Please wait while the transcript is being prepared...
0:00
Hi, everyone. My name
is Andreas Charidimou.
I'm a Neurologist at
Boston University
and I'm a researcher in
the field of cerebral
amyloid angiopathy.
My talk today as part of
these series is about
diagnostic aspects
with a heavy focus on
the Boston criteria and updates
on the Boston criteria.
0:23
I will cover some basics on
the clinical MRI
diagnosis of CAA,
especially the new
Boston criteria which
are termed version
2.0 and then go
through some very key
clinical questions
and frameworks and
challenges when we use
this criteria to make a
clinical MRI diagnosis of CAA.
I will not be going
into the details of
the Boston criteria version
2 validation study because
everything can be found in
the Lancet Urology paper from
2022 that you can see
here in my slide.
0:56
We all know that cerebral
amyloid angiopathy
now encompasses a
range of syndromes.
At the most basic form,
CAA denotes a common
neuropathology
in the brain which is affecting
the superficial
small vessels and is
very common in the
elderly individuals.
In most of these elderly
individuals, this pathology,
it's there but often causes
no symptoms and it's
an incidental MRI finding or
an MRI done for
any other reason.
In certain patients,
cerebral amyloid
angiopathy when it's
more advanced or when
it's interacting with
other pathologies can
present with a range of
symptoms and we can
conceptualize these
into three categories.
There are patients we see
in the stroke clinics or
the hemorrhagic stroke service
who present with
hemorrhagic stroke.
This includes lobar
intracerebral
hemorrhage or acute convexity
subarachnoid hemorrhage
which typically leads to
transient focal
neurological episodes.
The other big group
of presentations is
in a memory clinic and these
patients might present
either with vascular-type
cognitive impairment because of
advanced CAA or CAA
might be a co-pathology
in Alzheimer's disease.
A third group of
presentation is related to
CAA and inflammation and
we have two syndromes.
We have spontaneous CAA-related
inflammation and we
have ARIA or amyloid-related
imaging abnormalities,
which is essentially iatrogenic
CAA-related inflammation in
the setting of
anti-amyloid treatments
for patients with
Alzheimer's disease.
Drugs like lecanemab,
donanemab and anti-amyloid
antibodies in
general lead to this syndrome
of brain edema and
bleeding into the brain.
