Stroke and Depression
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Stroke and Depression Yu. P. Sivolap and I. V. Damulin
Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 119, No. 9, Iss. 1, pp. 143–147, September, 2019. Original article submitted March 28, 2019. Accepted May 13, 2019. Depression is a frequent complication of stroke and develops in about one third of survivors. It degrades the course of poststroke neurological impairments, increases the physical helplessness of patients, and decreases their quality of life, significantly reducing the efficacy of therapeutic and rehabilitation measures and increasing the risk of lethal outcomes. Antidepressants eliminate or decrease the symptoms of depression, promote reductions in neurological disorders, improve cognitive functions and patient’s overall status, increase the efficacy of treatment and rehabilitation, decrease the risk of repeat stroke, and decrease lethality. Preference in the treatment of poststroke depression is given to selective serotonin reuptake inhibitors; data have been obtained on the efficacy of other contemporary antidepressants, as well as tricyclic antidepressants. Unresolved aspects of this problem requiring further suitably designed controlled studies include the tolerance of antidepressants by elderly patients, selection of the appropriate drugs, and choice of treatment duration. Keywords: stroke, poststroke depression, outcomes, lethality, antidepressants, selective serotonin reuptake inhibitors.
Strokes, 80% of which are ischemic and 20% hemorrhagic, are in the category of diseases with high medical and social importance. In the US, stroke is the fifth most common cause of death and disability [1]. Depression, along with arterial hypertension, smoking, dyslipidemia, diabetes, insulin resistance, alcohol abuse, low physical activity, and other causes, is one of the risk factors for the development of stroke [1]. On the other hand, depression is a not infrequent and very undesirable complication of stroke and is regarded as its most typical psychosocial consequence. Poststroke depression has been known to clinicians for more than 100 years, though it is only since the 1970s that systematic controlled studies of this disorder have started [2]. The possible pathogenetic mechanisms for the development of depression after stroke include inflammation, lesions to the white matter of the brain, impairments to the mechanisms regulating cerebral vessel tone, changes in neuroplasticity, glutamatergic and other neurotransmitter disorders, and genetic and epigenetic factors [2].
In assessing the prevalence of poststroke depression, most authors give figures of 28–35% [3–7]; in other words, depression develops in about a third of survivors or a little more, though in some countries, particularly Iran, the prevalence is 1.5 times greater, at 47% [8]. On the basis of summarized published data, researchers at Minnesota University (USA) reported a wide range of prevalences of poststroke depression – from 25% to 79% [9, 10]. In the overall population, depression is encountered about twic
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