Tech Corner: Detection of Subarachnoid Hemorrhage Induced
Cerebral Vasospasm: Electroencephalography and Cranial
Accelerometry
By Fawaz Al-Mufti, MD
The authors have no actual or potential conflict
of interest in relation to the topics discussed in
this column. This article may discuss non-FDA
approved devices and “off-label” uses. The NCS
and Currents do not endorse any particular
device.
Brain ischemia secondary to cerebral
vasospasm is managed by increasing arterial
blood pressure, infusing vasodilators and performing cerebral
angioplasty. One can postulate that if cerebral vasospasm
is detected prior to the development of cerebral ischemia,
morbidity can be reduced or eliminated. Therefore, the reduction
in morbidity is dependent on the accurate and early detection of
cerebral vasospasm.
Real-time detection of cerebral vasospasm is challenging, and,
although cerebral vasospasm may be suspected by change in
clinical status, these changes may be nonspecific, resulting in high
false positive rate for predicting true cerebral vasospasm. Noninvasive
vascular and perfusion imaging can document vessel
caliber and alterations in cerebral perfusion; however, none of
these techniques are ideal and only provide episodic assessments.
The creation of a non-invasive, portable method that samples
more vascular territory is needed.
EEG can also be used to non-invasively collect information on
changes in cerebral autoregulation. A decrease in the alpha-delta
ratio (ADR) was shown to accurately predict delayed cerebral
ischemia (DCI) in subarachnoid hemorrhage patients.2-4 In some
of these studies, a single decrease in the ADR of greater than 50
percent was 89 percent sensitive and 84 percent specific for DCI,
and, in the other, a 38 percent decrease in either the ADR or
alpha variability was 100 percent sensitive and 83 percent specific
during the onset of DCI.2 4 Rots et. al also found that the changes
in alpha/delta ratio preceded clinical diagnosis of vasospasm
by an average of seven hours, indicating that continuous EEG
monitoring may allow for early treatment of this important
complication in subarachnoid hemorrhage patients.2 3
Gollwitzer et. al. did not study the ADR but found that a 40
percent decrease in alpha power for greater than five hours was
89 percent sensitive and 77 percent specific for the development
of DCI.3 Another paper demonstrated that patients who later
went on to develop delayed cerebral ischemia showed no change
(or a decrease) in the EEG signal while infused with sodium
nitrite. Those who did not develop delayed cerebral ischemia did
the exact opposite and showed a strong increase in EEG signal.
This paper highlighted how the nitric oxide pathway is important
in the development of delayed cerebral ischemia, but this also
means we now quite possibly may be able to relatively quickly
determine who is at risk for this life-threatening complication
and who is not.5
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