Updated: Aug 3, 2009
Sleep disorders are commonly underdiagnosed and a significant source of concern in the geriatric population.1 Several diverse factors may contribute to sleep disturbances in a large proportion of the elderly. These contributing factors include changes associated with aging, such as retirement, health problems, death of spouse/family members, as well as changes in circadian rythym.2 Changes in sleep patterns may be part of the normal aging process; however, many of these disturbances may be related to pathological processes that are not considered a normal part of aging.3,4
In addition to affecting quality of life (including excessive daytime sedation, physical, psychological, cognitive problems affecting overall health of the patient4 ), sleep disorders have been implicated with an increased mortality rate. Unfortunately, the number of medications increases with age, which in itself can lead to more morbidity, mortality, side effects such as falls5 , cognitive impairment, financial stressors, and even sleep disturbances.6 Treating insomnia in the elderly can improve the overall health of the patient, but care must be taken when medications are used in this particular population.1
Treatments for sleep disorders include over-the-counter and prescription medications, behavioral treatments, relaxation techniques, sleep hygiene, sleep restriction, light therapy7 , cognitive behavioral therapies3,8 , valerian, Tai Chi, yoga, meditation, acupuncture, and acupressure9 .
See Medscape's Insomnia and Sleep Health Resource Center.
Normal sleep is organized into different stages that cycle throughout the night. Polysomnographic studies have classified the sleep stages into the following categories:
The following definitions are provided:
Older people spend more time in bed to get the same amount of sleep they obtained when they were younger; however, the total sleep time, at most, is only slightly decreased, with an increase in nocturnal awakenings and daytime napping. They often report having earlier bedtimes and an increased sleep latency (time to fall asleep), but excessive daytime somnolence is not part of normal aging. Older subjects have been observed to be more easily aroused from sleep by auditory stimuli, suggesting increased sensitivity to environmental stimuli.
Sleep disturbance or insomnia is the third most common patient complaint, ranking behind headaches and the common cold. Approximately 15% of the adult population in the United States has insomnia of significant enough severity to seek medical attention. More than 50% of elderly people have insomnia.11 Of the US population, 1.7% receive a hypnotic prescription annually, and another 0.8% purchase nonprescription sleep aids. Fifty million Americans occasionally take some form of sleep medication.
In addition to affecting the quality of life, sleep disorders have been implicated with excess mortality. Two primary sleep disorders that increase with age are sleep apnea (SA) and periodic limb movements in sleep (PLMS). Sleep apnea can result in daytime hypersomnolence, systemic hypertension, cardiac arrhythmias, cor pulmonale, and sudden death. Among a random sample of 427 older volunteers, 45% had PLMS, and they each reported dissatisfaction with sleep, sleeping alone, and kicking at night.
In a study of sleep-disordered breathing (SDB) and nocturnal cardiac arrhythmias in older men, Mehra et al found that the likelihood of atrial fibrillation or complex ventricular ectopy (CVE) increased along with the severity of sleep-disordered breathing. In addition, different forms of sleep-disordered breathing were associated with the different types of arrhythmias.
Polysomnography in 2,911 participants showed that the odds of atrial fibrillation (P=0.01) and of complex ventricular ectopy (P <.001) increased with increasing quartiles of the respiratory disturbance index (a major index including all apneas and hypopneas). Central sleep apnea was more strongly associated with atrial fibrillation (odds ratio [OR], 2.69; 95% CI, 1.61-4.47) than with complex ventricular ectopy (OR, 1.27; 95% CI, 0.97-1.66). In contrast, obstructive sleep apnea and hypoxia was associated with complex ventricular ectopy; participants in the highest hypoxia category had an increased odds of CVE (OR, 1.62; 95% CI, 1.23-2.14) compared with the lowest quartile. The results suggest that different sleep-related stresses may contribute to atrial and ventricular arrhythmogenesis in older men.12
Older women are more likely to experience insomnia than older men. In a large epidemiological study of people older than 70 years, 35% of women reported moderate-to-severe insomnia, compared to only 13% of men.13
More than one half of people older than 64 years who live at home and two thirds of people older than 64 years who reside in a long-term care facility are estimated to have some form of sleep disturbance.
Evaluation begins with a complete sleep history. The assessment of this patient includes a detailed multidisciplinary approach. Sleep problems in the elderly include hypersomnia, disorientation, delirium, impaired intellect, decreased cognition, psychomotor complaints, increase accidents, falls, and financial issues.14 In the geriatric population, the most frequent complaints are problems initiating or maintaining sleep.15
Physical examination and the Mental Status Examination may give clues to the causes of sleep disturbance (eg, obesity with resulting obstructive sleep apnea [SA], depression). These are further discussed below in Causes. In addition, potential complications of sleep disorders, such as hypertension from obstructive SA, may also be discovered.
Obtain a complete medical history, and perform a complete mental status examination, physical examination, and neurologic examination to assist with the evaluation and rule out other disease processes.
Although the mental status examination varies for each patient, examples of items to assess are listed below. Because of the variability of the presentation of the disorder, any or all symptoms of insomnia or other sleep disorders may manifest depending on the presenting subtype.
Two primary sleep disorders that increase with age are sleep apnea (SA) and periodic limb movements in sleep (PLMS).
SA is the lack of breathing during sleep, and it can be obstructive (upper airway occlusion), central (primary neurologic disease), or mixed. People with SA may experience waking with gasping, confused wandering in the night, and thrashing during sleep.
Because waking resolves obstructive apnea, avoid sedatives and hypnotics in these patients because such agents can further relax the pharynx dilators, thereby worsening the apnea. Martin et al found that among healthy older adults living in community settings, the prevalence of SA (defined by > 5 apneas per h) was 28% in men and 20% in women.
Martin et al also found that among a random sample of patients in a medical ward, the prevalence of SA was higher (33%). This may be because of the high incidence of congestive heart failure (CHF) in this group. Significantly, many elderly inpatients are prescribed hypnotics, which can exacerbate SA. SA occurs in 42% of people with dementia who live in nursing homes and correlates with cognitive function.
An interaction between SA and the cognitive deterioration of dementia is likely, which could be exacerbated with the use of hypnotics and other CNS depressants. SA can result in daytime hypersomnolence, systemic hypertension, cardiac arrhythmias, cor pulmonale, and sudden death.
PLMS or nocturnal myoclonus is repetitive, unilateral, or bilateral stereotyped leg jerks that arouse the subject from sleep.
Among a random sample of 427 older volunteers, 45% had PLMS; this statistic correlated with dissatisfaction with sleep, sleeping alone, and kicking at night. The incidence of nocturnal myoclonus increases with age, and the likelihood of an associated sleep-wake complaint is related to the absolute number and intensity of the leg movements.
Psychiatric disorders
Circadian rhythm sleep disorders
Many abnormalities of the sleep-wake cycle manifest as sleep-wake disorders. These conditions include the following:
Psychophysiological insomnia
This is associated with acute emotional conflicts or reactions and is transient in nature. If it is associated with frustration to fall asleep, thereby resulting in arousal, it can be persistent in nature.
Environmental sleep disorders
Ferritin levels of less than 50 ng/mL were present in elderly patients with restless legs syndrome.
After a detailed history, a clinician may find it necessary to refer the patient to a sleep disorders center for evaluation of sleep apnea.
Consultation with appropriate specialists may be indicated, depending on the underlying causes of the sleep disorder, eg, psychiatric consultation for severe depression, pulmonary or surgical consultation for obstructive sleep apnea.
The first priority should be to determine the underlying cause of the sleep disorder, rather than just treat insomnia symptomatically. Usually, treatment on a short-term basis together with sleep hygiene is appropriate for transient insomnia, for example, second to bereavement or acute hospitalization. Insomnia in this population is treated with antidepressants, benzodiazepines, nonbenzodiazepines, melatonin agonist, and herbals. Medications, if used, should be started with low dose and monitored for side effects.16
In March of 2007, the FDA requested that the manufacturers of 13 sedative-hypnotic medications (such as, temazepam, flurazepam, triazolam, estazolam, zolpidem, zalepon, eszoplicone, quazepam, ramelton, butabarbitol, and secobarbitol) change their labeling to include stronger language about the risks of severe allergic reactions and complex sleep-related behaviors (eg, driving, making telephone calls, eating, having sex while not fully awake).
According to the 1990 National Institutes of Health (NIH) consensus statement, hypnotics should be used on a limited short-term period and should only be used for older adults with transient insomnia because of increased hypnotic-related adverse effects. Avoid over-the-counter hypnotics (eg, diphenhydramine) because they have strong anticholinergic effects.
Barbiturates also are not indicated for insomnia, and psychiatric consultation may become necessary for patients receiving barbiturates for many years. The advantage of chloral hydrate is its rapid onset and rapid metabolism, although whether it is safe and well tolerated in the older population is unclear. Barbiturates are effective only for short-term use, losing much of their effectiveness after 2 weeks of administration. They are not used for insomnia in older patients.
Benzodiazepines remain the most commonly prescribed agents for sleep. The major advantages of the benzodiazepines (short and intermediate acting) are their relative safety in overdose, lower addiction risk, and weak interaction with other drugs. They should be used for a maximum of 2-3 weeks, or, if used longer, they should be used for only 2-3 nights per week. Because continued use results in increasing tolerance and increasing dose, care must be taken to avoid dependence. While the short- and intermediate-acting benzodiazepines are less likely to be associated with falls and hips fractures than the barbiturates and the longer-acting benzodiazepines, they are still a risk factor for falls in the older population.
Benzodiazepines are also more likely to produce the most pronounced rebound and withdrawal symptoms after discontinuation of the drug. Tapering the dosage can reduce rebound insomnia after discontinuation of these agents. Do not use long-acting agents (eg, flurazepam) in the older population because of the long half-life (2-8 d) and the tendency to accumulate over several days or weeks. These drugs are associated with daytime sedation, lethargy, ataxia, falls, and cognitive and psychomotor impairment.
Newer nonbenzodiazepines hypnotics like zolpidem, zaleplon, and eszoplicone do not cause rebound insomnia or withdrawal symptoms at discontinuation. Eszoplicone is approved for prolonged use.
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Rapidly absorbed and eliminated and may cause rebound insomnia, anterograde amnesia, and confusion, especially in elderly individuals.
Older patient: 0.125 mg PO hs; use 0.25 mg only in patients who are exceptional and do not respond to a trial of lower dose; not to exceed 0.25 mg/d
Not established
Increased toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohol
Documented hypersensitivity; narrow-angle glaucoma; untreated obstructive SA; history of substance abuse
X - Contraindicated; benefit does not outweigh risk
Caution and close monitoring needed in hepatic disease, low albumin levels, renal or pulmonary disease; causes residual daytime sedation, impairs cognition, and increases risk of falls, especially in older people; caution with other CNS depressants
Structurally dissimilar to benzodiazepines but similar in activity with the exception of having reduced effects on skeletal muscle and seizure threshold. Advantage of no rebound insomnia or anxiety at discontinuation. At recommended doses, it is as effective as triazolam. Adverse CNS effects (eg, nightmares, agitation, drowsiness) noted in 10% of patients. As with benzodiazepine hypnotics, is approved only for short-term use (3-4 wk maximum) and, if used longer, for only 2-3 nights/wk.
5 mg PO hs; not to exceed 10 mg
Not established
Increases toxicity of alcohol and CNS depressants
Documented hypersensitivity; breastfeeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Monitor elderly people for impaired cognitive or motor performance
Short-acting pyrazolopyrimidine hypnotic with full agonistic activity on central benzodiazepine receptors (B21 type). At small doses, it is an affective sleep inducer with limited risk of disturbance in morning performance. Like zolpidem, zaleplon is particularly suitable for treatment of initial insomnia and does not cause rebound insomnia and withdrawal symptoms at discontinuation. Approved only for short-term use (3-4 wk maximum), and, if used longer, limit use to only 2-3 nights/wk.
5 mg PO hs
Not established
Cimetidine significantly increases levels
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Failure of insomnia to remit after 7-10 d of treatment may indicate need for evaluation of a primary psychiatric or medical illness; reevaluate patient if needs to be taken for >2-3 wk (not to prescribe in quantities exceeding a 1-mo supply); caution in patients exhibiting signs or symptoms of depression
Nonbenzodiazepine hypnotic pyrrolopyrazine derivative of the cyclopyrrolone class. The precise mechanism of action is unknown but is believed to interact with GABA-receptor at binding domains close to or allosterically coupled to benzodiazepine receptors. Indicated for insomnia to decrease sleep latency and improve sleep maintenance. Short half-life of 6 h. Higher doses (ie, 2 mg for elderly adults and 3 mg for nonelderly adults) are more effective for sleep maintenance, whereas lower doses (ie, 1 mg for elderly adults and 2 mg for nonelderly adults) are suitable for difficulty in falling asleep.
Nonelderly adults: 2 mg PO hs; may increase to 3 mg PO hs prn
Elderly adults: 1 mg PO hs initially; not to exceed 2 mg PO hs
Severe hepatic impairment: Do not exceed 2 mg PO hs
<18 years: Not established
>18 years: Administer as in adults
CYP3A4 and CYP2E1 substrate; potent CYP3A4 inhibitors (eg, ketoconazole, itraconazole, clarithromycin, nefazodone, ritonavir, nelfinavir) increase AUC, Cmax, and t1/2 and therefore potential toxicity (decrease dose); potent CYP3A4 inducers (eg, rifampicin) increase clearance; coadministration with alcohol or other CNS depressants may increase effect and toxicity (decrease dose); coadministration with olanzapine may decrease DSST scores; sleep onset may be delayed if taken with or immediately after a high-fat or heavy meal
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause dyspepsia, headache, or coldlike symptoms; rare adverse effects associated with hypnotics include short-term amnesia, confusion, agitation, hallucinations, worsened depression, or suicidal thoughts; high doses (ie, 6-12 mg) produce euphoric effects similar to those of diazepam 20 mg; anxiety, abnormal dreams, nausea, and upset stomach may occur within 48 h after discontinuing; alertness may be affected the following day; use caution while operating machinery or driving a car
Sedative hypnotic with short onset of effects and relatively long half-life. By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation. Helpful for sleep maintenance insomnia and should be taken 30 min before bedtime. Causes less withdrawal and rebound than short-acting benzodiazepines but may cause more daytime sedation.
0.5-1 mg PO hs
Not established
Toxicity of benzodiazepines in CNS increases when used concurrently with alcohol, phenothiazines, barbiturates
Documented hypersensitivity; preexisting CNS depression, hypotension, and narrow-angle glaucoma
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in renal or hepatic impairment, myasthenia gravis, organic brain syndrome, or Parkinson disease;
like all benzodiazepines, danger of abuse and physical dependence; avoid abrupt cessation
Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Intermediate-acting agent that is helpful for sleep-maintenance insomnia. If patients also have difficulty falling asleep, agent should be taken 30 min before bedtime. Causes less withdrawal and rebound than short-acting benzodiazepines but may cause more daytime sedation.
15 mg PO hs
Not established
Increased toxicity of benzodiazepines in CNS with coadministration of phenothiazines, barbiturates, alcohol
Documented hypersensitivity; narrow-angle glaucoma; untreated obstructive SA; history of substance abuse; severe uncontrolled pain
X - Contraindicated; benefit does not outweigh risk
Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity);
like all benzodiazepines, danger of abuse, addiction, and physical dependence; avoid abrupt cessation
Sedating antidepressants (eg, trazodone, nefazodone), in low doses, can also be prescribed at bedtime for insomnia. Indicated for use when patient has a previous history of substance abuse. As with other antidepressants, little scientific evidence supports efficacy in the treatment of insomnia without associated depression and their use in patients with insomnia but without depression is not FDA approved and should be considered off label use.
Increases concentration of serotonin and norepinephrine in the CNS by inhibiting their reuptake by presynaptic neuronal membrane. These effects are associated with a decrease in symptoms of depression.
30-150 mg/d PO hs or 2-3 divided doses; gradually increase dose to 300 mg/d prn
<12 years: Not recommended
>12 years: 25-50 mg/d PO hs or bid/tid and increase gradually to 100 mg/d
Decreases antihypertensive effects of clonidine but increases effects of sympathomimetics and benzodiazepines; effects of desipramine increase with phenytoin, carbamazepine, and barbiturates
Documented hypersensitivity; urinary retention; acute recovery phase following myocardial infarction; glaucoma
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in cardiovascular disease, conduction disturbances, seizure disorders, urinary retention, hyperthyroidism and patients receiving thyroid replacement
Exhibits both noradrenergic and serotonergic activity. In cases of depression associated with severe insomnia and anxiety, shown to be superior to other SSRI drugs.
15 mg PO hs initially; may increase by 15 mg increments q1-2wk, not to exceed 45 mg hs
Not established
May increase effect of CNS depressants; concurrent administration with MAOI may trigger hypertensive crisis
Documented hypersensitivity; MAOI within 14 d
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May cause drowsiness; discontinue use if patient develops sore throat, fever, or other signs of infection; suicide ideation is inherent in depression and may persist until significant remission occurs; severe neutropenia reported in clinical trials
Antagonist at the 5-HT2 receptor and minimally inhibits the reuptake of 5-HT. Has negligible affinity for cholinergic and histaminergic receptors. Not associated with tolerance or withdrawal effects. Associated orthostatic hypotension can be minimized by administration with food. Limited data exist regarding efficacy in patients who are not depressed, and the FDA does not approve it as a hypnotic.
50 mg PO hs
Not established
May enhance response to alcohol, barbiturates, and other CNS depressants; cimetidine significantly increases levels of trazodone; serotonin syndrome may occur when used with other serotonergic agents, such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, nefazodone, SSRIs, but especially with MAOIs
Documented hypersensitivity; MAOIs use within 14 d of initiating treatment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypotension has occurred, including orthostatic hypotension and syncope; may produce drowsiness, dizziness, or blurred vision; patients taking this medication should be cautious while driving or performing other tasks requiring alertness, coordination, or dexterity; caution in cardiac disease, cerebrovascular disease, or seizures; discontinue therapy and reevaluate if priapism occurs
Antagonist at the 5-HT2 receptor and inhibits the reuptake of 5-HT. Has negligible affinity for cholinergic and histaminergic receptors.
50 mg PO hs
Not established
Increases effects of digoxin, carbamazepine, triazolam, alprazolam, and protease inhibitors through its effect of inhibiting CYP450 3A4 enzyme; serotonin syndrome may occur when used with other serotonergic agents, such as buspirone, meperidine, tramadol, dextromethorphan, triptans, mirtazapine, SSRIs, but especially with MAOIs
Documented hypersensitivity; MAOIs use within 14 d of initiating treatment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in cardiac disease, cerebrovascular disease, or seizures
These agents may promote sleep. Ramelteon does not cause rebound insomnia or withdrawal symptoms at discontinuation. It is approved for prolonged use.
Melatonin receptor agonist with high selectivity for human melatonin MT1 and MT2 receptors. MT1 and MT2 are thought to promote sleep and be involved in maintaining circadian rhythm and normal sleep-wake cycle. Indicated for insomnia characterized by difficulty with sleep onset.
8 mg PO 30 min before bedtime on empty stomach
Not established
Major substrate of cytochrome P450 CYP1A2 and minor substrate of CYP2C and CYP3A4; strong CYP1A2 inhibitors (eg, fluvoxamine) increase AUC up to 190-fold and Cmax 70-fold; strong CYP inducers (eg, rifampin) decrease total exposure by mean of 80%; strong CYP3A4 inhibitors (eg, ketoconazole) and strong CYP2C9 inhibitors (eg, fluconazole) may increase serum levels
Documented hypersensitivity; strong cytochrome P450 CYP1A2 inhibitors (eg, fluvoxamine); severe hepatic impairment
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
May affect reproductive hormones in adults (eg, decreased testosterone levels, increased prolactin levels), further study required to determine safety in prepubescent and pubescent children; caution with mild hepatic impairment; adverse effects leading to discontinuation in clinical trials included: dizziness, nausea, fatigue, headache, and worsening insomnia
Health professionals must continually educate themselves on the topic of sleep disorders in the geriatric population so they can properly educate the patients and caregivers about insomnia. With the aid of clinical studies and various forms of research, a wealth of new information on insomnia is available. These data inform health professionals about the different types of insomnia, available treatments, and good sleep practices. However, if this information is not utilized, it will be a huge disservice to the elderly patient population.
When a person experiences significant and prolonged sleep disturbance, they will generally contact their primary care provider for an evaluation. This evaluation may consist of a medical history review, concomitant medications, physical examination, lab work, and a Mental Status Examination. If the provider is unable to determine the underlying causality of the sleep disturbance, referral to a psychiatrist or sleep specialist may be necessary. At this point, a more in-depth examination is performed to rule out other potential contributing factors and to reach a diagnosis. Determining the causality of the sleep disturbance is imperative to be able to educate patients and caregivers about treatment alternatives.
Individuals should be made aware that obtaining 8 hours of sleep a night is not crucial. Sleep needs are individualized. Although one person may need 10 hours of sleep, another person may only need 5 hours. The amount of sleep we require tends to change with age. If a significant change in amount of sleep occurs, yet there are no disturbances in daily functioning, there shouldn't be a cause for worry. When significant disturbance in daily functioning has occurred, it is time to educate the patient about available treatment options.
Today, a variety of options are available that do not necessarily include the use of prescription medications. However, if prescription medications are warranted, there are many to choose from. Certain medications should be avoided in the elderly population (see Medication section for further information). If medication is not preferred, healthcare professionals can educate patients about other alternatives.
Experts suggest stimulus control, which means using the bed for only sleep and sex. If people are used to reading or watching television in bed, they are encouraged to leave the bedroom and engage in a relaxing activity elsewhere until they are sleepy and ready to return to bed. Teaching patients muscular relaxation techniques to reduce tension and promote sleep is also useful. Regardless of the underlying causes of insomnia, general habits should be practiced for good sleep. Patients should be instructed to go to bed at the same time, wake up at the same time, and avoid daytime napping, caffeine, heavy meals, nicotine, alcohol, and exercise at bedtime. Another useful tool is to turn the bedroom into an environment that is quiet, dark, cool, and one that ultimately promotes sleep.
Please visit the following Web sites for further education on insomnia. These sites have information on signs and symptoms, causality, preventive measures, complications, treatments, and even current enrolling clinical trials for insomnia.
For other excellent patient education resources, visit eMedicine's Mental Health and Behavior Center and Sleep Disorders Center. Also, see eMedicine's patient education articles Sleep Disorders and Aging, Insomnia, REM Sleep Behavior Disorder, Understanding Insomnia Medications, Periodic Limb Movement Disorder, and Sleeplessness and Circadian Rhythm Disorder.
Failure to diagnose sleep apnea and periodic limb movements in sleep
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sleep disturbances, sleep problems, sleep changes, sleep disorders, insomnia, sleep apnea, SA, hypersomnolence, sleep latency, sleep efficiency, periodic limb-movement disorder, PLMD, periodic limb-movement syndrome, periodic limb movement syndrome, periodic limb movements in sleep, PLMS, nocturnal myoclonus, rapid eye movement, REM, non-REM, paradoxical desynchronized sleep, slow-wave sleep, SWS, conjugate gaze, dreams, dreaming, nocturnal penile tumescence, NPT, electrooculography, EOG, circadian rhythms
Guy E Brannon, MD, Associate Clinical Professor of Psychiatry, Louisiana State University Health Sciences Center; Director, Adult Psychiatry Unit, Chemical Dependency Unit, Clinical Research, Brentwood Behavior Health Company
Guy E Brannon, MD is a member of the following medical societies: American Medical Association, American Medical Writers Association, American Psychiatric Association, American Society of Addiction Medicine, Association of Clinical Research Professionals, Louisiana State Medical Society, and Southern Medical Association
Disclosure: AstraZeneca Honoraria Speaking and teaching; Takeda Honoraria Speaking and teaching; Wyeth Honoraria Speaking and teaching; Janssen Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
Subir Vij, MD, MPH, Assistant Professor, Department of Medicine, Eastern Virginia Medical School; Medical Director, Portsmouth Community Health Center
Subir Vij, MD, MPH is a member of the following medical societies: American College of Physician Executives, American College of Physicians, and American Medical Association
Disclosure: Nothing to disclose.
Angela Gentili, MD, Director of Geriatrics Fellowship Program, Associate Professor, Department of Internal Medicine, Virginia Commonwealth University Health System and McGuire Veterans Affairs Medical Center
Angela Gentili, MD is a member of the following medical societies: American Geriatrics Society
Disclosure: Nothing to disclose.
Sarah C Aronson, MD, Associate Professor, Departments of Psychiatry and Medicine, Case Western Reserve School of Medicine/University Hospitals of Cleveland
Sarah C Aronson, MD is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Iqbal Ahmed, MBBS, Professor, Department of Psychiatry, John A Burns School of Medicine, University of Hawaii
Iqbal Ahmed, MBBS is a member of the following medical societies: Academy of Psychosomatic Medicine, American Association for Geriatric Psychiatry, American Neuropsychiatric Association, and American Psychiatric Association
Disclosure: Nothing to disclose.
Harold H Harsch, MD, Program Director of Geropsychiatry, Department of Geriatrics/Gerontology, Associate Professor, Department of Psychiatry and Department of Medicine, Froedtert Hospital, Medical College of Wisconsin
Harold H Harsch, MD is a member of the following medical societies: American Psychiatric Association
Disclosure: lilly Honoraria Speaking and teaching; Forest Labs Honoraria Speaking and teaching; AstraZeneca Honoraria Speaking and teaching; Pfizer Grant/research funds Speaking and teaching; Northstar Grant/research funds Research; Novartis Grant/research funds research; Pfizer Speaking and teaching; Sanofi-avetis Grant/research funds research; Otsuke Grant/research funds reseach; GlaxoSmithKline Grant/research funds research
Stephen Soreff, MD, President of Education Initiatives, Nottingham, NH; Faculty, Metropolitan College of Boston University, Boston, MA
Stephen Soreff, MD is a member of the following medical societies: American College of Mental Health Administration and American Psychosomatic Society
Disclosure: Nothing to disclose.
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