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Drugs and Insomnia: 
The Use of Medications to Promote Sleep

National Institutes of Health
Consensus Development Conference Statement
November 15-17, 1983

Conference artwork, moon stars and a wide open eye on a purple background.

See more recent conference statement 
NIH State-of-the-Science Conference on 
Manifestations and Management of
Chronic Insomnia in Adults

This statement is more than five years old and is provided solely for historical purposes. Due to the cumulative nature of medical research, new knowledge has inevitably accumulated in this subject area in the time since the statement was initially prepared. Thus some of the material is likely to be out of date, and at worst simply wrong. For reliable, current information on this and other health topics, we recommend consulting the National Institutes of Health's MedlinePlus

This statement was originally published as: Drugs and Insomnia: The Use of Medications To Promote Sleep. NIH Consens Statement 1983 Nov 5-17;4(10):1-19.

For making bibliographic reference to the statement in the electronic form displayed here, it is recommended that the following format be used: Drugs and Insomnia: The Use of Medications To Promote Sleep. NIH Consens Statement Online 1983 Nov 5-17 [cited year month day];4(10):1-19.


The past decade has provided new developments and methodologies in sleep research, clinical practices, neuropharmacology, and psychiatric diagnoses. A taxonomy of sleep disorders has been advanced, and there are two newly marketed rapidly eliminated hypnotic drugs, as well as others under development. Use of a sleep-promoting medication is a decision that physicians and patients alike frequently encounter.

A recent national survey found that one-third of the population reported some degree of insomnia, and one-half of this group--17 percent of the population--considered the insomnia serious. Half of the group with "serious insomnia" reported a high level of emotional distress. Only ten percent of the subjects reporting "severe" insomnia received prescribed sleep-promoting medications; 5 percent used over-the-counter compounds. Surveys of primary care practice indicate that the bulk of hypnotic drug therapy is directed to women and the elderly with medical or mental disorders, and only a very small proportion with a primary diagnosis of insomnia.

Since insomnia appears in different diagnostic contexts and occurs under a variety of circumstances, it is often difficult for the physician to know whether, when, and how to select and use hypnotics and other sleep-promoting medications. Yet, with the more extensive pharmacological and clinical information now available, more effective day-to-day clinical decisionmaking is possible.

As an aid to clinicians, the National Institute of Mental Health and the Office of Medical Applications of Research of the National Institutes of Health convened a
Consensus Development Conference on November 15-17, 1983, to address these questions and develop principles to facilitate diagnosis and treatment. After a day and a half of presentation of data by experts, a
Consensus Panel consisting of psychiatrists, psychopharmacologists, biomedical researchers, epidemiologists, primary care physicians, and public representatives considered the evidence and agreed on answers to the following questions:

  1. Under what circumstances might a sleep-promoting medication be considered; in what types of sleep disturbances are sleep-promoting medications undesirable?
  2. What are the pharmacologic factors to be considered in the selection of sleep-promoting medications?
  3. What are the appropriate treatment strategies to be employed in using sleep-promoting medications on a short-term or long-term basis?
  4. What are the principal cautions and risks associated with prescribing these drugs; what special considerations should be applied in regard to medical status, age, concurrent drug use, or other factors?
  5. What research areas need further development?

Insomnia is a symptom or condition of heterogeneous origin. It signals the need for careful and systematic diagnostic inquiry. Primary medical, psychiatric, and other causes of insomnia should be identified and treated accordingly. Treatment of insomnia should start with the assessment and necessary correction of sleep hygiene and habits. Psychotherapeutic, behavioral approaches and pharmacotherapy, alone or in combination, should be considered in the formulation of a comprehensive treatment plan. When pharmacotherapy is indicated, benzodiazepines are preferable. Patients should receive the smallest effective dose for the shortest clinically necessary period of time; this recommendation applies especially to the elderly. The choice of a specific drug should be based upon its pharmacological properties in conjunction with the particular clinical situation and needs of the patient. Physicians should educate and monitor patients in order to evaluate and reduce the risks of dependence, side effects, and possible withdrawal difficulties. The treatment of insomnia will advance further with better understanding of the pathophysiologies of sleep disorders, as well as with the improvement of sleep-promoting agents and techniques.  

Under What Circumstances Might a Sleep-Promoting Medication Be Considered; In What Types of Sleep Disturbances Are Sleep-Promoting Medications Undesirable?

Accurate differential diagnosis is essential to effective management of patients with insomnia. The first obligation of the practitioner is to search for a specific psychiatric or medical disease as the underlying cause. This view considers insomnia as primarily one symptom of a symptom complex, which can be assessed by an appropriate medical history, physical examination, and laboratory procedures. Evaluation of the sleep history should include a review of the patient's usual sleeping habits with specific description of the sleep complaint (e.g., difficulty falling asleep, sleep disruptions, intermittent or persistent), bedtime routines and review of waking schedule, and use of prescription and non-prescription medications and alcohol, and may be aided by the use of a sleep diary. Treatment should be directed toward the medical or psychiatric condition and, if treatment is successful, the insomnia ordinarily responds concomitantly. This, however, may not be the case with medical conditions involving considerable pain or debility, where insomnia may remain as an unresponsive symptom. Adjunctive treatment with sleep-promoting medication may be of use in such cases.

Another strategy typically employed by tertiary referral sleep disorder clinics emphasizes not only a sleep-medical history and extensive review of 24-hour functioning, but also, when appropriate, application of sleep laboratory procedures to evaluate day and night sleep and physiological patterns. While a specialized taxonomy emphasizes primary sleep disorders and sleep disturbances associated with psychiatric, medical, or drug-related conditions, others find the DSM III psychiatric classifications adequate. To date, neither general clinical practice (which can manage the majority of disorders) nor special sleep disorder procedures have produced unambiguous indications for sleep-promoting medication.

At this stage of evolving knowledge, it is convenient for purposes of discussion to divide the insomnias into transient insomnia, short-term insomnia, and long-term insomnia. While there is not complete agreement in the field, many experts state that individuals with transient insomnia are normal sleepers who experience an acute stress or situation for several days (e.g., air travel to a new time zone, hospitalization for elective surgery) which affects their sleep adversely. Some advocate the use of sleep-promoting medication, especially if the situation can be anticipated or it will last only several days. Others feel that reasons for the transient insomnia should be explored or the situation should be dealt with by tolerating the sleep loss or observing good sleep hygiene (e.g., caffeine reduction, regulation of hours in bed, and, for the traveler, the bedtime hour).

Short-term insomnia is usually associated with a situational stress (e.g., acute personal loss) often related to work and family life or serious medical illness. Since this type of insomnia may last up to 3 weeks, sleep hygiene and non-drug procedures, sleep-promoting medications may be considered.

Controversy exists over the indication for medication in long-term insomnia. The clinician should undertake an extensive differential diagnostic workup prior to a treatment decision. The available data suggest that insomnia in one-third to one-half of patients in this category is related to underlying psychiatric conditions. A second group consists of individuals whose insomnia is related to chronic drug/alcohol dependence or abuse. Other causes of long-term insomnia include medical conditions, sleep apnea, periodic leg movement (myoclonus), 24-hour rhythm disturbances such as advanced and delayed sleep phase, or psychophysiological insomnia (no apparent psychiatric or medical syndrome). Since the prevalence of sleep apnea and nocturnal myoclonus increases in the elderly, patients suspected of having these disorders need careful inquiry and investigation, often in sleep disorders clinics, before sleep-promoting agents are prescribed.

Non-drug strategies such as exercise, decreased caffeine intake, elimination of alcohol and drugs, trial of biofeedback/relaxation or other stress reduction techniques are indicated as the initial approach to psychophysiological insomnia. A short trial (less than 1 month) of sleep-promoting medication concomitant with behavioral treatments may also be indicated.

Insomnia patients who have not responded to the aforementioned treatments and for whom major psychiatric or medical disorders have been specifically ruled out are the most appropriate for referral to a sleep disorders clinic. In addition to evaluation, such centers may provide specialized treatment. For example, the newer technique of chronotherapy for advanced and delayed sleep is warranted for selected individuals with work-shift schedule problems or other phase-shift sleep/wake problems, although qualified and interested practitioners can also learn and provide such treatment.

Several of the diagnostic categories of long-term insomnia may represent relative contraindications for sleep-promoting medications. While some practitioners have argued the case for sleep-promoting medication as an adjunct in psychiatric conditions, the appropriate treatment of the underlying condition usually will lead to improvement in sleep. One would only prescribe hypnotics to individuals with a known dependence on alcohol with considerable caution. The presence of sleep apnea, daytime sleepiness, or heavy snoring may also be reasons not to administer traditional sleep-promoting medications for long-term insomnia.  

What Are the Pharmacologic Factors To Be Considered in the Selection of Sleep-Promoting Medications?

Pharmacologic factors to be considered with hypnotic agents include the following: therapeutic index, dose, rate of absorption, lipophilicity, rate of tissue distribution, elimination half-life or clearance rate, presence or absence of active metabolites, presence or absence of drug interactions, and various pharmacodynamic characteristics which mediate drug effect.

The therapeutic index refers to the ratio of the lethal dose of a drug to its effective dose. The very favorable therapeutic index of the benzodiazepine class of hypnotic drugs more than any other factor accounts for the shift away from the barbiturates and related sleeping medications. Fatal overdoses are extremely rare unless these drugs are taken in combination with alcohol or other drugs. Since benzodiazepines largely have replaced other types of hypnotics, only pharmacologic characteristics of importance for this drug class will be discussed.

Dose is central to therapy because of the way it influences other pharmacologic factors. Although low lethality gives the physician considerable leeway in individualizing the dose for each patient, the principle of using the lowest effective dose is still a good guide in avoiding unwanted side effects.

Differences in rates of dissolution and absorption of benzodiazepine drugs from the gastrointestinal tract into the blood influence the time to peak plasma concentration and the time to onset of hypnotic effect. Significant differences in absorption rates have been reported for marketed benzodiazepine hypnotics, but sufficient clinical trial data are lacking to establish whether these are clinically meaningful. The rate of entry into the brain is governed largely by the solubility of drug in lipoid tissue, termed its lipophilicity. All benzodiazepines are relatively lipophilic. Where lipophilicity of two active agents is approximately equal, the rate of onset of hypnotic effect should be governed by dose and by rate of absorption from the GI tract into blood rather than by the rate of transfer from blood into the brain.

Along with dose, rate of tissue distribution and clearance rate of a drug determine its duration of action. A convenient way of estimating clearance is in terms of a drug's elimination half-life. The more slowly eliminated hypnotic is more apt to produce unwanted daytime sedation and to accumulate in the body with chronic administration. In recent years, drug development has focused on more rapidly eliminated (shorter half-life) benzodiazepine hypnotics in order to minimize these potential disadvantages. Two shorter half-life benzodiazepines are now approved as hypnotics: temazepam, with a half-life of 8-12 hours, and triazolam, with a half-life of 3-4 hours. Actually, several shorter acting benzodiazepines have been available for a number of years (e.g., oxazepam), but they have been promoted as anxiolytics. When given at appropriate dosage, these are effective hypnotics and are not associated with significant daytime sedation or cumulative effects. However, the short half-life may be associated with occasional next-day memory difficulties and with chronic use unwanted tolerance and decreased hypnotic effect may occur, as discussed in question 4.

Many benzodiazepines have several active metabolites. For example, flurazepam has two rapidly eliminated metabolic products, hydroxyethyl flurazepam and flurazepam aldehyde, and the slowly eliminated metabolite desalkylflurazepam with a half-life ranging from 40-100 hours. These various metabolites of flurazepam largely determine its clinical actions, both acute and chronic, but add complexity to its use with chronic administration and in the older patient. Triazolam and temazepam (like oxazepan and lorazepam) are not thought to have any significant active metabolites.

Although the benzodiazepines in therapeutic doses generally do not appear to inhibit or enhance the metabolism of other drugs, their effects do interact with those of ethanol and other sedative hypnotics. Thus CNS depressant effects of alcohol and the other benzodiazepines are additive. Furthermore, ethanol can slow the normal rate of liver metabolism of the benzodiazepine thereby increasing levels of the hypnotic drug. As another example, cimetidine significantly impairs the metabolism of most benzodiazepines, except for those metabolized exclusively by conjugation.

Finally, there are several pharmacodynamic factors that need to be considered. The problems of tolerance and neuronal adaptations, which are responsible for withdrawal symptoms and rebound insomnia, are discussed in question 4.

The interplay of these pharmacologic factors is important in achieving various clinical objectives, and often there is a balancing or tradeoff of one against the other. For example, it is possible to obtain a faster rate of onset by raising the dose, but this in turn may prolong duration of effect leading to unwanted daytime sedation, hangover, or memory problems. One drug may be preferred for a sleep latency problem and another for a problem of sleep maintenance or insomnia associated with high levels of anxiety. These differences in pharmacologic characteristics of the benzodiazepine hypnotics can be utilized in special clinical circumstances in order to individualize treatment.  

What Are the Appropriate Treatment Strategies To Be Employed in Using Sleep-Promoting Medications on a Short-Term or Long-Term Basis?

Patients should be considered for sleep-promoting drug therapy when they are significantly troubled by the presence or possibility of inadequate sleep or when the physician is concerned about the deleterious impact of disturbed or inadequate sleep on the patient's health, safety, and well-being.

As stated in question 1, the strategy should begin with an appropriate medical history and physical examination, with the identification, whenever possible, of potentially treatable causes of insomnia. The strategies for transient insomnia, short-term insomnia, and long-term insomnia will differ.

Transient insomnia refers to insomnia related to minor situational stress (e.g., hospitalization for elective surgery, jet travel). For this type of insomnia, drug treatment may or may not be necessary. Where elected, the treatment should be a small dose of a rapidly eliminated hypnotic unless sustained sedation is desired. Treatment may be needed for 1 to 3 nights.

Short-term insomnia is usually related to stress associated with work and family life, such as job loss, bereavement, or illness. For this type of insomnia, it is particularly important to educate the patient in regard to desirable sleep routines, including the avoidance of caffeine, alcohol, daytime naps, going to bed too early, etc. Simultaneously and during maintenance of good sleep hygiene, a benzodiazepine hypnotic may be used. If drug treatment is elected, the smallest effective dose should be used, with titration of dose if necessary, and for a treatment period usually of not more than 3 weeks.

Intermittent use of the drug is advisable, with skipping of nightly dosage after 1 or 2 good night's sleep. A benzodiazepine with a short half-life may be preferable if significant anxiety is not present, or to avoid unwanted daytime sedation. For other patients, a benzodiazepine with a long half-life may be preferable. Discontinuance of therapy should be carried out gradually.

Before a drug is chosen, the patient should be questioned about previous experience with specific medications. Therapy should also be individualized to take into account such factors as age and weight.

Patient/physician contact should be maintained, at least by phone, to achieve optimal dosage and monitor side effects. Patient education may include the use of written materials to reinforce verbal instruction on the benefits and hazards of drug therapy.

Long-term insomnia requires special medical, physiological, and psychiatric evaluation, as described under question 1. If a major psychiatric disorder exists, it needs to be treated appropriately. Specific treatment for chronic medical disorders may still leave a need for treatment of associated insomnia. In addition, certain specific sleep disturbances, such as sleep apnea, may need to be ruled out before treatment is undertaken for insomnia.

Long-term insomnia not attributable to disorders such as the above is best treated with a combined approach, employing sleep-promoting agents along with psychological-behavior therapies, such as relaxation techniques, sleep curtailment, or stimulus control therapy to undo negative conditioning related to sleep habits.

Benzodiazepines are the drugs of choice, and intermittent usage, such as 1 night in 3, is advised. This intermittent usage allows assessment of the possibility of discontinuing therapy. A benzodiazepine with a long half-life would seem appropriate in this circumstance. If benzodiazepines do not meet the patient's needs, the physician may elect to prescribe a sedative anti-depressant, e.g., amitriptyline 25-100 mg at bedtime.

For patients who respond to this program, it is wise to discontinue therapy gradually after 3 to 4 months. Patients who do not respond to treatment may have to be reevaluated for the possibility of other medical or psychiatric disorders or be referred to a sleep disorders clinic (see question 1).  

What Are the Principal Cautions and Risks Associated With Prescribing These Drugs; What Special Considerations Should Be Applied in Regard to Medical Status, Age, Concurrent Drug Use, or Other Factors?

The risks associated with pharmacologic treatment of sleep disturbance vary with the patient, the situation, the condition (type of sleep disturbance) being treated, and the specific agent selected. Since the benzodiazepines are now the sleep-promoting agents of choice, our discussion focuses on them.

Perhaps the most common risk associated with the use of the benzodiazepines is diminished daytime performance as a result of carryover effects. Despite the development of some degree of tolerance, cognitive or psychomotor impairment can be a significant problem for many patients when more slowly eliminated benzodiazepines are given over a period of weeks. Even with short term use of slowly eliminated drugs, decreased performance the next day is a potentially serious risk for individuals in those occupations requiring high levels of visual-motor coordination. This problem can be reduced by using lower doses or more rapidly eliminated drugs.

All sedative-hypnotics, including the benzodiazepines, cause systematic alterations in the architecture of sleep (e.g., decreased amount of delta wave sleep) and raise thresholds for arousal from sleep. The practical implications of these observations are presently unknown.

Benzodiazepines can interact with a number of other drugs commonly used by patients with insomnia (see question 2), but the practical significance of these interactions is uncertain. An important interaction is that with alcohol, where the psychomotor impairing effects are additive. This interaction is of concern since the subjective sense of intoxication may not be enhanced. Further, with the slowly eliminated benzodiazepines, plasma levels may persist for days after benzodiazepine use has ceased.

Drug dependence on sedative-hypnotics (i.e., psychological dependence and compulsive drug use) has been recognized for more than 100 years. The shorter-acting barbiturate and the shorter-acting non-barbiturate hypnotics (e.g., methaqualone, glutethimide) represent a greater risk in this respect than the more slowly eliminated benzodiazepines. There is as yet too little experience with the more rapidly eliminated benzodiazepines to gauge their dependence liability relative to other benzodiazepines when prescribed for sleep disturbance. The development of dependence can be minimized by limiting the amount prescribed and the duration of use and by careful monitoring of use and refills.

Adaptive changes to the actions of general CNS depressants and benzodiazepines probably begin with the first doses given. These changes are responsible for the partial tolerance that typically develops with the sleep-promoting and psychomotor-impairing effects of these drugs, as well as for rebound and withdrawal phenomena. Even after short periods of use, if the benzodiazepines could be abruptly removed from their sites of action, in most cases some rebound or withdrawal phenomena would be detectable with appropriate measuring instruments. Technically, this represents physical dependence. However, unless high doses of benzodiazepines are used for several weeks or lower doses are used for a number of months, physical dependence is not likely to be of sufficient severity to cause major clinical problems. With the more rapidly eliminated benzodiazepines, and to a far lesser degree, with the more slowly eliminated benzodiazepines, some rebound exacerbation of sleep disturbance may occur when the drugs are discontinued. Tapering the dose can reduce, but probably not eliminate, this problem entirely. The more rapid onset of these rebound effects after discontinuing the more rapidly eliminated drugs could, in theory, increase the tendency of the patient to believe they are needed for continued satisfactory sleep. Good management should include preparing the patient for this transient exacerbation of sleep disturbance when the drugs are reduced or stopped.

Clinically significant withdrawal phenomena of varying intensity can occur when benzodiazepines have been administered for prolonged periods especially if the daily dosage has exceeded the recommended amounts. Based on experience with barbiturates, the severity of withdrawal may prove to be considerably greater if more rapidly eliminated benzodiazepines are abused for prolonged periods and are then abruptly discontinued.

In the past, suicide was frequently accomplished by the ingestion of barbiturates and non-barbiturate hypnotics. Although the benzodiazepines carry less risk of fatality in such situations, caution is nevertheless indicated where suicide is a potential concern. Caution must be taken to write prescriptions for a limited period of time and to monitor refills so that the drugs cannot be readily utilized in a lethal fashion. When benzodiazepines are lethal, it is usually because they are combined with alcohol or other drugs.

Certain populations require special considerations. Aged patients, who tend to clear drugs more slowly and who are more sensitive to a given blood level of benzodiazepines, are more likely to develop cognitive and motor impairments when given the more slowly eliminated benzodiazepines. Ataxia and problems with memory and thinking are possible complications that may not appear until several weeks after beginning treatment. Similar problems may develop in younger patients on renal dialysis or with impaired hepatic function. Dosages for these populations must be carefully adjusted, and more rapidly eliminated drugs are preferable. The physician must be alert to the possibility of drug interactions for all patients, but most especially for this elderly group which is often being treated with other drugs.

Sleep apnea is more common among obese or elderly patients, especially males. Treatment with any hypnotic may exacerbate sleep apnea. While reports of death due to using hypnotics in therapeutic doses are rare, laboratory studies show an increase in frequency and duration of apnea episodes and a decreased 02 saturation of blood.

Pregnant patients also require special attention since all benzodiazepines carry special warnings for this population.

Patients with histories of alcoholism or other types of drug dependence are at higher risk for developing dependence on sedative hypnotics and benzodiazepines.  

What Research Areas Need Further Development?

A number of areas deserve research attention and support by health research agencies. These include epidemiologic studies on insomnia in the general population as well as in the primary care office setting, including specific complaints that bring insomniacs to doctors. Such studies should describe patients' demographic and medical characteristics and consider factors related to physicians' prescribing patterns for sleep-promoting drugs. Also needed are studies of the cost-effectiveness of various diagnostic and treatment approaches. The role of sleep disorders centers in providing diagnostic and therapeutic guidance, criteria for referral and, in particular, their potential for generating sound clinical research, should be studied. Also deserving of study is the process of self-treatment by insomniacs, including the magnitude, therapeutic performance, and adverse effect record of over-the-counter hypnotic drug usage. The nature and extent of daytime performance deficits in insomniacs, with and without treatment, is not adequately documented. We need to know the somatic, psychological, social, and economic costs of untreated insomnia, and the impact (positive or negative) on these costs of various therapeutic approaches, especially in long-term insomnia. Research should continue on the function and physiology of normal sleep and the pathophysiology of abnormal sleep. Finally, the search for new and better treatments for insomnia should continue.  

Consensus Development Panel

Daniel X. Freedman, M.D.
Judson Braun Professor of Psychiatry and Pharmacology
Director of the Division of Adult Psychiatry,
Neuropsychiatric Institute
University of California,
Los Angeles, Center for the Health Sciences
Los Angeles, California
John S. Derryberry, M.D.
Past President
American Academy of Family Physicians
Shelbyville, Tennessee
Daniel D. Federman, M.D.
Professor of Medicine
Harvard Medical School
Boston, Massachusetts
Jerome H. Jaffe, M.D.
Professor of Psychiatry
University of Connecticut Medical School, Farmington
Associate Chief of Staff for Education
Veterans Administration Medical Center
Newington, Connecticut
Elizabeth A. Jenkins, M.B.A.
Administrative Director
Clinical Laboratories
Mary Hitchcock Memorial Hospital
Hanover, New Hampshire
T. Byram Karasu, M.D.
Professor and Deputy Chairman
Department of Psychiatry
Albert Einstein College of Medicine
Montefiore Medical Center
Bronx, New York
C. James Klett, Ph.D.
Cooperative Studies Program Coordinating Center
Veterans Administration Medical Center
Perry Point, Maryland
Eleanor S. Kohn, M.S.W.
Past Member
National Institute of Mental Health Advisory Council
Danbury, Connecticut
David J. Kupfer, M.D.
Professor and Chairman
Department of Psychiatry
Western Psychiatric Institute and Clinic
University of Pittsburgh School of Medicine
Pittsburgh, Pennsylvania
Louis Lasagna, M.D.
Professor of Pharmacology and Medicine
University of Rochester Medical School
Rochester, New York
John H. Renner, M.D.
Director, S.S.M. Regional Family Practice Residency Program and National Family Practice Research and Development Center
Kansas City, Missouri
Donald S. Robinson, M.D.
Professor and Chairman
Department of Pharmacology
Marshall University
School of Medicine
Huntington, West Virginia
Bonnie L. Svarstad, Ph.D.
Associate Dean
Associate Professor of Social Studies of Pharmacy
University of Wisconsin-Madison School of Pharmacy
Madison, Wisconsin
Harold L. Williams, Ph.D.
Distinguished Professor of Psychiatry and Behavioral Science
University of Oklahoma
Health Sciences Center
Oklahoma City, Oklahoma


Mitchell B. Balter, Ph.D.
"Prevalence of Insomnia and Drug Treatment"
Chief Applied Therapeutics and Health Practices Program
National Institute of Mental Health
Rockville, Maryland
Douwe D. Breimer, Ph.D.
"Pharmacokinetics of the Non-Benzodiazepines"
Department of Pharmacology
University of Leiden Sylvius Laboratories
Jonathan O. Cole, M.D.
"Hypnotics and Major Psychiatric Disorders"
Chief of Psychopharmacology
McLean Hospital
Belmont, Massachusetts
William Dement, M.D., Ph.D.
"What, Why, and How to Treat with Medication"
Director Sleep Disorder Center
Stanford University School of Medicine
Stanford, California
David J. Greenblatt, M.D.
"Pharmacokinetics of the Benzodiazepines"
Professor of Psychiatry and Associate Professor of Medicine
Tufts University School of Medicine
Chief Division of Clinical Pharmacology
New England Medical Center Hospital
Boston, Massachusetts
Peter J. Hauri, Ph.D.
"Pharmacologic and Nonpharmacologic Strategies"
Dartmouth Sleep Disorder Center
Dartmouth Medical School
Hanover, New Hampshire
Leo E. Hollister, M.D.
"Management of Dosage Regimens"
Senior Medical Investigator
Veterans Administration Medical Center
Palo Alto, California
Herschel Jick, M.D.
"Adverse Drug Reactions"
Associate Professor of Medicine
Boston University School of Medicine
Director Boston Collaborative Drug Surveillance Program
Boston University Medical Center
Waltham, Massachusetts
Laverne Johnson, Ph.D.
"Residual Effects"
Chief Scientist Naval Health Research Center
San Diego, California
Anthony Kales, M.D.
"An Overview of Insomnia and the Use of Hypnotics"
Professor and Chairman
Department of Psychiatry Director
Sleep Research and Treatment Center
Pennsylvania State University College of Medicine
Hershey, Pennsylvania
John Marks, M.A., M.D., F.R.C.P., M.R.C.Psych.
"Measurement of Benefit and Risk"
Fellow, Tutor, and Director of Medical Studies
Girton College
Glen D. Mellinger, Ph.D.
"Prevalence of Insomnia and Drug Treatment"
Director Institute for Research in Social Behavior
Oakland, California
Wallace B. Mendelson, M.D.
"Clinical Risks: A Practical Appraisal"
Chief Unit on Sleep Studies
National Institute of Mental Health
Bethesda, Maryland
Anthony N. Nicholson, O.B.E., D.Sc.,M.B.,Ch.B., Ph.D., F.R.C.P.(ath)
"Hypnotics and Occupational Demands"
Consultant in Aviation Medicine
Royal Air Force Institute of Aviation Medicine
Farnborough, Hampshire
Robert E. Rakel, M.D.
"Practitioners' Perspective"
Professor and Head Department of Family Practice
University of Iowa
Iowa City, Iowa
Karl Rickels, M.D.
"Anxiety Insomnia and Withdrawal"
Stuart and Emily Mudd Professor of Human Behavior
Professor of Psychiatry
Department of Psychiatry
University of Pennsylvania School of Medicine
University Hospital
Philadelphia, Pennsylvania
Howard P. Roffwarg, M.D.
"Contexts in Which Insomnia Occurs"
Professor and Director of Research
Director Sleep Study Unit
Department of Psychiatry
Presbyterian Hospital of Dallas
University of Texas Health Science Center at Dallas
Dallas, Texas
Thomas Roth, Ph.D.
"Efficacy Criteria"
Director Sleep Disorders and Research Center
Henry Ford Hospital
Clinical Professor Department of Psychiatry
University of Michigan Medical School
Detroit, Michigan
John W. Rowe, M.D.
"Age as a Modulator of Adverse Drug Reactions"
Associate Professor and Director Division on Aging
Harvard Medical School
Director Geriatric Research Education
Clinical Center Veterans Administration
Boston, Massachusetts
Edward M. Sellers, M.D., Ph.D., F.R.C.P.(C)
"Alcohol and Drug Interactions"
Professor of Pharmacology and Medicine
University of Toronto
Director Clinical Institute Addiction Research
Toronto, Ontario
Constantin R. Soldatos, M.D.
"Relation of Elimination Half-Life to Efficacy and Side Effects of Benzodiazepine Hypnotics"
Director Sleep Research Unit
University of Athens School of Medicine
Athens, GREECE
Clinical Professor, Department of Psychiatry
Pennsylvania State University College of Medicine
Milton S. Hershey Medical Center
Hershey, Pennsylvania

Planning Committee

Mitchell B. Balter, Ph.D.
Chief, Applied Therapeutics and Health Practices Program
National Institute of Mental Health
Rockville, Maryland
Louis Aronow, Ph.D.
Professor and Chairman, Department of Pharmacology
Uniformed Services
University of the Health Sciences
Bethesda, Maryland
Daniel X. Freedman, M.D.
Judson Braun Professor of Psychiatry and Pharmacology
Director of the Division of Adult Psychiatry,
Neuropsychiatric Institute
University of California, Los Angeles,
Center for the Health Sciences
Los Angeles, California
J. Christian Gillin, M.D.
Professor of Psychiatry
University of California, San Diego
San Diego, California
Peter J. Hauri, Ph.D.
Dartmouth Sleep Disorder Center
Dartmouth Medical School
Hanover, New Hampshire
Harold A. Pincus, M.D.
Special Assistant to the Director
National Institute of Mental Health
Rockville, Maryland
Howard P. Roffwarg, M.D.
Professor and Director of Research
Director, Sleep Study Unit
Department of Psychiatry
University of Texas Health Science Center at Dallas
Presbyterian Hospital of Dallas
Dallas, Texas
Richard I. Shader, M.D.
Professor and Chairman
Department of Psychiatry
Tufts University School of Medicine
New England Medical Center Hospital
Boston, Massachusetts
Monica Walters
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland
Richard Jed Wyatt, M.D.
Adult Psychiatry Branch
Division of Special Mental Health Research
National Institute of Mental Health
St. Elizabeths Hospital
Washington, D.C.

Conference Sponsors

National Institute of Mental Health
Herbert Pardes, M.D. Director
Office of Medical Applications of Research
J. Richard Crout, M.D. Director

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