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Brainstem auditory evoked responses and alpha-patten coma.

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BRIEF COMMUNICATIONS A N D CASE REPORTS
Brainstem Auditory
Evoked Responses and
Alpha-Pattern Coma
Riitta Hari, MD,’ Raimo Sulkava, MD,”
and Matti Haltia, M D t
A young comatose man with an alpha-pattern electroencephalogram is reported. The brainstem auditory
evoked responses were severely abnormal, suggesting a
pontomesencephalic lesion which was confirmed at autopsy.
Hari R, Sulkava R, Haltia M: Brainstem auditory
evoked responses and alpha-pattern coma.
Ann Neurol 11:187-189, 1982
Rhythmic, nonreactive alpha-range activity in the
electroencephalogram (EEG) of comatose patients is
usually considered a poor prognostic sign [ l , 6, 13,
141. This “alpha-pattern coma” is most often due to
pontomesencephalic brainstem lesions or to postanoxic encephalopathy [4-8, 13, 141. However,
pharmacological intoxications (from benzodiazepines
and chlormethiazole) uncomplicated by hypoxia can
also induce comatose states associated with nonreactive alpha-range activity; in these cases recovery can
be complete [ 3 ] . Furthermore, some patients with
alpha-pattern coma due to brainstem lesions or postanoxic encephalopathy also have recovered with
minimal neurological defects [G, 71.
Brainstem auditory evoked responses (BAERs)
have proven helpful in determining the level of the
damage that has induced a comatose state [lo, 121.
We report a patient with an alpha-pattern EEG of
unknown cause. The BAERs were abnormal and
suggested a pontomesencephalic lesion, which was
confirmed at autopsy.
A 32-year-old man was admitted on February 18, 1980,
because of unconsciousness following “a seizure.” No
other history was available. Later the information was obtained that the patient had been healthy but a heavy drinker
for a couple of years.
O n admission the patient was unconscious but reacted to
noxious stimuli with extension of all limbs. Rectal temper-
ature was 40.0”C and blood pressure, 180/70 mm Hg. The
tendon reflexes were symmetrically brisk, with extensor
plantar responses. The pupils were equal, midposition, and
nonreactive to light. Conjugate oculocephalic responses
could not be elicited; only lateral eye movements were
produced with oculocephalic maneuvers. Corneal reflexes
were present. There were no signs of trauma, increased intracranial pressure, o r meningeal irritation, and the patient
breathed spontaneously.
A computerized tomographic scan was normal. Cerebrospinal fluid was clear, with normal cell count, protein of
47 mg/dl, and normal glucose content. Chest roentgenogram and electrocardiagram were normal. There was mild
leukocytosis (white blood cells, 12,500/mm3) and an elevated erythrocyte sedimentation rate (3 1 mm/hr). Other
blood tests were normal. A tentative diagnosis of drug intoxication was made, and forced diuresis was started in the
intensive care unit.
Two days later the patient’s condition was unchanged.
Multidrug screening of urine, including benzodiazepines,
barbiturates, salicylates, phenothiazines, and tricyclic antidepressant drugs, was negative. Cerebrospinal fluid
showed 108,000 erythrocytes and 8 white blood cells per
cubic millimeter and a protein content of 64 mg/dl. Encephalitis or ischemic brain damage was suspected, although the possibility of drug intoxication could not be
ruled out definitely.
The first EEG was recorded on the third hospital day.
T h e tracing showed rhythmic, 12 to 14 cps, 30 to 50 FV,
alpha-like activity with dominance over the posterior areas
(Fig 1).This rhythmic activity occurred in spindles of 1 to 2
seconds’ duration, varying with periods of desynchronized
activity. Reactivity of the EEG was absent: vigorous visual,
auditory, and tactile stimulation failed to modify the EEG
pattern. Some bursts of 5 to 7 cps activity were intermixed
with alpha-range activity.
BAERs were recorded on the same day. Only component 1, representing function of the cochlear nerve, was
present, its latency being normal; no other components
could be discerned (Fig 2). The BAER findings combined
with the alpha-pattern EEG indicated a large lesion of the
pontomesencephalic brainstem. Brainstem infarction was
suspected.
In a control EEG o n March 13, the dominant frequency
was slower (8 to 9 cps, 4 0 to 70 p V ) and was intermixed
with abundant frontal-dominant, 5 to 6 cps, 100 pV episodes. There was slight reactivity to noxious stimuli but no
driving with photostimulation. T h e next tracing, on April
3, was otherwise similar, but during photostimulation there
was temporary reduction in alpha-range activity in the right
hemisphere.
The patient remained stable until July 1, 1980, when he
died.
Autopsy Findings
From the Departments of *Neurology (Haartmaninkatu 4) and
?Pathology (Haartmaninkatu 3), University of Helsinki, SF-00290
Helsinki 29, Finland.
Received Feb 9, 1981, and in revised form Apr 22. Accepted for
publication Apr 24, 1981.
Address reprint requests to Dr Hari.
At postmortem examination an old organized thrombus
was found to be totally occluding the basilar artery at the
level of the superior cerebellar arteries. There was an associated cystic infarct involving the rostral half of the pons,
midbrain, and thalamus but sparing the caudal pons (Fig 3).
The midline lesion affected the rostral half of the pontine
0364-5 134/82/020187-03$01.25 @ 1981 by the American Neurological Association
187
tegmentum (including the pontine reticular formation in
toto). Most of the basis pontis was also symmetrically destroyed at this level. The lesion continued to the midbrain
tegmentum involving the ventral periaqueductal gray matter and the medial part of the mesencephalic reticular formation bilaterally. The substantia nigra was totally destroyed, as were the medial two-thirds of the crura cerebri
and the medial aspects of the thalami (including the ventral
part of the dorsomedial nuclei). The lateral thalami, including the reticular nuclei, were intact. Small, scattered,
ischemic lesions were found in the calcarine cortex, in the
left hippocampus, and in the dentate nuclei and cerebellar
cortex. The basal ganglia and the rest of the cerebral cortex
appeared intact. There was no evidence for Wernicke's encephalopath y.
Fig 1 . Electroencephalogram three duys after onset of the coma.
1
Discussion
T h e clinical findings in this young comatose patient
pointed t o the presence of a severe brainstem lesion
[9]. I t has been reported that t h e prognosis of alphapattern coma is better predicted by the neurological
examination than by EEG recordings and that there is
n o relationship between the distribution of alpha
rhythm and the clinical outcome of patients [ 7 ] .According to Grindal et a1 [ 7 ] ,clinical evidence of intact
brainstem function implies a favorable outcome in
patients who survive
coma. I n Our patient the
severity of the brainstem lesion, as quantified by the
abnormality of the BAERs, indicated a Poor Prognosis, in agreement with the clinical findings. It is
possible that BAERs will help to predict the outcome
188 Annals of Neurology
Vol 11 No 2
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2I
I
4I
I
6
I
I
8I
I
10
MSEC
Fig 2 . Brainstern aaditory evoked responses with click stimuli
(80 dB SPL, repetition rate lOlsec) presented binaurally t o the
patient (above) and t o a normal subject (below). Each curve
is the average of about 1,200 responses. The cawes begin 0.6
msec after stimulus onset. Derivation: Fpz-right mastoideum.
February 1982
has been unilateral [14]. O u r patient differed from
these cases because the massive bilateral destructive
lesions extended to the thalamic level. The finding
agrees with animal studies [2] indicating that medial
thalamic structures are not indispensable for generation of the cortical alpha rhythm.
References
1. Alving J, Moller M, Sindrup E, Nielsen BL: “Alpha pattern
F i g 3. Extent of ischemic brain damage (hatched areas). See
text forfurther explanation.
for patients with alpha-pattern coma of brainstem
origin.
Stockard and Sharbrough [ l l l reported a patient
with an alpha-pattern EEG who possibly was “locked
in” rather than being in alpha coma. The alpha
rhythm of the EEG was reactive, but all components
of the BAER were absent. An autopsy revealed acute
thrombosis of the upper cervical and intracranial
portions of the vertebral arteries and the basilar artery, with infarction of the acoustic nerves and
brainstem u p to the midbrain. In analogy with our
case, the severe abnormality of the brainstem responses indicated an irreversible lesion.
Most cases of alpha coma with brainstem lesions
reported in the literature have been due to abnormalities involving the pontomesencephalic junction.
In some patients the lesion has extended to the
mesencephalon and thalamus, but this rostra1 lesion
coma” following cerebral anoxia. Electroencephalogr Clin
Neurophysiol47:95-101, 1979
2. Andersen P, Andersson SA: Physiological Basis of the Alpha
Rhythm. New York, Appleton-Century-Crofts, 1968
3. Carrol WM, Mastaglia FL: Alpha and beta coma in drug intoxication uncomplicated by cerebral hypoxia. Electroencephalog Clin Neurophysiol 46:95- 105, 1979
4. Chase T N , Moretti L, Prensky AL: Clinical and electroencephalographic manifestations of vascular lesions of the pons.
Neurology (Minneap) 18:357-368, 1968
5. Chatrian GE, White LE, Shaw CM: EEG pattern resembling
wakefulness in unresponsive decerebrate state following
traumatic brainstem infarct. Electroencephalogr Clin Neurophysiol 16:28 5 -2 89, 1964
6. Chokroverty S: “Alpha-like” rhythms in electroencephalograms in coma after cardiac arrest. Neurology (Minneap)
25:655-663, 1975
7. Grindal AB, Suter C, Martinez AJ: Alpha-pattern coma: 24
cases with 9 survivors. Ann Neurol 1:371-377, 1977
8. Neundorfer B, Meyer-Wahl L, Meyer JG: Alpha-EEG
und Bewusstlosigkeit. Ein kasuistischer Beitrag zur lokaldiagnostischen Bedeutung des a-EEG beim bewusstlosen
Patienten. Z EEG-EMG 5:106-114, 1974
9. Plum F, Posner JB: The Diagnosis of Stupor and Coma. Third
edition. Philadelphia, Davis, 1980
10. Starr A, Achor J: Auditory brainstem responses in neurological disease. Arch Neurol 32:761-768, 1975
11. Stockard JJ. Sharbrough FW: Unique contributions of shortlatency auditory and somatosensory evoked potentials to
neurologic diagnosis. In Desmedt JE (ed): Clinical Uses of
Cerebral, Brainstem and Spinal Somatosensory Evoked Potentials. Basel, Karger, 1980, pp 231-263
12. Uziel A, Benezech J: Auditory brainstem responses in comatose patients: relationship with brain-stem reflexes and levels
of coma. Electroencephalogr Clin Neurophysiol45:5 15-524,
1978
13. Vignaendra V, Wilkus RJ, Copass MK, Chatrian GE: Electroencephalographic rhythms of alpha frequency in comatose
patients after cardiopulmonary arrest. Neurology (Minneap)
24:582-588, 1974
14. Westmoreland BF, Klass DW, Sharbrough FW, Reagan TJ:
Alpha-coma: electroencephalographic, clinical, pathologic and
etiologic correlations. Arch Neurol 32:713-718, 1975
Case Report: Hari et al: BAERs in Alpha-pattern Coma
189
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