Monitoring Neurological Injury by qEEG - Quantitative EEG Analysis Methods and Clinical Applications - page 181

It also compares the recovery for relatively mild (7-minute) versus severe (9-minute)
asphyxial arrest durations. The experiment demonstrates greater recovery of IQ in
rats treated with hypothermia compared to normothermic controls for both the
injury groups ( p 0.05) (Figure 7.7). Not surprisingly, the 9-minute CA results in a

slower progression of recovery.
Further, IQ levels in the normothermia cohort are compared with the hypother-
mia cohort, and in each case the recovery of the hypothermia cohort is greater; that
is, the IQ levels restore toward the normalized baseline. Baseline characteristics of
animals in the hypothermia and normothermia groups were similar, including
weight on the day of CA, duration of asphyxia prior to CA, duration of CPR prior
to ROSC, and baseline ABG data. The baseline control measures include arterial
pH, HCO 3 - , PCO 2 , PO 2 , and O 2 saturation.
Another way to assess the outcome is through NDS. In our studies, the 72-hour
NDS scores, an estimate of the long-term outcome of the animals, of the control and
hypothermia groups were compared. NDS significantly improved under hypother-
mia compared to the normothermia group ( p

<

0.05). There was a trend toward
improved survival rates and mean duration of survival hours in animals treated
with hypothermia in both the 7-minute and 9-minute groups. Another interesting
question worth asking is whether IQ values measured early (at 4 hours) correlate
with the primary neurological outcome measure later on (72 hours). The animal
studies presented here demonstrate the potential utility of qEEG-IQ to track the
response to neuroprotective hypothermia during the early phase of recovery from
CA.

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7.5.1 qEEG-IQ Analysis of Brain Recovery After Temperature Manipulation
Previous studies showed that temperature maintenance of the brain has profound
effects on the neurological recovery and survival of animals. It is evident that hypo-
thermia has a neuroprotective effect and, conversely, hyperthermia should have
harmful effects. Using the asphyxial CA rodent model, we tracked qEEG of 6-hour
immediate postresuscitation hypothermia ( T = 33°C), normothermia ( T = 37°C), or

hyperthermia ( T 8 per group). While hypothermia was implemented

as before, hyperthermia was achieved using a warming blanket and an automatic
warming lamp (Thermalet TH-5, model 6333, Physitemp, New Jersey) to achieve a
target temperature of 39ºC within 15 minutes and the temperature was maintained
at 38.5ºC to 39.5ºC for 6 hours. NDS cutoff for good outcome was NDS

= 39°C) ( N =

60 (char-
acterized as independently functioning animals) and poor outcome was NDS

=

< 60

(characterized as sluggish to unresponsive animals) [9, 10, 67].
To study the temperature effects on neurological outcomes, three groups of ani-
mals were evaluated: (1) cohort 1: 6 hours of hypothermia ( T

= 33°C); (2) cohort 2:

normothermia ( T 39°C) immediately

postresuscitation from 7-minute CA. Temperature was maintained as before using
surface cooling. Neurological recovery was defined by a 72-hour NDS assessment.
The key observations were that burst frequency was higher during the first 90 min-
utes in rats treated with hypothermia (25.6

= 37°C); and (3) cohort 3: hyperthermia ( T =

± 12.2/min) and hyperthermia (22.6 ±

8.3/min) compared to normothermia (16.9 0.001). The burst fre-

quency correlated strongly with 72-hour NDS in normothermic rats ( p

± 8.5/min) ( p <

< 0.05), but