The core of diagnosing and treating diseases in traditional Chinese medicine lies in syndrome differentiation. The eight principles of syndrome differentiation serve as guidance for syndrome differentiation. As one of the eight principles of syndrome differentiation， the differentiation of deficiency and excess is the basic and critical method. Ischemic stroke is currently the leading cause harming the health of Chinese residents. Although the hypotheses about the cause of ischemic stroke have evolved from external wind to the later internal wind and to the modern theory of toxin damaging the brain collaterals， they all believe that this disease is rooted in internal deficiency and external excess. According to available studies， although stroke is characterized by complex pathogenesis and rapid progression of syndromes， the key cause evolution has a regularity， that is， from excess to deficiency. This article analyzes the historical evolution of the etiology， pathogenesis， and syndrome differentiation schemes of stroke. There are diverse schemes for the syndrome differentiation of stroke， which make it difficult to choose in clinical practice. In view of this problem， this paper puts forward a new approach of staging sequential treatment of ischemic stroke based on the differentiation of deficiency and excess according to the evolution law of the key cause of stroke. Furthermore， we conducted a randomized controlled study on 100 patients with ischemic stroke to evaluate this new approach. The results showed that the staging sequential treatment of ischemic stroke based on the differentiation of deficiency and excess demonstrated definite clinical efficacy. In addition， this article reviews the previous research results of our team and the research achievements of other teams to preliminarily explore the relationship between stroke syndromes and biomarkers， aiming to provide an objective basis for unveiling the pathogenesis of stroke. In summary， according to the key cause evolution （from excess to deficiency）， the treatment of ischemic stroke by stages based on differentiation of deficiency and excess can facilitate the rapid intervention and improve the clinical efficacy on ischemic stroke.

ObjectiveTo establish a mouse model of basilar artery dolichoectasia （BAD） and explore the mechanism of modified Tongqiao Huoxuetang （JTQHX） in regulating BAD via phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt） pathway. MethodSixty C57/BL6 female mice were randomized into sham operation （injected with 10 U·mL^-1 inactivate elastase）， model， atorvastatin calcium tablets （2.6 mg·kg·d^-1）， and low- and high-dose （crude drug 3.4， 17 g·kg^-1·d^-1， respectively） JTQHX groups. The mouse model of BAD was established by injection with 10 U·mL^-1 elastase. After 14 days of modeling， the sham operation group and model group were administrated with equal volumes of pure water by gavage， and other groups with corresponding drugs for 2 months. The levels of interleukin-6 （IL-6） and calpain （LpA） in the serum were measured by enzyme-linked immunosorbent assay （ELISA）. Verhoeff 's Van Gieson （EVG） staining was employed to observe the pathological changes of blood vessels. Terminal-deoxynucleotidyl transferase mediated nick end labeling （TUNEL） was employed to examine the apoptosis rate of vascular smooth muscle cells （VSMCs）. Image Pro Plus was used to observe and calculate the curvature index， elongation length， percentage increase in vessel diameter， and curvature angle of the basilar artery vessels in mice. Western blot was employed to determine the expression levels of PI3K and Akt in the vascular tissue. ResultCompared with the sham operation group， the model group showed lowered IL-6 level （P<0.01）， no significant change in LpA level， increased apoptosis of VSMCs （P<0.01）， and increased curvature index， elongation length， percentage increase in vessel diameter， and curvature angle （P<0.01）. Furthermore， the modeling up-regulated the protein levels of PI3K and Akt in blood vessels （P<0.01） and aggravated the destruction of the inner elastic layer， atrophy of the muscular layer， and hyaline changes in the connective tissue of the medial membrane of the basilar artery wall. Compared with the model group， 2 months of treatment with JTQHX elevated the IL-6 level （P<0.01）， reduced the apoptosis of VSMCs （P<0.01）， decreased the curvature index， elongation length， percentage increase in vessel diameter， and curvature angle （P<0.05， P<0.01）， and down-regulated the protein levels of PI3K and Akt in blood vessels （P<0.01）. In addition， the treatment alleviated the destruction of the inner elastic layer， atrophy of the muscular layer， and hyaline changes in the connective tissue of the medial membrane of the basilar artery wall. ConclusionJTQHX inhibits the elongation， expansion， and curvature of basilar artery vessels and alleviates the pathological changes by reducing the apoptosis of VSMCs and down-regulating the expression of PI3K/Akt pathway.

Vestibular migraine(VM)is a common vestibular disorder in which vertigo and migraine coexist,and visually induced vertigo is one of the typical vestibular symptoms of VM.The clinical manifestations of VM re-lated visual vertigo are various,which are affected by anxiety,motion sickness,age and other factors.Multiple mechanisms such as anatomical and physiological connections,gaze instability,visual vestibular integration defects,impaired sensory remodeling,sensitization of the central vestibular pathway,5-hydroxytryptamine and glutamate-glutamine cycle and other neurotransmitters may lead to VM-related visual vertigo.

The comorbidities of vertebrobasilar dolichoectasia（VBD） and cerebral small vessel disease（CSVD） increase the poor prognosis of patients，and elucidating the mechanism underlying their comorbidities helps to explore effective treatment strategies. Therefore，based on the collateral disease theory and combining with the pathogenesis and research progress of traditional Chinese and Western medicine on the understanding of the two，this study proposes that both the disease locations are in the brain collaterals and the pathogenesis is deficiency in foundation and excess in symptoms. The main pathogenesis roots in the deficiency of original Qi and the emptiness of brain collaterals，which corresponds to the dysfunction of endothelial cells and neuro-endocrino-immune networks in modern medicine. The symptoms are cerebral blood stasis，occlusion of cerebral arteries and toxic lesion of cerebral arteries，corresponding to cerebrovascular atherosclerosis，hemodynamic changes，hypoperfusion and toxic metabolites-induced injury of white matter in modern medicine. Based on the collateral disease theory，exploring the common pathogenesis of the VBD and CSVD is expected to facilitate the establishment of TCM treatment scheme including the principles，methods and medicines，and improve the clinical prognosis of patients.

Migraine with brainstem aura is one of the subtype of migraine with aura, with varied etiology and complex mechanism. Migraine with brainstem aura and transient loss of consciousness (TLOC) often occur together clinically, seriously affect the social life of the patients. At present, relation between migraine with brainstem aura and TLOC has not been elucidated, and clinical manifestations between TLOC and syncope is similar and easily confused by physicians. In order to deeply explore the complex relations between migraine with brainstem aura and TLOC, this article summarizes the clinical association, pathogenesis and differential diagnosis of migraine with brainstem aura associated with TLOC, so as to further optimize the clinical diagnosis strategies and provide new ideas for exploring comprehensive treatment measures for migraine with brainstem aura associated with TLOC.

Astrocytes play a key role in maintaining the homeostasis and function of the central nervous system. Abnormal lipid accumulation, ferroptosis, elevated lactic acid, and high DNA methylation mediated by astrocytes in their own or toxic states are particularly closely related to seizures. In recent years, epilepsy treatment from astrocyte energy metabolism perspective has become a research hotspot. Metabolic therapy, such as ketogenic diet, can inhibit seizures via a variety of mechanisms as astrocyte homeostasis maintenance. This paper reviews the relationship between astrocyte energy metabolism and epilepsy pathogenesis and its related metabolic therapy, in order to provide new ideas for clinical treatment of drug-resistant epilepsy.

Vertebrobasilar dolichoectasia (VBD) is a cerebrovascular variant disease. Researches have shown that further development of VBD may lead to severe disability and even death. The pathogenesis of VBD is still unclear, and there is no specific clinical prevention and treatment scheme. Therefore, establishing a stable and reliable animal model helps to further understand the pathophysiological mechanisms and potential therapeutic targets of VBD. This article reviews the establishment methods and research progress of the available VBD animal models.

Vertebrobasilar dolichoectasia (VBD) is a disease characterized by the dilation, elongation, and tortuosity of the vertebrobasilar artery. Cerebral microbleeds (CMBs) are brain parenchymal injuries mainly caused by punctate microbleeds due to small vessel lesions. Recent studies have shown that VBD can increase the incidence rate of CMBs, but the correlation and pathophysiological mechanism of the two remain unclear. Multiple factors can induce VBD to accompany CMBs. A deep understanding of the causal relationship and related mechanisms between VBD and CMBs is helpful for the clinical prevention and treatment of such cerebrovascular diseases.

Diet can be both a trigger and a treatment for migraine. The effects of alcohol, dairy products and pickled foods on migraine have been highly recognized. The effects of plant foods and caffeine on migraine currently have 2 sides. Ketogenic diet (KD), modified Atkins diet (MAD), and high n-3 fatty acid/low n-6 fatty acid diet can improve migraine through protecting nerves, improving mitochondrial function and energy metabolism, reducing calcitonin gene-related peptide (CGRP) levels, and inhibiting neuroinflammation. In this paper, the recent advance in the above content is summarized as follows.

Whether Fanconi anemia (FA) heterozygotes are predisposed to bone marrow failure and hematologic neoplasm is a crucial but unsettled issue in cancer prevention and family consulting. We retrospectively analyzed rare possibly significant variations (PSVs) in the five most obligated FA genes, BRCA2, FANCA, FANCC, FANCD2, and FANCG, in 788 patients with aplastic anemia (AA) and hematologic malignancy. Sixty-eight variants were identified in 66 patients (8.38%). FANCA was the most frequently mutated gene (n = 29), followed by BRCA2 (n = 20). Compared with that of the ExAC East Asian dataset, the overall frequency of rare PSVs was higher in our cohort (P = 0.016). BRCA2 PSVs showed higher frequency in acute lymphocytic leukemia (P = 0.038), and FANCA PSVs were significantly enriched in AA and AML subgroups (P = 0.020; P = 0.008). FA-PSV-positive MDS/AML patients had a higher tumor mutation burden, higher rate of cytogenetic abnormalities, less epigenetic regulation, and fewer spliceosome gene mutations than those of FA-PSV-negative MDS/AML patients (P = 0.024, P = 0.029, P = 0.024, and P = 0.013). The overall PSV enrichment in our cohort suggests that heterozygous mutations of FA genes contribute to hematopoietic failure and leukemogenesis.
Anemia, Aplastic/genetics* ; Epigenesis, Genetic ; Fanconi Anemia/genetics* ; Germ Cells ; Hematologic Neoplasms/genetics* ; Humans ; Leukemia, Myeloid, Acute/genetics* ; Retrospective Studies