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*It is only for medical professionals to read and refer to the current hot topics of stroke research and intervention in the world.
Stroke has received more and more attention due to its high incidence and disability.
The recovery of function, cognition, mood and the improvement of quality of life after stroke have become important indicators for evaluating the effect of treatment and affecting the outcome of patients.
Post-stroke cognitive impairment (PSCI) can significantly increase the mortality of stroke patients and reduce the 5-year survival rate of patients.
It is a hot spot in current stroke research and intervention.
It is important to correctly identify PSCI and evaluate it regularly.
The concept PSCI refers to a clinical syndrome in which cognitive impairment occurs after a stroke event and persists to varying degrees of cognitive impairment until 6 months, emphasizing the potential causal relationship between stroke and cognitive impairment and the clinical relationship between the two The relevance of management includes cognitive impairment caused by stroke events such as multiple infarcts, key infarcts, subcortical infarctions, and cerebral hemorrhage, as well as brain degenerative diseases such as Alzheimer's disease (AD) after stroke 6 Cognitive impairment caused by progress within one month.
According to the severity of cognitive impairment, PSCI can be divided into post-stroke cognitive impairment non-dementia (PSCIND) and post-stroke dementia (PSD).
PSCI emphasizes the trigger-like event of stroke, which encompasses the continuous spectrum of cognitive impairment from PSCIND to PSD.
The clinical manifestations of clinical classification of PSCI are highly heterogeneous, not only related to the size and location of the stroke, but also affected by the patient's age, education, genetic background, and AD and other comorbidities.
It can be roughly divided into the following types.
1.
Multiple infarct type: multiple infarcts of different sizes in the cortex and under the cortex, mainly caused by thrombo-embolism or cardiogenic embolism caused by atherosclerosis of large-medium caliber.
The clinical manifestations are sudden onset, fluctuating or step-like course, focal neurological deficits (motor, sensory, visual impairment, and damage to advanced cortical functions).
2.
Infarct type of key parts: It is characterized by single or multiple infarcts in important functional brain areas, such as infarcts of the thalamus, frontal cortex, basal forebrain, medial temporal lobe and hippocampus, caudate nucleus and angular gyrus.
The clinical manifestations are related to the damaged functional areas, and both large and small blood vessels can be affected.
3.
Cerebral arteriole occlusion (cerebrovascular disease): Stroke is manifested by acute lacunar syndrome, with neuroimaging evidence of recent infarction in the perforator blood supply area, often accompanied by multiple old infarcts and varying degrees of white matter lesions .
Cognitive performance is characterized by prominent impairment of attention to executive function.
4.
Hemorrhagic cerebrovascular disease: cerebral parenchymal hemorrhage, subarachnoid hemorrhage, etc.
Cognitive impairment is related to the location of parenchymal hemorrhage and the size of hematoma, as well as the age of onset.
5.
Mixed type: a mixture of the above vascular diseases.
In addition, if the patient is accompanied by AD and other degenerative diseases, corresponding imaging findings can also be combined.
Risk factors Hypertension is an independent risk factor for cognitive impairment.
Studies have found that the rational use of antihypertensive drugs, lipid-lowering drugs or combination drugs after stroke can reduce the risk of long-term cognitive impairment.
A study published by Stroke in 2018 found that both low and high blood pressure in the early stage of acute ischemic stroke increased the risk of PSCI at 3 months; the systolic/diastolic blood pressure was maintained at (143~158)/(93~102) mmHg reduces PSCI; large atherosclerosis and anterior circulation complete infarction type increase the risk of PSCI at 3 months.
Current research shows that the left angular gyrus, left basal ganglia, and left basal ganglia surrounding white matter are the key structures of PSCI.
If infarcts or lesions occur in these parts, PSCI is more likely to occur, but there is currently no very good model based on the PSCI prediction model based on the infarcted part.
Because the occurrence of PSCI is not only related to infarction, some of its potential pathophysiological changes, including the pathophysiological changes of AD, are also of great significance, and the occurrence of PSCI is affected in many ways.
The Stroke and Cognition Alliance (STROKOG) evaluated 12,092 patients at risk of stroke or transient ischemic attack, including exploring the rate and pattern of cognitive decline, risk factors for PSCI, and biomarkers.
The results of the study show that PSCI has a high prevalence rate in the population, and there are ethnic differences.
PSCI is not only related to stroke size and location, but also affected by patient's age, education, genetic background, and AD and other comorbidities.
Among them, diabetes is considered an important risk factor for PSCI.
Table 1 Assessment and diagnosis of risk factors for post-stroke cognitive dysfunction.
Post-stroke delirium and transient cognitive impairment can be recovered early.
The diagnosis of PSCI is often finalized based on the results of cognitive assessment 3 to 6 months after stroke.
Cognitive tests for stroke patients need to evaluate at least 4 cognitive domains (executive function/attention, memory, language ability, visual space ability), and the impairment of daily living ability should be independent of the motor/sensory function impairment of the secondary vascular event .
The establishment of PSCI diagnosis should have three elements: clear stroke diagnosis: stroke diagnosis supported by clinical or imaging evidence, including transient ischemic attack, hemorrhagic stroke and ischemic stroke.
Cognitive impairment exists: the patient's main complaint or the insider's report or the experienced clinician judges that the cognitive impairment occurred after the stroke event, and neuropsychological evidence confirms that there is more than one cognitive domain functional impairment or evidence of cognitive decline compared with the previous.
The temporal relationship between stroke and cognitive impairment: it appears after the stroke event and lasts for 3 to 6 months.
The cognitive function change of PSCI is a dynamic process.
For stroke patients, the cognitive function needs to be routinely evaluated quickly.
Once diagnosed, comprehensive intervention measures should be taken as soon as possible, including intervention and prevention of known risk factors, drug treatment and recovery treatment. Figure 1 Flow chart of PSCI outpatient management Note: *PSCI high-risk population: medical history and questioning results show that living ability is reduced, comprehension, language, and use ability are significantly reduced, and may also be accompanied by depression in patients.
PSCI: cognitive impairment after stroke; PSCIND: PSCI non-dementia; PSD: post-stroke dementia; Cog: Cognitive Impairment Preliminary Evaluation Form; Mini-Cog: Simple Cognitive Assessment Scale; MMSE: Simple Mental State Examination Scale; MoCA: Montreal Cognitive Assessment Scale; NPI: Neuropsychiatric Symptom Questionnaire; NMDA: N-Methyl-D-Aspartic Acid Prevention and Treatment Controlling the risk factors of stroke, reducing the occurrence and development of stroke, and doing secondary prevention of stroke is the fundamental way to prevent PSCI.
The main purpose of PSCI treatment is to delay the further decline of cognitive impairment, improve cognitive level, improve mental behavior symptoms and improve the ability of daily living.
PSCI intervention should consider the time of stroke, the severity of cognitive impairment, whether there are comorbidities, and the needs of patients and caregivers.
Compared with AD, PSCI lacks treatment drugs that are consistently recommended by national guidelines.
Currently, the commonly used drugs in clinical practice are as follows: Cholinesterase inhibitors: donepezil, galantamine, rivastigmine; non-competitive N-methyl-D-aspartame Amino acid receptor antagonist: Memantine; other drugs: Niergoline, Nimodipine, Citicoline, etc.
PSCI can also have psycho-behavioral symptoms, such as depression, anxiety, delusions, hallucinations, sleep inversion, impulsive aggressive behavior, etc.
The treatment principles are as follows: non-drug treatment should be the first choice for mild psycho-behavioral symptoms; selective serotonin is recommended for depression Reuptake inhibitors; atypical antipsychotics are the first choice for antipsychotics, and the clinical benefits and potential risks of patients must be fully considered. Reference materials: [1]Xu Jun.
Practices for outpatient management of patients with cognitive impairment after stroke[J].
Chinese Journal of Stroke,2019,v.
14(09):65-78.
[2]Wang Yanjiang, Luo Benyan, Wang Jun.
Expert consensus on the prevention and treatment of cognitive impairment after stroke in China[J].
Chinese Journal of Stroke,2020(2):158-166.
[3]Dong Qiang,Guo Qihao, Luo Benyan, et al.
Expert consensus on management of cognitive impairment after stroke[J] .
Chinese Journal of Stroke, 2017.
[4] Professor Song Haiqing’s academic report: the concept and practice of post-stroke cognitive dysfunction [5] Professor Yu Jintai’s academic report: progress in the diagnosis and treatment of post-stroke cognitive dysfunction ：Nerve News Editor in charge: Mr.
Lu Li’s copyright statement.
This article is reprinted and forwarded to Moments-End-Call for papers.
Welcome to submit papers to the editor’s mailbox: yxjsjbx@yxj.
org.
cn.
Please specify: [Submission] Hospital + Department + Name.
Form, author's remuneration favorably edit WeChat: chenaFF0911
Stroke has received more and more attention due to its high incidence and disability.
The recovery of function, cognition, mood and the improvement of quality of life after stroke have become important indicators for evaluating the effect of treatment and affecting the outcome of patients.
Post-stroke cognitive impairment (PSCI) can significantly increase the mortality of stroke patients and reduce the 5-year survival rate of patients.
It is a hot spot in current stroke research and intervention.
It is important to correctly identify PSCI and evaluate it regularly.
The concept PSCI refers to a clinical syndrome in which cognitive impairment occurs after a stroke event and persists to varying degrees of cognitive impairment until 6 months, emphasizing the potential causal relationship between stroke and cognitive impairment and the clinical relationship between the two The relevance of management includes cognitive impairment caused by stroke events such as multiple infarcts, key infarcts, subcortical infarctions, and cerebral hemorrhage, as well as brain degenerative diseases such as Alzheimer's disease (AD) after stroke 6 Cognitive impairment caused by progress within one month.
According to the severity of cognitive impairment, PSCI can be divided into post-stroke cognitive impairment non-dementia (PSCIND) and post-stroke dementia (PSD).
PSCI emphasizes the trigger-like event of stroke, which encompasses the continuous spectrum of cognitive impairment from PSCIND to PSD.
The clinical manifestations of clinical classification of PSCI are highly heterogeneous, not only related to the size and location of the stroke, but also affected by the patient's age, education, genetic background, and AD and other comorbidities.
It can be roughly divided into the following types.
1.
Multiple infarct type: multiple infarcts of different sizes in the cortex and under the cortex, mainly caused by thrombo-embolism or cardiogenic embolism caused by atherosclerosis of large-medium caliber.
The clinical manifestations are sudden onset, fluctuating or step-like course, focal neurological deficits (motor, sensory, visual impairment, and damage to advanced cortical functions).
2.
Infarct type of key parts: It is characterized by single or multiple infarcts in important functional brain areas, such as infarcts of the thalamus, frontal cortex, basal forebrain, medial temporal lobe and hippocampus, caudate nucleus and angular gyrus.
The clinical manifestations are related to the damaged functional areas, and both large and small blood vessels can be affected.
3.
Cerebral arteriole occlusion (cerebrovascular disease): Stroke is manifested by acute lacunar syndrome, with neuroimaging evidence of recent infarction in the perforator blood supply area, often accompanied by multiple old infarcts and varying degrees of white matter lesions .
Cognitive performance is characterized by prominent impairment of attention to executive function.
4.
Hemorrhagic cerebrovascular disease: cerebral parenchymal hemorrhage, subarachnoid hemorrhage, etc.
Cognitive impairment is related to the location of parenchymal hemorrhage and the size of hematoma, as well as the age of onset.
5.
Mixed type: a mixture of the above vascular diseases.
In addition, if the patient is accompanied by AD and other degenerative diseases, corresponding imaging findings can also be combined.
Risk factors Hypertension is an independent risk factor for cognitive impairment.
Studies have found that the rational use of antihypertensive drugs, lipid-lowering drugs or combination drugs after stroke can reduce the risk of long-term cognitive impairment.
A study published by Stroke in 2018 found that both low and high blood pressure in the early stage of acute ischemic stroke increased the risk of PSCI at 3 months; the systolic/diastolic blood pressure was maintained at (143~158)/(93~102) mmHg reduces PSCI; large atherosclerosis and anterior circulation complete infarction type increase the risk of PSCI at 3 months.
Current research shows that the left angular gyrus, left basal ganglia, and left basal ganglia surrounding white matter are the key structures of PSCI.
If infarcts or lesions occur in these parts, PSCI is more likely to occur, but there is currently no very good model based on the PSCI prediction model based on the infarcted part.
Because the occurrence of PSCI is not only related to infarction, some of its potential pathophysiological changes, including the pathophysiological changes of AD, are also of great significance, and the occurrence of PSCI is affected in many ways.
The Stroke and Cognition Alliance (STROKOG) evaluated 12,092 patients at risk of stroke or transient ischemic attack, including exploring the rate and pattern of cognitive decline, risk factors for PSCI, and biomarkers.
The results of the study show that PSCI has a high prevalence rate in the population, and there are ethnic differences.
PSCI is not only related to stroke size and location, but also affected by patient's age, education, genetic background, and AD and other comorbidities.
Among them, diabetes is considered an important risk factor for PSCI.
Table 1 Assessment and diagnosis of risk factors for post-stroke cognitive dysfunction.
Post-stroke delirium and transient cognitive impairment can be recovered early.
The diagnosis of PSCI is often finalized based on the results of cognitive assessment 3 to 6 months after stroke.
Cognitive tests for stroke patients need to evaluate at least 4 cognitive domains (executive function/attention, memory, language ability, visual space ability), and the impairment of daily living ability should be independent of the motor/sensory function impairment of the secondary vascular event .
The establishment of PSCI diagnosis should have three elements: clear stroke diagnosis: stroke diagnosis supported by clinical or imaging evidence, including transient ischemic attack, hemorrhagic stroke and ischemic stroke.
Cognitive impairment exists: the patient's main complaint or the insider's report or the experienced clinician judges that the cognitive impairment occurred after the stroke event, and neuropsychological evidence confirms that there is more than one cognitive domain functional impairment or evidence of cognitive decline compared with the previous.
The temporal relationship between stroke and cognitive impairment: it appears after the stroke event and lasts for 3 to 6 months.
The cognitive function change of PSCI is a dynamic process.
For stroke patients, the cognitive function needs to be routinely evaluated quickly.
Once diagnosed, comprehensive intervention measures should be taken as soon as possible, including intervention and prevention of known risk factors, drug treatment and recovery treatment. Figure 1 Flow chart of PSCI outpatient management Note: *PSCI high-risk population: medical history and questioning results show that living ability is reduced, comprehension, language, and use ability are significantly reduced, and may also be accompanied by depression in patients.
PSCI: cognitive impairment after stroke; PSCIND: PSCI non-dementia; PSD: post-stroke dementia; Cog: Cognitive Impairment Preliminary Evaluation Form; Mini-Cog: Simple Cognitive Assessment Scale; MMSE: Simple Mental State Examination Scale; MoCA: Montreal Cognitive Assessment Scale; NPI: Neuropsychiatric Symptom Questionnaire; NMDA: N-Methyl-D-Aspartic Acid Prevention and Treatment Controlling the risk factors of stroke, reducing the occurrence and development of stroke, and doing secondary prevention of stroke is the fundamental way to prevent PSCI.
The main purpose of PSCI treatment is to delay the further decline of cognitive impairment, improve cognitive level, improve mental behavior symptoms and improve the ability of daily living.
PSCI intervention should consider the time of stroke, the severity of cognitive impairment, whether there are comorbidities, and the needs of patients and caregivers.
Compared with AD, PSCI lacks treatment drugs that are consistently recommended by national guidelines.
Currently, the commonly used drugs in clinical practice are as follows: Cholinesterase inhibitors: donepezil, galantamine, rivastigmine; non-competitive N-methyl-D-aspartame Amino acid receptor antagonist: Memantine; other drugs: Niergoline, Nimodipine, Citicoline, etc.
PSCI can also have psycho-behavioral symptoms, such as depression, anxiety, delusions, hallucinations, sleep inversion, impulsive aggressive behavior, etc.
The treatment principles are as follows: non-drug treatment should be the first choice for mild psycho-behavioral symptoms; selective serotonin is recommended for depression Reuptake inhibitors; atypical antipsychotics are the first choice for antipsychotics, and the clinical benefits and potential risks of patients must be fully considered. Reference materials: [1]Xu Jun.
Practices for outpatient management of patients with cognitive impairment after stroke[J].
Chinese Journal of Stroke,2019,v.
14(09):65-78.
[2]Wang Yanjiang, Luo Benyan, Wang Jun.
Expert consensus on the prevention and treatment of cognitive impairment after stroke in China[J].
Chinese Journal of Stroke,2020(2):158-166.
[3]Dong Qiang,Guo Qihao, Luo Benyan, et al.
Expert consensus on management of cognitive impairment after stroke[J] .
Chinese Journal of Stroke, 2017.
[4] Professor Song Haiqing’s academic report: the concept and practice of post-stroke cognitive dysfunction [5] Professor Yu Jintai’s academic report: progress in the diagnosis and treatment of post-stroke cognitive dysfunction ：Nerve News Editor in charge: Mr.
Lu Li’s copyright statement.
This article is reprinted and forwarded to Moments-End-Call for papers.
Welcome to submit papers to the editor’s mailbox: yxjsjbx@yxj.
org.
cn.
Please specify: [Submission] Hospital + Department + Name.
Form, author's remuneration favorably edit WeChat: chenaFF0911
