The "2024 Academic Annual Meeting of the Vertigo Medicine Branch of the China Association for the Promotion of International Exchange in Health Care and the 5th China Vertigo Medicine Forum" was held in Zhuhai, Guangdong Province from May 10 to 12, sponsored by the Vertigo Medicine Branch of the China Association for the Promotion of International Exchange in Health Care and undertaken by Zhuhai Hospital of Integrated Traditional Chinese and Western Medicine and Union Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology. This conference invited a number of experts from all over the country to conduct in-depth discussions on new concepts, new technologies and new products in the field of vertigo medicine, bringing a feast of academic gluttony with various forms and rich contents. At this conference, Professor Qi Xiaokun from the Sixth Medical Center of the General Hospital of the Chinese People's Liberation Army gave a wonderful sharing on the theme of "dizziness and cerebral small vessel disease".
The author of this article is the report team of the Yimaitong Vertigo Conference
Yimaitong collated the report, please do not reprint without authorization.
Concept, classification, and etiology of cerebral small vessel disease
Concept: Cerebral small vessel disease (CSVD) refers to a series of pathological and imaging changes (not all of which are small lesions) caused by various etiologies affecting arterioles, arterioles, capillaries, venules and venules in the brain.
Common symptoms: dizziness, gait disturbances, cognitive impairment, low quality of life, depression and anxiety, parkinson-like symptoms.
Common images: lacunar infarction, white matter hyperintensity (WMH), cortical microinfarction, enlarged perivascular space, cerebral microhemorrhage, cerebral atrophy.
Uncommon imaging: multiple large lesions in the brain, parenchymal hemorrhage, SAH, convex SAH, mass lesion like, meningeal thickening, etc.
Classification of CSVD:
(1) Arteriolar sclerosclerosis (age-related and vascular risk factors)
(2) Sporadic and hereditary cerebral amyloid angiopathy
(3) Hereditary small vessel disease
(4)炎症及免疫介导的(Wegener肉芽肿,Sneddon等)
(5) Intravenous collagen disease
(6) Other small vessel diseases (such as radiation-related encephalopathy)
Early influencing factors of CSVD:
Research published in Brain in 2021 explored the impact of life factors at birth and childhood on CSVD. The results of the study showed that life factors in childhood significantly increased the burden of CSVD after 50~80 years, and this association was independent of vascular risk factors and economic level in adulthood. Strengthening the shaping of children's living habits and intelligence level is helpful to reduce the incidence of CSVD in the future, and at the same time, it puts forward the direction of further exploration of the pathogenesis of CSVD.
CSVD的地区、种族、差异:
A study published in 2021 in Neurology explored the effects of subtypes and severity of CSVD across different ethnicities on the prognosis and risk of recurrence of intracranial hemorrhage. In this study, the overall CSVD burden score of patients was evaluated according to head MRI, and the CSVD burden score related to hypertension was counted separately, and the influencing factors of recurrence of intracerebral hemorrhage were further analyzed. The results showed that the recurrence rate of CVSD was significantly higher in blacks than whites in both the low and high CSVD burden groups.
Another large-scale cohort study confirmed that the phenotype, incidence and severity of CSVD among various ethnic groups and ethnic groups have their particularities, suggesting that there are many differences in the occurrence and development mechanism and treatment of CSVD in different countries. Therefore, further exploring the characteristics of CSVD in Asian yellow populations is helpful to form an effective treatment system and improve the prognosis of CSVD patients in mainland China.
Guidelines and expert consensus on the diagnosis of cerebral small vessel disease
European Stroke Organization (ESO) guidelines for the management of occult cerebral small vessel disease (ccSVD):
(1) ccSVD has clear signs of cerebral small vessel disease in imaging examination, but there are no obvious neurological symptoms in clinical practice, which will increase the risk of cognitive impairment, disability and death in future stroke. The guidelines provide guidance and recommendations for the management of ccSVD, particularly white matter hyperintensity and lacunar cerebral infarction (luminal infarction), to prevent adverse outcomes.
(2) The blood pressure of patients with ccSVD needs to be effectively controlled (<140/90mmHg), and the blood pressure drop can slow down the progression of ccSVD.
(3) It is not recommended for patients with ccSVD alone to take antiplatelet drugs such as aspirin.
(4) The evidence for lipid lowering in patients with ccSVD is also insufficient.
(5) Quitting smoking and exercising regularly were beneficial to the preservation of cognitive function; It is also recommended to have a good diet and sleep habits to avoid obesity and stress.
(6) Experts do not recommend blood glucose control in patients with ccSVD who do not have diabetes, nor do they recommend traditional Alzheimer's disease dementia drugs for patients with ccSVD.
Guidelines for the diagnosis and management of hereditary cerebral small vessel disease:
The guidelines mainly explore monogenic genetic diseases such as Fabry, CADASIL, CARASIL, HTRA1, RVCL, COL4A12 (including PADMAL) and hereditary CAA-related microbleeds, and describe in detail the clinical phenotype, imaging characteristics, genetic alterations and conventional drug treatment specifications of each monogenic genetic disease. How to manage patients with hereditary CSVD was systematically described, and the early warning indications of five major types of monogenic inherited diseases were summarized. Guidelines conclude that the diagnosis of monogenic cerebral small vessel disease should not be excluded even in patients with routine vascular risk factors.
Expert Consensus on the Diagnosis and Treatment of Cerebral Small Vessel Disease in China 2021:
The Expert Committee on Cerebral Small Vessel Disease of the Chinese Hospital Research Society compiled this guideline based on the latest research results at home and abroad, so as to reflect the latest progress in the field of CSVD research and provide guidance for the diagnosis and treatment of CSVD.
Laboratory tests and imaging markers of cerebral small vessel disease
Laboratory tests:
imaging markers:
· New subcortical infarct (≤20 mm): avascular necrosis of local brain tissue after perforator artery closure.
· 腔隙梗死（3~15mm）、微梗死（0.5~3mm）：缺血性梗死遗留残腔。
· Vasogenic white matter hyperintensity: slight lesions of white matter demyelination.
· Perivascular space (≤3 mm): The leptomeninges continue with the blood vessels in and out of the brain parenchyma.
· Cerebral microhemorrhage (2~5mm): endothelial cell destruction and blood-brain barrier damage.
· Brain atrophy: a decrease in brain volume unrelated to a specific focal injury.
Imaging Cases:
1. Male, 49 years old, dizzy for one week, history of hypertension.
Figure 1. Case 1
2. CSVD brain MRI images in patients with hypertension and diabetes.
Figure 2. Case 2
Clinical manifestations of cerebral small vessel disease and related research
CSVD Clinical Overview:
· Onset and course: 60% had an insidious onset and 80% had a progressive course.
· Age: Age-related disease, 70-year-old MRI found that 10%~30% had CSVD.
· Incidence: The incidence of CSVD is 5~6 times that of clinical stroke.
· Common clinical symptoms: vascular dementia (VCI), mainly subcortical vascular impairment, CSVD is present in 90% of VCI populations.
· CSVD is an important cause of affective disorders (vascular depression, anxiety, etc.).
· CSVD occurs in 30% of patients with Alzheimer's disease (AD).
Clinical manifestations of CSVD:
Related Research Progress:
One study analysed CSVD and dizziness in older adults. The study graded leukoencephalopathy (Figure 3), with grades 0-1 in the low small vessel burden group and grades 2-3 in the high small vessel burden group. The results of the study showed that the incidence of dizziness increased with increasing load, and the incidence of eye movement disorder was higher in the high-burden group.
Figure 3. Grading of leukoencephalopathy
In 2021, Alzheimer's & Dementia published a meta-analysis of cognitive symptoms in patients with CSVD, and came to a different conclusion from previous studies. The assessment included processing speed, executive function, memory, attention, reasoning, visuospatial ability, language and other aspects, and the conclusion showed that compared with the control group, CSVD cognitive dysfunction existed in all dimensions. The study also found that low educational attainment is a potentially modifiable risk factor for impaired cognitive function associated with CSVD. In future CSVD studies, it is necessary not only to adopt a multi-dimensional cognitive function assessment scheme, but also to collect the education level of subjects.
Specific cases of cerebral small vessel disease with dizziness
1. Female, 62 years old, with intermittent headache for more than 40 years, dizziness and vomiting for more than 20 years, diplopia, hemilimb numbness and weakness for 13 years, and diffuse lesions in the brain. Imaging showed long T1 and long T2 signals in the brainstem and basal ganglia, and "herringbone signs" in the basal ganglia, and GOM deposition was seen in electron microscopy. Diagnosis of CADASIL (Notch 3 gene) is an autochromic dominant cerebral artery disease with subcortical infarction of leukoencephalopathy.
Figure 4. Case 1
2. Female, 34 years old, with episodic low back pain 5 years ago; 3 years ago, hair loss, headache; Before May, the right limb was weak and numb. The patient has a BP110/65 mmHg and memory loss. The skin of the whole body is rough, the hair is slightly thin, and the skin of the hands is dry and keratinized. Right limb muscle strength level 5-. Hyperreflexia of the tendons in the extremities, leading to ankleclonus bilaterally. Bilateral pathological signs (+). The patient has symmetrical lesions in the white matter of the brain and a long T2 signal on the spinal cord. Diagnosis of CARASIL with leukoencephalopathy with subcortical infarction of autochromic recessive cerebral arteriopathy (HTRA1 gene).
Figure 5. Case 2
3. Male, 39 years old. Headache, dizziness, blurred vision, left limb weakness for 5 years with urine protein, decreased speech with right limb weakness for 1 month. The patient has vasculitis-like lesions in the brain; The patient's father had a large space-like lesion in the brain, and the brain pathology showed CSVD. Diagnosis of hereditary endothelial cell disease with retinopathy, kidney disease and stroke (HERNS) with leukoencephalopathy and systemic manifestations of retinal vascular disease (RVCL-S).
Figure 6. Case 3
4. Male, 40 years old, was admitted to the hospital mainly due to "numbness of the right limb for more than 8 months and aggravation for 1 month". Previous history of blurred vision, hypertension, anemia, renal insufficiency, and gastrointestinal bleeding. My father and younger brother were both diagnosed with brain tumors, kidney disease, and liver cirrhosis when they were about 30 years old. The patient's visual acuity is 0.3 on the left/0.25 on the right, and the visual field above the nasal side of both eyes is annular defect. There is bilateral optic neuropathy in the fundus of the protected eyes, and there is a space-like lesion on noncontrast MRI of the brain. Diagnosis of retinal vascular disease with leukoencephalopathy and systemic manifestations (RVCL-S).
Figure 7. Case 4: Fundus examination
Fig.8 Noncontrast MRI of the brain in case 4
5. Male, 27 years old, with dizziness, headache, syncope, right frontotemporal lobe mass, surgical resection treatment. Postoperative epilepsy, and at the same time found to have renal insufficiency, refractory anemia, hypoproteinemia. At the age of 29, the symptoms worsened again, the number of intracranial lesions increased, and he died after ineffective treatment. brain imaging shows a space-occupying lesion; Brain pathology showed thickening of the blood vessel wall, enlargement of the lumen, cell necrosis, and glial hyperplasia. Mutations in the TREX1 gene are present. Diagnosis of retinal vascular disease with leukoencephalopathy and systemic manifestations (RVCL-S).
Figure 9. Case 5
6. Female, 75 years old. Memory loss for more than 1 year, aggravation of 2 months accompanied by unsteady walking, occasional falls. IQ test MMSE 9 points, MOCA 5 points. EEG shows a large number and a large number of low-amplitude waves. CSF-Aβ42 protein was 414.56 pg/mL↓, and Aβ40 protein was 71.54 pg/m1↓. Diagnosis is considered to be inflammation associated with cerebral amyloid angiopathy (CAA-RI).
Figure 10. Case 6
7. Male, 45 years old. Intermittent dizziness for 1 month, nystagmus, and head CT showed ischemic foci in the left cerebellum. Chaddock's sign (+) on the left, the number of cells detected by CSF was 0, the number of eggs was 1g/L, and the rest were normal. SWI indicates hemorrhage, and PWI is hypoperfusion. MRS suggests a lactate peak at the lesion. Diagnosis of central nervous system vasculitis.
Figure 11. Case 7
8. Female, 62 years old, due to episodic facial finger withdrawal for more than 5 months, dizziness, and mobility disorders of both lower limbs for 2 months, accompanied by cognitive impairment. The patient is conscious and speaks slowly. Gross measurement of calculation and reaction are reduced. The right nasolabial fold is slightly shallow, the corners of the mouth are slanted to the left, the mandibular reflex is positive, and the tongue protrusion is centered. Muscle strength of both upper limbs is level 4, muscle strength of both lower limbs is level 2, and muscle tone is normal; The tendon reflex of the limbs is slightly higher, the double Babinski is positive, and the double finger nose and rotation test are not cooperative. CSF was yellowish, WBC 40, RBC 990, Pr1.8gL↑, and blood anti-Ma2/Ta antibody was positive. ESR 50 mm/h↑, LDH455.0UЛL↑, PET-CT showed patchy hypermetabolic foci in the right lateral fissure cortex. CT shows multiple lesions in the brain. Diagnosis of primary central nervous system intravascular lymphomatopathy.
Figure 12. Case 8
9. Female, 55 years old. Hearing loss in both ears for 2 years, aggravation with dizziness and unsteady walking was admitted to the hospital for half a year. Deafness in the left ear and severe hearing loss in the right ear. Imaging shows paramagnetic material deposition on the surface of the brain, particularly at the front of the brainstem. Diagnosis of central nervous system surface ferrodeposition.
Figure 13. Case 9
A special report on the 2024 Academic Annual Meeting of the Vertigo Medicine Branch of the China Association for the Promotion of International Exchange in Health Care and the 5th China Vertigo Medicine Forum
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