There are many other less frequent lacunar configurations but they can be identified by their similarity to one of the archetypal syndromes; they tend to affect one limited system or are fragments of a typical syndrome. Indeed, Fisher (1982) described 20 such variant types and several “miscellaneous” patterns. Some of these are difficult to accept, such as pure motor hemiparesis with confusion and loss of memory, but we have encountered many of the others, admittedly infrequently, including pure dysarthria, hemiballismus, virtual locked-in syndrome from bilateral lacunes in the base of the pons, and pure motor hemiplegia with sixth nerve palsy.
Some strokes that carry the term “lacune” are simply the result of larger deep cerebral infarctions along the lines of the striatocapsular stroke discussed earlier. In order to retain its clinical utility, the term lacune is probably best applied to small deep lesions that are the result of occlusion of a correspondingly small vessel and not to those strokes that result from occlusion of the orifices of several adjacent small vessels and are typically from larger atheromas in a parent vessel.
Multiple lacunar infarcts involving the corticospinal and corticobulbar tracts are a common cause of pseudobulbar palsy in clinical practice (trailed in frequency by amyotrophic lateral sclerosis and infiltrating tumors). Undoubtedly, an accumulation of lacunes deep in both hemispheres can give rise to gait disorders and also to mental dulling sometimes referred to as multiinfarct dementia (see further on and Chap. 20). The main differential diagnostic considerations are normal-pressure hydrocephalus (see Chap. 29) and the common degenerative brain conditions that affect the frontal lobes and basal ganglia (see Chap. 38).
Finally, it should be emphasized that what appears initially to be a lacunar syndrome may be the initial component or warning sign of a large deep territory infarction in the middle, posterior cerebral, or basilar arteries.
As mentioned earlier, MRI is more reliable than CT in demonstrating the lacunes. Initially, lacunes are seen on the MRI as deep oval or linear areas of T2, fluid-attenuated inversion recovery (FLAIR) and, especially, diffusion-weighted signal abnormality; later they become cavitated. Representative lacunar infarctions are shown in Fig. 33-17. The EEG, while little used for this purpose nowadays, may be helpful in a negative sense; in the case of lacunes in the pons or the internal capsule, there is a notable discrepancy between the unilateral paralysis or sensory loss and the negligible electrical changes over the affected hemisphere and, even with lacunes of the deep cerebrum, any EEG changes are disproportionately mild in comparison to the deficit.