9.29 Schizophrenia's Startling Story

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29. Schizophrenia (Update 17 Septr 2021.)  The following column has main headings in order as in text. Use to search & find or to scroll to the topic.

Schizophrenia

Contents of this Chapter in Order of Appearance

The Schizophrenia Spectrum

Genetic Factors

 Diagnosis of Schizophrenia
Schizophrenic Speech

Case Example of Schizophrenic Break

Lifetime risk of schizophrenia based on family relatedness

Identical Twin Studies
Other High Risk Factors

the peculiar course of schizophrenia

Prevention and Causes

what the illness is to its sufferer. 

statistics on schizophrenia.

 Advices

  Prevention of Schizophrenia

Treatment of schizophrenia

the anti psychotic drug therapy 

 psychotherapy

Letter from a Schizophrenic

Endnote Reading

Final note: The 2001 A Beautiful Mind 

The schizophrenia spectrum consists of full-blown Schizophrenia.

 Schizophreniform Disorder satisfies  the diagnosis requirements of Schizophrenia but duration of illness more than 1 month and less than 6 months), Schizo-Affective Disorder (Contains cases where Schizophrenia alternates with manic mood disorder), and Schizotypal Disorder (Schizoid personality disorder without the psychotic features of Schizophrenia). These are related genetically but do not satisfy the full diagnosis and have a better prognosis for full recovery than full-blown Schizophrenia which from now on I call: Schizophrenia.
 Eugene Bleuler, the famous Swiss Psychiatrist invented "schizophrenia" in a lecture in April 1908, to describe his insane-asylum patients whose affect seemed to be split from their actual behavior (despite acting-out crazily, they seemed unaffected by it and believed in their delusions and hallucinations).  Between 1908 and 1978, when the Feighner Report Criteria, which strictly defines a schizophrenia diagnosis as we know it today, came out, psychiatrists, especially in U.S.A. and much less so in U.K. were using the term, schizophrenia, to diagnose almost any crazy (psychotic) behavior pattern. As early as Dr Emil Kraepelin in the 1890s, it had been recognized that at the core of the schizophrenia diagnosis lay a major mental disorder limited to young adults, which showed a deteriorating picture of breakdowns with delusions and hallucinations starting under teenage stress and invariably worsening into early dementia (dementia praecox) and which could be separated from the other major psychosis —- manic-depressive —- with which it had previously been lumped, by its youthful course, its more frequent, bizarre hallucinations and delusions and its highly inappropriate, weird behavior.  But there remained a confusion with manic-depressive psychosis, pure paranoia, and drug induced psychotic states.

The Feighner Criteria required the illness to last at least 6 months with an at least 1-month active phase, it threw out all drug-induced states, and it described a core illness starting often with breakdowns in late teens and early 20s of almost pure psychotic behavior --- delusions, hallucinations, speech neologisms  and other forms of disordered thinking, but not mania ---plus a set of negative symptoms, alogia, apathy, anhedonia and loss of attention.  Since then (1978) with universal adoption of the Criteria, schizophrenia has settled into its familiar niche we see today that afflicts 1% of adults and has 10% suicides in all countries and runs a typical downward (In the untreated state which is rarely seen today.) course of intermittent breakdown with psychotic/delusional behavior.
   The current schizophrenia diagnosis is based on its psychotic (positive) symptoms (hallucinations, impossible delusions), its negative (apathetic, alogia, anhedonia) symptoms, and it’s weakening of intellectual (neurocognitives) abilities occurring in late teens and early adulthood and (without treatment) worsening in a series of breakdowns. (Latest DSM-5 does not require breakdown.& )

Schizophrenia in its classic form begins with dramatic psychotic breakdown in youth. It afflicts 1% of populations in all nations, in all religions and ethnic groups, which suggests an input of ancient genes.

Genetic factors account for part of the risk for schizophrenia. When one sibling has had a schizophrenic break, the risk in the other siblings is 7.5% to 10% and when a parent has had one, the risk in the child is 13% and if both parents the risk is 50% compared to a 1% risk of the general population. And in identical (monozygotic) twins where the one has a schizophrenic break the risk is 50% in the other. These genetic factors are strongest in ones who have a schizophrenic break during the teenage years compared to later breaks. The risk starts from age 15, and peaks in the 20s and progressively declines to age 55, a reflection that schizophrenic breaks occur between ages 15 and 55.   In considering the above statistics, especially for identical twins, it becomes obvious that the environment in which a twin is raised has an effect and this is an important observation because the environment can be altered for good or for bad while the genes cannot.

Twin studies suggest that parental genes transmit a vulnerability, the S-trait, to a child. Having it as part of your DNA does not doom you to schizophrenia but puts you at increased risk if you get exposed to environment stress (e.g. attending a college out of town).

The number of genes transmitting the S-trait is more than two. Although the S-trait seems to imply a bad quality, research suggests the genes may also have good qualities. (Explaining why they get passed on to future generations.) In recent years, the ability to view gene abnormalities electron-microscopically allows scientists to detect certain genes that give high risk for schizophrenia in offspring of carriers thereby opening the way for prospective mates to determine risks in their potential offspring.

Identical twin Studies in which only one twin shows schizophrenia suggest the S-trait is not in itself sufficient to predict that its bearer will develop schizophrenia since only half of the S-trait twins got schizophrenic during adult life. A Scandinavian study of identical twin-pairs with the S-trait who went on to each have their own children showed the percentage of children who would have a schizophrenic break was the same in offspring of the non-schizophrenic twin as in offspring of the schizophrenic twin. Thus the S-trait is from a carrier gene but it probably requires differential environmental conditions or epigenetic acquired physical damage to bring out the schizophrenia. This is of importance for eventual prevention and future treatment. Though the environmental factors and the physical damage that bring out schizophrenia in the S-trait individual are presently unclear, the successful search for them will be a key in preventing and treating. As yet, the genes that make the S-trait have not been clearly identified.

Other High Risk Factors Being born and raised in an urban environment for one`s first 15 years doubles the risk of schizophrenia, and a paternal age 50 or more increases the risk 3 to 4 times compared paternal age in 20s.  This can tack on to genetic risks and calls for special precautions in childbearing and upbringing.

The model is added to by the peculiar course of schizophrenia. It does not show before age c.15 or after c.55, occurs more frequently (3:2) and earlier (10 years for peak) in men than in women (so its occurrence must be affected by the differential sex hormones or the environment difference between boy and girl), and is made worse with each successive schizophrenic break. (Importance in preventing them and limiting the number; in this it also resembles epilepsy fit, cf. kindling.)

Diagnosis of Schizophrenia: “Having schizophrenia” today in 2021 is based on a set of signs and symptoms observed by a psychiatrist, the acute episode lasting at least a month and the total process at least 6 months. They must include positive psychotic symptoms including hallucinations and delusions, and often present as an acute psychotic break in young adulthood or late adolescence in reaction to a child separating from parent. Also important are so called negative symptoms like apathy, muteness, catatonia and language distortion. Overall the physician should be impressed in actual behavior by a separation of affect from actual behavior, e.g., the patient laughing as she conveys how her loved one died.  More and more it is observed that schizophrenic patients suffer an early significant ongoing loss of intellect (hence Dementia praecox, or “premature dementia).     

As knowledge of the metabolic and endocrinopathic causes of schizophrenia have deepened it has become obvious that schizophrenia is not a pure diagnosis of a single disease psychotic state; rather it is a set of crazy behaviors of a deteriorating frontal lobe function as distinguished from Bipolar mood-congruent psychosis characterized by mania and psychosis.

Having the S trait cannot be determined to be a plus or a minus: it is not digital, it is analog (i.e., one has risk of developing schizophrenia based on number and closeness of DNA relatives who had a schizophrenic break). Thus, all data on schizophrenia hinge on diagnosing the schizophrenia by uniformly trained psychiatrists from an agreed-upon worldwide criteria.

Schizophrenic Speech

Language disturbance referred to as alogia is a central negative symptom of schizophrenia. Grammar is reasonably intact, but content can wander or be incoherent, a symptom that is commonly referred to as "loosening of associations." More bizarre but less common patterns of speech include neologisms (idiosyncratically invented words), blocking (sudden spontaneous interruptions), or clanging (associations based on the sounds rather than the meanings of words, such as "If you can make sense out of nonsense, well, have fun. I'm trying to make cents out of sense. I'm not making cents anymore. I have to make dollars.")

Examples of loosening of associations are:

"I'm supposed to be making a film, but I don't know what is going to be the end of it. Jesus Christ is writing a book about me."

"I don't think they care for me because two million camels … 10 million taxis … Father Christmas on the rebound."

Question: "How does your head feel?" Answer: "My head, well that's the hardest part of the job. My memory is just as good as the next working man's. I tell you what my trouble is, I can't read. You can't learn anything if you can't read or write properly. You can't pick up a nice book, I don't just mean a sex book, a book about literature or about history or something like that. You can't pick up and read it and find things out for yourself."

Case Example of Schizophrenic Break: (Note: the dramatic breakdown described here is no longer required for diagnosis but is still very typical.)  John seemed a normal child. He was quieter than his older brother and shy but his mother valued that as part of his unique nature. By age 7 he had become an energetic child who excelled in school, was a good reader and performed well at sports. But he did not make friends well and was easily insulted due to his being hypercritical and argumentative. By high school he seemed more outgoing, was interested in politics and environmental causes, and had girlfriends. But he was still easily hurt emotionally and his relationships were uneven and stormy. And his parents were becoming aware of a developing roughness in his relations with them. There was no warmth but they considered it due to adolescent stress and were happy when he was accepted to an out-of-town university because they thought its challenge would help socialize John better. After 6 months away at university, despite his having been a top high school student, John failed all courses and dropped out.

Comment: A pre- or early-teenage, high-risk personality can be made out in the above childhood development: an irritable, picky-picky, offbeat, loner personality (schizoid). During teenage or early 20s a disorganization of personality development begins to be seen. This abnormal development is unmasked by the stressful adolescence due to hormone change and by a loss of parental control due to separation from the protective home environment. The data suggest that schizophrenia is a syndrome due to bad development of a normal-at-birth brain in the offspring of a mother affected by factors like late pregnancy, radiation or toxin, or due to trauma at birth by various bad influences like virus infection or nutritional deficiency; or caused by a gene effect on enzyme imbalance in brain leading to neuron fiber mal-connections. One hint of an infectious factor is the increased schizophrenia in persons born in temperate zones during winter months, particularly Feb. or March and especially in urban versus rural. (Conceived in mid spring, a time in temperate zones of high risk for measles, mumps, rubella, chickenpox.)

The case example continues: John told his mother something was sucking thoughts from his brain, and one morning she finds him attacking the refrigerator with a hammer because, he says, it has been bugged by the CIA in order to read his mind. This scares John's parents but they still do not want to admit he is seriously ill, and they keep him home, hoping that tender loving care will get him over his “nervous breakdown.” He stays in room, refuses to allow anyone to touch him, and has his food test-tasted before eating, claiming the CIA is trying to infect him with HIV and suspecting the persons who seem to be his mom and dad are actually cloned copies of his parents replaced by the CIA. (Capgras Syndrome) He says that voices from the TV set are discussing his sex life and broadcasting his thoughts. He begins to use a corner of his room for excretions. One morning his mother finds him standing mid room, mute, in strange pose. She calls ambulance and in hospital the diagnostic impression of schizophrenic break is applied to John.

The above is typical of schizophrenic break (But note that many schizophrenics do not have the classic break depicted here but simply deteriorate into the crazy inappropriate behavior) with fixed bizarre delusions and aural hallucination. (May in fewer cases be visual.) Content of schizophrenic delusion and hallucination has changed over time. Previously, it was religious and more often visual; today it incorporates technology and modern life and is almost always aural as accusatory voice. The CIA is frequent, suggesting influence of the Media on the schizophrenic mind.

  Prevention and Causes:  By identifying person with the trait (Targeting the chromosome and its gene electron-microscopically and using gene cloning technique; already being done in research), and then by having the at-risk victim with identifiable gene avoid the stress factors, we might prevent cases of schizophrenia. But present data are inadequate. So put on thinking cap, brilliant reader! Someone out there can become a Nobelist and savior of schizophrenic sufferers and families.

The commonsense idea that mom (or family) brings out schizophrenia by poor child care seemed to be confirmed by studies that showed moms of schizophrenics to have higher frequency of giving less than loving care and of being over-involved with the child. As a causation theory, this was shot down by a study on identical twins of schizophrenic parents that were adopted away, each of a pair being raised in different household yet each individual of the pairs coming down with almost the same incidence of schizophrenia regardless of the child care. It should not be taken to mean that child care is not important in schizophrenia but it does imply that the factors that channel vulnerable persons toward the schizophrenic break are subtle ones and not to be detected by questionnaire or interview and may not be limited to maternal practice. Studies also show parental attitude is affected by the feedback from the schizophrenic child (i.e., a child who will develop schizophrenia evokes in the mom a great degree of over-involvement in care and a coldness that originally was thought to be cause of the break rather than the reverse).

John's case shows what a schizophrenic break looks like; it does not show what the illness is to its sufferer. What we see in John is a behavior reaction process to what, to him, is internal evidence of losing his mind. 

Basically, symptoms of schizophrenia come from a disordered thought process due to physical change in a brain. The normal filter of incoming sensory information seems disabled causing the mind to be overwhelmed by too much sensory input. It's like a psychedelic trip except it builds more gradually and does not depend on taking drug. Also the cerebral cortex is partially disconnected from cerebellum and basal ganglia causing a loss of mental balance. What the victim reports and how we perceive him to act reflects his reaction to his own distorted perception. The hallucination is a distortion of sensory input; the paranoid delusion is an attempt to make reassuring sense of the frightening change a schizophrenic breakdown person is experiencing in his mind.

  We can further deduce important facts from the statistics on schizophrenia. It is a process that fluctuates, based on the balance between the dis-integrative vs. the integrative. External environment seems important. We may guess that absence of schizophrenic break before a child goes away to college is at least partly due to protective environment. From that it follows that parent may protect child by the right moves in upbringing. For example, not sending an at-risk youth to an out-of-town university seems correct because of the so-frequent story of a first break coming at live-away school.

The rarity of first schizophrenic break after age 55 suggests that earlier environmental factors have unmasked the S-trait at-risk population by age 55. Later age occurrence, lower incidence and milder course of schizophrenia in women favor a protective factor. But one may alternatively or additionally guess a sex hormone protective effect of estrogen and/or a worsening effect of androgen.

  Each repeated break worsens the disease and increases the probability of suicide and dementia and here it resembles epilepsy and this suggests some kind of structural deterioration caused by an active process. Since data show schizophrenic break may be provoked by recreational psychedelic or stimulant drug (LSD, amphets or cocaine) especially avoiding stimulant drugs is good advice. Another factor that has provoked the break is what is called a hypercritical home atmosphere, which means constant criticism of a lifestyle. So a tolerance ought to be shown in a family where there is a specific risk factor or a break has already occurred. Where family can't help but be destructive, a therapeutic community seems best.

Finally, more and more DNA genetic markers that cause neuro-metabolic diseases are showing schizophrenia, which suggests it is a disorder of mal-development starting with metabolic and other genetic defects. Also this suggests absolute care to avoid influences like MRI or CT or other x-ray during pregnancy because these influences may cause the developing neuron fiebers to mis-connect with the result: schizophrenia. 

  Advices: All humans can be pushed over a brink, depending on each person's degree of the S-trait genes and the extremes of a destructive environment.  A small percent are at high risk and may break down because the gene load for the S-trait is above normal and/or because sensitive brain defects present at birth are over-stressed overcoming a threshold of sensory stimulation of usual life. It follows that a vulnerable person should have protective environment and avoid excess criticism and other stimulation.

I have so far emphasized the positive or purely psychotic symptoms like hallucinations, delusions and disorganized thought and speech, which stand out and mark the patient as “crazy”. Today in 2021 these may be successfully reversed by anti-psychotic medication. But the negative symptoms —- apathy, movement deficiency —- and the loss of IQ intelligence factors like working memory, loss of logic and the poverty of language, are the most troublesome, because they more affect the quality of life and do not respond to treatments.

 Prevention of Schizophrenia ideally should span generations and involve all society. (Supportive social network and medical system that relieves patient and family of the financial burden of the illness.)  Emphasis should be on prevention. New parents should identify risk factors in each new pregnancy so they can estimate risk in a coming baby. History of psychosis or other mental disorder, hospitalization, or odd behavior or homelessness in DNA relation may be a marker. A striking risk factor is advanced paternal age (Like in Down Syndrome except there it is maternal age); also for parent to note is complicated pregnancy that ends with fetal distress or labor and delivery that gives a newborn needing intensive care. Such at-risk child should be raised with emphasis on avoiding separation anxiety (No nursery school, no summer camp, no away from home school), and fostering a home environment with control of sensory input. (Public & cable TV controlled or absent, selected video disc or cassette; no unsupervised internet and no intense childhood relationship) It is important that an at-risk child be brought into a therapeutic program. He or she should learn what it means to be at risk and actually view schizophrenic behavior or at least have family seminar about it to develop insight (Schizophrenics typically lack insight; it needs to be helped by therapist.) into the behavior. As child grows, parent should cultivate relaxed, non-critical loving relationship based on informality, which makes no demand  but has high hope, and a loving, trusting communication between parent schizophreniaand child should be fostered so that parent can spot a thought-process disturbance early on. The start of puberty should start vigilance and positive reinforcement training in resilience and self control. A child psychiatrist should do behavioral desensitization to criticism, and education at home should be fostered. 

Note: A so-called dimensional approach to schizophrenia is buzzing its cutting edge research. In contrast to the current categorical approach introduced by Kraepelin around 1900, which separates schizophrenia from other psychosis based on its absence of manic thinking and episodes, it uses the degree of psychosis, and that has tended to move schizophrenia back into the affective psychosis spectrum albeit on its outlier disorganized thought pattern. Watch this development!

Treatment of schizophrenia starts with the schizophrenic break.  Of course the drug treatment of schizophrenia should be initiated and supervised by a psychiatrist experienced with he latest in drug treatment of schizophrenia but that does not mean that a lay reader here should not be conversant with the principles of treatment This recognition of schizophrenia diagnosis is always a dramatic event that rapidly leads to emergency hospitalization and treatment with strong anti-psychotic drug. Note: in a first apparent schizophrenic break, the definite diagnosis of schizophrenia should not be made until 6 months has passed because many acute psychoses are  due to drugs or medication or are part of other mental illnesses that can resemble a schizophrenic break and need to be separated from the diagnosis of schizophrenia per se. (But that should not delay treatment for the psychotic symptoms, because delay may worsen the prognosis.) All acute psychotic breaks once they are in hospital and calmed by anti psychotic injections should have a fairly similar plan of treatment. (Note, what follows may be somewhat Utopian but still it is useful to see an ideal good approach even if circumstances prevent it in particular case) The goal of a therapist for a patient who has suffered a first psychotic break should be rapid relief by appropriate dose anti-psychotic medication (usually Haldol by injection) in hospital and start of a therapy program whose goal is to prevent or limit further psychotic breaks, to return the patient to his community in a condition that she or he can participate in normal life, and to start psychotherapy that will include non Freudian analysis (See Chapter 33 here). 

On the anti psychotic drug therapy there are 3 stages, each with somewhat different goal and approach. The first, given above, is to quickly relieve the acute psychosis so that the patient is manageabledrug against high L to start psychotherapy. This is done with an older, stronger antipsychotic drug, today usually haloperidol by injection in relatively high dose. This goal is usually successful. The 2nd stage of drug treatment is maintenance to keep the patient from lapsing back into psychosis. 

Because the longer use of the older anti psychotics have high bad side-effects; today, the newer anti psychotics (aka Second Generation Antopsychotics, SGAs, or Serotonin-Dopamine Antagonists, SDAs) led by olanzapine aka "Zyprexa", are being used. These have less serious side effects and a good effectiveness (70% cf placebo). But they pose another increased risk, the metabolic syndrome which can lead to DM-1 and CVS disease in brain and heart.

The question is raised in the 3rd stage of treatment —-  How long should a schizophrenic in remission continue medication? Most psychiatrists experienced in the treatment advise continuing for life. A recent 18-month study shows that almost all schizophrenics on these drugs discontinue them on their own. I think the oral medication can be used to good effect for setting the patient on a good road while in remission through the use of smart psychotherapy and psychoanalysis. After that it up to the therapist, but he or she needs medical degree. (No osteopaths or chiropractors, please!)

 The psychotherapy I outline is as follows: The patient should have a therapist (Does not need M.D.) he trusts and considers an authority figure, but the therapist should come on as sympathetic, empathetic, and not directive. Much of the psychotherapy is showing the patient about his disease and talking with him about what the patient's goals are. Most of all, the therapist needs to establish a close, trusting relation with the patient. The family and friends and the outside society also need to be dealt with. The psychotherapy of schizophrenia is hard; but, still, it is the best tool to bring the patient to an understanding of the disease and blunt or prevent future psychotic breaks.  

 I end with excerpt of letter from a Schizophrenic.

  “… I want people to know I have schizophrenia. I need medicine and psychotherapy and at some times I have required hospitalization. But I also want them to know I have been on the dean's list, and have friends, and expect to receive my M.D. degree from a major medical school. When you think about schizophrenia next time, please try to remember … there are more people like me out there trying  to overcome a poorly understood disease and doing the best they can with what medicine and psychotherapy have to offer them. And some of us are making it.” Killed

Final note: The 2001 “A Beautiful Mind” is a fairly accurate movie of schizophrenia although the hallucination/delusion has been romanticized and, over-visualized, and over-realized, in order to make it more movie-able. Incidentally, Dr. John Nash (who got a 1994 Memorial Prize for Economic Science) and wife were killed in a freak car accident in May 2015 due to neglecting seatbelts.

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