1 Acute Ischemic Stroke: Small Vessel Disease
Abstract
Small vessel disease (SVD) is the result of several pathophysiological mechanisms including lipohyalinosis, microatheroma, small emboli, and failure of cerebral autoregulation. Risk factors include aging, hypertension, diabetes mellitus, smoking, and genetics. Differential diagnoses include CADASIL, Susac′s disease, intraventricular lymphoma, sarcoidosis, and amyloid angiopathy. It mostly affects the brainstem (pons), basal ganglia, and internal capsule. Clinical presentation is variable and usually discrete. Classic presentations include pure motor or sensory hemiparesis, ataxic hemiparesis, and dysarthria–clumsy hand syndrome. Magnetic resonance imaging (MRI) is key to identify and manage SVD, and classic MRI findings include subcortical infarcts, lacunes, white matter hyperintensities, microbleeds, and brain atrophy. Main treatment in the acute phase includes alteplase (for those eligible patients). Secondary management consists of hypertension and dyslipidemia control, lifestyle modifications (reduce obesity and smoking cessation), and antiplatelet agents. Endovascular management has no role in the management of stroke and SVD.
Introduction
Small vessel disease (SVD) is responsible for approximately 20 to 30% of all strokes. They commonly occur in the basal ganglia, internal capsule, and pons. Recurrence is estimated to be relatively low at about 2% at 1 month and 3.4% at 3 months. The predominant cause of SVD is thought to be mostly lipohyalinosis secondary to fibrinoid necrosis. While advancing age is the most important risk factor, others include arterial hypertension, diabetes mellitus, and noncerebral vascular disease.
Several mechanisms for SVD and lacunar infarction have been described, and they include (1) lipohyalinosis of the penetrating arteries, particularly of smaller infarcts (3–7 mm in length); (2) microatheroma of the origin of the penetrating arteries coming off the middle cerebral artery (MCA) stem, circle of Willis, or distal basilar or vertebral arteries; (3) small emboli, which can be the cause of small vessel stroke; and (4) failure of the cerebral arteriolar and capillary endothelium and the associated blood–brain barrier.
Confluent SVD found on magnetic resonance imaging (MRI) shows faster progression than discrete lesions. Lacunar infarcts are small (0.2–15 mm in diameter), noncortical infarcts caused by occlusion of a single penetrating branch of a large cerebral artery. These branches arise at acute angles from the large arteries of the circle of Willis, stem of the MCA, or the basilar artery.
Major controversies in decision making addressed in this chapter include:
Indications for tissue-type plasminogen activator and the best medical treatment.
Workup necessary for differential diagnosis.
Lifestyle modifications.
Whether to Treat
Medical therapy is always indicated ( 1 in algorithm ). Acute ischemic stroke (AIS) should be considered a true neurological emergency. The decision to treat is based on many factors. Stroke severity, based on the level of the National Institutes of Health Stroke Scale (NIHSS) score, can be used to estimate the likelihood of AIS and confirmed with a noninvasive study.
Pathophysiology/Classification
SVD strokes are the result of two separate pathophysiologies that may occur separately or simultaneously. First, small penetrating arteries originate at right angles from large arteries to perforate the deep brain parenchyma. Hemodynamically, the structure of these perforating arteries undergoes great stress. The result is often called lipohyalinosis and results in gradual narrowing and occlusion of these arteries. Second, these small perforating arteries may be occluded by plaque forming in the large parent arteries and then occluding their origin. This is called intracranial branch atheromatous disease by Fisher and Caplan. Both lipohyalinotic and branch atheromatous diseases affect the deeper portions of the cerebral hemispheres to include the basal ganglia, thalamus, and brainstem. SVD can produce lacunar strokes in the superficial cortex/cerebellum. However, the pathophysiology of these strokes is more varied and includes hypertension, diabetes, CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy), Susac′s disease, intravascular lymphoma, cerebral amyloid angiopathy, and sarcoidosis ( 3 in algorithm ).
Workup
Workup for SVD should include a standard stroke workup: a complete physical and neurological examination, computed tomography (CT) of the head, CT angiogram, MRI including diffusion-weighted imaging, fluid-attenuated inversion recovery (FLAIR), apparent diffusion coefficient, gradient echo, carotid ultrasound, transthoracic echocardiogram with or without bubble study, lipid panel, and hemoglobin A1c.
Clinical Evaluation
There are more than 20 clinical syndromes associated with lacunar strokes. Clinical examination should demonstrate discrete, focal neurological deficits such as unilateral weakness, sensory loss without cortical findings of aphasia, visual deficits, or cognitive deficits. Importantly, these clinical syndromes can be produced by small hemorrhages. The four most classic clinical lacunar syndromes are described:
Pure motor hemiparesis: Unilateral motor deficit of the face, arm, and leg without cortical or sensory signs. The leg weakness is often less pronounced and a dysarthria may result from the facial weakness. The lesions are in the internal capsule, corona radiata, or basis pontis.
Pure sensory stroke: Unilateral hemisensory deficit of the face, arm, trunk, and leg. The sensory deficit is often subjective. Affected areas are the ventroposterolateral nucleus of the thalamus, corona radiate, parietal cortex, or medial lemniscus of the pons.
Ataxic hemiparesis: Paresis involves the leg more than the arm and much more than the face. Incoordination on the same side in the arm and leg. The affected toes are upgoing. The contralateral lesions are classically in the posterior limb of the internal capsule or basis pontis, and also include thalamocapsular, red nucleus, and superficial anterior cerebral artery lacunes.
Dysarthria–clumsy hand syndrome: Facial weakness, tongue deviation, dysarthria, dysphagia, loss of fine motor control of the hand, and upgoing toes. Lacunes are located contralaterally, usually in the basis pontis, and also in the internal capsule.
Imaging
MRI is key in identifying and managing SVD. Identifying features are subcortical infarcts, lacunes, white matter hyperintensities, microbleeds, and brain atrophy and may be coexistent with embolic strokes. About 30% of clinical lacunar syndromes are not accompanied by visible small subcortical infarcts (▶ Fig. 1.1 ). Lacunar infarcts are defined as those 3 to 20 mm in maximum diameter on axial imaging. Larger infarcts are not lacunar and smaller ones are likely to be perivascular spaces. Recent infarcts are those less than 2 weeks old. White matter hyperintensities are supportive of SVD and are best seen in FLAIR sequences. Microbleeds are 2 to 5 mm-diameter areas of hypointensity on T2 sequences. Microbleeds can be up to 10 mm in size. Brain atrophy unrelated to a specific infarction or trauma is supportive of SVD. This atrophy specifically affects the corpus callosum, white matter (vacuolar) shrinkage, increased ventricular size, basal ganglia, hippocampus, and cortical regions connected with subcortical infarcts.
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