What is Branch Atheromatous Disease (BAD)?

BAD refers to ischemic strokes caused by occlusion or stenosis of the origin og perforating arteries, usually due to atherosclerosis. It primarily affects the deep structures of the brain such as the basal ganglia, thalamus, and brainstem.

ISCHEMIC STROKE

Branch atheromatous disease (BAD)

David Goldemund M.D.
Updated on 08/10/2024, published on 24/09/2024

Branch atheromatous disease (BAD) or Branch Artery Disease is a subtype of ischemic stroke that results from the occlusion of small, penetrating arteries branching off major cerebral vessels. Unlike lacunar strokes caused by lipohyalinosis, BAD is attributed to microatheroma or plaque extension from parent arteries. Recognizing BAD is crucial due to its distinct pathophysiology, clinical presentation, and management implications.

Pathophysiology

BAD occurs when atherosclerotic plaques in the parent artery extend into the origin of penetrating branches, leading to their occlusion
this differs from small vessel disease (or penetrating artery disease) caused by lipohyalinosis, where intrinsic vessel wall degeneration is the primary cause
the occlusion in BAD affects a longer segment of the vessel, resulting in larger infarcts compared to lacunar strokes

Clinical presentation

the neurological deficit depends on the affected territory and the extent of ischemia
early neurological deterioration (END) is not uncommon (Li, 2024)
lesions typically involve the basal ganglia, thalamus, or brainstem

Diagnostic evaluation

Diffusion-weighted imaging (DWI) shows elongated or wedge-shaped infarcts extending from the parent artery
HR-MRI (3D CUBE T1 sequence) can detect pathological changes in the penetrating arteries (Li, 2016) (Yang, 2018)
computed tomography (CT) may show early signs of infarction but is less sensitive than MRI for small, deep infarcts
CT angiography may show atherosclerosis in the parent artery

Diagnostic criteria

progressive symptoms corresponding to deep penetrating artery territories
infarcts larger than 15 mm in length along the penetrating artery’s axis
cardioembolic sources and large artery atherosclerosis causing artery-to-artery embolism are excluded

Probable Branch Artery Disease (BAD) leading to pontine infarct.

Branch artery disese detected on high-resolution MRI (Miyaji, 2014)

Differential diagnosis

lacunar infarcts due to arteriolopathy (penetrating artery disease/small vessel disease)
- blockage occurs in small penetrating arteries due to wall thickening and subsequent lumen reduction
- lacunar infarcts are typically small (<15 mm) and rounded
- symptoms usually have an abrupt onset and are not progressive
- presentation: classic lacunar syndromes such as pure motor stroke, pure sensory stroke, or ataxic hemiparesis
atherosclerosis of large arteries – may cause cortical strokes or multiple infarcts
cardioembolic stroke – cortical involvement sometimes affecting multiple territories

Feature	Branch Atheromatous Disease (BAD)	Penetrating Artery Disease (PAD) / Small Vessel Disease (SVD)
Etiology	atherosclerosis	lipohyalinosis and fibrinoid necrosis
Pathophysiology	occlusion occurs at the origin of the penetrating artery due to plaque	occlusion occurs within the penetrating artery itself due to a diffuse vessel wall thickening
Infarct size and shape	larger, elongated, wedge-shaped infarcts along the axis of the penetrating artery (often >15 mm in length) infarcts often span the cortical-subcortical junction	smaller, rounded lacunar infarcts (typically <15 mm in diameter) in areas like the basal ganglia, thalamus, or internal capsule lesions are often isolated and do not extend to the cortex
Clinical onset and progression	symptoms may progress over hours due to gradual occlusion and extension of the infarct	symptoms usually have an abrupt onset and are typically non-progressive after the initial event
Common clinical presentations	progressive motor or sensory deficits brainstem syndromes if posterior circulation is involved	classic lacunar syndromes
Risk factors	atherosclerotic risk factors	atherosclerotic risk factors (particularly hypertension)
Prognosis	Generally worse than typical lacunar strokes larger infarct size with more significant deficits potential for symptom progression (early deterioration)	Generally better prognosis smaller infarct size less likelihood of symptom progression

Management

Acute stroke treatment

intravenous thrombolysis for eligible individuals
antiplatelet therapy (SAPT or short-term DAPT for mild stroke)

Stroke prevention

vascular risk factors control (hypertension, diabetes, dyslipidemia, and smoking cessation)
- high-dose statins for lipid control and plaque stabilization
long-term antiplatelet therapy to prevent recurrence

Prognosis

BAD-related strokes tend to have a worse prognosis than typical lacunar strokes due to larger infarct size and potential for progressive symptoms
early recognition and treatment are essential for improving outcomes