Schizophrenia Related Quotes

Research has also revealed that women who have developed PTSD in relation to early childhood sexual abuse often develop borderline personality disorder. Some severe cases will result in the development of dissociative identity disorder or depersonalization disorder. Patients who have been exposed to protracted and repeated sexual abuse may also develop schizophrenia simultaneously with PTSD.

State philosophy reposes on a double identity: of the thinking subject, and of the concepts it creates and to which it lends its own presumed attributes of sameness and constancy. The subjects, its concepts, and also the objects in the world to which the concepts are applied have a shared, internal essence: the self-resemblance at the basis of identity. Representational thought is analogical; its concern is to establish a correspondence between these symmetrically structured domains. The faculty of judgment is the policeman of analogy, assuring that each of these terms is honestly itself, and that the proper correspondences obtain. In thought its end is truth, in action justice. The weapons it wields in their pursuit are limitive distribution (the determination of the exclusive set of properties possessed by each term in contradistinction to the others: logos, law) and hierarchical ranking (the measurement of the degree of perfection of a term’s self-resemblance in relation to a supreme standard, man, god, or gold: value, morality). The modus operandi is negation: x = x = not y. Identity, resemblance, truth, justice, and negation. The rational foundation for order. The established order, of course: philosophers have traditionally been employees of the State. The collusion between philosophy and the State was most explicitly enacted in the first decade of the nineteenth century with the foundation of the University of Berlin, which was to become the model of higher learning throughout Europe and in the United States. The goal laid out for it by Wilhelm von Humboldt (based on proposals by Fichte and Schleiermacher) was the ‘spiritual and moral training of the nation,’ to be achieved by ‘deriving everything from an original principle’ (truth), by ‘relating everything to an ideal’ (justice), and by ‘unifying this principle and this ideal to a single Idea’ (the State). The end product would be ‘a fully legitimated subject of knowledge and society’ – each mind an analogously organized mini-State morally unified in the supermind of the State. More insidious than the well-known practical cooperation between university and government (the burgeoning military funding of research) is its philosophical role in the propagation of the form of representational thinking itself, that ‘properly spiritual absolute State’ endlessly reproduced and disseminated at every level of the social fabric.

I am relatively certain that religious faith alone doesn't prevent hallucinations because many patients try to save themselves by their faith. Observation would suggest useful social acts (charity) would come closer to preventing schizophrenia.

Sturtevant’s rudimentary genetic map would foreshadow the vast and elaborate efforts to map genes along the human genome in the 1990s. By using linkage to establish the relative positions of genes on chromosomes, Sturtevant would also lay the groundwork for the future cloning of genes tied to complex familial diseases, such as breast cancer, schizophrenia, and Alzheimer’s disease. In about twelve hours, in an undergraduate dorm room in New York, he had poured the foundation for the Human Genome Project.

Becoming is certainly not imitating, or identifying with something; neither is it regressing-progressing; neither is it corresponding, establishing corresponding relations; neither is it producing, producing a filiation or producing through filiation. Becoming is a verb with a consistency all its own; it does not reduce to, or lead back to, 'appearing:' 'being:' 'equaling:' or 'producing.

What if he could isolate the gene irregularity that caused people to react this way to the double-click test? If he could do that, and if those people were indeed diagnosed with schizophrenia, then he would have proven the existence of a gene related to the illness and opened the door to a genetic remedy.

Though diagnosis is unquestionably critical in treatment considerations for many severe conditions with a biological substrate (for example, schizophrenia, bipolar disorders, major affective disorders, temporal lobe epilepsy, drug toxicity, organic or brain disease from toxins, degenerative causes, or infectious agents), diagnosis is often counterproductive in the everyday psychotherapy of less severely impaired patients. Why? For one thing, psychotherapy consists of a gradual unfolding process wherein the therapist attempts to know the patient as fully as possible. A diagnosis limits vision; it diminishes ability to relate to the other as a person. Once we make a diagnosis, we tend to selectively inattend to aspects of the patient that do not fit into that particular diagnosis, and correspondingly overattend to subtle features that appear to confirm an initial diagnosis. What’s more, a diagnosis may act as a self-fulfilling prophecy. Relating to a patient as a “borderline” or a “hysteric” may serve to stimulate and perpetuate those very traits. Indeed, there is a long history of iatrogenic influence on the shape of clinical entities, including the current controversy about multiple-personality disorder and repressed memories of sexual abuse. And keep in mind, too, the low reliability of the DSM personality disorder category (the very patients often engaging in longer-term psychotherapy).

Strong selection for extreme mental capacities may have given us all minds like the legs of racehorses, fast but vulnerable to catastrophic failures. This model fits well with the idea that schizophrenia is intimately related to language and cognitive ability.93 It also fits well with the observation that schizophrenia may be intimately related to the human capacity for “theory of mind,” our ability to intuit other people’s motives and cognitive abilities in general.

Unfortunately, most researchers studying gating dynamics in children are, as with “schizophrenia,” focused on “normal” versus “abnormal” gating. And all children are expected to fit into the defined “normal” range of behavior. Sensory gating dynamics outside that culturally determined “norm” are defined as abnormal and researchers note that Individuals with these characteristics have been classified as having sensory processing deficits (SPD). Such behaviors disrupt an individual’s ability to achieve and maintain an optimal range of performance necessary to adapt to challenges in life. The manifestations of SPD may include distraction, impulsiveness, abnormal activity level, disorganization, anxiety, and emotional lability that produce deficient social participation, insufficient self-regulation and inadequate perceived competence.1 Those terms, if you look at them more closely, are exterior, “authority” generated terms; they relate directly to the paradigm in place in those authorities. They really don’t have much to say about the interior experience of the children so labeled.

Despite the growing clinical and research interest in dissociative symptoms and disorders, it is also true that the substantial prevalence rates for dissociative disorders are still disproportional to the number of studies addressing these conditions. For example, schizophrenia has a reported rate of 0.55% to 1% of the normal population (Goldner, Hus, Waraich, & Somers, more or less similar to the prevalence of DID. Yet a PubMed search generated 25,421 papers on research related to schizophrenia, whereas only 73 publications were found for DID-related research.

The clinical hallmark of manic-depressive illness is its recurrent, episodic nature. Byron had this in an almost textbook manner, showing frequent and pronounced fluctuations in mood, energy, sleep patterns, sexual behavior, alcohol and other drug use, and weight (Byron also exhibited extremes in dieting, obsession with his weight, eccentric eating patterns, and excessive use of epsom salts). Although these changes in mood and behavior were dramatic and disruptive when they occurred, it is important to note that Byron was clinically normal most of the time; this, too, is highly characteristic of manic-depressive illness. An inordinate amount of confusion about whether someone does or does not have manic-depressive illness stems from the popular misconception that irrationality of mood and reason are stable rather than fluctuating features of the disease. Some assume that because an individual such as Byron was sane and in impressive control of his reason most of the time, that he could not have been "mad" or have suffered from a major mental illness. Lucidity and normal functioning are, however, perfectly consistent with-indeed, characteristic of-the phasic nature of manic-depressive illness. This is in contrast to schizophrenia, which is usually a chronic and relatively unrelenting illness characterized by, among other things, an inability to reason clearly.

Both individuals who are manic and those who are writers, when evaluated with neuropsychological tests, tend to combine ideas or images in a way that "blurs, broadens, or shifts conceptual boundaries," a type of thinking known as conceptual overinclusiveness. They vary in this from normal subjects and from patients with schizophrenia. Researchers at the University of Iowa, for example, have shown that "both writers and manics tend to sort in large groups, change dimensions while in the process of sorting, arbitrarily change starting points, or use vague distantly related concepts as categorizing principles." The writers are better able than the manics to maintain control over their patterns of thinking, however, and to use "controlled flights of fancy" rather than the more bizarre sorting systems used by the patients.

If you can imagine this, perhaps you can understand that someone from another planet who came to visit us would have a similar experience with humans. But it isn’t our skin that is full of wounds. What the visitor would discover is that the human mind is sick with a disease called fear. Just like the description of the infected skin, the emotional body is full of wounds, and these wounds are infected with emotional poison. The manifestation of the disease of fear is anger, hate, sadness, envy, and hypocrisy; the result of the disease is all the emotions that make humans suffer. All humans are mentally sick with the same disease. We can even say that this world is a mental hospital. But this mental disease has been in this world for thousands of years, and the medical books, the psychiatric books, and the psychology books describe the disease as normal. They consider it normal, but I can tell you it is not normal. When the fear becomes too great, the reasoning mind starts to fail and can no longer take all those wounds with all the poison. In the psychology books we call this a mental illness. We call it schizophrenia, paranoia, psychosis, but these diseases are created when the reasoning mind is so frightened and the wounds so painful, that it becomes better to break contact with the outside world. Humans live in continuous fear of being hurt, and this creates a big drama wherever we go. The way humans relate to each other is so emotionally painful that for no apparent reason we get angry, jealous, envious, sad. To even say “I love you” can be frightening. But even if it’s painful and fearful to have an emotional interaction, still we keep going, we enter into a relationship, we get married, and we have children. In order to protect our emotional wounds, and because of our fear of being hurt, humans create something very sophisticated in the mind: a big denial system. In that denial system we become the perfect liars. We lie so perfectly that we lie to ourselves and we even believe our own lies. We don’t notice we are lying, and sometimes even when we know we are lying, we justify the lie and excuse the lie to protect ourselves from the pain of our wounds.

By the end of this decade, permutations and combinations of genetic variants will be used to predict variations in human phenotype, illness, and destiny. Some diseases might never be amenable to such a genetic test, but perhaps the severest variants of schizophrenia or heart disease, or the most penetrant forms of familial cancer, say, will be predictable by the combined effect of a handful of mutations. And once an understanding of "process" has been built into predictive algorithms, the interactions between various gene variants could be used to compute ultimate effects on a whole host of physical and mental characteristics beyond disease alone. Computational algorithms could determine the probability of the development of heart disease or asthma or sexual orientation and assign a level of relative risk for various fates to each genome. The genome will thus be read not in absolutes, but in likelihoods-like a report card that does not contain grades but probabilities, or a resume that does not list past experiences but future propensities. It will become a manual for previvorship.

Generally, the best way to determine the relative benefit of drugs is through comparative effectiveness studies, in which all drugs, or a representative selection, are compared. In the United States, the nonprofit Consumer Reports is dedicated to such unbiased testing of consumer products, but no equivalent exists for medicines. After a drug is approved by the FDA, there is no process for tracking how it stacks up against other medications currently in use." ― Jeff Lieberman, Malady of the Mind: Schizophrenia and the Path to Prevention

It is actually relatively common for someone to be diagnosed with multiple personality disorder after having visited the doctor for an eating issue. The eating issue cannot be resolved by the conventional approaches which most doctors use. Only when these approaches are all exhausted will the doctor look for alternatives and may well discover that the eating disorder is a symptom of a multiple personality disorder and not a disorder in its own right. •

The fading relevance of the nature–nurture argument has recently been revived by the rise of evolutionary psychology. A more sophisticated understanding of Darwinian evolution (survival of the fittest) has led to theories about the possible evolutionary value of some psychiatric disorders. A simplistic view would predict that all mental illnesses with a genetic component should lower survival and ought to die out. ‘Inclusive fitness’, however, assesses the evolutionary value of a characteristic not simply on whether it helps that individual to survive but whether it makes it more likely that their offspring will survive. Richard Dawkins’s 1976 book The Selfish Gene gives convincing explanations of the evolutionary advantages of group support and altruism when individuals sacrifice themselves for others. A range of speculative hypotheses have since been proposed for the evolutionary advantage of various behaviour differences and mental illnesses. Many of these draw on ethological games-theory (i.e. the benefits of any behaviour can only be understood in the context of the behaviour of other members of the group). So depression might be seen as a safe response to ‘defeat’ in a hierarchical group because it makes the individual withdraw from conflict while they recover. Mania, conversely, with its expansiveness and increased sexual activity, is proposed as a response to success in a hierarchical tussle promoting the propagation of that individual’s genes. Changes in behaviour that look like depression and hypomania can be clearly seen in primates as they move up and down the pecking order that dominates their lives. The habitual isolation and limited need for social contact of individuals with schizophrenia has been rather imaginatively proposed as adaptive to remote habitats with low food supplies (and also a protection against the risk of infectious diseases and epidemics). Evolutionary psychology will undoubtedly increasingly influence psychiatric thinking – many of our disorders fit poorly into a classical ‘medical model’. Already it has helped establish a less either–or approach to the discussion. It is, however, a highly controversial area – not so much around mental disorders but in relation to social behaviour and particularly to gender specific behaviour. Here it is often interpreted as excusing a very male-orientated, exploitative worldview. Luckily that is someone else’s battle.

A Family Affair: Essential Fatty Acids More chemical clues to the nature of alcoholism come from research focusing on alcoholics with at least one grandparent who was Welsh, Irish, Scottish, Scandinavian, or native American. Typically, these alcoholics have a history of depression going back to childhood and close relatives who suffered from depression or schizophrenia. Some may have relatives who committed suicide. There also may be a family history of eczema, cystic fibrosis, premenstrual syndrome, diabetes, irritable bowel syndrome, or benign breast disease. The common denominator here is a genetic abnormality in the way the body handles certain essential fatty acids (EFAs) derived from foods. Normally, these EFAs are converted in the brain to various metabolites such as prostaglandin E1 (PGE1), which plays a vital role in the prevention of depression, convulsions, and hyperexcitability. When the EFA conversion process is defective, brain levels of prostaglandin E1 are lower than normal, which results in depression. In affected individuals, alcohol acts as a double-edged sword. It activates the PGE1 within the brain, which immediately lifts depression and creates feelings of well-being. Because the brain cannot make new PGE1 efficiently, its meager supply of PGE1 is gradually depleted. Over time, the ability of alcohol to lift depression slowly diminishes. Several years ago, researchers hit upon a solution to this problem. They discovered that a natural substance, oil of evening primrose, contains large amounts of gamma-linolenic acid (GLA), which can help the brain convert EFAs to PGE1. The results are quite dramatic. In a recent study in Scotland, researcher David Horrobin, M.D., matched two groups of alcoholics whose EFA levels were 50 percent below normal. The first group got EFA replacement, the second, a placebo. Marked differences between the two groups emerged in the withdrawal stage. The group that got EFA replacement had far fewer symptoms, while the placebo group displayed the full range of withdrawal symptoms associated with prostaglandin deficiency: tremors, irritability, tension, hyperexcitability, and convulsions. At the outset of the study, members of both groups had some degree of alcohol-related liver damage. Three months later, the researchers found that liver function among the EFA replacement group was almost normal. There was no significant improvement among the placebo group. A year later, the placebo group was still deficient in the natural ability to convert essential fatty acids into PGE1. What’s more, only 28 percent of this group had remained sober; the rest had resumed drinking. Results were dramatically better among the EFA replacement group: 83 percent remained sober and depression free.

The bottom-line conclusion from the early work on the relation of monoamines to schizophrenia was this: Too much dopamine induces a psychological disorder, and too little, a movement disorder similar to Parkinson's disease. A balance must be maintained. When it is tipped, the brain does not function normally. Subsequent work, as we'll see in the following section, has drawn a more complex picture of the neural basis of schizophrenia. Dopamine is still believed to be involved, but not quite in so simple a way as the original imbalance hypothesis suggested.

In fact, regarding the relatively small percentage of individuals who do become addicted, co-occurring psychiatric disorders—such as excessive anxiety, depression, and schizophrenia—and socioeconomic factors—such as resource-deprived communities and un- and underemployment—account for a substantial proportion of these addictions.

Near-Psychotic Symptoms in Obsessive-Compulsive Disorder Despite clear-cut differences in psychopathology between schizophrenia and OCD, there is a substantial overlap, a “gray zone,” between the two disorders. Thus, unusual and “bizarre” obsessive themes exhibited by a subgroup of otherwise typical OCD patients might complicate the distinction between the obsessions and delusions. The difference between OCD-related pathologic slowness and the restrictive motor output associated with negative symptoms of schizophrenia or with catatonic motor disturbances is not straightforward. The differential diagnosis between OCD-related indecisiveness and pathologic doubt and schizophrenic ambivalence is also challenging. Patient insight into the senseless nature of OC symptoms is one of the hallmarks of the disorder. According to the DSM-5, at some point in the course of the illness, the patients must recognize that their obsessive beliefs are “definitely or probably not true.” Indeed, in typical OCD cases, patients readily acknowledge that their OC symptoms are illogical and pathologic. On the other hand, a significant majority of schizophrenia patients either do not believe that they are ill, or even if they do acknowledge symptoms, they misattribute them to other causes.6 Nevertheless, a significant subset of OCD patients can sometimes present without insight, or with conviction that their obsessions are true, thus complicating the differential diagnosis of obsessions from delusions. Overall, from the psychopathologic perspective, schizophrenia and OCD are distinct, despite their partially overlapping characteristics. Some symptoms, such as delusions and obsessions, pathologic doubt and ambivalence, rituals and motor stereotypy, may represent a continuum of OCD impairments, while others, such as negative and disorganized symptoms, are more schizophrenia-specific (Fig 3.1).

After immobilizing his head with two white straps, the neuroanatomist moved a figure eight–shaped instrument toward the crest of his skull—a coil that delivered magnetic impulses to a very precise area of the encephalon, so that the targeted neurons, like micromagnets, would react and rearrange themselves. Transcranial magnetic stimulation allowed them to attenuate, even eradicate, the hallucinations related to schizophrenia. The main difficulty was, of course, to target the right spot, as the area in question measured only a few centimeters, and being off by even a millimeter could make the patient start meowing or reciting the alphabet backward for the rest of his life.

rediscovered, a ketogenic diet is returning to mainstream acceptance and is again recognized as a highly effective therapy for seizure and neurologically related disorders. In fact, there are studies to show the strong benefits of ketogenic diets on virtually every manner of neurological disorder. Some examples of neurologic uses of a ketogenic diet other than epilepsy are migraines, Alzheimer’s disease, Parkinson’s disease, Lou Gehrig’s disease (ALS), autism, brain tumors, depression, sleep disorders, schizophrenia, postanoxic brain injury, posthypoxic myoclonus glycogenosis type V, and narcolepsy, to name a few.

So, again, with Kekkonen, we see how difficult it is for the Finns to maintain democracy. They are too inclined to follow and trust their leaders, they are disinclined to stand out from the crowd and risk social opprobrium, or, rather, there are too few per capita people who are prepared to behave in such a way or support those who are prepared to. Moreover, it could be argued that Kekkonen successfully took advantage of a kind of paranoia among the Finns. As we have discussed, they are relatively high in schizophrenia, meaning that the average Finn is further along the schizotypy spectrum than is the average person in many European countries. This would mean that a higher proportion of Finns, with their very high empathy, would read too much into the external signs of the mind of the Soviet Union and thus become paranoid, prepared to assume that an indication of displeasure was in fact an indication of fury, possibly leading to invasion. ‘Only President Kekkonen can deal with this crisis’ they might reason, ‘so I must support him.’ But, in reality, there isn’t really a crisis at all.

This hypothesis, referred to as the monoamine hypothesis, grew primarily out of two main observations made in the 1950s and ’60s.14 One was seen in patients being treated for tuberculosis who experienced mood-related side effects from the antitubercular drug iproniazid, which can change the levels of serotonin in the brain. Another was the claim that reserpine, a medication introduced for seizures and high blood pressure, depleted these chemicals and caused depression—that is, until there was a fifty-four person study that demonstrated that it resolved depression.15 From these preliminary and largely inconsistent observations a theory was born, crystallized by the work and writings of the late Dr. Joseph Schildkraut, who threw fairy dust into the field in 1965 with his speculative manifesto “The Catecholamine Hypothesis of Affective Disorders.”16 Dr. Schildkraut was a prominent psychiatrist at Harvard who studied catecholamines, a class of naturally occurring compounds that act as chemical messengers, or neurotransmitters, within the brain. He looked at one neurochemical in particular, norepinephrine, in people before and during treatment with antidepressants and found that depression suppressed its effectiveness as a chemical messenger. Based on his findings, he theorized broadly about the biochemical underpinnings of mental illnesses. In a field struggling to establish legitimacy (beyond the therapeutic lobotomy!), psychiatry was desperate for a rebranding, and the pharmaceutical industry was all too happy to partner in the effort. This idea that these medications correct an imbalance that has something to do with a brain chemical has been so universally accepted that no one bothers to question it or even research it using modern rigors of science. According to Dr. Joanna Moncrieff, we have been led to believe that these medications have disease-based effects—that they’re actually fixing, curing, correcting a real disease in human physiology. Six decades of study, however, have revealed conflicting, confusing, and inconclusive data.17 That’s right: there has never been a human study that successfully links low serotonin levels and depression. Imaging studies, blood and urine tests, postmortem suicide assessments, and even animal research have never validated the link between neurotransmitter levels and depression.18 In other words, the serotonin theory of depression is a total myth that has been unjustly supported by the manipulation of data. Much to the contrary, high serotonin levels have been linked to a range of problems, including schizophrenia and autism.19 Paul Andrews, an assistant professor

Schizophrenia is the absolute limit, but capitalism is the relative limit.

My aim for this archaeological project is twofold. Contrary to what many think, diagnoses are helpful but by no means necessary for the work of psychotherapy. They are crucial if one is to prescribe medication or bill an insurance provider, of course, but they don't play nearly as large of a role in two people talking to one another. When a client comes to me and tells me that they have bipolar disorder, depression, or the like, I file it away as necessary data. However, that categorization is far less interesting or meaningful to me than exploring what gives their life purpose and how they could better live into their values. To paraphrase the British psychoanalyst Donald Winnicott, the business of therapy is really just two people playing together. I have found that the fear of diagnosis, what it might mean to be labeled as "depressed" or "anxious," much less "psychotic," prevents many people from consulting a therapist when they need help. A label that isn't all that useful to my work serves as an impediment to those in need. Perhaps it's time to rethink the utility of those labels, or at least how we relate to them. Once I know the person sitting in front of me has schizophrenia, the focus becomes fixed on treating their hallucinations and delusions, on helping them best integrate into society. We thus exempt ourselves from considering everything that came before they entered our office. What if it was possible to both acknowledge their suffering while also condemning the injustices and inequalities that have helped lead them here? That is the task that I have set for myself in the following pages.

Let us call schizophrenia a successful attempt not to adapt to pseudo social realities. s ths also an objective fact? Schizophrenia is a failure of ego functioning. Is this a neutralist definition? But what is, or who s, the 'ego'? In order to get back to what the ego is, to what actual reality it most nearly relates to, we have to desegregate it, de-depersonalize it, de-extrapolate, de-abstract, de-objectify, de-reify, and we get back to you and me, to our particular idioms or styles of relating to each other in social context. The ego is by definition an instrument of adaptation, so we are back to all the questions this apparent neutralism is begging. Schizophrenia is a successful avoidance of ego-type adaptation? Schizophrenia is a label affixed by some people to others in situations where an interpersonal disjunction of a particular kind s occurring. This is the nearest one can get at the moment to something like an 'objective' statement, so called.