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Stroke is typically defined as the sudden onset of a neurologic deficit caused by vascular abnormalities. There are two main categories: (1) ischemia (infarction)—restricted blood flow due to vascular stenosis/occlusion and the consequent insufficient oxygen and glucose supply to an area of the central nervous system (CNS) and (2) hemorrhage—bleeding in or around the brain. Ischemic stroke is more common than hemorrhagic stroke (70% vs. 30% globally); a higher incidence of hemorrhagic stroke was noted in the Asian, Hispanic, and African–American populations .
Ischemic stroke can be further characterized into subtypes based on the different involved vascular territories, mechanisms, and causes. This chapter will introduce each subtype of stroke classified by each of these different methods. Each stroke subtype’s pathophysiology, clinical characteristics, and imaging will be discussed. Venous diseases, silent brain infarcts/hemorrhage, and retina or spinal strokes are not discussed in this chapter.
The brain tissue is perfused and given nutrition by two vascular systems, the anterior and posterior circulation. Based on the infarct location, ischemic stroke can be classified as anterior circulation ischemic stroke (ACIS) or posterior circulation ischemic stroke (PCIS). There are several differences between ACIS and PCIS; for example, atrial fibrillation is noted more frequently in ACIS in most studies and the rate of intracranial hemorrhage after intravenous thrombolysis is significantly less common in PCIS . Therefore, their evaluation and management strategies should be different. Patients with ACIS and PCIS often present their own localization-specific neurologic deficits. Magnetic resonance imaging with diffusion-weighted imaging sequences will often be needed to accurately differentiate these two categories of stroke.
The anterior circulation of the brain is supplied by the internal carotid arteries (ICAs) and their branches including large intracranial vessels, middle cerebral arteries (MCAs) and anterior cerebral arteries (ACAs), and small vessels (perforating arteries from intracranial ICAs, MCAs, and ACAs). The territory comprises most of the cerebrum except the occipital and medial temporal lobes. Ischemic stroke occurring in the anterior circulation accounts for 70–80% of all ischemic strokes.
The clinical features can present as MCA syndrome, ACA syndrome, or lacunar syndrome (LS). The common clinical manifestations are dysarthria, central facial palsy, and motor and/or sensory involvement of the contralateral extremities. The typical presentations of MCA territory infarction, the most common form of ACIS, are dysarthria, contralateral central facial palsy, ipsilateral deviation of eyes, contralateral hemianopsia, contralateral extremities weakness and sensory deficits, and cortical signs including aphasia (left MCA) or hemineglect (right MCA).
The three main causes of ACIS are large artery atherosclerosis (LAA), cardiac embolism (CE), and small vessel occlusion (SVO). The major mechanisms are (1) embolism: emboli can arise either from proximal atherosclerotic large artery lesions, mainly the extracranial and intracranial ICA and the mainstem MCA (artery-to-artery emboli), or from thrombi and other sources within the heart or the aorta (cardiogenic emboli); (2) thrombosis: in situ thrombosis at the site of atherosclerotic plaque in a large brain-supplying artery (usually over the vascular bifurcation region); and (3) hemodynamic compromise: a combination of large artery atherosclerotic severe stenosis/occlusion and generalized hypoperfusion caused by systemic conditions such as dehydration, blood loss, or cardiac failure. These cerebral infarct patterns can be single, multiple, or scattered; can involve the territory or subterritory; and can be isolated subcortical or cortical.
Lacunar infarction (small vessel occlusion) in the anterior circulation is caused by single perforating artery occlusion, and the associated small vascular pathologic conditions include lipohyalinosis or microatheroma. Perforating artery blood flow can also be blocked by large artery atheroma at the orifice of the branch (atheromatous branch occlusive disease).
Posterior circulation of the brain is the territory supplied by the vertebrobasilar arteries and their branches including the posteroinferior cerebellar arteries, anteroinferior cerebellar arteries, superior cerebellar arteries, posterior cerebral arteries, and perforating arteries. Brainstem, cerebellum, occipital lobe, medial temporal lobe, and thalamus are supplied by the posterior circulation.
The most common clinical features of PCIS are homolateral weakness and sensory deficits, which are hardly used for differentiating it from ACIS. Unique presentations of PCIS occur in less than 10% of patients, including crossed weakness or sensory deficits, hemianopia or quadrantanopsia, Horner syndrome, and cranial nerve signs, particularly oculomotor nerve palsy . Compared with ACIS, onset of stuttering neurologic deficits and nonfocal symptoms such as dizziness, vertigo, nausea/vomiting, and unsteadiness are more common in PCIS. These facts may result in delayed identification of PCIS in the clinical setting. Progressive stroke and precedent transient ischemic attack (TIA) symptoms have also been found more frequently in PCIS than in ACIS. The longest progression time being reported in PCIS is 14 days after the onset .
Besides LAA, CE, and SVO, there are two other causes that are reported more frequently in PCIS than in AICS. One is basilar artery atheromatous branch occlusive disease (BABO) with perforating artery occlusion at the openings. BABO results in paramedian brainstem (most commonly pontine) infarction, which mimics lacunar infarction (SVO) radiologically and clinically, although the former infarction is originated from large artery atherosclerotic disease and the latter is from small vessel disease . The other cause occurring more frequently in PCIS is arterial dissection, usually in younger individuals, than the other causes. Arterial dissections causing PCIS are most commonly initiated in the vertebral artery (VA). As in large artery atherosclerotic disease, intracranial arterial dissections [V4 part of VA and basilar artery (BA)] are involved more frequently in the Asian population with arterial dissection-related PCIS than in the Western population . Both BABO and arterial dissection need extensive or high-resolution imaging investigations of large artery vessel walls.
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