Sundowning Syndrome in the Older Patient


Paul Kim, MD, Coeurlida Louis, MD, Sunanda Muralee, MD, and Rajesh R. Tampi, MD, MS


Pages 32 - 36

In psychiatric literature, several terms including sundowning, sundowning syndrome, and nocturnal delirium have been used interchangeably to describe the same observations. The reason for this confusion is the lack of a clear and precise definition for the observed phenomenon along with indefinite sources of etiology. Sundowning is a descriptive term rather than a psychiatric diagnosis as defined in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition-text revision (DSM-IV-TR). This article reviews past investigations to characterize the observed phenomenon of sundowning. It also reviews the theories of etiology and the current approaches to its management.

Although there is no established definition, sundowning is widely used to describe a group of behaviors occurring in some older patients with or without dementia at the time of nightfall or sunset. These behaviors include confusion, anxiety, agitation, or aggressiveness with increased motor activity like pacing, wandering, resistance to redirection, and increased verbal activity such as yelling. Although some of these behaviors are also exhibited in dementia, delirium, and sleep disturbance, sundowning distinguishes itself from these conditions in that these disruptive behaviors are characteristically worse in the evening hours. Cameron1 described “delirium and agitation” within one hour of induced darkness, but these symptoms regressed within one hour of exposure to light; however, this study has never been replicated.2

There have been variations in defining the temporal pattern of sundowning within the literature. Evans3 observed that sundowning behaviors occurred more often during 4:00-6:00 pm as compared to 10:00 am-12:00 pm.3 Cohen-Mansfield et al4 found increased vocalizations and physically aggressive behaviors to occur 4:30-11:00 pm versus 4:30-7:00 pm. The same study found vocalizations to occur at higher rates between 11:00 pm and 6:00 am. Wandering was found to be more likely 7:00-10:00 pm.5 Twenty-four hour behavior logs kept by caregivers found patients with Alzheimer’s disease more likely to display agitated behaviors between 4:00 pm and 8:00 pm.

However, other studies did not observe such temporal patterns of behavior. Bliwise et al6 did not observe any convincing patterns of worsening agitation nocturnally or during sunset hours in nine nursing home residents with severe dementia, who were observed four times per hour for 12 hours. Rather, this study found a seasonal effect: sundowning was more likely to occur in the winter or fall.6 In contrast, Martin et al7 found no component of seasonality to agitation in 85 institutionalized patients with Alzheimer’s disease, yet the study found considerable variation in the timing of agitation, with the peak at 2: 38 pm (standard deviation, 3 hours and 23 minutes). Overall, the variances described most likely reflect the variety of methods used to assess sundowning behavior, the heterogeneity of populations studied, and the lack of a standard definition employed throughout these studies.

Sundowning is not an uncommon phenomenon, but establishing its prevalence has proved challenging given the various definitions and methods used to assess it. Reports have ranged between 2.4% and 25%.7 In patients with Alzheimer’s disease or dementia, the range is widened to 2.4-66%.8,9 Currently, not much is known about the existence of gender or race prevalences.

The risk factors associated with the occurrence of sundowning are both physiologic and environmental.

Physiologic factors
The circadian abnormalities in patients with Alzheimer’s disease progress concomitantly with their behavioral and cognitive dysfunction. In addition, sundowning is more common in this population. One explanation for this phenomenon is that the neurofibrillary tangles found in the hypothalamus of patients with Alzheimer’s disease may lead to the behavioral changes of sundowning through mechanical disruption of brain tissue.10 Specifically, pathologic damage to the suprachiasmatic nucleus (SCN), which is responsible for regulating our circadian rhythms, is believed to result in disruptive behaviors associated with sundowning.11

Environmental factors
Certain environmental factors have been shown to worsen the behavioral symptoms of sundowning. These include changes in the environment, amount of daily light exposure, activities during the day, noise level, disruptions at night, medications, and the patient’s medical comorbidities. One study found that nursing home residents with sundowning were more likely to have been recently admitted to the nursing facility, moved to a new room, and subjected to staff shift changes; exposed to low levels of lighting during the day and bright hallway lighting during the evening; had reduced physical and mental activity during the day; and had increased naptime during daytime hours and reduced nighttime sleep, due to either frequent nursing care for incontinence or to increased daytime napping.3 These factors alone or in combination are associated with increased evening and daytime agitation as well as other symptoms of sundowning. The strong effect of these environmental factors speaks to the importance of appropriate environmental input in the regulation of circadian rhythm. It also may account for variations in research outcomes, given that controlling for these environmental factors has not been done uniformly.

Although the cause of sundowning still remains unclear, there are several theories explaining these behaviors. The most accepted one is centered on the dysfunction of the circadian rhythm. This may result in increased agitation at night and other behaviors found in sundowning. Important components of the biological basis of the circadian rhythm include the SCN and melatonin. Deterioration of the SCN seen in patients with Alzheimer’s disease is actively investigated to be an important factor in the disruption of the circadian rhythms. Because the SCN is the principal circadian pacemaker of the body, its deregulation influences the core body temperature, heart rate, and hormone secretion. These alterations translate into disturbed sleep, agitation, and other manifestations of sundowning. Suprachiasmatic nucleus volume and cell number are found to be decreased in those between the ages of 80 and 100 years. These changes are even more pronounced in patients with dementia of the Alzheimer’s type.12 Melatonin, a hormonal regulator of circadian rhythm that is released by the pineal gland, is found to be decreased in the cerebrospinal fluid levels of patients with Alzheimer’s disease.13 This would not only result in deregulation of circadian rhythm but also reduce its neuroprotective effect on the SCN and other neural structures.14

Other theories describe the role of sleep fragmentation in sundowning. Bliwise et al6 found that awakenings during the post-sunset period, spontaneous or during nursing care, were more likely to result in agitated behavior in nursing home residents with dementia.6

Both pharmacologic and nonpharmacologic approaches have been considered in the management of patients with sundowning. The pharmacologic aim of treatment has been to attempt to correct deficiencies in the regulation of the circadian rhythm. These studies were focused primarily on melatonin. One multicenter, placebo-controlled trial revealed that there was no difference in sleep time among patients with Alzheimer’s disease when given placebo, slow-release melatonin 2.5 mg daily, or melatonin 10 mg daily for 2 months.15 This contrasts with an earlier study that showed decreased sundowning behaviors in 45 patients with Alzheimer’s disease with sleep disturbances after 4 months of melatonin 6 mg daily.16

Conventional therapy has tended to use hypnotics and benzodiazepines to control evening agitation and behavioral problems associated with sundowning. Generally, this style of management aims to maintain patient safety and comfort while addressing the behavioral disturbances, without necessarily producing sleep.17 Even such neuroleptics as low-dose haloperidol and thioridazine have been used with the assumption that the agitated behaviors are associated with dopamine level deregulation. Although they may be of benefit to some patients, these pharmacologic treatments are not without side effects and should be used carefully in the older patient. Haloperidol can lead to tardive dyskinesia, and thioridazine can cause orthostatic hypotension. The anticholinergic side effects of these medications can lead to increased heart rate. Atypical antipsychotics are effective in the treatment of psychosis and agitation in dementia.18-21 The average daily dose for an atypical antipsychotic such as risperidone is between 0.25 mg and 2.0 mg daily in divided doses. Risperidone is less likely than the other atypical antipsychotic drugs to cause metabolic complications like diabetes mellitus, although it can cause prolactin elevation and extrapyramidal side effects such as parkinsonism at higher doses. While there are no specific trials of these drugs in the treatment of sundowning, they should be as effective as conventional agents. Additionally, these drugs are better tolerated than typical antipsychotics, especially in the elderly.22

The negative side effects of benzodiazepines and other hypnotics make them poor drugs of choice for older patients who often have comorbidities. They may not only create drug dependence but can also increase the likelihood of respiratory and central nervous system depression.23 These drugs may cause disinhibition and confusion in elderly patients with agitation who have sundowning syndrome.

In a study using the Neuropsychiatric Inventory (NPI) as a secondary outcome, Feldman et al24 found that the NPI scores improved in patients with moderate-to-severe Alzheimer’s disease when treated with donepezil in comparison to those who were treated with placebo. Skjerve et al25 observed that donepezil decreased electronically measured evening agitation (sundowning) and increased daytime activity in a 71-year-old man with clinically diagnosed dementia with Lewy bodies. Treatment with donepezil also helped improve his cognitive function and parkinsonian symptoms. This effect was noted 10 days into treatment, and it continued during the following weeks. This patient had previously failed trials of melatonin, oxazepam, citalopram, and haloperidol. The authors postulated that the improvements seen in his behavior may actually have been secondary to improved cognitive functioning due to donepezil.

Nonpharmacologic treatments for sundowning include behavioral therapy, with some persons responding positively to this intervention. Successful behavioral management programs focus on ways of managing wandering, yelling, and aggressive behaviors.9 A pilot study found that providing bright light therapy in the late morning hours between 9:30 am and 11:30 am significantly lowered patients’ agitation during the evening.26 As already mentioned, many institutionalized elderly patients receive very little light exposure on a daily basis. This may account for the reversal in their day–night behavioral patterns. So, the positive effects of bright light exposure on circadian rhythms, documented in healthy individuals, may also be of benefit in sundowning.27

Although the exact definition of sundowning is still open to debate, the term is commonly used to describe disruptive behaviors seen in the older patient, usually in the evening hours. It is a descriptive term and not a psychiatric diagnosis, as defined in the DSM-IV-TR. It is believed to occur due to changes in the circadian rhythm caused by the degeneration of the suprachiasmatic nucleus of the hypothalamus. Despite the prevalence of this condition, there have been no large-scale, controlled trials of pharmacologic agents or nonpharmacologic treatments. Antipsychotic medications, melatonin, donepezil, bright light therapy, and behavioral modifications have been found to be helpful in the treatment of sundowning. A clearer definition and further research into etiology and treatments will help us decrease the morbidity from this condition, decrease caregiver burden, and avoid premature institutionalization.

This project is supported by funds from the Division of State, Community, and Public Health, Bureau of Health Professions (BHPr), Health Resources and Services Administration (HRSA), Department of Health and Human Services (DHHS) under grant number 1 K01 HP 00071-02 and Geriatric Academic Career Award. The information or content and conclusion are those of the author, Rajesh R. Tampi, MD, MS, and should not be construed as the official position or policy of, nor should be any endorsements be inferred by, the BHPr, HRSA, DHHS, or the U.S. government.