THE CLINICAL study of Cupini et al1 in this issue of the ARCHIVES addresses a long-standing and vexing question, namely, what is the relationship between arteriolar hemodynamics and subcortical stroke? At the center of this question is the controversial lacuna, a 3- to 15-mm lesion first described by DeChambre in 1838.2 It is found in characteristic locations in deep subcortical white matter tracts subserved by noncollateralizing penetrating arterioles arising from proximal cerebral arteries. It was C. Miller Fisher who advanced the lacunar concept with descriptions of pathologic features in these arterioles and associated clinical syndromes.2 With smaller lacunae he described a distal subintimal arteriolar degeneration termed "lipohyalinosis"; these lesions were likely to be symptomatic only if strategically located in a sensory or motor tract. Larger lacunae, however, were associated with proximal occlusion or stenosis of the arteriole by "a tiny bead" of microatheroma. These larger lacunae were more likely to be symptomatic regardless of location. In some arterioles he found no pathologic features and, thus, speculated a role for embolism in exceptional cases. Fisher3 correlated his findings with the description of 21 lacunar syndromes, of which the pure motor, pure sensory, clumsy hand–dysarthria, and ataxic hemiparesis syndromes survive as clinically useful. Finally, he associated hypertension as an important causal factor of lacunae.
Dulli DA. Subcortical Infarctions, Transcranial Doppler, and Cerebral Vasomotor Reactivity. Arch Neurol. 2001;58(4):551-552. doi:10.1001/archneur.58.4.551