With a low incidence and a non-specific clinical manifestation, medial medulary infarction (MMI) can often be misdiagnosed or missed diagnosis. Magnetic resonance imaging(MRI) played a major role in diagnosing the MMI. This article reviews the epidemiology, etiology, pathogenesis, clinical and imaging manifestations, diagnosis and differential diagnosis, and prognosis of MMI.

The relationship between thyroid diseases and cerebrovascular diseases is getting increasingly attention. Studies have shown that thyroid diseases are associated with many kinds of cerebrovascular diseases, such as ischemic cerebrovascular disease, moyamoya disease, cerebral venous thrombosis, and artery dissection. This article review the advances in research on the correlation between thyroid diseases and cerebrovascular diseases.

Inflammation plays a key role in the formation of intracranial aneurysm. At present, the pathophysiological processes of intracranial aneurysms are mainly caused by both hemodynamic abnormalities and inflammation. Studies have shown that the inflammatory cels in the intracranial aneurysm wal are mainly mononuclear macrophages, and can secrete various effector molecules, weakening and destroying the structures of the vessel wal . Therefore, the research of the roles of differences played in different subtypes of macrophages and their effector molecules in the pathophysiological processes of intracranial aneurysms wil provide clues for exploring the pathogenesis of intracranial aneurysms and effective targeted therapy.

Inflammation is involved in the pathogenesis of many vascular disorders. Hemodynamics cause the activation of inflammatory factors in the vascular wal , resulting in dysfunction of vascular endothelial cels and vascular smooth muscle cels, activating vascular wal inflammatory cascade. Inflammatory cels, especialy macrophage infiltration and secretion of enzymes gradualy weaken the vessel wal to form aneurysm, and even cause aneurysm rupture. Therefore, inflammation plays a key role in the formation and rupture of intracranial aneurysms.

Intracranial aneurysms are mainly caused by the local arterial wal defects and the increased intraluminal pressure. Usualy, the unruptured smal aneurysms are asymptomatic, and the ruptured aneurysms can cause subarachnoid hemorrhage. So far, the etiology and pathogenesis of intracranial aneurysms are not fuly understood. A lot of evidence has showed that intracranial aneurysms are a complex disease of environmental factors and multi-gene interaction. This article reviews the correlation between polymorphisms of elastin and colagen type Ⅰ α2 genes and intracranial aneurysm.

Infection is one of the common complications of stroke. It can seriously affect the prognosis of patients. Poststroke infection is closely associated with immune system imbalance, while the excessive activation of sympathetic nerve is an important factor of the occurrence of immunosuppression after stroke. The sympathetic nerve regulates immune cels primarily via β2 adrenergic receptors on the surface of the immune cels. There is evidence to show that β2 adrenergic receptor mediated immune function enhances rather than inhibits under certain conditions, but its specific molecular mechanism is unclear. This article reviews the molecular mechanisms of β2 adrenergic signaling pathway in regulation of inflammation after stroke.

High mobility group protein box 1 (HMGB1) is a typical nonhistone chromosomal protein. It has many celular functions in nucleus. Studies in recent years have showed that HMGB1 can be released to the outside of cels to exert a wide range of cytological effects. Ischemic stroke is one of the diseases with the highest morbidity and disability. More and more evidence has shown that HMGB1 plays a variety of important roles in the occurrence and development process of ischemic stroke. This article reviews the roles of HMGB1 in ischemic stroke.

As a cavola marker protein, caveolin-1 participates in many pathophysiological processes through its scaffolding domain oligomering many celular signal transduction molecules, and also regulates inflammation after cerebral ischemia through different pathways. This article reviews advances in caveolin-1 and inflammation after ischemic stroke in recent years, mainly focusing on its mechanism in regulating inflammation.

Caveolins are the major component proteins of the caveolae, and they are also the essential proteins to carry out the physiological functions of caveolae. Caveolins are expressed in smooth muscle cels, endothelial cels, and adipocytes. Caveolae are not only involved in the basic physiological processes, such as celular fat intake, endocytosis, and pinocytosis, but also play a very important role in cel signal transduction and transport and permeability of macromolecular substance. With the in-depth research on the molecular structure and biochemical function of caveolins, increasing studies have shown that caveolae and their main component caveolins play an important role in the pathophysiological process of cerebrovascular diseases. This article reviews the roles of caveolins in the blood-brain barrier destruction after cerebral ischemia.

Peroxisome proliferators-activated receptor γ (PPARγ) belongs to a nuclear receptor superfamily. Many studies have shown that PPARγ can help to improve the outcome of cerebrovascular disease. PPARγ can reduce inflammatory response, oxidative stress as wel as enhance the hematoma removal abilities of microglia and macrophages, and it plays an important protective role in intracerebral hemorrhage.