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Effects of hypothermia on the human brainstem auditory response.

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need for surgery. In view of their alert state of consciousness and compromised systemic status, we also
withheld surgery in our patients, although we fully
realized that precipitous decline can occur at times.
However, they had a benign outcome, thus underscoring the potential for spontaneous resolution in 3ome
of these patients. If we bear this potential in mind,
perhaps in the future we may be able to delineate
predictive features whereby patients with cerebellar
hemorrhage who are alert may be treated conservatively. At present, such a prediction is at best hazardous, even in fully alert patients.
Addendum
Recently a 74-yeu-old man presented to o u r institution
with headache, vertigo, and right-sided brainsrem signs of
sudden onset. C A T scan revealed a right cerebellar hemorrhage. He was treated conservatively since multiple medical contraindications existed. H i s neurological status slowly
improved over the ensuing four weeks. However, h e died
of widespread enterococcal septicemia emanating from a
posrobsrructive pneurnonra. A t autopsy h e had merasraric
carcinoma of the lung and a right c e r e b e h r hemorrhage.
References
1. Baker HL, Houser OW: Computed tomography in the diagnosis of posterior fossa lesions. Radio1 Clin North Am
14:129-146, 1976
2. Brennan RW, Bergland RM: Acute cerebellar hemorrhage:
analysis ofcltnical hndings and uurcome in I 2 cases. Neurology
(Minneap) 27:527-532, 1977
3. Dinsdale HB: Spontaneous hemorrhage in the porrerior fossa:
a study of primary cerebellar and pontine hemorrhage with
observations on the pathogenesis. Arch Neurol 10:200-2 17,
1964
4. Duncan GW, Parker SW, Fisher CM: Acute cerebellar infarction in the PICA territory. Arch Neurol 32:364-368, 1975
5. Fisher CM, Picard EH, Polak A, et al: Acute hypertensive
cerebellar hemorrhage: diagnosis and surgical management
treatment. J Nerv Menc Dis 140:38-57. I965
6. Lehrich JR: Cerebellar infarction with brainsrem compression.
Arch Neurol 22:490-498, 1970
7. Lichtenstein RS: Spontaneous cerebellar hematomas. Johns
Hopkins Med J 122:319-328, 1968
8. McKissock W, Richardson A, Walsh L Spontaneous cerebellar
hemorrhage: a study of 34 consecutive cases treated surgically.
Brain 83:l-9, 1960
9. Orr KH, Kase CS, Ojemann RG, eta]: Cerebellar hemorrhage:
diagnosis and treatment. A review of 56 cases. Arch Neurol
311160-167, 1974
10. Pressman BD, Kirkwood JR, Davis DO: Posterior fossa
hemorrhage localization by computed tomograph. JAMA
232:932-933, 1975
11. Rey-Bellet J: Cerebellar hemorrhage: a neuropathologic study.
Neurology (Minneap) 10:2 17-222, 1960
12. Sypert GW, Alvord EC: Cerebellar infarction. Arch Neurol
32:357-363, 1975
Effects of Hypothermia on
the Human Brainstem
Auditory Response
JamesJ. Stockard, MD, P h D , Prank W. Sharbrough, M D ,
and John A. Tinker, MD
Latency measurements between three potentials (waves
I, 111, and IV/V) of the human brainstem auditory response can allow early detection of certain posterior
fossa lesions. T h e diagnostic use o f these interwave
latencies requires knowledge of what factors may prolong rhem in the absence of disease. Hypothermia appears t~ be one such factor-in 5 neurologically and
audiometrically normal patients, mean esophageal
temperatures as high as 34.5"C resulted in prolongations of central auditory conduction time. Interwave
latency prolongations that were abnormal relative to an
age-matched normal population were seen a t 32.1" ?
0.3"C in patients with both spontaneous and induced
hyporhermia, and these abnormalities disappeared
after rewarming to norrnorhermia. Hypothermia often
accompanies intoxication and coma and should theref o r e be considered when brainstem auditory response
abnormalities are being interpreted in these two clinical conditions.
Stockard JJ, Sharbrough FW, T i n k e r J A . Effects of
hypothermia OR t h e human braktern auditory
response. Ann N e u r o l 3:368-370, 1978
The first five vertex-positive waves of the human auditory evoked response are volume-conducted potentials generated in subcortical structures distant from
the recording electrode at the scalp [l]. Clinicopathological correlarions indicate that waves 1, 111,
and V originate from the acoustic nerve, pons. and
midbrain, respectively, and that the 1-111 and 111-V
interwave latencies may be selectively prolonged by
lesions at different levels of the brainstem [4].The
present report demonstrates that hypothermia may
also prolong these interwave latencies and thus mimic
the effects of central structural lesions on brainstem
auditory evoked potentials (BAEPs).
Materials and Methods
O n e patient was studied w h o suffered accidental hypothermia d u e to cold exposure while taking high doses of
chlorpromazine. Five o t h e r patients were studied during
~
From the Departments of Neurology and Anesrhesiology, Mayo
C h i c , Ruchesrer, MN.
Accepted for publication Nov 23, 1777.
Address reprint requests to Dr Stockard, Department of Neurology, Division of Electroencephalography, Mayo Clinic, Rochester,
MN 55901.
368 0364-51~4/78/OOO$-O415$Ol.O0@ 1 9 7 8 by James J. Stockard
induced hypothermia at the time of open-heart surgery with
cardiopulmonary bypass (CPB). These patients ranged in
age from 42 to 63 years with a mean of 54.2 ? 3.5 (SEM)
years. All 6 had normal neurological examinations and
audiograms.
The patients undergoing induced hypothermia were
lightly anesthetized with combinations of intravenous
meperidine and diazepam and 70q1inspired nitrous oxide.
In this group, BAEPs were recorded at three different
steady-state temperatures, the steady state being defined by
constancy of esophageal and nasopharyngeal temperature at
a given value for more than 15 minutes. Because of
therapeutic requirements, BAEPs could be obtained at only
two steady-state esophageal temperatures in the patient who
had accidental hypothermia.
BAEPs were elicited with 100 psec clicks of 85 dBHL
(intensity above normal hearing threshold) presented binaurally at a rate of 10 per second. Bipolar electroencephalographic activity was recorded from vertex to mastoid
electrode pairs, amplified 500,000 times, and filtered
through a bandpass of 100 to 3,000 Hz (3 d B down points).
The EEG activity that was time-locked to the acoustic
stimuli was sampled with a computer at 13 to 25 kHz,
and four computer averages of 2,000 click-evoked responses were plotted at each steady-state temperature. In all
patients, wave IV fused with wave V into a single complex
wave that is hereafter designated wave IV/V. Latencies from
the stimulus to the peaks (peak latency) of waves I, 111, and
I V N and between the peaks of these waves (interpeak
latency) were measured to within 40 to 80 psec, and the
mean interpeak latency of four separate trials was rounded
off to the nearest 0.1 msec after statistical analysis. Averaging the interpeak latencies for the different patients resulted
in standard deviations of less than 0.2 msec at normothermia
( N = 6), 34.5"C ( N = 5 ) , and 32.1"C ( N = 6); SDs for the
different interpeak latencies were 0.2 to 0.4 msec at 27.9"C
( N = 5 ) . The concentrations or dosages of anesthetic and
tranquilizing agents to which patients in this study were
exposed d o not themselves significantly affect BAEP interpeak latencies when body temperature is controlled [53.
Results
The mean 1-111, 111-IV/V, and I-IV/V i n t e r p e a k
m
Te = 32.5"C
I
o a yv
l
I
A
m
( 1 hour later)
Te = 37.1" C
I
L 4 . 4 mt-'
'I
85 d9HL
clicks
BAEP.i before and after rewurniing i n a patient u'ho .iuffPred
ucridentul hypothermia. The patient waJ a 54-year-old man
known to be tuking large do.reJ of rhlorpromazine. Urine weening showed no drugs other than phenothiazine.i. Ethanol was
not detectable in the blood. The patient was lethargic at the
time ofthe top recording, crnd the 1-IVN interpeuk latency of'4.5
m e c exceeded the upper limit of normal of our 99% ronjidenre
interz'alfor this value in the sixth derade. Following rewarming
to normothermia one hour later, the patient was 1e.u lethargic
andl-IVN interpeak latency had returnedto normal. Note
slight sharpening of the uuueform with return to normothermia. T w o separate aueruRes are superimposed at each temperature t o demonstrate response reliability. Totalsweep is 10 mser
with 1 m.rec divisions. Vertexpositivity is repmenled by an upward pen dejlection. (T, = esophageal temperature.)
N o r m o t h e r m i a (37.1" 2 0.2"C): 1-111 = 2.1 msec;
= 1.8 msec; I-IVlV = 3.9 msec.
After induction of anesthesia but p r i o r t o CPB
(34.5" k 0.4"C): 1-111 = 2 . 3 msec; 111-IV/V = 2.0
msec; I-IV/V = 4.3 msec.*
D u r i n g CPB i n 5 patients and d u r i n g s p o n t a n e o u s
h y p o t h e r m i a i n 1 p a t i e n t (32.1" 2 0.3"C):1-111 = 2.5
msec; 111-IV/V = 2.2 msec;' and I-IV/V = 4.7
msec.? The first abnormal latency prolongations rela-
tive to a normal population [41 were seen at this
t e m p e r a t u r e , and later c o m p o n e n t s were affected
progressively m o r e . Also, as can be s e e n i n t h e Figure,
t h e s h a p e of t h e waves began to alter a t this temperature, the d u r a t i o n o f each w a v e increasing a n d the
p e a k s b e c o m i n g broader.
A t the lowest t e m p e r a t u r e reached by all patients
on CPB (27.9" -t 0.3"C):1-111 = 2.8 msec;" III-IV/V
= 2.7 msec;? and I-IV/V = 5.5 msec.: A t this t e m p e r a t u r e t h e peak latency o f w a v e I itself h a d increased
significantly f r o m its n o r m o t h e r m i c value o f 1.2 k 0.1
(SD) to 1.9 k 0.3" m s e c despite constancy of t h e
hearing threshold i n t h e room for n o r m a l persons.
Increase from normothermic latency significant at: "p < 0.05; t p <
0.01; z p < 0.005.
22" t o 24°C i n 2 of t h e surgical patients resulted i n
f u r t h e r prolongations i n the peak latency of wave I
latencies a t f o u r different esophageal t e m p e r a t u r e s
( m e a n 2 1 SD) w e r e as follows:
111-IV/V
F u r t h e r reductions i n esophageal t e m p e r a t u r e t o
Brief Communication: Stockard et al: Hypothermia and Evoked Potentials
369
relative to the stimulus and in the interwave latencies
of what were identified as waves I, 111, and IVlV. T h e
morphology of the last two components was so distorted at these temperatures that waves I11 and IV/V
could not be identified with certainty, and peak latency could not be meaningfully determined. All of
the changes in latency and shape of BAEPs that occurred with hypothermia reversed completely with
rewarming, and subsequent recordings from each patient at drug-free intervals of days to weeks showed no
changes from the normothermic tracings obtained
shortly after rewarming.
Discussion
T h e systematic prolongation of different human
BAEPs with decreasing temperature is qualitatively
similar to that seen in hypothermic rats [ 3 ] . T h e
present study indicates that temperature-induced alteration of human BAEPs may begin at temperatures
as high as 34.5"C (94.1"F) and that spontaneously
developing hypothermia of 32.5"C (90.5"F) can pro-
370 A n n a l s of Neurology
Vol 3
No 4
A p r i l 1978
duce central BAEP abnormalities in .the absence of
brainstem disorders. Hypothermia of this degree is
not uncommon in drug intoxication and in coma [2],
and therefore it is important to consider body temperature before interpreting BAEPs clinically.
References
1. Jewett DL, Romano MN, Williston JS: Human auditory evoked
potentials: possible brain stem components detected o n the
scalp. Science 167:1517-1518, 1970
2. Plum F, PosnerJB: Diagnosis of Stupor and Coma. Philadelphia,
FA Davis Company, 1972, pp 215-216
3. Schorn V, Lennon V, Bickford R: Temperature effects on the
brainstem auditory evoked responses (BAER's) of the rat.
Proc San Diego Biomed Symp 16:313-318, 19'7
4. Stockard JJ, Stockard JE, Sharbrough FW: Detection and
localization of occult lesions with brainstem auditory responses.
Mayo Clin Proc 52:761-769, 1977
5. Stockard JJ: Experimental and pathologic alteration of central
auditory conduction in man. clinical significance of the resultant
far-held (brainstem) response patterns, in Aminoff MJ (ed):
Electrophysiologic Approaches to Neurologic Diagnosis. Edinburgh and London, Churchill/Livingstone (in press)
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