Small Centrum ovale Infarcts – A Pathological Study

Abstract

There are limited data, mainly clinical and radiological, on small centrum ovale infarcts (SCOIs). From a consecutive series of 159 autopsy brains we identified 12 cases which on gross pathological examination harboured a total of 21 SCOIs. In the majority of lesions histology revealed a significant component of incompletely infarcted brain. Clinicopathological data suggested that the underlying mechanism was likely to have been cardioembolic in 3 cases, and possibly embolic from heart or aortic arch in a further 5. Two cases were due to ipsilateral carotid artery atheroma (i.e. 10 of 12 cases had possible embolic sources). The majority of lesions appeared to lie in arterial borderzones. The combined data suggest that SCOIs are pathologically and pathogenetically heterogeneous, and therefore that the term ‘lacune’ is inappropriate because this implies intrinsic small vessel disease as the underlying cause. Clinically, potentially treatable cardiac and large vessel pathology should be excluded.

Cavitation of Deep Lacunar Infarcts in Patients With First-Ever Lacunar Stroke

“…We did not include lacunar infarcts in the centrum semiovale in contrast to these 2 studies, because the centrum semiovale is generally supplied by medullary branches of the cortical arteries and these infarcts may have different causes than those arising in the territory of the deep perforators. [5][6][7] It may also be that the deep gray and white matter respond differently to lacunar damage, gray matter being more likely to cavitate than white matter. It would be interesting to directly compare cavitation rates between small deep and centrum semiovale infarcts.…”

“…There is some evidence that although lacunar infarcts in the deep brain regions are caused by cerebral small vessel disease, lacunar infarcts in the centrum semiovale have different causes. [5][6][7] We studied cavitation of symptomatic lacunar infarcts in the basal ganglia, pons, and internal capsule, for which there was no other cause than intrinsic cerebral small vessel disease, in patients with first-ever lacunar stroke, all of whom had a 2-year follow-up MRI.…”

Long Insular Artery Infarction: Characteristics of a Previously Unrecognized Entity

“…Most important, an embolic mechanism has also been suggested for WMMA infarction. [3][4][5][6] Because LIAs are a subtype of WMMA, the pathogenesis of the LIA infarction could be similar to that of the WMMA infarction. The size or shape of LIA and LSA infarcts corresponds with so-called lacunar infarction, for which stroke physicians often place a low priority for the evaluation of embolic sources and frequently recommend antiplatelet agents, because this pathology has been regarded as a small-vessel disease.…”

“…[1][2][3][4][5][6][7][8] Among the deep penetrating arteries, the lenticulostriate arteries (LSAs) arise from the M1 segment of the MCA and supply the lower part of the corona radiata. [7][8][9][10] The superficial penetrating arteries, namely the white matter medullary arteries (WMMAs), arise from the cortical branches of the MCA and feed the periventricular deep white matter.…”

“…[7][8][9][10] The superficial penetrating arteries, namely the white matter medullary arteries (WMMAs), arise from the cortical branches of the MCA and feed the periventricular deep white matter. [1][2][3][4][5][6] Several reports suggest that WMMA infarction should be distinguished from LSA infarction and treated differently because of their different clinical and etiologic backgrounds. [4][5][6] The long insular artery (LIA) is a unique supplier of the periventricular white matter.…”