5.1 Historical Role of Neurosurgery for Stroke

A stroke is a sudden critical function failure of the brain, which can result from ischemic causes or intracranial bleeding. The clinical implications regarding diagnosis and treatment are common to both types of stroke, ischemic and hemorrhagic. The aim of any treatment is the prevention of secondary brain damage. However, ischemic stroke is one of the most common causes of death worldwide and one of the main sources of disability. Stroke prevention and modern stroke treatment have decreased incidence and mortality in western countries during the last few decades. In spite of this progress, the expected demographic shift due to an aging population will only heighten the importance of ischemic stroke management in coming years. Neurosurgical treatment options are required in all stroke units. Particularly so since the cause of stroke is initially unknown and the occurrence of secondary bleeding complications is always possible. Aneurysms, AVMs, hematoma evacuation, and cerebral revascularization, including moyamoya, are summarized below. Many important stroke-related neurosurgical procedures are the subject of other chapters (e.g. decompressive craniectomy).

5.2 Surgery for Acute Hemorrhagic Stroke or Intracerebral Hematomas

Primary intracerebral hemorrhages occur in approximately 10% of strokes. The most common causes of hemorrhagic strokes are: hypertension (30–60%), cerebral amyloid angiopathy (10–30%), anticoagulation (1–20%), and vascular structural lesions (3–8%); idiopathic stroke comprises 5–20% of cases. Supratentorial intracerebral hemorrhages account for 85–95% of cases. Within this group, lobar hemorrhages represent 25–40% of cases, and deep brain structure hemorrhages 50–75%. The 30-day mortality is higher for deep hemorrhages than for lobar ones, and mortality rises with hemorrhage volume. Intracerebral hemorrhages may be associated with various complications such as rebleeding with expansion of the hematoma, hydrocephalus, intraventricular hemorrhage, and edema. Patients with a cerebellar hematoma are at particular risk of deterioration, specifically due to direct compression of the brainstem and cerebellum. The risk of hematoma expansion and hydrocephalus underlines the importance of careful neurological monitoring and 24-hour access to computed tomography scanning in cases of deterioration. Early surgical evacuation of supratentorial hematomas might be beneficial for patients with a Glasgow Coma Scale score of 9–12 who are treated within 8 hours after symptom onset. A minimally invasive drainage via catheter may represent a promising treatment option for deep hematomas. An external ventricular drain combined with topical fibrinolysis may reduce mortality, though it does not seem to be related to better functional outcomes in patients with intraventricular hemorrhage and hydrocephalus. Surgical evacuation of infratentorial intracerebral hemorrhages is typically indicated if the Glasgow Coma Scale score is lower than 14, the hematoma diameter greater than 30–40 mm, the hematoma volume greater than 7 cm³, or if there is an obliteration of the fourth ventricle. An external ventricular drain is usually inserted if there is an associated hydrocephalus. General recommendations to manage hemorrhagic stroke include: (7)

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  Stroke services should agree upon and share protocols for the monitoring, referral, and transfer of patients to regional neurosurgical centers for the management of symptomatic hydrocephalus.

  
  
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  Patients with intracranial hemorrhages should be monitored in neurosurgical or stroke care for deterioration in function, and referred immediately for brain imaging when necessary.

  
  
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  Previously healthy patients should be considered for surgical intervention if the intracranial hemorrhage causes hydrocephalus.

  
  
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  Patients with any of the following conditions rarely require surgical intervention and should receive medical treatment initially: small deep hemorrhages; lobar hemorrhages with neither hydrocephalus nor rapid neurological deterioration; a large intracerebral hemorrhage and concurrent with significant prior co-morbidities; a Glasgow Coma Scale (GCS) score below 8, unless due to hydrocephalus.

5.3 Aneurysm and Stroke

Unruptured intracranial aneurysms (UIA) presenting with ischemic events such as transient ischemic attacks (TIAs) or ischemic stroke are relatively rare. The number of patients with cerebral aneurysms who presented with TIAs and/or stroke amounts to 0.5–6.6%. Ischemic episodes in patients with intracranial aneurysms are caused by thrombosed aneurysms or occlusion of the parent vessel. Several reports have shown that no matter how small the aneurysm, a thrombotic mass can migrate from its dome to the distal region of symptomatic cerebral arteries or spread to the parent artery.

5.3.1 Pathophysiology

There are mainly two reasons for intra-aneurysmal thrombus formation. First, the flow pattern inside of the aneurysm can stimulate thrombus formation. Second, the aneurysmal lumen can stimulate thrombosis. Both of these causes of thrombus formation also play a role in aneurysmal wall pathophysiology. Additionally, there is the possibility for thrombosis to increase via neovascularization or growth of the aneurysm. Likewise, in large and giant aneurysms (Fig. 5‑1), intramural hemorrhages due to rupture of fragile vasa vasorum stimulate thrombus formation. The dynamics of thrombus formation and lysis result in the appearance of emboli, which subsequently makes stroke inevitable. Unfortunately the thrombus inside the aneurysm does not protect the patient from aneurysm rupture, but can actually advance it. It is complete obliteration of an aneurysm and thrombotic mass removal that protect the patient from stroke. This is why open microneurosurgery is preferred. In many cases revascularization is necessary for such large and giant aneurysms. This should be done in medical centers dedicated to neurovascular treatment.

5.4 Arteriovenous Malformation and Stroke

Most patients with cerebral arteriovenous malformation (AVM) are diagnosed during middle-age, meaning that they have potentially decades of life ahead. Helsinki study of the natural history of AVMs is in line with the ARUBA study (A Randomized trial of Unruptured Brain AVMs): there exists an approximately 2–3% annual risk of hemorrhage. The indications for treating these lesions are easy to understand and readily justified. The collective risk of rupture of AVMs will grow significantly over the span of a patient’s life and the only way to avoid such a hemorrhage is to remove the AVM. Originally, ARUBA investigators came to conclude that conservative treatment is superior to intervention at 33 months follow-up. Regrettably, the same investigators later extrapolated that the results of ARUBA were valid as follow-up data decades later. Fortunately for patients, the neurovascular community has woken up from this disastrous way of thinking and there are now many other studies which report more rational conclusions for patient care. No one can know the obliteration rate of AVMs in the ARUBA study, as it has not been reported. More than half of the intervention group either had on-going treatment or had not started treatment (53 and 20 patients, respectively) during the report of ARUBA. Meta-analysis by Liu X showed that 96% of AVMs are removable by microneurosurgery, 38% by radiation, and 13% by embolization. Despite this knowledge, only 17 patients out of 114 in the ARUBA intervention group were treated by microneurosurgery, even though 76 patients in the intervention group had Spetzler-Martin (SM) Grade I-II. Additionally, approximately one-third of patients in the ARUBA study were SM grade III-IV; as such this subgroup is overrepresented in the patient cohort. Obviously intervention in such cases is riskier than for lower grade AVMs. All this shows that complex diseases such as AVMs should be treated in medical centers dedicated to them by professionals who treat these lesions daily.