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*Only for medical professionals' reference to read "Minor Stroke", Great Harm
.
Cerebral small vessel disease (CSVD), with insidious clinical symptoms and slow progression of the disease, is often called "little strokes", but CSVD is a catastrophic damage involving small blood vessels throughout the brain, like a storm After that, there was a mess, and the subsequent damage continued
.
In addition, cognitive decline is the most common and important clinical manifestation of CSVD, and about half of vascular cognitive impairment is caused by CSVD
.
Therefore, CSVD has received more and more attention from scholars
.
At the 3rd Annual Meeting of the Professional Committee of Cerebral Small Vascular Diseases, Professor Xu Yun from the Drum Tower Hospital of Nanjing University gave a wonderful lecture on "Diagnosis and Treatment of Cerebral Small Vascular Diseases", which mainly covered the clinical manifestations and pathology of CSVD Features, imaging manifestations, diagnosis and differential diagnosis, early diagnosis and treatment are all covered, let’s take a look
.
1.
Introduction to Cerebral Small Vascular Disease CSVD refers to a group of clinical syndromes involving cerebral arterioles, branch arterioles, capillaries and venules, and clinical manifestations of abnormal mood, abnormal gait, abnormal urination, vascular cognitive impairment, etc.
.
The risk factors mainly include age, hypertension, diabetes, family history and so on
.
▌ The clinical features of CSVD 60% of patients with insidious onset, 80% of patients showed a progressive course; increased with age, MRI found that 10% to 30% of people over 70 years old have CSVD; the incidence of CSVD is 5-6 of clinical stroke Times; Subcortical vascular impairment caused by CSVD is the most common vascular dementia (VCI); CSVD is an important cause of vascular depression; CSVD exists in 90% of VCI populations; Alzheimer’s disease (AD) patients 30% of them have CSVD
.
▌ CSVD pathological classification (Europe) Type I: arteriolar sclerosis, manifested as fibrinoid necrosis, lipid hyaline degeneration, arteriolar atherosclerosis, microaneurysm, segmental structural disorder or disintegration of arterioles (80% is I Type, related to hypertension and age); type II: sporadic or hereditary cerebral amyloid angiopathy (CAA); type III: hereditary small vessel disease, such as autosomal dominant genetic disease combined with subcortical infarction and leukoencephalopathy ( CADASIL), autosomal recessive cerebral artery disease and arteriosclerosis with subcortical infarction and leukoencephalopathy (CARASIL), mitochondrial myopathic encephalopathy with lactic acidosis and stroke-like attacks (MELAS), Fabry disease (Fabry disease), Hereditary cerebral retinal small vessel disease; Type IV: inflammation or immune-mediated small vessel disease, such as Wegener's granulomatosis, rheumatism, vasculitis; Type V: venous collagen disease, causing thickening and occlusion of small veins; Type VI: Other Small vessel disease, such as small vessel disease after radiation
.
▌ The pathological changes of CSVD Professor Xu Yun pointed out that the pathological changes of CSVD mainly include: 1.
Arteriole atherosclerosis; 2.
Lipid hyaloid degeneration; 3.
Fibrinoid necrosis; 4.
Amyloidosis; 5.
Blood vessels Enlarged peripheral space; 6.
Small aneurysm; 7.
Blood-brain barrier (BBB) destruction; 8.
Vasculitis
.
Therefore, when choosing a treatment method, these pathologies can be targeted for clinical treatment
.
Figure 1: Pathological changes of CSVD From a pathological point of view, CSVD first causes cerebrovascular damage, intravascular compression, vascular smooth muscle damage, and then causes cerebral cortex damage; when smooth muscle damage causes ischemia, it will cause Lacunar infarction; if it is diffuse, it will cause brain white matter damage; if an aneurysm is formed with small hemorrhage, it is microhemorrhage; if a large blood vessel ruptures, it is hemorrhage.
The details can be seen in the figure below
.
Figure 2: Pathological changes of cerebral small blood vessels II.
The diagnosis of CSVD.
At present, the diagnosis of CSVD mainly depends on imaging.
Its imaging manifestations mainly include lacunar infarction (LI) and white matter hyperintensities (WMHs).
), perivascular space (PVS), cerebral microbleeds (CMBs) and brain atrophy
.
Figure 3: The imaging manifestations of CSVD clinically, when diagnosing CSVD, different sequence choices should be made for different clinical manifestations.
Professor Xu Yun gave some examples, such as: acute lacunar infarction-DWI is easy to recognize.
FLAIR is optional, but DWI has higher specificity; white matter damage-DWI and T2, FLAIR and T2 can also be used; pure lacunar infarction-FLAIR can see low signal and glial hyperplasia around it; enlarged Vascular space-FLAIR and T2; microbleeds-SWI is preferred, and T2*GRE imaging can also be used
.
Figure 4: The diagnosis of conventional imaging technology and CSVD▌ Old lacunar infarction T2 shows high signal, FLAIR shows low signal, and there is glial hyperplasia around it
.
Figure 5: Old lacunar infarction ▌ Old cerebral infarction DWI low signal, FLAIR low signal, T2 high signal, among which FLAIR is the most obvious
.
Figure 6: Old cerebral infarction ▌ Differentiation of acute lacunar infarction and enlarged perivascular space In clinical practice, when there is no reference, the enlarged peripheral space is often misdiagnosed as a small lacunar infarction
.
Therefore, it is more recommended to use the FLAIR phase for diagnosis
.
Figure 7: Differentiation of acute luminal infarction and enlarged perivascular space.
The red arrow is acute luminal infarction, T1 is not enhanced, and FLAIR is high signal; the blue arrow is the perivascular space, T1 is not enhanced, and FLAIR is low signal, which is close to the cerebrospinal fluid signal
.
▌ Old cerebral hemorrhage Figure 8: Old cerebral hemorrhage For old cerebral hemorrhage, DWI and T1W1 are sometimes difficult to distinguish
.
FLAIR phase is easier to distinguish, softening foci can be seen in bleeding, and glial hyperplasia should be seen in ischemia
.
T2W1 shows high signal with surrounding low signal ring (hemosiderin deposition)
.
▌ CSVD white matter hyperintensity features Figure 9: CSVD white matter hyperintensity features III.
Differential diagnosis of CSVD ▌ Differentiating from multiple sclerosis Typical multiple sclerosis is easier to differentiate and diagnose.
Both brain and spinal cord can have lesions, multiple lesions, and asymmetric It usually has a relatively fixed distribution pattern and shape; the lesion is vertically distributed to the lateral ventricle; T1WI low signal, T2WI high signal (fried egg-like, cloud-like), FLAIR high signal, DWI shows high signal in the acute phase, and C after enhancement Shaped or open ring to strengthen
.
Figure 10: MS (provided by Nanjing Gulou Hospital) Professor Xu Yun gave an example of an image of an acute phase patient in his hospital.
The DWI of the acute phase patient in the following image shows high signal, which is cloudy, and it is C-shaped after enhancement Or open ring enhancement, which can be used as a basis for differential diagnosis
.
Figure 11: Distinguishing between acute MS and hereditary diseases.
In clinical, hereditary diseases are generally seen in children and young adults.
Most of the white matter of the brain has diffuse and symmetrical white matter hyperintensity, such as metachromatic leukodystrophy and adrenal white matter Malnutrition is related to location.
The predominance of the frontal lobe may be Alexander disease, the periventricular advantage may be metachromatic leukodystrophy, the parieto-occipital advantage may be Krabbe disease, etc.
This can help us in the differential diagnosis.
According to Medical history, genetic testing to confirm the diagnosis, here are some genetic diseases and their distinguishing characteristics
.
Figure 12: Autosomal dominant cerebral arterial disease (CADASIL) with subcortical infarction and leukoencephalopathy, temporal pole and external capsule involvement on MRI are characteristic, skin biopsy vascular smooth muscle middle layer osmium particles (Notch3 protein) deposition map 13: Fabry disease (Fabry disease), cutaneous angiokeratoma, corneal opacity, cataract and retinal ischemic changes IV.
Early diagnosis of CSVD▌ quantitative method of white matter damage Dynamic monitoring of white matter damage helps predict lacunar infarction, For the occurrence of diseases such as cerebral hemorrhage and cognitive dysfunction, the Fazekas visual assessment is the simplest quantitative method, and the classification is as follows: Figure 14: Fazekas visual assessment around the ventricle: 0 = none; Ⅰ = cap-shaped or pencil-like thin layer lesions Ⅱ=smooth halo; Ⅲ=irregular periventricular WMH, which invades deep white matter of the brain
.
Deep (subcortical): 0 = none; Ⅰ = punctate lesions; Ⅱ = lesions begin to merge; Ⅲ = lesions fused with large areas
.
Professor Xu Yun mentioned that lacunar infarctions of grade II and above are more common, and that white matter can be automatically located, extracted and quantified, which is more accurate
.
Figure 15: White matter automatic location, extraction and quantification▌ White matter hyperintensity (WMH) outcome——Professor Xu Yun's team research Professor Xu Yun's team's research over the years has found that the severity of WMH is related to lacunar infarction, cerebral hemorrhage, and Pa The occurrence of depressive symptoms of Kinsen’s disease is closely related; the risk of lacunar infarction is the highest within 2 years after the onset of WMH; the size of WMH is related to the impairment of cognitive function
.
At the same time, for the early diagnosis of CSVD, Professor Xu Yun mentioned that some scales can be made to evaluate the influence markers (peripheral vascular space, microbleeds, etc.
)
.
Figure 16: CSVD impact marker evaluation scale▌ Cerebral small vessel disease MRI total score Total CSVD score items include: number of lacunar foci ≥1; number of microbleeds (CMBs) ≥1; EPVS (EPVS-BS); WMH Around the ventricle: Fazekas score ≥ 3 points or deep
.
Each of the above items counts 1 point, and the sum of each item is the total CSVD score.
If the score is more than 2 points, there may be executive function and language dysfunction
.
Figure 17: If the score is more than 2 points, there will be executive dysfunction and language dysfunction.
Professor Yun Xu's team research found that as long as the score is more than 2 points, there will be executive dysfunction and language dysfunction
.
At the same time, international studies have shown that this table can predict the severity of cerebral hemorrhage, gait disturbance and cognitive decline
.
Figure 18: International research on the total score of MRI for cerebral small vessel disease ▌ Other methods helpful for early diagnosis For clinical research on early prediction of CSVD, T1W1 can be used to judge the degree of atrophy on the macroscopic structure; DTI on the microstructure , SWI can see fiber changes, micro hemorrhage, etc.
; function, perfusion, etc.
can use BOLD
.
Next, Professor Xu Yun used BOLD to look at patients with hypertension and white matter damage, as shown in the figure below
.
Figure 19: BOLD to take a look at patients with hypertension and white matter damage.
A significant increase in functional connectivity (FC) can be seen in the core area and subsystems of the default network (DMN), suggesting dysfunction (cognitive function and FC in the DMN dorsal subsystem Shows a negative correlation)
.
5.
CSVD treatment Professor Xu Yun said that the current treatment of CSVD is very lacking and is still a bottleneck.
There is no specific medicine that can treat CSVD
.
Mainly through active control of hypertension and diabetes to prevent progression and recurrence
.
It is hoped that more CSVD drugs will be developed, especially some old drugs that are already in clinical application may be further developed
.
Aspirin can be used for CSVD with lacunar infarction, and it is not recommended for other types of CSVD, especially those with inheritance and degeneration
.
There are many controversies about statins, which may increase the risk of intracranial hemorrhage, especially CAA.
It is very important that you do not use statins when there is no indication for primary prevention or secondary prevention
.
[There is evidence that CSVD "asymptomatic" microbleeds can be transformed into massive intracranial hemorrhage
.
The SPARCL study suggests that the application of high-dose statin therapy for CSVD is beneficial to the primary endpoint (fatal or non-fatal stroke) event, and there is no significant increase in the risk of bleeding
.
It is currently believed that intensive statin therapy can indeed increase the risk of intracranial hemorrhage
.
] For the treatment of white matter damage, Professor Xu Yun mentioned the following 3 points: 1.
Active antihypertensive therapy delays or prevents the progress of white matter hyperintensity; 2.
When choosing antihypertensive drugs, it is recommended that long-acting calcium antagonists (CCB) are the first choice And renin-angiotensin system (RAS) blockers; 3.
Deal with known vascular risk factors (hypertension, obesity, diabetes, and hypercholesterolemia)
.
Regarding the study of CSVD treatment strategy, although there is no therapeutic drug, the current preliminary research has found that its white matter damage, microhemorrhage, and lacunar infarction are all related to vascular endothelial and vascular smooth muscle function damage
.
Therefore, Professor Xu Yun believes that we should screen clinical drugs to target the microvascular endothelium of the brain, blood-brain barrier, and neuroinflammation for treatment
.
Figure 20: Targeting of CSVD prevention and treatment
.
Cerebral small vessel disease (CSVD), with insidious clinical symptoms and slow progression of the disease, is often called "little strokes", but CSVD is a catastrophic damage involving small blood vessels throughout the brain, like a storm After that, there was a mess, and the subsequent damage continued
.
In addition, cognitive decline is the most common and important clinical manifestation of CSVD, and about half of vascular cognitive impairment is caused by CSVD
.
Therefore, CSVD has received more and more attention from scholars
.
At the 3rd Annual Meeting of the Professional Committee of Cerebral Small Vascular Diseases, Professor Xu Yun from the Drum Tower Hospital of Nanjing University gave a wonderful lecture on "Diagnosis and Treatment of Cerebral Small Vascular Diseases", which mainly covered the clinical manifestations and pathology of CSVD Features, imaging manifestations, diagnosis and differential diagnosis, early diagnosis and treatment are all covered, let’s take a look
.
1.
Introduction to Cerebral Small Vascular Disease CSVD refers to a group of clinical syndromes involving cerebral arterioles, branch arterioles, capillaries and venules, and clinical manifestations of abnormal mood, abnormal gait, abnormal urination, vascular cognitive impairment, etc.
.
The risk factors mainly include age, hypertension, diabetes, family history and so on
.
▌ The clinical features of CSVD 60% of patients with insidious onset, 80% of patients showed a progressive course; increased with age, MRI found that 10% to 30% of people over 70 years old have CSVD; the incidence of CSVD is 5-6 of clinical stroke Times; Subcortical vascular impairment caused by CSVD is the most common vascular dementia (VCI); CSVD is an important cause of vascular depression; CSVD exists in 90% of VCI populations; Alzheimer’s disease (AD) patients 30% of them have CSVD
.
▌ CSVD pathological classification (Europe) Type I: arteriolar sclerosis, manifested as fibrinoid necrosis, lipid hyaline degeneration, arteriolar atherosclerosis, microaneurysm, segmental structural disorder or disintegration of arterioles (80% is I Type, related to hypertension and age); type II: sporadic or hereditary cerebral amyloid angiopathy (CAA); type III: hereditary small vessel disease, such as autosomal dominant genetic disease combined with subcortical infarction and leukoencephalopathy ( CADASIL), autosomal recessive cerebral artery disease and arteriosclerosis with subcortical infarction and leukoencephalopathy (CARASIL), mitochondrial myopathic encephalopathy with lactic acidosis and stroke-like attacks (MELAS), Fabry disease (Fabry disease), Hereditary cerebral retinal small vessel disease; Type IV: inflammation or immune-mediated small vessel disease, such as Wegener's granulomatosis, rheumatism, vasculitis; Type V: venous collagen disease, causing thickening and occlusion of small veins; Type VI: Other Small vessel disease, such as small vessel disease after radiation
.
▌ The pathological changes of CSVD Professor Xu Yun pointed out that the pathological changes of CSVD mainly include: 1.
Arteriole atherosclerosis; 2.
Lipid hyaloid degeneration; 3.
Fibrinoid necrosis; 4.
Amyloidosis; 5.
Blood vessels Enlarged peripheral space; 6.
Small aneurysm; 7.
Blood-brain barrier (BBB) destruction; 8.
Vasculitis
.
Therefore, when choosing a treatment method, these pathologies can be targeted for clinical treatment
.
Figure 1: Pathological changes of CSVD From a pathological point of view, CSVD first causes cerebrovascular damage, intravascular compression, vascular smooth muscle damage, and then causes cerebral cortex damage; when smooth muscle damage causes ischemia, it will cause Lacunar infarction; if it is diffuse, it will cause brain white matter damage; if an aneurysm is formed with small hemorrhage, it is microhemorrhage; if a large blood vessel ruptures, it is hemorrhage.
The details can be seen in the figure below
.
Figure 2: Pathological changes of cerebral small blood vessels II.
The diagnosis of CSVD.
At present, the diagnosis of CSVD mainly depends on imaging.
Its imaging manifestations mainly include lacunar infarction (LI) and white matter hyperintensities (WMHs).
), perivascular space (PVS), cerebral microbleeds (CMBs) and brain atrophy
.
Figure 3: The imaging manifestations of CSVD clinically, when diagnosing CSVD, different sequence choices should be made for different clinical manifestations.
Professor Xu Yun gave some examples, such as: acute lacunar infarction-DWI is easy to recognize.
FLAIR is optional, but DWI has higher specificity; white matter damage-DWI and T2, FLAIR and T2 can also be used; pure lacunar infarction-FLAIR can see low signal and glial hyperplasia around it; enlarged Vascular space-FLAIR and T2; microbleeds-SWI is preferred, and T2*GRE imaging can also be used
.
Figure 4: The diagnosis of conventional imaging technology and CSVD▌ Old lacunar infarction T2 shows high signal, FLAIR shows low signal, and there is glial hyperplasia around it
.
Figure 5: Old lacunar infarction ▌ Old cerebral infarction DWI low signal, FLAIR low signal, T2 high signal, among which FLAIR is the most obvious
.
Figure 6: Old cerebral infarction ▌ Differentiation of acute lacunar infarction and enlarged perivascular space In clinical practice, when there is no reference, the enlarged peripheral space is often misdiagnosed as a small lacunar infarction
.
Therefore, it is more recommended to use the FLAIR phase for diagnosis
.
Figure 7: Differentiation of acute luminal infarction and enlarged perivascular space.
The red arrow is acute luminal infarction, T1 is not enhanced, and FLAIR is high signal; the blue arrow is the perivascular space, T1 is not enhanced, and FLAIR is low signal, which is close to the cerebrospinal fluid signal
.
▌ Old cerebral hemorrhage Figure 8: Old cerebral hemorrhage For old cerebral hemorrhage, DWI and T1W1 are sometimes difficult to distinguish
.
FLAIR phase is easier to distinguish, softening foci can be seen in bleeding, and glial hyperplasia should be seen in ischemia
.
T2W1 shows high signal with surrounding low signal ring (hemosiderin deposition)
.
▌ CSVD white matter hyperintensity features Figure 9: CSVD white matter hyperintensity features III.
Differential diagnosis of CSVD ▌ Differentiating from multiple sclerosis Typical multiple sclerosis is easier to differentiate and diagnose.
Both brain and spinal cord can have lesions, multiple lesions, and asymmetric It usually has a relatively fixed distribution pattern and shape; the lesion is vertically distributed to the lateral ventricle; T1WI low signal, T2WI high signal (fried egg-like, cloud-like), FLAIR high signal, DWI shows high signal in the acute phase, and C after enhancement Shaped or open ring to strengthen
.
Figure 10: MS (provided by Nanjing Gulou Hospital) Professor Xu Yun gave an example of an image of an acute phase patient in his hospital.
The DWI of the acute phase patient in the following image shows high signal, which is cloudy, and it is C-shaped after enhancement Or open ring enhancement, which can be used as a basis for differential diagnosis
.
Figure 11: Distinguishing between acute MS and hereditary diseases.
In clinical, hereditary diseases are generally seen in children and young adults.
Most of the white matter of the brain has diffuse and symmetrical white matter hyperintensity, such as metachromatic leukodystrophy and adrenal white matter Malnutrition is related to location.
The predominance of the frontal lobe may be Alexander disease, the periventricular advantage may be metachromatic leukodystrophy, the parieto-occipital advantage may be Krabbe disease, etc.
This can help us in the differential diagnosis.
According to Medical history, genetic testing to confirm the diagnosis, here are some genetic diseases and their distinguishing characteristics
.
Figure 12: Autosomal dominant cerebral arterial disease (CADASIL) with subcortical infarction and leukoencephalopathy, temporal pole and external capsule involvement on MRI are characteristic, skin biopsy vascular smooth muscle middle layer osmium particles (Notch3 protein) deposition map 13: Fabry disease (Fabry disease), cutaneous angiokeratoma, corneal opacity, cataract and retinal ischemic changes IV.
Early diagnosis of CSVD▌ quantitative method of white matter damage Dynamic monitoring of white matter damage helps predict lacunar infarction, For the occurrence of diseases such as cerebral hemorrhage and cognitive dysfunction, the Fazekas visual assessment is the simplest quantitative method, and the classification is as follows: Figure 14: Fazekas visual assessment around the ventricle: 0 = none; Ⅰ = cap-shaped or pencil-like thin layer lesions Ⅱ=smooth halo; Ⅲ=irregular periventricular WMH, which invades deep white matter of the brain
.
Deep (subcortical): 0 = none; Ⅰ = punctate lesions; Ⅱ = lesions begin to merge; Ⅲ = lesions fused with large areas
.
Professor Xu Yun mentioned that lacunar infarctions of grade II and above are more common, and that white matter can be automatically located, extracted and quantified, which is more accurate
.
Figure 15: White matter automatic location, extraction and quantification▌ White matter hyperintensity (WMH) outcome——Professor Xu Yun's team research Professor Xu Yun's team's research over the years has found that the severity of WMH is related to lacunar infarction, cerebral hemorrhage, and Pa The occurrence of depressive symptoms of Kinsen’s disease is closely related; the risk of lacunar infarction is the highest within 2 years after the onset of WMH; the size of WMH is related to the impairment of cognitive function
.
At the same time, for the early diagnosis of CSVD, Professor Xu Yun mentioned that some scales can be made to evaluate the influence markers (peripheral vascular space, microbleeds, etc.
)
.
Figure 16: CSVD impact marker evaluation scale▌ Cerebral small vessel disease MRI total score Total CSVD score items include: number of lacunar foci ≥1; number of microbleeds (CMBs) ≥1; EPVS (EPVS-BS); WMH Around the ventricle: Fazekas score ≥ 3 points or deep
.
Each of the above items counts 1 point, and the sum of each item is the total CSVD score.
If the score is more than 2 points, there may be executive function and language dysfunction
.
Figure 17: If the score is more than 2 points, there will be executive dysfunction and language dysfunction.
Professor Yun Xu's team research found that as long as the score is more than 2 points, there will be executive dysfunction and language dysfunction
.
At the same time, international studies have shown that this table can predict the severity of cerebral hemorrhage, gait disturbance and cognitive decline
.
Figure 18: International research on the total score of MRI for cerebral small vessel disease ▌ Other methods helpful for early diagnosis For clinical research on early prediction of CSVD, T1W1 can be used to judge the degree of atrophy on the macroscopic structure; DTI on the microstructure , SWI can see fiber changes, micro hemorrhage, etc.
; function, perfusion, etc.
can use BOLD
.
Next, Professor Xu Yun used BOLD to look at patients with hypertension and white matter damage, as shown in the figure below
.
Figure 19: BOLD to take a look at patients with hypertension and white matter damage.
A significant increase in functional connectivity (FC) can be seen in the core area and subsystems of the default network (DMN), suggesting dysfunction (cognitive function and FC in the DMN dorsal subsystem Shows a negative correlation)
.
5.
CSVD treatment Professor Xu Yun said that the current treatment of CSVD is very lacking and is still a bottleneck.
There is no specific medicine that can treat CSVD
.
Mainly through active control of hypertension and diabetes to prevent progression and recurrence
.
It is hoped that more CSVD drugs will be developed, especially some old drugs that are already in clinical application may be further developed
.
Aspirin can be used for CSVD with lacunar infarction, and it is not recommended for other types of CSVD, especially those with inheritance and degeneration
.
There are many controversies about statins, which may increase the risk of intracranial hemorrhage, especially CAA.
It is very important that you do not use statins when there is no indication for primary prevention or secondary prevention
.
[There is evidence that CSVD "asymptomatic" microbleeds can be transformed into massive intracranial hemorrhage
.
The SPARCL study suggests that the application of high-dose statin therapy for CSVD is beneficial to the primary endpoint (fatal or non-fatal stroke) event, and there is no significant increase in the risk of bleeding
.
It is currently believed that intensive statin therapy can indeed increase the risk of intracranial hemorrhage
.
] For the treatment of white matter damage, Professor Xu Yun mentioned the following 3 points: 1.
Active antihypertensive therapy delays or prevents the progress of white matter hyperintensity; 2.
When choosing antihypertensive drugs, it is recommended that long-acting calcium antagonists (CCB) are the first choice And renin-angiotensin system (RAS) blockers; 3.
Deal with known vascular risk factors (hypertension, obesity, diabetes, and hypercholesterolemia)
.
Regarding the study of CSVD treatment strategy, although there is no therapeutic drug, the current preliminary research has found that its white matter damage, microhemorrhage, and lacunar infarction are all related to vascular endothelial and vascular smooth muscle function damage
.
Therefore, Professor Xu Yun believes that we should screen clinical drugs to target the microvascular endothelium of the brain, blood-brain barrier, and neuroinflammation for treatment
.
Figure 20: Targeting of CSVD prevention and treatment
