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.

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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

We described an autopsy case of a ruptured aneurysmal subarachnoid hemorrhage treated with endovascular embolization by interlocking detachable coils. An 85-year-old male presented with sudden onset of severe subarachnoid hemorrhage. Cerebral angiogram revealed a right internal carotid-posterior communicating artery aneurysm. Post-operative angiogram revealed complete obliteration of the aneurysm, except for its orifice. Following the embolization of the aneurysm, tissue plasminogen activator was intrathecally perfused for anti-vasospasm treatment. Follow-up angiogram showed stable obliteration of the aneurysm, and no particular findings of cerebral vasospasm. The patient had been recovering without any neurological deficits, but died from pneumonia on the 25th day after the embolization. Autopsy findings revealed the disappearance of the subarachnoid hemorrhage, and no visible finding of cerebral infarction or edema. The inner lumen of the aneurysm was occupied by a mixture of the coils and the clots. The surface of the embolized coils was directly observed through the orifice of the aneurysm without any membranous substance from the inner lumen of the internal carotid artery. This pathological finding is different from the previously reported animal models in which the surface of the embolized coils was covered with endothelial membrane 2 weeks after embolization. Further examinations are required to clarify the pathogenesis of the endothelial regrowth.

An autopsy case of a ruptured cerebral aneurysm treated with interlocking detachable coils

https://www.jstage.jst.go.jp/article/scs/42/1/42_37/_pdf

Issues in Revascularization Surgery for Elderly Patients with Moyamoya Disease

Background: Management of hemorrhagic moyamoya disease (MMD) is one of the most challenging issues in neurosurgical practice. Recently, surgical revascularization by superficial temporal artery-middle cerebral artery anastomosis was reported to significantly reduce the risk of re-bleeding in hemorrhagic-onset MMD patients in the chronic state, but the optimal treatment strategy in the acute phase of hemorrhagic MMD is undetermined. Thus, we retrospectively analyzed our surgical results for hemorrhagic MMD in the acute stage, focusing on the efficacy of neuro-endoscopic management for hematoma removal. Materials and methods: Among 26 consecutive hemorrhagic MMD patients who were managed at our institution in the acute stage, 8 patients with intracerebral hemorrhage underwent surgical evacuation of the hematoma. All patients were diagnosed with MMD before surgery by magnetic resonance angiography and/or catheter angiography. Results: The initial surgical procedure was neuro-endoscopic hematoma removal in seven patients and microsurgical hematoma removal by craniotomy in one patient. One patient treated by the neuro-endoscopic procedure required subsequent small craniotomy due to difficulty in hemostasis. Satisfactory hematoma evacuation was achieved in all eight patients, as demonstrated by post-operative computed tomography, although one patient who was deeply comatose before surgery died in the early post-operative period. Conclusion: Neuro-endoscopic hematoma removal may be the optimal management method for hemorrhagic MMD in the acute stage in terms of the maximum preservation of pre-existing collateral anastomosis without affecting the potential donor vessels used for future revascularization surgery. Abbreviations: MMD: Moyamoya disease; STA: Superficial temporal artery; MCA: Middle cerebral artery; JAM: Japan Adult Moyamoya; ICH: Intracerebral hemorrhage; IVH: Intraventricular hemorrhage; SAH: Subarachnoid hemorrhage; CT: Computed tomography; TE: Total evacuation; PE: Partial evacuation; SMR: Light mass reduction; MR: Magnetic resonance; mRS: Modified Rankin scale; GCS: Glasgow Coma Scale; ICP: Intracranial pressure.

Neuro-endoscopic management of hemorrhagic moyamoya disease in the acute stage: single institute experience.

Moyamoya disease is a chronic, occlusive cerebrovascular disease with unknown etiology characterized by bilateral steno-occlusive changes at the terminal portion of the internal carotid artery and an abnormal vascular network at the base of the brain [1]. Clinical presentation of moyamoya disease includes transient ischemic attack (TIA), cerebral infarction, intracerebral hemorrhage, and seizure [2]. TIA is one of the most common clinical presentations of moyamoya disease both in pediatric and adult cases [2], while intracerebral hemorrhage is mostly seen among adult cases [3]. Recently, headache is also considered to be one of the common clinical presentations of moyamoya disease. Patients with moyamoya disease may complain of headache before and after revascularization surgery. In this chapter, the authors focus on headache as the clinical presentation of moyamoya disease, and discuss the incidence and mechanism of this symptom. We further discuss the efficacy of revascularization surgery for the improvement of headache.

Headache in Moyamoya Disease

A 61-year-old woman presented with aneurysmal subarachnoid hemorrhage (SAH) associated with multiple remote intracerebral hemorrhages (ICHs). She had undergone microsurgical neck clipping for ruptured right middle cerebral artery aneurysm and ventriculo-peritoneal shunting 16 years previously. Computed tomography revealed SAH predominantly in the basal cistern and ambient cistern, in association with multiple ICHs in the bilateral tegmentum of the brain stem and right caudate nucleus. Digital subtraction angiography revealed an aneurysm at the P1 segment of the left posterior cerebral artery. The ruptured aneurysm was microsurgically clipped via a left subtemporal approach without complications. Simultaneous occurrence of aneurysmal SAH and multiple remote ICHs is rare. The spatial pattern of the ICHs in the present case is apparently unique.

Subarachnoid Hemorrhage Due to Ruptured Posterior Cerebral Artery Aneurysm Simultaneously Associated With Multiple Remote Intracerebral Hemorrhages : Case Report

Miki Fujimura

Papers

An autopsy case of a ruptured cerebral aneurysm treated with interlocking detachable coils

Issues in Revascularization Surgery for Elderly Patients with Moyamoya Disease

Neuro-endoscopic management of hemorrhagic moyamoya disease in the acute stage: single institute experience.

Headache in Moyamoya Disease

Subarachnoid Hemorrhage Due to Ruptured Posterior Cerebral Artery Aneurysm Simultaneously Associated With Multiple Remote Intracerebral Hemorrhages : Case Report