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HOW I ESCAPED THE STRAITJACKET OF SERIOUS MENTAL ILLNESS
Contents:
  1. My Label, My Life
  2. Mental Illness cures: (EDS-7) Etiological Diagnostic Snapsheet
  3. Getting the diagnosis right when symptoms are confusing

A similar hierarchy of syndromes developed around manic-depressive illness. This view of the diagnostic categories as proper sets, recognized by symptoms that were singly necessary and jointly sufficient to define the diagnosis. And early editions of the DSM were at least implicitly structured around this conceptualization, in terms of the "textbook cases" it used to characterize each syndrome.

However, the traditional view quickly encountered problems of a sort that are familiar from the critique of the classical view of categories as proper sets discussed in the lectures on Thought and Language. The simple fact was that very few patients actually resembled the textbook descriptions of the various syndromes.

Accordingly, for the third edition of DSM DSM-III , published in , the diagnostic system was reformed to take into account a new understanding of the structure of natural categories offered by cognitive psychology. Under this "revisionist" view:. Consider, for example, several prominent psychiatric diagnoses, as listed in DSM-5 :. Schizophrenia may be diagnosed in the presence of any two "characteristic symptoms". Positive symptoms entail the presence of something normally absent, like delusions.

Negative symptoms entail the absence of something normally present, appropriate emotional responses. One patient may have delusions and hallucinations while another may have catatonic behavior and flat affect, but both are "schizophrenics". DSM-5 also abandons the Bleulerian subtypes, such as hebephrenic and catatonic schizophrenia, in favor of a distinction between acute and chronic schizophrenia, and whether the patient has had multiple episodes prior to the current one. Some clinicians and researchers promote a distinction between Type I schizophrenia, where positive symptoms predominate, and Type II schizophrenia, dominated by negative symptoms.

Similarly , Major Depressive Disorder can be diagnosed after observing any five of a large number of symptoms. Note that depression can be diagnosed even if the person doesn't feel depressed! All patients with Anxiety Disorder must display abnormal levels of anxiety, but this singly necessary symptom is not sufficient to make the diagnosis.

Other symptoms must also be present, but none of these additional symptoms is necessary for the diagnosis. Similarly, the diagnosis of Post-Traumatic Stress Disorder requires that the patient have been exposed to traumatic levels of stress, so this is another instance of a singly necessary defining feature. The exposure may take the form of directly experiencing, or "just" witnessing, the trauma; or learning about a trauma which occurred to a significant other.

The exposure can also be repeated or prolonged, not just a single episode. But none of the other symptoms are necessary to make the diagnosis. But there are lots of different ways to display these features, no particular manifestation is necessary. A statistical technique called network analysis can be used to show the relations among the various categories of psychopathology. Denny Borsboom, a Dutch psychologist, and his colleagues created a simple spreadsheet showing the co-occurrence of all the symptoms listed in DSM-IV -- that is, how many times insomnia and fatigue are listed as characteristic symptoms of the same syndrome such as sleep disorder or depression.

The obtained a graph in which each symptom is represented by a node, and nodes are connected whenever two symptoms are characteristic of the same disorder. They then colored each of the nodes, according to the major category of mental illness in which each symptom occurred. Regardless of diagnostic category, there was no expectation that all of the symptoms listed under a syndrome will be present in any particular case. In principle, we can observe all possible combinations of characteristic symptoms.

Diagnosis, then, is a matter of judgment under uncertainty. Studies of the diagnostic process by Nancy Cantor and her associates show that the certainty with which a diagnosis of schizophrenia is made, for example, will be a function of the number of the patient's symptoms that are highly characteristic of schizophrenia, and the number of symptoms that are more characteristic of other diagnostic categories. In this system, "textbook cases" serve as category prototypes, and there is explicit recognition of heterogeneity among actual patients.

Both manuals were as much literary productions as scientific ones. They were heavily influenced by Freudian psychoanalysis, centered on the distinction between psychoses and neuroses, and didn't really include clear criteria for making various diagnoses. In these editions, serious effort went into producing checklists of symptoms by which the various disorders could be reliably diagnosed.

SCHIZOPHRENIA & schizoaffective disorder - Mental Health therapist Kati Morton treatment & psychosis

The fifth edition of DSM , known as DSM-5 , retains the "fuzzy set" structure of the diagnostic categories, while sometimes revising the criteria for specific disorders. However, DSM-5 abandons certain other features of previous editions. Some commentators have expressed the fear of diagnostic inflation -- that these kind of changes may make it possible to diagnose anyone with a mental illness -- or, at least, that DSM threatens to "pathologize normality" by classifying normal mental states, like bereavement or even shyness which can resemble depression , as mental illnesses.

Benjamin Wolman, a leading psychoanalytic psychotherapist, once wrote a book entitled Call No Man Normal. Overdiagnosis, of course, inevitably leads to overtreatment. In addition, some of those responsible for formulating the DSM-5 criteria had unacknowledged links with the pharmaceutical industry, raising the possibility that increasing the number of people who can be diagnosed with some form of mental illness, however mild, will effectively expand the market for psychiatric medications.

At the very least, these affiliations might have biased the Manual developers toward biological diagnoses and treatments. At the worst, it raises the possibility that Big Pharma might encourage clinicians to formulate new diagnoses that expand the market for available psychotropic drugs -- what Marcia Angell, the former editor of the New England Journal of Medicine , has called a "patent-extending game" see her book, the Truth About Drug Companies: How They Deceive Us and What We Can Do About It , Other commentators worry that many DSM-5 diagnoses simply lack validity to begin with.

In an important early paper, Robins and Guze outlined the criteria for establishing the validity of any diagnostic category:. By these standards, more than 40 years later, many DSM diagnoses do not fare too well. For example, the American Psychiatric Association proposed to "field-test" DSM-5 before its actual publication, to make sure that clinicians could use it reliably to make diagnoses. Unfortunately, DSM-5 failed its field trials, in that the rate of disagreement between two clinicians, applying the same criteria to the same patient, was unacceptably high.

This state of affairs has led some investigators to propose alternatives to the DSM. For now, though, DSM-5 is what we've got. The Social Security administration won't pay disability benefits, insurance companies won't pay for treatment, and courts won't consider the insanity defense, in the absence of an official psychiatric diagnosis, and DSM is how psychiatrists officially diagnose patients. It's as simple as that. Instead of employing traditional diagnostic categories, such as schizophrenia and bipolar disorder, RDoC classifies mental processes into several domains, constructs, and sub-constructs, with each construct and sub-construct hypothetically linked to a different neural circuit in the brain.

Here is a list of the domains and subdomains, as listed in a document published by NIMH in Following the medical model, it's important to get beyond surface symptoms and signs to underlying pathology. DSM-5 doesn't do that, it's diagnoses are solely based on signs and symptoms. Diagnosis in the rest of medicine is of diseases , and the RDoC is a step in this direction. At the same time, we can worry about the underlying assumption, which is that each element of underlying pathology is linked to a dysfunction in some brain circuit Insel, "Faulty Circuits", Scientific American , April It's not at al clear that a faulty brain circuit must be involved in every instance of mental illness.

Moreover, the identification of such circuits is years, decades, maybe centuries away. The whole project of identifying the circuits of the brain, which is the raison d'etre of the Human Connectome Project announced by President Obama in , begins with extremely simple nervous systems, such as aplysia the sea slug studied by Eric Kandel and others , and then move up to the mouse, and only later to the human -- at which point the process of linking neural circuits to the various domains can begin.

Not in my lifetime, nor yours.


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In the meantime, diagnosis needs to move beyond signs and symptoms to the identification of underlying pathology through laboratory tests -- underlying psycho pathology. For now, though, and for the foreseeable future, psychiatric diagnosis is going to be based on symptoms and signs, and organized by something very much like DSM This line of research in experimental psychopathology has a long and distinguished history, going back to Emil Kraepelin's studies of schizophrenia using Donders's reaction-time methodology.

While the RDoC claims to be "agnostic" about the traditional diagnostic categories actually, far from being agnostic, it rejects them , experimental psychopathology takes them as a starting point, and tries to identify the pathological mental processes that underlie them. One result of this work should be the more fine-grained classification, moving beyond superficial symptoms and signs, that the RDoC seeks -- but without the excessive biologizing.

Current diagnostic practices classify illness based on surface symptoms, but the symptoms are not the disease. Rather, symptoms are assumed to be caused by some underlying disease process -- pathology. In medicine, symptoms are not the disease, and progress in medical understanding is marked by a shift in focus from symptoms to underlying disease processes -- to underlying pathology revealed by laboratory analyses of structure and function whose results are interpreted in the light of a theoretical understanding of normal function.

Consider the example of fever , manifested by chills a symptom about which patients complain and increased body temperature a sign, indicated by a thermometer. Well into the 19th century the medical nosology included a large number of different "types" of fever, based on the symptoms accompanying the fever and the circumstances under which the fever occurred. In fact, Benjamin Rush, the pioneering American physician of the Revolutionary War era, thought there was only one disease -- fever. But nobody diagnoses and treats fever anymore, because fever is viewed as a symptom of an underlying bacterial infection.

Physicians may try to reduce a patient's fever, as an emergency measure, but most of their efforts are devoted to identifying the underlying infection through blood tests and then treating it through antibiotics. In "Rocky Mountain spotted fever" the patient presents with chills and elevated body temperature, as well as a petechial rash beginning on the wrists and ankles; the illness was first diagnosed in the Rocky Mountain area of the United States.

Initially, treatment focused on bring the fever down with cold compresses, or else simply letting the fever "run its course". Now, however, a physician who suspects that a patient suffers from this disease will order a laboratory test to look for serum antibodies to the Rickettsia rickettsii virus, which is transmitted by a wood tick found in the western United States.

Treatment entails finding the tick and removing it from the patient's skin, followed by a course of antibiotics to eliminate the infection. This treatment, applied in a timely fashion, results in a complete cure, not just symptom relief. Similarly, efforts at preventing the disease are aimed at eliminating the tick from the environment through insecticide sprays. Lisa Sanders, a physician on the faculty of the Yale School of Medicine, occasionally contributes a column to the New York Times Magazine in which she shows how a puzzling medical diagnosis was resolved through the interpretation of laboratory tests that went beyond the usual symptoms, signs, and history.

Here are a couple of examples from her columns:. These examples illustrate how diagnosis is done in advanced, scientific medicine:. In any event, the patient's response to treatment is assessed by laboratory tests: if the diagnosis is correct, and the treatment is working, the patient's scores will improve on the very tests that generated the diagnosis in the first place. On occasion, the correlation between symptoms and disease may be so high that no tests are ordered.

But in most cases, medical diagnosis is based on laboratory tests, not presenting symptoms, and the success of treatment is confirmed by laboratory tests as well. In medicine, pathology affects bodily functions through lesions in anatomical structures e. Modern medical diagnosis is based on evidence of these pathological conditions, as revealed by objective laboratory tests. There are parallels in the medical model of psychopathology:. In medicine, underlying pathology is revealed by laboratory analyses interpreted in the light of our understanding of normal structure and function.

In psychopathology, such laboratory research is known as experimental psychopathology. Experimental psychopathology tries to identify the causes of the patient's manifest symptoms. It is basic research on psychopathology, as opposed to applied research on diagnosis and treatment, and it comes in two major forms:. Studies of psychological deficit in schizophrenia have a long history, dating back to experimental work by Kraepelin, in Wundt's laboratory, who used Donders' reaction time technique to measure the speed of mental processes in patients with dementia praecox presenile dementia , the syndrome later renamed schizophrenia.

One highly prominent theory of schizophrenia holds that the psychological deficit underlying the patient's presenting symptoms affects the attentional system. According to this theory, schizophrenics suffer from a breakdown in selective attention that renders them highly distractable and unable to filter out irrelevant ideas. The patient shows thought and language disorder because he cannot keep track of what he is thinking and saying; he withdraws socially to shut out this chaos of stimulation.

And, in fact, laboratory tests confirm that patients with schizophrenia have a number of difficulties with attention. The information-processing deficits in schizophrenia appear to begin at the very beginning of the information-processing sequence. Think of the multi-store model discussed in the lectures on memory. In that model, stimulus information is briefly held in modality-specific sensory registers, from which it is extracted into short-term or working memory for further processing, and then encoded into long-term memory.

Studies of information-processing in schizophrenia have focused on the sensory registers, working memory, and attention. If things go wrong at these earliest stages of information processing, lots of other things will go wrong as well. Consider, for example, a study by Wishner and Wahl of dichotic listening in schizophrenia there are other studies of this topic, but I chose this one because Wishner was a teacher of mine in graduate school and Wahl was a graduate-student colleague.

In this paradigm, different messages are played through earphones to the two ears, and the subject is instructed to shadow one message, repeating its words aloud as they are spoken, and ignore the other. There is little or no impairment when normal subjects shadow a single message, with no distracting message coming over the other ear.

When the distracting channel is added, however, subjects begin to make shadowing errors: omissions of parts of the target message and intrusions of the irrelevant message, and recall of the target message. Wishner and Wahl found that schizophrenics were particularly prone to make shadowing errors: more omissions and more intrusions, especially when the target message was played at a relatively fast speed;, and poorer recall of words from the target message, even when no distractor was present.

These results are consistent with the hypothesis that schizophrenics suffer from an attentional deficit. Comparable findings were obtained in a study of visual attention by Saccuzzo and Shubert employing the backward masking paradigm. In this procedure, an array of digits or letters is presented very briefly, so that there is not much opportunity for it to register in a very short-term memory store known as iconic memory see the lecture supplements on Memory.

Presentation of this array is followed by a "masking" stimulus that effectively displaces the array from iconic memory, preventing it from being further processed in "primary", "short-term, or "working" memory. Therefore, identification of the elements in the array requires highly focused attention, so that the subject can process the information from the array into primary memory before its representation disappears from iconic memory.

In the experiment, subjects had to search for the letter T in an array of A s, or for the letter A in an array of T s: if it is present, they simply say "yes" and another trial begins. The investigators varied the "stimulus-onset asynchrony" SOA , or the interval between the onset of the array and the onset of the mask -- essentially, the amount of time that a representation of the array resides in iconic memory. They found that schizophrenics were generally poorer at target detection than controls, especially at longer SOAs.

They concluded that it takes longer for schizophrenics to transfer information from iconic to primary memory. By virtue of this slower rate of information processing, schizophrenics miss a lot of what goes on around them, and are more distractable. In recent years, much attention has focused on working memory in schizophrenia. This information may be extracted from perception or retrieved from memory. As such, working memory is critical for a wide variety of cognitive processes, such as selective attention, including both focusing on needed information and inhibition of irrelevant information.

A problem in working memory can permeate far into cognitive function, affecting memory, reasoning, problem-solving, and language. Working memory is often studied with variants of the Sternberg task, discussed at length in the lecture on methods and statistics. In the Sternberg task, a subject is asked to memorize a small set of items, and then to search that set for a particular target. In the Sperling task, subjects have to inspect a study set presented as a visual array.

In the Sternberg task, they have to hold a representation of the study set in working memory while they search it. An experiment by Paul Metzak and his colleagues compared schizophrenic patients with a group of normal control subjects who had been matched with the patients on such demographic variables as age and education. Like Sternberg, Metzak found that accuracy decreased, and response latency increased, with the size of the study set.

But this variable had a greater effect on the performance of the schizophrenic patients than on the normal subjects. Performance especially deteriorated at the largest set size. Working memory consists of several different components. First, there are modality-specific buffers which maintain information in an active state. These elements are similar to the traditional concept of short-term memory, and there appears to be no problem with them in schizophrenia. Then there is a central executive, which actually guides various information-processing tasks, manipulating and transforming information held by the buffers.

Here is where the psychological deficit in schizophrenia appears to be located. This central executive appears to be mediated by the dorsolateral prefrontal cortex. Interestingly, this region of the brain is part of a system modulated by dopamine, and the antipsychotic drugs used in the treatment of schizophrenia are antagonists of this neurotransmitter. Studies of dichotic listening, backward masking, and working memory illuminate schizophrenic deficiencies in central mechanisms of attention, but attention is also regulated by peripheral mechanisms -- as when we turn our heads or eyes to shift our attention from one object to another.

Holzman and his colleagues have studied the peripheral mechanisms of attention with an eye-tracking paradigm in which subjects are asked to hold their head in a fixed position and move their eyes to track a target moving smoothly across a screen; they then examine the subjects' pursuit eye movements PEMs as they follow the target. Some aspects of these eye movements are not consciously perceptible to the subject, but can be recorded by an electrooculogram EOG similar to that used in sleep research, or by special infrared devices.

Holzman et al. Accordingly, Holzman has suggested that abnormal PEMs might be a biological marker for schizophrenia, perhaps indicating an underlying malfunction in the frontal-lobe of the brain, particularly in those centers involved in the peripheral control of attention. Interestingly, Holzman and his colleagues have found that abnormal PEMs are related to various aspects of thought disorder, as measured in patients' verbal protocols. However, abnormal PEMs are associated with thought disorder across a wide variety of diagnoses, so this aspect of attentional deficit may not be specific to schizophrenia.

My Label, My Life

Most experimental studies of schizophrenia focus on various aspects of cognitive function, such as attentional deficits, but schizophrenia can involve problems with emotional function as well. Consider anhedonia , one of the classic "Four As" of schizophrenia. Many schizophrenics show flat or bunted affect, or else affect that is inappropriate to the situation. But that's their display of affect. Recall Lang's multiple systems view of attention, according to which emotional responses have three different components: a subjective feeling state, overt behavior, and covert physiological response.

I n one experiment, Kring and Neale showed emotional positive and negative and neutral films to schizophrenic patients and controls, and measured all three components of emotional response. In terms of facial expressions, schizophrenics were, indeed, less reactive than controls -- in terms of the frequency, intensity, and duration. But they were actually more reactive when their covert physiological responses were measured by a psychophysiological index known as skin conductance.

The self-reported emotional responses of schizophrenic patients were somewhat muted, compared to controls, but both patients and controls showed the same pattern of response to positive and negative films. So, schizophrenics do not appear to be emotionally responsive, in terms of their facial expressions. But in terms of their subjective feeling states, and their physiological response to emotional stimuli, they appear to be experiencing emotion -- even if they aren't showing it in their behavior.

The problem with diagnosing mental illness based on symptoms is illustrated by attention deficit hyperactivity disorder ADHD , which is typically diagnosed in children based on such symptoms as failure to pay attention in school or play, running around the room, climbing on things, fidgeting and squirming, and the like. But adults with ADHD don't necessarily do these things. Instead, they display other, more age-appropriate symptoms such as difficulties in "wrapping up" the final details of a project, getting and keeping things in order, remembering appointments, and the like.

Both sets of symptoms may have a common origin in some attentional dysfunction, and perhaps a common standard for diagnosis, applicable to children and adults alike, could be achieved by the development of laboratory tests that assess attentional functions directly. In addition to studies of psychological deficit, it is sometimes possible to create laboratory models of psychopathology, inducing in normal individuals a syndrome that, in at least some respects, resembles some form of actual mental illness.

Laboratory models are rarely if ever exact replicas of mental illnesses, down to the last detail; rather, they usual mimic one or more characteristic symptoms of some syndrome. In a sense, laboratory models constitute theories of how symptoms arise in actual patients, because they are based on the assumption that the causative agents that effectively produce symptoms in the lab parallel those that are present in the real world outside the laboratory.

Thus laboratory models can be used to test proposals concerning the origins, treatment, and prevention of mental illness. As such, they can be evaluated on a number of dimensions:. Like studies of psychological deficit, laboratory models of psychopathology have a history that goes fairly far back in time -- but this time, to Pavlov's laboratory rather than Wundt's. In some early studies of discrimination learning, dogs were conditioned to salivate to a circle or an ellipse, and then the axes of the stimulus were progressively changed, so that the circle became more elliptical, or the ellipse more circular.

The result was that, at some point, the dogs became distressed -- seemingly anxious -- a phenomenon that became known as experimental neurosis. One explanation proposed by Sue Mineka and myself was that this increase in anxiety occurred because the animals could no longer predict the onset of the food US. Unpredictability causes anxiety hold this thought, because in a little while we'll discuss another laboratory model that indicates that uncontrollability causes depression.

In addition, conditioned fear has served as a laboratory model of phobia, while conditioned avoidance has served as a laboratory model for obsessive-compulsive disorder. Of particular interest is the development of learned helplessness as a laboratory model of depression. As discussed earlier in the lectures on Learning , learned helplessness was initially observed in studies designed to test Mowrer's "two-factor" theory of avoidance learning.

In avoidance learning, a conditioned stimulus such as a tone is followed by prolonged shock as an unconditioned stimulus. If the animal makes a certain conditioned response such as moving from one side of the shuttlebox to the other after the onset of the US, it can turn the US off; termination of the US constitutes reinforcement of an escape response. If it makes the CR after the onset of the CS, but before the onset of the US, the US is prevented from occurring at all; this reinforces an avoidance response.

Martin Seligman and his colleagues discovered that prior exposure to inescapable shock interfered with escape and avoidance learning. In their analysis, prior experience with inescapable shock taught the animal that shock was uncontrollable, and this learning generalized to the new situation of the shuttlebox. The learned helplessness experiments underscore the principle that in instrumental conditioning the organism is learning to control its environment.

The animals in these experiments learned to be helpless, but Seligman and his colleagues also observed that they looked and behaved as if they were "depressed" if you've ever seen a sad dog, you know what they meant. This led Seligman to propose that learned helplessness is a laboratory model for some forms of depression -- i. Subsequent research by Seligman and others, including Steven Maier, Lyn Abramson, and Lauren Alloy, identified a number of parallels between learned helplessness and depression:. The learned helplessness model of depression, as originally formulated, is not complete, and nobody claims that LH underlies all forms of depression.

But Abramson and Alloy have suggested that a certain type of depression, which they label helplessness depression , is caused by the kinds of experiences modeled in the LH experiments. Abramson, Alloy, and their colleagues subsequently modified Seligman's theory with the hopelessness theory of depression. They argued that the experience of uncontrollable aversive events was not enough to make people or dogs, for that matter depressed.

Sometimes, people and dogs respond to uncontrollable aversive events with anger, instead. Abramson and Alloy proposed that uncontrollability led to depression only when the individual made a certain causal attribution concerning the uncontrollability. They argued that the explanations that people make for various events vary on certain dimensions:. They proposed that uncontrollability causes depression only when the individual makes an internal, stable, global attribution for the helplessness -- as if to say, I can't control this thing, it's my fault that I can't control it, I can never control this or anything else.

If you thought like this, you'd get depressed, too, and that's the point. Abramson and Alloy pointed out that, in contrast to non-depressed people, depressed people are often starkly realistic about their inability to control events -- a characteristic of depressive realism that they contrasted to the illusion of control that is characteristic of non-depressed thought. That is, non-depressed individuals often have an unrealistically elevated sense of control which is why many of us think we can control chance events by picking "lucky" lottery numbers , while depressed individuals are often quite realistic about the prospects.

Abramson and Alloy identified this pessimistic attributional style as a risk factor for what they called hopelessness depression. They and their colleagues also constructed a personality questionnaire, the Attributional Style Questionnaire ASQ to identify people who might be "at risk" for depression, based on this aspect of cognitive style. Seligman, for his part, took off from his studies of helplessness and depression to focus on the other side of things, and proposed that positive psychology should focus on the sunny side of life, and the positive characteristics that enabled people to be resilient in the face of unpleasant circumstances.

In particular, Seligman has proposed that giving experiences of control to children who are at risk for depression by virtue of their pessimistic attributional style may help these children avoid actual episodes of depression. In the domain of the psychoses, amphetamine psychosis can serve as a laboratory model of schizophrenia. High doses of amphetamines, which increase dopamine activity in the brain, lead to psychological symptoms similar to those found in acute schizophrenia -- hallucinations, thought disorder, and paranoid delusions.

The behavioral parallels between amphetamine psychosis and schizophrenia is one source of the dopamine hypothesis of schizophrenia , discussed below. While most laboratory modeling has focused on various anxiety disorders, some investigators -- again, beginning in the late 19th and early 20th century -- noticed a phenotypic similarity between some of the phenomena of hypnosis e.

This has suggested that understanding the mechanisms of hypnosis might help us to understand these forms of mental illness as well. In fact, it's been proposed that both the dissociative and conversion disorders result from a division of consciousness that prevents certain percepts and memories from being represented in conscious awareness. Sometimes, laboratory models and studies of psychological deficit go hand-in-hand. Consider experimental research on psychopathy , or antisocial personality disorder.

One feature of psychopathy is that these individuals tend not to be responsive to aversive stimulation. On experimental tests, psychopaths often show a failure of avoidance learning, and they also show a failure to respond to punishment. Gorenstein and Newman observed a similar pattern of behavior in laboratory rats who had surgical lesions in a subcortical area of the brain known as the septum.

Rats with septal lesions do not freeze when they are punished, they have difficulty with passive avoidance learning i. All of these phenomena, of course, closely resemble the characteristic symptoms of psychopathy. This has led to a theory that, by virtue of some kind of brain disorder, psychopaths, like septal rats, are unable to suppress habitual behaviors in order in order to avoid the aversive consequences of these behaviors.

Experimental research by Newman and others have further clarified the psychological deficit in psychopathy to problems linking attention to the reward system. In one experiment, subjects played a computerized card game: if they turned over a card they would gain a point if it was a face card, and lose a point if not. The deck was arranged so that 9 of the first 10 cards were face cards, then 8 of the next ten, 7 of the next 10, and so on, and they could stop whenever they wanted.

Of course, with the deck arranged in this manner, the subjects began accruing lots of points, and then started losing. Normal subjects generally stopped playing after about 50 cards, while they were still ahead; but the psychopaths continued playing, losing everything they had won -- and more. Newman's latest theory of psychopathy implicates attention rather than reward per se. The general idea is that psychopaths have difficulty updating working memory with new information, once their attention has been engaged.

They can focus attention, but they can't disengage and shift it very easily. Still, there does seem to be something missing in psychopaths' emotional lives. They don't accurately pick up on other people's facial and vocal expressions of emotion, especially fear; don't respond normally to words with positive or negative emotional connotations. Returning to Newman's septal rats, Kent Kiehl has used fMRI to record brain activity in psychopaths during various types of tasks. He has found deficits in a a system of subcortical brain areas known as the paralimbic system :.

Kiehl and Joshua W. We're going to get back to the clinic in a moment, but the point of this whole exercise is that the clinical enterprise of understanding and treating mental illness is not divorced from the sort of basic research that goes on in university laboratories. We can use various research paradigms of the sort discussed earlier in this course -- classical and instrumental conditioning, dichotic listening, and the like -- to understand the basic mechanisms by which mental illness occurs -- as well as ways in which we might more effectively treat mental illness and prevent it from occurring in the first place.

By virtue of basic laboratory research we can move beyond the surface signs and symptoms of mental illness to understand its underlying pathology. And by better understanding its underlying pathology, we will be able to formulate better theories of the causes and cure of mental illness, and better tools for diagnosis, treatment, and prevention.

In fact, laboratory research helps us to identify two different ways that mental illness can occur. Where mental illness appears to reflect maladaptive social learning, we generally assume that the architecture of the individual's basic mental structures and processes is largely intact, as are the neural substrates of that mental architecture. However, where mental illness appears to reflect an underlying psychological deficit, there are good reasons to think that the neural substrates of that mental architecture are malfunctioning as well -- that is, that the mental disorders are ultimately neurological disorders.

This idea is expressed in Ralph Gerard's old adage that. The idea that mental illness have underlying biological causes goes back at least as far as the 19th century -- which is to say, it is almost as old as scientific medicine and scientific psychology themselves. In fact, the history of psychiatry and clinical psychology may be characterized as a cycle in which prevailing views alternate between "somatogenic" theories that mental illness is due to biological causes i. The earliest scientific theories of mental illness were neurological theories, based on the assumption, mostly unproven, that patients' symptoms were due to lesions or infections affecting brain tissue.

With the emergence of Freudian psychoanalysis, in the late 19th and early 20th centuries, the predominant theory of mental illness shifted from somatogenic to psychogenic. Put briefly, Freud and his followers taught that mental illnesses, particularly the neuroses, had their origins in conflict and defense. Psychoanalysis, both Freudian and neo-Freudian, dominated psychiatry well into the s. Another important influence on American psychiatry was Adolph Meyer, who argued that mental patients' problems had their origins in their life histories, not their biology. The pendulum began to shift back toward somatogenesis in the s, with the introduction of the first psychotropic "mind-moving" drugs: Thorazine , a "major tranquilizer" used in the treatment of schizophrenia; Milltown , a "minor tranquilizer" used to treat anxiety; and Marsilid , a "psychic energizer" used in the treatment of depression.

These drugs were discovered more or less accidentally, but it was soon learned that they and other drugs like them altered the levels of certain neurotransmiters in the brain. This led to the hypothesis that schizophrenia, depression, and other forms of major mental illness were caused by abnormal levels of these substances. Let us just note, in passing, that the logic of this inference is far from airtight. In fact, it's a variant on the logical error of denying the antecedent , discussed in the Lecture Supplement on Thinking.

The logic seems to go something like this. The problem is that the efficacy of a treatment says nothing about the cause of the illness. Nobody thinks that a lack of aspirin causes fever to occur. And, as it happens, the evidence for the dopamine theory of schizophrenia, and similar theories, is not completely convincing. There has never been any convincing demonstration that, prior to treatment, schizophrenics or depressives actually suffer from any kind of chemical imbalance in their brains. Still, theories about chemical imbalances remain very popular.

In fact, over the past years or so, biological causes have been uncovered for a number of mental illnesses, whose biological causes were unknown at the time they were described, and which had previously been attributed to environmental causes. In this way, some "functional" mental illnesses have been reclassified as "organic" in nature. According to the dopamine hypothesis of schizophrenia , the symptoms of schizophrenia, and their underlying psychopathology, are caused by excess activity of dopamine, a neurotransmitter substance. Evidence for the dopamine hypothesis includes:.

In fact, autopsy studies, and also some brain imaging studies, indicate that there are increased levels of dopamine metabolites in schizophrenic patients. And that's consistent with the dopamine hypothesis. Moreover, phenothiazine drugs, which are used in the treatment of schizophrenia, block the neural receptors for dopamine, impairing the uptake of dopamine by post-synaptic neurons.

So the fact that there are increased levels of dopamine metabolites found in schizophrenic patients, and that antipsychotic medications operate to reduce dopamine levels -- these are both factors that are consistent with the dopamine hypothesis of schizophrenia. But another piece of evidence comes from a laboratory model of schizophrenia known as amphetamine psychosis.

Solomon Snyder and his colleagues, working at the National Institute of Mental Health, found that the administration of certain drugs known as amphetamines can actually produce some of the symptoms of psychosis, particularly schizophrenia, in rats and other laboratory animals. They also noticed that the habitual heavy use of amphetamines by humans can produce some of the symptoms of schizophrenia as well -- particularly hallucinations, thought disorder, and delusions.

These amphetamine drugs, such as Benzedrine amphetamine , Dexedrine dextroamphetamine , and methedrine methamphetamine may cause the user to experience hallucinations, while habitual, heavy use can cause thought disorder and paranoid symptoms as well. So this laboratory model -- first studied in rats, then in monkeys, and then in humans who abuse amphetamine recreationally -- provides further support for the dopamine hypothesis of schizophrenia. In these ways, amphetamine psychosis seems to mimic at least some of the symptoms usually associated with schizophrenia.

According to the monoamine hypothesis of depression , the symptoms of depression, and their underlying psychopathology, are caused by lowered levels of another class of neurotransmitters, the monoamines, which include norepinephrine and serotonin. Evidence for the monoamine hypothesis includes:.

Depression is so frequent it has been called "the common cold of psychiatry" , and has been around for so long Robert Burton published The Anatomy of Melancholy in , that some evolutionary psychologists have suggested that, counter-intuitively, a tendency toward depression might actually be an adaptive trait. According to one argument, the ruminative thinking that is one of the characteristic symptoms of depression facilitates problem-solving. The only problem is that depressives don't solve their problems -- they just stay depressed. Actually, that's just one of the problems with the evolutionary argument.

Here are some others:. This points out the problem with the adaptationist fallacy that lies at the heart of so many speculations by evolutionary psychologists. Depression exists as a human psychological trait, human psychological traits, like human physical traits, a product of natural selection; therefore, depression must be adaptive in the Darwinian sense. A similar argument has been made about homosexuality which, of course, isn't a mental illness , and even about grandmothers who aren't necessarily mentally ill either!

But the whole thing begins with a fallacious assumption, which is that every human trait, whether biological or psychological, but be adaptive. It should be understood that these are only hypotheses about the underlying biology of these syndromes, and that these hypotheses are surely incomplete. And sometimes biological hypotheses are just wrong. In , a paper published in Lancet by Andrew Wakefield, a British physician, suggested a link between autism and the childhood vaccine for measles, mumps, and rubella MMR.

The resulting concern led to a worldwide reduction in MMR vaccination, as parents hoped to prevent their children from getting autism. The methodology of the study was subsequently criticized, and 10 of Wakefield's 12 co-authors subsequently retracted the paper -- as did the journal in which it was originally published, and Wakefield lost his license to practice medicine in Britain he relocated to the US. In , an investigation published in the British Medical Journal asserted that Wakefield's paper was not just methodologically weak but actually fraudulent.

In fact, subsequent, better designed studies show that there is no evidence for a role of MMR or any other childhood vaccination in autism. Nevertheless, as of , Wakefield who has relocated to the US continues to assert such a link, and worldwide MMR vaccination rates have never returned to their pre levels -- increasing the risk of childhood diseases that are entirely preventable. For an excellent introduction to the roe of neurotransmitters in mental illness, and the basics of psychopharmacology, see Drugs and the Brain Rev.

Because the pharmaceutical industry is constantly developing new products, the information on specific drugs is necessarily a little dated. But the basic ideas haven't changed much, and neither has the underlying neuroscience. It's a good place to sstart.. Somatogenic and psychogenic theories of mental illness are, first and foremost, theories about the role of nature and nurture, and we have now learned that the proper formulation is nature-nurture questions is not "Which is right? The etiology of mental illness is no exception.

One place to look for the origins of psychopathology is in the genes: perhaps certain forms of mental illness, or at least risk factors for them, are passed through families through genetic inheritance. We know that, for many diagnoses, having a family member with mental illness increases the risk for mental illness in other family members. Of course, this effect could be environmental as well as genetic. The genetic contribution to mental illness can be assessed by means of the twin-study method described in the lectures on Psychological Development : by comparing the similarity of MZ and DZ twins, we can estimate the contributions of genetics, the shared environment, and the nonshared environment.

When it comes to personality characteristics, such as the Big Five personality traits, similarity is measured by means of the correlation coefficient. In psychiatric genetics, similarity is more commonly measured by means of the concordance rate -- that is, the probability that two twins will have the same psychiatric disorder. The calculations for heritability differ a little, but the underlying logic is the same:. This table reflects our best understanding of the heritability of major forms of mental disorder, as of The heritability coefficients vary widely, from a low of. Note, however, two points about this table:.

So, as is generally the case, the origins of mental illness are not to be found in the genotype alone. Rather, they will have to be found in gene-by-environment interactions GxE of the sort discussed under the heading of epigenesis in the lectures on Psychological Development. Still, once researchers have established a significant level of heritability for a mental illness, it makes sense to start searching for the genes responsible for a review, see Duncan et al.

Before the 21st century, this was not really possible. We didn't know enough about the human genome, and we didn't have the technology. And even with the mapping of the human genome, and the availability of relatively inexpensive technology, the task is daunting:. Until recently, researchers had to propose, on the basis of some theory, what genes to look for. So, for example, if they were interested in schizophrenia, they might look at genes that are involved in the production and metabolism of the neurotransmitter dopamine; for depression, they might look for genes involved with the production and metabolism of the neurotransmiters norepinephrine or serotonin.

This is known as the candidate gene strategy. However, advances in technology have permitted researchers to go on "fishing expeditions" in which they cast their nets more widely, over thousands or millions of candidate genes and their variants, in what are known as genome-wide association studies GWAS. These studies have begun to yield results -- and, interestingly, they have been turning up evidence of genes involved in mental illness other than those "candidates" hypothesized by various biochemical theories of mental illness! It's pretty clear that the search for "the gene" that is "for" schizophrenia, or any other form of mental illness, is going to be complicated Duncan et al.

Once we've determined that there is, in fact, a genetic contribution to some mental illness, the next step is to determine what genes are involved. I say "genes", plural, because it's clear that there's no single gene "for" schizophrenia, like the gene for blue or brown eyes presented in standard elementary accounts of Mendelian genetics.

Rather, much as wth intelligence, the genetic basis for schizophrenia is most likely to involve the cumulative effects of many genes -- dozens, perhaps hundreds. Recent advances in understanding the genetics of schizophrenia offer interesting insights into the genetic contribution to mental illness more generally. These advances have been made possible by the Human Genome Project, which in delivered a map of the human genome, indicating the location of each of our roughly 22, genes on our 23 chromosome pairs.

Then began the process of determining the function of each of these genes. Over the years, gene-mapping has become less expensive and time-consuming, so it is now possible to search the genomes of large numbers of individuals for genes that are associated with various illnesses, employing such techniques candidate gene association , common variant association , and copy number variation. This discussion is largely drawn from these sources. With data available on a very large number of individuals, investigators are able to identify asociations between schizophrenia and other forms of major mental illness, such as bipolar disorder and autism with various portions of the human genome.

The "Manhattan plot" at left so named because it looks like the New York City Skyline , taken from one such study involving more almost 37, patients and more than , controls, sampled from 20 countries, shows which specific locus on each chromosome is significantly associated with schizophrenia Sekar et al. Of course, with 22, genes, a number of these associations could appear just by chance, so the investigators employed appropriate statistical corrections.

These sorts of findings would be expected if, as most theorists believe, major mental illness is fundamentally a disorder of the central nervous system. But other findings were more surprising. For example, the strongest association the talest "skyscraper" in the Manhattan plot above was on Chromosome 6, in a region known as the major histocompatibility complex MHC , whose genes are linked to the immune system. But how do we get from the immune system to schizophrenia? Here's one prominent theory Sekar et al.

Mental Illness cures: (EDS-7) Etiological Diagnostic Snapsheet

Understand: I'm not saying that this theory is the neuroimmunological cue to the secret of the origins of schizophrenia. It might very well be wrong -- just like most past hypotheses concerning the genetic origins of schizophrenia. Another multinational group of researchers, known as the Brainstorm Consortium performed a GWAS of 25 different neurological and psychiatric disorders, involging more than , patients and more than , healthy controls -- thanks mostly to European countries whose national health systems maintain large databases Anttila et al.

Science , ; see also Gandal et al. As had proved to be the case in previous, smaller-scale studies, the psychiatric syndromes showed substantial genetic overlap the only exception was post-traumatic stress disorder, which by definition has a substantial environmental cause. That is to say, a number of genetic markers were identified for each syndrome, but the same makers tended to appear from one syndrome to another.

By contrast, the 15 neurological syndromes studied, including Alzheimer's disease and Parkinson's disease, showed much more distinct genetic profiles. And there was little overlap between the psychiatric conditions and the neurological ones. What to make of this isn't clear. One possibility is that there is a genetic component to risk for mental illness in general, and other factors, whether biological or environmental, determine which specific mental illness a person will suffer.

Another possibility is that the GWAS method, and genetics in general, isn't going to tell us much about the etiology of mental illness. At the same time, other researchers have turned their attention to the environment, and in particular to those features of the environment that interact with one's genetic heritage. The origins psychopathology etiology may be viewed within the framework of the diathesis-stress model of psychopathology proposed initially by Meehl and Rosenthal , and elaborated more recently by Monroe and Simons and Belsky and Pleuss According to the model:. I do not understand how a hospital admitted me and diagnosed me instantly with bipolar and I was on medication the same day!!!

I think you misinterpreted the issue of the average length of time for an accurate bipolar diagnosis. Bipolar Disorder can present in many different ways, especially when symptom acuity is mild to moderate It can even initially manifest though depression with an absence of any hypomanic or manic symptoms. When the initial symptom presentation is not clear cut, the disorder is often misdiagnosed and people do not receive appropriate treatment. Additionally, someone can experience mild to moderate symptoms and due to their own denial or their resistance to seeking help, it may take them a long time before they finally do choose to see a mental health professional.

This too contributes to that long duration of time before someone receives an accurate diagnosis. But if an individual's manic symptoms are acute enough to require hospitalization, and if there there's an absence of other confounding symptoms that can make the picture more complex, the diagnosis can be determined relatively rapidly.

I am most definitely not "bipolar" or whatever the latest catch all diagnosis du-jour might be. I thank God I have the love, support and good sense of my husband of 31 years or I would otherwise be dead. It's all about money. No compassion. Your diagnosis becomes your own strait-jacket with a medication Lobotomy. It is easy to see who is protected and what parties benefit from our current laws.

My own six-foot-one psychiatrist brother-in-law, full of hate, envy, and scorn manipulates family members recklessly for his own benefit as he slips into slinky dresses and high-heels after hours to satisfy his own perverted desires. Also violating through theft of the psychiatric records of own mother without any accountability or disciplinary action!

His personal quest traumatized her up to her death bed and our entire family and we are to respect his "credentials" even while the AMA turns their ethics cheek? I appreciate your article and the opportunity to add my first comment. His diagnosis was unspecified but recommended I stay on the current Rx not providing me any relief from the anxiety I came to learn was being caused or made worse BY these medications. I am grateful the internet has these new studies and information, it is very confusing but when a patient is willing to take the risk to see how they might do without the Rx the "professionals" should be more accommodating to help them heal rather than keep them drugged.

In MY professional arena, customs compliance, I could not and would never try, to get away with steering any client in a reckless position yet this is exactly what happened to me by all of my paid qualified professionals. Getting diagnosed and labeled as such should never be rushed or taken lightly as was done at least in my case and your article helps to drive that point home. Thank you. Now aged 50 I too was diagnosed in haste 5 years ago - more meds I was given - massive mood swings - never experienced before. Hospitalized 3 times- lost job as teacher.

Getting assessed by female hormone clinic in London as now use HRT- severe Premenstrual syndrome manifests massive mood swings!!!! Yes, you are spot on. This whole diagnosis nonsense has made big pharma filthy rich. It has made psychiatry some absurd profession where doctors try to guess what works. Imagine a doctor telling you, 'Well, it seems your leg hurts and we will just try to treat it all kinds of ways and hopefully something works. That's what you get with psychiatry. It's fraud at best and a joke at worst.


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  • Sure, whatever. What a farce. We've got more people doped up on meds than ever before. More homeless, more drugged out of their minds on pain meds and psychotropics and we are not one bit better as a society or individuals. Hi my best friend lost her job and her 8 year marriage within one week. She went into deep depression and no one could help her. Thanks Russ. A very clarifying article. The best I've seen on differentiation of these overlapping disorders. At the same time one point you make merits further thought.

    You mention that all the data you have comes from one person who is in one mood at the time of the interview. How often do you include family members in at least some part of the diagnostic process? My general experience has been that people with bipolar are often fairly poor at self-awareness. Hearing from others who live with that person about what they see can present a quite different, or at least augmented, symptom picture. I would suggest everyone to get a second opinion just to be safe. For the time and price its well worth it.

    Very professional and saved me a bunch of money. I recommend getting a second opinion because it can potentially save your life. I'm 34 and been through a few wringers between different doctors. Until yesterday, I had never seen a doctor outside of primary care. I have tried many different drugs for sleep problems, most of which made me gain quit a bit of weight and left me groggy in the morning.

    I get overwhelmed at times and my anxiety levels raises, leading me to get violent. My older sister was severely bipolar. My primary doc prescribed me Zoloft to help keep my anxiety levels down. I was severely emotional, my mind was going miles an hour normal is miles an hour for me , I could not sit still, I was nasueas, and could not focus on any one thing for more than a few seconds.

    Luckily one of the psychiatrists squeezed me in and said I should never take Zoloft again.

    Getting the diagnosis right when symptoms are confusing

    She gave me Xanax to help my mind calm down and said she it's very possible I have some bipolar tendencies, something about hypo manic something. I work with her, and very rarely am I not happy go lucky. Apparently you can be bipolar where most of the time you are on an up level. We are going to meet again in a couple weeks before deciding on a starting game plan. I was "unofficially" diagnosed with bipolar at 22, even though I wasn't presenting any bipolar symptoms, because of an acute manic episode of my father's twenty years earlier. That started me on a long and very disheartening path of thinking I had bipolar and not realizing what was actually going on: undiagnosed ADD.

    Yep, turns out that's what caused the distress and anxiety that sent me to the doctor in the first place. I wish I'd been wise enough to ask for a second opinion, but after 30 minutes of discussion of my family history and "mood swings" meaning, in my case, being more emotionally reactive than most people, a classic ADD symptom I came out of the office with a prescription for lithium.

    And when I started a stressful postsecondary course of study and the lithium didn't "work," they raised the dose! Nobody ever asked "What is this diagnosis based on? It took ten years to straighten everything out and discover that those "mood swings" were just a normal, predictable, and very regulable part of ADD--not, to my profound relief, a sign of serious mental illness. By then I'd been afraid of my feelings for so long that learning how to regulate them was a welcome challenge, and it started to work right away.

    Not only would I have gained self-understanding and practical management skills much quicker, I'd have been spared the terrible toll of believing my emotions were not only invalid, but dangerous. So yes--do be careful, a lot of these different problems can mimic each other, both in childhood and in adulthood. Don't assume that "mood swings" automatically means grandiosity and depression: they could just be a kid whose emotional regulation isn't as mature as everyone else's Same word, different symptoms. Thanks for all your work in making this information available to the public: being your own best advocate and researcher can go a long way toward preventing these life-changing mistakes and finding the life-changing solutions!

    Inattentive, Limbic and Over Focused. I don't know what. I don't know "you" beyond being very limited description you've provided. Also, given that. I am a psychologist and I do not prescribe medication. I was digging through my email and saw this from a long time ago. Remembering your article and your response, its time to update you on what is going on. In my opinion, I think medical science needs to put a lot of work and research into why anti depressants or similar drugs even drugs like Lamictal put me into " angry " , " Rage-y " type moods, my first psych could not figure out why.

    I fired him Sept I was prescribed Lamictal Jan when the anti depressants put me into mania, cycling put us non bipolars into " manic " like behaviors. My Modereate-Severe A. I hope this response is seen by many doctors, like yourself, so it helps bring new attention as to why these crazy meds makes people respond the way they do and to end this over diagnoses of Bipolar disorder and the ridiculous amounts of pill combos that these people get thinking it helps them.

    I really appreciate your time with this! I was misdiagnosed as bipolar and I was subsequently harmed as a result. What are the correct steps that a patient should take in this situation, now that I have escaped the mental hospital, followed up with a regular physician, and with doctor supervision discontinued my bipolar meds? It is my understanding that once something is placed in a medical record it cannot be removed. However, if you desire legal certainty on the issue, I would suggest you consult with a lawyer who specializes in medical record documentation.

    This could be helpful in the event you should ever encounter future difficulties due to the bipolar diagnosis. Facing the limitations of parental influence with adult children's bipolarity. Understanding contributions of mood, environment and personality upon bipolarity. Back Psychology Today. Back Find a Therapist. Back Get Help. Back Magazine. Subscribe Issue Archive. Back Today. The Psychology of Creativity. Russ Federman Ph. The URL is below. D, Blog Author - "Bipolar You".

    Response to comment about misdiagnosis Submitted by Russ Federman, Ph. Blog Author - "Bipolar You". Burned Submitted by Anonymous on July 8, - pm. You have got to be kidding Submitted by jjj on May 28, - am. Agreed kinda Submitted by Blu on August 12, - am. Longitudinal studies have shown Submitted by Anonymous on July 8, - pm. Anonymous wrote:. Response to comment Submitted by Russ Federman, Ph. It should be called "Fraud". Hi my best friend lost her Submitted by Anonymous on September 29, - pm. Excellent article Submitted by Susan Heitler Ph.

    I would suggest everyone to Submitted by Elli K. Wow that sounds just like me Submitted by Cj hartman on September 26, - pm. I was "unofficially" Submitted by DC on September 25, - pm.