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	<title>Psychiatry / Neurology Book Reviews &#187; anxiety</title>
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	<link>http://psychiatry.com.ua</link>
	<description>The book reviews provides critical synopses of medical literature in three categories: brief or extended reviews of recently published books and reviews of books that are of historical interest.</description>
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		<title>Les troubles anxieux</title>
		<link>http://psychiatry.com.ua/index.php/psychiatry/les-troubles-anxieux#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
		<comments>http://psychiatry.com.ua/index.php/psychiatry/les-troubles-anxieux#comments</comments>
		<pubDate>Tue, 29 Dec 2009 05:13:02 +0000</pubDate>
		<dc:creator>Canadian</dc:creator>
				<category><![CDATA[Psychiatry]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[anxiety disorders]]></category>
		<category><![CDATA[mental health]]></category>
		<category><![CDATA[obsessive-compulsive disorder]]></category>

		<guid isPermaLink="false">http://psychiatry.com.ua/?p=635</guid>
		<description><![CDATA[Les troubles anxieux : approche cognitive et comportementale
Ladouceur R, Marchand A, Bois-vert J, editors
Montreal: Gaetan Morin Editeur; 1999. 213 pp
ISBN 2-89105-736-8 (paper)
This book addresses anxiety disorders and their treatment with cognitive-behaviour therapy. Each of the 6 chapters, coauthored by 1 of the 3 main authors, covers a different anxiety disorder The authors (Robert Ladouceur of [...]]]></description>
			<content:encoded><![CDATA[<p>Les troubles anxieux : approche cognitive et comportementale</p>
<p>Ladouceur R, Marchand A, Bois-vert J, editors</p>
<p>Montreal: Gaetan Morin Editeur; 1999. 213 pp</p>
<p>ISBN 2-89105-736-8 (paper)</p>
<p>This book addresses <strong>anxiety disorders</strong> and their treatment with cognitive-behaviour therapy. Each of the 6 chapters, coauthored by 1 of the 3 main authors, covers a different <strong>anxiety disorder</strong> The authors (Robert Ladouceur of Université Laval, André Marchand of Université du Québec a Montréal and Jean-Marie Boisvert of Université Laval) are renowned researchers and have considerable international reputations. Several chapter coauthors are also well-known in their areas of expertise (e.g., Michel Dugas in generalized <strong>anxiety disorders</strong>, and Mark Freeston in <strong>obsessive-compulsive disorders</strong>, among others).</p>
<p>The introduction details the theories, the difference between normal and abnormal <strong>anxiety</strong>, the different causes of <strong>anxiety</strong> and finally, the outline of the book. The content of each chapter follows somewhat the same format: a review of diagnostic criteria, a clinical description, prevalence and precipitating factors and comorbidity. Then, evaluation and rating scales for each specific disorder are reviewed. Finally, theoretical models of etiology and therapeutic strategies are discussed.</p>
<p>The authors review the current literature well, and research avenues to be pursued are also elicited. Several chapters have extended clinical examples of therapeutic techniques and detail the objectives and content of therapeutic sessions.</p>
<p>Some chapters — for example the one on generalized <strong>anxiety disorder</strong> — also propose some very innovative models of explanation of the disorder. Obviously, these proposals are in accordance with cognitive-behavioural therapy theory.</p>
<p>This book is manifestly meant for <strong>mental health</strong> professionals who do cognitive-behaviour therapy with patients suffering from <strong>anxiety disorders</strong>. Psychologists, <strong>psychiatrists</strong>, family physicians, social workers and others who feel a need to better understand cognitive-behaviour therapy will also find this book very helpful.</p>
<p>Because it is written in French with a North American flavour, it will be popular with French-speaking Canadians and in Europe where several of the coauthors are very well known. It should be of interest to all <strong>psychiatrists</strong> and clinicians who see patients with <strong>anxiety disorders</strong> in consultations and are aware from the literature of cognitive-behavioural therapy&#8217;s encouraging results.</p>
<p>This is an excellent multiauthored book which reviews the up-to-date theories and therapeutic approaches for the treatment of <strong>anxiety disorders</strong> within a cognitive-behavioural framework. It is clearly written and readable by all health professionals. The format and presentation make it an agreeable work to consult. Finally, because it is so well documented, it could well become a very useful work of reference in the French literature.</p>
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		<item>
		<title>A Primer of Supportive Psychotherapy</title>
		<link>http://psychiatry.com.ua/index.php/psychotherapy/a-primer-of-supportive-psychotherapy#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
		<comments>http://psychiatry.com.ua/index.php/psychotherapy/a-primer-of-supportive-psychotherapy#comments</comments>
		<pubDate>Sat, 12 Dec 2009 04:27:22 +0000</pubDate>
		<dc:creator>Canadian</dc:creator>
				<category><![CDATA[Psychotherapy]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[mental disorders]]></category>
		<category><![CDATA[mental health]]></category>
		<category><![CDATA[obsessive-compulsive disorder]]></category>
		<category><![CDATA[panic]]></category>

		<guid isPermaLink="false">http://psychiatry.com.ua/?p=586</guid>
		<description><![CDATA[A Primer of Supportive Psychotherapy
Pinsker H
Hillsdale (NJ): The  Analytic Press; 1997. 278 pp. with index
ISBN 0-88163-274-0  (cloth)
Convincing evidence  has accumulated that the supportive or nonspecific component, common to most  forms of psychotherapy, is  responsible for most of the change that results from psychotherapeutic  interventions. This component appears to be [...]]]></description>
			<content:encoded><![CDATA[<p>A Primer of Supportive Psychotherapy</p>
<p>Pinsker H</p>
<p>Hillsdale (NJ): The  Analytic Press; 1997. 278 pp. with index</p>
<p>ISBN 0-88163-274-0  (cloth)</p>
<p>Convincing evidence  has accumulated that the supportive or nonspecific component, common to most  forms of <strong>psychotherapy</strong>, is  responsible for most of the change that results from psychotherapeutic  interventions. This component appears to be both supportive — in that it is derived from the quality  of the therapeutic relationship — and technical — in that it stems from the  contract established with the patient and the use of nonspecific interventions.  Specific interventions drawn from different schools of thought account for  surprisingly little of the variance in outcome for most disorders, with the  possible exceptions of <strong>panic</strong> and <strong>obsessive-compulsive disorders</strong>. The  implications of these findings are clear. All <strong>mental health</strong> clinicians, regardless of their field, should be well  versed in nonspecific interventions, and clinical training should emphasize  integrated or so-called transtheoretical perspectives. Unfortunately, both  practice and training tend to lag behind research. Many clinicians continue to  rely on specific psychotherapeutic models, and training rarely gives  nonspecific interventions the weight that they deserve, although there is some  evidence that this is changing.</p>
<p>In this context, Dr.  Pinsker&#8217;s very practical little volume is a useful addition to the growing  number of texts on supportive therapy. Although one might disagree with some of  the ideas and with the theoretical model that lies behind the volume, one must  agree with the tone. This is the work of a sensitive and humane clinician who  respects his patients. The approach emphasizes a conversational style and a  responsive approach, rather than listening silently or interrogating the  patient. The volume offers a model worth emulating. Anyone who adheres to the  spirit of this work will not go far wrong, nor will his or her patients come to  harm.</p>
<p>The value of this  work lies in the large number of examples of the kinds of statements patients  typically make and the clinician&#8217;s possible responses. The topics discussed  include most of the key issues in therapy: increasing self-esteem, reducing and  preventing <strong>anxiety</strong>, promoting  adaptive skills, building a treatment alliance, and so on. These topics are  explored through specific examples that include illustrations of helpful and  less helpful responses that therapists may make. It is these examples that make  this book especially helpful as an introductory text. Here is an experienced  clinician talking in a common-sense way about the nuts and bolts of therapy.  This makes for a style that is at times a little dull but replete with clinical  wisdom. The simple practical examples will be helpful to a neophyte clinician  who is learning how to conduct assessment and therapy interviews. They may also  be worth a brief perusal by those who are much more experienced, who may be  surprised to recognize bad habits unwittingly accumulated over the years.</p>
<p>The volume is not  without limitations. Two issues are worthy of comment. First, some of the  examples are a little sparse, and the discussion of alternative responses by  the clinician is a little limited. Hence, the implications of the different  possible therapist responses may not always be clear to the beginning  therapist. More problematic is the theoretical perspective that runs through  the volume. This is classically psychodynamic; hence, much is made of the  distinction between supportive and expressive therapy. With increasing emphasis  on integrated approaches, this distinction is less important. It may also be a  little dated. The problem emerges on the first page when supportive therapy is  differentiated from expressive therapy in terms of technical considerations.  These are defined as using a conversational style, viewing the  patient-therapist relationship as a real relationship that is not analysed, and  supporting defences that are not maladaptive. Perhaps the important issue is  not the distinction between supportive and exploratory therapy — which is important only to those who  espouse the psychoanalytic tradition — but rather the degree of intrusiveness  and the extent to which generic mechanisms are used to effect change. Dr.  Pinsker describes these clearly, although in different terms. Consequently, it  is easy to put theoretical issues to one side and concentrate on the practical  component of the book. In this regard, the volume meets its goal of being a is  a useful primer.</p>
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		<item>
		<title>Handbook of Behavioral State Control</title>
		<link>http://psychiatry.com.ua/index.php/neurology/handbook-of-behavioral-state-control#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
		<comments>http://psychiatry.com.ua/index.php/neurology/handbook-of-behavioral-state-control#comments</comments>
		<pubDate>Fri, 04 Dec 2009 04:06:43 +0000</pubDate>
		<dc:creator>Old Physician</dc:creator>
				<category><![CDATA[Neurology]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[depression]]></category>
		<category><![CDATA[neurologists]]></category>
		<category><![CDATA[neuropsychiatric disorders]]></category>
		<category><![CDATA[neuropsychologists]]></category>
		<category><![CDATA[panic]]></category>

		<guid isPermaLink="false">http://psychiatry.com.ua/?p=562</guid>
		<description><![CDATA[Handbook of Behavioral State Control: Cellular and Molecular Mechanisms
Lydic R, Baghdoyan  HA, editors
Boca Raton (FL): CRC  Press LLC; 1999. 700 pp. with index
ISBN 0-8493-3151-X  (hard cover)
Although one may  argue that any change in neuronal activity may ultimately lead to behavioural  alterations, a closer relation between single cell function and behavioural [...]]]></description>
			<content:encoded><![CDATA[<p>Handbook of Behavioral State Control: Cellular and Molecular Mechanisms</p>
<p>Lydic R, Baghdoyan  HA, editors</p>
<p>Boca Raton (FL): CRC  Press LLC; 1999. 700 pp. with index</p>
<p>ISBN 0-8493-3151-X  (hard cover)</p>
<p>Although one may  argue that any change in neuronal activity may ultimately lead to behavioural  alterations, a closer relation between single cell function and behavioural  consequences is needed. This relation is complex, and there are numerous and  inter-related regulatory levels between cellular/molecular processes and  behavioural outcome. It is therefore not surprising that there is a remarkable  lack of exhaustive textbooks that explain cellular mechanisms underlying  behavioural activity more globally. This book, edited by Lydic and Boghdoyan,  both from Pennsylvania State University, partially fills this gap. It is a  carefully planned handbook divided into 38 chapters organized in 8 sections,  and written by 95 authors. The book&#8217;s major goal is to provide updated material  on the cellular and molecular mechanisms generating diverse behavioural states.  The authors do not explain cellular mechanisms of particular behaviours but  rather provide information about the neural processes that regulate behavioural  states, such as sleep, wakefulness, consciousness, arousal, etc. Different  behavioural states, in turn, determine a subset of possible behavioural  outcomes. The dominating theme of the book is sleep, wakefulness, arousal, and  vigilance; this theme is compatible with the research interest and experience  of the editors in the neurobiology of sleep mechanisms.</p>
<p>The handbook represents  a working reference for numerous topics relating to physiological,  psychological and pathophysiological states, including information on  epidemiology, diagnosis, and treatment of common state disorders. The chapters  in the first section discuss mammalian circadian rhythms, structure and  function of the suprachiasmatic nuclei, melatonin rhythm-generation systems,  and genetic circadian clock mechanisms. The subsequent chapters of the second  section describe daily alterations in the arousal state, REM sleep dreaming,  NREM sleep mentation, and neurological disorders of sleep. Section 3 deals with  the anatomical substrate, neurochemical coding, and functional organization of  components of the ascending reticular activating system, which includes  ascending cholinergic, monoaminergic, and glutamatergic pathways. Particular  attention is paid to the mesopontine cholinergic system and its role in REM  sleep, wakefulness and cortical activation, and the noradrenergic and  serotonergic pathways and their role in sleep, wakefulness, regulation of motor  output and sensory information processing. The same systems are further  discussed in more detail in the next section. Successive chapters deal with  intrinsic membrane properties, synaptic activity, membrane current characteristics  and excitability of cholinergic, noradrenergic, and serotonergic neurons.  Particular attention is focused on the state-dependent cellular oscillations in  the corticothalamic system and on the rhythmic oscillations in the hippocampal  formation.</p>
<p>Mechanisms of  behavioural state control may be altered by centrally active drugs. Several  chapters in the section entitled &#8220;Molecules modulating mental state&#8221;  discuss this issue. Neuronal and neurochemical mediation of addictive  behaviour, and alterations in behavioural state caused by benzodiazepines,  barbiturates, ethanol, caffeine, nicotine, marijuana, and <strong>serotonin</strong> antagonists are discussed.</p>
<p>The following 2  sections of the handbook review the current knowledge regarding state-dependent  processing in somatosensory pathways and the role of the rostral ventromedial  medulla in regulating ascending sensory transmission. Several chapters of the  last 2 sections of the handbook deal with pathophysiological states. There is a  particular emphasis on pain sensation, anesthesia, pharmacological and surgical  treatment of pain, and immunological alterations in the arousal state. The  topics cover cytokines in sleep regulation, immune effects on  neurotransmission, and finally, body temperature, fever and microbial modulations  of arousal.</p>
<p>Although the textbook  covers vast areas of behavioural neuroscience, there are several important  areas that are not represented. Results of the vast research concerning  emotional states, such as <strong>anxiety</strong> or  fear, and relevant regulatory functions of the limbic structures are not  included. Also, psychopathological states of <strong>panic</strong>, <strong>depression</strong>, or  euphoria are not described, except in parts of one chapter about addictive  behaviour and neural mechanisms of reward. This topical selection was probably  necessary to keep the textbook at the manageable size.</p>
<p>The textbook is well  illustrated and contains overall 3500 references, more than 90 references per  chapter. The book may serve as an excellent resource for advanced undergraduate  and graduate students, postdoctoral fellows and biomedical researchers working  with animal models of neurological and <strong>neuropsychiatric  disorders</strong>. It will also be highly useful for medical residents, lecturers  in neuroscience courses, and other professionals interested in problems of  behavioural neuroscience and general neural principles governing animal and  human behaviour.</p>
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		</item>
		<item>
		<title>The Maudsley Handbook of Practical Psychiatry</title>
		<link>http://psychiatry.com.ua/index.php/psychiatry/the-maudsley-handbook-of-practical-psychiatry#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
		<comments>http://psychiatry.com.ua/index.php/psychiatry/the-maudsley-handbook-of-practical-psychiatry#comments</comments>
		<pubDate>Tue, 17 Nov 2009 04:43:05 +0000</pubDate>
		<dc:creator>Old Physician</dc:creator>
				<category><![CDATA[Psychiatry]]></category>
		<category><![CDATA[antidepressants]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[medications]]></category>
		<category><![CDATA[psychiatric disorders]]></category>

		<guid isPermaLink="false">http://psychiatry.com.ua/?p=508</guid>
		<description><![CDATA[The Maudsley Handbook of Practical Psychiatry, 3rd edition
D. Goldberg, editor
New York: Oxford  University Press; 1997
ISBN 0192628534 (hard  cover)
Often when residents  begin training in psychiatry there  is a great deal of anxiety,  particularly related to the first on-call experience. Most training in medical  school focuses on the skills used to [...]]]></description>
			<content:encoded><![CDATA[<p>The Maudsley Handbook of Practical Psychiatry, 3rd edition</p>
<p>D. Goldberg, editor</p>
<p>New York: Oxford  University Press; 1997</p>
<p>ISBN 0192628534 (hard  cover)</p>
<p>Often when residents  begin training in <strong>psychiatry</strong> there  is a great deal of <strong>anxiety</strong>,  particularly related to the first on-call experience. Most training in medical  school focuses on the skills used to take patient histories and conduct medical  examinations; these need to be modified when dealing with psychiatric patients.</p>
<p>Residents who have  been comfortable with the medical model are frequently unsure about how to  elicit information from patients with psychiatric difficulties. And most  introductory <strong>psychiatry</strong> textbooks  contain a great deal of factual information but do not provide practical  advice. The widely used <em>Synopsis of the Comprehensive Textbook of Psychiatry </em>by Kaplan and Saddock is an example of a work that began as a condensed  version of a larger textbook but has grown to such a size that there will soon  be a need for a synopsis of the <em>Synopsis of the Comprehensive Textbook.</em></p>
<p>In the <em>Maudsley  Handbook of Practical Psychiatry, </em>David Goldberg, director of medical  education at the Bethlehem Maudsley NHS Trust in London, has attempted to  provide a comprehensive yet accessible introductory textbook for residents as  they begin training. The book was developed in consultation with staff <strong>psychiatrists</strong> and house officers from  the Maudsley to ensure that the book meets the needs of house officers and  residents. It attempts to provide a comprehensive guide to psychiatric and neuropsychiatric  examinations and guidelines for the clinical management of common psychiatric  presentations in the emergency setting and in the early phases of treatment. It  is meant to be a guide for doctors beginning their training in <strong>psychiatry</strong> and for those preparing for  professional examinations, and although written in the United Kingdom, is  intended to be used elsewhere.</p>
<p>The structure of the  book reflects these objectives. There is a section on the psychiatric interview  and assessment, which includes the mental status examination as well as some  aspects of neuropsychiatric assessment. The section on early treatment is less  extensive and focuses primarily on the initial stages of management. There are  also sections on referring patients to specialists and on the medicolegal  issues related to <strong>psychiatry</strong> in the  UK.</p>
<p>The most valuable  section of the book is on interview and assessment; it provides practical  guidelines for the assessment of children, adults and geriatric patients.  Although written for the beginning trainee, a review of this section would be  valuable for residents preparing for their oral examinations. There are  well-written discussions of difficult situations in the interview setting, and  of issues such as gifts, disinhibited patients, violence and sexual involvement  with patients.</p>
<p>The issue of false  memory and repressed memory is certainly a controversial one in the field of <strong>psychiatry</strong>. This handbook provides one  of the better overviews of this area, discussing the evidence for repressed memory  and for concerns about false memory. Practical discussions about the impact of  these issues on the psychiatric interview are clear, as are discussions of  cross-cultural issues and their impact on the psychiatric assessment.</p>
<p>Unfortunately, other  sections of the book are not as helpful. The sections on medico-legal issues  are relevant largely to the UK. Although there is some interesting discussion  of such things as consent and hospitalization, these are presented within the  context of UK laws rather than in terms of general principles. The section on  referral is largely unhelpful in the Canadian context; many of the suggested  indications for specialist referral are in fact issues that residents are  directly involved with.</p>
<p>Because <strong>drug therapy</strong> evolves so rapidly, by the  time a book is in print, aspects of it are already out of date. This fact has  limited the usefulness of the section on early treatment. For example,  haloperidol is recommended for patients who present with acute psychosis, and  for patients who are unresponsive, treatment with chlorpromazine and clozapine  is recommended. Obviously, this does not take into account the impact of newer  atypical antipsychotic agents on the management of patients in the acute  treatment setting or in first-episode psychoses. There is even less discussion  of <strong>medication</strong> use, probably because  the goal of the book is to focus on early management, the assumption being that  residents will discuss the initiation of such treatments as <strong>antidepressant</strong> <strong>medication</strong> with a staff <strong>psychiatrist</strong>.  In many cases the treatment plans outlined are general, probably insufficient  to allay the <strong>anxiety</strong> of a beginning  resident, and lack sufficient complexity to be of use to a senior resident.</p>
<p>The final difficulty  I had with this book is related to one of its strengths. As noted above, there  is an unfortunate tendency in the medical field for handbooks and synopses to  rapidly balloon into tomes large enough that no hand could easily encircle  their girth. The <em>Maudsley Handbook </em>is in fact a book that could slip  quite comfortably into the pocket of a lab coat. Because of that, however, the  layout is very tight and the margins are small. This makes it difficult to find  things quickly when leafing through it. Breaks are not obvious and sections blend  together.</p>
<p>The <em>Maudsley  Handbook </em>is, I believe, a valuable introductory handbook in terms of its  discussion of the psychiatric interview and assessment. For this reason alone I  would recommend it for beginning residents and those preparing for their oral  examinations. It does not, however, live up to its billing as a provider of  extensive and practical management guidelines for a variety of psychiatric  conditions, and is limited by the fact that it is written primarily for the UK  audience, despite its claim to do otherwise.</p>
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		</item>
		<item>
		<title>The Neuropsychiatry of Limbic and Subcortical Disorders</title>
		<link>http://psychiatry.com.ua/index.php/neuropsychiatry/the-neuropsychiatry-of-limbic-and-subcortical-disorders#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
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		<pubDate>Sat, 14 Nov 2009 04:40:58 +0000</pubDate>
		<dc:creator>Old Physician</dc:creator>
				<category><![CDATA[Neuropsychiatry]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[epilepsy]]></category>
		<category><![CDATA[neurologists]]></category>
		<category><![CDATA[psychiatric disorders]]></category>
		<category><![CDATA[psychiatrists]]></category>

		<guid isPermaLink="false">http://psychiatry.com.ua/?p=516</guid>
		<description><![CDATA[The Neuropsychiatry of Limbic and Subcortical Disorders
Salloway S, Malloy P,  Cummings JL, editors
Washington (DC):  American Psychiatric Press; 1997. 217 pp with index
ISBN 0-88048-942-1  (cloth)
The limbic system is  a topic of considerable interest to both psychiatrists and neurologists. For biologically  oriented clinicians, one can barely go a week without encountering some [...]]]></description>
			<content:encoded><![CDATA[<p>The Neuropsychiatry of Limbic and Subcortical Disorders</p>
<p>Salloway S, Malloy P,  Cummings JL, editors</p>
<p>Washington (DC):  American Psychiatric Press; 1997. 217 pp with index</p>
<p>ISBN 0-88048-942-1  (cloth)</p>
<p>The limbic system is  a topic of considerable interest to both <strong>psychiatrists</strong> and <strong>neurologists</strong>. For biologically  oriented clinicians, one can barely go a week without encountering some  reference to a limbic disorder. The explosion of information about the  interconnectedness of various brain regions is forcing both practising clinicians  and neuroscientists to grapple with all brain regions, not just a favorite few.  Inevitably, one is confronted with the need to understand the function of the  limbic system. The definition of the limbic system has steadily broadened over  time to include not just the medial circuit of Papez, but structures that are  functionally associated with it. In common usage then, the term &#8220;limbic  system&#8221; speaks to a set of cognitive functions; these functions are  subserved by a network of cortical and subcortical structures.</p>
<p>In this spirit, <em>The  Neuropsychiatry of Limbic and Subcortical Disorders </em>represents a snapshot  of the state of knowledge of the limbic system. This book expands on the summer  1997 special issue of <em>The journal of Neuropsychiatry and Clinical Neurosciences </em>on the same topic. Published by the American Psychiatric Press, it is a  high-quality book at a reasonable price, with many colour figures and  photomicrographs.</p>
<p>This book is not an  easy introduction to the anatomy and function of the limbic system. As the  editors state in their introduction, &#8220;The essays in the volume cover a  broad range of basic and clinical material at various levels of difficulty. &#8230;  Some of the chapters present complex material requiring careful study and  perhaps a second reading.&#8221; This is not an understatement. The book is  divided into 2 sections: Anatomy and Neurochemistry, and Clinical Syndromes. It  is the first, more technical section that presents the most difficult material.  For neuroscientists familiar with the terminology, these chapters represent an  excellent resource. They are good summaries of the anatomical literature with  extensive references. Most chapters have 50 to 100 well-selected references,  though a few contain up to 300. There is an abundance of photomicrographs, many  of which have been previously published and retain an alphabet soup of  anatomical abbreviations. This may present a problem, primarily to the student  of behaviour wanting to learn more about the neural substrates.</p>
<p>If the anatomy  section suffers from over-inclusion of information, then the clinical section  suffers from a lack of rigour, and must be taken as hypothetical in many cases.  There are interesting ideas here, and the authors have put forth several  theories regarding the pathology of syndromes including temporal lobe <strong>epilepsy</strong>, emotional experience,  recovered memory and religious experience.</p>
<p>While many of the  chapters focus purely on the anatomical or clinical aspects of the limbic  system, a few successfully link anatomy and function. The chapter entitled  &#8220;Neurobiology of Fear Responses,&#8221; by Michael Davis, is a particularly  cogent exposition of the role of the amygdala in fear. This chapter,  appropriately positioned between the 2 major sections, introduces concepts such  as classical conditioning, and outlines the evidence from lesion and excitation  studies for the amgydala&#8217;s function. It is accessible to both anatomists and  behaviourists. The chapter entitled &#8220;The Neurobiology of Emotional  Experience,&#8221; by Kenneth Heilman, lucidly outlines several theories of  emotion, ultimately arriving at the modular theory. One version of the modular  theory states that emotions are mediated by anatomically distributed modular  networks, and it is the relative activation of these modules that gives rise to  the variety of human emotion. The location of the modules, of course, overlaps  with the limbic system. The chapter entitled &#8220;Limbic-Cortical  Dysregulation,&#8221; by Helen Mayberg, is an excellent exposition of a theory  of the functional organization of medial cortical and limbic structures. This  theory, based largely on human functional imaging (positron emission tomography  and functional magnetic resonance imaging), is quite successful in unifying  often contradictory studies regarding cingulate function. Finally, the chapter  by Koob and Nestler entitled &#8220;The Neurobiology of Drug Addiction&#8221; is  a good summary of the neural substrates that underlie reward behaviour, and how  drugs of abuse affect them.</p>
<p>All of the authors in  this book have published extensively in their fields. Consequently, most of the  material has appeared in other review articles. Nevertheless, it is convenient  to have the information all in one place, together with the colour  reproductions.</p>
<p>In a book that  juxtaposes both anatomical and syndromic chapters, it becomes painfully obvious  that our knowledge of brain wiring is fast outpacing our ability to describe  behaviour. A great deal is known about connectivity, neurotransmitters and gene  expression, but how can these be related to only a crude description of human  experience? Saver and Rabin, in their chapter on religious experience, offer  several convincing descriptions that would suggest that the mystical quality of  a religious experience is a manifestation of limbic activity, if not outright seizure  activity. While quite reductionist, it may even be true, but something is lost  in the characterization of the experience. It is no coincidence that virtually  every work of fiction is fundamentally concerned with &#8220;limbic  function.&#8221; The conclusions of all classical tragedies are known — it is the human experience that captures  our interest. When speaking about the function of the limbic system, one  quickly realizes that the putative functions, emotion, memory and motivation,  are difficult to describe, let alone quantify — hence, an unlimited supply of  literature. Unlike other cognitive functions such as perception, language and  motor behaviour, these limbic processes do not lend themselves easily to  experimentation.</p>
<p>Are these processes  unquantifiable? Perhaps the language is wrong. For example, <strong>anxiety</strong> is an emotion variously  localized to the limbic system. One can go to great lengths using different  rating scales to quantify the severity of <strong>anxiety</strong>,  but ultimately one relies upon individual interpretation of crude descriptions.  What if an emotion like <strong>anxiety</strong> were  compacted to a measure of probability? For example, &#8220;I feel like I&#8217;m going  to die,&#8221; represents the assignment of a non-zero probability to the  outcome of death. While the individual may know death is unlikely, it  nevertheless creates a situation of uncertainty: &#8220;I know I won&#8217;t die, but  then again, what if I do?&#8221; Measures of uncertainty, while not in the usual  parlance of emotion, do lend themselves to quantification, and ultimately correlation  with neural activity. Perhaps it is time for a shift in the description of  limbic behaviour. Only when these phenomena are accurately described will we be  able to relate them to brain function and dysfunction.</p>
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		<title>Akathisia and Restless Legs</title>
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		<pubDate>Tue, 20 Oct 2009 05:14:03 +0000</pubDate>
		<dc:creator>Canadian</dc:creator>
				<category><![CDATA[Neurology]]></category>
		<category><![CDATA[Psychiatry]]></category>
		<category><![CDATA[affective disorders]]></category>
		<category><![CDATA[antidepressants]]></category>
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		<category><![CDATA[anxiety disorders]]></category>
		<category><![CDATA[delirium]]></category>
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		<category><![CDATA[medications]]></category>
		<category><![CDATA[psychiatric disorders]]></category>
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		<description><![CDATA[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 [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Akathisia and Restless Legs</strong></p>
<p>P Sachdev</p>
<p>New York: Cambridge University Press; 1995. 425 p</p>
<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, <strong>pathophysiology</strong>, 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.</p>
<p>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 &#8220;akathisia&#8221; translated from its Greek root, however, means &#8220;not to sit&#8221; and was 1st used by Lad Haskovec in 1902. Ekbom introduced the term &#8220;restless legs syndrome (RLS)&#8221; in 1945 and described the most characteristic symptom of this disorder as &#8220;creeping or crawling sensations most frequently localized to the lower leg.&#8221; 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 <strong>medication</strong>.</p>
<p>Acute akathisia (AA) refers to akathisia that develops soon after the introduction of neuroleptic drugs; by contrast, <strong>tardive akathisia</strong> develops as a delayed side effect of long-term neuroleptic <strong>medication</strong>.</p>
<p>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, <strong>delirium</strong>, dementia, head injury, hypoglycemia, and RLS), and nonorganic <strong>psychiatric disorders</strong> (<strong>affective disorders</strong>, psychotic disorders, <strong>anxiety disorders</strong>, and childhood disorders like attention-deficit hyperactivity disorder).</p>
<p>The author distinguishes 2 aspects of restlessness — a motor (objective) component and a mental (subjective) component — and suggests a comprehensive operational definition.</p>
<p>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 <strong>neuroanatomy</strong> 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 <strong>delirium</strong>. Benzodiazepines are used quite extensively in the treatment of agitation, and a number of studies attest to their efficacy in some patients.</p>
<p>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 &#8220;the drug disagrees with me&#8221; and &#8220;I feel emotionally unresponsive&#8221; to neuroleptic noncompliance, <strong>anxiety</strong> and dere-alization, school and work avoidance, painful sensory symptoms, and even <strong>depression</strong>. The question of whether or not NID can also manifest as a cause of or contributor to <strong>depression</strong> is a controversial issue that remains to be resolved.</p>
<p>NID may result in a poor outcome, but while many NID patients become noncompliant, others benefit from dysphoria by negotiating with their <strong>psychiatrists</strong> for lower yet effective doses of neuroleptics, resulting in less severe EPS. The neurobiological basis of NID remains poorly understood.</p>
<p>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 <strong>tardive akathisia</strong>. 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, <strong>tardive akathisia</strong> should be diagnosed. Akathisia that continues for 3 mo or longer is considered to be chronic.</p>
<p>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 <strong>serotonin</strong> reuptake inhibitors, <strong>serotonin</strong> antagonists, heterocyclic <strong>antidepressants</strong>, anticonvulsants, calcium channel antagonists, and lithium carbonate.</p>
<p>There are no accurate estimates available as to the prevalence or incidence of <strong>tardive akathisia</strong>, 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 <strong>medication</strong>, 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.</p>
<p>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 <strong>suicide</strong>. 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.</p>
<p><strong>Tardive akathisia</strong> has not been universally accepted as a distinct syndrome. The phenomenological examination of patients on long-term neuroleptic <strong>medication</strong> suggests that <strong>tardive akathisia</strong> is distinct from <strong>tardive dyskinesia</strong>, with overlap between the 2. &#8220;Chronic,&#8221; in terms of describing akathisia, refers to the duration of the disorder, irrespective of the nature of onset, whereas &#8220;tardive&#8221; denotes a delayed onset.</p>
<p>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.</p>
<p>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. <strong>tardive akathisia</strong> and withdrawal akathisia have not been reported with nonneuroleptic drugs, suggesting that, unlike AA, they may be purely neuroleptic-related syndromes.</p>
<p>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 (<strong>ristanserin, amantadine, piracetam, tricyclic antidepressants, and sodium valproate</strong>). The treatment of <strong>tardive akathisia</strong> is, in general, unsatisfactory and the main emphasis should be on its prevention.</p>
<p>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.</p>
<p>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 <strong>psychiatrists</strong> and <strong>neurologists</strong>.</p>
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		<title>The Schedules for Clinical Assessment in Neuropsychiatry</title>
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		<pubDate>Sat, 03 Oct 2009 04:08:49 +0000</pubDate>
		<dc:creator>Old Physician</dc:creator>
				<category><![CDATA[Neurology]]></category>
		<category><![CDATA[Neuropsychiatry]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[mental disorders]]></category>
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		<description><![CDATA[The Schedules for Clinical Assessment in Neuropsychiatry. Version 2
Wing JK, chief editor
Geneva: World Health Organization—Division of Mental Health; 1994.331 p.
The Schedules for Clinical Assessment in Neuropsychiatry (SCAN) is a manual published by the World Health Organization designed to assess, measure, and classify the psycho-pathology and behavior associated with the major psychiatric syndromes of adult life. [...]]]></description>
			<content:encoded><![CDATA[<p><strong>The Schedules for Clinical Assessment in Neuropsychiatry. Version 2</strong></p>
<p><strong>Wing JK, chief editor</strong></p>
<p>Geneva: World Health Organization—Division of Mental Health; 1994.331 p.</p>
<p><em>The Schedules for Clinical Assessment in Neuropsychiatry </em>(SCAN) is a manual published by the World Health Organization designed to assess, measure, and classify the psycho-pathology and behavior associated with the major psychiatric syndromes of adult life. SCAN had its origins in the 9th edition of the <em>Present State Examination </em>(PSE 9). SCAN consists of 4 components: the 10th edition of the &#8220;Present State Examination&#8221; (PSE 10), the &#8220;Item Group Check List,&#8221; the &#8220;Clinical History Schedule,&#8221; and the &#8220;Glossary of Differential Definitions.&#8221; Only the first 3 were reviewed. The PSE 10, which forms the greater part of SCAN, covers phenomenology. The &#8220;Item Group Check List&#8221; is a method of obtaining information from case records and informants other than the patient himself or herself. The &#8220;Clinical History Schedule&#8221; is a method of checking or entering data relevant to the broader clinical and social history.</p>
<p>The PSE itemizes various domains and categories of psychopathology. For each phenomenological category an appropriate probe question is provided. The PSE does not give detailed definitions. These are contained in the &#8220;Glossary of Differential Definitions&#8221; which was unfortunately not available for review. This is regrettable since the SCAN can only be fully appreciated in the context of the glossary.</p>
<p>The SCAN is designed for epidemiological research rather than day-to-day clinical care. Data from the schedules are intended to be entered into a computer algorithm (C ATEGO-5) which processes the data. The output is a series of options including a range of profiles of symptoms, an index of definitions and ICD-10, and DSM-III-R diagnostic categories.</p>
<p>Interviewers who use SCAN must first address those factors that would interfere with access to psychopathology or indicate a need to adopt specific interview strategies. These include severe language disorders, cognitive impairment, severe behavioral disturbance, uncooperativeness, or the likelihood of a premature termination. The PSE 10 rating scales address various domains and categories of psychopathology. The domains contain overlapping phenomenological categories that can be confusing. For example, depersonalization and derealization, which are rightfully disturbances of perception, are also included in the domain of nervous tension. While this may be useful for research purposes and computerized programs, overlapping phenomenological categories muddy the analysis of the mental state. This is akin to describing motor weakness in a neurological patient within the domain of sensory changes. It is preferable to keep phenomenological categories within their rightful domains. Elicited psychopathology can then be extracted and linked together within the context of a biopsychosocial framework to reach a diagnosis.</p>
<p>The domains of the mental state identified by the PSE include: somatic symptoms, nervous tension, <strong>panic</strong>, <strong>anxiety</strong> and <strong>phobia</strong>, obsessional symptoms, depressed mood and ideation, thinking, concentration, energy and interests, body functions, eating disorders, expansive mood and ideation, alcohol and substance abuse, language difficulties, perceptual disorders other than hallucinations, hallucinations, subjectively described thought disorder and experience of replacement of will, delusions, cognitive impairment and/or decline, motor and behavioral phenomenology, observed affect, speech abnormalities, and social impairment.</p>
<p>SCAN contains a separate section for evaluating stress-causing acute reactions and posttraumatic stress disorders, the course of <strong>schizophrenia</strong> as described by either DSM-III-R or ICD-10, acute psychosis, induced psychotic disorder, schizotypal disorder, simple <strong>schizophrenia</strong> (an ICD-10 but not a DSM-III-R diagnosis), and the negative syndrome of <strong>schizophrenia</strong>. The latter has been included in SCAN for research purposes.</p>
<p>The section on cognitive impairment and/or decline includes the well-known Mini-Mental State Examination (MMSE) as well as the less well-known Verbal Trails Test. This section also contains probes to assess language, calculation, praxis, abstraction, fiind-of-knowledge, frontal-sub-cortical function, and level of consciousness. The section on dementia includes specific etiologies such as Alzheimer disease and Parkinson disease.</p>
<p>SCAN was developed by an international panel of researchers. Various groups of collaborators were responsible for the design and field trials of particular sections of SCAN. This presumably accounts for the lack of integration and the overlap of phenomenological categories across various psychopathological domains. In addition SCAN, unlike PSE 9, shifts out of the context of the mental state examination and includes sections that rate specific <strong>psychiatric disorders</strong> and disease course as well as identifies specific etiologies. SCAN is, therefore, much more than a rating scale for the mental state examination. Users of the SCAN may find this confusing and would be wise to look elsewhere for a clear and integrated conceptual understanding of the various domains and categories of the abnormal mental state. Nonetheless SCAN does list much of the psychopathology of <strong>mental disorders</strong> and can be used as a reference by clinicians to enrich and polish their own mental state evaluations.</p>
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		<title>Seminars in Basic Neurosciences</title>
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		<pubDate>Wed, 23 Sep 2009 03:28:40 +0000</pubDate>
		<dc:creator>Old Physician</dc:creator>
				<category><![CDATA[Neurology]]></category>
		<category><![CDATA[Neuropsychology]]></category>
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		<description><![CDATA[Seminars in Basic Neurosciences 
Gethin Morgan and Stuart Butler
College Seminars Series (Royal College of Psychiatrists), London: Gaskell, 328 p., 1993.
The following remarks fall into two parts: first, a review of the book listed above; second, some comments on the place of the neurosciences in current psychiatry.
The title (with &#8220;Basic Neurosciences&#8221; placed in a prominent box [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Seminars in Basic Neurosciences </strong></p>
<p><strong>Gethin Morgan and Stuart Butler</strong></p>
<p>College Seminars Series (Royal College of Psychiatrists), London: Gaskell, 328 p., 1993.</p>
<p>The following remarks fall into two parts: first, a review of the book listed above; second, some comments on the place of the neurosciences in current <strong>psychiatry</strong>.</p>
<p>The title (with &#8220;Basic Neurosciences&#8221; placed in a prominent box on the cover) might suggest that this book is a rival to such a text as that by Kandel et al (1991) on &#8220;Principles of Neural Sciences&#8221;. This small volume, however, has a different purpose, namely, that of instructing clinical trainees in <strong>psychiatry</strong> to those aspects of neuroscience which may be of value to the practising clinician (and in meeting examination demands). In fact, it incorporates far more than the basic neurosciences as conventionally understood for it includes, in addition, a concise course in clinical <strong>neurology</strong>. Perhaps a future addition might reflect this in the title. Two important features should be noted at the outset. First, it is written by &#8220;contributors&#8230;experienced as teachers of clinical trainees.&#8221; Second, &#8220;there are many figures, diagrams, tables and boxes to make the information accessible and more easily absorbed&#8221;.</p>
<p>The contents of the book fall into nine chapters with short reference lists. They will now be considered <em>seriatim; </em>(the figures in parentheses indicate the page lengths of each).</p>
<p>&#8220;Functional neuroanatomy&#8221; (41) Butler: This chapter provides, in brief form, a standard account of relevant <strong>neuroanatomy</strong>. It includes an excellent diagram (Figure 1.14) on the limbic system and its connections.</p>
<p>&#8220;Neurophysiology&#8221; (28) Logan: This chapter is a concise account of synaptic transmission and, thereafter, reflex phenomena in the sensory and motor sphere. Diagrams are less plentiful but usually useful (for example, Figure 2.5 as opposed to Figure 2.4) (One wonders if the busy clinician will ever have recourse to the complex connections of the cerebellum portrayed in Figure 2.4 &#8211; unless it is a particularly slow day).</p>
<p>&#8220;Neurochemistry and neuropharmacology&#8221; (40) Nutt: This chapter is one of the best chapters in the book. Written by the Director of the Psychopharmacology Unit in the School of Medical Sciences at Bristol University, it deals succinctly with receptors and the mechanisms by which the ever-increasing numbers of psychotropic drugs are presumed to work. While the diagrams are excellent, the tables are outstanding. Figures 3.6 and 3.8 together with Tables 3.1,3.2 and 3.6 are superb summaries of current knowledge and Dr. Nutt deserves our gratitude and congratulations. The book is worth buying for these alone.</p>
<p>&#8220;Neurological examination and neurological syndromes&#8221; (38) Barrett: This chapter gives a remarkably complete account of clinical <strong>neurology</strong> as well as the neurological examination. Here summarized information given in &#8220;boxes&#8221; varies in utility from good 4.3 (classification of epileptic seizures), 4.5 (causes of dementia) to poor 4.4 (causes of <strong>epilepsy</strong>), 4.6 (causes of <strong>delirium</strong>). Simply listing seventeen or thirteen items in a &#8220;box&#8221; without any attempt at organization is daunting, not helpful. Nonetheless, to cover so well a wide area in such a small space does credit to the author.</p>
<p>&#8220;Neuropsychology&#8221; (34) Hallett: This is another excellent chapter. In Hallett&#8217;s own words, &#8220;<strong>neuropsychology</strong> offers a robust system for the measurement and quantification of cognitive function, emotional state and behavioural repertoire&#8230;&#8221; and is a &#8220;complementary system of analysis to <strong>psychiatry</strong>.&#8221; The chapter goes on to detail what <strong>psychology</strong> can and cannot do in this area. As an even-handed exposition in a small space I doubt if this chapter could be bettered. The appendices are admirable summaries of relevant tests.</p>
<p>&#8220;Neuropathology&#8221; (34) Luthert: This chapter provides the pathological complement to Barrett&#8217;s chapter. After discussing techniques and basic pathological processes, the writer then surveys most of the common neurological diseases. Most relevant to <strong>psychiatry</strong> is the excellent and concise account (in six paragraphs and one table) of the changes in <strong>Alzheimer’s disease</strong>. The &#8220;boxes&#8221; in this chapter are outstandingly good, for example, 6.2 (time course of events following focal occlusion of a cerebral vessel) and 6.3 (routes of infection.)</p>
<p>&#8220;Neuroendocrinology&#8221; (25) Gilbey and Macrae: This chapter provides a good survey of the field and here excellent diagrams are a feature (Figures 7.1, 7.3, 7.4 and 7.7). This section is particularly valuable since it collects together in one place information which is much less accessible to most of us than the content of many other chapters of this volume. Table 7.4 and 7.5 (psychiatric manifestations of endocrine disorder and endocrine manifestations of <strong>psychiatric disorders</strong>) are very helpful.</p>
<p>&#8220;Clinical neurophysiology&#8221; (SS) Hilary Morgan: This chapter deals successively with techniques of recording the EEG, its normal appearance and the changes occurring in metabolic and toxic states and following treatment (including ECT). After an account of changes in the various neurological disorders, there is then a special section devoted to <strong>epilepsy</strong>. The facts are encapsulated in the &#8220;mother of all tables&#8221; 8.1 which runs over four pages. Pages 281 to 283 contain important summaries on violence, <strong>epilepsy</strong> and the EEG; the EEG and episodic behavioural changes and <strong>schizophrenia</strong> and <strong>affective disorders</strong>. There is a short account of sleep and the EEG (now a subspecialty of <strong>psychiatry</strong> with its own testing examination) and the chapter concludes with mapping (including power spectral analysis) event-related potentials and evoked potentials. Instead of boxes there are numerous illustrations of the EEG in various conditions.</p>
<p>&#8220;Neuroradiology&#8221; (12) Bradshaw and Lewis: After discussing the various techniques in this chapter (plain radiography, angiography, CT, MRI, PET and SPECT), the authors survey successively the spine, congenital lesions, vascular disease, trauma, neoplasia and finally degenerative, metabolic and toxic disorders. There is an introductory and minatory warning against the temptation to scan large numbers of psychiatric patients in the hope of &#8220;finding something&#8221;. But there are replicable findings, for example, the ventricular changes in <strong>schizophrenia</strong> and changes in rCBF and glucose metabolism in dementia which deserve discussion. This could with profit replace the account of radiology of the spine. And the use of PET and SPECT to study a wide variety of neuroreceptors is surely of interest (Daniel et al). There are missed opportunities here.</p>
<p>&#8220;Appendix and index&#8221; The former contains a map of cutaneous innervation and a table of reflexes. There is an excellent index compiled by Linda English.</p>
<p>At first sight, the chapters appear uneven but to a degree this reflects the subject matter. It is easier to be enthusiastic about the latest findings in the brains of patients suffering from <strong>Alzheimer’s disease</strong> than to get excited over the corticothalamic tracts which haven&#8217;t changed much in the last few centuries. But this would be a very unfair reflection on the authors who have produced remarkably good summaries of their areas which, despite brevity, are readable, thanks in large part to the lavish use of boxes and diagrams which contribute to the success of this enterprise.</p>
<p>One could always argue with the editors about allocation of space to the different subjects. Thus, in considering diagnosis, many would put <strong>neuropsychology</strong> first followed by radiology, endocrinology and the EEG last; yet the pages allotted are 34, 12, 25 and 55 respectively. But the editors are presumably tuned to local needs and the requirements of examinations. (And the pages on the EEG are inflated by numberous multichannel illustrations).</p>
<p>In sum, this excellent volume provides in one place an extremely useful, concise and up-to-date compendium of clinical neuroscience and <strong>neurology</strong>. If the trainees absorb the contents then they will be well-equipped to deal with the increasing pace of change due to new research findings which, judiciously and selectively, they may wish to incorporate into their clinical practice.</p>
<p>If we accept the view that mental activity is based on brain activity then a knowledge of the basic neurosciences becomes essential. It is true that a few still hold to the dualist view, notably Sir John Eccles and the late Sir Karl Poppers, but most in the field are less defeatist and believe that eventually most mental activity will correlate with neuronal events. There are indeed notable successes to date which are recounted in the volume by Kandel et al (1991) already cited. Kandel&#8217;s work on <strong>anxiety</strong> and the synapse is a classical example of the progress being made.</p>
<p>Nonetheless, to the practising clinician the different neurosciences have varying relevance. Can we not, then, leave some to the specialist? While it is customary to defer to individual experts in, say, radiology or endocrinology, it is still essential, in this reviewer&#8217;s opinion, that the clinician have enough general knowledge not only to know what the different disciplines can provide but also to be able to interpret oneself in relation to any individual patient and at times overide the expert.</p>
<p>Some would even go further and deny the need for medical training. Thus, <strong>psychologists</strong> in the US have sought admission privileges and the right to prescribe drugs. Without full medical training including the neurosciences such a course is fraught with hazard. But if clinicians themselves do not use their medical skills then it becomes more difficult to answer the pressures of competitive professions. However, there is an increasing shift from <strong>consultation-liaison psychiatry</strong> to medical <strong>psychiatry</strong> defined by Stoudemire and Fogel (1987) as &#8220;a medical specialist who assumes primary responsibility for the diagnosis and treatment of <strong>psychiatric disorders</strong> within the medically ill population.&#8221; They go on to list the reasons for its growing importance as follows: &#8220;(1) the increasing prevalence of chronic disease and the aging of the population, (2) advances in neurodiagnostic techniques and <strong>psychopharmacology</strong>, permitting more rational biological therapy of <strong>psychiatric disorders</strong> in the medically ill, (3) the development and implementation of brief, focused dynamic <strong>psychotherapy</strong> techniques appropriate for the medical setting, (4) the development of specialized medical-psychiatric inpatient units, (5) increasing time pressures on other medical specialists, leaving the <strong>psychiatrist</strong> as the only medical specialist with the time, knowledge, and skills to develop a comprehensive understanding of the emotional dimensions of medical patients&#8217; illnesses, and (6) increased competitive pressures from non-medical <strong>psychotherapists</strong>, causing <strong>psychiatrists</strong> to emphasize their medical training and skills.&#8221; The role of the basic neurosciences in the above needs no emphasis.</p>
<p>If, indeed, <strong>psychiatrists</strong> do not pay attention to these areas then <strong>psychiatry</strong> as a discipline will diminish and may vanish. Our patients will be the big losers. That dire consequences are already upon us is exemplified in a recent editorial by Robin Eastwood (1994). He notes that both by competition from other specialties and by default <strong>psychiatry</strong> is losing its place in dementia research in Canada. This displacement is occurring elsewhere too and he quotes a Lancet editorial which &#8220;says that dementia, especially basic research, is now indeed the domain of <strong>neurologists</strong> and that even <strong>schizophrenia</strong> is not exclusive to <strong>psychiatry</strong> anymore.&#8221; If, in fact, <strong>psychiatry</strong> has decided to concentrate on the &#8220;functional&#8221; psychoses, he concludes &#8220;how sad that the magnificent start given by Kraepelin and Alzheimer at the beginning of the century, at the Ludwig-Maximilians-Universitat in Munich, has come to this in Canada.&#8221;</p>
<p>This reviewer hopes the volume edited by Morgan and Butler will help stop the rot.</p>
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		<title>Brain Biochemistry and Brain Disorders</title>
		<link>http://psychiatry.com.ua/index.php/psychiatry/278#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
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		<pubDate>Wed, 16 Sep 2009 17:46:07 +0000</pubDate>
		<dc:creator>Old Physician</dc:creator>
				<category><![CDATA[Psychiatry]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[depression]]></category>
		<category><![CDATA[dopamine]]></category>
		<category><![CDATA[schizophrenia]]></category>

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		<description><![CDATA[Brain Biochemistry and Brain Disorders
Philip G. Strange
Oxford, New York, Tokyo: Oxford University Press, 342 pp, 1992
I read and re-read this book several times — it is easy to read. On my first survey, I noted numerous excusable and many unforgiveable omissions (for example, only a brief mention of the dopamine D-3 receptors on page 239 [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Brain Biochemistry and Brain Disorders</strong></p>
<p><strong>Philip G. Strange</strong></p>
<p>Oxford, New York, Tokyo: Oxford University Press, 342 pp, 1992</p>
<p>I read and re-read this book several times — it is easy to read. On my first survey, I noted numerous excusable and many unforgiveable omissions (for example, only a brief mention of the <strong>dopamine</strong> D-3 receptors on page 239 and not even a word on the D-4 receptors that had been described by then). But I came to the realization that one cannot be an excessively critical judge. Any book of this size that comprises biochemistry, structure, research methodology and a wide range of pathologies of the brain can only be somewhat of a smorgasbord. There is nothing wrong with a neuroscience buffet, however, provided it is nutritious and served with style. And this must be recognized about this book, including the extremley well chosen cover illustration of Edward Munch&#8217;s &#8220;The Dance of Life&#8221;.</p>
<p>The first seven chapters provide sufficient amounts of basic information and neuroscience facts that are required for the grasp of the second part of the book, which focuses on six different disorders.</p>
<p>The author discusses artfully and, for purposes of psychiatric residents and practitioners, sufficiently the cellular aspects of the brain tissue, the chemical and electrical signalling, the neurotransmitter and receptor systems as well as some research technologies, although the description of the restriction-fragment length polymorphism (RFLP) could have been made clearer.</p>
<p>The author chose six diverse pathologies that are connected along the mesostriatal, mesolimbic and mesofrontal tracts. The totality of these six pathologies, and some others mentioned <em>en passant, </em>provides a base not only for the understanding of these illnesses but also for the comprehension of these brain parts. The discussion of <strong>Parkinson’s disease</strong>, including the MPTP, genetic aspects, rationale of tissue transplant, etc. is fairly complete, as is the chapter on Huntington&#8217;s disease and <strong>Alzheimer’s disease</strong>. The chapter on <strong>schizophrenia</strong>, as a brain disease, competently deals with the subject, although the contribution of Weinberger (mentioned briefly on page 256) could have been more extensive. The chapter on <strong>depression</strong>, although thorough and interesting, is too speculative in relation to the septohippocampal system. The last chapter, on <strong>anxiety</strong>, is probably the weakest.</p>
<p>The illustrations, including the CT scans, are of good quality. There are aspects of the quotations of original contributors where one could disagree with the author. Considering that books rapidly become outdated, this book has a certain philosophy and appeal — not to mention a modest price — that will assure a measure of longevity.</p>
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		<title>Headache and Depression: Serotonin Pathways as a Common Clue</title>
		<link>http://psychiatry.com.ua/index.php/psychiatry/headache-and-depression-serotonin-pathways-as-a-common-clue#utm_source=feed&amp;utm_medium=feed&amp;utm_campaign=feed</link>
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		<pubDate>Fri, 04 Sep 2009 11:28:51 +0000</pubDate>
		<dc:creator>Canadian</dc:creator>
				<category><![CDATA[Neurology]]></category>
		<category><![CDATA[Psychiatry]]></category>
		<category><![CDATA[anxiety]]></category>
		<category><![CDATA[depression]]></category>
		<category><![CDATA[mood disorders]]></category>
		<category><![CDATA[neurologists]]></category>
		<category><![CDATA[psychiatrists]]></category>
		<category><![CDATA[serotonin]]></category>

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		<description><![CDATA[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, [...]]]></description>
			<content:encoded><![CDATA[<p><strong>Headache and Depression: Serotonin Pathways as a Common Clue</strong></p>
<p><strong>G. Nappi, G. Bono, G. Sandrini, G. Micieli</strong></p>
<p>New York, NY: Raven Press, 345 pp., 1991</p>
<p><strong>Serotonin</strong> (5-HT) is an ubiquitous substance, found throughout the body, which has become a common focus of interest for <strong>psychiatrists</strong>, <strong>neurologists</strong> 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 <strong>serotonin</strong> receptors which are found in different tissues and organs.</p>
<p>This book examines the role of <strong>serotonin</strong> in <strong>depression</strong>, headaches and related conditions. The editors are all from Italy, where much research into <strong>serotonin</strong> has been conducted, but they have enlisted authorities from around the world to add chapters on their own fields.</p>
<p>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 <strong>serotonin</strong> pathways in headaches, and Cassano and Marazitti, its role in <strong>depression</strong>. The subject of chronic daily headaches is presented by Mathew. The possible role of <strong>serotonin</strong> and neuroendocrine factors in this condition and in cluster headaches are explored by several authors.</p>
<p>The role of <strong>serotonin</strong> in migraines is extremely complex. IV 5-HT can both precipitate and relieve migraine headaches. Blockage of <strong>serotonin</strong> synthesis can cause a panalgesia syndrome. While reserpine-induced <strong>serotonin</strong> depletion in platelets is associated with the precipitation of acute headaches, there is a reduction in migraine attacks during the subsequent month while <strong>serotonin</strong> 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.</p>
<p>In the case of <strong>mood disorders</strong>, the situation is even less clear. Both high and low levels of <strong>serotonin</strong> activity have been found in patients with <strong>depression</strong>. Again, the receptors may hold the key. 5-HT-2 receptors seem to be important in <strong>depression</strong>, while <strong>anxiety</strong> is related to 5-HT-l receptor activity. Up and down regulation of receptors are likely responsible for <strong>depression</strong> and the effects of antidepressive <strong>medications</strong>.</p>
<p>In trying to untangle this complex scheme, one may be forgiven for concluding that the only common factor in headaches, <strong>depression</strong> and <strong>serotonin</strong> perturbation is the nervous system itself.</p>
<p>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 <strong>depression</strong>, presumably as a result of the loss of melotonin, which is metabolized to <strong>serotonin</strong>. Melotonin may also play a role in some features of cluster headaches. Studies in chronobiology may give new insights into the basis of <strong>mood disorders</strong>, 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 <strong>depression</strong> are often part of <strong>premenstrual syndrome</strong>. There are several chapters in the book on this subject.</p>
<p>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 <strong>serotonin</strong>, <strong>depression</strong> 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 <strong>psychiatrists</strong> who wish to have up-to-date information on some of the biochemical bases and the mechanisms of current therapeutic agents for treating <strong>depression</strong>. Headache specialists and behavioral <strong>neurologists</strong> may also find it useful. It will be of less interest to others in the profession.</p>
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