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The 7th Annual Conference of the Chinese Stroke Society and the Tiantan International Cerebrovascular Disease Conference 2021 (CSA & TISC 2021) will be held on July 9, 2021
.
At the China Cerebrovascular Disease Roundtable Special Review (CNSR) sub-forum of this conference, Professor Xu Yun from Nanjing University Drum Tower Hospital gave a sharing report on the status and prospects of basic and clinical research on cerebrovascular disease.
The articles are organized as follows
.
Cerebral small blood vessels and cerebrovascular disease Small cerebral blood vessels refer to small perforating arteries and small arteries (40-200μm in diameter), capillaries and venules, which constitute the basic unit of blood supply of brain tissue and maintain brain function Plays an important role
.
Cerebral Small Vascular Disease (CSVD): involving cerebral arterioles, branch arterioles, capillaries and venules, the clinical manifestations are abnormal mood, abnormal gait, abnormal urination, stroke, dementia and other clinical syndromes
.
Imaging manifestations: lacunar infarction, white matter hyperintensity, microhemorrhage, perivascular space enlargement and brain atrophy (as shown in the figure below)
.
Pathological changes of CSVD The pathological changes of CSVD mainly include: small arterial atherosclerosis, lipid hyaline degeneration, fibrinoid necrosis, amyloidosis, expansion of the perivascular space, small aneurysms, BBB destruction and vasculitis, etc.
(as shown in the figure below) )
.
Pathological classification of SVD: Type I: arteriolar sclerosis, manifested as fibrinoid necrosis, lipid hyaline degeneration, arteriolar atherosclerosis, microaneurysm, segmental structural disorder or disintegration of arterioles; 80% are type I, Related to high blood pressure and age
.
Type II: sporadic or hereditary cerebral amyloid angiopathy (CAA); Type III: hereditary small vessel disease, such as CADASIL, CARASIL, MELAS, Fabry, hereditary cerebral retinal small vessel disease; Type IV: inflammation or immune-mediated Leading small vessel diseases, such as Wegener's granulomatosis, rheumatism, and vasculitis; Type V: venous collagen disease, causing thickening and occlusion of small veins; Type VI: Other small vessel diseases, such as post-radiation small vessel disease
.
CSVD animal model research is currently used to study animal models of cerebral small vessel disease as shown below: CSVD pathological mechanism research ① Potassium channel disease-like defects are the basis of hereditary CSVD early vascular dysfunction; ② CSVD-related brain white matter damage mechanism research: CSVD mechanism is complex; White matter hyperintensity (WMH) is the most common imaging change in CSVD, and it is often the basis of other pathological changes in CSVD; the prevalence of WMH in people aged 60-90 is 92%
.
Myelin/white matter anatomy basis: White matter damage is mainly the damage of myelin, and myelin is formed by oligodendrocytes, which are derived from their precursor cells (OPCs)
.
Myelin formation and repair are affected by many factors, such as the functions of oligodendrocyte precursor cells, astrocytes and microglia, and the integrity of the blood-brain barrier
.
Part of the white matter damage can be reversed
.
Overall, CSVD clinical and scientific problems mainly in the following points: pathogenesis is unclear, the lack of animal models to clinical use, the lack of objective quantitative clinical diagnostic criteria, lack of early warning, predicting prognosis evaluation techniques
.
Secondly, the current clinical research is characterized by more imaging studies
.
Lock the medlive-neurology channel to view the latest information of CSA & TISC 2021 at the same time! Long press the QR code to follow the CSA & TISC 2021 special report ☟☟☟ You can also click "Read the original text" to view More CSA & TISC 2021 topics related content!
.
At the China Cerebrovascular Disease Roundtable Special Review (CNSR) sub-forum of this conference, Professor Xu Yun from Nanjing University Drum Tower Hospital gave a sharing report on the status and prospects of basic and clinical research on cerebrovascular disease.
The articles are organized as follows
.
Cerebral small blood vessels and cerebrovascular disease Small cerebral blood vessels refer to small perforating arteries and small arteries (40-200μm in diameter), capillaries and venules, which constitute the basic unit of blood supply of brain tissue and maintain brain function Plays an important role
.
Cerebral Small Vascular Disease (CSVD): involving cerebral arterioles, branch arterioles, capillaries and venules, the clinical manifestations are abnormal mood, abnormal gait, abnormal urination, stroke, dementia and other clinical syndromes
.
Imaging manifestations: lacunar infarction, white matter hyperintensity, microhemorrhage, perivascular space enlargement and brain atrophy (as shown in the figure below)
.
Pathological changes of CSVD The pathological changes of CSVD mainly include: small arterial atherosclerosis, lipid hyaline degeneration, fibrinoid necrosis, amyloidosis, expansion of the perivascular space, small aneurysms, BBB destruction and vasculitis, etc.
(as shown in the figure below) )
.
Pathological classification of SVD: Type I: arteriolar sclerosis, manifested as fibrinoid necrosis, lipid hyaline degeneration, arteriolar atherosclerosis, microaneurysm, segmental structural disorder or disintegration of arterioles; 80% are type I, Related to high blood pressure and age
.
Type II: sporadic or hereditary cerebral amyloid angiopathy (CAA); Type III: hereditary small vessel disease, such as CADASIL, CARASIL, MELAS, Fabry, hereditary cerebral retinal small vessel disease; Type IV: inflammation or immune-mediated Leading small vessel diseases, such as Wegener's granulomatosis, rheumatism, and vasculitis; Type V: venous collagen disease, causing thickening and occlusion of small veins; Type VI: Other small vessel diseases, such as post-radiation small vessel disease
.
CSVD animal model research is currently used to study animal models of cerebral small vessel disease as shown below: CSVD pathological mechanism research ① Potassium channel disease-like defects are the basis of hereditary CSVD early vascular dysfunction; ② CSVD-related brain white matter damage mechanism research: CSVD mechanism is complex; White matter hyperintensity (WMH) is the most common imaging change in CSVD, and it is often the basis of other pathological changes in CSVD; the prevalence of WMH in people aged 60-90 is 92%
.
Myelin/white matter anatomy basis: White matter damage is mainly the damage of myelin, and myelin is formed by oligodendrocytes, which are derived from their precursor cells (OPCs)
.
Myelin formation and repair are affected by many factors, such as the functions of oligodendrocyte precursor cells, astrocytes and microglia, and the integrity of the blood-brain barrier
.
Part of the white matter damage can be reversed
.
Overall, CSVD clinical and scientific problems mainly in the following points: pathogenesis is unclear, the lack of animal models to clinical use, the lack of objective quantitative clinical diagnostic criteria, lack of early warning, predicting prognosis evaluation techniques
.
Secondly, the current clinical research is characterized by more imaging studies
.
Lock the medlive-neurology channel to view the latest information of CSA & TISC 2021 at the same time! Long press the QR code to follow the CSA & TISC 2021 special report ☟☟☟ You can also click "Read the original text" to view More CSA & TISC 2021 topics related content!
