Modern Classification of Introspective Psychopharmacological Drug Profiles?

In the effort to better relate neuronal mechanisms to states of mind, it makes sense to have - in addition to pharmacological classifications of drugs and imaging/physiology classifications of their effects - classifications of the states of mind they evoke, according to introspective reports.

I have been unable to find such a data-driven classification in the literature (I would imagine a cluster analysis of reported terms, or a factor analysis of ratings on statements could be appropriate). Instead, "subjective effects" classification seems to be restricted to single-substance profiling, and elsewise is remarkably top-down - based on ad hoc models by the same authoritative people or entities which commonly make psychoactive substances available to consumers (introducing confirmation bais). I'm wondering if there's anything else out there?

Cultural Aspects of Major Mental Disorders: A Critical Review from an Indian Perspective

Major mental disorders such as schizophrenia and affective disorders are highly disabling illnesses. The cultural factors that influence the diagnosis and treatment of these disorders are of paramount clinical significance. We attempted to critically review the cultural factors in relation to the epidemiology, phenomenology, treatment, and outcome of major mental disorders from an Indian perspective, and tried to compare these with the cultural factors identified in major international studies. The clinical expression of major mental disorders was noted to vary across cultures in the review. In addition, the outcome of major mental disorders is reported to be better in developing nations than in the developed countries. Transcultural variations are also noted to exist in pharmacokinetics, pharmacodynamics, traditional healing practices, and psychotherapeutic approaches. The role of cultural factors in severe mental illnesses needs adequate attention from mental health professionals. Continued research on the cultural aspects is required to understand the interplay of all social, cultural, and biological factors. It is important to consider other cultural, traditional, and folk methods for understanding and management of mental illnesses.


Claude Bernard (1865/1961) noted that the maintenance of life is critically dependent on keeping our internal milieu constant in the face of a changing environment. Cannon (1929) called this “homeostasis.” Selye (1956) used the term “stress” to represent the effects of anything that seriously threatens homeostasis. The actual or perceived threat to an organism is referred to as the “stressor” and the response to the stressor is called the “stress response.” Although stress responses evolved as adaptive processes, Selye observed that severe, prolonged stress responses might lead to tissue damage and disease.

Based on the appraisal of perceived threat, humans and other animals invoke coping responses (Lazarus & Folkman 1984). Our central nervous system (CNS) tends to produce integrated coping responses rather than single, isolated response changes (Hilton 1975). Thus, when immediate fight-or-flight appears feasible, mammals tend to show increased autonomic and hormonal activities that maximize the possibilities for muscular exertion (Cannon 1929, Hess 1957). In contrast, during aversive situations in which an active coping response is not available, mammals may engage in a vigilance response that involves sympathetic nervous system (SNS) arousal accompanied by an active inhibition of movement and shunting of blood away from the periphery (Adams et al. 1968). The extent to which various situations elicit different patterns of biologic response is called “situational stereotypy” (Lacey 1967).

Although various situations tend to elicit different patterns of stress responses, there are also individual differences in stress responses to the same situation. This tendency to exhibit a particular pattern of stress responses across a variety of stressors is referred to as “response stereotypy” (Lacey & Lacey 1958). Across a variety of situations, some individuals tend to show stress responses associated with active coping, whereas others tend to show stress responses more associated with aversive vigilance (Kasprowicz et al. 1990, Llabre et al. 1998).

Although genetic inheritance undoubtedly plays a role in determining individual differences in response stereotypy, neonatal experiences in rats have been shown to produce long-term effects in cognitive-emotional responses (Levine 1957). For example, Meaney et al. (1993) showed that rats raised by nurturing mothers have increased levels of central serotonin activity compared with rats raised by less nurturing mothers. The increased serotonin activity leads to increased expression of a central glucocorticoid receptor gene. This, in turn, leads to higher numbers of glucocorticoid receptors in the limbic system and improved glucocorticoid feedback into the CNS throughout the rat’s life. Interestingly, female rats who receive a high level of nurturing in turn become highly nurturing mothers whose offspring also have high levels of glucocorticoid receptors. This example of behaviorally induced gene expression shows how highly nurtured rats develop into low-anxiety adults, who in turn become nurturing mothers with reduced stress responses.

In contrast to highly nurtured rats, pups separated from their mothers for several hours per day during early life have a highly active hypothalamic-pituitary adrenocortical axis and elevated SNS arousal (Ladd et al. 2000). These deprived rats tend to show larger and more frequent stress responses to the environment than do less deprived animals.

Because evolution has provided mammals with reasonably effective homeostatic mechanisms (e.g., baroreceptor reflex) for dealing with short-term stressors, acute stress responses in young, healthy individuals typically do not impose a health burden. However, if the threat is persistent, particularly in older or unhealthy individuals, the long-term effects of the response to stress may damage health (Schneiderman 1983). Adverse effects of chronic stressors are particularly common in humans, possibly because their high capacity for symbolic thought may elicit persistent stress responses to a broad range of adverse living and working conditions. The relationship between psychosocial stressors and chronic disease is complex. It is affected, for example, by the nature, number, and persistence of the stressors as well as by the individual’s biological vulnerability (i.e., genetics, constitutional factors) and learned patterns of coping. In this review, we focus on some of the psychological, behavioral, and biological effects of specific stressors, the mediating psychophysiological pathways, and the variables known to mediate these relationships. We conclude with a consideration of treatment implications.


As these arguments make clear, it is intriguing to suggest that insofar as psychotherapy is successful in bringing about substantive changes in behavior, it does so by producing alterations in gene expression that produce new structural changes in the brain. This obviously should also be true of psychopharmacological treatment. Treatment of neurosis or character disorders by psychotherapeutic intervention should, if successful, also produce functional and structural changes. We face the interesting possibility that as brain imaging techniques improve, these techniques might be useful not only for diagnosing various neurotic illnesses but also for monitoring the progress of psychotherapy. The joint use of pharmacological and psychotherapeutic interventions might be especially successful because of a potentially interactive and synergistic—not only additive—effect of the two interventions. Psychopharmacological treatment may help consolidate the biological changes caused by psychotherapy.

One example of this congruence is now evident in obsessive-compulsive disorder (OCD). This common debilitating psychiatric illness is characterized by recurrent unwanted thoughts, obsessions, and conscious ritualized acts and compulsions that are usually attributed to attempts to deal with the anxiety generated by the obsessions. Medications that are selective serotonin reuptake inhibitors (SSRIs) and specific behavioral therapies that use the principles of deconditioning, involving exposure and response prevention, are effective in reducing the symptoms of many patients with OCD.

Many investigators have postulated a role for the cortical-striatal-thalamic brain system in the mediation of OCD symptoms. OCD is associated with functional hyperactivity of the head of the right caudate nucleus. After effective treatment of OCD with either an SSRI (such as fluoxetine) alone or with behavioral modification alone (with exposure and response prevention techniques), there is a substantial decrease in activity (measured as glucose metabolic rate) in the head of the right caudate nucleus. In one study (29) patients who responded to behavior therapy had a significant decrease in glucose metabolic rate in the caudate nucleus bilaterally compared to those who did not respond to treatment.

These arguments suggest that when a therapist speaks to a patient and the patient listens, the therapist is not only making eye contact and voice contact, but the action of neuronal machinery in the therapist's brain is having an indirect and, one hopes, long-lasting effect on the neuronal machinery in the patient's brain and quite likely, vice versa. Insofar as our words produce changes in our patient's mind, it is likely that these psychotherapeutic interventions produce changes in the patient's brain. From this perspective, the biological and sociopsychological approaches are joined.

Chlorpromazine after 50 Years

I entered psychiatry in my native country, Hungary, in 1954 and was among the last of a generation who used “insulin coma” in the treatment of schizophrenia and “opium” in the treatment of depression. Chlorpromazine became available on our service in the first months of 1955, but in spite of the favorable reports, it was received incredulously by some of our senior staff. As far as I was concerned, CPZ was great! It worked better than the morphine-scopolamine combination we used in controlling agitation, and it could also relieve psychotic symptoms regardless of patient’s diagnosis. It was especially effective for some schizophrenics. For me, the most junior member of the staff, at the National Institute of Nervous and Mental Diseases in Hungary, CPZ was a miracle drug.

Chlorpromazine was synthesized by Paul Charpentier in the laboratories of Rhône-Poulenc in December, 1950 and released for clinical investigation as a potentiator of general anesthesia in May, 1951 (Caldwell 1970). Its importance for psychiatry was recognized by the scientific community in 1957 with the presentation of the prestigious Albert Lasker Award to the three key players in the clinical development of the drug: Henri Laborit, for using CPZ as a therapeutic agent first and recognizing its potential for psychiatry Pierre Deniker, for his leading role in introducing CPZ into psychiatry and demonstrating its influence on the clinical course of psychosis and Heinz Lehmann for bringing the full practical significance of CPZ to the attention of the Western World. In the same year Daniel Bovet was awarded the Nobel Prize in Medicine for his major contributions to the synthesis of antihistamines which, through Laborit’s observations of promethazine, an antihistaminic phenothiazine, promethazine, led to the development of CPZ (Ban 1994).

The pharmacological bridge from antihistamines to “antipsychotics” was provided by a test with a potential to detect the central effects of antihistamines by the increase in time required for trained rats to climb a vertical rope for food (Charpentier et al. 1952). But the first test procedure for the prediction of antipsychotic effects which readily translated from animal to man was introduced by Leonard Cook in the United States (Cook 2004). It was based on his findings that CPZ differs from the old sedatives by selectively blocking the conditioned avoidance response, while leaving the unconditional motor reflex unaffected. Employment of Cook’s procedure was instrumental in the development of a rapidly growing number of antipsychotic drugs.

The large number of antipsychotic drugs developed by the late 1950 was reflected in the communications at the first CINP Congress in Rome, in 1958. Frank Ayd reported on clinical findings of 25 (Ayd 1959), and in Hanns Hippius’of 12. It was in Rome where Hippius first focused attention on the lack of a relationship between the preclinical pharmacological profile and the therapeutic efficacy of these drugs (Hippius and Selbach 1959). By emphasizing that the therapeutic usefulness of a substance must be measured in terms of the relationship between therapeutic efficacy and somatic side effects, without any theoretical preconception, he opened the path for a development which led from CPZ to clozapine (Hippius 2004).

Simultaneously with the development of CPZ there was a shift in understanding of the nature of synaptic transmission from a purely electrical to a chemically mediated event and by the end of the 1950s, six neurotransmitters were identified in the central nervous system. Recognition of chemical mediation at the site of the synapse, coupled with the introduction of the spectrophotofluorimeter, triggered the development of neuropharmacology. There were high expectations that CPZ combined with spectrophotofluorimetry would provide a royal road to the understanding of the pathophysiology of schizophrenia. It was also hoped that there would be feedback from the clinical psychopharmacologists to the neuropharmacologists, which would help to develop clinically more selective and thereby more effective pharmacological treatments (Ban 2001).

Early neuropharmacological studies with CPZ were conducted in the periphery. In one of the first publications Laszlo Gyermek a Hungarian pharmacologist, reported on the potent anti-serotonin effects of the drug.(Gyermek 1955). In the early 1960s interest shifted from the anti-serotonin to the antidopamine effects of CPZ, after Carlsson and Lindqvist eported that CPZ stimulated the turnover of catecholamines in the mice by a hypothesized blockade of catecholamine receptors (Carlsson and Lindqvist 1963). Postulation of a relationship between DA receptor blockade and antipsychotic effects provided the rationale for the research which led to the demonstration that antipsychotics block DA receptors (Creese, Burt and Snyder 1975).

However, the confounding of antipsychotic properties with therapeutic effects in schizophrenia has been counterproductive. Introduction of CPZ focused attention on the heterogeneity of schizophrenia in terms of responsiveness to treatment and persistence on a unitary concept of schizophrenia was conflicting with clinical experience and with findings in clinical psychopharmacological research. To disentangle whether the difference in responsiveness to treatment is due to individual idiosyncrasies in responding to neuroleptics, or to differences in the biology of the different forms of the disease, Frank Fish, a British professor of psychiatry, examined, the therapeutic response profile of neuroleptics with the employment of the different forms of schizophrenia in the classification of Karl Leonhard, a German professor of psychiatry (Fish 1964 Leonhard 1957). The significant differences he found in responsiveness to neuroleptics between some of the groups could not be explained by idiosyncratic individual variations in responsiveness to the drugs.. The differences were so great that in one group, more than 4 in 5 patients responded to treatment, whereas in another, less than 1 patient responded in 4. Fish published his findings in 1964 in Encephale, a French journal, but with his untimely death, coupled with reservations towards Leonhard’s classification, his findings were summarily dismissed. Nevertheless, by the end of the 1960s, there was sufficient evidence to believe that ignoring the heterogeneity of schizophrenia deprived neuropharmacology from the necessary feedback for developing clinically more selective and thereby more effective treatments (Ban 1969) and by the mid-1980s, there was sufficient evidence to conclude that resolving the heterogeneity of schizophrenia is an essential prerequisite for progress in the understanding of the biology of the different illnesses pooled together in schizophrenia (Ban 1987).

Since the first time I used CPZ in a schizophrenic patient, almost 50 years have passed and during these years pharmacotherapy has become the primary treatment in psychiatry. The success of CPZ was instrumental to the development which led to the reintegration of psychiatry with the other medical disciplines by turning psychiatrists from care givers to full-fledged physicians who can help their patients and not only listen to their problems.

Introduction of CPZ was also instrumental to the development of neuropsychopharmacology, a new discipline which has forced psychiatry to examine and change its theoretical foundation. By the end of the 20 th century, Wilhelm Griesinger’s contention that mental illness is a symptom of brain disease, has become an accepted reality, and Moreau de Tours’ vision of understanding mental pathology by studying the effect of centrally acting drugs, an accepted methodology Griesinger 1845 Moreau de Tours 1845). Yet, in spite of all the progress made in the understanding signal transduction, and designing drugs, if an agitated and aggressive psychotic patient in the emergency fails to respond to the new medications I have no hesitation in recommending good old CPZ. This is why we are celebrating 50 years CPZ!

Ayd FJ. 1959. A clinical analysis of the differential effects of phenothiazine derivatives. In Bradley PB, Deniker P, Radouco-Thomas C (eds). Neuropsychopharmacology. Amsterdam: Elsevier. p 487-8.

Ban TA. 1969. Psychopharmacology. Baltimore: Williams & Wilkins. p 431

Ban TA. 1987. Prolegomenon to the clinical prerequisite. Psychopharmacology and the classification of mental disorders. Prog. Neuro-Psychopharmacol. & Biol. Psychiat., 11: 527-80.

Ban TA. 1994. Nobel Prize and Albert Lasker Award. In Ban TA, Hippius H (eds). Towards CINP. Brentwood: JM Productions. p 8-14.

Ban TA. 2001. Pharmacotherapy of mental illness. A historical analysis. Prog. Neuro-Psychopharmacol. & Biol. Psychiat., 25: 709-27.

Caldwell AE. 1970. Origins of Psychopharmacology From CPZ to LSD. Springfield: Charles C. Thomas. p 23-55.

Carlsson A, Lindqvist M. 1963. Effect of chlorpromazine and haloperidol on formation of 3-methoxytyramine and normetanephrine on mouse brain. Acta Pharmacol. Toxicol., 20: 140-4.

Charpentier P, Gailliot P, Jacob R, Gaudechon J, Buisson P. 1952. Recherches sur les diméthylaminopropyl-N phénothiazines substituées. CR. Acad. Sci. (Paris), 235: 59-60.

Cook L. 2004b. Early pharmacology of chlorpromazine. The International Journal of Neuropsychopharmacology 7 (supplement 1): 21.

Creese I, Burt R, Snyder SH. 1975. Dopamine receptor binding differentiation of agonist and antagonist states with 3 H-dopamine and 3 H-haloperidol. Life Science, 17: 993-1001..

Fish FJ. 1964. The influence of the tranquilizers on the Leonhard schizophrenic syndromes. Encephale, 53: 245-9.

Griesinger W.1845. Die Pathologie und Therapie des Psychischen Krankheiten. Wreden: Braunschweig.

Gyermek L. 1955. Chlorpromazine: A serotonin antagonist? The Lancet, 2: 724.

Hippius H. 2004. From chlorpromazine to modern (“atypical”) antipsychotics. The International Journal of Neuropsychopharmacology, 7 (supplement 1): 21-2.

Hippius H, Selbach H. 1959. On the correlation of the pharmacologically effective qualities of a drug to its therapeutic effect in psychoses. In Bradley PB, Deniker P, Radouco-Thomas C (eds). Neuropsychopharmacology. Amsterdam: Elsevier. p 598-601.

Leonhard K. 1957. Aufteilung der endogenen Psychosen. Berlin: Academie Verlag. p 155-396

Moreau de Tours J. 1845. Du Hachich et de L’Alienation Mentale. Etude Psychologiques. Paris: Fortin & Mason.

Donald F. Klein, Rachel Gittelman, Frederic Quitkin and Arthur Rifkin, editors

Donald F. Klein, Rachel Gittelman, Frederic Quitkin and Arthur Rifkin, editors. Diagnosis and Drug Treatment of Psychiatric Disorders: Adults and Children. Williams & Wilkins, Baltimore, 1983. (849 pages.)

Introduction: Brief historical summary of somatic psychiatric care “We may be fortunate to be entering a period in which rational comparative study will become the standard for therapeutic decision…”, “We are looking forward to the publication of the American Psychiatric Association Diagnostic and Statistical Manual III”.

I.Diagnosis, the Diagnostic Process, and Common Errors II. Psychotropic Drug Management, General Principles III. The Concept of Psychosis - This was a unique, we think still fruitful, hypothesis developing the term Psychosis as due to a flaw in inferential process yielding an unwarranted sense of certainty through the failure of innate skepticism IV. Diagnosis of Schizophrenia V. Review of Nosological Schemes in Schizophrenia V1. Review on the Pharmacotherapy and Psychotherapy of Schizophrenia: A Review of the Literature VII. Clinical Management of the Various Stages and Subtypes of SchizophreniaVIII. Side Effects of Antipsychotic Drugs and their Treatment IX. Antipsychotics in non-schizophrenic conditions X. Diagnosis of Affective Disorders: Clinical Considerations XI. Diagnosis of Affective Disorders : Review of Nosological Schemata XII. Review of the Literature on Mood-Stabilizing Drugs XIII. Clinical Management of Affective Disorders XIV. Side Effects of Mood Stabilizing Drugs and Treatments XV Diagnosis of Anxiety, Personality, Somatoform, and Factitious Disorders XVI. Review of the Literature on Antianxiety Drugs XVII. Treatment of Anxiety, Personality, Somatoform and Factitious Disorders XVIII. Assessment and Treatment of Childhood Disorders: General Considerations XIX. Diagnosis and Drug Treatment of Childhood Disorders XX. Critique of Treatment Studies XXI. Theoretical Inferences Concerning Clinical Groupings and Psychotropic Drugs.

Author Index Subject Index Glossary of Drugs.

ONE OF THE EDITOR’S STATEMENT: This second edition of this book is organized somewhat differently from the first edition, which was co-authored by John M Davis MD. (First edition: Donald F. Klein and John M. Davis: Diagnosis and Drug Treatment of Psychiatric Disorders. Williams & Wilkins, Baltimore, 1969 – See, INHN “Books”, November 28, 2013). In 1969 there was still considerable doubt within the psychiatric professions concerning the scientific basis for the uses of antipsychotics. antidepressants and antianxiety agents. It was not unusual to hear the firm assertion that there were more studies proving that these drugs do not work than demonstrating that they were effective. We felt at that time that the presentation of extensive tabulated reviews of studies of drug efficacy would be a worthwhile contribution. In fact the evidence of drug efficacy was well-nigh overwhelming .This work had been done largely through the efforts of John Davis, who has since continued to contribute brilliantly to systematic critical reviews of psychopharmacological studies.

For this edition we decided this tactical goal had been accomplished and that it didn't pay to belabor what had become the obvious, although a recent spurt of lay books have endeavored to muddy the waters. Unfortunately these efforts have been reinforced by the recent evidence concerning the deletion of important negative clinical data by industry. We believe that only release of the raw patient level data will restore the publics’ justified confidence.

Therefore, for the Second Edition, critical reviews and tabulations focused on narrower specific questions that were, circa 1983, (and still are) controversial.

Yet another change is a unique section on pediatric psychopharmacology ably managed by Rachel Gittelman. Negative feelings towards the use of psychiatric medication reach their apogee in the treatment of children. Our review dealt systematically with realistic concerns. It should help dispel largely irrational fears. The section on affective disorders was largely the work of the late Frederick Quitkin. The section on schizophrenia was based on the efforts of Art Rifkin.

It is recognized that many of the descriptions of psychiatric syndromes are abstract and the reader might well have benefited from representative case illustrations .This proved impractical. The reader is referred to Klein DF. Psychiatric Case Studies: Treatments, Drugs and Outcomes, Williams & Wilkins, Baltimore, 1972 (see, INHN “Books”, January 2, 2014), which remains the only set of full case presentations addressing the long-term effects of the range of psychopharmacological treatments.

Ethnomedicine and Drug Discovery

S Mbua Ngale Efange , in Advances in Phytomedicine , 2002

II. Example 1: Design of ibogaine analogs

Ibogaine (1, Figure 1 ) is the major constituent of the root of Tabernanthe iboga , a shrub commonly found in West and Central Africa. 4,5 Ibogaine has been shown to reduce cocaine and morphine self-administration in laboratory animals (reviewed in Ref. 6 ), and to attenuate alcohol intake by alcohol-preferring rats. 7 The compound also reduces the rewarding effects of nicotine in animals. 8,9 In addition, the compound reduces craving in humans. 10–13 Ibogaine is thus a potentially useful anti-addictive agent.

Fig. 1 . Ibogaine and selected ibogaine fragments.

The goal of this study was to develop synthetic ibogaine-like compounds that might be more effective than the parent compound. Due to the fact that ibogaine is a relatively complex structure, our immediate objective was to identify the simplest ibogaine fragment that retains anti-addictive activity. The fragmentation approach has been used extensively in medicinal chemistry to probe ligand–receptor interactions and to generate novel molecular entities. 14 A close inspection of ibogaine reveals that the latter is composed of two major fragments, 2 and 3 ( Figure 1 ), derived from 5-methoxytryptamine and isoquinuclidine. An intermediate structure, which incorporates elements of both fragments, is the tricyclic heterocycle 4 ( Figure 1 ). In previous studies of conformationally restricted tryptamines, compounds derived from this basic skeleton had been found to antagonize aggressive behavior in animals 15 and to display potential antidepressant activity. 16 The current study investigated the biological activities of the corresponding azepino[4,5-b]bezothiophenes.

The target compounds (12a–d) were synthesized as shown in Figure 2 . When tested in vitro ( Table 1 ), all four compounds displayed moderately high affinity for dopamine and serotonin transporters, 17 two molecular targets implicated in the mode of action of cocaine 18,19 and ibogaine. 20,21 The compounds also interact with other molecular targets with varying degrees of effectiveness and thus appear to mimic the parent compound. In subsequent studies, compounds 12a, 12c and 12d were found to dose-dependently reduce cocaine self-administration in rats without affecting general locomotor activity (Efange et al., unpublished). Taken together, the foregoing investigations confirmed that the tricyclic ibogaine fragment 4 retains anti-addictive activity and is thus a useful platform for developing new anti-addictive agents.

Fig. 2 . Synthesis of substituted hexahydroazepino[4,5-b]benzothiophenes.

Table 1 . Relative Affinities (IC50 ± SD, μM) of hexahydroazepino[4,5-b]benzothiophenes and Reference Compounds at Selected Molecular Targets *


The universality vs. distinctiveness dilemma implicit in the elaboration of diagnostic and classification systems across history has an emblematic angle in the debate about incorporation of culture and cultural factors in the forthcoming editions of DSM and ICD. The internationalization of the health and mental health fields due to globalization, nourished, in turn, by seemingly unstoppable migrations, has led to the acceptance and practical concerns of diversity in clinical settings around the world. While generally accepted, this effort is not free of difficulties in many areas: conceptual, methodological, clinical, financial, administrative, and political. Nevertheless, a historical opportunity for the materialization of old promises is now present, and must be decisively grabbed by all individuals, groups and organizations involved.

The trajectory of today’s two main nosological systems has made clear that culture, as an etiopathogenic and pathoplastic factor, and as a contributing component of severity, has a significant impact on psychiatric diagnosis. But, such impact goes even beyond: every clinician needs to know about, and assess pertinent cultural variables, family data, explanatory models, strengths and weaknesses of individual patients and their communities of origin. Cultural psychiatry, as a young but robust discipline, helps in the systematization of these pieces of knowledge, thanks to its growing connections with both neurobiological and social sciences.

Together with an explicit declaration of a cultural referent (𠇌ultural discordances”) in a new definition of mental disorder, the use and refinement of, and additional field research on tools such as DSM-IV-TR’s cultural formulation are needed for a new and pragmatic clinical interview, that should include an exploration of cultural factors in both history-taking and diagnosis-building phases. This article has elaborated on the theoretical/conceptual and logistic/pragmatic components of the effort.

Janusz Rybakowski: The Faces of Manic-Depressive Illness

INFORMATION ON CONTENTS: Chapter 1 presents a fascinating illness, the symptoms of which are the manifestation of very basic as well as unusually sublime aspect of existence and human experience. Chapter 2 describes ancient and modern history of the illness, from Hippocrates and Areteus of Cappadocia up to the contemporary classification of Emil Kraepelin and a separation from recurrent depression by Jules Angst and Carlo Perris. Chapter 3 characterizes mania when nothing is impossible and Chapter 4 describes depression when life has no sense. Chapter 5 presents mania and depression in various configurations and Chapter 5 defines what is the risk of becoming ill. Chapter 7 describes what is going on in the brain during the illness, Chapter 8 presents the past and present of the illness genetics and Chapter 9 shows the illness from the evolutionary perspective. Chapter 10 raises an issue of a connection between bipolar disorder and creativity. Lithium remains the most specific drug for the illness what is discussed in chapter 11. Chapter 12 further elaborates the management of the illness with special focus on mood-stabilizing drugs, mentioning also psychotherapeutic approaches. In Chapter 13, an attempt is made for using the illness as a metaphor of the American society. Finally, Chapter 14 put forward the research and treatment perspectives.

AUTHOR’S STATEMENT: The book was based on my 40 years’ experience with mood disorders and lithium treatment. My interest in bipolar illness extends from epidemiology and clinics, to neurobiology, genetics and psychopharmacological treatment. I was in charge of two epidemiological Polish projects: DEP-BI and TRES-DEP. In the first, which included 880 patients with depression remaining in ambulatory treatment by Polish psychiatrists, we demonstrated that in more than 60% of them, some kind of bipolar disorder can be diagnosed. In the second, covering 1,051 patients with diagnosed unipolar depression, in one third of them the features of bipolarity were found, as assessed by the Hypomania Checklist (HCL-32). Furthermore, patients with bipolar features were more resistant to treatment with antidepressant drugs than the remaining ones. My enterprise with lithium started in 1971 and has been going on until now. I am the author of more than 100 papers on different aspects of lithium treatment. Recently, we have reported on five patients being the excellent lithium responders, receiving the drug for 40 years or more. In 2012, I received the Lifetime Achievement Award from the European Bipolar Forum and in 2015 – the Lifetime Achievement Award of the World Federation of Biological Psychiatry.

Diagnosis and Drug Treatment of Psychiatric Disorders

Introduction: Brief historical summary of somatic psychiatric care I. Diagnosis and the diagnostic process II. Psychotropic drug management III.Diagnosis of schizophrenia IV.Review of antipsychotic drug literature V. Treatment of Schizophrenia VI.Diagnosis of affective disorders VII.Review of mood-stabilizing drug literature VII.Treatment of affective disorders VIII.Diagnosis of neuroses and personality disorders IX.Review of minor tranquilizer literature X. Treatment of neuroses and personality disorders XI.Critique of treatment studies XII.Theoretical inferences on clinical groupings of psychotropic drugs Author Index Subject Index. 36 tables detailing the treatment reviews 10 figures.

About 1964 John Davis suggested this book to me as a collaboration of clinical trials expertise with a depth of literature review and theoretical concerns.

The initial material included an unusually detailed discussion of the theory of diagnosis and the importance of syndromes. The belief that psychiatric diagnosis could arise from the multivariate study of scales was criticized.

There was a general chapter on psychotropic drug management followed by a series of three layer cakes regarding schizophrenia, affective disorders, and neuroses and personality disorders. Each first section was a critical statement about the development of this diagnosis and its substantiation. A critical review of the drug literaturefollowed documenting each trial. Such reviews have been effectivelysuperseded by meta-analyses. However, a detailed comparison of trial designs, analyses and outcome measures is a necessary precursor for fleshing out anonymous effect sizes. An attempt to integrate clinical trials data, clinical experience and practical matters follows, providing detailed treatment guidance.

Following these data rich chapters was acritique of the design of treatment studies . A scheme for large clinical research facilities to facilitate psychopharmacological development was outlined. Unfortunately this proved Utopian. The last chapter emphasized the utility of psychopharmacological dissection. It emphasized the existence of syndromes and the fact of remission was critical to nosology. This material shrinks the current over emphasis on endophenotypes and dimensions. That current psychopathological theory emphasizes either an excess or deficiency of some neurotransmitter --in rheostat fashion-- was also criticized as incompatible with known clinical data. A theory of cybernetic deficiencies of control feedback mechanisms was suggested that is still largely unremarked

Published in 1969, it was the first clinical textbook of psychopharmacology. The title of the book was unique in that it emphasized drug treatment. It was upsetting when we were told by the eminent publisher that due to some incomprehensible technical difficulty that the word “Drug” had been omitted from the book’s cover .They hoped that I would agree that this was of little consequence. However,myreaction led to a re-embossed cover. A corrected stick-on was provided for the spine, which promptly peeled off.

The book sold well as academic texts go. We were frequently told by residents that it served as an indispensable solitary, resource.

Over the next decade the exponential psychopharmacologic development warranted a second edition. In particular the entire field of childhood psychopharmacology had blossomed.

Watch the video: classification of psychopharmacological agentspsycopharmacological agnt (December 2021).