following atherothrombotic or lipohyalinotic occlusion of a small artery(
30 to 300 _m) in the brain. The term small-vessel stroke denotes
occlusion of such a small penetrating arteryand is now the preferred
term. Small-vessel strokes account for _20% of all strokes.
PATHOPHYSIOLOGY The MCA stem, the arteries comprising the circle of
Willis (A1 segment, anterior and posterior communicating arteries,
and P1 segment), and the basilar and vertebral arteries all give rise to
30- to 300-_m branches that penetrate the deep grayand white matter
of the cerebrum or brainstem (Fig. 349-3). Each of these small
branches can occlude either byatherothrombotic disease at its origin
or bythe development of lipohyalinotic thickening.
Thrombosis of
these vessels causes small infarcts that are referred to as lacunes (Latin
for “lake” of fluid noted at autopsy). They range in size from 3 mm
to 2 cm. Hypertension and age are the principal risk factors.
CLINICAL MANIFESTATIONS The most common lacunar syndromes are the
following: (1) Pure Motor Hemiparesis from an infarct in the posterior
limb of the Internal Capsule or basis pontis; the face, arm, and leg are
almost always involved; (2) pure sensory stroke from an infarct in the
ventrolateral thalamus; (3) ataxic hemiparesis from an infarct in the
base of the pons; (4) dysarthria and a clumsy hand or arm due to
infarction in the base of the pons or in the genu of the internal capsule;
and (5) pure Motor Hemiparesis with “motor (Broca’s) aphasia” due
to thrombotic occlusion of a lenticulostriate branch supplying the genu
and anterior limb of the internal capsule and adjacent white matter of
the corona radiata.
Transient symptoms (small vessel TIAs) may herald a small-vessel
infarct; theymay occur several times a day and last only a few minutes.
Recoveryfrom a small-vessel stroke often begins within hours or days,
and over weeks or months maybe nearly complete; in some cases,
however, there is severe permanent disability. Often, institution of
combined antithrombotic treatments does not prevent eventual stroke
in “stuttering lacunes.”
A large-vessel source (either thrombosis or embolism) maymanifest
initiallyas a lacunar syndrome with small-vessel infarction. Therefore,
the search for embolic sources (carotid and heart) should not be
completelyabandoned in the evaluation of these patients. Secondary
prevention of lacunar stroke involves risk factor modification, specificallyreduction
in blood pressure (see “Primary and Secondary Prevention,”
below).
