The etiology of poststroke depression: a review of the literature and a new hypothesis involving inflammatory cytokines

Abstract

Although poststroke depression is unlikely to represent a single disorder and numerous etiologies for different kinds of poststroke depression will likely emerge as the result of future research, we believe that a number of poststroke depressive disorders are likely to be the result of specific changes in brain pathology and neurophysiology. Nevertheless, there are relatively few hypotheses about the pathophysiology of poststroke depression. This paper, therefore, proposes a new hypothesis for poststroke depression involving increased production of proinflammatory cytokines resulting from brain ischemia in cerebral areas linked to the pathogenesis of mood disorders. This paper reviews the evidence supporting the hypothesis that proinflammatory cytokines are involved in the occurrence of stroke as well as mood disorders linked to the brain damage. The increased production of proinflammatory cytokines such as IL-1b, TNF-a or IL-18 resulting from stroke may lead to an amplification of the inflammatory process, particularly in limbic areas, and widespread activation of indoleamine 2,3-dioxygenase (IDO) and subsequently to depletion of serotonin in paralimbic regions such as the ventral lateral frontal cortex, polar temporal cortex and basal ganglia. The resultant physiological dysfunction may lead to poststroke depression. Future investigations may explore this hypothesis through more extensive studies on the role of proinflammatory cytokines, such as IL-1b, TNF-a or even IL-18, in patients with poststroke depression. Molecular Psychiatry (2006) 11, 984-991.

Literature and Art Therapy in Post-Stroke Psychological Disorders

“…It is likely that depression increases stroke morbidity and mortality through biological mechanisms such as increased activity in the hypothalamic-pituitary-adrenal (HPA) axis, sympathetic stimulation, pro-inflammatory cytokine levels, and behaviors such as diminished adherence to medical treatment regimens, neglect of self-care, physical inactivity, poor diet, and substance abuse (Katon 2003). Stroke lesions or brain ischemia increases the risk of depression through similar biological mechanisms including increased production of HPA axis hormones and pro-inflammatory cytokines in addition to the disruption of neural circuits underlying emotional regulation (Bhogal et al 2004;Spalletta et al 2006). The comorbid bidirectional relationship between stroke and depression indirectly indicates that treatment or preventive intervention of one may have a positive impact on both, and modifying shared causative factors may have preventive potential for both disorders.…”

Post-stroke depression

“…A PSD-t gyakran nem ismerik fel, ezért kezelése elmarad [10], pedig az irodalomban számos utalást találha-tunk rá, hogy a depresszív irányú hangulatzavar meghosszabbítja a kórházi akut ellátás időtartamát [11], rontja a beteg rehabilitációját, funkcionális felépülését [12,13], napi aktivitását [14], életminőségét [15] és nö-veli a stroke utáni mortalitást [15,16,17]. Ezenkívül a depresszív irányú hangulatváltozás negatív hatással van a párkapcsolatra [14] és növeli egy újabb stroke kockázatát [18].…”

“…Általánosan elfogadott, hogy röviddel a stroke után az endogén faktorok szerepe jelentősebb, tehát a károsodott anatómiai struktúrák, illetve a neurotranszmitter és neuroendokrin rendszerek szerepét hangsúlyozzák [30,31]. Egy másik lehetséges elmélet szerint a stroke következtében megemelkedett citokintermelés gátolja a szerotoninprodukciót az agy több területén, ami a depresszió kialakulásához vezethet [16]. Ezzel szemben a késői fázisban a pszichoszociális faktorok elsődlegességét emelik ki.…”

There is No Association Between the Omega-3 Index and Depressive Symptoms in Patients With Heart Disease Who Are Low Fish Consumers

“…LCn3PUFAs may also increase levels of monoaminergic neurotransmitters in the brain [11], and inhibit inflammation that is associated with depression [9]. The mechanisms underlying depression are complex and, while there is some evidence linking change to cerebrovascular structure and function with depression [12], other evidence suggests that inflammatory changes are central [13]. Changes in inflammatory markers following supplementation with LCn3PUFAs have been proposed to be central to improvements seen in vascular function in adults with metabolic syndrome [14].…”