Poststroke depression (PSD) is a frequent psychiatric sequela after stroke, and its influence is detrimental. However, the etiology of PSD is still not clear. Although many studies have indicated that immune dysregulation plays an important role in the pathophysiology of depression, it is still unknown if PSD involves the same mechanism. Thus, the current study objectives were to evaluate whether there were cytokine changes when patients with ischemic stroke suffered from PSD.
We included ischemic stroke patients without depression when the stroke occurred and followed them for 1 year. The Hamilton Depression Rating Scale score and cytokines were assessed at baseline and at the 1st, 3rd, 6th, 9th and 12th months after stroke.
One hundred four patients with ischemic stroke participated and completed the study, and 12 suffered from PSD during the 1-year study period. There were significant increases in the cytokines interleukin-6 (IL-6), interleukin-10 (IL-10), tumor necrosis factor α (TNF-α) and interferon-γ, and the ratios of IL-6/IL-10 and TNF-α/IL-10 were also elevated. Interleukin-1β was too low to show any difference.
Our study suggested that immune imbalance plays a possible role in the pathophysiology of PSD and that IL-6 and TNF-α are key cytokines.
"In this study, poststroke depression was not associated with a bias towards peripheral production of IL-17. Relationships between poststroke depression and peripheral concentrations of other cytokines have been inconsistent, with increases noted in some    but not all previous studies   . "
[Show abstract][Hide abstract] ABSTRACT: Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-] γ), anti-inflammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status (F 1,46 = 8.44, P = 0.006). IL-17 concentrations did not differ between subjects with and without depressive symptoms (F 1,46 = 8.44, P = 0.572); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms (F 1,46 = 9.29, P = 0.004). In those subjects with depressive symptoms, IL-17 was associated with higher LPH (ρ = 0.518, P = 0.023) and lower IL-10 (ρ = -0.484, P = 0.036), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinflammatory and anti-inflammatory activity and increased oxidative stress.
BioMed Research International 06/2014; 2014:245210. DOI:10.1155/2014/245210 · 2.71 Impact Factor
"Nevertheless, a prospective examination of cytokine changes during post-stroke recovery revealed that among those patients that expressed depressive symptoms one year after stroke, serum concentrations of IL-6, IL-10, TNF-α, and IFN-γ were concomitantly increased, supporting the supposition that these key cytokines might contribute to, or be an index of, post-stroke depressive symptoms (Su et al., 2012). Although in this study serum IL-1β levels were too low to be detected (Su et al., 2012), a role for IL-1β in post-stroke depressive symptoms has been confirmed in animal models in which the anhedonia elicited by middle cerebral artery occlusion was attenuated by intracerebrovascular injection of IL-1ra (Craft and DeVries, 2006). As in the case of major depression, the mood symptoms that follow stroke have been related to impairments of BDNF. "
[Show abstract][Hide abstract] ABSTRACT: The development of depressive disorders had long been attributed to monoamine variations, and pharmacological treatment strategies likewise focused on methods of altering monoamine availability. However, the limited success achieved by treatments that altered these processes spurred the search for alternative mechanisms and treatments. Here we provide a brief overview concerning a possible role for pro-inflammatory cytokines and growth factors in major depression, as well as the possibility of targeting these factors in treating this disorder. The data suggest that focusing on one or another cytokine or growth factor might be counterproductive, especially as these factors may act sequentially or in parallel in affecting depressive disorders. It is also suggested that cytokines and growth factors might be useful biomarkers for individualized treatments of depressive illnesses.
[Show abstract][Hide abstract] ABSTRACT: Introduction:
Post-stroke depression (PSD) is the most common mood disorder following a stroke, and also the main factor limiting recovery and rehabilitation in stroke patients. In addition, it may increase mortality by up to ten times.
PSD occurs in 1 in 3 stroke patients and more than half of all cases are neither diagnosed nor treated. Several mechanisms, including biological, behavioral, and social factors, are involved in its pathogenesis. Symptoms usually occur within the first three months after stroke (early onset PSD), and less frequently at a later time (late onset PSD). Symptoms resemble those of other types of depression, although there are some differences: PSD patients experience more sleep disturbances, vegetative symptoms, and social withdrawal. For PSD diagnosis, we recommended vigilance and use of specific diagnostic tools such as the Patient Health Questionnaire-2 (PHQ-2). The treatments of choice are selective serotonin reuptake inhibitors (SSRI). However, there are still many unanswered questions in the treatment of PSD, such as the best time to start treatment or the effects of antidepressants on cognition and motor function, among others.
Neurologists play a pivotal role in the care and management of patients recovering from stroke. They must be familiar with methods for early detection and treatment of PSD, as this can facilitate a patient's functional recovery and social reintegration, and improve quality of life for patients and their families.
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