Pathophysiology Of Multiple Sclerosis

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The risk of stroke increases with age and is higher in men than in women at any age. Major risk factors include arterial hypertension (> 140mmHg systolic, > 90mmHg diastolic), diabetes mellitus, heart disease, cigarette smoking, hyperlipoproteinemia (total cholesterol > 5.0 mmol/l, LDL > 3mmol/l, HDL < 0.9-1.2 mmol/l), elevated plasma fibrinogen, and obesity. Symptomatic or asymptomatic carotid artery stenosis, elevated plasma homocysteine levels, erythrocytosis, anti-phospholipid antibodies, alcohol abuse (>60g of alcohol @ 75 cl of wine per day in men, > 40 g in women). Drug abuse (amphetamines, heroin, cocaine), a sedentary lifestyle, and low socioeconomic status (unemployment, poverty) also increase the risk of stroke.

Embolism (ca. 70%) is the most common cause of stroke. Emboli arise from local atheromatous lesions (atheromatous thromboembolism) on the walls of large arteries (macroangiopathy) of the brain or heart (cardiac embolism in atrial fibrillation, valvular heart disease, ventricular thrombus, and myxoma). Thrombosis (ca. 25%). Occlusion of a small end-artery (microangiopathy, small vessel disease) causes lacunar infarction. The cause is hyaline (lipohyalinosis)orproximalsclerosisof penetrating arteries (lenticulostriate, thalamoperforating or pontine arteries, central branches). Causal factors include hypertension, diabetes, and blood-brain barrier disruption leading to deposition of plasma proteins in the arterial wall. Microan-giopathy-related hemodynamic changes sometimes cause hemodynamic infarction. Rare causes (ca. 5 %) include hematological diseases (e. g., coagulopathy, abnormal blood viscosity, anemia, leukemia) and arterial processes (dissection, vasculitis, migraine, fibromuscular dysplasia, moyamoya, vasospasm, amyloid angiopathy, and CADASIL = cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy).

■ Infarct Types

Lacunar infarcts ("small deep infarcts"). Lacunes are small (< 1.5 cm in diameter), round or oval infarcts in the subcortical periventricular region or brain stem. Classic lacunar syndromes include purely motor hemiparesis (internal capsule, corona radiata, pons), contralateral purely sensory deficit (thalamus, internal capsule), ataxic hemiparesis (internal capsule, corona radiata, pons), and dysarthria with clumsiness of one hand (= clumsy hand-dysarthria syndrome; internal capsule, pons). The presence of multiple supratentorial and infratentorial lacunes is termed the lacunar state ("état lacunaire") and is clinically characterized by pseudobulbar palsy (p. 367), small-step gait ("marche à petit pas"), urinary incontinence, and affective disorders (compulsive crying). For leukoaraiosis, see p. 298.

Territorial infarcts are those limited to the distribution of the ACA, MCA, or PCA. With the exception of striatocapsular infarcts (internal capsule, basal ganglia), these infarcts are predominantly cortical. Embolic territorial infarcts often undergo secondary hemorrhage ("hemorrhagic conversion").

End zone infarcts. Low-flow infarction in the subcortical white matter is due to extracranial high-grade vessel stenosis and/or inadequate collateral flow.

Border zone infarcts (p. 168) also result from hemodynamic disturbances due to microan-giopathy. They are found at the interface ("watershed") between adjacent vascular territories, and can be either anterior (MCA-ACA ^ contralateral hemiparesis and hemisensory deficit, mainly in the lower limb and sparing the face, with or without aphasia) or posterior (MCA-PCA ^ contralateral hemianopsia and cortical sensory deficit, with or without aphasia). Global cerebral hypoxia/ischemia. The causes include cardiac arrest with delayed resuscitation, hemorrhagic shock, suffocation, and carbon monoxide poisoning. Global cerebral hy-poxia/ischemia causes bilateral necrosis of brain tissue, particularly in the basal ganglia and white matter.

Basal ganglia Thalamus

Arterio-arterial thrombo-emboli

Thrombus (source of embolism) -

Atherosclerosis (plaque)-

Thrombi Embolus

Basal ganglia Thalamus

Arterio-arterial thrombo-emboli

Territorial Infarction

genic thromboemboli

Sources of thromboembolism

Border zone infarcts

genic thromboemboli

Sources of thromboembolism

Territorial infarct

(middle cerebral a.)

End zone infarcts

Border zone infarcts

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