Delayed-onset Depression Research Articles

Abstract TP414: Early and Delayed Onset Poststroke Depression

Background and aim: We aimed to investigate the predictors for early (3-month) and delayed (3-year) depression after stroke. Methods: Stroke or transient ischemic attack (TIA) subjects (n=1023) were recruited from the C hinese U niversity of Hong Kong - ST roke R egistry I nvestigating cognitive DE cline (CU-STRIDE). Clinical factors, drug use and neuroimaging markers of small vessel diseases (SVD) were collected at baseline. Geriatric depressive score (GDS) 15-items (≥ 6) was used to ascertain the presence of depression. Logistic regression was used to explore risk factors for presence of depression at 3-month and delayed-onset depression at 3-year, respectively. Results: A total of 394 (38.5%) patients had depression at 3-month after stroke/TIA, leaving 629 depression-free subjects. Among these 629 subjects, 350 received re-assessment of GDS at 3-year, and 49 (14%) developed depression. At 3-month, National Institute of Health Stroke Scale (NIHSS) score (OR=1.09, 95% CI: 1.04-1.14, p<0.001), Montreal Cognitive Assessment performance (MoCA) (OR=0.92, 95% CI: 0.89-0.96, p<0.001), and younger age (OR=0.979, 95% CI: 0.961-0.997, p=0.024) were associated with depression, while statins use (OR=0.69, 95% CI: 0.49-0.96, p=0.028) was associated with a decreased risk. At 3-year, presence of lacunes at baseline (OR=2.2, 95% CI: 1.1-4.3, p=0.022) and MoCA performance (OR=0.88, 95% CI: 0.81-0.96, p=0.003) were significant risk factors for development of delayed-onset depression, while long-term use of statins (OR=0.4, 95% CI: 0.2-0.9, P=0.021) was associated with a reduced risk of delayed-onset depression. Conclusion: Clinical severity and age influence early-onset depression, while SVD and cognitive impairment increase risk of delayed-onset depression. Statins use protects from development of depression.

Expression of Concern on “Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents”

Expression of Concern on “Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents”

Response to: Comment on “Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents”

Response to: Comment on “Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents”

Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents.

The relationship of elevated depression risk recently discovered among adult persons raised by same-sex parents with possible precipitating conditions in childhood has not previously been acknowledged. This study tests whether such inattention is supportable. Logistic regression based risk ratios were estimated from longitudinal measures of mental health outcomes observed in three waves (at ages 15, 22, and 28) of the US National Survey of Adolescent to Adult Health (n = 15,701). At age 28, the adults raised by same-sex parents were at over twice the risk of depression (CES-D: risk ratio 2.6, 95% CI 1.4–4.6) as persons raised by man-woman parents. These findings should be interpreted with caution. Elevated risk was associated with imbalanced parental closeness and parental child abuse in family of origin; depression, suicidality, and anxiety at age 15; and stigma and obesity. More research and policy attention to potentially problematic conditions for children with same-sex parents appears warranted.

Comment on "Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents".

Comment on "Invisible Victims: Delayed Onset Depression among Adults with Same-Sex Parents".

One-year follow up of PTSD and depression in elderly aboriginal people in Taiwan after Typhoon Morakot.

This paper describes a 1-year follow-up of post-traumatic stress disorder (PTSD) symptomatology and depression in an elderly minority population who experienced Typhoon Morakot in Taiwan. The PTSD Symptom Scale--Interview and the 10-item short form Center for Epidemiological Studies Depression Scale were used to examine PTSD symptomatology and depression in 120 victims at 3-6 months and in 88 victims (73.3% reinterview rate) at 11-12 months after the disaster. Further, we looked for associations between stress, prognosis, and development of PTSD symptomatology and depression. The prevalence of PTSD symptomatology decreased from 29.2% (35/120) at 3-6 months to 15.9% (14/88) at 11-12 months. The prevalence of depression, however, increased from 43.3% (52/120) to 46.6% (41/88). No factor was associated with follow-up PTSD symptomatology, and only the level of education was related to follow-up depression. Generally, the risk factors of age, sex, symptomatology of PTSD and depression at baseline, and stressor of unemployment predicted new-onset or chronic PTSD symptomatology and depression. Delayed-onset depression 48.0% (24/50) was more common than delayed-onset PTSD symptomatology 11.3% (7/62). Chronic and delayed-onset PTSD symptomatology were more easily developed with depression. Although PTSD and depression were separate consequences of trauma, they emerged and affected mental health together. We documented the courses of PTSD and depression among elderly aboriginal people, and the possible effects of demographic, symptomatology, and adverse life stressors were discussed.

Risk Factors for and Correlates of Poststroke Depression Following Discontinuation of Antidepressants

Risk Factors for and Correlates of Poststroke Depression Following Discontinuation of Antidepressants

Comparison between acute and delayed onset major depression after spinal cord injury.

Sixty patients with spinal cord injury were examined to assess major depression during the in-hospital period and at 3- and 6-month follow-up. Thirteen patients had depression during the initial in-hospital evaluation (acute onset depression) and eight had depression first diagnosed at either 3- or 6-month follow-up (delayed onset depression). Acute onset depression was related to the severity of impairment and premorbid history of psychiatric disorder, suggesting a psychological reaction to impairment or premorbid vulnerability as a possible mechanism for developing depression. Delayed onset depression was not related to severity of physical impairment but was associated with more rostral spinal injury, suggesting the possibility that neurophysiological response to injury more proximal to the brain may play a role in delayed onset depression. These data also suggest that the etiology and pathophysiology of these two types of depression may be different.

Comparison between acute- and delayed-onset depression following traumatic brain injury

Sixty-six patients admitted for the treatment of acute closed head injury were assessed for the presence of mood disorders during the in-hospital period and at 3-, 6-, and 12-month follow-ups. Diagnosis was made using a structured psychiatric interview and DSM-III criteria. A total of 28 patients had major depression at some time during the study: 17 had acute-onset depression and 11 had delayed-onset depression. Acute-onset depressions are related to lesion location and may have their etiology in biological responses of the injured brain, whereas delayed depressions may be mediated by psychosocial factors, suggesting psychological reaction as a possible mechanism.

Two-year longitudinal study of post-stroke mood disorders: comparison of acute-onset with delayed-onset depression.

Patients who developed post-stroke depression 3 to 24 months after hospital discharge (N = 21) were compared with patients who developed depression during hospitalization (N = 26) and patients who never developed depression over 24 months of follow-up (N = 15). During the acute hospitalization and at follow-up, the three groups were not significantly different in their demographic characteristics, neurological impairment, intellectual impairment, or quality of social support. The acute depression group, however, showed an increased correlation between impairment and depression from hospitalization to follow-up. Findings suggest that impairment does not produce depression, but, once depression occurs, it may interact with impairment to influence post-stroke recovery.