World Health Organization

New York: Cambridge University Press; 1996. 302 pp with index

ISBN 0-521-58133-8 (cloth)

For many decades, psychiatric epidemiology involving comparisons among countries has been handicapped by different classification systems. North Americans tend to use the Diagnostic and Statistical Manual of Mental Disorders, 4th edition, (DSM-IV) criteria, developed primarily by committees of the American Psychiatric Association, whereas western European countries use the International Classification of Diseases system, now in its 10th revision (ICD-10). This book is the ICD-10 equivalent of the big green DSM-IV manual that lists the multi-axial classification of psychiatric disorders, together with the brief description of signs and symptoms that make up the essence of the diagnoses.

The introduction, by the eminent child psychiatrist Michael Rutter, is first-rate. It indicates that there has been serious corroboration with DSM-IV. The similarities, including the use of a multi-axial description of each diagnosis and brief descriptions of signs and symptoms, are much more evident than any differences. As with DSM-IV, the diagnoses are based on clinical description and not on etiology, since precise causation in psychiatric disorders cannot be determined in most diagnostic categories.

As is often the case with British medical textbooks, the language is more succinct and the book is shorter than its North American counterpart.

A compare-and-contrast exercise does reveal some interesting, although relative minor, differences. Autism or pervasive development disorder and mental retardation are placed on axis II, instead of on axis I, in the ICD-10 system.

Under conduct disorders, always a problematic diagnostic category, there is an intriguing and possibly useful category called “conduct disorder confined to the family context.” In the section on affective disorders, the ICD-10 system does not include rapid cycling bipolar disorder.

The ICD-10 system has maintained a category of neurotic disorders, which are virtually identical to the personality disorders in DSM-IV. Among the neurotic disorders described by ICD-10 is “neurasthenia.” This concept, which feels outdated from a North American perspective, is related in a fairly modern way to postviral fatigue states and depression. “Neurasthenia” appears to have resurfaced in North America as chronic fatigue syndrome.

The section in ICD-10 on personality disorders suggests that these disorders can be diagnosed as early as 16 years of age, in contrast to the North American view that personality disorders begin only at age 18. The North American approach takes into account the flexibility of adolescent minds, which we hope will not settle into permanent personality structures prematurely. The use of the term “anankastic” for obsessive-compulsive disorders is another example of the way that traditional psychiatric phenomenology is maintained in the ICD-10.

Another example of a difference in terminology, which is illustrative of British brevity, is “clumsy child syndrome,” which is the same as “developmental coordination disorder,” described in DSM-IV.

In contrast with DSM-IV, ICD-10 does not set up lists of symptoms with the instruction that 3 or more must be present. There is usually a description of the general presentation of the problem. Instead of counting up symptoms, the clinician then forms personal impressions and makes his or her own judgements.

Axis V in ICD-10 refers to associated abnormal psychosocial situations. This is virtually the same as axis IV in DSM-IV, which refers to psychosocial and environmental problems. I found, however, that the ICD-10 axis V was more specific and clearer in describing the precise problems that children and families have. For instance, there is a specific category for lack of warmth in parent-child relationships, for scapegoating of a child, for disability in a sibling, for experiential privation and even for parental overprotection. Such clear categories allow family dysfunction to be introduced diagnostically in a clearer way.

The ICD-10 text on multi-axial classification of child and adolescent psychiatric disorders is a parallel but not identical effort to the DSM-IV currently in use in North America. Each system has something to teach the other. The continuing collaboration between the two evolving systems can only be of benefit. This book is not exactly a thriller to read, but for those interested in international collaboration in clarity of diagnostic categories, it is a very important sourcebook.

SJ Watson, editor

Washington (DC): American Psychiatric Press; 1996. 540 p

Over the past 30 y and particularly over this last decade — the decade of the brain — there has been marked acceleration of research efforts in the fields of neuroscience, molecular genetics, and biochemistry of mental disorders. Coupled with increasing sophistication in clinical observations, there has been an explosion of information about mechanisms of normal and pathological brain function. Although we are still far away from a clear understanding of the psychopathology behind 2 of the major psychiatric disorders, schizophrenia and affective disorders, substantial information already exists linking subcellular biological activities and the functioning of the neurons. The integration of information from molecular genetics, biochemistry, pharmacology, brain anatomy, and neuroimaging has advanced our knowledge about the impact of mental illness on specific brain neural circuits and their response to treatment. The recent and evolving knowledge about such specific brain circuits has inspired a new strategy of pharmacological targeting in the treatment of mental disorders. In this context, this book has its major strength focusing on the interface between several mental disorders and the genetics, pharmacology, neurochemistry, brain imaging, and postmortem studies reported by the researchers themselves, who are active in these fields.

The book emanates from contributions by a number of well-known and accomplished researchers in neuroscience to the 73rd meeting of the Association for Research in Nervous and Mental Disease, which took place in New York in 1993. One major feature of that meeting was that speakers were asked not only to present an overview of their field and their own work but also to provide their views on future developments. The book includes 17 chapters that deal with topics related to schizophrenia, affective disorders, infantile autism, an introductory chapter by the editor himself, and an overview chapter with discussions at the end. The introductory chapter by Watson presents an overview of mood disorders, autism, and schizophrenia from a clinical perspective and sets the stage for the basic science chapters that follow. The chapter written by Akil, “Biology of Stress from Periphery to the Brain,” explores the concept of “stress” as a trigger for psychiatric illnesses. The contributor documents her extensive work on the regulation of the limbic-hypothalamic pituitary-adrenal access and makes clear the well-known point that “the stressful nature of any given stimulus resides less in its objective characteristics and more in the organism’s ability to cope with it” (p 15).

The 5 chapters that relate to affective disorders include a contribution by Blakely about norepinephrine and serotonin transporters that highlights the progress on the molecular targeting of antidepressant effects. Another chapter, by Owens and others, deals with peptides and affective disorders and concludes with an account of future directions in the area based on the development of such new approaches as the application of ribonuclease (RNASE) protection assay, the expanding knowledge of the peptidergic brain circuits, and the ability to image central nervous system tissue with magnetic resonance imaging and positron emission tomography technology. The chapter about the mechanism of action of antidepressants by Berman and others elegantly reviews information, both basic and clinical, about well-known monoamines that have been explored in terms of their mechanism of action: serotonin, norepinephrine, dopamine, and neuropeptides. The chapter delves beyond the monoamines theory, however, by exploring postreceptors signal transduc-tion and neuroanatomy of antidepressant action and their relevance for the development of novel treatment approaches to depressive disorders. The chapter by Raichle and Drevets maps brain circuits relative to brain function and explores its implication for psychiatric illnesses. Another excellent chapter, by Mann and others, presents an up-to-date review of available information spanning more than 2 decades about postmortem studies of suicide victims.

The book includes 8 chapters related to schizophrenia. The chapter by Benes entitled “Excitotoxicity in the Development of Cortico Limbic Alterations in Schizophrenia” examines both the proposition that schizophrenia is a neurodegenerative disorder and the evidence for glutamatergeric dysfunction in schizophrenia. Goldman-Rakic, in her chapter, “Dissolution of Cerebral Cortical Mechanisms in Schizophrenia,” advances the argument from a neurocognitive perspective about the importance of frontal cortex and the role of working memory in the disordered thinking of patients with schizophrenia. Using postmortem studies, Kleinman and Nawroz provide evidence for the involvement of dorsal lateral prefrontal cortex, the hippocampus, and the entrorhinal cortex in the pathology of schizophrenia. An up-to-date review of the “Epidemiology and Behavioral Genetics of Schizophrenia” is provided by Tsuang and Faraone. Khan and her colleagues, in their excellent chapter, “Revisiting the Dopamine Hypothesis in Schizophrenia,” advance the argument for schizophrenia as both a hyper- and hypodopamine state, thus linking such diverse elements of the broad spectrum of symptomatology as positive and negative symptoms as well as neurocognitive deficits. The contributions of neuroimaging to the understanding of the psychopathology of schizophrenia is well presented in a chapter by Van Horn and colleagues. “Abnormal Frontotemporal Interactions in Patients with Schizophrenia,” by Friston and others, provides results of their extensive work using neuroimaging in examining functional connectivity by studying corticocortical interactions in patients with schizophrenia. The last contribution related to schizophrenia is the excellent chapter by Meltzer and others, “Exploring the Mechanism of Atypical Anti-psychotic Medications,” which provides evidence for Meltzer’s recent argument for a major role for serotonergic mechanics in the improved therapeutic effects of atypical antipsychotics, particularly their tendency to produce significantly fewer extrapyramidal side effects.

The chapter devoted to “Linkage and Molecular Genetics of Infantile Autism” by Ciaranello reports the results of extensive linkage studies of 1 of the least understood disorders: infantile autism. This chapter, coming after the recent sudden and untimely death of its author, serves as a memorial to a distinguished scientist.

Overall, the book is a significant contribution, providing valuable information for understanding the mechanisms of normal and pathological brain function and its relevance to schizophrenia and affective disorders. The book makes a good attempt to integrate information at the level of functional neurocircuits. It should be of interest not only to neuroscientists but also to psychiatrists, neurologists, and psychologists. Although the book is about basic neuroscience, its relevance to clinicians is obvious because it explores the basic biological brain functions in relation to mental

illness. The book reads well, which reflects the skills of its editor, Stanley Watson. The only regret I have is that it took 3 y to publish the proceedings of that 73rd meeting of the Association for Research in Nervous and Mental Disease, which is rather a relatively long time in terms of the rapidly evolving neuroscience research. Nevertheless, the book is a valuable contribution and continues to be equally relevant today.

P Sachdev

New York: Cambridge University Press; 1995. 425 p

This book provides the most comprehensive review to date on akathisia, restless legs, and neuroleptic-induced dysphoria. The volume is divided into 4 distinct parts. Part 1 provides a historical review of akathisia and restlessness as well as a concise and excellent review of neuroleptic-induced dysphoria. Part 2 focuses extensively on drug-induced akathisia. The definition, epidemiology, differential diagnosis, and clinical characteristics of both acute and tardive akathisia are well presented. Assessment procedures are discussed, as are the etiology, pathogenesis, and treatment of the disorder. Part 3 reviews the clinical features, pathophysiology, and treatment of restless legs syndrome. Part 4 offers the reader a summary and recommendations for future research followed by appendices of 4 akathisia clinical rating scales.

In part 1, the book offers a detailed introduction to the development of the concept of akathisia, which was 1st reported by Thomas Willis (1621-1675). The term “akathisia” translated from its Greek root, however, means “not to sit” and was 1st used by Lad Haskovec in 1902. Ekbom introduced the term “restless legs syndrome (RLS)” in 1945 and described the most characteristic symptom of this disorder as “creeping or crawling sensations most frequently localized to the lower leg.” By the 1960s, RLS was firmly established as a neurological disorder, albeit of unknown etiology. After antipsychotic drugs became widely available, a number of reports of akathisia appeared in the literature, with descriptions of patients being restless, being unable to sit, or marching like soldiers. In spite of the few interesting papers examining the psychological and psychodynamic meaning of the akathisic reaction, consensus emerged in the early 1960s that akathisia was an extrapyramidal side effect (EPS) of neuroleptic medication.

Acute akathisia (AA) refers to akathisia that develops soon after the introduction of neuroleptic drugs; by contrast, tardive akathisia develops as a delayed side effect of long-term neuroleptic medication.

Akathisia is often used synonymously with neuroleptic-induced restlessness, yet the term was introduced well before neuroleptic drugs became available. In the clinical setting, restlessness can be caused by psychological factors, organic disorders (drug-induced disorders, drug withdrawal reactions, delirium, dementia, head injury, hypoglycemia, and RLS), and nonorganic psychiatric disorders (affective disorders, psychotic disorders, anxiety disorders, and childhood disorders like attention-deficit hyperactivity disorder).

The author distinguishes 2 aspects of restlessness — a motor (objective) component and a mental (subjective) component — and suggests a comprehensive operational definition.

The motor component of restlessness is typically considered to be under voluntary control; there is, however, a compelling need to move, and suppression of movement results in mounting distress. Sachdev reminds us that the functional neuroanatomy and the neurochemical basis of restlessness remain poorly understood. In many cases, restlessness must be treated because of its negative impact on the patient and caregivers. It is important, however, to identify and, if possible, to rectify the various psychological, social, and environmental determinants of restlessness. Drug therapy may be required to reduce motor activity and subjective distress. The choice of a particular drug is guided by the setting and the possible etiology. Neuroleptics are probably the drugs most commonly used for the management of agitation in dementia and delirium. Benzodiazepines are used quite extensively in the treatment of agitation, and a number of studies attest to their efficacy in some patients.

Neuroleptic drugs induce unpleasant subjective effects among healthy controls and in many psychiatric patients. A dysphoric response is often a predictor of neuroleptic non-compliance. The manifestations of neuroleptic-induced dysphoria (NID) are varied and range from complaints like “the drug disagrees with me” and “I feel emotionally unresponsive” to neuroleptic noncompliance, anxiety and dere-alization, school and work avoidance, painful sensory symptoms, and even depression. The question of whether or not NID can also manifest as a cause of or contributor to depression is a controversial issue that remains to be resolved.

NID may result in a poor outcome, but while many NID patients become noncompliant, others benefit from dysphoria by negotiating with their psychiatrists for lower yet effective doses of neuroleptics, resulting in less severe EPS. The neurobiological basis of NID remains poorly understood.

While the importance of akathisia is now well recognized, there is no consensus on its essential characteristics and hence its diagnostic criteria. The essential features of drug-induced akathisia (DIA) are: 1) exposure to neuroleptic drugs; 2) subjective component: feelings of restlessness, constant urge to move the legs, difficulty or inability to maintain a posture for several minutes; 3) objective component: movements while sitting, standing, or lying. The assessment scale Sachdev uses is the Prince Henry Hospital Akathisia Scale, which includes 3 subjective items, 7 objective items, and a global akathisia score. Sachdev also proposes detailed criteria to diagnose akathisia. It is appropriate to consider onset of symptoms after 3 mo of continuous use of the drug without change in dose or type as tardive akathisia. Onset within 6 weeks of stopping or significantly reducing the dosage of a neuroleptic drug should be considered a withdrawal akathisia, and if the diagnosis of akathisia persists beyond 3 mo after drug cessation or reduction, tardive akathisia should be diagnosed. Akathisia that continues for 3 mo or longer is considered to be chronic.

The published rates of AA with conventional neuroleptics vary from 8% to 76%. A conservative estimate of the incidence of akathisia with classical neuroleptics at clinical dosage levels is about 20% to 30%, but this rate is significantly affected by treatment-related and other variables (parenteral administration and drug potency, for example). Akathisia can also be induced by novel or atypical neuroleptic drugs. Current evidence suggests a reduced rate of AA with these novel agents, and further systematic work is necessary. Nonneuroleptic drugs that can also induce AA include serotonin reuptake inhibitors, serotonin antagonists, heterocyclic antidepressants, anticonvulsants, calcium channel antagonists, and lithium carbonate.

There are no accurate estimates available as to the prevalence or incidence of tardive akathisia, and data on the epidemiology of withdrawal akathisia are extremely limited. In children and adolescents, drug-induced movement disorders have been poorly documented, and akathisia has been relatively neglected. In individuals with developmental disabilities on long-term neuroleptic medication, akathisia appears to be common, but the overall data are too few to make comparisons with nondisabled populations. In the geriatric population, reports of akathisia have been few.

The main feature of AA is subjective distress. In its milder form, it is experienced as a vague feeling of apprehension, irritability, dysphoria, impatience, or general unease. While the restlessness of akathisia may be felt in the mind or body or both, the characteristic that distinguishes it from restlessness of other etiology is its reference to the lower limbs. The movements are described as a response to an irresistible urge to move, but the movement alleviates the urge and the distress only temporarily. Akathisia has been associated with psychotic exacerbation, violence, and suicide. Fidgetiness is perhaps the most common motor sign of akathisia and is usually manifest as semipurposive or purposeless movements of legs, feet, and toes. While the emphasis is on leg and postural movements, semipurposeful or purposeless arm and hand movements may occur. Upper limb movements are less prominent and virtually never occur in isolation. Activating maneuvers in the case of akathisia tend to diminish or suppress movements.

Tardive akathisia has not been universally accepted as a distinct syndrome. The phenomenological examination of patients on long-term neuroleptic medication suggests that tardive akathisia is distinct from tardive dyskinesia, with overlap between the 2. “Chronic,” in terms of describing akathisia, refers to the duration of the disorder, irrespective of the nature of onset, whereas “tardive” denotes a delayed onset.

The most popular method of measuring akathisia is with the multiitem rating scales such as the Barnes Akathisia Rating Scale, the Hillside Akathisia Scale, and the Prince Henry Hospital Akathisia Scale. The measurement of akathisia presents a number of difficulties owing to the complex manifestations of the disorder, the lack of a well-accepted definition, and its variability. No instrumental method is totally satisfactory, but a combination of strain-gauge measurements and actigraphy can provide an accurate measurement of the motor component of akathisia.

The etiology of akathisia must be understood in terms of the drugs that are directly causative and in view of a number of background variables that are likely to increase the risk of its development. Its pathogenesis is incompletely understood, and many competing hypotheses exist. tardive akathisia and withdrawal akathisia have not been reported with nonneuroleptic drugs, suggesting that, unlike AA, they may be purely neuroleptic-related syndromes.

Treatments for AA include modification of the offending drug (cessation, dosage reduction, change to another type, reduction in rate of increment); modification of risk factors; and introduction of benzodiazepines, anticholinergic, antiadrenergic (β-antagonists, α2-agonists), or other agents (ristanserin, amantadine, piracetam, tricyclic antidepressants, and sodium valproate). The treatment of tardive akathisia is, in general, unsatisfactory and the main emphasis should be on its prevention.

There is still no consensus on the incidence and prevalence of RLS. Like akathisia, it is characterized by sensory and motor features. The restlessness in RLS is different from the movements seen in DIA. The other main motor feature in RLS is myoclonic jerks. RLS often leads to sleep disruption. The course of idiopathic RLS is variable — starting in childhood, adulthood, or old age, being progressive or staying the same or even getting better. Table 12.5 (p 317-318) contrasts the DIA and RLS disorders clearly. In RLS treatment, clonazepam remains the drug of 1st choice. Although evidence supports the use of 1-dopa, problems with the long-term use of this drug make clonazepam a better initial agent. If 1-dopa is not tolerated, bromocriptine can be used.

In summary, this is a timely, well-written, and well-researched volume. Dr Sachdev is to be congratulated for offering readers the 1st book-length review of akathisia and related syndromes. Undoubtedly, this book will be a welcome reference for psychiatrists and neurologists.

A Takada, G Curzon, editors

Amsterdam: Elsevier Science BV; 1995. 260 p

This book is part of the International Congress Series and contains the proceedings of the Symposium on Serotonin in the Central Nervous System and Periphery held in Nagoya, Japan, on April 1 -2, 1995. It is comprised of papers presented at the symposium and contains up-to-date information on the area, written by some of its top researchers, who were selected to participate in the symposium based on their expertise. It has become necessary for clinicians and scientists to focus on the basic science and fundamental actions of the new serotonin-acting drugs in order to understand their functions. This book attempts to provide such information in a timely fashion.

There are 7 sections in the book: Regulatory Mechanisms, Relationship with Feeding, Amines and Stress, Depression and Anxiety, Other Central Aspects, Vascular System, and Lung. The most useful and important section is the first, which covers the regulation of serotonin release, genes, and the pathophysiology of affective disorders. Even with a minimum of prior knowledge of the area, the clinician, by reading this section, can gain an understanding of how serotonergic drugs work. The section on depression and anxiety is a must-read for psychiatrists, though the majority of information refers to animal models. The relationship of serotonin and feeding behavior, pre- and postnatal stress reactions, antipsychotic medications, the psychoprotective effect of estrogen, learning and memory, Alzheimer’s disease, and physical health are also covered in the book.

Although this book suffers stylistically because of the number of different authors, it is, overall, a succinct, well-written, and extremely informative text. It provides recent information in the field of serotonin research and could prove to be a valuable teaching and research reference. We highly recommend this book to clinicians, who could apply it in their use of psychopharmacology, to biological researchers, who will find it a useful reference, and to residents in psychiatry, who may appreciate it as a learning tool.

A.-M. Ghadirian and E.H. Lehmann

New York, NY: Springer Publishing Company, 188 pp, 1993

When I initially browsed through this book, I wondered how topics as diverse as seasonal affective disorder, taijin kyofu sho, the homeless, and terrorism could be tied together in a cohesive mental health theme. After completing it, I believe the editors deserve credit for doing just that. Drs. Ghadirian and Lehmann are well-known and respected clinician researchers from McGill who are eminently qualified to examine the interaction between our environment and the expression of mental illness. As they point out in the introduction, this interaction is complex and difficult to study, but is essential for understanding stress and coping. Their book is divided into three sections: physical factors and psychopathology; social and cultural forces; and catastrophic forces. The first section includes chapters on how light, noise, pollution, and nutrition may contribute to psychopathology. The second section looks at the relationship between mental illness and culture-bound syndromes (taijin kyofu sho is a form of Japanese social phobia), the “postwar generation”, homelessness, and substance abuse. The psychological effects of natural disasters, terrorism and torture, and concentration camps are addressed in the final section.

Overall, the writing and editing are good, the quality of the book is excellent, and the price is very reasonable. The usual problem with multi-authored books (that of overlap between chapters) is a non-issue because of the diversity of topics. My one criticism of the technical aspects is that the references in the text include all the authors’ names. While I very much prefer text references in this author/year style instead of numbers, I find it annoying to have to wade through five or six author names for a single reference, especially when several references are cited.

The chapters are succinct and well-written by authorities in each field. As expected in a book with this theme, the authors range from psychobiologists, to sociologists, to epidemiologists. Sometimes the chapters are a bit too sparse. Gerald Klerman has a chapter on the fascinating epidemiologic data showing increasing depression rates in younger age cohorts in the 20th century. He describes the methodology in detail, but does not elaborate on possible explanations for these findings. Unfortunately Dr. Klerman died last year, but his ideas and speculations on the matter would have been very interesting. Other topics such as environmental illness, or “20th century disease” seem conspicuous by their absence. Dr. Lehmann has not contributed a chapter, but Dr. Ghadirian penned the chapter on psychoactive substance abuse and psychopathology, a nice summary of the available literature. The chapter on homelessness and psychopathology by Wallace, Streuning and Susser offers a well-thought out treatise that limited effective social networks leading to spiralling feedback loops that result in homelessness. The final chapter by John Sigal on concentration camps points out that all of the literature on survivors of concentration camps is based on people from Western industrialized nations, and that we have very little understanding of the psychological effects of atrocities on Third World people. He pointedly suggests that this may be merciful, but I wonder about this restricted focus that we have in the “First World”.

One small omission from the book’s introduction is a clear statement of the target audience, i.e. who should read the book. This is important, because I think of books as meals. Choosing a meal depends on your appetite and interest. For example, reference books are like smorgasbords — there is lots of variety and everything is available in vast quantities. Researchers prefer gourmet fare, like nouvelle cuisine — small portions, but carefully and exquisitely prepared with only quality ingredients. Residents tend to favour health food — lean and spare, with all the vital nutrients but no frills. Medical students like easily digestible food that has been strained of birdseed. In this analogy, I would classify this book as an appetizer course — small, varied, tasty nibbles that whet your appetite for more. When thinking about environmental effects on mental illness, one tends to forget broader issues like culture or disasters, and ubiquitous factors like light or noise. I would therefore recommend this book to readers interested in brief essays on the way selected environmental factors can affect psychopathology and mental illness.

J. Mendlewicz, Paris: Masson, 160 pp., 1991

During the past four decades, research in biological psychiatry and neuroscience has made unprecedented progress. New research methods and technologies in areas such as molecular biology and brain imaging have contributed to an extraordinary explosion of knowledge in the pathophysiology and treatment of many mental disorders. The timing of this book is appropriate, since we are in what has been named “the decade of the brain.”

This collaborative volume, edited by J. Mendlewicz, brings together 15 chapters on selected topics in biological psychiatry. The chapters covered include: a historical review of psychiatric nosology; the chronobiology of affective and schizophrenic disorders; hemispheric laterality and psychopathology; sleep disturbances; a review of the clinical use of neuroendocrine markers in psychiatry; the neurobiology of anxiety disorders; molecular genetics of affective disorders and schizophrenia, respectively; the pathophysiology of schizophrenia; dopaminergic mechanisms in the action of antipsychotic drugs; a general overview on tardive dyskinesia; receptor mechanisms in depression and the mode of action of antidepressant medication; a review of benzodiazepine receptors and anxiety and a final chapter on the status of biological psychiatry in developing countries.

Some chapters, which could have been grouped around a common theme, such as the chapter on the neurobiology of anxiety disorders and the chapter on benzodiazepine receptors and anxiety, are 58 pages apart. This contributes to a lack of unity in the volume. However, this book is ideally suited to the reader who is unfamiliar with and wishes a “glimpse” at some of the many developments that have occurred in the field of biological psychiatry.

John Madden IV

New York, NY: Raven Press, 368 pp, 1991

This book comes at a time of progress and exciting new discoveries in the field of research involving the neural basis of learning, emotion and affect. The study of learning and memory has flourished for many years within the neuroscientific community. Although long neglected by all but a handful of neuroscientists, emotion and affect have begun to attract attention. A clear summary of the status of this recent work is therefore particularly welcomed.

The book is divided into three parts. The first part is devoted to recent advances in the research of the neural mechanisms of fear conditioning, in both invertebrates and vertebrates. Most exteroceptive stimuli we encounter in our life are affectively “neutral”. However, they can take on emotional properties and elicit emotional reactions, such as defence or approach responses, through association with other stimuli or events that are affectively charged. It is possible to study experimentally the ways in which the brain forms such associations through the use of Pavlovian conditioning techniques, whereby a “neutral” stimulus, the conditioned, or conditional stimulus (CS), is paired with a biologically significant (affectively charged) stimulus, the unconditional or unconditioned stimulus (US).

Pavlovian conditioning procedures have been used to study the biology of learning in many species. Whether or not it is reasonable to speak of Pavlovian conditioning as a process of emotional learning is debatable for invertebrates, many vertebrates, and even many mammalian species, if emotion is restricted to subjective, experiential factors. However, if by emotion we also mean the neural mechanisms by which stimuli are evaluated for their significance (LeDoux 1990), it is possible to view all animals as engaging in a form of emotional processing. What is different about humans and possibly higher primates is that the emotional processing of stimulus significance becomes represented as conscious content. This view is advantageous in that it places emotional processes on a continuum and allows for studies of emotion throughout the animal kingdom.

In the Aplysia model, described in detail by Hawkins, the cellular mechanisms and neural loci responsible for associative learning are, without a doubt, understood more than in any other animal model. Are the same basic mechanisms discovered in this simple model in operation also in more complex organisms? Hawkins believes that classical conditioning in Aplysia, Hermissenda, cat and rabbit involve the same neural mechanisms. In Aplysia, the US plays a modulatory role in stimulating the facilitator neurons. The convergence of this input with the appropriate CS input (the one that was paired with the US) increases presynaptic facilitation and produces classical conditioning. A similar mechanism is acting in vertebrate models as well, Hawkins suggests. The aminergic and cholinergic systems in the vertebrate nervous system can behave like the facilitator neurons of Aplysia. One challenge for the future is to test this simple and attractive theory.

Another elegant invertebrate model is Drosophila melanogaster. An advantage of this model is the possibility of using genetic tools. In recent years, the isolation of mutations that affect an aversive conditioning task in the fruit fly has considerably increased our understanding of the molecular mechanisms of learning and memory. Tim Tully reminds us that with Drosophila research, we probably have the only evidence that short-term and long-term memory are indeed two genetically distinct processes.

Our understanding of the molecular and underlying elementary neural mechanisms which make learning possible in an individual is far less developed in vertebrate models. In recent years, however, simple vertebrate model systems have been worked out, and important neural structures and pathways essential in learning have been shown. It now appears that different types of learning are mediated by different but, in some cases, overlapping neural circuits.

One promising vertebrate model is the conditioned fear-potentiated startle paradigm. In this behavioral model, the conditioned stimulus (usually a light) is paired with a shock and startle response elicited by a noise burst in either the presence or absence of the light. If the startle response is greater when elicited in the presence of the light, the fear-potentiated startle has occurred.

The role of the amygdala in this reflex has been demonstrated by Davis and collaborators; in this book they review the current state of affairs. The amygdala is the centerpiece of the neural pathway involved in fear-potentiated startle, as well as in other fear conditioning situations (Kapp et al 1990; LeDoux 1990). Davis and collaborators show that the activation of the amygdala from the visual conditioned stimulus pathway triggers the startle reflex pathway. The central nucleus of the amygdala carries this out through its connection with the nucleus reticularis pontis caudalis (a nucleus in the startle circuit). Davis and colleagues believe that the visual input comes to the amygdala through cortical pathways. However, findings from our laboratory suggest that visual fear conditioning can be mediated by subcortical visual inputs to the amygdala (LeDoux 1990).

There is a general consensus about the involvement of the amygdala in mediating the acquisition of autonomic responses in the aversive classical conditioning. These responses are defined as “non-specific” and include heart rate, generalized motor activity (freezing, startle response) and skin resistance. They all develop rapidly after a few trials, sometimes requiring just a single contingent pairing. “Specific” responses, on the other hand, are discrete, skeletal muscle responses elicited by specific aversive stimuli. They are much slower to develop and are more specifically adaptive for the organism.

Steinmetz and Thompson describe how the cerebellum, in particular the interpositus nucleus, is an important site for the acquisition of these discrete, specific responses. Using a multi-technique approach (recording, stimulation, lesion studies) they developed a detailed anatomical map of the circuitry involved in the adaptation to aversive events for these behavioral responses. According to Steinmetz and Thompson, the cerebellum plays an “informational” role in the learning of the organism. It is activated in conjunction with the aversive system that involves higher brain regions (the amygdala, for example). These two systems in the brain are distinct, but they interact in the adaptive learning phase. The US pathway activates both systems. And while the cerebellum appears to play an important role in learning the specific response, recent studies also suggest that the amygdala is involved in the early phases of learning. The final attempts to relate these ideas to the popular Rescorla-Wagner learning theory.

Part II of the book deals with experimental situations in which the animal is allowed little or no control over the aversive stimulation How do the subjects cope with stressful events when species-specific defense responses are not helpful? What kind of behavioral and biochemical changes will stressful events elicit? Results from these experimental studies are particularly valuable for their clinical implications. Weiss, using an uncontrollable shock paradigm, suggests in fact that stressed animals show symptoms closely corresponding to those developed by depressed individuals. Moreover, the author proposes that stressful events (for example, uncontrollable shock) elicit both anxiety and behavioral depression. In his analysis, Weiss shows how the locus coeruleus seems to be a key structure in the neurochemical unbalance produced by the uncontrollable shock.

Cognitive deficits may also occur as part of the response to stress. Animals that are exposed to shocks that they cannot avoid or escape later fail to escape shock in a situation in which escape is possible. They also fall well behind control animals (that were allowed to escape or avoid shock in the first phase of the experiment) in Y-maze or water-maze learning tests. Some researchers have explained these results in terms of a simple motoric impairment: the shocked animals learn a coping response in the new situation, but they cannot perform it. Maier rejects this hypothesis; his work suggests that inescapable shock gives rise to learning deficits that cannot be explained by a motor activity deficit.

However, the impairment is not the result of associational learning between the first phase of the experiment and later test situations, as it was suggested in the early explanations of this phenomenon. What is impaired in these subjects, according to Maier, is the capacity to attend the salient external cues; the deficit is then a cognitive one, not an associative one (the learned helplessness hypothesis). Whether this cognitive deficit will be connected to some neural loci or biochemical systems will have to be determined in future studies.

More complex issues of depression and human affect disorders, which involve multiple interactions between emotional and cognitive systems operating at conscious and unconscious levels, are difficult to probe with vertebrates too distant from us in the evolutionary ladder and in social habits. Suomi describes a primate model of affective disorders, the separation model. Humans share over 90% of non-replicated DNA material with higher primates. In addition, the behavior of these animals is characterized by advanced and dynamic social interactions among members of the same species. Rhesus monkeys, in particular, have been studied extensively in the wild and in laboratory settings. Stressful events caused by social relationships among individuals closely resemble human social life. Separation from an attachment object, such as a mother or a loved conspecific, produces profound behavioral and physiological effects, both in the wild and in the laboratory. The evidence of individual differences in these animals makes this model particularly interesting. Not all subjects respond to the same social separation in the same manner. There is also consistency in this behavior in individuals. The same monkeys “at risk” are more readily aroused by and behaviorally fearful of other stressful events. Having individuated the groups “at risk” in the rhesus monkeys population, it may be possible to forecast or even prevent the affective disorder. The “separation/risk” model in monkeys, as Suomi defines it, seems to be extremely promising for improving our understanding of the psychobiology of human affective disorders.

There is evidence from this primate model that the noradrenergic system is involved in mediating depressive states. Matthysse reaches the same conclusion in his analysis of mood disorders. In particular, the locus coeruleus, an important source of forebrain noradrenalin, is advanced as a candidate for depression, as Weiss also proposed for the helplessness model. According to Matthysse, this nucleus becomes activated by excited unhappy memories, which are the result of early loss or other traumatic events. Cerebral activation is then reduced by the increased firing of the locus coeruleus. At this point, physostigmine, the cholinergic agent, enters the circuit to produce the physiological symptoms of depression. In Matthysse’s view, while the memories are the primary cause of noradrenergic changes, the biogenic amines are only the effectors in this theory. Matthysse points out that human studies suggest that decreased cerebral activation is produced by physiostigmine in normal subjects (for example, the subjects feel “apathy, slowness of speech and movement”). Physiostigmine physiological symptoms closely resemble those of depression. In his fascinating theory, however, Matthysse does not tell us where these memories may be stored in the brain or why, at a certain point, they overflow to reach the locus coeruleus. Also, it will be interesting to try to define the role of anxiety in this context. Under identical conditions of stress some people respond only with anxiety; do they have the capacity to deal with the unhappy memories activation in a different way? Interesting questions arise from this theory that only future experiments can elucidate.

Control over stressors is a critical factor that influences biological functions which regulate adaptive and maladaptive behaviors. Bandura states that the ability to control stress effects is the principal factor that makes a person cope with stress events. It is the ability to control the stress effects that prevents the release of stress-related hormones or the impairment of the immune system. With the support of human quasi-experimental studies, Bandura describes the effect of being able to gain control over the stressful situation. For instance, catecholamine levels in phobic patients dropped after allowing them to acquire controlling efficacy. Pain tolerance was increased in normal subjects when there was self-efficacy, even in those subjects to whom naloxone was administered to block opioid activation. Self-efficacy mechanisms play an essential role in the individual’s well-being. Bandura’s theory proposes an entire psychological approach to deal with stressful events that deteriorate our biological systems. This approach provides an intelligent stimulus to operate in the sphere of human maladaptive behaviors with “clean” psychological tools but with an attentive eye on the neurobiological domain.

Part III of the book explores broader issues in the field of emotion and affect and presents two models. Gray describes three systems that control emotional behavior. Each of these systems is associated with a particular area in the brain. One of these systems, the behavioral inhibition system, is thought by Gray to be centered around the hippocampal formation. This system is responsive to stimuli associated with punishment or with the conditioned aversive stimuli and is involved in increasing the level of arousal and increasing attention to the environment to cope with the new situation. Anxiolytic drugs affect the septohippocampal system, and lesions of this system lead to a behavioral syndrome similar to that seen after the administration of anxiolytic drugs. These results are the strong-hold of Gray’s theory. The amygdala, a structure that has long been considered to play a pivital role in fear, including fear learning, is not included in the behavioral inhibition system. It is involved instead in the second system, the fight/flight system, which is responsive to unconditioned punishment and non-reward, that is, to issue commands either for fight or for flight depending on the context and type of punishment received. Gray dismisses fear conditioning studies as irrelevant to the problem of anxiety and relegates them to elicitor of a more species-specific type of defence or attack responses. We do not agree with such a view. Nevertheless, Gray’s model is commendable in its breadth and attempt to synthesize divergent findings into a unified theory of anxiety. The second model uses the opponent-process theory to explain a large set of affective phenomena, taken from everyday life and experimental settings. This model states that it is possible to produce acquired motives by non-associative mechanisms alone. The mechanism is repetition, not conditioning (association). Solomon believes that his approach can explain food intake, drug addiction and related phenomena that Pavlovian conditioning is not able to explain. An important question that the author raises is whether or not the opponent-process states are predictable. He is convinced that they are and analyzes the process of food intake and obesity following the logic of opponent-process theory.

Neurobiology of Learning, Emotion, and Affect is a well organized, multi-disciplinary book. It presents a range of approaches and contributions. The literature on behavioral neuroscience, in general, has increased tremendously in the last few years. Moreover, there is a growing interest in research on emotion, which has been somewhat neglected in the age of cognition. This book will help bring research on emotion into the limelight. The book will be very useful as an introduction to research on the biology of emotion and learning and will also be useful as reference point for future research.

Stanley W. Jackson

New Haven, CT: Yale University Press, 441 pp., 1990

“Melancholia is one of the great words of psychiatry. Suffering many mutations, at one time the tenacious guardian of outworn schemes or errant theories; presently misused, cavilled at, dispossessed, it has endured into our own times, a part of medical terminology no less than of common speech.” With such magisterial prose did Sir Aubrey Lewis start his historical review of the subject. Now, over half a century later, Dr. Jackson gives us a splendid volume to flesh out the skeleton which Sir Aubrey provided. And one of the excellent features of this book is the ample use of quotations from the various authors thus enabling the reader to form his or her own opinion on the clinical entity being described.

In his first chapter Jackson makes it clear that he is concerned with the disease or syndrome, not the symptom. But equally, consideration of the developing concepts of disease, knowledge of “the passions,” explanatory systems in medicine and, at times, the relevance of contemporary “belief-action systems other than medicine” receive attention to elucidate the main subject.

Greeks, Arabs and Others

Like Sir Aubrey, Jackson begins with Hippocrates and Greek medicine. This is of necessity as ‘melancholia‘ is formed from the Greek words for black bile an excess of which was supposed to account for the condition. This is not to say that earlier peoples had no notion of this enduring aberration of the human condition. The skulls of many neolithic men showed trephine holes made, it is conjectured, to let out spirits supposedly inserted to cause disease. (As Ackerknecht points out thought insertion may be a legitimate explanation of disease in some primitives and not a sign of illness.) Nonetheless, there is little recognizable reference to affective disorders in either primitive medicine or the ancient civilizations of Egypt, Sumeria, Mexico or Peru. The concept of disease as retribution for offending the gods, however, was prevalent in all cultures and the equating of disease with sin was particularly characteristic of the Babylonians.

But it is entirely appropriate for Jackson to start with Greek medicine because, in the words of Ackernecht, it “is incomparably closer to modern medicine than any other historical form of medicine.” “Disease was no longer regarded as a supernatural phenomenon; it was approached from a rational, naturalistic and scientific point of view” and he wonders why “a small group of people in the eastern Mediterranean took this important and radical step in human thought.”

As Jackson recounts, the Hippocratic writings of the fifth century B.C. describe melancholia as an “aversion to food, despondency, sleeplessness, irritability, restlessness” and “fear or depression that is prolonged.” The cause was located squarely in the body due to an excess of black bile. (The latter, together with yellow bile, blood and phlegm, formed the explanatory system of four humors which was to last for another two millennia. Had the subject started in our present day one wonders if ‘indolia’ or ‘catecholia’ would be equally durable). Subsequently Aristotle speculated why those who became “eminent in philosophy or politics or poetry or the arts” were apparently prone. The disease was distinguished from both the temperament and the despondency “which occurs in everyday life.” Yet supernatural or dualist views still persisted in that some forms of melancholia were believed to be a “divine madness” associated with gifts of prophecy. Aristotle also noted sexual intercourse as a cause. Subsequent writers elaborating on these ideas included Celsus, Soranus and Rufus of Ephesus who, in contrast to Aristotle, regarded coitus as “the most helpful remedy of all against melancholia.” These views were later extended by Aretaeus, (c. 150 A.D.) and in particular by Galen (A.D. 131-201).

This teaching was preserved and nurtured in translation during the “Golden Age” of Arabic medicine and the names of Constantine, Oribasus, Alexander of Tralle and Paul of Aegina deserve honor. Throughout the clinical descriptions remained remarkably consistent from Soranus’ account at the beginning of the second century A.D. to that of Bartholomaeus Anglicus in the thirteenth century (summarizing Greco-Arabic views) and which, hardly changed, persisted to the seventeenth century.

The Early Church

Powerful religious views, on the other hand, took a different direction. Whilst the humoral theory obviously anchored symptoms to changes in the body, many were of a dualist persuasion (from Plato to Descartes), and the spiritual side was emphasized by the early Christian church through the notion of “acedia.” This condition was first described in Egyptian desert monks near Alexandria in the fourth century A.D., and the symptoms included dejection, sorrow, lassitude, weariness, carelessness and neglect. This result of cenobitic life was considered a sin and hence the cure lay in religion. An important part of Jackson’s work is the separation of the concept of acedia (which was blameworthy) from melancholia (for which the sufferer was to be pitied). It is one of the banes of sufferers from depressive illness that the milder manifestations are often categorized as sloth, a fate which those suffering from many mild forms of physical illness escape. (If one has a mild rash one simply has fewer or less ostentatious spots). In contemporary terms, it is illustrated by the debate about the “chronic fatigue syndrome.” But certainly the idea of “accidie” as a cardinal sin had great influence and, together with the often proffered guilt of the sufferers themselves and theological notions of demonic possession, not infrequently led to burning of many depressed women as witches. It is to Dr. Jackson’s great credit that he teases out from the very confusing and conflicting notions of medieval writers these two concepts of sin and illness.

Renaissance to the Eighteenth Century

The early years of the Renaissance saw little change in the humoral theories of Hippocrates and Galen. There were, however, comprehensive accounts including Burton’s well-known “Anatomy of Melancholy” and also, as Jackson points out, the lesser-known but equally deserving notebooks of Richard Napier, which contained records of more than 2000 mentally disturbed patients and which have been analyzed by MacDonald. An exception was the fiery Paracelsus. He objected to the system of Galen but had to replace it with an equally speculative “chymistrie.” (He also disagreed with the clergy who espoused supernatural causes.) And Thomas Willis in the later seventeenth century tried to shift explanatory schemes for the first time in two thousand years from humors to chemistry. For Willis, melancholia was “a complicated Distemper of the Brain and Heart: for as Melancholick people talk idly, it proceeds from the vice or fault of the Brain, and the inordination of the Animal Spirits dwelling in it.” The latter, which were normally transparent, became thick and dark, “Acetous and Corrosive, like those liquors drawn out of Vinegar,” and were instilled into the brain. Iatro-chemistry, however, was short-lived and replaced by iatro-mechanics, reflecting both the advances in physics pioneered by Newton and in physiology by Harvey. Thus melancholia for Pitcairn was due to a defect of the normal “vivid motions” of the blood, part of which became sluggish. Similar views were espoused by Hoffman and Boerhaave, the black bile being transmuted into a sort of dark sludge from the blood. In turn, mechanistic views were criticized or often held pari passu with electrical and vitalist theories.

More important, Jackson suggests, was the clinical separation of hypochondriasis from depression, the former consisting of “a syndrome of physical complaints and a non-psychotic depressed state…. It seems likely that the logic of separating nonmad dejected states from mad dejected states was more compelling to clinical observers than any effect of mechanical explanations.” The notion of melancholia had also penetrated the literary world and was ascribed to Addison, Thomas Gray and Cowper. Jackson considers in detail the autobiographical accounts of two other supposed sufferers, namely Timothy Rogers and Samuel Johnson. The latter defined Melancholy in his dictionary as “a kind of madness, in which the mind is always fixed on one object.” (Shakespeare, incidentally, was also considered afflicted by the careful and critical Sir Aubrey Lewis on the basis of the sonnets. A “heartfelt utterance of shame and self-disgust” was thought to be expressed in sonnets 110 and 111 to be distinguished from the “contrived woe” of sonnet 66).

The Nineteenth Century to the Present

In the nineteenth and twentieth centuries we reach more familiar ground. The fresh insights which Jackson’s work provides show that Rush departed from his contemporaries in both terminology and concepts. He advocated a theory of an excited cardiovascular system which he derived from Cullen who had previously abandoned it. Jackson reaffirms the central place of Pinel, whose 1801 scheme of mental disorders comprised the quartet of mania, melancholia, dementia and idiotism. Pinel’s use of the term “mania” reflected the understood meaning of his time but must not obscure the fact that he obviously recognized the manic component (in present-day terminology) commenting: “sometimes it is distinguished by an exulted sentiment of self-importance, associated with chimerical pretensions to unbounded power or inexhaustible riches.” Esquirol, the pupil of Pinel, introduced the term monomania to denote any form of insanity “in which the delirium is partial, permanent, gay or sad.” It is to Griesinger that we owe both the use of the word depression in a technical psychiatric sense and the concept of the unitary psychosis (Einheitspsychose) currently being resuscitated by British workers. His views on an organic pathology were far more sophisticated and less dogmatic than many think. Others receiving mention include Tuke, Bucknill, Maudsley, Krafft-Ebing, Mercier and Savage.

Kraepelin’s name is given primacy at the start of the chapter on the twentieth century which is just since his views have continued to hold influence to the present day. Adolf Meyer, Freud and others take us up to DSM-III and our current preoccupations.

The book’s concluding sections comprise a thoughtful discussion of the relationships of melancholia to mania, hypochondriasis, grief and religion; accounts of three variants of the syndrome, namely, lycanthropy, love and nostalgia, (none of which have yet appeared in DSM formulations); and an overview and afterthoughts.

The Value of History

Many, preoccupied with the minutiae of advancing technology, will be impatient with an exploration of the ideas of bygone years; some may even be suspicious — remarking that whilst God cannot change the past historians can. But this book clearly exemplifies the values of an historical approach.

First, the volume shows, through quotations of the various authors across two millennia, that melancholia or depression is an enduring and recognizable clinical entity surviving all translations and known as far back as recorded history will take us. It is a biological phenomenon capable of description, and remarkably consistent in its main features. To regard it as a professional construct or a mode of behavior imposed by society or physicians, as some of the more outre* and otiose sociological and Marxist theories profess, is to adopt a viewpoint of marginal and tangential significance.

Second, not only has the notion survived down the centuries but it is equally evident that it has occurred in all cultures where there are adequate records. It has affected ancient Greeks, monks in Egyptian monasteries, medieval Englishmen and modern Americans.

A third value of chronicling the past is, one hopes, the encouragement of humility in those who espouse particular causes and/or treatments.

Fourth, the story of melancholia displays beautifully the four perspectives of psychiatry enunciated by McHugh and Slavney. It can be a disease, a temperament, a learned form of behavior, and, in all cases, an individual’s life story.

Fifth, it directs us to look carefully at our current approach to nosology. The strength of the Kraepelinian view was to base disease distinctions on carefully observed natural histories. The psychoanalytical approach on the other hand introduced interpretation which influenced DSM-I and -II to be replaced by the operational criteria provided in DSM-III. Now that we have improved reliability surely the next step in nosology is empirical biological validation rather than committee reviews of the literature. Science should proceed from individual studies which can be replicated rather than consensus and democratic opinion. One has a rising anxiety, not yet of DSM-III proportions, that we are currently in danger of allotting vast amounts of money and human effort to an enterprise where the shifting sands of categorization are determined by political process (cf. the pre-menstmal syndrome) and not by scientific method. Further whilst DSM-III and III-R gave us a more reliable vocabulary, frequent repetition of the undertaking may be self-defeating. The case has been well argued by Zimmerman. In fact committee confusion and conflation of conflicting concepts are evident in the DSM-IH-R definition of delusions — the veritable keystone of psychopathology — a matter lucidly exposed by Manfred Spitzer. It would logically follow, as cogently argued by Costello, that such careful examination of symptoms may be more fruitful than constantly changing the syndromes.

At the end, an exemplary volume such as Jackson’s reminds all of us engaged in day-to-day practice or research that from time to time it is imperative to stand back and look at the subject from afar. This is the final message of the historical approach. It should ensure that our broader objectives are sensible and worthwhile, and that our energies are channelled in the most appropriate way to the elucidation and alleviation of suffering in our patients. Dr. Jackson’s excellent exegesis provides a scholarly and even-tempered survey for our future guidance.

J. Montplaisir and R. Godbout

New York: Oxford University Press, 240 pp., 1991

The editors are to be congratulated for assembling a collection of important papers by key Canadian and U.S. contributors dealing with fundamental mechanisms involved in biologic rhythms and sleep and their applications to psychiatry. This volume is a record of the proceedings of the Tenth Symposium of the Centre de Recherches en Science Neurologiques and the Departement de Psychiatrie of the Universite de Montreal.

The first part of the book is devoted to biologic rhythms. Robert Moore provides a brief overview of the role of the supra-chiasmatic nucleus (SCN) and its influence on circadian sleep-wake behavior. This theme is expanded by Benjamin Rusak who describes a complex hierarchical feedback model of photic and nonphotic behavioral oscillators that are linked to the SCN and circadian functions. Roger Broughton and colleagues briefly summarize aspects of the chronobiology of sleep. They focus attention on their studies of the extended sleep paradigm that indicate 24, 12, 3-4, and 1.5-2 hour periodicities in the human sleep-wake rhythm. Thomas Wehr’s chapter provides a superb detailed review of the reciprocal influences of sleep-wake physiology on affective disorders. The chapter by Charles Czeisler and associates on the use of a time isolation facility to measure human physiologic aspects of the endogenous circadian pace maker is followed by Lewy and colleagues’ review of their work on the influence of bright light on melatonin secretion and the light-dark cycle in patients with winter depression. This section on biologic rhythms concludes with Michael Terman and David Schlager’s description of a novel apparatus that simulates naturally graded dawn twilight exposures of light in treating winter depression.

The second part of the book on sleep follows the same format as the first part. The initial two chapters by Robert McCarley, and by Mircea Steriade and Denis Pare, detail descriptions of brainstem electrophysiologic and neurotransmitter mechanisms in rapid eye movement sleep in animals and possible implications for dreaming. James Krueger and colleagues provide an excellent brief overview of endogenous sleep neuro-modulating substances that involve aspects of the immune and neuroendocrine systems. Psychophysiologic features of sleep and wakefulness in chronic insomnia and the effects of hypnotics on sleep and waking cognitive function are reviewed by Wallace Mendelson. The final chapter by Roger Godbout, Jacques Montplaisir and associates addresses the purported mechanisms and current treatments of periodic movements in sleep and restless legs syndrome and narcolepsy.

The book suffers from the expected unevenness in presentations and overlap between chapters that characterize published proceedings of meetings. But students of the neurosciences and clinicians interested in key contemporary concepts in biologic psychiatry will find this a useful overview of the implications of chronobiology and sleep-wake physiology for fundamental behavioral states, affective and some sleep-related disorders.

S.W. Hurt, M. Reznikoff, J.F. Clarking

New York: Brunner/Mazel Publishers, 506 pp., 1991

This book begins with an overview of psychological testing. It establishes perspective by regarding the historical role of assessment in the general field of mental health. It first presents the history of the psychological testing movement, reviews the development of the American Psychiatric Association Diagnostic and Statistical manuals, and then relates the two. The remainder of the book is organized according to the DSM-III-R manual, discussing first the Axis-I disorders focussing on the disorders of infancy, childhood and adolescence, the schizophrenias, major affective disorders, anxiety disorders, and adjustment disorders, and then Axis-II disorders focussing primarily on paranoid, borderline, and narcissistic personality disorders.

The book uses the case method as a vehicle for teaching psychological assessment, and describes ways in which these assessment results might be analyzed, interpreted, and applied to treatment planning. It will be of particular interest for the student of clinical psychology who is attempting to acquire assessment skills that are relevant and applicable in the clinical situation. The book, while of interest to others in the mental health field, will probably not be as relevant as it is to the clinical psychologist. Those in other mental health disciplines, such as psychiatric nursing, psychiatry, and occupational therapy, would also be interested in this book since it offers a clear discussion of psychological assessment. However, the detail of its coverage would preclude its general use for these disciplines.

This book bridges a gap which has been present for many years in clinical application of psychological assessment. There is concern among members of the health care team that clinical psychology assessments do not go far enough in aiding the treatment team to generate an effective treatment plan This book enables the clinical psychologist to extend his/her capabilities and be better able to make significant input into the treatment planning process, aiding the team to make a useful plan.

In summary, this book is well written, readable, and important, especially in the area of training of clinical psychologists to provide more relevant, effective, and applicable assessment of psychiatric patients.