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*For medical professionals' reference only, read the express delivery of the exciting content of the 14th Annual Meeting of Neurologists of the Chinese Medical Doctor Association! The "14th Annual Meeting of Neurologists of the Chinese Medical Doctor Association" hosted by the Chinese Medical Doctor Association and the Neurologist Branch of the Chinese Medical Doctor Association was successfully held in Nanjing on June 11, 2021
.
In today’s Cerebrovascular Disease Forum, Professor Lu Zhengqi from the Neurology Department of the Third Affiliated Hospital of Sun Yat-sen University gave us a wonderful lecture entitled "Progress in Diagnosis and Treatment of Perforating Atherosclerosis" (Background: May 2021 Professor Yue Lu Zhengqi published the "Chinese Expert Consensus on Perforator Atherosclerosis" as a co-corresponding author)
.
Perforating branch atheromatous disease (BAD) refers to the cerebrovascular disease caused by the pathological changes of the perforating artery itself.
The common ones are atherosclerosis that occurs at the proximal end of the perforating artery and the fibers that occur at the distal end.
Hyalinotic arteriole sclerosis
.
Common perforating arteries include lenticulostriate arteries (LSA), paramedian pontine arteries (PPA), thalamic geniculate artery, anterior choroidal artery, Heubner's artery and thalamic perforating artery
.
Cerebral infarction caused by perforator atherosclerosis is a common type of ischemic stroke patients in Asia
.
At present, most clinical researches are on cerebral infarction caused by the pathological changes of the lenticular artery and the parapontine artery
.
1.
Epidemiological research and risk factors So far, the incidence of BAD in the population of acute ischemic stroke is not clear.
According to the current literature, it is estimated that BAD accounts for 10% to 15% of all ischemic stroke causes, and it is common.
Between 54 and 75 years old, males are the majority
.
The risk factors of BAD are basically the same as those of large-vessel atherosclerosis, including hypertension, diabetes, hyperlipidemia, smoking, hyperhomocysteinemia, etc.
Studies have suggested that the location of large-vessel atherosclerotic plaque is similar to BAD The patient has an obvious relationship, and the current understanding of BAD tends to be more closely related to large vessel atherosclerosis
.
2.
Pathology and pathogenesis At present, there are very few pathological studies on BAD
.
In 2010, Tatsumi et al.
reported that the brain MRA of patients with infarction on one side of the pons showed that the basilar artery was normal, but the pathological results suggested that there was thrombus and macrophage infiltration from the basilar artery to the opening of the perforating artery
.
LSA and PPA are emitted vertically from the carrier artery.
Due to the large diameter of the main artery, large blood flow, fast blood flow, and high pressure, the PPA and LSA emitted at right angles are significantly thinner than the main artery.
This hemodynamics The change causes the endothelium to be damaged first and promotes the formation of atherosclerosis.
Vascular risk factors promote the formation of this process, which leads to cerebral infarction in the relevant area
.
There are four main pathological forms of BAD: ①The atherosclerotic plaque of the carrier artery blocks the opening of the perforating artery (Figure 1B) ②The atherosclerotic plaque of the carrier artery extends to the opening of the perforating artery and causes vascular occlusion (Figure 1 C) ③The atherosclerotic plaque at the opening of the perforator artery causes vascular occlusion (Figure 1D), which is theoretically BAD ④The unstable plaque at the opening of the perforator artery falls off and causes vascular occlusion (Figure 1E) Clinical manifestations 1 Classification by blood supply area ① Ischemic cerebrovascular disease in the blood supply area of LSA (diameter 300～840μm): lateral movement disorder (appears in almost all patients, with severe symptoms), sensory dysfunction, cognitive decline, advantages Hemispheric lesions can cause aphasia and mental and psychological disorders, and non-dominant hemispheric lesions can cause hemispheric neglect
.
②Ischemic cerebrovascular disease in the blood supply area of PPA (200～300μm in diameter): hemimotor disorder (hemiparesis-complete paralysis, multiple upper limbs than lower limbs), dysarthria, hemisensory disorder, ataxia, central facial paralysis And other symptoms
.
The blood supply area of PPA is relatively limited, but the pontine nucleus and fiber bundles are relatively concentrated.
Due to anatomical changes, the clinical manifestations of infarction in the upper, middle, and lower pons are slightly different, and the clinical manifestations of the lower pons are more important
.
2 According to the manifestation, there are the following three forms: ① Stereotypical transient ischemic attack (TIA): Typical representatives include internal capsule warning syndrome and pons warning syndrome
.
The clinical manifestations are recurrent stereotyped sensations and/or dyskinesias, involving 2 or more of the hemilateral area, upper limbs, and lower limbs.
Pure motor hemiplegia and paresthesias.
No cortical branch involvement.
Infarcts are mostly located Internal capsule
.
② acute lacunar infarction: similar to the classic lacunar syndrome caused by small vessel disease, clinical manifestations such as pure motor hemiparesis, ataxic hemiparesis, dysarthria - clumsy hand syndrome
.
③ Deterioration of early neurological function: symptoms of cerebral infarction appear in the acute phase, followed by deterioration of early neurological function, leading to aggravation of the disease, and even total paralysis of the hemiplegia
.
4.
Auxiliary examination 1.
High resolution magnetic resonance (HR-MRI): It is recommended to perform enhanced sequence to observe the composition and stability of plaque on the blood vessel wall 2.
Vascular disease and cardiac examination: examination of intracranial and extracranial vascular disease It is helpful to identify the pathogenesis and etiology of stroke to further select treatment methods
.
The TCD foam test can rule out abnormal emboli from the heart and lungs
.
3.
Laboratory examination: complete blood count (including platelet count); blood lipids, blood sugar, glycosylated hemoglobin, homocysteine, cystatin C; coagulation function (including D-dimer); exclusion indicators include rheumatic immunity and tumor indicators
.
V.
Diagnosis 1.
LSA regional ischemic stroke: ① Meet the diagnostic criteria for acute ischemic stroke; ②DWI shows that the infarct in the corresponding blood supply area involves 3 levels and above (diameter ≥15mm) in the horizontal position; ③The LSA blood supply area is : Most of the putamen, the outer part of the globus pallidus, the head and body of the caudate nucleus, the forelimbs of the internal capsule, the upper part of the internal capsule and the radial corona around the ventricle
.
(Image manifestations of perforating branch atherosclerosis in the region of the legislature artery blood supply) 2.
PPA regional ischemic stroke: DWI shows that the infarct is connected to the ventral surface of the pons, and the lesion is close to the midline, on one side and not exceeding the midline
.
(Imaging manifestations of perforating atherosclerosis in the area of the parapontine middle artery blood supply) 3.
Exclusion criteria: ①imaging shows that the responsible large vessels are stenosis ≥50%; ②imaging shows that the intracranial aorta, external carotid artery and vertebral artery may exist Unstable plaques that cause arterial-arterial embolism; ③DWI shows cortical infarction, watershed infarction, and multiple cerebral infarctions; ④Cerebral infarction caused by other clear causes, such as immune or infectious vasculitis, cardiogenic cerebral embolism, fat embolism, Causes such as abnormal platelet and coagulation function
.
It is worth noting that traditional magnetic resonance imaging cannot clearly display LSA, and the WB-VWI technology that has emerged in recent years can clearly display LSA with a larger diameter
.
With the development of technology, WB-VWI should be able to further display other perforating arteries including PPA.
This breakthrough may continuously update and rewrite the diagnostic criteria for BAD
.
6.
Treatment 1 Treatment of repeated TIA ① Intravenous thrombolysis: Alteplase (rt-PA) and urokinase are the main thrombolytic drugs currently used in China
.
The indications, contraindications and precautions for recurrent TIA thrombolytic therapy are the same as the guidelines for the diagnosis and treatment of acute ischemic stroke
.
Studies have shown that rt-PA cannot prevent the progression of BAD patients during the fluctuating symptoms, but can temporarily improve the clinical symptoms and improve the 3-month prognosis
.
②Antiplatelet therapy: Although the curative effect is uncertain and controversial, domestic scholars have found that tirofiban is more than 70% effective
.
③Anticoagulation: Used for early warning treatment of recurrent attacks in Japan, effective in preventing and curing BAD
.
④Statins: Observational studies suggest that high-intensity statins can improve the prognosis of patients with acute ischemic stroke, but the efficacy of BAD needs to be confirmed by further high-quality randomized controlled studies
.
2 Treatment of acute ischemic cerebral infarction It is recommended to follow the treatment plan for TIA or mild stroke in the CHANCE study, with the first dose of clopidogrel 300 mg, followed by 75 mg per day, combined with aspirin 100 mg per day for 21 days
.
3 Treatments for early deterioration of neurological function Specific treatments include intravenous thrombolysis, antiplatelet, anticoagulation, statins and neuroprotective treatments
.
①Intravenous thrombolysis: rt-PA can temporarily improve the clinical symptoms of BAD patients, but it cannot avoid the deterioration of early neurological function.
About 57.
1% of patients will experience symptoms worsening again after treatment
.
②Antiplatelet therapy: A group of controlled studies of cilostazol combined with antiplatelet drugs found that cilostazol 200 mg daily combined with aspirin 100 mg daily (load 300 mg) or clopidogrel 75 daily was used in the early stage of BAD.
The mg (load 225 mg) combination treatment regimen was changed to any antiplatelet drug alone after 1 week, which can significantly reduce the progression of the disease without increasing the risk of bleeding
.
③Anticoagulation: Because the lumen of BAD arteriosclerosis is narrow, it is easy to form red thrombus after platelets adhere to the lumen, causing the disease to progress.
Therefore, anticoagulant drugs such as Amethtroban are also recommended for the treatment of advanced BAD
.
④Statin drugs and neuroprotective drugs: If statin drugs are used, statin therapy needs to be strengthened
.
7.
Outlook With the popularization of high-resolution magnetic resonance, we have an in-depth understanding of BAD
.
On the one hand, the current newer WB-VWI technology can display LSA, but it cannot display other smaller diameter perforating arteries, such as PPA; on the other hand, the mechanism and treatment of clinical BAD patients’ disease progression is still in the research stage
.
It is recommended to develop WB-VWI visualization and multi-modal technology research and development in the future to promote the display of other perforating arteries by WB-VWI; to carry out multi-center, large-scale clinical treatment experiments to improve the prognosis of BAD patients
.
With the continuous advancement of science and technology, I believe that the diagnostic criteria and treatment guidelines for BAD can be continuously updated and rewritten
.
References: [1] Men Xuejiao, Chen Weiqi, Xu Yuyuan, Zhu Yicheng, Hu Wenli, Cheng Xin, Bai Feng, Wang Lihua, Mao Ling, Qu Hui, Lu Peiyuan, Liu Jun, Sun Zhongwu, Sun Li, Li Yusheng, Wu Zhongliang, Wu Danhong, Wu Bo,Gu Wenping,Fan Yuhua,Zhou Guoyu,Ni Jun,Gao Feng,Huang Shixiong,Cao Yongjun,Peng Dantao,Xie Chunming,Cai Zhiyou,Xu Yun,Wang Yilong,Lu Zhengqi.
Consensus of Chinese Experts on Perforating Atherosclerosis[J].
Chinese Journal of Stroke ,2021,16(05):508-514.
.
In today’s Cerebrovascular Disease Forum, Professor Lu Zhengqi from the Neurology Department of the Third Affiliated Hospital of Sun Yat-sen University gave us a wonderful lecture entitled "Progress in Diagnosis and Treatment of Perforating Atherosclerosis" (Background: May 2021 Professor Yue Lu Zhengqi published the "Chinese Expert Consensus on Perforator Atherosclerosis" as a co-corresponding author)
.
Perforating branch atheromatous disease (BAD) refers to the cerebrovascular disease caused by the pathological changes of the perforating artery itself.
The common ones are atherosclerosis that occurs at the proximal end of the perforating artery and the fibers that occur at the distal end.
Hyalinotic arteriole sclerosis
.
Common perforating arteries include lenticulostriate arteries (LSA), paramedian pontine arteries (PPA), thalamic geniculate artery, anterior choroidal artery, Heubner's artery and thalamic perforating artery
.
Cerebral infarction caused by perforator atherosclerosis is a common type of ischemic stroke patients in Asia
.
At present, most clinical researches are on cerebral infarction caused by the pathological changes of the lenticular artery and the parapontine artery
.
1.
Epidemiological research and risk factors So far, the incidence of BAD in the population of acute ischemic stroke is not clear.
According to the current literature, it is estimated that BAD accounts for 10% to 15% of all ischemic stroke causes, and it is common.
Between 54 and 75 years old, males are the majority
.
The risk factors of BAD are basically the same as those of large-vessel atherosclerosis, including hypertension, diabetes, hyperlipidemia, smoking, hyperhomocysteinemia, etc.
Studies have suggested that the location of large-vessel atherosclerotic plaque is similar to BAD The patient has an obvious relationship, and the current understanding of BAD tends to be more closely related to large vessel atherosclerosis
.
2.
Pathology and pathogenesis At present, there are very few pathological studies on BAD
.
In 2010, Tatsumi et al.
reported that the brain MRA of patients with infarction on one side of the pons showed that the basilar artery was normal, but the pathological results suggested that there was thrombus and macrophage infiltration from the basilar artery to the opening of the perforating artery
.
LSA and PPA are emitted vertically from the carrier artery.
Due to the large diameter of the main artery, large blood flow, fast blood flow, and high pressure, the PPA and LSA emitted at right angles are significantly thinner than the main artery.
This hemodynamics The change causes the endothelium to be damaged first and promotes the formation of atherosclerosis.
Vascular risk factors promote the formation of this process, which leads to cerebral infarction in the relevant area
.
There are four main pathological forms of BAD: ①The atherosclerotic plaque of the carrier artery blocks the opening of the perforating artery (Figure 1B) ②The atherosclerotic plaque of the carrier artery extends to the opening of the perforating artery and causes vascular occlusion (Figure 1 C) ③The atherosclerotic plaque at the opening of the perforator artery causes vascular occlusion (Figure 1D), which is theoretically BAD ④The unstable plaque at the opening of the perforator artery falls off and causes vascular occlusion (Figure 1E) Clinical manifestations 1 Classification by blood supply area ① Ischemic cerebrovascular disease in the blood supply area of LSA (diameter 300～840μm): lateral movement disorder (appears in almost all patients, with severe symptoms), sensory dysfunction, cognitive decline, advantages Hemispheric lesions can cause aphasia and mental and psychological disorders, and non-dominant hemispheric lesions can cause hemispheric neglect
.
②Ischemic cerebrovascular disease in the blood supply area of PPA (200～300μm in diameter): hemimotor disorder (hemiparesis-complete paralysis, multiple upper limbs than lower limbs), dysarthria, hemisensory disorder, ataxia, central facial paralysis And other symptoms
.
The blood supply area of PPA is relatively limited, but the pontine nucleus and fiber bundles are relatively concentrated.
Due to anatomical changes, the clinical manifestations of infarction in the upper, middle, and lower pons are slightly different, and the clinical manifestations of the lower pons are more important
.
2 According to the manifestation, there are the following three forms: ① Stereotypical transient ischemic attack (TIA): Typical representatives include internal capsule warning syndrome and pons warning syndrome
.
The clinical manifestations are recurrent stereotyped sensations and/or dyskinesias, involving 2 or more of the hemilateral area, upper limbs, and lower limbs.
Pure motor hemiplegia and paresthesias.
No cortical branch involvement.
Infarcts are mostly located Internal capsule
.
② acute lacunar infarction: similar to the classic lacunar syndrome caused by small vessel disease, clinical manifestations such as pure motor hemiparesis, ataxic hemiparesis, dysarthria - clumsy hand syndrome
.
③ Deterioration of early neurological function: symptoms of cerebral infarction appear in the acute phase, followed by deterioration of early neurological function, leading to aggravation of the disease, and even total paralysis of the hemiplegia
.
4.
Auxiliary examination 1.
High resolution magnetic resonance (HR-MRI): It is recommended to perform enhanced sequence to observe the composition and stability of plaque on the blood vessel wall 2.
Vascular disease and cardiac examination: examination of intracranial and extracranial vascular disease It is helpful to identify the pathogenesis and etiology of stroke to further select treatment methods
.
The TCD foam test can rule out abnormal emboli from the heart and lungs
.
3.
Laboratory examination: complete blood count (including platelet count); blood lipids, blood sugar, glycosylated hemoglobin, homocysteine, cystatin C; coagulation function (including D-dimer); exclusion indicators include rheumatic immunity and tumor indicators
.
V.
Diagnosis 1.
LSA regional ischemic stroke: ① Meet the diagnostic criteria for acute ischemic stroke; ②DWI shows that the infarct in the corresponding blood supply area involves 3 levels and above (diameter ≥15mm) in the horizontal position; ③The LSA blood supply area is : Most of the putamen, the outer part of the globus pallidus, the head and body of the caudate nucleus, the forelimbs of the internal capsule, the upper part of the internal capsule and the radial corona around the ventricle
.
(Image manifestations of perforating branch atherosclerosis in the region of the legislature artery blood supply) 2.
PPA regional ischemic stroke: DWI shows that the infarct is connected to the ventral surface of the pons, and the lesion is close to the midline, on one side and not exceeding the midline
.
(Imaging manifestations of perforating atherosclerosis in the area of the parapontine middle artery blood supply) 3.
Exclusion criteria: ①imaging shows that the responsible large vessels are stenosis ≥50%; ②imaging shows that the intracranial aorta, external carotid artery and vertebral artery may exist Unstable plaques that cause arterial-arterial embolism; ③DWI shows cortical infarction, watershed infarction, and multiple cerebral infarctions; ④Cerebral infarction caused by other clear causes, such as immune or infectious vasculitis, cardiogenic cerebral embolism, fat embolism, Causes such as abnormal platelet and coagulation function
.
It is worth noting that traditional magnetic resonance imaging cannot clearly display LSA, and the WB-VWI technology that has emerged in recent years can clearly display LSA with a larger diameter
.
With the development of technology, WB-VWI should be able to further display other perforating arteries including PPA.
This breakthrough may continuously update and rewrite the diagnostic criteria for BAD
.
6.
Treatment 1 Treatment of repeated TIA ① Intravenous thrombolysis: Alteplase (rt-PA) and urokinase are the main thrombolytic drugs currently used in China
.
The indications, contraindications and precautions for recurrent TIA thrombolytic therapy are the same as the guidelines for the diagnosis and treatment of acute ischemic stroke
.
Studies have shown that rt-PA cannot prevent the progression of BAD patients during the fluctuating symptoms, but can temporarily improve the clinical symptoms and improve the 3-month prognosis
.
②Antiplatelet therapy: Although the curative effect is uncertain and controversial, domestic scholars have found that tirofiban is more than 70% effective
.
③Anticoagulation: Used for early warning treatment of recurrent attacks in Japan, effective in preventing and curing BAD
.
④Statins: Observational studies suggest that high-intensity statins can improve the prognosis of patients with acute ischemic stroke, but the efficacy of BAD needs to be confirmed by further high-quality randomized controlled studies
.
2 Treatment of acute ischemic cerebral infarction It is recommended to follow the treatment plan for TIA or mild stroke in the CHANCE study, with the first dose of clopidogrel 300 mg, followed by 75 mg per day, combined with aspirin 100 mg per day for 21 days
.
3 Treatments for early deterioration of neurological function Specific treatments include intravenous thrombolysis, antiplatelet, anticoagulation, statins and neuroprotective treatments
.
①Intravenous thrombolysis: rt-PA can temporarily improve the clinical symptoms of BAD patients, but it cannot avoid the deterioration of early neurological function.
About 57.
1% of patients will experience symptoms worsening again after treatment
.
②Antiplatelet therapy: A group of controlled studies of cilostazol combined with antiplatelet drugs found that cilostazol 200 mg daily combined with aspirin 100 mg daily (load 300 mg) or clopidogrel 75 daily was used in the early stage of BAD.
The mg (load 225 mg) combination treatment regimen was changed to any antiplatelet drug alone after 1 week, which can significantly reduce the progression of the disease without increasing the risk of bleeding
.
③Anticoagulation: Because the lumen of BAD arteriosclerosis is narrow, it is easy to form red thrombus after platelets adhere to the lumen, causing the disease to progress.
Therefore, anticoagulant drugs such as Amethtroban are also recommended for the treatment of advanced BAD
.
④Statin drugs and neuroprotective drugs: If statin drugs are used, statin therapy needs to be strengthened
.
7.
Outlook With the popularization of high-resolution magnetic resonance, we have an in-depth understanding of BAD
.
On the one hand, the current newer WB-VWI technology can display LSA, but it cannot display other smaller diameter perforating arteries, such as PPA; on the other hand, the mechanism and treatment of clinical BAD patients’ disease progression is still in the research stage
.
It is recommended to develop WB-VWI visualization and multi-modal technology research and development in the future to promote the display of other perforating arteries by WB-VWI; to carry out multi-center, large-scale clinical treatment experiments to improve the prognosis of BAD patients
.
With the continuous advancement of science and technology, I believe that the diagnostic criteria and treatment guidelines for BAD can be continuously updated and rewritten
.
References: [1] Men Xuejiao, Chen Weiqi, Xu Yuyuan, Zhu Yicheng, Hu Wenli, Cheng Xin, Bai Feng, Wang Lihua, Mao Ling, Qu Hui, Lu Peiyuan, Liu Jun, Sun Zhongwu, Sun Li, Li Yusheng, Wu Zhongliang, Wu Danhong, Wu Bo,Gu Wenping,Fan Yuhua,Zhou Guoyu,Ni Jun,Gao Feng,Huang Shixiong,Cao Yongjun,Peng Dantao,Xie Chunming,Cai Zhiyou,Xu Yun,Wang Yilong,Lu Zhengqi.
Consensus of Chinese Experts on Perforating Atherosclerosis[J].
Chinese Journal of Stroke ,2021,16(05):508-514.
