Joseph A Fisher1,2,3, Olivia Sobczyk1, Adrian P Crawley4, Julien Poublanc4, Paul Dufort1, Lashmi Venkatraghavan5, David J Mikulis1,4, and James Duffin2,3
1Institute of Medical Sciences, University of Toronto, Toronto, ON, Canada, 2Department of Physiology, University of Toronto, Toronto, ON, Canada, 3Departments of Anaesthesia, University Health Network, Toronto, ON, Canada, 4Joint Department of Medical Imaging and the Functional Neuroimaging Laboratory, University Health Network, Toronto, ON, Canada, 5Department of Anaesthesia, University Health Network, Toronto, ON, Canada
Synopsis
We surveyed
the varied patterns of BOLD changes in response to a ramp CO2 stimulus ranging
from hypocapnia to hypercapnia in 10 healthy individuals and 10 patients with
steno-occlusive disease. The patterns of
response fell into 4 types, based on the two linear slopes fitted to each range. Maps of these types on a voxel by voxel basis
were compared to cerebrovascular reactivity (CVR) calculated as the linear slope
over the whole ramp. We suggest that for
assessing cerebrovascular reactivity, CVR and type scoring enhance the
interpretation of each other, and that modeling the possible underlying
patho/physiologies to explain the type patterns is the portal to further work.
Purpose
To classify the varied BOLD
responses to progressive hypercapnia in patients with known cerebrovascular
steno-occlusive disease (SOD).
Introduction
Increasing
the partial pressure of CO
2 (PCO
2) in the arterial blood reduces
vascular resistance and increases cerebral blood flow (CBF). When the stimulated CBF exceeds the inflow
capacity of the major arterial vessels, competition for flow is established between
vascular regions. In healthy brains, the
regional resistances are balanced and the pattern of the flow response to CO
2
is sigmoidal in shape. However, in the
presence of cerebrovascular disease, flow is preferentially redistributed to the
healthier vessels, and produces various patterns of flow response to progressive
hypercapnia (ramp) in various regions. We
set out to classify these patterns of flow response to a ramp stimulus of
increasing end-tidal PCO
2 (P
ETCO
2), for
each voxel in patients with SOD, and map them to the corresponding location on
the anatomical scan.
Methods
We
monitored the BOLD response as a surrogate measure of cerebral blood flow, in 10 healthy
subjects and 10 patients with SOD. The
BOLD signals were divided into those corresponding to the upper and lower halves
of a ramp P
ETCO
2 from 5-10
mmHg below resting to10-15 mmHg above resting.
A linear least squares fit of each part was used to calculate the two slopes. These slopes were then categorised as
positive (+) or negative (-).
Results
We found
that the changes in BOLD signal as a function of P
ETCO
2
in each voxel could be categorised into one of four types based on the two
slopes of the lower and upper range of the CO
2 stimulus as follows: (A)
+/+, (B) +/-, (C) -/-, (D) -/+, as illustrated in Figure 1. Each of the four types of BOLD response
patterns shown in Figure 2 were color coded (A = red, B = light blue, C = dark
blue, and D = yellow) and the colors were superimposed on the corresponding
voxel of the anatomical scan to produce ‘type’ maps. Figure 2 shows an example. For
comparison, we also calculated the CVR in
the classical form where CVR = Δ BOLD / Δ P
ETCO
2. The type map shows an area of abnormality over a greater
extent than the steal alone. However C types indicate negative CVR and
true steal.
Discussion/Conclusion
This is the
first report of BOLD response patterns to a ramp P
ETCO
2 stimulus.
We found that all voxels in healthy subjects, and patients show one of four
flow response patterns to a ramp CO
2 stimulus that we call ‘types’, two of which are biphasic. CVR is a subset of ‘types’ with the best
correlation to types A and C, which are linear.
Biphasic types B and D have small values of CVR because of an averaging
of the two slopes. We suggest that for
assessing cerebrovascular reactivity, CVR and type scoring enhance the
interpretation of each other, and that modeling the possible underlying
patho/physiologies to explain the type patterns is the portal to further work.
Acknowledgements
No acknowledgement found.References
No reference found.