, 118–127.
Pubmed Abstract | Pubmed Full Text
Fraiberg, S. (1977). Insights from the Blind. London: Souvenir.
Garg, A., Schwartz, D., and Stevens, A. A. (2007). Orienting auditory spatial attention engages frontal eye fields and medial occipital cortex in congenitally blind humans. Neuropsychologia 45, 2307–2321.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Geenens, D. L. (1999). “Neurobiological development and cognition in the deafblind,” in A Guide to Planning and Support for Individuals Who are Deafblind, ed. J. M. McInnes (Toronto: University of Toronto Press), 150–174.
Genevsky, A., Garrett, C. T., Alexander, P. P., and Vinogradov, S. (2010). Cognitive training in schizophrenia: a neuroscience-based approach. Dialogues Clin. Neurosci. 12, 416–421.
Pubmed Abstract | Pubmed Full Text
Gold, R., Butler, P., Revheim, N., Leitman, D. I., Hansen, J. A., Gur, R. C., et al. (2012). Auditory emotion recognition impairments in schizophrenia: relationship to acoustic features and cognition. Am. J. Psychiatry 169, 424–432.
Pubmed Abstract | Pubmed Full Text
Goodale, M. A. (1993). Visual pathways supporting perception and action in the primate cerebral cortex. Curr. Opin. Neurobiol. 3, 578–585.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Goodale, M. A., Kroliczak, G., and Westwood, D. A. (2005). Dual routes to action: contributions of the dorsal and ventral streams to adaptive behavior. Prog. Brain Res. 149, 269–283.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Goodin-Jones, B. L., Eiben, L. A., and Anders, T. F. (1997). Maternal, well-being and sleep-wake behaviors in infants: an intervention using maternal odor. Infant Ment. Health J. 18, 378–393.
CrossRef Full Text
Gorwood, P., Pouchot, J., Vinceneux, P., Puechal, X., Flipo, R. M., De Bandt, M., et al. (2004). Rheumatoid arthritis and schizophrenia: a negative association at a dimensional level. Schizophr. Res. 66, 21–29.
Pubmed Abstract | Pubmed Full Text
Green, M. F. (1996). What are the functional consequences of neurocognitive deficits in schizophrenia? Am. J. Psychiatry 153, 321–330.
Pubmed Abstract | Pubmed Full Text
Green, M. F., Hugdahl, K., and Mitchell, S. (1994). Dichotic listening during auditory hallucinations in patients with schizophrenia. Am. J. Psychiatry 151, 357–362.
Pubmed Abstract | Pubmed Full Text
Griskova-Bulanova, I., Dapsys, K., Maciulis, V., and Arnfred, S. M. (2012). Closed eyes condition increases auditory brain responses in schizophrenia. Psychiatry Res. doi:10.1016/j.pscychresns.2012.04.004
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Harvey, P. D., Earle-Boyer, E. A., Weilgus, M. S., and Levinson, J. C. (1986). Encoding, memory, and thought disorder in schizophrenia and mania. Schizophr. Bull. 12, 252–261.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Hasan, A., Nitsche, M. A., Herrmann, M., Schneider-Axmann, T., Marshall, L., Gruber, O., et al. (2012). Impaired long-term depression in schizophrenia: a cathodal tDCS pilot study. Brain Stimul. 5, 475–483.
Pubmed Abstract | Pubmed Full Text
Hasan, A., Nitsche, M. A., Rein, B., Schneider-Axmann, T., Guse, B., Gruber, O., et al. (2011). Dysfunctional long-term potentiation-like plasticity in schizophrenia revealed by transcranial direct current stimulation. Behav. Brain Res. 224, 15–22.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Heinrichs, R. W., and Zakzanis, K. K. (1998). Neurocognitive deficit in schizophrenia: a quantitative review of the evidence. Neuropsychology 12, 426–445.
Pubmed Abstract | Pubmed Full Text
Hemsley, D. R. (1996). Schizophrenia. A cognitive model and its implications for psychological intervention. Behav. Modif. 20, 139–169.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Herssens, J. (2010). “Haptic design research: a blind sense of place,” in Proceedings of the 7th ARCC/EAAE 2010 International Conference on Architectural Research (Washington, DC: EAAE-ARCC). Available at: http://www.aia.org/aiaucmp/groups/aia/d … 087187.pdf [accessed December 27, 2012].
Hertrich, I., Dietrich, S., Moos, A., Trouvain, J., and Ackermann, H. (2009). Enhanced speech perception capabilities in a blind listener are associated with activation of fusiform gyrus and primary visual cortex. Neurocase 15, 163–170.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Hirano, S., Hirano, Y., Maekawa, T., Obayashi, C., Oribe, N., Kuroki, T., et al. (2008). Abnormal neural oscillatory activity to speech sounds in schizophrenia: a magnetoencephalography study. J. Neurosci. 28, 4897–4903.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Horan, W. P., Braff, D. L., Nuechterlein, K. H., Sugar, C. A., Cadenhead, K. S., Calkins, M. E., et al. (2008). Verbal working memory impairments in individuals with schizophrenia and their first-degree relatives: findings from the Consortium on the Genetics of Schizophrenia. Schizophr. Res. 103, 218–228.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Horrobin, D. F. (1979). Schizophrenia: reconciliation of the dopamine, prostaglandin, and opioid concepts and the role of the pineal. Lancet 1, 529–531.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Horton, H. K., and Silverstein, S. M. (2007). Cognition and functional outcome among deaf and hearing people with schizophrenia. Schizophr. Res. 94, 187–196.
Pubmed Abstract | Pubmed Full Text
Horton, H. K., and Silverstein, S. M. (2011). Visual context processing deficits in schizophrenia: effects of deafness and disorganization. Schizophr. Bull. 37, 716–726.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Hotting, K., and Roder, B. (2004). Hearing cheats touch, but less in congenitally blind than in sighted individuals. Psychol. Sci. 15, 60–64.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Hugdahl, K., Ek, M., Takio, F., Rintee, T., Tuomainen, J., Haarala, C., et al. (2004). Blind individuals show enhanced perceptual and attentional sensitivity for identification of speech sounds. Brain Res. Cogn. Brain Res. 19, 28–32.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Hull, T., and Mason, H. (1995). Performance of blind children on digit span tests. J. Vis. Impair. Blind. 89, 166–169.
Ilankovic, L. M., Allen, P. P., Engel, R., Kambeitz, J., Riedel, M., Muller, N., et al. (2011). Attentional modulation of external speech attribution in patients with hallucinations and delusions. Neuropsychologia 49, 805–812.
Pubmed Abstract | Pubmed Full Text
Iyer, D., Boutros, N. N., and Zouridakis, G. (2012). Single-trial analysis of auditory evoked potentials improves separation of normal and schizophrenia subjects. Clin. Neurophysiol. 123, 1810–1820.
Pubmed Abstract | Pubmed Full Text
Javitt, D. C., Strous, R. D., Grochowski, S., Ritter, W., and Cowan, N. (1997). Impaired precision, but normal retention, of auditory sensory (“echoic”) memory information in schizophrenia. J. Abnorm. Psychol. 106, 315–324.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Jiang, J., Zhu, W., Shi, F., Liu, Y., Li, J., Qin, W., et al. (2009). Thick visual cortex in the early blind. J. Neurosci. 29, 2205–2211.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Johns, L. C., Rossell, S., Frith, C., Ahmad, F., Hemsley, D., Kuipers, E., et al. (2001). Verbal self-monitoring and auditory verbal hallucinations in patients with schizophrenia. Psychol. Med. 31, 705–715.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Kallstrand, J., Montnemery, P., Nielzen, S., and Olsson, O. (2002). Auditory masking experiments in schizophrenia. Psychiatry Res 113, 115–125.
Pubmed Abstract | Pubmed Full Text
Kamath, V., Turetsky, B. I., Calkins, M. E., Kohler, C. G., Conroy, C. G., Borgmann-Winter, K., et al. (2011). Olfactory processing in schizophrenia, non-ill first-degree family members, and young people at-risk for psychosis. World J. Biol. Psychiatry. [Epub ahead of print]. .
Pubmed Abstract | Pubmed Full Text
Kantrowitz, J. T., Leitman, D. I., Lehrfeld, J. M., Laukka, P., Juslin, P. N., Butler, P. D., et al. (2013). Reduction in tonal discriminations predicts receptive emotion processing deficits in schizophrenia and schizoaffective disorder. Schizophr Bull. 39, 86–93.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Kayser, J., Bruder, G. E., Tenke, C. E., Stuart, B. K., Amador, X. F., and Gorman, J. M. (2001). Event-related brain potentials (ERPs) in schizophrenia for tonal and phonetic oddball tasks. Biol. Psychiatry 49, 832–847.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Keeler, W. R. (1958). Autistic Patterns and Defective Communication in Blind Children with Retrolental Fibroplasia. New York: Grune & Stratton.
Keller, H. (1908). The World I Live In. New York: Grosset and Dunlop.
Khan, R. (in press). “Why Kraepelin was right: schizophrenia as a cognitive disorder,” in Schizophrenia: Evolution and Synthesis, eds S. Silverstein, B. Moghaddam, and T. Wykes (Cambridge: MIT Press).
Kim, D., Burge, J., Lane, T., Pearlson, G. D., Kiehl, K. A., and Calhoun, V. D. (2008). Hybrid ICA-Bayesian network approach reveals distinct effective connectivity differences in schizophrenia. Neuroimage 42, 1560–1568.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
King, J. P., Christensen, B. K., and Westwood, D. A. (2008). Grasping behavior in schizophrenia suggests selective impairment in the dorsal visual pathway. J. Abnorm. Psychol. 117, 799–811.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Kitson, N., and Fry, R. (1990). Prelingual deafness and psychiatry. Br. J. Hosp. Med. 44, 353–356.
Pubmed Abstract | Pubmed Full Text
Klosterkotter, J. (1992). The meaning of basic symptoms for the genesis of the schizophrenic nuclear syndrome. Jpn. J. Psychiatry Neurol. 46, 609–630.
Pubmed Abstract | Pubmed Full Text
Knight, R. A. (1984). “Converging models of cognitive deficits in schizophrenia,” in Nebraska Symposium on Motivation: Theories of Schizophrenia and Psychosis, ed. J. C. W. Spaulding (Lincoln, NE: University of Nebraska Press), 93–156.
Knight, R. A., and Silverstein, S. M. (1998). “The role of cognitive psychology in guiding research on cognitive deficits in schizophrenia,” in Origins and Development of Schizophrenia: Advances in Experimental Psychopathology, ed. R. H. D. M. Lenzenweger (Washington, DC: APA Press), 247–295.
Kocourkova, J., Soltysova, M., Mohaplova, M., and Hrdlicka, M. (2011). Anorexia nervosa in a blind girl. Neuro Endocrinol. Lett. 32, 748–750.
Pubmed Abstract | Pubmed Full Text
Koerts, J., Tucha, L., Lange, K. W., and Tucha, O. (2012). The influence of cognitive reserve on cognition in Parkinson’s disease. J. Neural Transm. [Epub ahead of print]..
Pubmed Abstract | Pubmed Full Text
Kraepelin, E. (1903). Lehrbuch der Psychiatrie. Leipzig: Barth.
Kreher, D. A., Holcomb, P. J., Goff, D., and Kuperberg, G. R. (2008). Neural evidence for faster and further automatic spreading activation in schizophrenic thought disorder. Schizophr. Bull. 34, 473–482.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Kujala, T., Alho, K., Kekoni, J., Hamalainen, H., Reinikainen, K., Salonen, O., et al. (1995). Auditory and somatosensory event-related brain potentials in early blind humans. Exp. Brain Res. 104, 519–526.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Kupers, R., Beaulieu-Lefebvre, M., Schneider, F. C., Kassuba, T., Paulson, O. B., Siebner, H. R., et al. (2011). Neural correlates of olfactory processing in congenital blindness. Neuropsychologia 49, 2037–2044.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Lalor, E. C., De Sanctis, P., Krakowski, M. I., and Foxe, J. J. (2012). Visual sensory processing deficits in schizophrenia: is there anything to the magnocellular account? Schizophr. Res. 139, 246–252.
Pubmed Abstract | Pubmed Full Text
Landgraf, S., Amado, I., Berthoz, A., Krebs, M., and Van Der Meer, E. (2012). Cognitive identify in schizophrenia: vision, space, and body perception from prodrome to syndrome. Curr. Psychiatry Rev. 8, 119–139.
Landgraf, S., Steingen, J., Eppert, Y., Niedermeyer, U., Van Der Meer, E., and Krueger, F. (2011). Temporal information processing in short- and long-term memory of patients with schizophrenia. PLoS ONE 6:e26140. doi:10.1371/journal.pone.0026140
CrossRef Full Text
Leclerc, C., Segalowitz, S. J., Desjardins, J., Lassonde, M., and Lepore, F. (2005). EEG coherence in early-blind humans during sound localization. Neurosci. Lett. 376, 154–159.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Lee, H., Dvorak, D., Kao, H.-Y., Duffy, A. M., Scharfman, H. E., and Fenton, A. A. (2012). Early cognitive experience prevents adult deficits in a neurodevelopmental schizophrenia model. Neuron. 75, 714–724.
Pubmed Abstract | Pubmed Full Text
Leitman, D. I., Hoptman, M. J., Foxe, J. J., Saccente, E., Wylie, G. R., Nierenberg, J., et al. (2007). The neural substrates of impaired prosodic detection in schizophrenia and its sensorial antecedents. Am. J. Psychiatry 164, 474–482.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Leitman, D. I., Wolf, D. H., Laukka, P., Ragland, J. D., Valdez, J. N., Turetsky, B. I., et al. (2011). Not pitch perfect: sensory contributions to affective communication impairment in schizophrenia. Biol. Psychiatry 70, 611–618.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Lerner, I., Bentin, S., and Shriki, O. (2012). Excessive attractor instability accounts for semantic priming in schizophrenia. PLoS ONE 7:e40663. doi:10.1371/journal.pone.0040663
CrossRef Full Text
Li, C. S., Chen, M. C., Yang, Y. Y., and Tsay, P. K. (2002). Altered performance of schizophrenia patients in an auditory detection and discrimination task: exploring the ‘self-monitoring’ model of hallucination. Schizophr. Res. 55, 115–128.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Light, G. A., and Braff, D. L. (2005a). Mismatch negativity deficits are associated with poor functioning in schizophrenia patients. Arch. Gen. Psychiatry 62, 127–136.
CrossRef Full Text
Light, G. A., and Braff, D. L. (2005b). Stability of mismatch negativity deficits and their relationship to functional impairments in chronic schizophrenia. Am. J. Psychiatry 162, 1741–1743.
CrossRef Full Text
Maher, B. A. (1974). Delusional thinking and perceptual disorder. J. Individ. Psychol. 30, 98–113.
Pubmed Abstract | Pubmed Full Text
Mahncke, H. W., Connor, B. B., Appelman, J., Ahsanuddin, O. N., Hardy, J. L., Wood, R. A., et al. (2006). Memory enhancement in healthy older adults using a brain plasticity-based training program: a randomized, controlled study. Proc. Natl. Acad. Sci. U.S.A. 103, 12523–12528.
Pubmed Abstract | Pubmed Full Text
Matteau, I., Kupers, R., Ricciardi, E., Pietrini, P., and Ptito, M. (2010). Beyond visual, aural and haptic movement perception: hMT+ is activated by electrotactile motion stimulation of the tongue in sighted and in congenitally blind individuals. Brain Res. Bull. 82, 264–270.
Pubmed Abstract | Pubmed Full Text
McGorry, P. D. (2010). Risk syndromes, clinical staging and DSM V: new diagnostic infrastructure for early intervention in psychiatry. Schizophr. Res. 120, 49–53.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
McGorry, P. D., Nelson, B., Goldstone, S., and Yung, A. R. (2010). Clinical staging: a heuristic and practical strategy for new research and better health and social outcomes for psychotic and related mood disorders. Can. J. Psychiatry 55, 486–497.
Pubmed Abstract | Pubmed Full Text
McNeil, T. F., and Kaij, L. (1987). Swedish high-risk study: sample characteristics at age 6. Schizophr. Bull. 13, 373–381.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Mears, R. P., and Spencer, K. M. (2012). Electrophysiological assessment of auditory stimulus-specific plasticity in schizophrenia. Biol. Psychiatry 71, 503–511.
Pubmed Abstract | Pubmed Full Text
Mittal, V. A., Neumann, C., Saczawa, M., and Walker, E. F. (2008). Longitudinal progression of movement abnormalities in relation to psychotic symptoms in adolescents at high risk of schizophrenia. Arch. Gen. Psychiatry 65, 165–171.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Morgan, C., O’Donovan, M., Bittner, R., Cadenhead, K., Jones, P., McGrath, J., et al. (in press). “How can risk and resilience factors be leveraged to optimize discovery pathways,” in Schizophrenia: Evolution and Synthesis, eds M. B. Silverstein and T. Wykes (Cambridge: MIT Press).
Mors, O., Mortensen, P. B., and Ewald, H. (1999). A population-based register study of the association between schizophrenia and rheumatoid arthritis. Schizophr. Res. 40, 67–74.
Pubmed Abstract | Pubmed Full Text
Muchnik, C., Efrati, M., Nemeth, E., Malin, M., and Hildesheimer, M. (1991). Central auditory skills in blind and sighted subjects. Scand. Audiol. 20, 19–23.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Muller, N., Myint, A. M., and Schwarz, M. J. (2012). Inflammation in schizophrenia. Adv. Protein Chem. Struct. Biol. 88, 49–68.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Musial, F., Kolassa, I. T., Sulzenbruck, S., and Miltner, W. H. (2007). A case of spider phobia in a congenitally blind person. Psychiatry Res. 153, 97–101.
Pubmed Abstract | Pubmed Full Text
Myin-Germeys, I., and van Os, J. (2007). Stress-reactivity in psychosis: evidence for an affective pathway to psychosis. Clin. Psychol. Rev. 27, 409–424.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Naslund, B., Persson-Blennow, I., McNeil, T., Kaij, L., and Malmquist-Larsson, A. (1984). Offspring of women with nonorganic psychosis: infant attachment to the mother at one year of age. Acta Psychiatr. Scand. 69, 231–241.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Neumann, C. S., Grimes, K., Walker, E. F., and Baum, K. (1995). Developmental pathways to schizophrenia: behavioral subtypes. J. Abnorm. Psychol. 104, 558–566.
Pubmed Abstract | Pubmed Full Text
Ngan, E. T., Vouloumanos, A., Cairo, T. A., Laurens, K. R., Bates, A. T., Anderson, C. M., et al. (2003). Abnormal processing of speech during oddball target detection in schizophrenia. Neuroimage 20, 889–897.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Nguyen, A. D., Shenton, M. E., and Levitt, J. J. (2010). Olfactory dysfunction in schizophrenia: a review of neuroanatomy and psychophysiological measurements. Harv. Rev. Psychiatry 18, 279–292.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Niemeyer, W., and Starlinger, I. (1981). Do the blind hear better – investigations on auditory processing in congenital or early acquired blindness. II. Central functions. Audiology 20, 510–515.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Noppeney, U., Friston, K. J., and Price, C. J. (2003). Effects of visual deprivation on the organization of the semantic system. Brain 126, 1620–1627.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Nuechterlein, K. H., Subotnik, K. L., Ventura, J., Green, M. F., Gretchen-Doorly, D., and Asarnow, R. F. (2012). The puzzle of schizophrenia: tracking the core role of cognitive deficits. Dev. Psychopathol. 24, 529–536.
Pubmed Abstract | Pubmed Full Text
Oken, R. J., and Schulzer, M. (1999). At issue: schizophrenia and rheumatoid arthritis: the negative association revisited. Schizophr. Bull. 25, 625–638.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ortiz, T., Poch, J., Santos, J. M., Requena, C., Martinez, A. M., Ortiz-Teran, L., et al. (2011). Recruitment of occipital cortex during sensory substitution training linked to subjective experience of seeing in people with blindness. PLoS ONE 6:e23264. doi:10.1371/journal.pone.0023264
CrossRef Full Text
Oxley, T., Fitzgerald, P. B., Brown, T. L., De Castella, A., Daskalakis, Z. J., and Kulkarni, J. (2004). Repetitive transcranial magnetic stimulation reveals abnormal plastic response to premotor cortex stimulation in schizophrenia. Biol. Psychiatry 56, 628–633.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Palmer, B. W., Dawes, S. E., and Heaton, R. K. (2009). What do we know about neuropsychological aspects of schizophrenia? Neuropsychol. Rev. 19, 365–384.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Peck, J. S., Legoff, D. B., Ahmed, I., and Goebert, D. (2004). Cognitive effects of exogenous melatonin administration in elderly persons: a pilot study. Am. J. Geriatr. Psychiatry 12, 432–436.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Perez-Pereira, M., and Conti-Ramsden, G. (1999). Social Interaction and Language Development in Blind Children. Hove: Psychology Press.
Perrin, M. A., Butler, P. D., Dicostanzo, J., Forchelli, G., Silipo, G., and Javitt, D. C. (2010). Spatial localization deficits and auditory cortical dysfunction in schizophrenia. Schizophr. Res. 124, 161–168.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Persson-Blennow, I., Naslund, B., McNeil, T. F., Kaij, L., and Malmquist-Larsson, A. (1984). Offspring of women with nonorganic psychosis: mother-infant interaction at three days of age. Acta Psychiatr. Scand. 70, 149–159.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Petkova, V. I., Zetterberg, H., and Ehrsson, H. H. (2012). Rubber hands feel touch, but not in blind individuals. PLoS ONE 7:e35912. doi:10.1371/journal.pone.0035912
CrossRef Full Text
Phillips, W. A., and Silverstein, S. M. (2003). Convergence of biological and psychological perspectives on cognitive coordination in schizophrenia. Behav. Brain Sci. 26, 65–82; discussion 82–137.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Pietrini, P., Furey, M. L., Ricciardi, E., Gobbini, M. I., Wu, W. H., Cohen, L., et al. (2004). Beyond sensory images: object-based representation in the human ventral pathway. Proc. Natl. Acad. Sci. U.S.A. 101, 5658–5663.
Pubmed Abstract | Pubmed Full Text
Pietrini, P., Ptito, M., and Kupers, R. (2009). Blindness and Consciousness: New Light from the Dark. Amsterdam: Elsevier.
Plomp, G., Roinishvili, M., Chkonia, E., Kapanadze, G., Kereselidze, M., Brand, A., et al. (2012). Electrophysiological evidence for ventral stream deficits in schizophrenia patients. Schizophr. Bull. [Epub ahead of print]..
Pubmed Abstract | Pubmed Full Text
Polley, D. B., Steinberg, E. E., and Merzenich, M. M. (2006). Perceptual learning directs auditory cortical map reorganization through top-down influences. J. Neurosci. 26, 4970–4982.
Pubmed Abstract | Pubmed Full Text
Pring, L. (1988). The ‘reverse-generation’ effect: a comparison of memory performance between blind and sighted children. Br. J. Psychol. 79(Pt 3), 387–400.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Proksch, J., and Bavelier, D. (2002). Changes in the spatial distribution of visual attention after early deafness. J. Cogn. Neurosci. 14, 687–701.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ptito, M., Fumal, A., De Noordhout, A. M., Schoenen, J., Gjedde, A., and Kupers, R. (2008). TMS of the occipital cortex induces tactile sensations in the fingers of blind Braille readers. Exp. Brain Res. 184, 193–200.
Pubmed Abstract | Pubmed Full Text
Ptito, M., Matteau, I., Gjedde, A., and Kupers, R. (2009). Recruitment of the middle temporal area by tactile motion in congenital blindness. Neuroreport 20, 543–547.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ptito, M., Matteau, I., Zhi Wang, A., Paulson, O. B., Siebner, H. R., and Kupers, R. (2012). Crossmodal recruitment of the ventral visual stream in congenital blindness. Neural Plast. 2012, 304045.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Putzhammer, A., and Klein, H. E. (2006). Quantitative analysis of motor disturbances in schizophrenic patients. Dialogues Clin. Neurosci. 8, 123–130.
Pubmed Abstract | Pubmed Full Text
Rabinowicz, E. F., Silipo, G., Goldman, R., and Javitt, D. C. (2000). Auditory sensory dysfunction in schizophrenia: imprecision or distractibility? Arch. Gen. Psychiatry 57, 1149–1155.
Pubmed Abstract | Pubmed Full Text
Raz, N., Amedi, A., and Zohary, E. (2005). V1 activation in congenitally blind humans is associated with episodic retrieval. Cereb. Cortex 15, 1459–1468.
Pubmed Abstract | Pubmed Full Text
Raz, N., Striem, E., Pundak, G., Orlov, T., and Zohary, E. (2007). Superior serial memory in the blind: a case of cognitive compensatory adjustment. Curr. Biol. 17, 1129–1133.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Rettenbach, R., Diller, G., and Sireteanu, R. (1999). Do deaf people see better? Texture segmentation and visual search compensate in adult but not in juvenile subjects. J. Cogn. Neurosci. 11, 560–583.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Rigucci, S., Rossi-Espagnet, C., Ferracuti, S., De Carolis, A., Corigliano, V., Carducci, F., et al. (2012). Anatomical substrates of cognitive and clinical dimensions in first episode schizophrenia. Acta Psychiatr. Scand. doi:10.1111/acps.12051
CrossRef Full Text
Riscalla, L. M. (1980). Blindness and schizophrenia. Med. Hypotheses 6, 1327–1328.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Roder, B., Kusmierek, A., Spence, C., and Schicke, T. (2007). Developmental vision determines the reference frame for the multisensory control of action. Proc. Natl. Acad. Sci. U.S.A. 104, 4753–4758.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Roder, B., and Neville, H. (2003). Developmental Functional Plasticity. Amsterdam: Elsevier.
Roder, B., Rosler, F., and Hennighausen, E. (1997). Different cortical activation patterns in blind and sighted humans during encoding and transformation of haptic images. Psychophysiology 34, 292–307.
Pubmed Abstract | Pubmed Full Text
Roder, B., Rosler, F., Hennighausen, E., and Nacker, F. (1996). Event-related potentials during auditory and somatosensory discrimination in sighted and blind human subjects. Brain Res. Cogn. Brain Res. 4, 77–93.
Pubmed Abstract | Pubmed Full Text
Roder, B., Rosler, F., and Neville, H. J. (1999). Effects of interstimulus interval on auditory event-related potentials in congenitally blind and normally sighted humans. Neurosci. Lett. 264, 53–56.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Roder, B., Rosler, F., and Neville, H. J. (2001). Auditory memory in congenitally blind adults: a behavioral-electrophysiological investigation. Brain Res. Cogn. Brain Res. 11, 289–303.
Pubmed Abstract | Pubmed Full Text
Roder, B., Rosler, F., and Spence, C. (2004). Early vision impairs tactile perception in the blind. Curr. Biol. 14, 121–124.
Pubmed Abstract | Pubmed Full Text
Roder, B., Stock, O., Bien, S., Neville, H., and Rosler, F. (2002). Speech processing activates visual cortex in congenitally blind humans. Eur. J. Neurosci. 16, 930–936.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Rogers, S. J., and Newhart-Larson, S. (1989). Characteristics of infantile autism in five children with Leber’s congenital amaurosis. Dev. Med. Child Neurol. 31, 598–608.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Rojas, D. C., Slason, E., Teale, P. D., and Reite, M. L. (2007). Neuromagnetic evidence of broader auditory cortical tuning in schizophrenia. Schizophr. Res. 97, 206–214.
Pubmed Abstract | Pubmed Full Text
Rokem, A., and Ahissar, M. (2009). Interactions of cognitive and auditory abilities in congenitally blind individuals. Neuropsychologia 47, 843–848.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Salillas, E., Grana, A., El-Yagoubi, R., and Semenza, C. (2009). Numbers in the blind’s “eye”. PLoS ONE 4:e6357. doi:10.1371/journal.pone.0006357
CrossRef Full Text
Sanders, G. S., Platek, S. M., and Gallup, G. G. (2003). No blind schizophrenics: are NMDA-receptor dynamics involved? Behav. Brain Sci. 26, 103.
CrossRef Full Text
Sathian, K. (2005). Visual cortical activity during tactile perception in the sighted and the visually deprived. Dev. Psychobiol. 46, 279–286.
Pubmed Abstract | Pubmed Full Text
Schenkel, L. S., and Silverstein, S. M. (2004). Dimensions of premorbid functioning in schizophrenia: a review of neuromotor, cognitive, social, and behavioral domains. Genet. Soc. Gen. Psychol. Monogr. 130, 241–270.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Schiffman, J., Maeda, J. A., Hayashi, K., Michelsen, N., Sorensen, H. J., Ekstrom, M., et al. (2006). Premorbid childhood ocular alignment abnormalities and adult schizophrenia-spectrum disorder. Schizophr. Res. 81, 253–260.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Scholes, K. E., and Martin-Iverson, M. T. (2010). Disturbed prepulse inhibition in patients with schizophrenia is consequential to dysfunction of selective attention. Psychophysiology 47, 223–235.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Schubert, E. W., Henriksson, K. M., and McNeil, T. F. (2005). A prospective study of offspring of women with psychosis: visual dysfunction in early childhood predicts schizophrenia-spectrum disorders in adulthood. Acta Psychiatr. Scand. 112, 385–393.
Pubmed Abstract | Pubmed Full Text
Sehatpour, P., Dias, E. C., Butler, P. D., Revheim, N., Guilfoyle, D. N., Foxe, J. J., et al. (2010). Impaired visual object processing across an occipital-frontal-hippocampal brain network in schizophrenia: an integrated neuroimaging study. Arch. Gen. Psychiatry 67, 772–782.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Sevik, A. E., Anil Yagcioglu, A. E., Yagcioglu, S., Karahan, S., Gurses, N., and Yildiz, M. (2011). Neuropsychological performance and auditory event related potentials in schizophrenia patients and their siblings: a family study. Schizophr. Res. 130, 195–202.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Shamma, S. A., Elhilali, M., and Micheyl, C. (2011). Temporal coherence and attention in auditory scene analysis. Trends Neurosci. 34, 114–123.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Sharma, A. K., Mehta, A. K., Rathor, N., Chalawadi Hanumantappa, M. K., Khanna, N., and Bhattacharya, S. K. (2012). Melatonin attenuates cognitive dysfunction and reduces neural oxidative stress induced by phosphamidon. Fundam. Clin. Pharmacol. doi:10.1111/j.1472-8206.2011.00977.x
CrossRef Full Text
Sharp, C. W. (1993). Anorexia nervosa and depression in a woman blind since the age of nine months. Can. J. Psychiatry 38, 469–471.
Pubmed Abstract | Pubmed Full Text
Siekmeier, P. J., and Hoffman, R. E. (2002). Enhanced semantic priming in schizophrenia: a computer model based on excessive pruning of local connections in association cortex. Br. J. Psychiatry 180, 345–350.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Silver, H., Feldman, P., Bilker, W., and Gur, R. C. (2003). Working memory deficit as a core neuropsychological dysfunction in schizophrenia. Am. J. Psychiatry 160, 1809–1816.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Silverstein, S. M. (in press). Cognitive coordination and psychotic phenomena pose challenges to Clark’s theory emphasizing propagation of prediction error and inhibition of correlated stimuli. Behav. Brain Sci.
Silverstein, S. M., Berten, S., Essex, B., Kovacs, I., Susmaras, T., and Little, D. M. (2009). An fMRI examination of visual integration in schizophrenia. J. Integr. Neurosci. 8, 175–202.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Silverstein, S. M., Jaeger, J., Donovan-Lepore, A. M., Wilkniss, S. M., Savitz, A., Malinovsky, I., et al. (2010). A comparative study of the MATRICS and IntegNeuro cognitive assessment batteries. J. Clin. Exp. Neuropsychol. 32, 937–952.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Silverstein, S. M., and Keane, B. P. (2009). Perceptual organization in schizophrenia: plasticity and state-related change. Learn. Percept. 1, 229–261.
Silverstein, S. M., and Keane, B. P. (2011a). Perceptual organization impairment in schizophrenia and associated brain mechanisms: review of research from 2005 to 2010. Schizophr. Bull. 37, 690–699.
Silverstein, S. M., and Keane, B. P. (2011b). Vision science and schizophrenia research: toward a re-view of the disorder editors’ introduction to special section. Schizophr. Bull. 37, 681–689.
CrossRef Full Text
Silverstein, S. M., Schenkel, L. S., Valone, C., and Nuernberger, S. W. (1998). Cognitive deficits and psychiatric rehabilitation outcomes in schizophrenia. Psychiatr. Q. 69, 169–191.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Slotnick, S. D., Thompson, W. L., and Kosslyn, S. M. (2005). Visual mental imagery induces retinotopically organized activation of early visual areas. Cereb. Cortex 15, 1570–1583.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Solovay, M. R., Shenton, M. E., and Holzman, P. S. (1987). Comparative studies of thought disorders. I. Mania and schizophrenia. Arch. Gen. Psychiatry 44, 13–20.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Steffener, J., and Stern, Y. (2012). Exploring the neural basis of cognitive reserve in aging. Biochim. Biophys. Acta 1822, 467–473.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Stern, Y. (2012). Cognitive reserve in ageing and Alzheimer’s disease. Lancet Neurol. 11, 1006–1012.
Pubmed Abstract | Pubmed Full Text
Sterr, A., Green, L., and Elbert, T. (2003). Blind Braille readers mislocate tactile stimuli. Biol. Psychol. 63, 117–127.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Sterr, A., Muller, M. M., Elbert, T., Rockstroh, B., Pantev, C., and Taub, E. (1998). Perceptual correlates of changes in cortical representation of fingers in blind multifinger Braille readers. J. Neurosci. 18, 4417–4423.
Pubmed Abstract | Pubmed Full Text
Stevens, A. A., and Weaver, K. (2005). Auditory perceptual consolidation in early-onset blindness. Neuropsychologia 43, 1901–1910.
Pubmed Abstract | Pubmed Full Text
Stevens, A. A., and Weaver, K. E. (2009). Functional characteristics of auditory cortex in the blind. Behav. Brain Res. 196, 134–138.
Pubmed Abstract | Pubmed Full Text
Stewart, R. H., and Sardo, R. (1965). The psychotherapy of a blind schizophrenic child. J. Am. Acad. Child Psychiatry 4, 123–132.
Pubmed Abstract | Pubmed Full Text
Stolt, P., Bengtsson, C., Nordmark, B., Lindblad, S., Lundberg, I., Klareskog, L., et al. (2003). Quantification of the influence of cigarette smoking on rheumatoid arthritis: results from a population based case-control study, using incident cases. Ann. Rheum. Dis. 62, 835–841.
Pubmed Abstract | Pubmed Full Text
Sullivan, R. (2000). Review: Olfaction in the Human Infant. New York: The Fragrance Foundation. Available at: http://www.senseofsmell.org/research/R. … -Paper.pdf
Sullivan, R. M. (2003). Developing a sense of safety: the neurobiology of neonatal attachment. Ann. N. Y. Acad. Sci. 1008, 122–131.
Pubmed Abstract | Pubmed Full Text
Sullivan, R. M., and Toubas, P. (1998). Clinical usefulness of maternal odor in newborns: soothing and feeding preparatory responses. Biol. Neonate 74, 402–408.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Tamminga, C. (2013). Psychosis is emerging as a learning and memory disorder. Neuropsychopharmacol. Rev. 38, 247.
CrossRef Full Text
Tek, C., Gold, J., Blaxton, T., Wilk, C., McMahon, R. P., and Buchanan, R. W. (2002). Visual perceptual and working memory impairments in schizophrenia. Arch. Gen. Psychiatry 59, 146–153.
Pubmed Abstract | Pubmed Full Text
Temple, E., Deutsch, G. K., Poldrack, R. A., Miller, S. L., Tallal, P., Merzenich, M. M., et al. (2003). Neural deficits in children with dyslexia ameliorated by behavioral remediation: evidence from functional MRI. Proc. Natl. Acad. Sci. U.S.A. 100, 2860–2865.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Tendolkar, I., Ruhrmann, S., Brockhaus, A., Pukrop, R., and Klosterkotter, J. (2002). Remembering or knowing: electrophysiological evidence for an episodic memory deficit in schizophrenia. Psychol. Med. 32, 1261–1271.
Pubmed Abstract | Pubmed Full Text
Thakkar, K. N., Nichols, H. S., McIntosh, L. G., and Park, S. (2011). Disturbances in body ownership in schizophrenia: evidence from the rubber hand illusion and case study of a spontaneous out-of-body experience. PLoS ONE 6:e27089. doi:10.1371/journal.pone.0027089
CrossRef Full Text
Thewissen, V., Myin-Germeys, I., Bentall, R., De Graaf, R., Vollebergh, W., and Van Os, J. (2005). Hearing impairment and psychosis revisited. Schizophr. Res. 76, 99–103.
Pubmed Abstract | Pubmed Full Text
Turetsky, B. I., Bilker, W. B., Siegel, S. J., Kohler, C. G., and Gur, R. E. (2009). Profile of auditory information-processing deficits in schizophrenia. Psychiatry Res. 165, 27–37.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Uhlhaas, P. J., and Mishara, A. L. (2007). Perceptual anomalies in schizophrenia: integrating phenomenology and cognitive neuroscience. Schizophr. Bull. 33, 142–156.
Pubmed Abstract | Pubmed Full Text
Uhlhaas, P. J., and Silverstein, S. M. (2005). Perceptual organization in schizophrenia spectrum disorders: empirical research and theoretical implications. Psychol. Bull. 131, 618–632.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Ullman, S. (1984). Visual routines. Cognition 18, 97–159.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Umbricht, D., Koller, R., Schmid, L., Skrabo, A., Grubel, C., Huber, T., et al. (2003). How specific are deficits in mismatch negativity generation to schizophrenia? Biol. Psychiatry 53, 1120–1131.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Van Snellenberg, J. X. (2009). Working memory and long-term memory deficits in schizophrenia: is there a common substrate? Psychiatry Res. 174, 89–96.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Vanlierde, A., De Volder, A. G., Wanet-Defalque, M. C., and Veraart, C. (2003). Occipito-parietal cortex activation during visuo-spatial imagery in early blind humans. Neuroimage 19, 698–709.
Pubmed Abstract | Pubmed Full Text
Vecchi, T., Tinti, C., and Cornoldi, C. (2004). Spatial memory and integration processes in congenital blindness. Neuroreport 15, 2787–2790.
Pubmed Abstract | Pubmed Full Text
Velasques, B., Machado, S., Paes, F., Cunha, M., Sanfim, A., Budde, H., et al. (2011). Sensorimotor integration and psychopathology: motor control abnormalities related to psychiatric disorders. World J. Biol. Psychiatry 12, 560–573.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Vercammen, A., De Haan, E. H., and Aleman, A. (2008). Hearing a voice in the noise: auditory hallucinations and speech perception. Psychol. Med. 38, 1177–1184.
Pubmed Abstract | Pubmed Full Text
Wakefield, C. E., Homewood, J., and Taylor, A. J. (2004). Cognitive compensations for blindness in children: an investigation using odour naming. Perception 33, 429–442.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Wan, C. Y., Wood, A. G., Reutens, D. C., and Wilson, S. J. (2010). Early but not late-blindness leads to enhanced auditory perception. Neuropsychologia 48, 344–348.
Pubmed Abstract | Pubmed Full Text
Ward, J., and Meijer, P. (2010). Visual experiences in the blind induced by an auditory sensory substitution device. Conscious. Cogn. 19, 492–500.
Pubmed Abstract | Pubmed Full Text
Ward, P. B., Catts, S. V., Fox, A. M., Michie, P. T., and McConaghy, N. (1991). Auditory selective attention and event-related potentials in schizophrenia. Br. J. Psychiatry 158, 534–539.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Weiss, K. M. (1989). Advantages of abandoning symptom-based diagnostic systems of research in schizophrenia. Am. J. Orthopsychiatry 59, 324–330.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Williams, L. E., Light, G. A., Braff, D. L., and Ramachandran, V. S. (2010). Reduced multisensory integration in patients with schizophrenia on a target detection task. Neuropsychologia 48, 3128–3136.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Williams-Gray, C. H., Foltynie, T., Lewis, S. J., and Barker, R. A. (2006). Cognitive deficits and psychosis in Parkinson’s disease: a review of pathophysiology and therapeutic options. CNS Drugs 20, 477–505.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Wing, L. (1969). The handicaps of autistic children – a comparative study. J. Child. Psychol. Psychiatry 10, 1–40.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Wong, M., Gnanakumaran, V., and Goldreich, D. (2011). Tactile spatial acuity enhancement in blindness: evidence for experience-dependent mechanisms. J. Neurosci. 31, 7028–7037.
Pubmed Abstract | Pubmed Full Text
Yung, A. R., and Nelson, B. (2011). Young people at ultra high risk for psychosis: a research update. Early Interv. Psychiatry 5(Suppl 1), 52–57.
Pubmed Abstract | Pubmed Full Text
Zhou, X., Panizzutti, R., De Villers-Sidani, E., Madeira, C., and Merzenich, M. M. (2011). Natural restoration of critical period plasticity in the juvenile and adult primary auditory cortex. J. Neurosci. 31, 5625–5634.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Zimler, J., and Keenan, J. M. (1983). Imagery in the congenitally blind: how visual are visual images? J. Exp. Psychol. Learn. Mem. Cogn. 9, 269–282.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Zimmer, U., Lewald, J., Erb, M., Grodd, W., and Karnath, H. O. (2004). Is there a role of visual cortex in spatial hearing? Eur. J. Neurosci. 20, 3148–3156.
Pubmed Abstract | Pubmed Full Text | CrossRef Full Text
Keywords: schizophrenia, blindness, perception, cognition, vision, vision disorders, plasticity
Citation: Silverstein SM, Wang Y and Keane BP (2013) Cognitive and neuroplasticity mechanisms by which congenital or early blindness may confer a protective effect against schizophrenia. Front. Psychology 3:624. doi: 10.3389/fpsyg.2012.00624
Received: 03 November 2012; Accepted: 31 December 2012;
Published online: 21 January 2013.
Edited by:
Michael Green, University of California Los Angeles, USA
Reviewed by:
Yue Chen, McLean Hospital, USA
Jonathan K. Wynn, University of California Los Angeles, USA
Copyright: © 2013 Silverstein, Wang and Keane. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
*Correspondence: Steven M. Silverstein, University Behavioral HealthCare, University of Medicine and Dentistry of New Jersey, 151 Centennial Avenue, Piscataway, NJ 08854, USA. e-mail: [email protected]
1 Comments - Bill Newbold.
overview
Bill Newbold Right, I didn't like having to sign in to write a comment. Somehow I found a way. I have schizophrenia, - onset age, 21. At twenty one I started organizing and positioning clips from magazines and papers on my walls visually. This is similar with some schizophrenics, exactly, I have schizoaffective depressed. This visual process was made public in it's ritual form by Graham Nash in the movie "A beautiful Mind." I was 21 in 1984 going to Rutgers at Livingston during my onset which is when my paper picture and article writings placement and organizing on my home walls was the greatest. This is something that I think relates to the effects of schizophrenia. I have been doing this process to my walls since 1984 no matter where I have lived, or what institution I was in. I understand this process well. Somehow the cognitive stress of schizophrenia is relieved from doing this. It is helpful helpful to me and my eye movement and control, I know this. I do this now, with music as well but that is different in a way. There is new research based on the paper above in relation to this process that I can help with. I think the fact that people born blind don't get schizophrenia as their brain is able to rework the cognitive maps to use the extra "processing" space or thinking area once used for vision.

Thank You for your research in this.

Forgive the lack of scientific jargon in my comment, college did not go well simultaneously with the onset of the Schizoaffective disorder. As such the research into these ideas could end here.
Yesterday at 4:22 AM

Write a comment...
Add
COMMENTARY
Base rates, blindness, and schizophrenia
Steven Silverstein, Yushi Wang and Matthew W Roche

2020-02-14 22:33:15

I know of one practicing blind psychologist, and my best friend is about to become a licensed clinical counselor as well. One of the future career paths I toyed with in high school was the field of psychology, in fact, a decision I greatly regret now because once people found out, they never got off my back about it, and still love to tell me to this day I'm selling myself short and oh, isn't it just a shame how you threw away a chance to make tons of money? But I digress.

My belief is that spirituality and/or religion should not enter into a counseling relationship unless the client is seeking out that type of support willingly, i.e. seeing a Christian counselor, and knowing exactly what that entails, or the client makes it very clear that they would benefit from that type of support, or needs to discuss traumas related to religion. In either case, especially if there are traumas involved, some pretty clear boundaries would have to be established around those topics. So, no, the psychiatric model may be busted in some ways, but I definitely do not believe adding more holistic healing, for lack of a better term, to the mix is the catch-all solution that was espoused a couple of posts ago. Leaning too far into the spiritual side can be just as, if not more, harmful than the all mental health diagnoses need to be medicated, no exceptions, way of thinking.

The glass is neither half empty nor half full. It's just holding half the amount it can potentially hold.

2020-02-14 23:27:26 (edited by bashue 2020-02-15 00:20:06)

Greetings turtlepower17. Thank you for making that good point. Even though I don't agree, I do understand the point you're making and I do respect it. @Everyone, below are articles taken from dsm.htm update.htm and ADHD.htm. While the below articles aren't elated to blindness and schizophrenia, they explain why I believe what I believe. I've quoted the authors and marked them with their respective urls. Kind regards, Amin Abdullah.

Clemencia Barnes wrote:

DSM.htm

~ THE ERROR OF PSYCHIATRY & PSYCHOLOGY ~
In the treatment of what is termed 'mental illness.'
&
The spiritual causes now revealed in this web site and in the 'Testament of Truth' Suicide document linked at the end.
In a recently produced CD 'Making a killing' aimed at raising awareness of Mental Health issues, a number of eminent professionals from the medical, legal, psychiatric and psychological professions presented a very strong case for investigating the validity of the system of mental health practices particularly as they relate to the reliance upon and utilisation of the Diagnostic Classification of Mental Diseases commonly referred to as the Diagnostic Statistics Manual (DSM).
A synopsis of the CD issued by the 'Citizens Commission on Human Rights' is set out in this document as is a link to a valuable Mental Health resource on the spiritual cause of Suicide and aggressive tendencies.
The content on theCD speaks of a 'Tale of deception' in the use of psychotropic drugs to 'manage' mental health problems and it exposes that there has been no 'cure' to date resulting from the use of said drugs, drugsthat have in fact killed people and caused untold harm and misery to 'millions.' The CD also speaks of "Psychiatry's prescription for Violence" due to so many users of prescription drugs becoming more depressed, irrational and violent rather than being a benefit to the user of said 'legal' drugs.
What is perhaps most alarming is that accordingto many of the participating mental health experts presenting on this CD, any aspect of human behaviour can, and now is,  labelled as a mental illness by the psychiatric DSM 'bible.' For example, such behaviour as exhibiting signs of being upset after a marital breakup, feeling nervous due to some important event, being sad or anxious when speaking in public, being shy, talking too much or simply being fearful, are now all classified as mental health "Disorders?"
In fact, GP's are now being instructed on how to assess whether a patient is exhibiting behaviours that are 'classifiable as a mental disease' and therefore required to be referred to the mental health professionals for diagnosis and medication.
If we look quickly at the many ordinary human emotions, sorrows and life difficulties which can be classified as 'disorders' according to the Mental health Diagnostic System of Mental Disorders (hereafter referred to as the DSM Fourth addition), we may well be astounded to find that the latest edition of this manual contains 943 pages of diagnostic categories under which are 'classified' all human feelings and behaviours in various computations, but all of them being labelled as Disorders of or diseases of mental states.
In other words, normal human emotional reactions to life stresses, challenges, uncertainties or even such major stressors as marriage disintegration, dealing with a problem child, or just feeling overwhelmed, are now given a mental 'dis-ease' label. This label is always accompanied by a drug usually having the effect of numbing the individual's emotional state. This in itself is madness as the majority of 'behaviours' listed are normal human emotions being displayed.
Let me name a very small sample of those 'disorders' which are in fact categorised as Mental Diseases..... stuttering, cigarette addiction, nightmares, fear of spiders and currently there is a wave sweeping the profession to include a disorder of infancy under the banner of paediatric mental health! How any individual could possibly 'diagnose' an infant with a mental Disease is surely beyond the comprehension of any rational person.
It is the spirit within the individual which contains both the positive LIGHT and the DARK inner emotions seen in times of despair and it is mostly the dark thoughts which infect the soul of man. The gambit of emotions in the minds of people are fear, greed, criticism, hatred, jealousy, anger, revenge and a multitude of other feelings and as such are a causal feature of the inner, ceaseless 'turmoil' that produce the behaviour we then label as mental disease. The other side of this concerns the spirit soul of the individual (which is also ignored by professionals) that is the core of LOVE, love that brings with it joy and happiness and inner PEACE.
I am quite aware that there are material as well as emotional occurrences that result in people suffering great mental and emotional trauma and that this together with physical abuse leads them to 'hospital' or other institutions for help or counselling.
And yes, we as a community are required, when faced with an individual who is disturbed by an abnormal situation causing them to  experience mental and emotional stress, to assist them as best we can. I am also aware that in many cases their normal reaction to abnormal circumstances is being turned into a diagnosis of mental illness, and that their cry for help can lead to medical abuse via the drug route.
Naturally a physical abuse 'incident' can be the cause of the present 'mental anguish' being felt by the 'victim' but equally, a person who has not been subjected to 'rape, violence or system abuse' can suffer mental and emotional problems which 'man' labels as a psychiatric disorder or mental illness but, which may have a causal factor of matters to do with the spirit soul of the individual's journey through time.
So in fact there are two separate causes for 'stress' or intensification of disturbing emotions which can increase the thought processes to a point where they reach the state of uncontrollable turbulence. One of these is solely the result of the consequence  of some form of violence aimed at the individual.
The other intensification disturbance in emotional states is aroused 'fearful or depressing' emotions which seem simply to 'happen' with no apparent external influence but which nevertheless are beyond the capacity of the individual to halt in terms of the revolving thoughts that go on endlessly and may lead to out of control emotions.
In both of the above 'cases' the mental and emotional disturbances result in the person feeling themselves to be out of control and  beyond their capacity to cope. This state often ends in the person being 'labelled' under the mental health umbrella but  the question that is seldom asked is 'why are the individuals thoughts and emotions unable to be controlled?'
The answer is simple. It is due to the intrusive 'nature' of the Dark energy essence which, being the consequence of their Dark emotions can, and mostly does, override individual thought processes. Without reason to enable a person to come to grips with their emotional response thoughts are compound by out of control emotions, emotions that can only be halted when the individual understands the process fully namely by taking the necessary 'steps' to fortify their minds against the incoming thoughts that constantly revolve in their mind.
~ Spiritual Clarification ~
As an EDUCATOR it is my 'task' to expose the fact that any inner turmoil which had NO outside causal factor is indeed the result of the spirit soul of the person having become "infected" as it were by Dark inner emotions. It is my 'task' to also expose the fact that any inner turmoil caused by an external factor is greatly exacerbated by negative emotions within the individual and this can result in 'non-acceptance' and un-forgiveness or blame. It is these  ongoing 'depressive' processes that are difficult to surmount or 'heal.'
These emotions are the sign of the negative emotional energy drawn into that persons spirit soul over a period of time, possibly an eternity of time. The result of this is that the individual's negative emotions begin to influence their mental state.  In this statethe thought processes become fixated on the negative feelings existing within their soul.
This fixation ultimately results in dark energy which in turn feeds the emotional turmoil and this process can go on endlessly.  What is so hard for the medical profession to accept is that these negative emotions existed within that persons soul long before the person's spirit entered this  material world.
I say this because 'unbeknown' to mankind, having emotions of fear, greed, criticism, hatred, jealousy, anger, revenge and a multitude of other DARK feelings within one's spirit soul is an 'unnatural' state of being.  (It is a state referred to as the SIN in man).
For those souls who have never defied  God's "peace, love, mercy, compassion and forgiveness" Command, negative emotions are not within their soul which means these people are therefore at 'Peace' both mentally and emotionally at all times and in all situations even when 'confronted' or abused. Without the negative feelings these individuals remain mentally and emotional steady and stable resulting in them being capable of being merciful and forgiving of any who become their oppressor.
There is no judgment being made in stating that dark inner emotions infest and infect the soul of a person. This is simply a reality  being experienced by the spirit of most individuals walking the earth today.  It is the reality of telepathic intrusion of the Dark that can cause an individual to become totally irrational for a time until they ''come to themselves" as it were.
Once they become 'rational' and more aware of their own thoughts they often have no cognitive memory of what it is they may have done while in the state of utter despair due to the telepathic control associated with the Dark intrusion into their mind.
It is the time for all mortals, especially 'helpers,' to understand that it is not a 'normal' state of affairs to have this DARK energy within our souls being expressed negatively from our mouths. It is also the time for 'troubled' (mentally disturbed) people to realise that IF they are not in control of their thoughts then these thoughts do 'stem' from outside the self, a state which in the past was correctly recognised as telepathic subjugation of the mind of man by intrusive spirit forces overriding the person's individual consciousness. The time now is for everyone to learn how to stem this process of 'spirit possession' and the means of doing so is available through the 'Suicide document.' The link thereto is available at the end of this document.
Further to the above, everyone needs to learn about 'The God factor,' for 'invited or not God will attend.' Understanding the God factor educates us about the immutable 'Law of God' which is in operation at all times. 
The Law of God is simply that what we put out in terms of our actions towards others does come back to us at the time and in the place so ordained by God consequently, a person 'suffering' physical, mental, emotional or any other form of abuse is simply receiving their 'Just dues' within said law whichis imposed on them through the 'hands' of ignorant and arrogant vain mortals or, stemming from within their own minds and negative emotions.
The individuals who use 'darkness' to intrude, control, rob, rape, pillage, abuse and destroy others are ignorant and have absolutely no knowledge that they themselves will later 'suffer' the same fate, a 'fate in the same form of suffering' which they imposed on others, whether that is to be imposed upon them in this life 'time' or in another realm in the afterlife.
However, the relevance of this 'DSM' outreach article is to 'awaken' all psychiatrists and psychologists to the error of their promotion via their mis-understanding of the spiritual truth surrounding mental and emotional issues. If these professionals are to become true 'helpers' then it is imperative that they reprogram their mind  and 'enlighten' it to the facts given so that the mental and emotionally 'needy' become educated and are then able to 'extract' themselves from their 'suffering' and move forwards.
Another reason for this outreach article is to 'awaken' all psychiatrists to the error of their promotion of mind-altering drugs and to assist them to address their own mis-understanding of the spiritual truth surrounding mental and emotional issues.
At this stage of history every true 'helper' needs to re-program their current 'programmed' mind by 'enlightening' it to the facts given so that the 'needy' become educated and they are then able to 'extricate' themselves from their 'suffering' and move forwards.
For too long the false belief of psychiatry has held mankind in suffering and as a consequence, and due to the psychiatrists own ignorance, they have caused ongoing trauma through their drug induced control. Through such control psychiatrists themselves are accruing a similar 'due' within God's Law, namely, that the physical or mental or emotional suffering you impose on others is the suffering you will have imposed upon yourself.
Clemencia
LINK: The Suicide document: suicide.htm

update.htm

~ Mental health revelations update - 2010 ~
What have we failed to do in all of our attempts to deal with the problem?
By Clemencia.

Introduction
As a practitioner in the field of mental health for a period of 43 years, I discovered some time ago that millions of dollars spent on 'interventions' and strategies to deal with mental illness were wasted.
I now know that this waste was not because individuals introducing those strategies as interventions were not desirous of assisting those with mental illness but, because those in positions of 'authority,' the decision makers on issues of mental health, refuse to accept that a spiritual malaise as well as the loss of the sacred in the lives of individuals are also causal factor in mental illness.
It has been my understanding of the reality of the spirit and spirit influence on the minds of individuals that led me on a personal search to find a better way to assist all who suffer from the unstoppable negative thought processes so prevalent in mental illness.
That journey has concluded and this 'update' added to this web site is simply an addition to the information already available. I wrote this article as a 'circular' for the many people dealing with mental illness so that they can truly give the mentally 'disturbed' the means to assist themselves.
During my working life I devoted much time to learning about methods of interventions best suited to individuals suffering from mental disturbances. What I was seeking was a strategic intervention that would assist individuals to deal with the emotional, psychological and distorted cognitive processes so prevalent in mental breakdown.
I found myself pushed to keep searching because prior to finding the current information concerning the impact of spirit reality on mental health, there were an increasing number of very successful and 'seemingly together’ individuals exhibiting evidence of destructive thought processes which rendered them incapable of making healthy emotional, psychological or cognitively sound life choices.
The conclusion reached is that, no matter what the interventions different professionals were utilizing, the best they could do was to ameliorate the mental stress in the minds of the mentally disturbed for a time. While this was helpful the fact is that the mental 'dis-ease' always remained and often required more treatment using whatever intervention the practitioner was utilising at the time. In short, there was no evidence of a ‘cure.'
What is Mental 'breakdown'?
Present psychiatric understanding of mental illness is based on the Diagnosis and Statistics Manual of Mental Illness (DSM). The DSM was created to attempt to classify and describe mental illness. While early editions contained some 50 diagnosis describing mental illnesses, the current issue of the latest edition, DSM 4 TR contains over 400 diagnoses. Should we not question how a ‘science’ legitimises the constant shifts in the descriptor assigned to behaviours to incorporate into the category of ‘mental illness’ particularly when the increase in new diagnoses seem more concerned with social control than any real ‘mental’ disturbance?
Basically it appears that psychiatrists, as agents of social control, have manufactured "madness" more to suit legitimate ways of controlling those who may disagree with the control of ‘systems’ of control than with a true science such as that carried out by the objective measurements of physical diseases via independent laboratory tests.
While diagnosis of mental illness is classified via the DSM by most health professions it is my experience that accepting this restricted interpretation of mental illness persistently ignores the role our spirit plays in the ‘thought processes’ involved when mental illness becomes apparent.
It is now time to readjust the 'belief' that mental illness is 'that which is down in the DSM 4, because those diagnoses are merely classifications ‘voted’ on by psychiatrists. Behaviour, whether misbehaviour or acceptable behaviour, cannot be described as a disease, it is always simply behaviour which is either acceptable or unacceptable in the social milieu of the time. What mental illness can be described as is a process of constant intrusive thoughts which disturb the peace of the individual experiencing them and which frequently do not seem to belong to the individual thinking them.
It is true to say that the medical and psychological professions do not accept that despite an explosion of interventions assisting with the treatment of mental illness over the decades, the inundation of personally ‘un-thought’ thoughts intruding into the minds of ordinary individuals who are not considered to be suffering ‘mental
health’ problems, keeps on increasing globally and at a rate not previously experienced.
Equally true is the fact that the increase in mental illness is occurring in spite of the plethora of therapeutic interventions and ‘new’ diagnosis with accompanying ‘treatments.’
It is my considered opinion that there are very deep reasons for the escalation of mental 'breakdown' and this is explained in the article titled 'Minds Under Siege' within the body of my web site. In this Treatise there is an exposition on how and why the mind of individuals is being subjugated and controlled from other realms of consciousness.
The means to a greater understanding of the processes outlined in that Treatise, together with information on ways of stemming the tide of intrusive thoughts is found therein.
To obtain greater understanding of the processes outlined in that Treatise, together with information on ways of stemming the tide of intrusive thoughts is found within:
Treatise 5 - Soul Survival and The Carer’s Manual found within :
Item 18 - The Treatise of Truth - 85 pages - The Mental Health Carer's Manual
Summary of Failed implementation Strategies in Mental Health
The first significant government intervention during my time as a practitioner was the National Youth Suicide Prevention Strategy (introduced in response to the alarming increase in youth suicides). This was an effort by the Commonwealth Government to provide a comprehensive, coordinated approach to youth suicide prevention.
Prevention Strategy were to:
• prevent premature death from suicide among young people
• reduce rates of injury and self-harm
• reduce the incidence and prevalence of suicidal ideation and behaviour
A total of $31 million was allocated to the Strategy from July 1995 to June 1999. Many earnest individuals, groups and organisations tendered for the process of delivering services with the aid of government funds allocated for the purpose.
At the time the NYSPS adopted strategies focused on Primary prevention, cultural change and early interventions
If Primary here refers to the root or source as for example in early childhood, then the strategies utilised failed if we consider the alarming number of very young children on drugs for mental health issues such as ADHD as at the year 2010.
It is my observation that the end point of the primary preventions implemented during the 1990’s have resulted in the ‘medicalization’ of childhood behaviour rather than in preventions leading to positive behavioural or cultural change that being the stated aim of the government's primary intervention.
The next major national intervention was the push by governments to establish a more cohesive approach in dealing with mental illness. The results of this intervention injected in excess of $250 million from 1993 to 1998 to assist with the implementation of the National Mental Health Strategy. The philosophy of the Strategy and recommendations for action in twelve priority areas for reform are articulated in five major documents: (cf. Appendix I)
The focus of these changes centred on the service mix for delivery of mental health services. The most dramatic shift was that of a resources shift from hospital-based services to community-based services, a shift from stand-alone psychiatric hospitals to general hospitals and health services, and an increased diversity of community-based services.
In the year 2010 we are experiencing the fall out of these shifts. There are currently a greater number of mentally ill people in jail than at other times in history. While an evaluation of the NMHS completed in December 1997 reported considerable impacts on the substantial shift of resources from stand-alone psychiatric hospitals to community based mental health services they did not foresee the catastrophic fallout of care for the mentally ill that would follow in the next 25 years.
In the First Mental Health Strategy in 1999, a further $328 million was spent by governments to improve mental health services and again in the year 2010 we cannot fail to note that mental illness is being exhibited in an ever increasing number in the younger children and teenagers as well as from within the older generations.
In summary, while a total of $906 million tax payer money has been spent on many different strategies over the past 25 years, there appears little evidence of where or how those funds have improved the state of mental illness in Australia.
Current comments from most professionals working in mental health areas report a general increase in the number of individuals generally, and the younger population specifically, seeking assistance for the treatment of mental health issues.
Where Do the Problems Lie
To me the question mental health professionals need to put to themselves is; "What is it they have failed to do or what area of investigation are they ignoring, that has led us to the stark reality that our children are not surviving adolescence in an emotionally healthy way"?
Given all our efforts, the good will of many people, professionals and lay folk alike and despite the substantial funds given out to resolve the problem of family break down, of increasing mental ill health and escalating suicidal, demanding, selfish and aggressive behaviour, what is it we as a nation have failed to do in all of our attempts to deal with the problem?
My response to that question is complex and therefore bound to be lengthy because there are many areas in the lives of our children and young adults where we have failed them.
Let me set out the bare facts as I see and experience them from within my practice.
In most wealthy Western Nations we now have the third generation of children who have received little or no input to provided them with a counter-point to the ideology or creed of ‘materialism.’
This Creed centres on the divine rights of the individual. The right to own, to acquire, to possess and to purchase.
These generations of children have been raised in times of corporate greed, political unaccountability, moral bankruptcy and religious betrayal.
Anything remotely connected with Spirit, soul, the sacred, alternate philosophies, truths or anything other than ‘materialism’ has been banished from the education  of most of our children.
Concepts or ideologies dealing with such things as mercy, forgiveness, compassion or love; ideas about self-sacrifice for the good of all, of caring for others and sharing resources are concepts alien to many of the young people who present for treatment around mental health issues.
What we have given our children in enormous doses is the 'New Religion which is best named the creed of greed. For at least three generations now children have been bombarded with the ideology of the superficial - ‘possession leads to happiness' – ‘to look good is to be good' –‘ownership of things’ is somehow considered to lead to "internal transformation"! The latter is a belief in the fact that the right make-up, clothes, toys, gadgets or an endless array of material acquisitions leads to one becoming a ‘better person,’ one with a 'status' concerning 'stuff' which give one value!
The indoctrination of children is now centres on the art of consumerism where acquisition of more leads to an obsession to have more. For any astute person it is impossible to deny that today there is no 'god' worshipped as voraciously as the God of "materialism."
Given that many members of the scientific profession make rather scathing comments about individuals who have a belief in God it is surprising that they have failed to address the mentally unhealthy impact on our young people through their worship at the feet of the "God of consumerism."!
Many of the problems faced by children today are as a direct consequence of our failure to give them a counterbalancing point of view by encouraging them to question the validity of material worth. When some of the mental and emotional stress on our children stems from not having the latest ‘material’ item are we not denying them some basic human rights about life? - for example - possessions are only a momentary ‘release’ from the inner turmoil? It is becoming more and more clear that our failure to give children some of the life's core values means that the inheritance we pass onto them today is a paucity of understanding regarding matters of the sacred, of spiritual strength and humility and of the wisdom to discern what is of value in a life simply and honestly lived.
The questions we now need to answer are firstly, how does this creed of materiality or lack of it affect the emotional state of the minds of individuals? Secondly, how do we account for individuals who, 'having it all' still succumb to mental illness, depression and suicidal thoughts?
The answer to the first question is that the negative emotions of selfishness and greed can grow. This is clearly evidenced as we see children becoming more demanding and increasingly aggressive, rude and disrespectful if their demands are not met.
Sadly, children also exhibit signs of feelings of 'inadequacy' or 'jealousy' when others are in ‘possession’ of the latest ‘in’ object and they do not posses the same. The 'have nots' today genuinely feel themselves to be inferior not because they do not have the same talent or other achievements but because the do not own the 'in' possession!
My point is that when we ponder over why there is this alarming increase in the deteriorating mental health in so many people we need go no further than the realization that we have failed to give people/children any sense of meaning beyond the material. The selfish 'creed of greed' has left individuals rudderless in the increasing storms of life.
In summary it is not until we introduce education enabling children to search for meaning in their lives outside of the ‘self’ or outside of materialism; not until we allow them to explore ideas such as an understanding of the meaning of existence; teach them how to search for understanding about the spirit of man and an understanding of the impact of negative actions on their emotional well-being; only when these are incorporated into children’s education do we provide them with the tools to assist them make mentally healthy choices.
The lack of such teaching has led to an intensification of the negative emotions within people, emotions leading to accompanying negative thoughts often beyond the individual’s capacity to control or override.
How are we going to deal with the explosion of mental illness currently rife throughout our population?
As a teacher in matters of the spirit I state quite categorically that unless we incorporate an understanding of the influence of spirit in our lives, any attempt to halt the progress of mental breakdown is futile and we will once again fail as surely as we did with the introduction of strategies implemented from the period 1993 to 2000. (1)
Men of science consistently deny the existence of a God, the Source or a universal Energy that impacts us and do so predominantly because they are unable to produce a scientific method to ‘prove the existence of such a being.' I on the other hand hold that if we keep ignoring the fact that mankind is not merely physical but is also a being of emotional, spiritual, psychological and mental energy, we will continue to exacerbate the increasing escalation in mental illness.
I would also go so far as to say that what is currently not understood or accepted is that man's mental processes of thought best exposes the presence of that aspect of man called spirit. That being so means that the consequence if we continue to ignore the spirit in our attempts to deal mental ill health can only result in the increase of endless new interpretations of mental illness being added to the DSM because to date there are not many theories of intervention other then an increasing dependency upon medication, that have proven a capacity to halt the increase in mental illness.
Incorporating an understanding of the spirit when grappling with mental illness assists in treating the whole person because, as with all other physical characteristics of life, man is made up of energy and it is both our cognitive and emotional state that reveals that energy and its invisible power.
Walk into a room where a couple are engaged in a verbal battle and although they stop well before you enter, you can ‘cut the air with a knife.’ We call this picking up a ‘vibe’ but in actuality what we feel is the vibration of the energy that human emotions emit. All of us ‘sense’ that energy either internally from within the self or, externally as in the above example. When I share this insight with people they often identify such energy with a constant 'stream of thought' and that these thoughts seem to feed upon themselves and can lead to actions that are often irrational or "not like me!"
While the idea that we are comprised of energy within our physical form and that the use of that energy does determine our physical well-being is not new, what is new is the understanding that the energy used by our emotions and thought processes are also determinants of our overall well-being. Negative thoughts and emotions do lead to negative actions while positive thoughts and emotions lead to positive actions.
If we combine the information about thought processes as 'energy in action' with the fact that man is also comprised of spirit and add to that statement the fact that man also produces energy during the process of turning thought into action, we may begin to grasp that energy, positive or negative can be, and I believe is, projected by spirit as thoughts into the minds of others.
Let me try and clarify what I am stating:
• Our thoughts create energy just as our actions create energy
• We are comprised of matter and spirit and our thoughts create energy that vibrates at various frequencies.
• We live in a universe where there are also other spirits, not incarnate, whose energies have the same vibrations as the frequency at which our energy is vibrating at any time.
• Incarnate spirits have the capacity to lock into the frequency of the vibration of energy coming from our thoughts and emotions and when they do so they can project their thoughts into our minds.
If we can accept that spirits project thoughts to other spirits {which includes spirits not incarnate inspiring ‘thoughts’ into the minds of spirits in the flesh} then truly, for the first time, we have a clearer understanding of just what is happening in the area of mental ill health. In the past this concept was referred to as 'spirit possession’ a belief that remains part of many religions today.
Energy is both positive and negative that is having both a dark (malignant - negative) and a light (benign - positive) side. Given this, when a negative stream of conscious thought is projected into the mind of an individual by someone ‘other’ than the self, this must inevitably lead to a belief that one is in a state of delusional thought processes. Specialist mental health practitioners would hold that to be so but what if the spirit reality is as ‘real’ as the ‘scientific’ reality and none of us know that? Would it not be incumbent upon us to examine, under clinical conditions, whether this is a truth or a proposition so preposterous that it must be disproved?
I find it hard to accept that the above interpretation concerning the increase of negative emotions in a greater number of people (generally termed ‘mental illness) is any less credible than the endless interpretations of what constitutes mental illness held by medical specialists who have spent many decades trying to find a method for understanding and successfully treating mental illness.
To date the best they have come up with is a plethora of diagnosis and medically based pharmaceutical interventions that do not cure mental illness but only change the bio-chemical balance in the brain of patients and while these certainly dull the mind of those diagnosed as mentally ill, they only do so for the duration of the medically induced changes wrought in the brain.
It is well documented that when patients withdraw from their medication they are again tormented by their endless thought processes which resume upon withdrawal of all medications.
To date no scientist has explored the possibility that it is the spirit of man which is also participating factor in mental illness where patients exhibit irrational and uncontrollable thought processes. This is most probably because scientists find it too ‘far-fetched’ to accept that there is such a thing as a Prime Source (which we call God or whatever that is named in ,various earthly interpretations).
Unfortunately this limited view by scientists of our mental functioning excludes them from accepting a basic human experience namely that people do experience themselves as spirit and that they do have experiences of spirits.
Without an understanding of the human spirit and the fact that spirits do interact with people we can always only try to treat the individual but we never actually give them the tools to treat themselves.
To help individuals to help themselves there are some basics that are taken as a given. These are:-
• There exists a Source variously called God, Buddha, Yahweh, Allah, Krishna and with many other names.
• That this Source is comprised of energy in all expressions thereof from positive to negative.
• That each individual spirit is created with both the positive and negative energy contained within the Source.
It is the negative or dark energy essence which remains 'unknowable' except by the pure of heart being those with a compassionate, merciful and forgiving nature who never retaliate thereby allowing them to become freed of the dark influence until they have no dark energy within. Such a person has been able to 'expose' the true nature of the Source namely, that the Source is comprised of energy and that the Source has a duality of both Light and Dark energy within Its frame.
What has compelled me to seek greater understanding of this insight into God as energy, and as having a duality, is the significance of how that Dark side is reflected within ourselves where it becomes the conduit activating our inner darkness, or demons, as we often refer to them.
This interest in the Dark side of both man and God stems from the revelation written over the past 15 years of that "Dark side of the Source" and is contained in a book titled "The Testament of Truth." It is this revelation which forms the basis of my personal insight into understanding of mental illness.
The Source as Energy – Positive and Negative
Light and Dark - Merciful and Judging
If we are genuinely searching for answers to the processes involved at the root of mental illness we need to understand how the mind and its content impacts on our mental well being and the fact that we can leave no stone unturned in that search even if it includes the ‘possibility’ that it is all about spirit.
As stated by a prominent psychiatrist from the past, ‘invited or not, God will attend.’ By quoting that statement what I mean is that the Source does indeed ‘attend’ to everything we do but not in the way that has been propounded by various philosophical, scientific, psychological or religions theories.
What I mean when I state that invited or not God will attend is that God is energy in every aspect of that term whether we utilize the term as implying positive and negative, light and dark or merciful and judging.
The emphasis is not on the adjectives but on the 'AND' since the Source is energy in totality therefore containing within Itself every aspect of energy. Of equal importance is the need for us to understand that there is a spiritual consequence resulting from our use of either aspect of God's energy in our interaction with others.
In accepting the evolutionary process we also accept that energy was produced with the ‘big bang.’ Of equal importance is that energy does not disappear and it is the assertion of this paper that mankind is also comprised of energy both in the aspects of our physical and spirit selves.
As energy we emit 'energy' frequencies according to the nature of the energy we utilize in our daily interactions with each other whether that interaction is benign or malignant.
When we are positive in terms of what the Source (who many call God) requires of us, namely to be peaceful, forgiving, compassionate, loving and non-judging of the 'offensive' actions of others, we are using the positive energy of the Source. The energy we chose to use in this situation produces a vibration at a particular frequency from the whole spectrum of energy.
When we are forgiving and non-judging it is the 'Light' or positive energy used in that moment of interaction with others which results in vibration at a positive frequency. Often we ‘feel’ this vibration when we meet someone for the first time as for example when we feel an instant connection or alternatively, when we feel an instant sense of being repelled.
The positive energy used in that interaction attracts a like vibration of an equal positive energy back towards us.
When we are negative in terms of God’s requirement of us, namely when we contravene the Command to be forgiving and loving and we choose instead to become cruel, retributive, punitive, critical or judgmental, we are using God’s Dark negative energy.
When we choose to be forceful, controlling or destructive the "Dark" negative energy used in that moment vibrates at a negative frequency and there attracts an equal negative energy back towards us.
Naturally utilizing the positive energy results in a steady mind as positive energy flows back to us but the reverse is true when we choose to use God’s negative energy. Negative energy used by us attracts a like vibration back to us and as it does so it places us under/within God’s one Law mostly referred to as the Law of Karma. (We reap what we Sow)
When we use either the Light or the Dark energy some of the energy we so use remains within our spirit soul thereby causing our soul to either 'brighten ' with more Light or ‘darken’ with more Dark.
It is the dark energy we use in interaction with others which attracts increased thought processes into our minds as spirit others, trapped in their own level of existence, are inspired to supposedly help us but in reality often make us fear for our sanity as our thoughts go endlessly around with concepts we thought we were incapable of thinking.
Man-Made Systems & Accountability for Spirit Reality
Solutions
Ultimately criticism remains a negative if we cannot offer an alternative, positive solution therefore the question becomes what do I have to offer those working in the mental health field to assist them in a manner that has to date not been utilized?
In the first instance I am cognisant that we are born not only with a physical body but also with a spirit that is more or less positive, more or less negative or a combination of both and that the nature of that spirit energy strongly influences our emotions and behaviour.
I am equally aware that the existence of a spirit and the influence of that spirit on human endeavours is consistently ignored by all mental health interventionists and that if if we do not deal with the ‘whole being’ we will always fail in ameliorating the current crisis in the field of mental illness whether that is via an increase in negative behaviour, in the escalating abuse of children, the careless regard for life or for the indifference we show in the face of the suffering and adversity of others.
Spirit is made of energy, energy no less real than the palpable energy emanating from heightened emotions which we readily pick up from others. When the spirit energy is predominantly negative the individual is more vulnerable to negative influences from both the physical and the spirit level. All negative energy may be directed outwardly (as in the abuse of others), or inwardly (self-abuse). The more negative we are in our actions, the more we are driven to be negative until it appears that we lose the capacity for choice. In many instances, continued use of negative energy does result in our negative behaviour becoming compulsive or automatic.
At a level of spirit we are at all times totally responsible for our actions. This is the law of Karma. The ‘dealer’ of negative acts must pay for all the acts of control, abuse, punishment or retribution that causes another to feel abused, controlled or punished.
Our secular and religious systems are now far removed from the nurturing and caring role for which they were initially set up and funded. These ‘caring’ systems now utilize the negative energy of control enforced by either the secular legally sanctioned punishment of fines to imprisonment or, the religious punishment of banishment 'for non-compliance.
Fines and the reasons to impose fines have increased exponentially as secular courts maintain that retribution is a right ‘enshrined’ in the legal system as are the "rights" to sue, to control and to seek retribution. The control imposed by Public liability insurance is so pervasive that events conducted by the community can no longer operate. These examples highlight only one of the realities reflecting a population totally under the control of a system of governance predicated upon the negative.
That ultimately all negative control must be ‘paid’ for is apparent when we observe the number of ‘leading’ figures in varying public institutions, individuals who orchestrated control in the past, being made publicly accountable for past actions. Lawyers, doctors, priests, ministers, teachers, public servants, welfare people, nurses, magistrates, judges; in all these professions individuals are dealing with public exposure resulting from past abuses of negative control.
Unfortunately we have been lulled into falsely believing that when our actions are carried out under some statutory rule or mandated regulation, that we are not held ‘personally’ responsible for the negative results of the ‘collective’ action.
That may be true in the secular world of ‘buck-passing’ but does not hold true for the world of the spirit. There is only one universal Law – what we put out will return to us.
The ‘implementers' of social control, be they decision makers or those carrying out the decisions, are responsible for the negative consequences of that control. Equally, since we the public fund the systems carrying out such control on our behalf, we must not be surprised to find that our lives are ever more circumscribed by controls from one system or another.
Responsibility is a personal issue and we are not exonerated in the spirit world from actions funded by us and taken on our behalf by one or other ‘system’ acting on our behalf with funds we have provided via our tax.
Being aware of the reality of spirit I am aware that there is a universal Law stating that we are accountable to a higher Source for all our actions and that for all our positive or negative actions there is a similar return.
I am also aware that all systems can presently be seen to be failing as they run in ever increasing circles without success because they always return to the same mistakes, mandatory controls enforced by punitive measures.
Please click onto this web site http://www.the-testament-of-truth.co.uk/clem/index.htm  to gain all the information you need to explore all the information in this document further.
The information concerns the spiritual reality of the actions we take either personally, or for actions taken on our behalf by some system. The time has arrived for us to truly educate those dealing with the care of children and adults.
Sincerely
Clemencia
References
Australian Health Ministers (1991) Mental Health Statement of Rights and Responsibilities. AGPS, Canberra.
Australian Health Ministers (1992) The National Mental Health Policy. AGPS, Canberra.
Australian Health Ministers (1992) The National Mental Health Plan. AGPS, Canberra.
Australian Health Ministers (1995) The Health of Young Australians: A national health policy for children and young people. AGPS, Canberra.
Australian Health Ministers, Second National Mental Health Plan. Mental Health Branch, Commonwealth Department of Health and Family Services, July 1998.
Burdekin B (1993) Human rights and mental illness: Report of the National inquiry into the human rights of people with mental illness. Human Rights and Equal Opportunity Commission, AGPS, Canberra.
The Testament of Truth - http://www.the-testament-of-truth.co.uk
ALLOCATION OF FUNDS TO PREVENT YOUTH SUICIDE
A total of $31 million was allocated to the Strategy from July 1995 to June 1999.
• The Commonwealth provided in excess of $250 million over the period 1 January 1993 to 30 June 1998 to assist implementation of the National Mental Health Strategy. Community development.
The new National Suicide Prevention Strategy entitled Living is for Everybody (LIFE) adopts a whole of life span approach to suicide prevention, however young people remain a major focus of the new Strategy.
The Government has committed $240 million to the Stronger Families and Communities Strategy over a period of 4 years. These funds are being allocated across nine different initiatives:
• The Stronger Families Fund ($40 million) — which aims to boost support for parents and families caring for young children especially in the area of parenting and early childhood development;
• Early intervention, parenting and family relationship support ($47.3 million) — which will expand the availability of prevention and early intervention programs aimed at preventing family breakdown;
• Greater flexibility and choice in child care ($65.4 million) — will provide more than 7000 places over four years and provide an expanded range of care options for families that have difficulty accessing existing services.
~ end. ~

Terence Malaher wrote:

ADHD.htm

~ Spiritual truth paper ~
The true causes behind the following purported to be mental and brain disorders.
ADHD - Autism - DRBB
There is an apparent 'common' link in the first two above that can be seen if one goes to the following paragraphs wherein is listed a little on the apparent 'nature' of each disease. All show a 'lack' of rational control and none of the sufferers are at peace mentally and they are unable to 'focus' calmly.
In reality they all show 'involuntary' movements and aggression at times. There is also lack of concentration with subsequent learning disabilities, and negative emotions are seen to be at 'play,' be they fear, criticism, anger, jealousy - etc. The last one DRBB is the most insidious and dangerous, for it is not seen as a 'disease,' but in fact those displaying its 'symptoms' do cause others a lot of pain and they see not that what they daily do is to be 'suffered' by them too.
ADHD - First, problems with Attention - Second, problems with a lack of impulse control - Third, problems with over-activity or motor restlessness - - Fourth, being easily bored - - anti-social behaviours are common - - many ADHD are also oppositional or defiant - - impulsive behaviours, quick temper, poor decision making, fractional hyperactivity, and so on.
Autism - Isolated in worlds of their own - - many engage in repetitive activities like rocking or banging their heads, or rigidly following familiar patterns in their everyday routines. Some are painfully sensitive to sound, touch, sight or smell.
(Reports) - He has always been obsessed with order. As a child, he lined up blocks, straightened chairs, kept his toothbrush in the exact same spot on the sink, and threw a tantrum when anything was moved - - could also become aggressive - - when upset or anxious, he would suddenly explode, throwing a nearby object or smashing a window - - he was often out of control -
(Another) sitting alone in the kitchen - - he didn't respond when called - - it was as if someone had pulled a shade over him - - he stopped talking and relating to others - - he often tore around the house like a demon - when made to stop, he threw a tantrum, kicking and biting anyone within reach -
(Another) sat motionless in her crib - screamed to get what she wanted - immense powers of concentration etc. - - -
It now is the 'time' for the human race to become more fully aware of the spiritual nature of man and to see that the biological fleshly body is but the 'vehicle' for the spirit soul within to be 'able' to function on this level of consciousness.
If "you" dismiss the word spiritual as pertaining to religious "hype" in having no "value" in this "modern" scientific world, then you miss the most important aspect of "holistic" healing. The "healing" of the spirit soul.
page 2
It needs now be understood that the spirit soul with its 'energetic' nature and mental and emotional bodies stands apart from the biological brain and flesh. The brain function is to 'translate' the impulses from the spiritual mind into physical actions.
The brain also 'holds' memories from all input received during this life's experiences as well as incoming thoughts from other levels of consciousness, be it divine inspiration, or demonic control over the psyche of man causing anti-social behaviour.
The brain also 'processes' thoughts flowing within its own 'this life' consciousness storehouse of information that is impinged upon by our senses. Thoughts flow through the brain that links the 'intent' into biological responses by motivating muscles through the nervous system that transmits energy impulses.
All must now try and see that there is an 'influx' of thoughts received into the mind of man and also it needs be seen that the 'nature' of intrusive thoughts depends on the energy 'forces' of the negative emotions within, be they fear, anger, etc. (Positive inspiration occurs through the positive 'love' emotion).
Yes, there may at times be a biological problem within man's biological body or brain so that messages received from ones own unique consciousness cannot be properly 'translated' into motivating speech or body movement etc, but there is also a far greater 'influence' over the actions of all that to date have not been 'seen' nor understood by man.
People, be they child or adult are perceived as 'normal' when they are kind and responsive and positive. When they are 'less' than that then man assumes they have a 'dietary' or other deficiency or they are mentally 'disturbed' in some way.
What is not seen, is the true cause of mental 'disability' wherein a person cannot 'maintain' a clear, rational, and positive expression and thus appear normal. In every 'case' of the above spoken 'disorders' there is an apparent 'spell' binding the mind of the person that controls their actions in some way.
Be it by placing them in a 'catatonic' state, or inducing negative speech with accompanying negative physical outbursts. There is also an apparent 'dislocation' of their mind from being able to maintain a 'pure' constant thought stream as telepathically induced 'thought' disruption takes place.
Every 'one' of these disorders come under the same 'umbrella' of "Minds Under Siege" wherein the psyche of the sufferer is being imposed upon or 'linking-in' to other realms of consciousness from where they are being 'hypnotised' into either action or non-action by other spirits who themselves are in a 'controlled' state.
Much have I already written on the subject so that all Carer's and parents can aid themselves with the necessary wisdom to aid others and themselves, for all humanity will now be 'impacted upon' from other levels of consciousness and there will be a great increase in insanity and destructive intent.
This will be accompanied by an increase in 'depression' through fear and many will become 'frozen' into immobility. All 'improper' acts are to a greater or lesser degree acts of insanity brought on by spirit possession.
Yes, prior to the new 'scientific' way it was 'known' that man could become 'possessed' by spirits abiding in other realms, thus losing "control" of his unique consciousness for a certain length of time and being "subjected" to telepathic control from others living in other realms of consciousness. The clear 'picture' is now revealed by me, and it is the time to see the reality of what is to be and what to do about it.
Note: The administering of, or lack of, certain chemicals and foods or drugs etc can and do 'influence' the capacity of the biological body to operate satisfactorily, or to hinder or aid the 'energy' flow of input from brain to body via the neurone system.
But this in no way effects the real cause of the problem that can only be 'arrested' and or changed by adhering to the 'program' given on my web site, in the knowledge that the cause 'stems' from the inner 'Sin' within man that grows or diminishes depending on the expression of each soul.
page 3
Age Activated Attention Deficit Disorder - and example of:
Minds Under Siege by multiple intruding thought processes.
This is how it manifests itself:
I decide to wash my car. As I start toward to the garage, I notice that there is mail on the hall table. I decide to go through the mail before I wash the car. I lay my car keys down on the table, put the junk mail in the trash can under the table, and notice that the trash can is full.
So, I decide to put the bills back on the table and take out the trash first, but then I think that since I'm going to be near the mailbox when I take out the trash anyway, I may as well pay the bills first. I take my chequebook off the table and see that there is only one check left. My extra checks are in my desk in the study, so I go to my desk where I find the can of Coke that I had been drinking.
I'm going to look for my checks, but first I need to push the Coke aside so that I don't accidentally knock it over. I see that the Coke is getting warm, and I decide I should put it in the refrigerator to keep it cold. As I head toward the kitchen with the Coke, a vase of flowers on the counter catches my eye--they need to be watered.
I set the Coke down on the counter and I discover my reading glasses that I've been searching for all morning. I decide I'd better put them back on my desk, but first I'm going to water the flowers. I set the glasses back down on the counter, fill a container with water and suddenly I spot the TV remote. Someone left it on the kitchen table.
I realise that tonight, when we go to watch TV, we will be looking for the remote, but nobody will remember that it's on the kitchen table, so I decide to put it back in the den where it belongs, but first I'll water the flowers. I splash some water on the flowers, but most of it spills on the floor. So, I set the remote back down on the table, get some towels and wipe up the spill. Then I head down the hall trying to remember what I was planning to do.
At the end of the day; the car isn't washed, the bills aren't paid, there is a warm can of Coke sitting on the counter, the flowers aren't watered, there is still only one check in my chequebook, I can't find the remote, I can't find my glasses, and I don't remember what I did with the car keys.
Then, when I try to figure out why nothing got done today, I'm really baffled because I know I was busy all day long, and I'm really tired. I realise this is a serious problem, and I'll try to get some help for it, but first I'll check my e-mail.
Do me a favour, will you? Forward this message to close friends you know, because I don't remember to whom it has been sent. Don't laugh - if this isn't you yet your day is coming and, if I have sent this to you before - - - well, now you know why you're getting it again!
page 4
There are a "number" of probabilities around the "Minds Under Siege" process:
1 - Lack of maintaining mental "thought" focus due to intrusive thoughts that "take over" the mind and lead it 'hither & thither' and, the "sufferer's" own consciousness is overridden and thus they cannot retain any focus on the matter at hand.
This "coupled" to the emotional "state" of the invisible intruder compounds the negative emotions within the sufferer and "jointly" through frustration and or fear or anger etc there may be an "ejaculation" of verbal or physical negativity.
2 - Total "possession" of the mind may be a reality as it is "overridden" totally by incoming thoughts. The "nature" of these thoughts and the emotional "state" of the invisible projector will show itself in the actions or non-action of the fleshly one.
Let it here be known that depending on the size or "volume" of the "attracting" emotions within the fleshly child or adult, they may be able to be helped or they may not, and if not, then their ongoing "state" is totally in the hands of God, and their "bondage" to the dark spirit realms will only be "broken" by the grace of God when God draws out the particular "sinful" emotion from their soul.
Let it here also be known, that the "common" acts of mankind perceived as "normal" whereby man is "justifiably" at war or "justifiably" merciless and unforgiving and retributionary, that this "way" also indicates minds under siege from dark realms, as in the "case" of "youths" running "amok" and displaying a lack of respect and consideration for others and being anti-social in their behaviour.
For the "natural" spiritual state is one whereby no "sin" exists in the spirit soul and it is only loving and kind and peaceful and calm in its expression. (Sin= the negative emotions within man that the human race 'perceive' as normal).
Man "classifies" mental "problems" into a few different categories, when in reality there are infinite possibilities due to the multiplicity of different factors, and each "case" is unique.
Please assist yourselves by reading my 'SUICIDE' document found on my web site below, read Item 6 (Thoughts sane or insane) and at the end of the Suicide document you will find your way to the new way "Mental Health Carer's Manual."
For a 'quick' insight of what is now to be, and what to do about any mental disorder, please go to the 'Brief Summary' of God's message that is found at the end of my front Index page.
It needs be understood, that the erupting negativity or violence or 'bad' behaviour in children associated in any of these supposed brain 'disorders' all stem from their emotions and 'open' minds. It is also obvious that as they grow older, that they will cause much harm to self or others, that will bring them within the 'punitive' arm of man's rules.
It is therefore important for all children displaying 'inattentiveness, confusion, disorderly conduct, violent conduct' to attend a 3 hour 'Feeling Easier Seminar' that will enable them and their parents to begin to be able to understand the process and to help themselves to maintain 'mental' stability until the spiritual disease has passed.
For details of Seminar go to 'Seminar'
Page 5
~ DRBB Syndrome ~
DRBB - This stands for 'Divine Right Bully Boy,' and is a 'disorder' caused primarily due to false ideological belief programming. The programming that has stemmed from precedents set whereby some members of the community believe that they do have a 'Divine Right' to bully and punish you and you and you into paying up any monetary demands that their 'organisation' wishes to impose and, to enforce their 'desired' code of daily conduct.
It is similar in some ways to the other listed 'brain' disorders as it also displays: - - - All show a 'lack' of rational control and none of the sufferers are at peace mentally and they are unable to 'focus' calmly. - - - For if any 'other' person is not 'conforming' to the conduct or 'standard' required by the rules contained in their 'rule books,' they become very agitated and 'bullish' and they use force of arms and guns to attain their demands.
These 'enforcers' are the 'armed' forces & judiciary & legislative men or women employed by 'State' authorities. They all live in a 'delusional' anti-God state whereby their minds are filled with vain thoughts, whereby they perceive themselves and their 'rules' as God or above God. For in the course of their duty to a 'wage,' they are prepared to defy God's "Walk in peace and love one another" Command and, they 'interfere, dictate, control, berate, invade, extort, seize and steal goods and money, fine people, kidnap people, hold people hostage in cells, and even kill people.'
So in fact, these 'bully boys' are the 'ultimate' aggressors that see not that the use of their dark force divorces their own soul from God's Light and paves the way for their own great suffering of pain on a later day. For as they are not God, it is they as all that are 'subject' to God's Divine and Rightful Law 'As you do is done unto you.'
These people are in fact 'spell bound' to a greater degree than most of those suffering ADHD and, most certainly all 'bully boys' need to attend my 'Feeling Easier Seminar' so that they can learn about 'karma' and the fact that God and God's Law is real.
The mentality of every DRBB is one whereby they are in fact 'spell-bound' from the devilish 'voice' of Satan that lives in the 'pit,' for only the truly arrogant, ignorant, and lost would take a 'mercenary' wage of 'silver' coins and perpetrate family violence against their own sisters, brothers, mothers, and fathers for and on behalf of 'text' in some unholy book of 'legislated' rules, that are the scourge and abomination of all humanity today.
All police and other enforcers today are simply 'political' pawns used to extract money from and to control the 'sleeping' populace but, they also need to see that they as many are all controlled mentally in some way to the point, that they cannot 'respect' themselves or others. Thus they all need the good 'counsel' of God before the day they will walk in shame in the 'bad' lands below.
If you wish to assist these 'lost' souls then please stop funding their iniquities, for in so doing you are complicit to their deeds that become your own misdeeds. All walk in ignorance, all are mentally bound in some way as within every mind dark thoughts exert their power play. Please go to the 'Spiritual result of action' < suaction.htm >
Education is the way forward, not 'punishment.'

2020-02-15 12:34:10

well, I hate to be a party pooper, but I'm totally blind and frequently go through pretty disturbing halluscinations, mostly of horror based stuff, screams, otherworldly shreeks, things like that.