Stroke and depression, they go hand in hand! Stroke and depression are brothers and sisters in arms. Stroke and depression are the most common and threatening disorders in neuropsychiatry. China has about 2 million new stroke patients every year (reportedly 5 times the incidence of coronary heart disease), of which 70% to 80% of those with disabilities cannot live independently; there are about 120 to 200 million patients with depression worldwide, and 10% to 15% of these patients are at risk of suicide. The relationship between cerebrovascular disease and depressive disorders is complex, and stroke and depression intersect in many ways, including post-stroke depression (PSD) and vascular depression. Post-stroke depression (PSD) is a risk factor for stroke, and depression can lead to stroke. PSD is a post-stroke psychological disorder characterized by persistent emotional depression, decreased interest, and behavioral withdrawal, with an overall incidence rate of 40% to 50%, of which 15% is severe depression, which can be accompanied by suicidal tendencies or even suicidal behavior. 2 years after stroke is the high-risk period for the development of depression, with a peak in the incidence of the disease at 3-6 months after stroke; vascular depression refers to the development of depression in old age. Depression refers to depressive symptoms or depressive disorders presumed to be caused by vascular lesions occurring in old age. Cerebrovascular disease patients with depressive symptoms are very common in clinical practice, manifested by headache, dizziness, generalized weakness, decreased interest, insomnia, and decreased mental activity, which are not well treated with cerebrovascular disease medication alone, and are significantly more effective with the addition of antidepressant treatment. What symptoms suggest the presence of post-stroke depression and vascular depression? When the patient is found to be unresponsive, indifferent and passive to the surrounding environment, emotional response and expression become less, will requirement decreases and interest is lost, self-evaluation is low, work ability decreases, social activity retreats, attention is poor, agitation, pleasure decreases, etc. (psychological symptoms), accompanied by insomnia or excessive sleep, sleepiness, fatigue and weakness, headaches, chest pains, back pains, arthralgias and muscular pains, appetite disorders, and changes in body mass, muscle tension, and gastrointestinal dysfunction (somatic symptoms), the presence of a depressive disorder should be considered. A large proportion of neurologic outpatients are actually related to this disorder and require vigilance and attention. Some PSDs may present early with somatic complaints as the first symptom, such as fatigue and unwillingness to cooperate with rehabilitation, headache and dizziness, palpitations and chest tightness, or gastrointestinal symptoms, which are often overlooked by both physicians and patients.PSDs are prone to be accompanied by a wide range of somatic symptoms, especially signs and symptoms of neurological deficits, but depressed mood and loss of interest remain the core symptoms. Individuals with vasovagal depression are less likely to have classic sadness, self-guilt, and milder depression, but are more likely to have attention deficits, apathy, psychomotor retardation, and cognitive impairments predominantly impairments in executive functioning. Vasovagal depression is different from classic depressive disorders: 1. Patients rarely actively complain of mood symptoms or seek medical attention for them, but instead complain of somatic symptoms such as sleep problems, fatigue, weakness, headache, dizziness, or pain; 2. Instead of having intense symptoms of low self-esteem, suicidality, and self-blame as in classic cases, patients tend to have a mild form of depression, a poor state of mind, or do not meet the diagnostic criteria of “The patients’ affective symptoms are a continuum from mild to severe, rather than a binary distinction between normal and episodic; 4. In contrast to classic patients who recognize emotional depression, these patients “hide” or refuse to admit to depression. Vascular factors underlie the pathology of both depression and stroke! Strokes are a group of cerebrovascular diseases with sudden onset and focal neurological deficits as a common feature of cerebrovascular dysfunction from various causes.PSD occurs as a result of abnormal changes in cerebral blood flow, with frontal lobe and limbic system suffering from damage, resulting in abnormal metabolism of neuronal transmitters such as 5-hydroxytryptophan and norepinephrine, which can lead to depression. The occurrence of vascular depression (age >50 years) may be associated with vascular damage to the frontal-subcortical pathways responsible for emotion regulation and cognition. Thus, vascular lesions are the common pathological basis of stroke and depression, and the prevention and treatment of vascular depression should not be neglected while emphasizing the comprehensive management of stroke patients. Diagnosis of vascular depression? Diagnostic criteria for vascular depression: 1) the presence of cerebrovascular disorder or risk factors for cerebrovascular disorder; 2) the presence of white matter high signal in the region of penetrating branches, cerebral infarction, internal carotid artery stenosis or occlusion, and the stenosis of the circumflex of the Willis artery; 3) the occurrence of depression after the age of 65 years, or the increase in the frequency of depressive episodes after the occurrence of depression in combination with cerebrovascular disorder in the younger years, or the persistence of depression symptoms; 4) the presence of cognitive 4, cognitive dysfunction, psychomotor block, lack of self-awareness, and feelings of powerlessness; and 5, no family history of affective disorders. Post-stroke depression is relatively simple to determine, and the presence of post-stroke depression can be determined. Clinically, the recognition rate of depression caused by cerebrovascular disease is very low, and the rate of underdiagnosis is very high, due to the following reasons: 1. The majority of patients’ family members and doctors lack relevant knowledge, and they often interpret patients’ “unhappiness” and “displeasure” as natural psychological reactions after stroke, and think that “more comforting” is better than “more comforting”, and that “more comforting” is not enough. The majority of patients’ family members and doctors lack relevant knowledge, and often interpret patients’ “unhappiness” and “unhappiness” as natural psychological reactions after stroke, and think that “more comfort will make you feel better, and it’s not a disease”; 2. Although PSD is common, patients are often not recognized at an early stage because of aphasia, motor or cognitive impairments that are difficult to be actively expressed; 3. The physical symptoms of depression are easy to confuse with the physical symptoms of depression caused by stroke, such as poor concentration, poor sleepiness, insomnia, and psychomotor retardation; and 4. Denials of the patients and their families. The Hamilton Depression Scale or a specific post-stroke depression rating scale should be used in the diagnosis, with reference to the Chinese Classification and Diagnostic Criteria for Mental Disorders (CCMD-3) or international recommendations for the diagnosis of vascular depression. What is the treatment for post-stroke depression? For patients with a clear diagnosis of PSD or vasovagal depression, the aims of treatment are to: alleviate symptoms, achieve clinical cure, minimize disability and suicide rates, improve quality of life, restore social functioning, and prevent recurrence. The following principles should be adhered to: 1) prevention and treatment should be combined; 2) social and family support and medical intervention should be combined; 3) pharmacological and non-pharmacological interventions should be combined; 4) pharmacological treatment should follow the evidence and guidelines; and 5) drug selection should be fully weighed in terms of efficacy versus safety and tolerability. Pharmacological treatment, in addition to the early individual use of tricyclic antidepressants, mostly use 5-hydroxytryptamine reuptake inhibitors (SSRI). Medication can prevent the occurrence of PSD and improve its symptoms, and the combination of SSRI and cognitive-behavioral therapy is superior to SSRI treatment alone. For vascular depression, the addition of nimodipine, which improves small blood vessels, to an SSRI can improve the efficacy of treatment. The Five Golden Flowers of Antidepressants The Five Golden Flowers of antidepressants are: fluoxetine (Benadryl), paroxetine (Seroquel), sertraline (Zoloft), fluvoxamine (Lanxess), and citalopram (Xipramil). Escitalopram has been described as the “sixth golden flower”, its effect is 100 times the effect of citalopram dextrose, the adverse effects are more mild than citalopram. 1, Prozac. Fluoxetine hydrochloride, domestically produced, there are Youke, Omeren. The effect is basically the same. Prozac can make people energetic, but there are side effects of insomnia and light mania. Fluoxetine is slow to work for some people, some even take six weeks to work gradually, you need to be patient to wait for the effect. Fluoxetine tends to cause mania. Fluoxetine may cause weight loss within one year of taking it, and has a greater impact on sexual function. Fluoxetine is not suitable for patients with insomnia. 2, Zoloft (sertraline). SSRI in the dopamine reuptake inhibition effect is the strongest, and its strength of action can even be compared with Ritalin. Sertraline is suitable for people who lack a sense of pleasure, with relatively little inhibition of movement and alertness. It has a fast onset of action (effects can usually be seen in 7 days). Sertraline is effective for people with emotional deficits. Sertraline is more effective in treating depression in women than in men. Sertraline has less effect on sexual function. 3, Xipomia (citalopram). Citalopram is a highly selective 5 hydroxytryptamine in the uptake inhibitor, because it has almost no affinity for receptors other than 5 hydroxytryptamine, so it is highly selective and relatively few side effects. Its ability to inhibit 5 hydroxytryptamine reuptake is weaker than paroxetine sertraline. Long-term administration of citalopram restores expression. The literature says that long-term citalopram use is rarely resistant, and the eventual treatment of depression is more effective and less likely to be resistant. Citalopram is also effective against anxiety. Citalopram is also suitable for unresponsive depressed patients. 4, selleck (paroxetine). 5 hydroxytryptamine reuptake inhibition of the strongest drug. Anxiolytic strong, can treat generalized anxiety disorder and social anxiety disorder, the efficacy of generalized anxiety disorder is good. It has a slight anticholinergic effect, which is the only antidepressant among SSRIs that has an anticholinergic effect. Paroxetine is less prone to excitability and is a better choice for people with insomnia. Ranking of domestic antidepressants: in terms of sales scale, the first is escitalopram, followed by paroxetine, and the third is sertraline. New drugs are opening up As the prospect of antidepressants is favored by pharmaceutical companies, it also makes the new drug research and development of this class of drugs very active and rich in results, such as NE-ergic and specific 5-HT-ergic (NaSSAs class of drugs), 5-HT and NE reuptake inhibitors (SNRIs class of drugs) and so on. Venlafaxine (Bolusin, Enox) is the world’s first drug in the SNRIs class with dual uptake inhibition of 5-HT and norepinephrine, with the fewest adverse effects and the most definitive efficacy in relieving anxiety states, and is the drug of choice for mixed anxiety and depression. For any poor response to treatment and serious clinical condition, timely psychiatric consultation or referral must be requested. Attention should be paid to the selection of drugs that have a small effect on blood pressure, blood glucose, and metabolic syndrome. It should also be noted that the antihypertensive agents rifampicin, methyldopa, calcium antagonists, and beta-blockers all carry the risk of exacerbating depressive disorders. Depression can either be a combination of multiple factors that lead to depression after stroke or it can be a vascular disease (vascular depression). The relationship between cerebrovascular disease and depression is complex, but the clinical dangers are serious and the medical-economic implications are significant and must be emphasized. Early identification and active and effective control of depressive disorders in patients with cerebrovascular disease should become one of the core clinical tasks of neurologists. The prevention and treatment of depressive disorders is based on pharmacotherapy, which should follow the evidence and weigh the pros and cons.