Occlusive Disease of Small Penetrating Arteries

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The small penetrating arteries deep within the brain parenchyma are the sites of various occlusive processes that are different from those of the larger arteries.

Pathogenesis and Pathophysiology. Lipohyalinosis, a destructive vasculopathy linked to severe hypertension, affects arteries 40 to 200 pm in diameter. The arterial lumen is compromised not by an intimal process but by thickening of the vessel wall itself. Subintimal lipid-laden foam cells and pink-staining fibrinoid material thicken the arterial walls, sometimes compressing the lumen. In places, the arteries are replaced by tangles and wisps of connective tissue that obliterate the usual vascular layers. The small, deep infarcts that result from occlusion of these arteries are usually called lacunes. [1 , y , y Small, deep infarcts can also result from miniature atheromas (microatheromas) that form at the origin of penetrating arteries, as well as by plaques within the parent arteries that obstruct or extend into the branches (junctional plaques). Rarely, they are occluded by microemboli (Fig. 45-5 (Figure Not Available) ). Vascular lesions involving the mouths of penetrating arteries are called intracranial branch atheromatous disease. [25]

A recently recognized entity named CADASIL (cerebral

Figure 45-5 (Figure Not Available) Branch atheromatous diseases of the basilar artery. (A) Plaque within parent artery blocking the branch artery orifice. (B) Plaque extends into the branch from the parent artery (junctional plaque). (C) Microatheroma originating in orifice of branch.(Adapted from Caplan LR: Intracranial branch atheromatous disease: A neglected, understudied, and underused concept. Neurology 1989:39:1246-1250: with permission.)

autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is a familial arterial disease of the brain that begins in early adult life. Its gene is mapped to chromosome 19. The CADASIL vasculopathy affects the media of leptomeningeal and perforating arteries of the brain. The media is thickened by an eosinophilic granular material of unknown origin. Clinically, patients present with recurrent subcortical infarcts, progressive or stepwise dementia, migraine with aura, and depression. Usually, there is no hypertension or other vascular risk factors. Prominent subcortical white matter and basal ganglia hyperintensities are noted on T2-weighted MRI. Vascular studies are usually not helpful diagnostically. y

Epidemiology and Risk Factors. Hypertension is the most significant risk factor for small vessel occlusive diseases and is responsible for about 80 to 90 percent of lacunar infarctions. In addition to hypertension, diabetes mellitus and smoking are also significantly associated with small vessel occlusive disease, particularly with branch atheromatous disease. Blacks and Asians, races with a predilection for hypertension, also have a higher frequency of penetrating artery disease and lacunar infarction than whites.

Clinical Features and Associated Disorders. The arteries commonly affected are the lenticulostriate branches of the MCAs, the thalamogeniculate and thalamoperforant branches of the PCAs, and midline and paramedian penetrating branches of the vertebral and basilar arteries ( .Fig 45-6 ). Infarcts do not involve the cerebral cortex but usually affect the subcortical structures such as the basal ganglia, thalamus, internal capsule, subcortical white matter, and brain stem. Clinical findings are characteristically less severe, neurological dysfunctions are restricted within a few systems, and cognitive and behavioral abnormalities

Figure 45-6 Penetrating arteries prone to lipohyalinosis and microaneurysms; the thalamogeniculate and lenticulostriate vessels and arteries to the (Adapted from Jones EF, Kalman JM, Calafiore P, et al: Proximal aortic atheroma. An independent risk factor for cerebral ischemia. Stroke 1995;26:218-224; with permission.)

are less common. Lacunar infarcts present diverse clinical syndromes. y

Deep infarcts in some regions such as the caudate nucleus, anterior thalamus, and genu of the internal capsule can produce apathy, inertia, and reduced interest in the environment. Bilateral extensive lacunar infarcts are often associated with white matter damage and clinical dementia. Neurological deficits in patients with lacunar infarction can progress gradually or stepwise for 1 to 7 days.

Differential Diagnosis and Evaluation. The major differential diagnostic considerations are restricted cortical and brain stem infarcts due to large artery occlusive disease or embolism and small ICHs. The diagnosis of penetrating artery disease is based on (1) the presence of risk factors, especially present or past hypertension, and diabetes; (2) clinical neurological symptoms and signs typical for or compatible with occlusion of a single perforating artery; and (3) CT or MRI showing a lacunar cerebral infarct or a brain stem infarct in the territory of a single penetrator, or at least no cortical infarct. In uncertain cases, vascular and cardiac imaging may be needed to clarify the diagnosis of penetrating versus large artery occlusive disease. [ii

Management. Treatment consists primarily of controlling the underlying causative process--hypertension. Antiplatelet agents have not been shown to be effective in this condition but are frequently prescribed. Heparin and warfarin anticoagulants are probably ineffective. No specific treatment is currently available for CADASIL.

Prognosis and Future Perspectives. Recovery from lacunar infarctions or branch atheromatous diseases is usually better than that from cortical infarctions. However, many patients develop recurrent lacunar infarcts and white matter ischemia. Dementia, pseudobulbar dysarthria and dysphagia, gait abnormalities, and parkinsonian-like stiffness are common features in patients with extensive brain damage caused by penetrating artery disease.

To date, there have been no controlled trials of patients with acute lacunar infarcts, but these are badly needed in the future. Also badly needed are studies of prevention of further brain damage in patients who already have lacunar infarcts and white matter damage.

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