Intracranial Branch Atheromatous Disease (iBAD)

Intracranial Branch
Atheromatous Disease (iBAD)
Ross L Levine MD, FAHA, FAAN
Spring 2012

Case
78 yo man
Onset of slurred speech, increasing
dysphagia, and R-sided weakness
about 7 days PTA
Initially refused to come to the ED
but because of progressive worsening
and an inability to walk was
eventually convinced to be evaluated

PMHx
Prior R capsular stroke
HBP
DM
CAD
Dyslipidemia
Former smoker and heavy drinker

Exam
No bruits
BP, HR okay
Fairly sleepy but when aroused had
severe, mixed dysarthria (spastic-plusscanning)
Bifacial diplegia, brisk jaw jerk
R > L UMN signs

Case
57 yo man awoke with severe
R-sided weakness and dysarthria
Initial BP of 233/126
On exam
R F/UE/LE flaccid weakness
Flaccid dysarthria

PMHx
Untreated HBP
Untreated dyslipidemia
Smoking
Depression

Neurology 1989;39:1246-1250

Pathology of iBAD
Three proposed disease states
Luminal plaques
Obstructing a branch artery
Functional plaques
Extending into a branch artery
Microatheroma
Forming within the orifice of a branch
artery

In the final narrowing of a branch artery
Micro-dissection
Hemorrhage into a plaque
Platelet and platelet-fibrin plugs
The infarct resulting from occlusion of
the mouth of a branch artery
Can extend to the basal surface
Forms an ‘island’ of ischemic tissue within
the parenchyma

Clinical Issues that Suggest the
Likelihood of iBAD
Branch disease is inferred clinically
when
The infarcts are small and deep
Confined to the territory of 1 or a few
penetrating arteries
The infarct abuts the basal surface
The pace and tempo of the ischemia
TIAs or gradual or stepwise progression of
SSx suggests intrinsic ‘thrombotic’ disease
rather than occult embolism

Branch disease inferred clinically
when
Vascular diagnostic studies
Show no important large vessel athero
Show no cardiogenic source of embolism
There is no past or present
HBP
Evidence of end-organ effects of HBP
such as retinopathy or LVH

Specific Arteries and Syndromes
Lenticulostriate branches
Series of curving vessels that originate from
the mainstem MCA or its upper division
Features favoring branch disease
Not hypertensive
Often diabetic, non-white
Often with infarcts that are larger than the
expected infarct with a single lenticulostriate
occlusion
Do not have MCA disease or proximal embolic
source

Thalamogeniculate branches
Usually there is a ‘fan’ of
thalamogeniculate arteries arising from
the PCA
Features favoring branch disease
Diabetic, dyslipidemic
Normal angiography
Contralateral sensory stroke of F/UE/LE
and ataxia or chorea in the same limbs

Anterior choroidal artery
Branches directly from the ICA at the siphon
Larger than the previous infarcts
Prevalent in DM, non-whites
Clinical picture
Many w/o SSx
Many w/ isolated hemiparesis, hemianopia, or
combined hemiparetic/hemisensory/hemianopic
SSx contralateral to the infarct
NEG angios, no proximal embolic source

Huebner’s artery
Usually there are 2 and sometimes 4
or more parallel recurrent arteries
arising from the proximal ACA
Supplies anterior basal ganglia and
basal frontal areas
Occlusion of 1 or more
Infarction in the caudate
Sometimes also in capsule, putamen

Huebner’s-cont-
Clinical picture
Dysarthria
Slight or moderate hemi-motor dysfunction
Abulia, agitation, neglect, or dysphasia
Features
MOST are hypertensive and/or diabetic
NO severe ACA occlusive disease

Thalamoperforating artery branches
Polar artery (tuberothalamic)
From PComm
Supplies anteromedial, anterolateral
thalamus
Infarctions result in abulia, minor motor
changes, facial asymmetries, subtle
dysphasia or left visual neglect
OFTEN
Basilar plaquing and no proximal embolic
source

Thalamic-subthalamic artery
Arises from proximal PCA
Supplies medial thalamus with R and L
arteries or both off a common trunk
Unilateral infarction
Amnestic, upgaze palsy
Bilateral infarction
Decreased LOC, hypersomnolence

Thalamic-subthalamic a.-cont-
OFTEN
Basilar plaquing
No proximal embolic source
IF an embolic source and ‘top of the BA
syndrome’, then the occipital and temporal
lobes are infarcted to some degree as well

Paramedian and short circumferential
basilar artery branches
Pontine paramedian branches
ONLY proven branch disease to date
Pure motor hemiplegia
Or motor deficits w/ ataxia and dysarthria
And occasionally diplopia and paresthesias

Dx of Branch Atheromatous
Disease
By exclusion of alternative
possibilities
And by recognizing a presentation
that might fit into the syndromes so
described

Doubters Often Argue
Since hypertensive patients are also
predisposed to accelerated athero
and thus branch disease
Branch disease and lipohyalinosis cannot
easily be distinguished in HBP-patients
Branch disease cannot be easily be
separated from occlusion of branches
by emboli arising in irregular proximal
large artery plaques

Does the Treatment Differ?
Need to Rx HBP, if it is present,
anyway
If proximal and non-stenotic large
vessels are present,
statins/antiplatelet agents
Once we are able to DEFINE branch
atheromatous disease clinically and
CONFIRM the Dx technologically, we
can then decide BETTER therapies

Neurology 2012;78:888-896

Analyzed 201 consecutive pts w acute
MCA infarcts but with no demonstrable
carotid or cardiac embolism source
BOD (n=46)
Subcortical infarcts w MCA stenosis
Non-BOD (n=52)
Infarcts beyond the subcortical area
w MCA stenosis
SAD (n=103)

HBP and current smoking were more
prevalent in the non-BOD group
The relevant MCA had more severe
and focal stenosis in the non-BOD
than in the BOD group
76.9% vs 28.3%
Non-relevant stenosis was more
prevalent in the BOD than in the
SAD group