Monitoring Neurological Injury by qEEG - Quantitative EEG Analysis Methods and Clinical Applications - page 170

aptic transmission, axonal conduction, and cellular action potential firing of the
neurons in the brain [7].
Controlled animal studies can be helpful in elucidating the mechanisms and
developing the methods to monitor brain injury. This chapter reviews the studies
done in an animal model of global ischemic brain injury, monitoring brain response
using EEG and analyzing the response using qEEG methods. These studies show
that the rate of return of EEG activity after CA is highly correlated with behavioral
outcome [8-10]. The proposed EEG monitoring technique is based on the hypothe-
sis that brain injury reduces the entropy of the EEG, also measured by its informa-
tion content (defined classically as bits per second of information rate [11]) in the
signal. As brain function is impaired, its ability to generate complex
electrophysiologic activity is diminished, leading to a reduction in the entropy of
EEG signals. Given this observation, recent studies support the hypothesis that neu-
rological recovery can be predicted by monitoring the recovery of entropy, or equiv-
alently, a derived measure called information quantity (IQ) [12, 13] of the EEG
signals. Information can be quantified by calculating EEG entropy [11, 14]. This
information theory-based qEEG analysis method has produced promising results in
predicting outcomes from CA [15-18].
7.1.1 Hypothermia Therapy and the Effects on Outcome After Cardiac Arrest
The neurological consequences of CA in survivors are devastating. In spite of
numerous clinical trials, neuroprotective agents have failed to improve outcome sta-
tistics after CA [19, 20]. Recent clinical trials using therapeutic hypothermia after
CA showed a substantial improvement in survival and functional outcomes com-
pared to normothermic controls [19, 21, 22]. As a result, the International Liaison
Committee on Resuscitation and the American Heart Association recommended
cooling down the body temperature to 32ºC to 34°C for 12 to 24 hours in
out-of-hospital patients with an initial rhythm of ventricular fibrillation who remain
unconscious even after resuscitation [23].
Ischemic brain injury affects neurons at many levels: synaptic transmission,
axonal conduction, and cellular action potential firing. Together these cellular
changes contribute to altered characteristics of EEGs [24]. Cellular mechanisms of
neuroprotective hypothermia are complex and may include retarding the initial rate
of ATP depletion [25, 26], reduction of excitotoxic neurotransmitter release [27],
alteration of intracellular messengers [28], reduction of inflammatory responses
[29], and alteration of gene expression and protein synthesis [30, 31]. Hypothermia
reduces the excitatory postsynaptic potential (EPSP) slope in a temperature-depend-
ent manner [32]. A recent study done on parietal cortex slice preparation subjected
to different temperatures showed greater spontaneous spike amplitude and fre-
quency in the range of mild hypothermia (32ºC to 34°C) [32]. However, more
detailed cellular information about neural activity in different brain regions is not
available and the neural basis to the effects of hypothermia therapy remains poorly
understood.
The ischemic brain is sensitive to temperature and even small differences can
critically influence neuropathological outcomes [33]. Hyperthermia, for example,
has been demonstrated to worsen the ischemic outcome and is associated with