Small Artery Occlusive Diseases

Introduction

Two Different Subtypes of Small Artery Occlusive Diseases

Small artery occlusive diseases, known as lacunar stroke, constitute approximately 25% of ischemic strokes and are particularly frequent among Hispanics and Asians. C. Miller Fisher performed detailed clinicopathological examinations and described two different subtypes of lacunar strokes: those caused by an intrinsic disease of the small arteries (40–200 μm diameter) categorized as small artery disease such as arteriolosclerosis, lipohyalinosis, or fibrinoid necrosis, and those caused by proximal atherosclerotic disease of the larger-caliber perforating arteries (200–850 μm diameter) .

Small Multiple Lacunar Infarctions

Intrinsic disease of the small arteries tends to occur as small multiple infarcts with leukoaraiosis and usually asymptomatic lacunar infarcts. Prognosis for mortality, recurrent stroke, cognitive impairment, and overall functional outcome in patients with lacunar stroke with multiple silent lacunar lesions is known to be more unfavorable than in patients with single lacunar infarction .

Branch Atheromatous Disease and Progressive Motor Deficits

Conversely, a single lacunar infarction associated with proximal atherosclerotic disease tends to show progressive motor deficits during the acute stage. Single perforating artery territory infarction caused by focal atherosclerotic disease of the termed branch atheromatous disease (BAD) . For example, single infarction in the territory of the lenticulostriate artery (LSA) with BAD mechanism may be located adjacent to the middle cerebral artery (MCA) and visible in multiple axial slices on MRI. Unilateral infarction in the territory of the paramedian pontine arteries with BAD mechanism may extend to the surface of the pontine base. Studies reported BAD was more often associated with atherosclerotic markers such as coronary artery disease and intracranial atherosclerosis but had a lower prevalence of small artery disease markers such as leukoaraiosis, multiple small lacunar infarcts, and microbleeds . In our study of 394 consecutive patients with penetrating artery territory infarcts, 95 patients in the territory of LSA (36.1%) and 78 patients in the territory of paramedian pontine artery (59.5%) were classified as BAD. Among BAD type, progressive motor deficits were found in 40% in the LSA and 41% in the paramedian pontine artery . A single lacunar infarct associated with atherosclerosis should be treated so as not to lead to progressive motor deficits in the acute stage, whereas small multiple infarcts should be carefully tracked to avoid recurrent stroke and progressive cognitive decline.

Characteristics of Small Artery Occlusive Diseases on Specific Arteries

Anterior Choroidal Arteries

Vascular Supply

The anterior choroidal artery (AChA) is a small artery that originates from the internal carotid artery (ICA) 2–5 mm distal to the posterior communicant artery (PComA) in diameter between 90 and 600 μm. The AChA supplies the zone between the striatum anterolaterally and the thalamus posteromedially. The AChAs initially course posteromedially within the carotid cistern and run posterolaterally within the crural cistern and terminate at the inferior limit of the choroidal fissure to supply the choroid plexus. The very proximal perforators supply the optic tract, medial segment of the globus pallidus, and the genu of the internal capsule. The next branches supply the temporal structures, such as the uncus, piriform cortex, amygdala, and head of the hippocampus. The third branches supply the middle third of the cerebral peduncle, substantia nigra, and red nucleus. The most distal perforating arteries vary in size from 200 to 610 μm, supply the posterior two-thirds of the posterior limb of the internal capsule, the tail of the caudate nucleus, the lateral geniculate body, the retrolenticular part including the origin of the geniculocalcarine tract, and the auditory radiation and lateral thalamic nuclei .

The posterior limb of the internal capsule, optic tract, lateral geniculate body, medial temporal lobe, and medial part of the pallidum are universally recognized as AChA supplied areas . Whether or not the vascular supply to the anterior limb of the internal capsule, genu of the internal capsule, posterior part of the putamen, substantia nigra, red nucleus, and posterior corona radiata is derived from the AChA remains a source of controversy.

Clinical Symptoms

The clinical symptoms related to AChA territory infarcts are variable because the AChA supplies various anatomical areas. The most common findings are contralateral hemiparesis, contralateral hemihypesthesia, and dysarthria. Sohn et al. studied 127 patients with AChA infarction and found dysarthria in 108 patients (85.0%), hemiparesis in 103 patients (81.1%), and facial palsy in 93 patients (73.2%) . In our study of 192 consecutive patients with AChA territory infarction, progressive motor deficits were found in 31 patients (16.3%), whereas progressive motor deficits were noted in 27.4% in 431 patients with lenticulostriate artery territory infarction during the same period. Contralateral sensory abnormalities are variable and mostly identified as sensorimotor syndrome. Ipsilateral visual field defect (homonymous hemianopia/quadrantanopia/sectoranopia) is variable depending on the involvement of the lateral geniculate body and the geniculocalcarine tract. Although the AChA supply the hilum and the anterolateral portion of the lateral geniculate body, the lateral choroidal arteries from the posterior cerebral artery (PCA) supply the medial and posterior portions. The most common visual field defects are a homonymous hemianopia, an upper quadrantanopia, and a quadruple sectoranopia.

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