Schizophrenia Development

I read once in an article that schizophrenia symptoms started ‘flourishing’ around the age of 18-20. Therefore, I’d like to know if to-be schizophrenics present some kind of odd behaviour or customs before fully developing it. Example: will a to-be schizophrenic child be totally normal until his late teen years, or will he have strange ideas, etc.

I’m sorry the question is quite vague.

The stage before a syndrome/illness or whatever full manifests is often called the prodromal stage. Back when I was a research assistant in an functional MRI lab, we studied executive function disorders, of which schizophrenia is one. We would often compare prodromes with patients and controls, to see if we could find things in the brain processing that might predict who becomes schizophrenic. The problem with doing such experiments is that since you don’t really know who is going to become schizophrenic, you test a bunch of people who have the risk factors we know about (first degree relative with sz, other things), and kind of morbidly hope for the best. I’d google Prodrome and Schizophrenia and see what comes up. But I can tell you, that out of a study of say, 30-40 or so, we had maybe 2 or 3 who would convert. You’re taking a condition that affects a small %age of the population, and then trying to find things that can predict for it. Not an easy task.

There’s been a surge of interest in schizophrenia prevention (treatment begins in the prodromal phase before the onset of psychosis) which has led to an increased number of studies on how to better identify predictive risk factors. These studies usually involve a group of young adults at risk for schizophrenia because of genetic factors and a group of age and gender matched control subjects. While these studies aren’t conclusive (follow through takes years and some researchers have called for larger samples) they suggest that those who later develop schizophrenia do display certain characteristic types of strange behavior before a formal diagnosis is appropriate. These include odd/disordered speech, magical thinking, interpersonal sensitivity, social withdrawal/isolation, and paranoid thoughts.
Additionally, those at high risk for developing schizophrenia are more likely to have previous psychiatric history and higher rates of juvenile delinquency than their peers in the control group.

On a recent Oprah show, she had a young girl (I think about 7) on, who was fully schizophrenic. The family had to adapt to her in some really major ways . . . like getting two separate apartments and taking turns being with her, while the other took care of their normal child. And they couldn’t leave her alone for a minute. It was very sad.

In general, there are two major categories of onset of thought disorders. The first is termed process or chronic, and that’s the type when a person has premorbid symptomology such as odd behaviors or thought patterns prior to the actual diagnosis, sometimes for years. The second is known as acute or reactive, which is a more rapid onset and generally occurs in people who don’t have a recognized pattern of premorbid symptomology prior to diagnosis.

I was wondering, audiobottle and miss eliss, if you were aware of the fairly recent discovery of the enormous and previously unrecognized importance of myelin (white matter) and myelin sheathing (and to a lesser extent, Schwann and other type of glia cells) in the brain. I read two absolutely compelling articles on the topic in a 2004 and 2008 Scientific American by R. Douglas Fields, chief of the Nervous System Development ad Plasticity Section at the National Institute of Child Health and Human Development and an adjunct professor in Neuroscience and Cognitive Science Program at the University of Maryland.

In the 2008 piece (which I seem to have misplaced), I recall that Fields writes that problems with myelin sheathing, including improper sheathing depth, appear to be important factors in some neurological as well as behavioral problems, including Alzheimer’s and various types of autism, and (here’s the point): very likely schizophrenia as well. If that were true, I seem to recall that Fields remarked that that would be the first known organic explanation for schizophrenia.

Do you think that last would be true? In other words, do you know of any other known or widely speculated organic cause of the disease?

I recall Fields noting that myelin sheathing is particularly sensitive to cigarette smoke, first or second-hand, and that this was a vital clue as to the cause of schizophrenia since that period of very high sensitivity (in susceptible individuals) corresponded remarkably well with the onset of young adulthood.

Do you happen to have any idea if that’s being seriously investigated yet? Or perhaps that hypothesis didn’t pan out…

What about the chromosome deletion syndrome where a lot of kids become sz?
I am VERY surprised that there’s not a lot of research trying to find the connection between Down’s and Alizheimer’s, or the chromosome deletion syndrome where a lot of them become sz.
So apparently familial history isn’t too much of a predictor? I do remember if sz is genetic it can be REALLY bad or cause childhood schiezophernia.

On the other hand…I have the mylination of a baby and while I have some ADD-ish issues, as well as bipolar, I don’t have a risk for Alzheimers (most Alz is spordiatic) and I’m not autistic…

There’s another disease called Childhood Schizophrenia. Although the symptoms appear to be the same, some people feel these are two distinct diseases with different causes. Of course, others feel that childhood schizophrenia is the same disease as the regular variety.

Schizophrenia starts to manifest itself about the age of 18 through 23. Earlier ages tend to get what is called “Simple” schizophrenia while older ages tend towards paranoia. However, brain scans for regular schizophrenia appear to be the result of the same types of problems.

And, if you are between the ages of 16 to 23 and worry you might be getting schizophrenia, you’re absolutely normal.

I’m no expert on the field of schizophrenia, but I understand that the link between toxoplasmosis and schizophrenia is a hot topic at the moment.

Webster, et al, 2006

(bolding added)
What the bolded part refers to is how Toxoplasma infection changes the behavior of infected rodents. Toxo’s definitive host is the cat, and it “wants” to be in cats. Affected rodents do not fear cats and are even attracted to them, which is theorized to be a mechanism for the Toxo to make its way from the intermediate host (rodent) to the definitive host (cat) so that it can continue its life cycle.
Toxo and rodents

Here’s an article on the relation between the genetics of schizophrenia and host-pathogen interactions.

That’s interesting info, horsetech. Thanks.

If you’ve been diagnosed with schizotypal personality disorder, you have about a 35% chance of developing schizophrenia. The disorder is characterized by odd communication styles, magical thinking, non-conformity, strange appearance and behavior, poor social skills and social withdrawal, restricted affect, and a propensity towards ego-syntonic obsessions. There’s also schizoid PD, which is similar to schizotypal PD except the weirdness is milder and the negative symptoms (like flat affect, apathy, dysphoria, withdrawal) are more apparent. Its link to schizophrenia isn’t as strong, but it shows up in families with schizophrenic relatives more frequently than random.

The early 20s is usually onset for men, but for women it generally hits in the early 30s. Estrogen has some kind of protective effect, apparently.

People who develop paranoid schizophrenia later in life (like in their 40s) generally have a rapid onset of the disease and a better prognosis.

I recall reading about a study in which researchers studied home videos of children and predicted which ones were going to develop schizophrenia. Turns out that the would-be schizophrenics tended to have more soft motor abnormalities (clumsiness) than the non-schizophrenics. Also, not related to this study, is that mixed-handedness is another risk factor. Another thing to look out for is obsessive-compulsive behaviors.

There are few things that set my teeth on edge like the word non-comformity being used as part of a list of symptoms or signs of disorders or mental diseases; yet I’m sure that there are many published guidelines that do exactly that.

But surely you don’t imagine Fields or myself have argued that there’s a perfect, one-for-one correlation between myelin sheathing thickness and autism, Alzheimer’s, schizophrenia or anything else, right?

In any case, it’s never the myelin sheathing thickness alone that causes problems. What matters in these maladies is that the synchronization in arrival times at essential points in the brain of critical nerve transmissions is not adequately close. The thickness of the myelin sheathing must vary according to speed and distance and “gaps” between nerve signal pathways in order to achieve good synchronization.

If you think of nerves to be like a spider web, the high speed between distant points must be matched by lower speeds between points that are closer together if close synchronization is to be achieved. Greater myelin thickness increases the speed of transmission, and consequently lesser thickness results in slower transmission; what matters is not absolute speeds but rather relative speed differences.

The gaps I spoke of are somewhat akin to breaks in a copper electrical wire, except that copper wire gaps effectively break the circuit while gaps in myelin sheathing serve to just slow the transmission speeds even more than low sheathing thickness does. The end result must be close synchronization of nerve signals at crucial points in the brain if the maladies I mentioned are to be avoided, and this is so even in those whose brains have lower than average myelin thickness. It’s just that in those instances, the sheathing thickness of other nerves must be relatively thinner still if the maladies are to be avoided.

If good synchronization is not achieved, the highly probable consequence will include symptoms just like those seen in various classes of autism, Alzheimer’s, and schizophrenia. That’s what’s so exciting about this very, very recent discovery of the critical importance of proper synchronization in the brain and the varying thickness of myelin sheathing that is necessary to achieve that. For without understanding of the organic causes of these maladies, effective treatments cannot be properly designed.

I consider this to have quite earthshaking ramifications!

I don’t know about the latter (after the semicolon), but I very much tend to agree with the rest.

On the other hand, in science fiction author Larry Niven’s “Known Space” universe, there exists a species that humans call “Puppeteers” (for their appearance, if not more) who are known for what we humans would call cowardice. They consider even the merest risk-takers among their own species to be mentally ill. When human characters in Niven’s stories challenge that contention, the Puppeteers reply: “The majority must always be considered sane”.

Putting such a thesis in the mouths of science fiction aliens is a prime example of the most valuable contribution of science fiction to our wider culture, in my view. Transferring a controversy out of the human realm is an extraordinarily good way to allow clearer thinking to be brought to the topic. In that light, I find that the Puppeteers’s definition of sanity is rather hard to argue against.

This article

http://www.neuropsychiatryreviews.com/dec00/npr_dec00_schizo.html

Talks about a study involving children in the prodromal stage of sz. They gave some kids low dose antipsychotics, counseling and if needed meds for depression and anxiety. With the other kids they just watched and waited. The kids with the intervention only had 13% develop full blown sz within 6 months vs 36% for the kids with nothing but people watching.

The study, the only schizophrenia prevention trial completed thus far, involved 59 persons with prodromal symptoms who received either “supportive following” or a multimodal treatment regimen consisting of low-dose risperidone, cognitive behavioral therapy, and (if necessary) antianxiety or antidepressant medications. After six months in the study, schizophrenia was diagnosed in 10 of the 28 control participants (36%) but in only four of the 31 of treated subjects (13%).
This one talks about 3 studies on prodrome interventions. The one above and 2 others. All saw significant decreases in the numbers who went on to develop full blown psychosis.

http://www.freshpatents.com/-dt20090827ptan20090215842.php

Only three studies thus far have addressed treatment needs of prodromal patients. The first two studied antipsychotic medication. A recently completed trial randomized 59 patients to open-label risperidone plus cognitive therapy plus usual care versus usual care alone (McGorry et al., 2002). Six month conversion to psychosis rates were 9.7% for the risperidone containing treatment and 35.7% for usual care (p<0.05). Our group has completed a 12 month trial randomizing 60 patients to olanzapine vs placebo (McGlashan et al., 2004; Woods et al., 2003). Twelve month conversion rates were 16% for olanzapine and 38% for placebo, a statistically significant difference when controlling for baseline severity imbalance. The third study randomized 58 prodromal patients to cognitive therapy vs monitoring (Morrison et al., 2004). Cognitive therapy group showed significantly lower rates when two patients later believed to have been already psychotic were excluded.

There are clinical studies on using NMDA agonists like glycine as an intervention during the prodromal phase to prevent development of full blown sz.


Also, this may not be what you are looking for but this website has a list of risk factors of developing sz.

http://www.schizophrenia.com/hypo.php

Things like being born in winter (because of maternal vitamin D levels), being born in urban areas, low birth weight, various infections, etc. all increase the risk of developing sz down the road.

In all honesty, I appreciate that I am on a board full of people mature enough to discuss an issue like this intelligently. Mental illness is surrounded by ridicule, blaming the victim and learned helplessness. Seeing people try to be intelligently proactive is really gratifying. My personal experience has been that most people are either too inept or immature to deal with these problems head on.

I don’t know what mental illness I had as a teenager (it developed into full blown psychosis a few months before I turned 18) but for several months beforehand I became socially withdrawn and started losing interest in hygiene and school. Having competent people willing and able to help me out would’ve made a huge difference. Maybe if I’d gotten low dose antipsychotics, stress/anxiety medications and counseling (like they gave the kids in the earlier study) it would’ve been arrested before it went too far. My experience with mental illness was a big factor in why I chose to study biochemistry in college.

Well, guidelines would probably use words like “unconventional beliefs and behavior” and then go on to decribe them, but I used “non-conformity” as short-hand for this. A person with brow piercings is a non-conformist in societal context–and would not ping on a psychiatric radar. A person who believes brow piercings generate psychic energy would be a non-conformist in a psychological sense, and may be a schizotype.

After reading Fields and others (most of it being reports of the research of others), I would think that cigarette smoke exposure levels would be at least as prominent a factor in increasing the risk of schizophrenia as the others you list. I’m not an anti-cigarette fanatic, and it probably would have never occurred to me that such smoke might have have a significant role in the production of mental illnesses such as these had I not read these articles, which highlight the dramatic role cigarette smoke very likely plays in this.

When I first read of this, I couldn’t help but think of Kurt Vonnegut’s son, whose young-adult onset of schizophrenia cut his father to the quick. Why did I think of Vonnegut? Because his excessive smoking is very well known, and I could only imagine the overwhelming emotional pain and guilt Kurt would likely feel if he had learned his habit was a major contributing factor in his son’s illness. Of such things are tragedies made, including Vonnegut’s own bitter fictional tragedies.

I’m not sure whether you meant sufferers or caregivers or the wider public, but I would think that all of those would suffer considerably more due to such negative social factors. I feel that the social stigmas have been, fortunately, rapidly diminishing in the first world for several decades now. But other, more damaging factors have arisen to take their place.

I speak of the tremendous dominance of pseudoscience, quackery, wishful thinking, con jobs, and terrible misinformation on the Internet. It would likely not be so bad if these had only a minority presence on the net, but we don’t even have that to hang our hats on. It always seems quite a contradiction to employ such an advanced technology to bring back medieval worldviews, but, as with bees living in one’s head, there they are.

The Internet is the number one promulgator of dangerous, anti-scientific bullshit in the realm of mental illness (and countless other things), but nowhere is it worse than the arena of autism. The front section of the Chicago Tribune of November 22 of this year included a wonderfully honest characterization of what autism crackpots are heavily pushing parents to do: Perform reckless, mad-scientist experiments on their own children!

So I certainly share your view of this board in particular. Parents would be well-advised to turn here to GQ before pursuing underinformed “treatments” for their children, whether autistic or suffering from other mental illnesses. At a guess, I’d speculate that the OP did exactly that, and he should be commended for his inquiry.

That is quite interesting. So basicly it’s the timing of the signals, rather then the equipment that may be the problem? Someone could have not top of the line equiptment but still have decent sychonization?
What about the indication that some autism/scheziopheria can respond to dietary intervention . For example there is a study I read that indicated that people taken off of milk and bread who are schzieophernic recover faster then those who don’t go off milk/bread. What do you think of orthomucular (sp?) therapy?
It really does seem to be a chicken or the egg thing. Is the signal causing the disorder or is the brain responding abnormaly to stuff like cigerette smoke.
And if cigerette smoke is a trigger then a lot of scheizopherincis are engaging in negative self medication…I think I read the nicotene acts theraputicly but there’s also something else in the smoke that may be triggering their psycosis.

Yes, I read that. Quite a good article. However…I do think that the DAN docs aren’t completely crackpot. I think that mainstream medical docs tend to not look for alternative causes of things…Like for example, if they are in a state that doesn’t screen for a condition if left untreated can mimic autism, they could just lump the kid into autistic.