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Hello. My name is
Jean-Claude Baron.
I'm a Neurologist,
and Neuroscientist
with two affiliations,
one in Paris University
and Sainte-Anne Hospital,
and the other one as
Emeritus Professor of
Stroke Medicine at the
University of Cambridge, UK.
My talk today will be about "Positron Emission Tomography, PET
in Cerebral Amyloid Angiopathy" which is acronymed as CAA.
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Before going into PET,
let's go quickly over
the main challenges
currently facing CAA
in the clinical world.
The first main
challenge is how to
diagnose these conditions
without pathological material,
which is the most common
situation by far.
The correct diagnosis is
based on the so-called
Boston criteria,
which are mainly based on
MRI, hemorrhagic markers.
These Boston criteria have
very good specificity
around 90%,
meaning there are
few false positives.
But the sensitivity
is not very good,
around 70% with many
false negatives.
A recent update of
the Boston criteria
has included some white
matter changes on MRI,
which has improved
sensitivity to 75%,
but at the cost of losing
some specificity at 85%.
This means we are currently
able to make a diagnosis
of probable CAA,
which is a probabilistic
diagnosis,
which can be wrong
by definition.
When the criteria for
probable CAA are not met,
we talk about possible CAA,
which really is not helpful
in managing patients.
This situation is
because there are
many other causes of
lobar haemorrhage,
which is the main
presentation of CAA.
Of course, there
are local causes
which can be diagnosed usually
quite easily using
advanced imaging.
But the main
differential diagnosis
is with hypertensive
arteriolopathy,
which is the other main type
of cerebral small
vessel disease.
Knowing that CAA accounts for
only about half of all
nuclear cause lobar ICH.
Why is it important to
make the diagnosis of CAA?
It's mainly because
of the high risk
of recurrent ICH,
intracerebral haemorrhage,
which can be precipitated
by antithrombotics,
which as you know,
are highly prescribed
in elderly people.
Therefore there is a real
need to differentiate
CAA-related ICH from hypertensive
arteriolopathy-related ICH.
There are also non-ICH
presentations of
CAA such as cognitive
complaints.
Sometimes it's an incidental
finding on MRI don't fall.
Other things,
inflammatory form of CAA,
transient, focal
neurological episode,
TFNEs, sulcal
subarachnoid haemorrhage
and several more presentations.
It looks like the Boston
criteria may not be very
helpful for all of these
non-ICH presentations.
An operational diagnosis is
required for clinical research,
notably for drug trials.
Diagnosis is very important
in the clinical setting.
But also for clinical research.
You need to be almost
sure that it is CAA
patients that are
recruited into your trial.
The other main
challenge regarding
CAA is the mechanisms
of this condition.
Why is there a vascular
amyloid-beta 40 accumulation?
Still unclear.
The causes or mechanisms of
the various symptoms and
presentations, phenotypes,
and the mechanisms underlying
the imaging markers,
haemorrhagic or white
matter markers.
All this remains quite unclear
and it's very important to
understand the
mechanisms because
this may lead to
novel therapies.
The topic of my talk today is,
can PET help to address
these challenges,
both diagnosis and mechanisms?
