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Prior to the routine use of vertebral angiography, posterior fossa AVMs were usually found unexpectedly during the evacuation of posterior fossa hematomas [1]. In 1932 (May 5th), Olivecrona had reported their first successful radical removal of a left cerebellar AVM in a 37-year-old male who was misdiagnosed of having a posterior fossa tumor. After an 8-h-long marathon surgery under local anesthesia and with a blood transfusion of 2000 ml, the AVM was removed. The postoperative course was uneventful and the patient left the hospital 3 months later [2]. As vertebral angiography became more widely used, the preoperative diagnosis of posterior fossa AVMs became possible. Even so, at that time, neurosurgeons thought that it was possible to operate on small-to-moderate-sized AVMs in silent areas of the brain but were reluctant to touch AVMs in nonsilent areas [2], including the more demanding posterior fossa. Neurosurgeons were, however, disappointed that only very few AVMs could be removed entirely without great risk, which led to the development of other, ineffectual techniques, such as vertebral artery or feeder ligation [1].

Since the development of Guglielmi detachable coil (GDC), endovascular technique for coiling has become widely accepted as one of the option treatments of intracranial aneurysms.

Neuroendoscopic procedures for spontaneous cerebral hemorrhage have recently increased. This is a result of the reports published by Nishihara et al. in 2000 [1], describing how to use the neuroendoscopic to evacuate the intracerebral hematoma by using a transparent sheath. Following this, 300 surgical cases of spontaneous intracerebral hemorrhage have been performed with an endoscope in our institution, and in related facilities, between 2000 and 2015. This procedure is commonly performed with only one or two burr holes under local anesthesia. If the transparent sheaths are introduced into hematoma safely, endoscopic procedures will be successful in any location of spontaneous hematomas.

Spontaneous intracerebral hemorrhage (ICH) due to uncontrolled hypertension is a common clinical entity that affects up to four million people annually [1]. Hemodynamic injury to perforating end arteries (100–400 μm) results in pathological lesions such as lipohyalinosis, fibrinoid necrosis, and Charcot-Bouchard microaneurysm which may predispose to rupture. Common locations where these hemorrhages may occur include the basal ganglia, pons, thalamus, cerebellum, or subcortical white matter (lobar) [2].

Intracranial dural arteriovenous fistulas (DAVFs) are acquired lesions characterized by a region of abnormal arteriovenous fistulous connection within the dura. DAVFs contribute to 10–15% of all AVM intracranially as reported by Newton et al. from 1969 [1]. In common population the probable rates were 0.15–0.29 per 100,000 people per year [2, 3]. Median age of DAVF patients is between 50 and 60 years, but it may present at any age [4, 5].

Moyamoya disease (MMD) is a rare condition where the supraclinoid part of internal carotid artery is slowly and progressively becoming stenotic, and also it often involves both middle cerebral arteries and anterior cerebral arteries (Fig. 26.1) [1]. The term moyamoya means in Japanese, and it was first reported by Takeuchi and Shimizu in 1957 with Japanese language [2].

The term complex intracranial aneurysms (CIAs) refers to aneurysm at a narrow and difficult location, difficult shape, and also giant size (aneurysm that is bigger than 25 mm in diameter) [1]. Giant aneurysms are more likely to bleed and present as subarachnoid hemorrhage, or sometimes they become partly thrombosed with ischemic brain causing mass effect with progressive symptoms or even death. Microsurgery and clip ligation can be challenging in CIAs because it is very difficult to have a panoramic view of the aneurysm, where sometimes the parent vessel is laid beneath the aneurysm, difficult to identify all branches and perforators, and also the surgical corridor could be very deep and narrow and surrounded by important neurovascular structures. During the clipping, it is important to make sure the aneurysm is well clipped to prevent injury from any perforator (Figs. 27.1, 27.2, and 27.3). Flow arrest can be induced by using adenosine; it will briefly reduce cerebral perfusion pressure and the tension on aneurysm, thereby facilitating the clip ligation. The length of time for the flow arrest will provide the surgeon to work at the aneurysm and the parts surrounding it or even reduce the bleed if it was ruptured during dissection. It will provide the time interval for the surgeon to be able to secure the neck of the aneurysm. The adenosine is working by inducing the transient asystole for a few minutes.

Clinical signs and symptoms of spinal arteriovenous malformation (AVM) have different characteristics according to the type of the AVM. Various classifications have been proposed for this complex lesion [1–3]; we use our own modified classification just to simplify our work-up discussion. We divide the spinal arteriovenous (AV) malformations by their fistula or nidus locations into dural, perimedullary, and intramedullary type and by fistulas or true malformations. Authors identify the dural AV fistulas (dAVF) (Fig. 28.1), perimedullary AV fistulas (AVF) (Fig. 28.2), and spinal cord true AV malformation (AVM) that is either juvenile-type AVM or glomus-type AVM.

Majority of morbidity and mortality due to aneurysmal subarachnoid hemorrhage (aSAH) is secondary to cerebral ischemia. Classically, the angiographic arterial narrowing following aSAH has been termed as angiographic vasospasm, which may or may not lead to clinical manifestations and cerebral ischemia, in which case it would be called symptomatic vasospasm. This concept has recently been questioned. Not always angiographic vasospasm leads to cerebral ischemia, which, in turn, may occur in a territory different from the one irrigated by the narrowed artery or even in the absence of any angiographic vasospasm, i.e., cerebral ischemia that occurs late (days after aSAH) cannot be attributed solely to the arterial narrowing seen on angiography [1]. Currently, the term “delayed cerebral ischemia” (DCI) has been proposed to replace the previously used “symptomatic vasospasm.” The clinician should be able to recognize and differentiate the radiological vasospasm from the clinical worsening secondary to DCI, whose etiology is multifactorial and includes angiographic arterial narrowing (Fig. 29.1). Alternative mechanisms have been proposed and include microvascular spasm and failure of cerebral blood flow (CBF) autoregulation, microthrombosis and microembolism, cortical spreading depolarization and ischemia, and delayed neuronal apoptosis resulting from acute brain injury. A more extensive review of the pathophysiology of DCI is out of the scope of this review.

The introduction of the operating microscope enabled modern neurosurgery. For usually deep-seated vascular lesions and confining, overhanging brain parenchyma walls, self-retaining retractors were necessary to enable open and safe dissection corridors. However, retractors also exert secondary pressure effects and can limit the degree of manual freedom [1].