Characteristics of intracranial branch atheromatous disease and its association with progressive motor deficits

Abstract

Background

Small deep brain infarcts are often caused by two different vascular pathologies: 1. atheromatous occlusion at the orifice of large caliber penetrating arteries termed branch atheromatous disease (BAD) and 2. lipohyalinotic degenerative changes termed lipohyalinotic degeneration (LD). We herein analyze and describe the characteristics of these 2 different pathologies.

Methods

We studied 394 patients with penetrating artery territory infarcts in the territories of the lenticulostriate arteries and anterior pontine arteries. Radiologically defined BAD of the lenticulostriate arteries was defined as infarcts with size more than 10 mm in diameter on axial slice and visible for 3 or more axial slices, and that of the anterior pontine arteries was defined as unilateral infarcts extending to the basal surface of the pons. Within each of the 2 territory groups, differences between BAD and LD were compared.

Results

Ninety five patients in the lenticulostriate arteries group (36.1%) and 78 patients in anterior pontine arteries group (59.5%) were classified as BAD. Initial NIHSS, incidence of progressive motor deficits and poor functional outcome were significantly higher and incidence of concomitant silent lacunar infarcts tended to be lower in BAD than LD. In logistic regression analysis, BAD compared with LD was independently associated with PMD, in lenticulostriate arteries group (OR: 4.21, p = 0.0001) and in anterior pontine arteries group (OR: 5.32, p = 0.0018).

Conclusions

Radiologically defined BAD and LD had different characteristics. BAD was significantly associated with progressive motor deficits and considered as a major vascular mechanism of progressive motor deficits in penetrating artery infarcts.

Introduction

Small deep brain infarcts that are predominantly caused by occlusion at the vessel orifices of lager caliber penetrating arteries by atheromatous plaque have been proposed as different stroke type from lipohyalinotic degeneration (LD), which is predominantly caused by lipohyalinotic degenerative changes within the course of penetrating arteries, coined as intracranial branch atheromatous disease (BAD) [1], [2], [3], [4].

Patients with pontine infarcts extending to the surface of the pontine base with atheromatous plaque occluding the orifice of the perforating branch of the basilar artery have been reported [5]. The validity of this condition has been confirmed by subsequent studies, and termed basilar artery branch disease [6], [7], [8], [9]. Basilar artery branch disease is often correlated with a progressive and fluctuating condition [5], [6], [9]. Atheromatous changes at the origin or proximal portion of a penetrating artery of larger caliber can also be observed in infarcts of the lenticulostriate as well as the anterior pontine arteries [10], [11]. The notion of basilar artery branch disease was then extended to the idea of intracranial BAD, encompassing not only basilar artery branch disease but also other specific arteries of larger caliber, such as the lenticulostriate, anterior choroidal, and thalamogenuculate arteries [4]. Platelet and platelet-fibrin plugs are presumed to play roles in the final narrowing or obstruction of the larger caliber penetrating arteries in BAD, often causing transient ischemic attacks (TIAs) or stepwise progression.

Branch atheromatous disease represents one of the important underlying mechanisms for progressive motor deficits in penetrating artery infarcts. Although various factors have been suggested to be correlated with progressive motor deficits [12], [13], [14], [15], [16], [17], [18], [19], only a limited number of reports address the mechanism of progressive motor deficits in terms of the vascular process. We conducted the present study to delineate the characteristics of radiologically defined BAD in reference to those of radiologically defined LD using the cohort on which we previously studied progressive motor deficits in penetrating artery territory infarcts [18].