Post stroke depression (PSD) is a depression that may occur after stroke, which has a significant impact on the healing process and overall quality of life of the affected persons.Studies have shown that poststroke depression is particularly associated with damage to the basal ganglia or the anterior brain region, including the hippocampal gyrus and the prefrontal cortex.Treatment of this condition generally includes selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), tricyclic antidepressants and cognitive behavioral therapy.
The symptoms of depression after stroke are the same as those of the main depression. The patient's symptoms and severity vary from person to person, but are usually manifested as depression and a decrease in interest in activities or a sense of happiness.
By definition, these symptoms include:
The incidence of post-stroke depression is reported to be between 18% and 33%, but this condition is often underestimated due to overlapping symptoms of stroke and depression.
Many risk factors can increase the likelihood of post-stroke depression, including:
The location, size, overall severity of stroke and its impact on cognitive function can predict the possibility of post-stroke depression than other risk factors.
The exact mechanism of post-stroke depression is not fully understood, and this condition is caused by the complex interaction of multiple factors such as neurochemistry, structure and inflammation.In particular, limbic system functions associated with major depression may be directly or indirectly affected by stroke.
Glutamate is an excitatory neurotransmitter substance. Excessive amounts can lead to neuronal death, aggravated impairment of mood regulation and reward pathways, especially in the prefrontal cortex, tonsils and hippocampal gyrus.
The hypothalamic-pituitary-adrenal (HPA) axis is responsible for regulating stress responses.HPA axis dysfunction is associated with elevated cortisol levels and chronic inflammation, which are all related to major depression.
The neurotrophic factor function in patients with depression after stroke is impaired, which affects the nerve growth and plasticity of the hippocampal gyrus and prefrontal lobes, which may lead to decreased emotional regulation and cognitive function.
After stroke depression is usually associated with a decrease in levels of conducting substances such as serotonin, dopamine and norepinephrine, which will affect mood regulation, cognitive function and intracerebral reward system.
Screen screening for poststroke depression should be a standard procedure for poststroke care, and tools such as the Hamilton Melancholy Score Scale (HDRS) and Patient Health Questionnaire-9 (PHQ-9) should be used.
The diagnosis is clinical, and any patient who has persistent depression symptoms after stroke can be diagnosed with poststroke depression.While these criteria may seem simple, the diagnosis can be challenging due to the overlap between stroke-related neurological symptoms and depression.
The difference between post-stroke depression and post-stroke apathy (PSA) is crucial.Apathy after stroke involves a reduction in goal-oriented behavior and a lack of spontaneous exercise or speech, but does not include symptoms related to depression such as depression, suicidal thoughts or guilt.
The treatment strategies for post-stroke depression usually include the following:
The mortality rate of patients with depression after stroke and baseline cognitive function is higher than that of patients with undepressed stroke.However, these consequences can be significantly improved by antidepressants such as SSRIs.Disability remains a challenge for many stroke patients, and post-stroke depression may aggravate medical problems and further affect disability.Faced with the challenge of post-stroke depression, we should think about: How to more effectively identify and treat the mental health problems of these patients to promote their recovery and quality of life?