In persons with dementia, cognitive decline is usually accompanied by challenging symptoms such as sleep-wake disturbances, inability to manage daily activities, communication difficulties, depression, mood swings, agitation, aggression, and wandering (Department of Health 2009, 7-8). The stress of these symptoms on family caregivers is a major risk factor for institutionalization of the person with dementia (Hogan et al. 2007, 366). Managing these symptoms can not only enhance the well-being of those with dementia and their family caregivers but can also have cost benefits for them and the health care system (Alzheimer Society of Canada 2010, 8-9; Hux et al. 1998,457).
Because of the increased risk of falls and fractures, increased confusion, decrements in self-care (McCurry et al. 2000, 611), and risk of death among older adults with some medications (e.g., conventional and atypical antipsychotic drugs; Wang et al. 2005, 2335), nonpharmaceutical interventions should be the first choice of treatment. Drug treatment should be considered only after nonpharmaceutical approaches have failed and reversible medical and environmental causes have been ruled out (Hogan et al. 2007, 369; McCurry et al. 2000, 611). Although the evidence is insufficient regarding the effectiveness of several nonpharmacological interventions, such as music, snoezelen (multisensory stimulation), reminiscence therapy, validation therapy, aroma therapy, massage therapy, and light therapy, the relative risk of using these approaches is low (McCurry et al. 2000, 611) and persons with dementia may benefit from them (Hogan et al. 2007, 369). This post examines the evidence specifically related to light therapy in managing symptoms of dementia.
With normal aging, people aged 65 years and over may experience changes in core body temperature, melatonin rhythm, and the circadian rest-activity cycle, which may present as fragmented nocturnal sleep, multiple and prolonged awakenings in the second half of the night, and increased daytime napping (Campbell et al. 1995, 151, 154; McCurry et al. 2000, 613) . These abnormalities and other related disturbances such as rest-activity cycle disruptions and sundowning are more frequent and pronounced in older adults with Alzheimer’ s disease (AD) (McCurry et al. 2000, 604). The neurobiological basis of these behavioral disorders is related to degenerative changes in the suprachiasmatic nucleus (SCN) of the hypothalamus that result in the loss of the expression of vasopressin (AVP) mRNA. Indeed, Liu et al. (2000, 314, 318) revealed that the total amount of AVP-mRNA expressed in the SCN was three times lower in persons with AD than in age- and time-of-death matched controls. In addition, the amount of AVP-mRNA was three times higher during the daytime than at night in control adults aged 60 to 80 years whereas no clear diurnal rhythm was observed in persons with AD. These findings suggest that the neurological basis of the circadian-rhythm disturbances that are responsible for behavioral rhythm disorders is located in the SCN. Liu and colleagues (2000, 320) emphasize that the loss of neurons expressing AVP- mRNA in the SCN does not necessarily mean that the neurons have died; they may still be present but inactive and no longer able to express AVP- mRNA. Reactivation of SCN neurons expressing AVP-mRNA was shown to be possible in studies of aged rats. Lucassen, Hofman, and Swabb (1995, 263) revealed that exposure to bright light appeared to reverse age-associated decrease in AVP-mRNA in old rats. As in the studies of aged rats, stimulation with light may positively affect the SCN neurons in aging humans and specifically in persons with dementia.
The circadian pacemaker in the SCN is synchronized with the 24-hour day by “zeitgebers” or triggers of which light is the most important. Light impinging on the retina is transduced into neural activity that reaches the SCN through the retinohypothalamic and possibly the geniculo-hypo- thalamic tracts. Light leads to changes in the firing rates of specialized neurons in the SCN that in turn affect circadian rhythms (van Someren et al. 1996, 260). However, in older adults with dementia most zeitgebers are reduced due to diminished social contacts, age-related deficiencies in the eye (e.g., macular degeneration, cataracts, blindness), day-length (e.g., winter months have fewer external light cues), and less exposure to sufficient outdoor or bright light (Burns et al. 2009, 718; Gasio et al. 2003, 3; McCurry et al. 2000, 607). Reduced sensory input is likely to lower the “general level of excitement” that is thought to play an important role in the entrainment of circadian rhythms (Burns et al. 2009, 711-712; van Someren et al. 1996, 260). Thus, an environment weak in phase prompts coupled with neuropathological damage causing poor sensitivity to such prompts can result in rhythm disorders. A decreased ability to maintain a stable circadian pattern of daytime arousal and nocturnal quiescence may contribute to sleep disruptions (Ancoli-Israel et al. 2002, 282; Burns et al. 2009, 711-712; McCurry et al. 2000, 604), cognitive dysfunction (Liu et al. 2000, 314; McCurry et al. 2000, 604), behavioral disturbances (e.g., agitation and sundowning; Burns et al. 2009, 711-712; Haffmans et al. 2001, 106; McCurry et al. 2000, 605), functional impairment (McCurry et al. 2000, 604), and depression (Liu et al. 2000, 314; McCurry et al. 2000, 608) in persons with dementia.
Trials that Examined the Effectiveness of Light Therapy
The following description of the evidence builds on a recent Cochrane Review (Forbes et al. 2009) with the addition of one study (Burns et al. 2009) which was retrieved following the Cochrane Review publication. In total, nine randomized controlled trials (RCTs; eleven articles) that examined the effectiveness of light therapy in managing the symptoms of dementia are included (Ancoli-Israel, Gehrman, et al. 2003; Ancoli-Israel, Martin, et al. 2003; Burns et al. 2009; Dowling et al. 2005, 2007, 2008; Gasio et al. 2003; Graf et al. 2001; Lyketsos et al. 1999; Mishima, Hishikawa, and Okawa 1998; Riemersma-van der Lek et al. 2008), with a total of 421 participants, of whom 324 completed the studies. Participants in the included trials were diagnosed with dementia (n = 13, 3%), probable AD (n = 318, 76%), vascular dementia (n = 55, 13%), mixed dementia (n = 5, 1%) or another type of dementia (n = 30, 7%). It is interesting to note that few participants were diagnosed with mixed dementia, defined as the coexistence of AD and vascular dementia. Mixed dementia is one of the most common forms of dementia with a prevalence range of 20-40% of persons with dementia (Zekry, Hauw, and Gold 2002, 1431, 1432).
Four of the trials were conducted in the United States (Ancoli-Israel, Gehrman et al. 2003, 22) Ancoli-Israel, Martin, et al. 2003, 194) Dowling et al. 2005, 738; Dowling et al. 2007, 961; Dowling et al. 2008,239; Lyketsos et al. 1999, 520), one was conducted in Austria (Graf et al. 2001, 726), one in Japan (Mishima, Hishikawa, and Okawa 1998, 647), one in the Netherlands (Riemersma-van der Lek et al. 2008, 2642), one in Switzerland (Gasio et al. 2003, 207), and one in the United Kingdom (Burns et al. 2009, 711). All participants were residents in a long-term care/seniors facility.
Sources of Bright Light
Seven trials used a Brite-Lite box (e.g., Apollo Light Systems, Orem, Utah) which was approximately 24 inches wide by 12 inches high by 3 inches deep and placed one meter from the participant’s head. The Brite- Lite utilized cool-white florescent, nonultraviolet, full-spectrum light bulbs with special ballast to augment the brightness. The treatment groups received light therapy ranging from 2,500 to 10,000 lux and the control groups received dim red light or dim, low-frequency blinking light, less than 300 lux, either in the morning or evening, for 1-2 hours, for 10 days to 10 weeks. There were two exceptions: the use of dawn-dusk simulation (maximum 400 lux) or placebo dim red light (< 5 lux) (Gasio et al. 2003, 211) and the use of ceiling mounted light fixtures (Riemersma-van der Lek et al. 2008, 2643). The Dawn-Dusk Simulator included a computer algorithm that drove an electronic controller connected to an overhead halogen lamp placed behind a diffusing membrane behind each participant’s bed. The ceiling-mounted fixtures were Plexiglas diffusers containing an equal amount of Philips TLD840 and TLD940 florescent tubes, which were installed in the common living area. The lights were kept on between approximately 0900 and 1800 hours with the aim of an exposure of ±1000 lux (Riemersma-van der Lek et al. 2008, 2643-2644).
Effects of the Light Therapy
Several outcomes were measured following exposure to light therapy: cognition, function, sleep, behavioral disturbances, and psychiatric disturbances. These are each discussed below.
Cognition
Four studies ( Burns et al. 2009, 712 ; Gasio et al. 2003, 208 ; Graf et al. 2001, 726; Riemersma-van der Lek et al. 2008, 2646) used the Mini-Mental State Examination (MMSE), a commonly used screening tool that concentrates on the cognitive aspects of mental function: orientation, immediate recall, attention and calculation, delayed recall, and language (Folstein, Folstein, and McHugh 1975). Morning bright light (10,000 lux) was compared with standard fluorescent-tube light (100 lux) in Burns et al. (2009, 713), evening bright light (3,000 lux) was compared with dim light (100 lux) in Graf et al. (2001, 726), all-day bright light (1,000 lux) was compared with dim light (300 lux) in Riemersma-van der Lek et al. (2008, 2643-2644), and dawn-dusk simulation with light up to 400 lux was compared with dawn-dusk simulation with dim red light (<5 lux) in Gasio et al. (2003, 209-210). The data in the Burns et al. (2009, 715) and Riemersma-van der Lek et al. (2008, 2647) studies were combined because the light therapy was administered in the morning or all day and their light intensities were considered bright light. The pooled data revealed no effect following 14 to 42 days of treatment (MD = 1.34, 95% CI -0.89 to 3.57, p = 0.24). Riemers- ma-van der Lek et al. (2008, 2647) data revealed similar results after one year of treatment (MD = 1.70, 95% CI -1.03 to 4.43, p = 0.22), and after two years of treatment (MD = 3.60, 95% CI -1.05 to 8.25, p = 0.13). Graf et al. (2001, 726) administered evening bright light for 10 days that had no effect on cognition (MD = 0.70, 95% CI -4.90 to 6.3, p = 0.81). Similarly, the Gasio et al. (2003, unpublished data provided by authors) study employing the dawn-dusk simulation revealed no effect at endpoint (MD = 0.46, 95% CI -14.14 to 15.06, p = 0.95) and at follow up (three weeks after treatment) (MD = -0.50, 95% CI -10.68 to 9.67, p = 0.92). Thus, none of the trials demonstrated a significant change in cognition as a result of the light therapy.
Function
One study (Riemersma-van der Lek et al. 2008, 2646) measured functional limitations using Nurse-Informant Activities of Daily Living (NI- ADL). This scale was an adaptation of the Katz ADL scale (Katz et al. 1963) and includes six items that measure competence in feeding, continence, transferring, going to toilet, dressing, and bathing (Holmes et al. 1990). After six weeks of treatment, light therapy had a positive effect in attenuating the increase in functional limitations (MD = -5.00, 95% CI -9.87 to -0.13, p = 0.04). After one year of treatment, there was no significant effect (MD -5.00, 95% CI -11.16 to 1.16, p = 0.11); however, a significantly less steep increase in functional decline was observed after two years of light therapy (MD = -16.00, 95% CI -26.21 to -5.79, p = 0.002). These significant findings show support for the benefit of light therapy in lessening functional decline in persons with dementia.
Sleep
Sleep latency, defined as the amount of time between reclining in bed and the onset of sleep (Venes 2001, 1200), was measured using wristwatch- size actigraphs in trials conducted by Gasio et al. (2003, 215) and Riem- ersma-van der Lek et al. (2008, 2646) . However the data from these two studies could not be pooled due to differences in light intensity. Findings from Riemersma-van der Lek et al. (2008, 2651) revealed that there were no significant improvements in sleep onset latency after six weeks of treatment (MD = 6.00, 95% CI -12.34 to 24.34, p = 0.52), one year of treatment (MD = 5.00, 95% CI -24.79 to 34.79, p = 0.74), and after two years of treatment (MD = 10.00, 95% CI -11.33 to 31.33, p = 0.36). Similarly, data from Gasio et al. (2003, 214) revealed that dawn-dusk simulation did not significantly reduce sleep latency after three weeks of treatment (MD = -79.00, 95% CI -327.17, 169.17, p = 0.53) and after three weeks of follow-up (MD = -62.00, 95% CI -216.55 to 92.55, p = 0.43).
Seven studies measured total night sleep duration following ten days (Ancoli-Israel, Gehrman, et al. 2003, 26), two weeks (Burns et al. 2009, 712), three weeks (Gasio et al. 2003, 207), four weeks (Lyketsos et al. 1999, 521), ten weeks (Dowling et al. 2005, 740; Dowling et al. 2008, 240), and one and two years of treatment (Riemersma-van der Lek et al. 2008, 2646) that consisted of bright-light therapy (>2500 to 10,000 lux) for one to two hours in the morning (Ancoli-Israel, Gehrman, et al. 2003, 26; Burns et al. 2009, 713; Dowling et al. 2008, 240; Lyketsos et al. 1999, 521), afternoon/evening (Ancoli-Israel, Gehrman, et al. 2003, 26; Dowling et al. 2005, 740), all day bright light (1000 lux) (Riemersma-van der Lek et al. 2008, 2643), or dawn- dusk simulation (400 lux) morning and evening (Gasio et al. 2003, 209-210). The treatment groups were compared with control groups who received dim light. Unfortunately, Ancoli-Israel, Gehrman, et al. (2003, 30) reported only the combined findings from the treatment and control groups data, and Lyketsos et al.’s (1999, 521) study was a crossover design and did not appear to have utilized analyses appropriate to a paired design. Thus, the data from these studies were excluded from the analyses. Combined data from Burns et al. (2009, unpublished data provided by authors), Dowling et al. (2005, 741), Dowling et al. (2008, 243), and Riemersma-van der Lek et al. (2008, 2648) combined data revealed no effect of morning to all-day bright light on total night sleep duration (MD = 18.16, 95% CI -5.63 to 41.95, p = .13). Evening bright light (Dowling et al. 2005, 741) revealed similar findings (MD = 10.00, 95% CI -59.22 to 79.22, p = .78). Data from Riemersma-van der Lek et al. (2008, 2648) also revealed that bright light had no effect on night-sleep duration after one year (MD = -36.00, 95% CI -84.21 to 12.21, p = .14) and two years of treatment (MD = -36.00, 95% CI -121.69 to 49.69, p = .41). Data from Gasio et al. (2003, 214) were analyzed separately due to the lower intensity of treatment light. No effect was found after three weeks of treatment (MD = 143.00, 95% CI -637.66 to 923.66, p = .72), or at follow-up (MD = 110.00, 95% CI -77.22 to 297.22, p = .25).
Four studies (Ancoli-Israel, Gehrman, et al. 2003, 25) Dowling et al. 2005, 740) Gasio et al. 2003, 210) Mishima, Hishikawa, and Okawa 1998, 649) measured night-time activity counts. Unfortunately, reported data from Ancoli-Israel, Gehrman, et al. (2003, 30) and Mishima, Hishikawa, and Okawa (1998, 650) were not appropriate for inclusion in the metaanalyses. The findings from Dowling et al. (2005, 740) and Gasio et al. (2003, 214) could not be combined due to the differences in intensity of the light therapy. Dowling et al. (2005, 740) measured activity scores per night for both morning and afternoon treatment groups compared with control groups after 10 weeks of treatment. No effect on nighttime activity scores was found when bright light was administered in the morning (MD = 855.78, 95% CI -867.84 to 2579.40, p = .33), or afternoon (MD = -78.60, 95% CI -627.17 to 469.97, p = .78). In Gasio et al. (2003, 214) activity for each participant was averaged in one-hour bins and then over seven consecutive days of baseline, treatment, and follow-up. No effect on night activity was found after three weeks of treatment (MD = -20.60, 95% CI -46.52 to 5.32, p = .12) and after three weeks of follow-up (MD = -24.70, 95% CI -52.70 to 3.30, p = .08). Dowling et al. (2005, 740, and 2008, 243) also measured the number of nighttime awakenings. Again, there was no effect on the number of nighttime awakenings after 10 weeks of treatment in either the morning bright-light exposure (MD = -2.37, 95% CI -8.75 to 4.01, p = .47) or evening exposure (MD = -4.38, 95% CI -11.61, 2.86, p = .24). In summary, a significant change in sleep latency, total nighttime duration, nighttime activity counts, and number of nighttime awakenings was not observed following light therapy.
Behavioral Disturbances
Behavioral disturbances (e.g., agitation) were measured in six studies using several instruments: (1) Agitated Behavior Rating scale (ABRS; Ancoli-Israel, Martin, et al. 2003, 196), which measured agitation, manual manipulation, searching and wandering, escape behaviors, tapping and banging, and verbal agitation (Bliwise and Lee 1993); (2) Behavioral Pathology in AD scale (Behave-AD; Lyketsos et al. 1999, 522), which measured paranoid and delusion ideation, hallucinations, activity disturbances, aggressiveness, and anxiety and phobias (Reisberg et al. 1987); (3) Neuropsychiatric Inventory (NPI; Gasio et al. 2003, 208, Dowling et al. 2007, 964-965), which measured the severity and frequency of delusions, hallucinations, dysphoria, anxiety, agitation/aggression, euphoria, disinhibi- tion, irritability/lability, apathy, and aberrant motor activity (Cummings et al. 1994); and (4) Cohen-Mansfield Agitation Inventory (CMAI; Burns et al. 2009, 712; Riemersma-van der Lek et al. 2008, 2646), which measured aggressive behavior, physically nonaggressive behavior, verbal agitation, and a global rating of agitation (Cohen-Mansfield, Marx, and Rosenthal 1989). In two studies (Ancoli-Israel, Martin, et al. 2003, 199; Dowling et al. 2007, 968) behavioral disturbances were compared between morning light therapy exposure and afternoon/evening light therapy and assessed in the morning and evening shifts (Ancoli-Israel, Martin, et al. 2003, 199). The findings from Lyketsos et al. (1999, 522-523) could not be included in the analyses for reasons cited above.
With light therapy administered during the morning or day time, behavioral disturbances measured by ABRS scores (Ancoli-Israel, Martin, et al. 2003, 196), NPI scores (Dowling et al. 2007, 964-965), and CMAI scores (Burns et al. 2009, 712, Riemersma-van der Lek et al. 2008, 2646) were pooled. The results revealed that light therapy administered during the morning or daytime had no effect on behavioral disturbances (SMD = -0.04, 95% CI -0.33 to 0.26, p = .80) following 10 to 50 days of light therapy. Similarly, no effect on behavioral disturbances was observed in the evening assessment following 10 days of treatment (MD = 0.11, 95% CI -0.23 to 0.45, p = .52; Ancoli-Israel, Martin, et al. 2003, 199), after five days of follow-up measured in the morning (MD 0.02, 95% CI -0.23 to 0.27, p = .87; Ancoli- Israel, Martin, et al. 2003, 199), in the evening (MD 0.07, 95% CL -0.26, 0.40, p = .67; Ancoli-Israel, Martin et al. 2003, 199), following one year of treatment (MD = -2.00, 95% CI -11.71to 7.71, p = .69; Riemersma-van der Lek et al. 2008, 2647), and after two years of light therapy (MD = -9.00, 95% CI -21.34 to 3.34, p = .15; Riemersma-van der Lek et al. 2008, 2647).
To assess behavioral disturbances following the administration of afternoon or evening light therapy, ABRS scores (Ancoli-Israel, Martin, et al. 2003, 199) and NPI scores (Dowling et al. 2007, 968) were pooled. The results revealed that light therapy administered in the afternoon or evening had no effect on reducing behavioral disturbances when assessed during the morning (SMD = 0.16, 95% CI -0.31 to 0.64, p = .50) following 10 to 50 days of light therapy (Ancoli-Israel, Martin et al. 2003, 199; Dowling et al. 2007, 968) or when assessed during the evening (MD 0.07, 95% CI -0.26 to 0.40, p = .67) following 10 days of treatment (Ancoli-Israel, Martin, et al. 2003, 199). Similar results were found after five days of follow-up during morning assessments (MD 0.10, 95% CI -0.16 to 0.36, p = .46; Ancoli-Israel, Martin, et al. 2003, 199) and during evening assessments (MD 0.11, 95% CI -0.23 to 0.45, p = .53; Ancoli-Israel, Martin et al. 2003, 199). In summary, light therapy whether administered in the morning/all day or afternoon/evening had no significant effect on behavioral disturbances at the end of treatment or on follow-up when assessed during the morning and evening.
Psychiatric Disturbances
Dowling et al. (2007, 964-965) and Riemersma-van der Lek et al. (2008, 2646) used the NPI to measure psychiatric disturbances. Their pooled data revealed no significant change after 42 to 50 days of light therapy (MD = 1.77, 95% CI -6.34 to 9.87, p = .67), after one year (MD = -0.30, 95% CI -2.73 to 2.13, p = .81), and after two years (MD = -3.30, 95% CI -7.03 to 0.43, p = .08). In addition, there was no effect when light therapy was administered in the afternoon (MD = 7.90, 95% CI, -0.46 to 16.26, p = .06; Dowling et al. 2007, 969). Gasio et al. (2003, 208) also used the NPI to examine psychiatric symptoms following three weeks of dawn-dusk simulation or dim red light therapy. No effect was observed following the treatment (MD = -3.19, 95% CI -9.83 to 3.45, p = .35) and after three weeks of follow-up (MD = -4.17, 95% CI -13.37 to 5.03, p = .37).
Five studies measured depression: Dowling et al. (2007, 964-965) used the depression/dysphoria domain of the NPI-Nursing Home version (NPI-NH), a modified version of the NPI (Iverson et al. 2002); Gasio et al. (2003, 208) used the Geriatric Depression Scale (GDS; Sheikh and Yesvage 1986); and Burns et al. (2009, 712), Lyketsos et al. (1999, 522), and Riemers- ma-van der Lek et al. (2008, 2646) used the Cornell Scale for Depression in Dementia (CSDD; Alexopoulos et al. 1988). Lyketsos et al. (1999, 524) reported that no significant differences in scores of depression were found between groups at each time point. However, raw data were not reported and could not be retrieved. Pooled data (Burns et al. 2009, 715) Dowling et al. 2007, 968; Riemersma-van der Lek et al. 2008, 2647) revealed no effect on depression following 14 to 50 days of light therapy (SMD = 0.06, 95% CI -0.55 to 0.67, p = .85). In addition, Riemersma-van der Lek et al. (2008,
2647) data revealed no effect on depression using CSDD scores at one year (MD = -.30, 95% CI -4.36 to 3.76, p = .88) and after two years of treatment (MD -4.40, 95% CI -10.82 to 2.02, p = .18). However, administering the light therapy in the afternoon resulted in an effect after 50 days of treatment (MD = 3.20, 95% CI 0.86 to 5.51, p = .007) favoring the control group (Dowling et al. 2007, 968). These results should be viewed with caution due to the small sample size (n = 17). Analysis of the data provided to the authors by Gasio et al. (2003) revealed no effect on depression scores after three weeks of treatment (MD = -0.82, 95% CI -4.33 to 2.69, p = .65) or at follow-up (MD = -1.29, 95% CL -3.99, 1.41, p = .35).
Apathy and indifference were measured using a domain of the NPI-NH (Iverson et al. 2002) following 50 days of treatment (Dowling et al. 2007, 969). There was no effect on apathy or indifference in either the morning administration of bright light (MD = 1.00, 95% CI -2.21 to 4.21, p = .54) or afternoon administration (MD = 0.40, 95% CI -3.00 to 3.80, p = .82). In summary, there is no significant evidence that bright light improves psychiatric symptoms in persons with dementia.
The Cochrane Review on light therapy and dementia (Forbes et al. 2009) with the addition of the trial by Burns et al. (2009) revealed little significant evidence of benefit of light therapy on cognition, function, sleep, behavioral disturbances, and psychiatric disturbances associated with dementia. Light therapy was shown to have an effect on two outcomes of interest. The Riemersma-van der Lek et al. (2008, 2647) data revealed that light therapy had a positive effect in attenuating the increase in functional limitations after six weeks and after two years of light therapy. The sample size was adequate at six weeks (n = 87) but by two years the sample size was only 26 participants. By ensuring an adequate sample size at follow-up, the effect of light therapy in limiting functional decline may be even greater as the power to detect a difference would be increased. The Dowling et al. (2007, 968) data revealed that the lack of afternoon bright- light therapy improved depression in the control group. However, these results should be viewed with caution as the sample size was small (n = 17; Dowling et al. 2007, 968). No significant evidence was found that light therapy decreases the decline in cognition, shortens sleep latency time, increases nocturnal sleep time, decreases nighttime activity, decreases behavioral disturbances, or improves psychiatric symptoms. These nonsignificant results may have been related to small sample sizes that contribute to insufficient power to detect a difference, if one is present. Notable exceptions were the Ancoli-Israel, Gehrman, et al. (2003, 25) and Ancoli-Israel, Martin, et al. (2003, 195) trials that included 92 participants and the Riemersma-van der Lek et al. (2008, 2645) study that included 94 participants at baseline. Clearly further research with larger sample sizes is required which examines all of the outcomes of interest.
Only one trial (Riemersma-van der Lek et al. 2008, 2653) examined adverse effects of light therapy. No adverse effects were reported; on the contrary, light therapy significantly reduced the ratings of irritability, dizziness, headache, constipation, and inability to sleep (Riemersma-van der Lek et al. 2008, 2653). Reporting of adverse events should be included in every intervention trial.
Unfortunately, Ancoli-Israel, Gehrman, et al. (2003), Lyketsos et al. (1999), and Mishima, Hishikawa, and Okawa (1998) did not report the data needed to conduct a meta-analysis (e.g., means and standard deviations at baseline and endpoints for the treatment and control groups) for some of the outcomes of interest. Authors need to report these data or be willing to provide the data on request. In addition, two studies (Lyketsos et al. 1999, 521, Mishima, Hishikawa, and Okawa 1998, 649) used crossover designs and did not conduct analyses appropriate to a paired design. Although participants received no light treatment for one to four weeks prior to being crossed over to the other group, it is unknown if there is a carry-over effect from the two to four weeks of exposure to the light therapy. Some studies (e.g., Ancoli-Israel, Gehrman, et al. 2003, 32) suggest that the effects of light therapy on nocturnal sleep may persist beyond the five-day treatment, while McCurry et al. (2000, 614) concluded that the benefits to sleep from increased bright light decline almost immediately once exposure is discontinued. Until the evidence is stronger, participants should not be regarded as generating independent data in the two phases of a crossover design.
Another plausible reason for the lack of strong evidence of the effectiveness of light therapy was the heterogeneity within several of the trials in regard to participants’ diagnosis and severity of dementia. Three trials (Ancoli-Israel, Gehrman, et al. 2003, 25; Ancoli-Israel, Martin, et al. 2003, 201; Dowling et al. 2005, 2008) were notable exceptions as only participants with AD were included. Persons with AD have a degenerative disease that is characterized by neurofibrillary tangles, usually in the hippocampus as well as the entorhinal cortex. As AD progresses, the pathology spreads to the lateral temporal cortex as well. Senile plaques occur later on (Chert- kow et al. 2007, 274). On the other hand, persons with vascular dementia have heterogeneous brain pathology; their response to light therapy may depend on the areas in which ischemic damage has occurred (Mishima, Hishikawa, and Okawa 1998, 653). Few participants were diagnosed with mixed dementia (1%), although it is now recognized that mixed dementia is one of the most common forms of dementia (Zekry, Hauw, and Gold 2002, 1432). It may be that those with AD with a vascular component were included with participants diagnosed with only AD. This was the practice in the Canadian Study of Health and Aging (Zekry, Hauw, and Gold 2002, 1432). Attempts should be made to accurately diagnose the participants with diagnostic procedures such as positron emission tomography (PET) neuroimaging, which have been recognized as key diagnostic modalities (Zekry, Hauw, and Gold 2002, 1435). In addition, accurately determining the severity of the disease is also important as it is possible that persons with mild to moderate AD with more intact SCNs and who are more receptive to other “zeitgebers” or triggers will have a greater response to light therapy than persons with severe AD (Ancoli-Israel, Martin, et al. 2003, 201).
Culture and geographic location are other factors that may influence the results of the review as trials were conducted in six different countries. For example, the participants from Japan may have experienced close family ties and well-developed informal care that may mask the symptoms of dementia (Zekry, Hauw, and Gold 2002, 1435). Geographic location is also a potential risk factor as participants in the United Kingdom may have experienced longer winters that resulted in fewer opportunities to be exposed to natural light than participants in more southern countries (Burns et al. 2009, 719). Subgroup analyses in the review could not be completed due to the small sample sizes. Investigators need to be sensitive to the importance of controlling for these differences in pathology, severity of dementia, and culture when designing studies that examine the effectiveness of light therapy. Otherwise, the degree of influence these factors may have on the effectiveness of bright-light exposure is unknown, making it difficult to predict who is most likely to benefit from the treatment.
Shochat et al. (2000) examined light exposure among elderly residents living in nursing homes. On average, healthy older adults are exposed to light above 2000 lux for 59 minutes a day. People with AD living at home are exposed to 29 minutes a day of light above 2000 lux, while institutionalized residents with dementia spent a median of 10.5 minutes per day (mean = 34; SD = 63) exposed to light above 1000 lux and a median of 4 minutes (mean = 19; SD = 39) per day exposed to light over 2000 lux (Shochat et al. 2000, 373, 374, 375). Clearly, there is a need to enhance residents’ natural exposure to light and to bright-light exposure in long-term care facilities. How best to carry this out is less clear.
Most trials in the review incorporated some form of a Brite Lite box, and two trials used other forms of light therapy. Gasio et al. (2003, 211) used dawn-dusk simulated light therapy that exposed the participants to natural amounts of light at dawn and dusk. However, the intensity (<400 lux) and duration of the natural light at dawn and dusk may be insufficient to be effective in changing sleep, behavior, and/or psychiatric disturbances. Indeed, several studies have revealed that the minimum therapeutic dose of light for treating depression and regulating circadian rhythms is approximately 2000 lux over one to two hours (e.g., Sloane et al. 2005, 280-281). Riemersma-van der Lek et al. (2008, 2643) used ceiling-mounted light fixtures with Plexiglas diffusers in the common living room.
These approaches to enhancing light exposure for long-term care residents are less invasive and demanding of the residents and staff than the traditional Brite-Lite box. Use of a Brite Lite box requires participants to sit in front of the box for one to two hours. However, persons with moderate to severe dementia may find it difficult to remain seated and to stay awake for this period of time (Ancoli-Israel et al. 2002, 286; Sloane et al. 2005, 281). Some studies (e.g., Burns et al. 2009, 713) attempted to overcome this problem by having a research nurse present during the treatment period to engage all participants in conversation and to distract them if they attempted to leave. Under usual circumstances, it may be difficult to find the resources to have a staff member sit with and engage the residents for one to two hours. Burns et al. (2009, 719) recommends wall-mounted light boxes placed at eye level for the residents seated during breakfast. Ancoli-Israel, Gehrman, et al. (2003, 34) suggests increasing ambient light to 2000 lux in multipurpose rooms where residents spend much of their time may be the most efficient approach for improving the symptoms of dementia related to circadian activity rhythms. Since studies that evaluate the impact of increasing ambient light on the symptoms of dementia often incorporate a non-RCT design (e.g., Sloane et al. 2007, 1525), systematic reviews should also include these study designs to ensure that all of the best available evidence is presented.
The best time of day to offer light therapy remains inconclusive although trials that administered light therapy in the morning, afternoon, evening, and all day were included in this systematic review. Evening bright-light treatment is beneficial for sleep-maintenance problems in older adults as well as for persons who are phase-advanced, that is, falling asleep in the early evening and awakening too early in the morning (Campbell et al. 1995, 153). Morning light exposure is most beneficial for persons who are phase-delayed, that is whose sleep onset and morning rising are pushed to later hours (McCurry et al. 2000, 613). Individuals with AD have been reported to have phase-delayed activity (Satlin et al. 1995, 769) . However, other studies (e.g., Ancoli-Israel et al. 2002, 282) have not supported the expected direction of change in individuals with AD. Ancoli-Israel, Gehrman, et al. (2003, 33-34) report that the timing of light required to achieve a phase advance or phase delay may be different in people with AD owing to the deterioration of the SCN, and recommends increasing light exposure throughout the day and evening. Most recently, Burns et al. (2009, 719) report that their use of light therapy at 10:00 am for two hours reduced the chance of residents receiving light therapy on or before their temperature nadir (lowest point), which has been suggested to shift the diurnal rhythm in the opposite expected direction. Burns et al. (2009, 719) also found that light therapy was only effective during the winter months and not during the summer months when there was increased opportunity to natural exposure of light. Clearly further research is required in this area.
In addition, community-based light-therapy research is needed. All of the participants in the included studies resided in long-term care/seniors facilities. However, light-therapy modalities implemented in residential facilities may not translate readily to a home setting as they may be impractical, unacceptable, and/or overly expensive for the family caregiver and person with dementia residing in the community (McCurry et al. 2000, 614). Although there is no known research that has examined the impact of being exposed to natural daylight, persons residing in the community (and those residing in long-term care facilities with assistance of healthcare aides or volunteers) can greatly increase their daily light exposure by spending time outdoors. For example, typical lux levels outside on a cloudy day range from 8,000 to 10,000 lux; interior daytime exposure sitting near windows equals approximately 1000 lux (McCurry et al. 2000, 614). As with all dementia care, a light-therapy plan that makes sense to the person with dementia, the family caregiver and healthcare provider,
and which targets factors that are both relevant and modifiable in their situation, is more likely to be effective than a “one size fits all” approach (McCurry et al. 2000, 621).
Given the methodological shortcomings of the trials included in this review, there is not good evidence that light therapy is effective or ineffective. An exception is the well-designed longitudinal RCT by Riemersma-van der Lek et al. (2008, 2643), which found that light therapy had a positive effect in attenuating the increase in functional limitations. Further well-designed research is required to compare different light-therapy approaches (e.g., light boxes, ambient light, natural light), to determine the most appropriate illumination intensity, frequency, time of day, and duration of the intervention with persons with AD, vascular dementia, and mixed dementia at different levels of severity of the disease (see Table 1). Outcomes that contribute to the quality of life of persons with dementia, cost implications, and adverse effects of light therapy also need to be examined. What is clear from the evidence is that older adults and especially persons with dementia should be spending more time outdoors in natural light (see Table 1). Healthcare aides, volunteers, and family caregivers are in an ideal position to take persons with dementia for a daily walk that would increase their exposure to light and possibly alleviate some of their challenging symptoms. This is a potentially easy solution to managing very difficult symptoms of dementia.
Table 1
Recommendations to Improve Methodological Quality of Trials
Well-designed RCTs that include random generation of subjects and concealed allocation to groups are the preferred design of choice. When RCTs are not feasible, the best available evidence should also be included in a systematic review, recognizing the potential risk of biases.
Sample sizes should be large enough to detect a difference if one is present.
Samples should be as homogenous as possible in terms of dementia diagnosis, level of severity, culture, and geography.
Trial authors should report the information needed to conduct a meta-analysis or be willing to share this information with the authors of a review.
Further research is needed to determine the most effective and feasible bright-light modality, time of day to administer the treatment, length of treatment, and the influence of season on the outcomes.
Reporting of adverse events should be included in every intervention trial.
Research on the effectiveness of light-therapy modalities in the home setting is also needed.
In long-term care facilities, increase the use of BriteLite boxes mounted to the wall at residents’ eye level during breakfast.
Increase the use of ceiling-mounted light fixtures with Plexiglas diffusers in the common living rooms.
Healthcare aides, volunteers, and family caregivers are in an ideal position to take persons with dementia for a daily walk, which will increase their exposure to natural light.
Increasing exposure to light is especially important after the autumn equinox and before the spring equinox.
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