Lacunar strokes tend to evolve quickly but not typically as suddenly as an embolus, for example. These clinical aspects are discussed extensively in the earlier section “Lacunar TIA.” In broad terms, the essential feature of these deep strokes is the striking absence of cortical deficits; that is, seizures, aphasia or amnesia (except in limited circumstances of small thalamic infarction), agnosia, apraxia, dysgraphia, alexia, and a number of cognitive changes. Multiple deep strokes can result in a dementia of the type discussed in Chap. 20. Furthermore, because of the small size of the strokes, certain clinical syndromes that might be expected to result from deep lesions, such as hemianopia, also do not occur. Fisher, in several papers (1965a, 1967, 1979) and in an iconic review 1965b, delineated the most frequent symptomatic forms of lacunar stroke: 1. Pure motor hemiplegia 2. Pure sensory stroke 3. Clumsy hand–dysarthria 4. Ipsilateral hemiparesis–ataxia
A lacune in the territory of a lenticulostriate artery, that is, in the internal capsule or adjacent corona radiata, usually causes a highly characteristic syndrome of pure motor hemiplegia involving the opposite face, arm, hand, leg, and foot in approximately equal measure. A lacune situated in the ventral pons causes an identical syndrome as discussed in an earlier section (Fig. 33-17). Most often the symptoms begin abruptly but not as rapidly as in embolic infarction, or evolve over several hours; in rare instances the neurologic deficit evolves stepwise and relatively slowly, exceptionally over as long a period as 2 to 3 days. Our experience has tended toward the shorter time frame, with most patients reporting that the full deficit is present not instantaneously but within minutes. Recovery, which may begin within hours, days, or weeks, is sometimes nearly complete even in the face of a severe initial stroke. However, many patients are left with some degree of clumsiness or slowness of movement of the affected side.
The motor disorder may take the form of a hemiparesis of the face and arm or arm and leg, or predominantly arm and proximal leg weakness; these fragmented patterns are indicative of a lesion located higher than the internal capsule, in the centrum semiovale. In these cases, the stroke simulates an embolic stroke affecting the cortex.
A lacune of the lateral thalamus or (less often of the deep parietal white matter) is the cause of hemisensory defect involving the limbs, face, and trunk extending to the midline with no motor or language difficulty, a pure sensory stroke. Partial sensory syndromes involving only parts of the hemibody are less frequent than in motor lacunar strokes. The incidence, course, and outcome are much the same as in a pure hemiplegia.
As mentioned, in the ventral pons, the lacunar syndrome may be one of pure motor hemiplegia, mimicking that of internal capsular infarction except at times for relative sparing of the face and the presence of an ipsilateral paresis of conjugate gaze in some cases; or there is another highly characteristic lacunar syndrome of a combination of dysarthria and clumsiness of one hand. This “clumsy hand–dysarthria” stroke is usually located in the paramedian midpons or in the posterior portion of the internal capsule opposite the affected limb. Occasionally, a lacunar infarction of the pons, midbrain, internal capsule, or parietal white matter gives rise to a hemiparesis with ataxia on the same side as the weakness (Fisher, 1965a; Sage and Lepore). Some of the brainstem syndromes may blend with basilar branch syndromes.