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1.4 Treatment for acute stroke
Gerhard Schroth, Christoph Ozdoba, Marwan El-Koussy
1.4.1 Clinical picture
According to the definition established by the World Health Organization, stroke is characterized by the acute onset of focal or global disturbances of brain function due to vascular causes. Synonyms for acute stroke include apoplexy, cerebrovascular accident, cerebral infarction, and ictus.
In Europe, cerebral infarction is the most frequent cause of disability among adults. After cardiac diseases and cancer, stroke is the third most frequent cause of death and it is one of the main causes of epilepsy and dementia in the elderly.
The incidence of stroke increases with age. Approximately two cases of stroke per year can be expected per 1000 population. In the over-50s age group, the incidence increases approximately two- to threefold in each decade of life.
Approximately 15–20% of stroke cases are caused by intracerebral or subarachnoid bleeding. The remaining 80% have ischemic causes, with occlusion of the cerebral arterial vessels. These two entities cannot be distinguished clinically; therefore every patient with stroke needs to undergo computed tomography (CT) or magnetic resonance imaging (MRI) as quickly as possible. If bleeding is excluded by the imaging examinations, then intravenous thrombolysis can be started on the CT/MRI table even while the location and effects of the vascular occlusion are demonstrated using CT angiography (CTA) or MR angiography (MRA).
The causes of acute vascular occlusion differ fundamentally between myocardial infarction and cerebral infarction, and require different treatment approaches. Heart attacks are due to local, and usually longstanding, arteriosclerotic changes in the vascular walls in over 90% of cases. This leads directly to acute occlusion of the coronary artery due to rupture of the plaque and secondary in situ thrombosis. In addition to rapid recanalization with thrombectomy and/or angioplasty, coronary stents are also used to stabilize the local vascular process.
By contrast, occlusions in the cerebral vessels are caused by arterio-arterial embolism in approximately 75% of cases. The aim of treatment for cerebral stroke is to remove the thrombus from an otherwise healthy cerebral vessel. Thrombi that are transported to the cerebral circulation often originate in the heart, but may also have formed on plaques in the aortic arch or cervical vessels. Thrombi that form in the pelvic and crural veins can be transported to the cerebral circulation via a right-to-left circulation defect such as a patent oval foramen. This phenomenon is termed “paradoxical” embolism.
The brain weighs approximately 1200 g, equivalent to around 2% of body weight, but it requires roughly 20% of cardiac output and oxygen consumption. The brain initially responds to a reduction in regional cerebral blood flow (CBF) with reversible cerebral dysfunction, which may progress to an irreversible defect—infarction—depending on the duration and extent of the drop in CBF (Fig. 1.4-1).
1.4.2 Clinical findings
A global interruption of blood supply to the brain (global ischemia)—e.g., due to cardiovascular arrest—leads to unconsciousness after approximately 10 seconds, and the cerebral tissue is already irreversibly damaged after only a few minutes. These intervals can be prolonged by hypothermia which acts as in a neuroprotective fashion.
In focal cerebral ischemia, cerebral blood flow is only reduced in the area supplied by the occluded cerebral vessel. The associated neurological deficits depend on the size, location, and collateral supply in the underperfused areas of the brain.
Fig. 1.4–1 Diagram showing threshold values for cerebral blood flow (CBF).
Occlusion of the main trunk of the middle cerebral artery (M1 occlusion) or its proximal (M2) or peripheral (M3) branches is by far the most frequent form of cerebral infarction. The main symptoms are contralateral predominantly arm and facial hemiparesis along with speech disorders if the dominant hemisphere is affected (Fig. 1.4-2).
Circulatory disturbances in the basilar artery lead to infarction of the brainstem, cerebellum, and thalamus. The main symptoms are vertigo, ataxia, and gaze paralyses, which can quickly progress to coma, quadriplegia, or “locked-in syndrome,” in which there is complete paralysis of the body and cranial nerves, but with preservation of cerebral cognitive function, and communication is only possibly using eye movements (Fig. 1.4-3).
Fig. 1.4–2a-f Acute stroke with left-sided hemiparesis in a 13-year-old boy. The diffusion-weighted image (DWI) (a) and apparent diffusion coefficient (ADC) map (b) show cytotoxic edema in the anterior territory of the middle cerebral artery (MCA). (c) On the mean transit time (MTT) map, the entire MCA area and parts of the posterior territory show a perfusion deficit. (d) The T2-weighted spin-echo image only shows discrete signal enhancement in the right insula. (e) First-pass contrast magnetic resonance angiography reveals the cause as an occlusion of the MCA. (f) On susceptibility-weighted imaging (SWI), the thrombus in the MCA leads to a flow void that demarcates the occlusion in an enlarged form (a round frontal artefact caused by the adjoining sphenoid sinus).
Fig. 1.4–3a-e A 64-year-old man with somnolence. The CT 85 minutes after the onset of symptoms shows an occlusion in the basilar artery. Intravenous thrombolysis was started 105 minutes after the onset of symptoms. The noncontrast CT (a) shows a hyperdense basilar artery that does not enhance after contrast administration (b). Magnetic resonance imaging 4 h 15 min after the onset of symptoms shows areas of acute ischemia in the brainstem and cerebellum on the diffusion-weighted image (c), which are already demarcated on the T2w image. Contrast-enhanced first-pass MRA of the cerebral arteries (e) shows the occlusion in the basilar artery.
Fig. 1.4–4a-c Sudden paralysis of the right leg by a thromboembolic occlusion in the left anterior cerebral artery. (a) The diffusion-weighted MRI shows cytotoxic edema in the anterior cerebral artery territory. Occlusion of the left anterior artery was confirmed on MRA (b) and digital subtraction angiography (c) before endovascular mechanical removal of the thrombus.
In occlusions of the anterior cerebral artery (Fig. 1.4-4), the main symptom is central paralysis of the legs, while with posterior infarction (Fig. 1.4-5) the main symptom is narrowing of the visual field (homonymous hemianopia).
The