Posterior Circulation Stroke

Approximately 15 to 20% of ischemic strokes affect the posterior circulation. Acute basilar artery (BA) occlusion, either by arterial embolism or local atherosclerotic occlusion, accounts for less than 1% of ischemic strokes and is associated with a high mortality rate. ^{4 , 5} Distal BA occlusion is typically caused by thromboembolism, because vascular segments with a clinically significant reduction in vessel diameter are predilection sites for embolic occlusions. ⁶ Occlusion of the distal BA leads to ischemia of the thalami, midbrain, inferior temporal lobes, and occipital lobes.

Embolic Stroke

Artery-to-artery and cardiac embolisms are the two most common causes of embolic stroke. ² Embolism occurs most commonly via cardiac sources and from atherosclerotic wall degeneration of the aortic arch, ⁷ the common carotid artery, and the ICA. ^{8 , 9}

Cardioembolism is responsible for 15 to 30% of nonhemorrhagic strokes. ^{10 , 11} The three primary mechanisms of cardioembolism are blood stasis and thrombus formation in the left cardiac chamber (due to atrial fibrillation, myocardial infarction, or heart failure); thrombus formation on a valvular surface (due more rarely to endocarditis, rheumatic mitral valve disease, mitral valve prolapse, mitral annulus calcification, or aortic valve disease); and paradoxical embolism (caused by residual patent foramen ovale).

Carotid artery atherosclerosis causes approximately 20% of ischemic strokes in the anterior circulation. ^{8 , 9} Important mechanisms in this scenario are luminal thrombus formation after plaque surface rupture and the downstream flow of thrombus material in the bloodstream to distal vascular territories.

Anterior Circulation

The embolic occlusion of the ICA, the anterior cerebral artery, or the middle cerebral artery (MCA) is associated with contralateral paralysis, aphasia (left hemisphere), and contralateral central facial nerve (cranial nerve [CN] VII) paralysis. Malignant brain infarction with consecutive transtentorial herniation is life threatening.

Posterior Circulation

Acute occlusion of the BA affects the function of the inferior temporal and occipital lobes, the midbrain, and the bilateral thalami. Conscious patients may experience the following symptoms: vertical gaze disturbance, convergence disorders, slowed pursuit movements, skew deviation, slowed or incomplete light reaction, dizziness, vomiting, dysarthria, dysmetria, and gait ataxia. ^{5 , 12 , 13}

Ipsilateral posterior cerebral artery (PCA) occlusion can lead to contralateral loss of vision, whereas bilateral PCA occlusion can result in cortical blindness. Midbrain infarction can result in oculomotor nerve (CN III) palsy, crossed hemiplegia, and hemiataxia; lower midbrain infarction can result in internuclear ophthalmoplegia and trochlear nerve (CN IV) palsy. ^{5 , 12 , 13}

Time Management

Time management before and during hospitalization is the most critical modifiable factor affecting patient outcome. In particular, immediate transfer of the patient to a stroke center with facilities for interventional and surgical stroke management is of great importance, as hemorrhagic stroke cannot currently be fully excluded during the prehospitalization phase. ¹⁴ Even in modern countries with a well-organized emergency system, only 10 to 20% of stroke patients arrive at a stroke center quickly enough to undergo stroke revascularization therapy.

Imaging

Vascular imaging with computed tomography (CT) and magnetic resonance imaging (MRI) is time-consuming but invaluable in the decision-making process for revascularization. ^{15 , 16 , 17 , 18 , 19} The infarct core and the salvageable tissue at risk must be carefully estimated. Furthermore, care must be taken to distinguish an embolic occlusion from a local atherosclerotic occlusion ( Fig. 24.1 ). For example, only up to 35% of basilar occlusions are caused by cardiac or artery-to-artery embolization. ^{10 , 11}

Medical Treatment

For the treatment of acute ischemic stroke in patients presenting within a 4.5-hour time window, intravenous application of recombinant tissue plasminogen activator (rTPA) is a level IA recommendation included in the treatment guidelines of several countries. ^{20 , 21 , 22 , 23} Contraindications to rTPA are summarized in Table 24.1 .

When an indication is present, 0.9 mg/kg rTPA is administered intravenously, to a maximum dose of 90 mg. The dose is divided as follows: 10% injected as a bolus and 90% administered continuously via a syringe pump over the course of the next hour. However, intravenous thrombolysis with rTPA has a limited effect on main branch occlusions (ICA, proximal MCA, and BA). ^{24 , 25 , 26}

Endovascular Treatment

During the last decade, endovascular treatment of major intracranial vessel occlusion has gained increasing importance. At first, intra-arterial lysis with rTPA or urokinase were treatment options, with some studies showing a beneficial effect regarding recanalization and improved outcomes. ^{27 , 28} During the last few years, rapid development of mechanical embolectomy devices has led to greater application of these techniques. ^{11 , 29 , 30} Stent retriever technology, in particular, has led to significant improvement in recanalization rates and outcomes. ^{31 , 32 , 33 , 34 , 35} The application criteria for endovascular mechanical revascularization (based on the AHA/ASA [American Heart Association/American Stroke Association] guideline) are listed in Table 24.2 . ^{36 , 37}