Can Lacunar Infarcts be Caused by Carotid Stenosis?
Abstracts & Commentary
Sources: Overell JR, et al. Association between carotid disease and ipsilateral lacunar stroke. Poster 187, p. 60. Abstract from the 25th International Stroke Conference, February 2000; Inzitari D, et al. Risk factors and outcome of patients with carotid artery stenosis presenting with lacunar stroke. Neurology 2000;54: 660-666.
Lacunar strokes have traditionally been con-sidered to arise from microcirculatory disturbances at the level of the small perforating arteries. Published literature does not support extracranial carotid disease as an etiological factor. However, two recent reports indicate that ipsilateral carotid stenosis may be a contributing factor in producing a significant subset of lacunar strokes.
Overell and colleagues report on 98 patients presenting with clinical or neuroimaging (CT/MRI) evidence of unilateral subcortical disease and a single stenotic carotid artery. Sixty-four patients had carotid stenosis ipsilateral to their stroke, compared to 34 who had a contralateral stenosis. Lacunes had a chi-square association of P < 0.003 with the ipsilateral strokes. These data suggest that lacunes could be a manifestation of symptomatic carotid stenosis.
Inzitari and associates also examine the relationship between carotid artery stenosis and lacunar stroke. A total of 43% of patients in the North American Symptomatic Carotid Endarterectomy Trial (NASCET) group had lacunar strokes as their entry event, defined by their clinical syndrome. The majority of these were confirmed on neuroimaging. Infarctions in the deep subcortical internal carotid artery border zone territory were not classified as lacunes. Patients with lacunar strokes tended to have lesser degrees of carotid stenosis. However, among patients with the most severe degrees of carotid stenoses (70-99%), one-third presented with a lacune. The benefit of carotid endarterectomy (CE) for patients with a lacune as their qualifying event was a 35% stroke risk reduction at three years. This reduction is several orders of magnitude lower than what is reported among patients presenting with a cortical hemispheric stroke (61%). Both Overell et al and Inzitari et al nevertheless conclude that CE is indicated for patients with ipsilateral carotid stenosis and a corresponding lacune. They suggest that stroke in these patients is due to small emboli from stenotic carotid lesions lodging in the deep penetrating arteries.
These data demonstrate that emboli and low flow may be alternative pathophysiologic mechanisms in lacunar stroke. Subcortical areas such as the anterior limb of the internal capsule and the caudate head are in a border zone between the deep and cortical perforating branches of the anterior and middle cerebral arteries. Strokes in these territories may thus be hemodynamic insults mediated by severe carotid stenosis.
The alternative mechanism as speculated by the NASCET investigators is artery-to-artery embolism from the carotid to a penetrating artery.
Given these possibilities, a carotid evaluation should be strongly considered in the investigation of what has, until now, been largely believed to be a local microcirculatory disease. —ak & azs (Dr. Ayeesha Kamal is a Chief Resident of Neurology at New York Presbyterian Hospital.)
Cerebral lacunes ipsilateral to a stenotic carotid artery are equal to or more than approximately what percentage as frequent than on the nonstenotic carotid artery hemisphere?