We found that PST prevented depressive disorders as a short-term preventive treatment but that its effect did not persist over time. There was, nevertheless, substantial evidence that PST was not the same as usual care. For one, we observed the hypothesized 50% risk reduction at 2 months and found that preventing the loss of valued activities mediated the relationship between PST and depression. We underestimated, however, the incidence of depression following cessation of treatment. This suggests that booster treatments for all PST subjects, or rescue treatments for those with low-level depressive symptoms, may have been necessary to sustain PST’s ability to prevent depressive disorders. The former is a continuation of the selective intervention strategy that targets an asymptomatic high risk group, whereas the latter is an indicated preventive strategy in that it targets patients with what may be early signs of depression.3
When we examined depression as a continuous measure of symptoms, we found no significant changes or differences between treatment groups. This was expected given that we enrolled nondepressed subjects; although a notable minority developed a depressive disorder over time, the preponderance of HDRS scores in the sample remained low throughout the study.
From a research design perspective, the clinical trial demonstrated that systematic sampling, successful randomization and masking, protocol-driven treatment, assessment of multiple relevant outcomes, and maintenance of treatment fidelity are feasible in psychosocial intervention studies. It adds to other studies demonstrating the value of depression management strategies to treat and, as our data suggest, prevent depression in older patients.10–13
The study also suggested that a practical, problem-solving intervention like PST may prevent depression in other disabling conditions such as heart disease, cancer, and stroke, where disability and loss of valued activities increase the risk for depression.
Minimal Depression Is Disabling and Increases the Risk for Depressive Disorders
In a secondary analysis of our data, we examined the effect of minimal depressive symptoms on levels of disability and the incidence of more severe depressive disorders.14
Many studies have identified the high prevalence and disabling consequences of depressive symptoms that do not meet criteria for major depression (variably termed minor, subthreshold, or subsyndromal depression).15
Lyness et al. recently found that subsyndromal depression produces clinically significant impairments and increases health service utilization and medical costs.16
Relying on Diagnostic and Statistical Manual of Mental Disorders – Fourth Edition
definitions of major or minor depression only, however, would omit a substantial proportion of affected older persons. Others have similarly reported that depressive symptoms predict future declines in functional status and onset of major depression.17–21
Although the “Preventing Depression in AMD” trial did not enroll patients with clinically significant depressive symptoms, subjects did have varying low levels of symptoms that we quantified using the HDRS.8
Total possible scale scores range from 0 to 50; scores greater than 14 indicate moderate-severe depression and scores less than 7 are normal. The mean for our sample was 2.2 (SD: 2.2) and 95.5% of subjects had scores within the normal range.
We identified 49 subjects (23.8%) whose baseline HDRS scores were one SD above the mean for this sample (i.e., ≥4). Their average HDRS score was 5.4 (SD 1.7); median: 5.0; range: (4, 12). We called these subjects “minimally depressed” and found that they had significantly greater difficulty performing vision-dependent daily living activities than subjects with fewer symptoms even though they had similar visual acuity and medical problems.14
We also found that minimal depressive symptoms strongly predicted incident depressive disorders. Thirty-four of the 49 (69%) subjects with HDRS greater than 4 (versus 24.4% with scores less than 4) developed a depressive disorder over the next 6 months. Their mean HDRS score, in fact, although in the top 25th percentile of the sample, was less than the HDRS score of seven that is taken as normal. The incidence rate for depressive disorders at 2 or 6 months for these subjects, compared with those with lower HDRS scores were: 75.6% versus 17.8%, respectively (OR = 14.27; 95% CI [6.40, 31.80]). shows the baseline HDRS symptoms that a regression analysis demonstrated independently and significantly predicted incident depression at 2 or 6 months. Subjects who reported a “depressed mood” alone were significantly more likely to develop a depressive disorder than those who denied depressed mood and correctly predicted 74.9% of the cases. Endorsing hypochondria, insomnia, and guilt identified an additional 6.8% of cases. Adding other HDRS symptoms did not improve the model. These data suggest that these four symptoms, taken together, correctly classified 81.7% of patients who developed a depressive disorder and may identify patients at risk.
Hamilton Depression Rating Scale Symptoms at Baseline that Predict Depressive Disorders at 2 or 6 Months
Thus, minimally depressed patients with AMD, who would not be considered depressed according to current diagnostic criteria, are at high risk to develop more severe depressive disorders and to suffer decrements in vision function that cannot be accounted for by the severity of their eye disease or general medical problems. Although we and others have previously reported the adverse effects of severe depression in AMD and other disorders, we now find that even minimal depressive symptoms adversely affect function.17–22
Future Directions for Prevention Depression in AMD
Although PST prevented depression, we believe its effect was short-lived because its emphasis on independent problem-solving (i.e., having subjects develop their own solutions, often without knowledge of low vision resources) did not optimize their remaining vision and thereby limited its effectiveness. We found, for example, that PST did not increase optical device use, low vision rehabilitation consultation, or home modifications. We believe that PST as a “talking treatment,” rather than one of education and demonstration, restricted its ability to access these compensatory strategies. To prevent depression more effectively over time, we believe that an intervention that builds on the strengths of a problem-solving framework (i.e., reframing problems into goal-oriented tasks) and enhances rehabilitative skills may be necessary.
We are now developing a low vision rehabilitation intervention that is designed to improve patients’ ability to continue valued activities and prevent depressive disorders. In it, an occupational therapist (OT) will collaborate with a low vision optometrist to develop and implement a care plan based on a patient’s rehabilitation potential and personal rehabilitation goals. The optometrist will evaluate remaining vision and magnification needs, prescribe optical devices, and provide the OT with an initial care plan. The OT will subsequently meet with subjects in their homes and use a problem-solving approach that reframes patients’ depressive perceptions (over which they feel they have no control) into goal-directed tasks that they can control. The hypothesis is that this treatment will enable patients with AMD to continue valued goals via enhanced compensatory strategies and problem-solving skills, and thereby to prevent depression. Because depression in AMD is a frequent, painful consequence of vision loss, integrating disease management strategies for both conditions is necessary. Our plan to incorporate depression management directly into low vision care provides, we believe, an optimal approach to meet this need and may well serve as a model for other rehabilitative interventions.
We plan to recruit patients with subthreshold depressive symptoms because of their increased risk for more severe depressive disorders. This then is an indicated prevention intervention because it targets people who already have detectable signs of depression but do not meet diagnostic criteria.3
The primary research question of the intervention’s efficacy drives our plan to use categorical diagnoses rather than depressive symptoms as the primary outcome. Although we recognize that depressive phenomena are not easily fitted to categories, the categorical approach seems best suited to assess a clinical treatment’s efficacy because it generates syndromes with discernable treatment and prognostic implications. Where we to rely on change in depressive symptoms as the primary outcome, we would obtain only a relative, not an explicit, sense of the intervention’s efficacy that may lack clinical meaning.
Our approach to disability assessment is innovative in that we will measure targeted vision outcomes, which identifies and quantifies specific vision-related goals as outcomes.23,24
This approach is likely to be more sensitive to treatment effects than summary scores on multisymptom measures that mix unvalued and valued activities and may obscure improvements in specific valued activities. It recognizes that different subjects select different goals and pinpoints and evaluates change in the goals that subjects value, and has the face validity, clinical relevance, and flexibility to convey meaningful change in response to rehabilitative interventions. The secondary study hypothesis is that intervention subjects will report less difficulty with targeted vision goals compared with controls over time.