Branch Atheromatous Disease: A Clinically Meaningful, Yet Unproven Concept

Abstract

Background: In 1989, Louis Caplan first used the term branch atheromatous disease (BAD) to describe an occlusion or stenosis at the origin of a deep penetrating artery of the brain, associated with a microatheroma or a junctional plaque, and leading to an internal capsule or pontine small infarct. BAD remained an understudied concept for decades. In recent years, the increasing diffusion of high-resolution magnetic resonance imaging (HRMRI) techniques brought new attention to the BAD debate. We have reviewed clinical studies dealing with BAD-related stroke checking whether a univocal definition of BAD existed, as well as to what extent were consistently associated clinical and imaging features reported. Summary: We conducted a search of the available literature published up to October 20, 2015 via PubMed using the following search terms: ‘branch atheromatous disease,' ‘intracranial branch atheromatous disease,' ‘cerebral branch atheromatous disease,' combined with ‘stroke.' Forty-six articles were included. We found discrepant definitions and a large variation among clinical features reported in BAD-related stroke patients: among others, a consistent association between BAD and any specific vascular risk factor profile was not detected. Despite this, early neurological deterioration (END) was consistently reported to occur frequently in such patients, although no clear-cut rate range or specific predictor or mechanism of progression was established. In a majority of the studies reporting imaging data, BAD diagnosis was not based on the selective site or type of arterial walls changes, but was inferred based on the vascular territory, size and/or shape of the ischemic lesion. Following the concept that these changes are seated proximally along the perforator artery, differently from to lipohyalinosis changes located distally, the consequent ischemic lesion was hypothesized to be larger in BAD than in lacunar infarcts. However, across reviewed studies, there was little consistency on the dimensional cutoff used to define BAD-related infarcts. In the last few years, a still limited number of studies using HRMRI techniques is providing preliminary proofs that atheromatous changes causing selective remodeling in the parent vessel and extending through the proximal segment of perforating vessel may subtend BAD. Key Messages: Our literature search showed the lack of a clear-cut definition of BAD, although BAD-related strokes were consistently considered a high risk of END. The use of high-resolution imaging techniques in the assessment of small subcortical strokes may represent the cornerstone in the perspective to better delimiting the boundaries of BAD as a nosological entity.

Greater periventricular white matter hyperintensity severity in basilar artery branch atheromatous disease

“…Consistent with the pathological and clinical evidence for atherosclerotic large-artery disease involvement in BABAD [3, 4, 18], we also found a high frequency of severe large artery atherosclerotic stenosis (ICA and MCA) in BABAD patients. Considering WMH is a commonly used SVD marker [7–13], the vascular risk factor-adjusted finding of greater WMH severity in the BABAD group compared to the NS and LAA groups implies that SVD is also involvement in the pathophysiology of BABAD.…”

Microbleeds of Lacunar Infarction and Middle Cerebral Artery Flow Velocity of Branch Atheromatous Disease Are Essential Factors of Stroke Etiology

“…The definition of larger size has the same meaning as branch atheromatous disease (BAD). Although the term BAD was originally created based on pathological findings [15], studies based on neuroimaging have increased in accordance with the progress of MRI [16]. In many studies, BAD was defined as a diameter > 1.5 mm and/or the appearance of a lesion on > 3 consecutive slices on MRI [7,17].…”

Ultra-Early Combination Antiplatelet Therapy with Cilostazol for the Prevention of Branch Atheromatous Disease: A Multicenter Prospective Study

“…Regarding obesity, although a significant difference was shown in multivariate analysis, perhaps due to the smaller sample size compared to other factors, obesity may be less likely to be a direct factor involved in the poor BAD prognosis. Moreover, it is interesting to note that results from a recent review by Inzitari and colleagues [8] showed no consistent associated vascular risk factors or predictors of progression for BAD. Finally, reports on the use of intravenous medication have been controversial.…”

“…1a, b). Historically, pathological studies have been used to identify mechanisms of stroke; however, in recent years, high-resolution and high-field magnetic resonance imaging (MRI) have been used to further delineate the intracranial vessel wall morphology in small-vessel occlusive disease [7,8]. However, currently there is no corresponding cerebrovascular disorder classification in the National Institute of Neurological Disorders and Stroke (NINDS) [9] or diagnostic criteria in the Trial of Org 10172 in Acute Stroke Treatment (TOAST) [10].…”

“…However, currently there is no corresponding cerebrovascular disorder classification in the National Institute of Neurological Disorders and Stroke (NINDS) [9] or diagnostic criteria in the Trial of Org 10172 in Acute Stroke Treatment (TOAST) [10]. Moreover, a recent review of BAD studies concluded that the fundamental definition of BAD as well as the mechanisms and rate of clinical progression are still unclear, yet BAD was frequently reported to be associated with early neurological deterioration [8]. …”