Since depression is so obviously a component of normal daily life one may assume that it has a function. This problem may be approached by first considering the function of affects in general. I have suggested elsewhere that affects might be considered labels by which individuals might anticipate the results of any proposed course of action. Thus, given any set of environmental circumstances, the individual attempts experimentally to ascertain what opportunity these circumstances offer for the gratification of instinctual wishes. For example, a sexually active male, introduced to a woman he has not known before will automatically want to know what she would be like as a sex partner. He proceeds to imagine the liaison accomplished and as he does so becomes aware of an effect. The experiment is performed swiftly, almost instantaneously and none of it may arise to the level of awareness save for the affect. If the affect is a pleasant one, the individual may proceed to live out his fantasy. If on the other hand considerations of morality, propriety, or personal safety, or the difficulty of accomplishment veto the project, one of the negative affects appears in consciousness and the project is not only abandoned but often its consideration is not acknowledged. In this way the affect is used as a guide for ascertaining the suitability of environmental circumstances for the gratification of instinctual wishes. However, affects appear not only during experimental contemplation of proposed behavior, but also in the course of actual living. Just as the affect which appears during experimental contemplation determines whether that or a similar fantasy is to be pursued or elaborated on the one hand or whether an entirely different mode of procedure is to be used on the other, so the affect which appears during an actual experience determines whether the individual shall strive to continue or intensify that experience or to change or replace it.

In light of this discussion we may ask what kind of activity is anticipated with the feeling of depression, and further, in what type of experience depression is likely to appear. Merely by referring to the conditions under which depression appears in normal life we are able to offer prompt replies. Obviously, when the consequence of any act is the loss of something or someone which one loves, the individual is warned by anticipation depression. Also following the actual experience of loss, the affect of depression conspires to undo the loss or at least the impact of the loss.

We may now ask, what is the nature of the loss against which anticipatory depression warns us and which post hoc depression attempts to undo. Addressing ourselves once more to the occasions on which normal depression appears, the most obvious instance, we realize is the loss of a loved person, in psychoanalytic terminology, the love object. The love may be based on family ties as in the parent-child or in the sibling relation, or it may be a romantic love. The loss may be occasioned by death, departure, separation or by rejection. Depression is equally likely to be concerned with a loss of the physical integrity of the person himself. Such losses include for example the amputation of a limb or the surgical removal of some organ which formed part of the individual’s mental image of himself, such as an eye or a breast. Even the realization of the gradual loss of youth as for example on the occasion of some biologic or chronologic landmark may be associated with depression. A loss of physical attractiveness whether gradually by aging or abruptly by a disfiguring injury may be a cogent cause of depression. Capacity for sexual performance is thought of in the same way. Moreover since the individual usually considers his social and economic status and his personal property to be in a sense a part of himself, their loss too may be associated with depression. It is interesting that even a loss of physical integrity or social prestige can be understood in terms of a loss of love object. In the first place the individual always reserves a sizable proportion of his capacity to love for himself, that is, for his body, his social position and his intellectual creations. Therefore a loss in any of these spheres may be considered a loss of love object. Secondly, since these features make for the individual’s attractiveness to others as a love object, a loss of any of them makes him less desirable to others and therefore less able to attract and hold a love object.

November 9, 1954

Depression is one of the common affective phenomena of daily living and it is also one of the most common symptoms of serious psychic illness. When a symptom consists of the pathologic exaggeration of a normal function, studies of physiology and pathology are mutually illuminating. The phenomenon of depression is therefore presented here in the contexts of both normal function and disease. The formulations offered are derived from observations made during psychoanalytic and psychiatric practice and correspond fairly closely, I believe, to classic psychoanalytic theory. The approach, however, is primarily clinical.

Definition and Description

Depression is an affect. The word affect refers to the pure subjective feeling component of the somewhat more general concept of emotion which is often considered to include elements of thoughts, fantasies, wishes and prejudices. Affects in general may be divided into those that are pleasurable and those that are painful. Depression is clearly one of the latter group which includes also, for example, anxiety, guilt, shame, embarrassment, resentment and anger. The distinction between depression and other painful affects cannot be made without resort to the use of some question begging term as sadness to characterize depression. Since the essence of every affect is a subjective and intangible sensation, the definition of an affect can distinguish one from the others only by appeal to ancillary data such as physical concomitants, circumstances of evocation and behavioral consequences. In a sense then, the definition of depression will have to be completed by the remainder of this paper.

Nevertheless there are certain visible signs by which an affect may declare itself to an observer. These signs become more pronounced and their number increased the more pronounced the affect. Depression is usually betrayed by a fairly characteristic facial expression. It is usually accompanied by weeping especially when the subject is alone. A psychic and physical inertia usually accompanies depression. The depressed individual is inclined neither to think, nor to imagine, nor to plan, nor to work, nor even to move. Such psychic and physical activity as does appear, is performed slowly and with a sense of great effort. Anorexia is fairly constant and in severe cases may be replaced by a positive aversion to food, or nausea. Unusual and unpleasant sensations may be referred to the gastrointestinal tract in instances of pronounced depression, a frequent complaint being a sense of “gnawing.” The depressed individual will sometimes compare his “stomach” sensations to those which might be produced by some living organism restlessly churning about and clawing. Sexual desire is diminished in mild depression and completely abolished in severe depression. Sexual performance is often impaired as well. In some seriously depressed individuals the usual inertia is replaced by a visible restlessness which often precludes sleep, and it betrays a pronounced psychic agitation. Confessions of unwarranted or exaggerated guilt especially toward loved ones are common. In instances of serious depression there may be feelings of worthlessness and wickedness. Of course the greatest threat in cases of pathologic depression is suicide. There are no signs by which a physician can be assured in any given case that a suicidal outcome is not possible. In general it seems that suicidal outcomes are more likely in cases in which there is a family history of suicide or a previous personal attempt at suicide. However, the absence of such a history cannot be depended upon to exclude the possibility of suicide.

The occasions upon which depression characteristically appears may also serve to distinguish depression from other painful affects. During the course of normal day to day living, depression is most frequently encountered following some serious loss or disappointment. The depression following the death of a loved person is typical. Mild depression persisting a few days or weeks often follows childbirth especially among women who have enjoyed their pregnancy. Depression falls into the category of disease when it occurs in the absence of any overt loss or when its persistence or severity is immoderate even though the precipitating loss be significant. The sixth decade of life is the period in which pathologic depression is most likely to appear or is likely to be most severe if episodes of depression have occurred earlier.

Question. Can you please give me your opinion on the P450 inhibitory effects of SSRIs, namely, fluoxetine, paroxetine, citalopram, sertraline and fluvoxamine? Which appears to have the least clinically significant effects on this and other liver enzymes? How do these effects demonstrate themselves to patients? How clinically significant are the effects?

Answer. I’ll give you the bottom line first, then fill in some of the details: if you are only worried about inhibitory effects of SSRIs on the cytochromes, it’s best to avoid using fluoxetine [Prozac], fluvoxamine [Luvox], and paroxetine [Paxil]. Instead, go to either sertraline [Zoloft] or citalopram [Celexa]. Neither of these latter two SSRIs have substantial inhibitory effects on the cytochromes, though that doesn’t mean they are fail-safe medications.

Furthermore, for many patients, Prozac, Luvox, or Paxil may simply work better for depression. To cite some data from Dr. Sheldon Preskorn [see Harvey & Preskorn, Journal of Clinical Psychopharmacology, 1996; 16:273-85], “both fluoxetine and paroxetine have substantial inhibitory effects on the cytochrome P450 2D6 (CYP 2D6) system. Fluoxetine also has substantial inhibitory effects on CYP 2C9 and moderate inhibitory effects on CYP 2C19. Fluvoxamine has substantial inhibitory effects on CYP 1A2 and 2C19, and moderate effects on CYP 3A3/4.”

In and of themselves, these inhibitory effects rarely are felt by patients, unless they are taking some other medication whose blood levels rise in the presence of one of these strongly-inhibiting SSRIs. For example, someone taking the antipsychotic clozapine [Clozaril] may experience marked side effects (sedation, dizziness) if fluvoxamine [Luvox] is added. This is because clozapine is metabolized (in part) through CYP 1A2, which fluvoxamine strongly inhibits. In other cases, the psychiatrist may actually take advantage of these inhibiting effects, by using the SSRI as a kind of magnifying glass, that is, using it to boost blood levels of some other therapeutic agent, which is prescribed in a very small dose.

In other cases, the rise in blood levels effected by one of these SSRIs is clinically insignificant, from the patient’s standpoint. It is always a matter of the particular drugs involved, and the particular patient. For example, some patients may lack the CYP enzymes required to break down a particular drug, or have an unusually active form of the enzyme. You might want to get hold of some of Dr. Preskorn’s recent articles on this subject for further details.

Question. I am a 33-year-old male who has suffered from major depression for about 10 years. I was also anorexic and bulimic around age 25. I have been in lengthy therapy several times, but every few years I seem to cycle back into a very depressed, immobilizing state. Medications (Prozac, Zoloft, Paxil, Serzone, anti-anxiety) don’t seem to help. I’ve always been emotional and sensitive. I am interested in hypnotherapy – do you think it might be beneficial? What other treatments might you suggest?

Answer. I don’t want to burst your balloon regarding hypnotherapy, but I know of no credible evidence that it helps depression. In the first place, hypnosis is not really a therapy, but rather a technique used in the context of a broader therapeutic approach, such as psychotherapy and/or medication. While hypnosis may be useful in certain post-traumatic and dissociative disorders, phobic disorders, some chronic pain states, and in the treatment of “habit” disorders like smoking, there’s no research to show that it is helpful either in the treatment of acute depression or the prevention of further episodes.

Since you say you “cycle” into depression, I would certainly make sure that you do not have a cyclical mood disorder, such as bipolar (manic-depressive) disorder. (You did not mention any mood stabilizers in your list of medications, and these might be worth discussing with your psychiatrist.) There are many new medications available for depression, such as venlafaxine (Effexor), mirtazepine (Remeron), and citalopram (Celexa), and the fact that you did not respond well to the ones you mentioned does not mean that you will not respond to these newer agents.

A MAOI (a special type of antidepressant) would also be worth considering. Both ECT (electroconvulsive therapy) and a new technique called TMS (transcranial magnetic stimulation) could be beneficial as well. Any medication should be used in the context of a supportive therapeutic relationship with a mental health professional. You could also benefit from participating in a support group for depressed individuals. And if you have not yet joined the National Depressive and Manic-Depressive Association, I would encourage you to do so. Don’t give up – there is effective help out there!

Cohen S, Kessler RC, Underwood Gordon L, editors

New York: Oxford University Press; 1997. 236 pp. with index

ISBN 0-19-512120-1 (paper)

“Stress” has become such an overused word that it is now almost a cliché. The Oxford English Dictionary has 10 different meanings for it. Because of these terminological difficulties, some consider that it should be discarded from the medical lexicon altogether. Nevertheless, “stress” has developed a widely understood meaning in common parlance, and it would appear acceptable to use the word technically as long as clear definitions are followed. In the psychosocial and biological sciences it has come to refer to the external events and changes that impinge on an individual and the reaction of the individual to those events. Over the last 50 years a huge volume of psychobiological research has been carried out on stress and its effects on health. It is ironic that, despite mounting clinical, epidemiological and pathophysiological evidence that stress has adverse effects on health, there still are sceptics who doubt the connection or — worse — fail to recognize and assist patients whose clinical problems are caused or aggravated by stress.

A probable reason for the existence of such scepticism is the very real difficulty in measuring stress in a valid and replicable way. This book tackles this problem in a pragmatic and comprehensive manner. Stress is defined as “a process in which environmental demands tax or exceed the adaptive capacity of an organism, resulting in psychological and biological changes that may place persons at risk for disease.” This process is examined from 3 perspectives: environmental, subjective and biological. The “environmental” perspective includes the external life events that impinge on an individual; the “subjective” factors are the psychological and emotional perception and evaluation of those events; and the “biological” factors refer to the physiological responses induced by these environmental and psychological changes. There are helpful introductory and summary chapters to each of the sections.

Two types of tests are used to measure the intensity of environmental events: those that depend on self-report ratings and those that depend on interviewer ratings. Self-report ratings have the major advantage of simplicity and efficiency of administration. However, some environmental events may not be listed in the inventories given to the patient, and earlier stressful events may be poorly remembered and evaluated. Interview methods have the advantages of being able to measure the timing and intensity of life events more accurately, and are also more comprehensive. However, they are much more expensive and time-consuming to administer.

The chapters on psychological response describe the measurement of stress “appraisal” and the measurement of the “affective response.” The book describes a variety of questionnaire-type tests that measure each of these responses. Two final fascinating chapters deal with physiological reactions to stress. These reactions affect 3 systems: the sympathetic-adrenal medullary system, the hypothalamic-pituitary-adrenocortical axis, and the immunological response. Each is important, because each is a likely means by which environmental events cause pathophysiological reactions.

This book is a must-read for those involved or wishing to be involved in stress research. The authors are all actively engaged in experimental research in this area or have helped to develop many of the tests in use. The chapters are comprehensive and well written and referenced. Although the book is expensive, it can be highly recommended as a compendium to those with an interest in this field.

Citalopram (Celexa, Forest Laboratories, Parke-Davis) has been approved by FDA for treatment of depression. A highly selective serotonin reuptake inhibitor, citalopram is the best-selling antidepressant in 13 countries, including eight in Europe. Citalopram has proven effective in treatment of depression in clinical trials involving 23,000 patients and has been used in some 8 million patients in 64 countries where the drug is already approved. Two, six-month, double-blind, placebo-controlled studies indicated that citalopram is significantly more effective than placebo in preventing relapse of depression.

Side effects include nausea, dry mouth, and sleepiness. As with all SSRIs, citalopram should not be taken with monoamine oxidase inhibitors.

Depression And The Social Environment: Research And Intervention With Neglected Populations
Editors: Philippe CappeUez; Robert J. Flyrm McGill
Queen’s University Press, 3430 McTavish St, Montreal, QCH3A 1X9, 1993, 428 ppl

The title of this book clearly expresses the concepts within. It is well written and includes fairly complete literature reviews, along with some of the authors’ personal work on research related to depression in specific populations. Most of the populations studied are often neglected by health planners and service providers.

This book is valuable for all mental health professionals in general psychiatric practices and for family physicians who subspecialize. It is, however, highly academic and slow to read. Although it promises to be practical, it is not necessarily so in all chapters. Chapter 3 on adolescent depression and chapter 6 on depression among patients attending a general practice are exceptions. These chapters are extremely good and are valuable reading for family physicians. In fact, both chapters should be mandatory reading for family practice residents.

Chapter 1 is an introduction to the text. It explains that the information in the book is psychosocially based and will be the foundation for policy recommendations and individual practical interventions. The book largely ignores biological considerations, a fact that reduces its relevance for the average family physician.

Chapters 2, 3, and 4, respectively, are related to childhood depression, adolescent depression, and suicide in young adults. For childhood depression, comprehensive assessment and treatment planning is stressed. The authors suggest that there is a “lack of evidence for efficacy of any specific treatment,” and therefore “sound clinical judgement” is required. They suggest that increased training of professionals, along with increased resources for treatment and further research, are required to make advances in this field.

In the chapter on adolescent depression, the phenomenology of depression in adolescents is compared with that in adults. However, hypersomnia; negative thoughts; irritability; and increased anxiety, especially in younger teens, are seen perhaps more often. The course of depression is also slighdy different. Depressed moods appear to last between 20 and 40 days in younger adolescents and increase in length in those who are older. The authors stress that rating scales should not be used to make a diagnosis but rather to follow patients once a clinical assessment is completed.

The chapter on suicide reviews the increase in suicide attempts in Canada during recent years. The difficulties of preventing suicide among young adults is discussed and strategies to make teens “more active and engage… in projects with other people” are suggested.

It is also suggested that the period of crisis immediately after a suicide attempt is crucial for restoring self-confidence, and therefore emergency services should be available and trained to assist at that time.

Other chapters address sex issues, the effects of unemployment, depression among Canadian Natives, depression among immigrants and refugees, depression among people with physical disabilities, depression among caregivers of impaired elderly family members, depression among elderly persons themselves, and mediators of depression in community-based seniors. Themes common to all the chapters emphasize the difficulty of separating depressive symptoms from syndromes and the importance of recognizing this as a problem to be researched itself. It would appear that the more specialized the population the bigger problem this distinction becomes. All of the chapters emphasize the need for further general study of these populations.

Chapter 14 is really the conclusion. In it the editors summarize and integrate material from all the other chapters and come to conclusions and recommendations. Reading the last chapter first puts the whole book into perspective. The editors suggest improving the training of professionals in both diagnosis and treatment of depressive illness. In particular, the focus should be on a comprehensive multidisciplinary approach. I believe this book is a helpful tool for working toward those goals.

Risk Management with Suicidal Patients

Bongar B, Berman AL, Mavis RW, Silverman MM, Harris EA, Pakman WL, editors

New York: The Guilford Press; 1998.197 pp with index

ISBN 1-57230-302-6 (cloth)

This book was written in response to the fact that most psychiatrists lose a patient to suicide sometime during their professional life. Suicide cases are a leading reason for malpractice action against mental health professionals. Dr. Bongar begins by suggesting that this book is “a forum for the exploration of avoiding liability in working with the suicidal patient.” In his introduction, Bongar stresses that the book is not intended as a standard of care, but rather “a rich and wide-ranging set of opinions and guidelines.” However, the book is quite contradictory on this point — Chapters 1, 3 and 4 are dedicated to discussing standards of care and the suicidal patient. Since this book, authored by experts in suicidology, and based on work published in the American Association for Suicidology’s official journal, will have an important impact on the care of suicidal patients, its deficiencies must be addressed.

This book includes 3 chapters based on articles previously published in Suicide and Life-threatening Behavior, and 4 new chapters. The contributors include many of the most prominent American suicidologists, including Drs. Alan Berman, Bruce Bongar, Robert Litman, Ronald Maris, Morton Silverman and Andrew Slaby. Chapter 1 is dedicated to the outpatient management of suicidal patients. It discusses common failure scenarios from malpractice proceedings and goes on to outline an outpatient standard of care. Bongar and coauthors originally published this paper in Suicide and Life-threatening Behavior in 1992. In Chapter 2, Dr. Slaby presents the essential elements of outpatient care of the suicidal patient. However, given its all-encompassing goal, the chapter ends up being a cursory discussion of many important issues. For example, when discussing the management of patients with borderline personality disorder, Dr. Slaby simply concludes, “Clinicians are not gods and are not able to predict or prevent all deaths by suicide. This is most true when they are dealing with Axis II personality disorders.” (page 35). Fortunately, the American Psychiatric Association is developing practice guidelines for the care of patients with borderline personality disorder. This will provide a more comprehensive statement about what is known and not known about the care of these patients. Chapters 3 and 4 are based on articles that were published in 1993 and 1994, respectively, in Suicide and Life-Threatening Behavior. The editors have included a commentary of Chapters 3 and 4 from Dr. Robert Litman, who criticizes Dr. Silverman’s Chapter 4 for providing good clinical practice standards, but not the minimal standards that are often the reference point for court proceedings. Chapter 5 is a new contribution by Drs. Goldblatt, Silverman and Schatz-berg, dealing with the psychopharmacological treatment of suicidal inpatients. However, the chapter is disturbingly incomplete. For example, the value of lithium maintenance treatment in reducing the risk of suicide for bipolar disorder and clozapine treatment in reducing the risk of suicide in schizophrenia are inadequately addressed. These treatments may have important indications in the suicidal behaviour of individuals with these specific diagnoses. Also, the discussion of borderline personality disorder is badly outdated; for instance, their most recent reference is from 1986 and recent evidence for using selective serotonin reuptake inhibitors for individuals with impulsive aggressiveness is ignored. Chapter 6, a new contribution by Dr. Silverman, purports to be a model for psychopharmacological interventions for hospitalized patients. A psychiatrist will find this discussion broad and uninformative. I suspect that the target audience for this chapter is the psychologist, who may find discussion of the steps that are needed to determine appropriate psychopharmacotherapy informative. The last chapter on the risk management of suicidal patients, by Drs. Packman and Harris, contains very practical suggestions for minimizing liability. For example, the authors provide an approach for discussing, at the outset of therapy, breach of confidentiality when a highly suicidal patient is in crisis and there is a need to inform the patient’s family. This chapter is more current, as it discusses the issues of liability in the managed care environment. A document that includes in its title “standard of care” for suicidal patients has the potential to do more harm than good. This book is primarily based on data from malpractice claims to develop “standards of care” for suicidal inpatients and outpatients. As a result, most of the chapters are outdated with regard to recent scientific evidence. The 3 reprinted chapters appear to have been published without any attempt to update the references. The new contributions do not provide a clear statement of the nature of the supporting evidence used to develop their approach, and do not appear to include the evidence based on empirical research. Therefore, this book eschews the scientific evidence that has accumulated to guide clinical practice. Drs. Rudd and Joiner have recently published a paper on the assessment, management and treatment of suicidality based on existing literature, and provide an important alternative to the approach by Bongar and colleagues.

The book is under 200 pages, well produced and contains no production errors. Although this book will attain prominence in the fields of psychiatry and psychology, the reviewer cautions that it has employed a very limited methodology to determine standards of care for suicidal patients. This contribution must be seen as only one facet in the development of the appropriate care for suicidal patients.

Question. My 18-year-old son was diagnosed schizophrenic two years ago. Currently hospitalized, he is receiving clozapine and Haldol as anti-psychotics and Paxil for depression. He was moved directly to clozapine from Risperdal and has gained over 60 lbs. in three months. I’ve heard that olanzapine acts much like clozapine, but with fewer side effects. Is it normal to move to “older” drugs before exhausting newer ones?

Answer. I appreciate how confusing some of these medication issues can be for parents and families of individuals with schizophrenia. Terms like “older” and “newer” can be confusing when applied to medications for psychosis or mood. For example, how “new” or “old” an antipsychotic is has more to do with marketing and approval processes than with how effective or safe it is.

Generally speaking, clinicians distinguish two broad groups of antipsychotic agents: older “typical” agents, also called neuroleptics, and the newer “atypical” agents. The latter group includes clozapine (Clozaril), the first atypical released; risperidone (Risperdal), which came out next; and then olanzapine (Zyprexa) and quetiapine (Seroquel). As a group, the atypicals are generally more effective for so-called negative symptoms of schizophrenia (apathy, social withdrawal), and are less likely to cause neuro-muscular problems like muscle spasms, stiffness, and abnormal movements (tardive dyskinesia).

However, the atypical agents are not without side effects. On rare occasion clozapine can cause a serious white blood cell problem called agranulocytosis, and it does tend to promote significant weight gain. On the other hand, many clinicians believe clozapine to be the most effective agent, old or new, for severe, refractory schizophrenia. Several studies do suggest clozapine is somewhat more effective than risperidone, though risperidone tends to have fewer side effects (such as weight gain). Olanzapine, as you note, is closely related to clozapine, but it is not yet known if it is as effective. Though olanzapine is generally better tolerated than clozapine and does not cause the white blood cell problem, it can also contribute to weight gain.

Regarding your son, many clinicians would argue that a failure to respond well to risperidone justifies a direct move to “the gold standard,” clozapine. Others (probably including me) might give olanzapine a try first, then go to clozapine. But this isn’t a matter of old vs. new as much as a matter of balancing risks and benefits on a case-by-case basis. The same applies to Paxil (which, compared to many agents on the market, is actually quite “new”). By the way, sometimes the older agents (such as haloperidol) are used to augment newer agents, as seems to be the case with your son.

To summarize, the changes in medication you have described aren’t “wrong,” but your son’s response is hard to predict. Clozapine certainly gives him a very good chance of recovery. The other atypical agent now available, quetiapine, has not really been compared in good studies with clozapine; my own impression is that quetiapine is a useful agent, but “no clozapine.” We are expecting yet another atypical agent, ziprasidone, in the next 6-10 months, and this agent appears to cause little if any weight gain. It may also have antidepressant properties, and could be useful for your son. But it’s not at all clear that it will out-perform clozapine.

Please keep the following information in mind when taking Seroquel®(Quetiapine Fumarate).

Making Seroquel tablets work for you

• Seroquel is available as tablets you take by mouth. You should take Seroquel tablets every day or as your doctor has directed. To gain the most benefits from Seroquel tablets, take the exact number of tablets your doctor has prescribed for you each day at the appropriate times. Regardless of how good or how bad you feel, do not stop taking Seroquel tablets without notifying your doctor.
• If you miss a dose, take it as soon as possible. If it is almost time for your next dose, skip the missed dose and return to your regular dosing schedule. Do not take two doses at once. If you are unsure, speak with your doctor.
• During therapy with Seroquel tablets, especially during the initial dosing period, you may experience light-headedness or dizziness, especially when standing up quickly or getting out of bed. To help prevent this feeling, rise slowly from your chair or bed.
• Drowsiness can be a side-effect of Seroquel tablets especially during the first 3-5 days after you begin taking Seroquel tablets. Use caution when performing any activity requiring alertness, including operating an automobile or other hazardous machinery, until you are reasonably certain Seroquel tablets do not cause you to be drowsy.
• You should avoid drinking alcoholic beverages while taking Seroquel tablets.
• Avoid becoming overheated or dehydrated while you are taking Seroquel tablets.
• It is very important to take your doses of Seroquel tablets every day or as your doctor recommends, even once your symptoms go away and as you’re feeling better.
• Seroquel tablets may be taken with or without food.

Consulting with your doctor and pharmacist

• Keep your doctor informed of how you are feeling on Seroquel tablets.
• Discuss any side-effects or other symptoms you are experiencing or questions you have regarding your treatment with Seroquel tablets.
• Ask about scheduling periodic eye exams.
• Talk to your doctor and pharmacist about any other prescription or nonprescription drugs you are currently taking, since certain medications may affect the way they work.
• Notify your doctor if you are pregnant or plan on becoming pregnant while taking Seroquel tablets.
• Tell your doctor if you are planning to breast-feed – You should not breast-feed while taking Seroquel tablets.
• You should call your doctor right away if you have any questions or concerns about your symptoms, treatment, or how you are feeling in general.
• Remember to take your Seroquel tablets every day as directed, and do NOT stop taking Seroquel tablets without notifying your doctor. Seroquel tablets, when taken as directed, can help you achieve a more normal life.