Biology Reference
In-Depth Information
Chapter 22
Physiological Assessments of Subarachnoid Hemorrhage
Jens P. Dreier
Abstract
Brain injury after subarachnoid hemorrhage (SAH) shows a multiphasic evolution with a global ischemic
insult at the time of the initial hemorrhage, complications of early surgical or endovascular aneurism treatment
thereafter, followed by a time period with a high risk for secondary focal ischemic events. This so-called
delayed cerebral ischemia (DCI) peaks around day 7 after the initial hemorrhage and is a multiphasic
condition by itself as it often shows a gradually progressing, waxing, and waning pattern before the
neurological defi cits become permanent. This chapter provides an introduction to Chaps.
23
-
29
in which
a number of methods are described to study the pathophysiological basis of different components that
contribute to brain damage during and following SAH.
Key words:
Sustained depolarization, Spreading ischemia, Calcium, Microthrombosis, Blood-brain
barrier, Hippocampus, Intracranial pressure, Vasospasm, Subarachnoid hemorrhage
1. Brain Damage
After
Subarachnoid
Hemorrhage
Clinical evidence suggests that the initial brain damage is the most
important factor for death and disability after subarachnoid hemorrhage
(SAH) (
1-3
); e.g., in a more recent population-based European
study, 16% of the patients with SAH died before reaching the hospital.
Another 5% of patients deceased on the day of hemorrhage after
admission to hospital (
4
). Clinical neuromonitoring studies using
microdialysis or electrocorticography suggest that the processes of
early brain damage continue into the early post-interventional
period which provides the theoretical option for treatment (
5, 6
).
Therefore, clinical and basic research is mandatory to understand
the pathophysiological basis of this early phase of brain damage (
7
).
DCI is less important for the overall outcome after SAH. However,
the unique constellation that DCI occurs after SAH while the patient
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