Astrocytes are specialized glial cells that outnumber neurons by over fivefold. They contiguously tile the entire central nervous system (CNS) and exert many essential complex functions in the healthy CNS. Astrocytes respond to all forms of CNS insults through a process referred to as reactive astrogliosis, which has become a pathological hallmark of CNS structural lesions. Substantial progress has been made recently in determining functions and mechanisms of reactive astrogliosis and in identifying roles of astrocytes in CNS disorders and pathologies. A vast molecular arsenal at the disposal of reactive astrocytes is being defined. Transgenic mouse models are dissecting specific aspects of reactive astrocytosis and glial scar formation in vivo. Astrocyte involvement in specific clinicopathological entities is being defined. It is now clear that reactive astrogliosis is not a simple all-or-none phenomenon but is a finely gradated continuum of changes that occur in context-dependent manners regulated by specific signaling events. These changes range from reversible alterations in gene expression and cell hypertrophy with preservation of cellular domains and tissue structure, to long-lasting scar formation with rearrangement of tissue structure. Increasing evidence points towards the potential of reactive astrogliosis to play either primary or contributing roles in CNS disorders via loss of normal astrocyte functions or gain of abnormal effects. This article reviews (1) astrocyte functions in healthy CNS, (2) mechanisms and functions of reactive astrogliosis and glial scar formation, and (3) ways in which reactive astrocytes may cause or contribute to specific CNS disorders and lesions.

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Astrocytes: biology and pathology

Pathobiology of ischaemic stroke: an integrated view

This review is directed at understanding how neuronal death occurs in two distinct insults, global ischemia and focal ischemia. These are the two principal rodent models for human disease. Cell dea...

Ischemic Cell Death in Brain Neurons

Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that selectively affects optic nerves and spinal cord. It is considered a severe variant of multiple sclerosis (MS), and frequently is misdiagnosed as MS, but prognosis and optimal treatments differ. A serum immunoglobulin G autoantibody (NMO-IgG) serves as a specific marker for NMO. Here we show that NMO-IgG binds selectively to the aquaporin-4 water channel, a component of the dystroglycan protein complex located in astrocytic foot processes at the blood-brain barrier. NMO may represent the first example of a novel class of autoimmune channelopathy.

/pdf/igg-marker-of-optic-spinal-multiple-sclerosis-binds-to-the-5cre8njxbr.pdf

IgG marker of optic-spinal multiple sclerosis binds to the aquaporin-4 water channel.

Over the past two decades, research has heavily emphasized basic mechanisms that irreversibly damage brain cells after stroke. Much attention has focused on what makes neurons die easily and what strategies render neurons resistant to ischaemic injury. In the past few years, clinical experience with clot-lysing drugs has confirmed expectations that early reperfusion improves clinical outcome. With recent research emphasizing ways to reduce tissue damage by both vascular and cell-based mechanisms, the spotlight is now shifting towards the study of how blood vessels and brain cells communicate with each other. This new research focus addresses an important need in stroke research, and provides challenges and opportunities that can be used to therapeutic advantage.

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Mechanisms, challenges and opportunities in stroke

Efficacy and Limitation of Prophylactic Blood Pressure Lowering to Avoid Hyperperfusion Syndrome after Revascularization Surgery for Moyamoya Disease

During microvascular decompression (MVD) for trigeminal neuralgia (TGN), the mastoid emissary veins (MEV) are routinely sacrificed using the suboccipital retrosigmoid approach. The technical nuances when the MEV is an important collateral venous pathway for the obstructive internal jugular vein (IJV) have not been described thus far. Herein, we demonstrate for the first time a modified surgical technique for MVD to preserve the MEV. A 62-year-old man with a 10-year history of TGN refractory to carbamazepine was referred to our hospital for MVD. Preoperative imaging revealed that the superior cerebellar artery was the offending vessel. Computed tomography angiography also revealed that his contralateral IJV pathway was hypoplastic, and the ipsilateral pathway was severely stenosed by the external compression of the elongated styloid process and the transverse process of the first cervical vertebra. The ipsilateral MEV and the connecting occipital veins were enlarged as the sole collateral pathways of intracranial venous drainage. A modified MVD technique, including an upside-down L-shaped skin incision, layer-by-layer dissection of the occipital muscles, and denuding of the intraosseous part of the MEV, was used to cure the TGN with the preservation of the venous pathway. After surgery, the pain completely diminished without any complications. In conclusion, such technical modifications would be applicable in cases where the MEV needs to be preserved during posterior fossa surgery. Preoperative screening of the venous system is also recommended.

/pdf/preservation-of-enlarged-mastoid-emissary-vein-during-8hvkbjve.pdf

Preservation of Enlarged Mastoid Emissary Vein during Microvascular Decompression for Trigeminal Neuralgia Accompanied by Abnormal Venous Drainage: A Technical Case Report

BACKGROUND
Human immunodeficiency virus (HIV)-associated vasculopathy can cause ischemic cerebral stroke; however, there is limited evidence on optimal management. Herein, we report a case of acute ischemic stroke due to progressive internal carotid artery (ICA) stenosis in an HIV-positive patient. Superficial temporal artery to middle cerebral artery (STA-MCA) bypass, in addition to the best medical treatments, prevented stroke progression. Clinical Description: A 39-year-old man with HIV infection presented with a sudden onset of aphasia and right hemiparesis. Magnetic resonance imaging revealed an ischemic lesion in the left basal ganglia and concentric thickening of the vessel wall in the terminal portion of the bilateral ICAs. Despite maximal medical treatments for HIV-associated vasculopathy and possible opportunistic infections, bilateral ICA stenoses progressed, leading to a second hemodynamic stroke event. Because tissue plasminogen activator treatment failed, we performed STA-MCA bypass. A significant improvement in neurological symptoms and cerebral blood flow was observed after surgery. No further stroke events occurred during the continuation of medical treatments.


CONCLUSION
This is the first case of STA-MCA bypass performed in a patient with recurrent ischemic stroke caused by HIV-associated vasculopathy. Although further evidence is needed, such treatment options can shed new light on the management of progressive HIV-associated vasculopathy, which is refractory to maximal medical treatment.

Rescue extracranial-intracranial bypass for ischemic stroke secondary to progressive human immunodeficiency virus-associated vasculopathy.

Evaluation of cholesterol crystals in carotid plaque by dual energy computed tomography

https://www.jstage.jst.go.jp/article/scs/43/3/43_212/_pdf

Miki Fujimura

Papers

Efficacy and Limitation of Prophylactic Blood Pressure Lowering to Avoid Hyperperfusion Syndrome after Revascularization Surgery for Moyamoya Disease

Preservation of Enlarged Mastoid Emissary Vein during Microvascular Decompression for Trigeminal Neuralgia Accompanied by Abnormal Venous Drainage: A Technical Case Report

Rescue extracranial-intracranial bypass for ischemic stroke secondary to progressive human immunodeficiency virus-associated vasculopathy.

Evaluation of cholesterol crystals in carotid plaque by dual energy computed tomography

Surgery for Aneurysms that are Residual or Recurrent after Open or Endovascular Surgery