Posts Tagged ‘serotonin’

Biology of Schizophrenia and Affective Disease

Biology of Schizophrenia and Affective Disease

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.

Akathisia and Restless Legs

Akathisia and Restless Legs

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.

Serotonin in the Central Nervous System and Periphery

Serotonin in the Central Nervous System and Periphery

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.

Novel Antipsychotic Drugs

Novel Antipsychotic Drugs

H. Y. Meltzer

New York, NY: Raven Press, 288 pp., 1992

Traditionally, the development of antipsychotic drugs has entailed looking for agents that produced catalepsy and blocked amphetamine-induced stereotypic movements in rodents. This produced a generation of drugs that were therapeutically antipsychotic but produced unacceptably high rates of neurological adverse effects. The atypical antipsychotics are a new generation of drugs that, through novel pharmacological properties, promise a lower rate of extrapyramidal side-effects and, in some cases, therapeutic superiority over the typical agents.

This volume, edited by psychiatrist and psychopharmacologist Herbert Meltzer, represents the proceedings of a symposium held in late 1990 which detailed the atypical agents being developed. For the most part, the volume is a status report on agents in various stages of development. These include clozapine and the related drug amperozide, the substituted benzamides remoxipride and raclopride, a number of dopamine agonists; drugs that mediate glutamine, “sigma” receptor antagonists, and serotonin antagonists such as respiridone and ondansetron. There are also three conceptual articles: Meltzer’s review of research into the efficacy and favorable extrapyramidal side-effect profile of clozapine, Philip Seeman’s review of receptor selectivities, which unfortunately predates the work on the D4 receptor, and Daniel Casey’s review of classification and directions for future research.

Although some of the articles appear to have been updated with material and references more recent than 1990, most of the book suffers from being a step out of date. Despite this, I found the volume more helpful than I anticipated, particularly the articles by Casey and Meltzer. This volume may be most significant as a historical work, since it heralds a welcome turning point in the pharmacotherapy of schizophrenia. For the first time, there is the promise of agents that offer novel therapeutic profiles, without the disabling neurologic effects we and our patients have had to learn to live with. Not only do these agents offer optimism, they also lead us to new models of pathophysiology for understanding schizophrenia and related disorders.

Headache and Depression: Serotonin Pathways as a Common Clue

Headache and Depression: Serotonin Pathways as a Common Clue

G. Nappi, G. Bono, G. Sandrini, G. Micieli

New York, NY: Raven Press, 345 pp., 1991

Serotonin (5-HT) is an ubiquitous substance, found throughout the body, which has become a common focus of interest for psychiatrists, neurologists and neuroscientists. Although originally discovered in the 1930s and isolated in 1948, only in the past decade has it caught the imagination of clinicians and basic scientists, particularly those exploring the basis of behaviour, mood, pain and headaches. The secret of how such a simple chemical substance could have such a variety of different physiological effects resides in the various kinds of serotonin receptors which are found in different tissues and organs.

This book examines the role of serotonin in depression, headaches and related conditions. The editors are all from Italy, where much research into serotonin has been conducted, but they have enlisted authorities from around the world to add chapters on their own fields.

The chapters vary in quality, but some contain excellent reviews and new material to which I will refer frequently. Feniuk and Humphrey give a nearly up-to-date account of 5-HT receptors. Since this book was published, they have added to the research on receptors, which is advancing at a furious pace. Edvinson describes the particular receptors involved in the cranial circulation. Sicuteri has written an excellent review of the role of serotonin pathways in headaches, and Cassano and Marazitti, its role in depression. The subject of chronic daily headaches is presented by Mathew. The possible role of serotonin and neuroendocrine factors in this condition and in cluster headaches are explored by several authors.

The role of serotonin in migraines is extremely complex. IV 5-HT can both precipitate and relieve migraine headaches. Blockage of serotonin synthesis can cause a panalgesia syndrome. While reserpine-induced serotonin depletion in platelets is associated with the precipitation of acute headaches, there is a reduction in migraine attacks during the subsequent month while serotonin is slowly restored. Certain 5-HT receptor agonists precipitate headaches in people who suffer from migraines, while most relieve acute attacks. The answer may be found in receptor specificity, with 5-HT-ID agonists generally relieving migraines. 5-HT-2 antagonists are used as prophylactic agents for migraines. Clearly, there is still much to be learned in this field.

In the case of mood disorders, the situation is even less clear. Both high and low levels of serotonin activity have been found in patients with depression. Again, the receptors may hold the key. 5-HT-2 receptors seem to be important in depression, while anxiety is related to 5-HT-l receptor activity. Up and down regulation of receptors are likely responsible for depression and the effects of antidepressive medications.

In trying to untangle this complex scheme, one may be forgiven for concluding that the only common factor in headaches, depression and serotonin perturbation is the nervous system itself.

I found many of the chapters on topics that were somewhat outside the main theme of the book to be very interesting. Chazot, from Lyon, reports on their experience with pinealectomized patients who have headaches and depression, presumably as a result of the loss of melotonin, which is metabolized to serotonin. Melotonin may also play a role in some features of cluster headaches. Studies in chronobiology may give new insights into the basis of mood disorders, cluster headaches and perhaps even migraines. Serotonin is undoubtedly involved as well in these cyclic conditions. It is less clear whether or not it is involved in menstrual syndromes, but headaches and depression are often part of premenstrual syndrome. There are several chapters in the book on this subject.

The book would have been of greater value to the casual reader had the editor added a concluding chapter summarizing the information. Nevertheless, this book provides a wealth of information on serotonin, depression and headaches, but only those who are specifically interested in the topics covered will find it worth the price of $130.00. However, I recommend it to psychiatrists who wish to have up-to-date information on some of the biochemical bases and the mechanisms of current therapeutic agents for treating depression. Headache specialists and behavioral neurologists may also find it useful. It will be of less interest to others in the profession.

Selective Serotonin Reuptake Inhibitors

Selective Serotonin Reuptake Inhibitors

J.P. Feighner and W.F. Boyer

Toronto, ON: John Wiley and Sons, 168 pp, 1991

In the past five years, there has been the appearance and use of new antidepressants called specific serotonin reuptake inhibitors. Dr. J.P. Feighner and Dr. W.F. Boyer, who are leading authorities and world respected clinicians, have conducted many clinical drug trials using these drugs. They have written a complete review of these drugs, which is now available in book form.

Specific serotonin reuptake inhibitors have been found to be effective in major depressive illness, panic disorder, obsessive compulsive disorder and bulimia, as well as other indications. These drugs are extremely powerful and should be used with an understanding of their indications and side-effect profile. To properly use these drugs, an understanding of the neuropharmacology of serotonin in the nervous system is essential.

Chapter 1 covers the neuropharmacology of serotonin in the central nervous system and gives a complete and detailed review of the theory, literature and latest information on what is known as the serotonin system. Dr. Marsden does this extremely well and in a very clear, concise manner.

In Chapter 2, there is a complete review of the pharmacological properties of SSRIs in the literature on animals.

Dr. Boyer and Dr. Feighner, in Chapter 3, explain why the serotonin hypothesis is necessary but not sufficient to explain some psychiatric disorders. This is done in a very easy-to-read and logical way. Even novices to the serotonin neurotransmitter system hypothesis can understand the basic foundations of this hypothesis.

Chapter 4 details the pharmacokinetics and drug interactions of the SSRIs. This is very useful as a reference work for cases where there are some untoward interactions in clinical practice.

The remaining chapters show the efficacy of the selective serotonin reuptake inhibitors in depression, panic disorder, generalized anxiety, obsessive compulsive disorder as well as other indications. These are very well documented with the appropriate studies and thus are a very useful reference source for anyone who is interested in more detailed studies of these indications.

The side-effects of the SSRIs are reviewed in detail in Chapter 8. Chapter 9 describes the clinical experiences of Drs. Boyer, McFadden and Feighner in the use of these agents. They have a great deal of valuable clinical experience.

As well, there is an interesting subchapter on combination treatment which is important in the treatment of resistant patients.

The book is a concise and useful distillation of the state of the art in the use of SSRIs. I recommend this book for any practising psychiatrists who want to help their patients with this most modern treatment in a safe and effective way. It has my highest recommendation for both its practical and academic aspects.

The Role of Serotonin in Psychiatric Disorders

The Role of Serotonin in Psychiatric Disorders

Serena-Lynn Brown, Herman M. Van Praag

New York, NY: Brunner/Mazel Publishers, 349 pp., 1991

I have had the pleasure of reviewing a wonderful book which reviews the state of the art of The Role of Serotonin in Psychiatric Disorders. This book is extremely well arranged and easy to read.

Psychiatrists and physicians who have forgotten their basic neurochemistry are gently reintroduced to it in the introductory chapter. The book is then divided into two major sections. The first one, is a complete review of the present state of the art in the neurochemistry of Serotonin and Serotonin Receptors. The second section is a chapter by chapter review of the role of serotonin in different psychiatric disorders.

These disorders range from anxiety, depression to schizophrenia, obsessive compulsive disorder, aggression, bulimia and disorders of childhood.

This book is well written and the references are all clearly documented for those who wish to pursue their topic in more detail.

I would strongly recommend this book as must reading for any physician who treats any type of psychiatric disorder. A final but important comment is that the price is extremely reasonable for such a wealth of information.