To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
This volume presents up-to-date, comprehensive and high quality reviews of the psychopharmacological evidence-base for each of the major psychiatric disorders, written by expert psychopharmacologists from around the world. Building on the success of the first edition, the volume summarizes the wealth of new developments in the field and sets them within the context of day-to-day clinical practice. All chapters have been fully updated and new contributions on personality disorders and substance dependence added. Each chapter provides information about optimal first line pharmacological interventions, maintenance pharmacotherapy and the management of treatment-refractory patients. The content is organized according to the DSM-V listing of psychiatric disorders, and covers all major conditions including schizophrenia, mood disorders, anxiety disorders, eating disorders and Alzheimer's disorder. These issues lie at the heart of clinical psychopharmacology, making this book invaluable to all practising and trainee clinicians, in a mental health setting or a less specialised environment.
Pharmacogenetics and pharmacogenomics are areas of significant importance at the interface of molecular genetics and psychopharmacology, with implications for drug development and clinical practice. This 2002 book provides a conceptual framework for understanding and studying the pharmacogenetics of psychotropic drugs, reviews advances in the field, and describes the established findings. Coverage extends to antipsychotics, antidepressants, mood stabilising, cognitive-enhancing and anxiolytic drugs. Chapters also examine the interface of pharmacogenetics with substance dependence and brain imaging, and consider its impact on the biotechnology and pharmaceutical industries. This book defines the young field of pharmacogenetics as it applies to psychotropic drugs, and is therefore of interest to all clinicians and researchers working in this field.
This chapter serves as a general introduction to psychopharmacogenetics and to the topics covered in this book, which provides the researcher and clinician with an overview of the pivotal topics in psychopharmacogenetics. For much of its history, the focus of pharmacogenetics has been on drug-metabolizing enzymes. This was because of the availability of techniques to detect phenotypic differences between individuals in the plasma level of drugs and to study their genetic basis. The chapter focuses on the methodological issues in pharmacogenetic research design. The interface between psychopharmacology and molecular genetics is already a focus of considerable research activity and this is likely to intensify as anticipated technological advances provide the tools for even more sophisticated studies. It may take longer than originally thought, but ultimately pharmacogenetics and pharmacogenomics will revolutionize the field of clinical psychopharmacology and the development of psychotropic drugs.
Specific psychotropic drugs and disorders
Ronnen H. Segman, Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel,
Bernard Lerer, Department of Psychiatry, Hadassah-Hebrew University Medical Center, Jerusalem, Israel
Bernard Lerer, Hadassah-Hebrew Medical Center, Jerusalem
Tardive dyskinesia (TD) affects about one fifth of schizophrenia patients following chronic exposure to dopamine receptor antagonist drugs. Drug- and patient-related risk factors for the development of TD have received much research attention but appear to predict only a minor part of the variance in the incidence of TD. This chapter reviews this rapidly developing field, incorporating recently available molecular genetic tools for a renewed exploration of the biological basis of TD. Genes coding for known drug targets can be directly explored for involvement in TD susceptibility. Genetic variability in dopamine receptors may predict functional differences in response patterns to neuroleptic agents and may be relevant to the expression of idiosyncratic reactions. Other promising findings, including the reported associations with 5-HT2A receptor (5-HTR2A) and 5-HTR2C and manganese superoxide dismutase (MnSOD) genetic polymorphic sites, require independent replications.