Intraoperative
Loss of Auditory Function Relieved By Microvascular Decompression
of the Cochlear Nerve
John
B. Wahlig, Anthony M. Kaufmann, Jeffrey Balzer, Thomas J.
Lovely and Peter J. Jannetta
Abstract:
Background: Brainstem auditory evoked potentials
(BAEP) are useful indicators of auditory function during posterior
fossa surgery. Several potential mechanisms of injury may
affect the cochlear nerve, and complete loss of BAEP is often
associated with postoperative hearing loss. We report two
cases of intraoperative auditory loss related to vascular
compression upon the cochlear nerve. Methods: Intra-operative
BAEP were monitored in a consecutive series of over 300 microvascular
decompressions (MVD) performed in a recent twelve-month period.
In two patients undergoing treatment for trigeminal neuralgia,
BAEP waveforms suddenly disappeared completely during closure
of the dura. Results: The cerebello-pontine
angle was immediately re-explored and there was no evidence
of hemorrhage or cerebellar swelling. The cochlear nerve and
brainstem were inspected, and prominent vascular compression
was identified in both patients. A cochlear nerve MVD resulted
in immediate restoration of BAEP, and both patients recovered
without hearing loss. Conclusion: These cases
illustrate that vascular compression upon the cochlear nerve
may disrupt function, and is reversible with MVD. Awareness
of this event and recognition of BAEP changes alert the neurosurgeon
to a potential reversible cause of hearing loss during posterior
fossa surgery.
Résumé:
Perte de la fonction auditive peropératoire soulagée
par décompression microvasculaire du nerf cochléaire.
Introduction: Les potentiels évoqués
auditifs du tronc cérébral (PÉATC) sont
des indicateurs de la fonction auditive qui sont utiles pendant
la chirurgie de la fosse postérieure. Une lésion
du nerf cochléaire peut survenir par différents
mécanismes et une perte complète des PÉATC
est souvent associée à une perte auditive postopératoire.
Nous rapportons deux cas de perte auditive peropératoire
reliée à une compression vasculaire du nerf
cochléaire. Méthodes: Les PÉATC
ont été surveillés peropératoire
dans une série consécutive de plus de 300 décompressions
microvasculaires (DMV) effectuées sur une période
de 12 mois récemment. Chez deux patients qui subissaient
un traitement pour névralgie du trijumeau, les ondes
ont disparu complètement pendant la fermeture de la
dure-mère. Résultats: L'angle
ponto-cérébelleux a été réexploré
immédiatement. Il n'y avait par d'évidence d'hémorragie
ou d'oedème cérébelleux. Le nerf cochléaire
et le tronc cérébral ont été inspectés
et une compression vasculaire évidente a été
identifiée chez les deux patients. Une DMV du nerf
cochléaire a provoqué une restauration immédiate
des PÉATC et les deux patients ont récupéré
sans perte auditive. Conclusion: Ces cas illustrent
qu'une compression vasculaire du nerf cochléaire peut
affecter sa fonction et qu'elle est réversible par
DMV. La connaissance de cette complication et l'observation
des changements des PÉATC alertent le neurochirurgien
à une cause réversible potentielle de perte
auditive pendant la chirurgie de la fosse postérieure.
Can.
J. Neurol. Sci. 1999; 26:44-47
The
relative efficacy and safety of microvascular decompression
(MVD) for a variety of cranial nerve compression syndromes
has been well established.(1-5) While postoperative neurological
deficits have been uncommon, hearing loss has been a serious
albeit infrequent complication of MVD for trigeminal neuralgia.
Various series have quoted incidences of hearing loss between
0-18%.(1,6-9) Several intraoperative events may result in
cochlear nerve dysfunction, including surgical manipulation,
retraction, and thermal injury from irrigation fluids.(10-13)
Intraoperative monitoring of brainstem auditory evoked potentials
(BAEP) has been widely employed to detect alteration of auditory
function which may respond to adjustment of surgical technique,
and has successfully reduced the occurrence of postoperative
hearing loss.(14-16)
MVD
procedures for the treatment of cranial nerve compression
syndromes have been carried out at the University of Pittsburgh
since 1972, and intraoperative monitoring of BAEP has been
routinely employed since 1984. During a recent 12-month period,
three neurosurgeons (PJJ, TJL, and AMK) performed over 300
of these procedures, 212 for trigeminal neuralgia. In two
cases, BAEP were suddenly lost during final dura closure.
Successful intraoperative measures were employed to restore
normal responses and maintain postoperative hearing. The mechanism
of acute cochlear nerve microvascular compression is described,
and the importance of attention to intraoperative monitoring
changes is highlighted.
Patient
1
A
66-year-old gentleman with a three-year history of typical
trigeminal neuralgia (V2,3), refractory to medical
therapy, underwent a retromastoid craniectomy and MVD. A branch
of the petrosal vein that coursed between the rostral fascicles
of the trigeminal nerve was coagulated and divided. Also,
an anterior inferior cerebellar artery (AICA) branch compressing
the lateral aspect of the nerve was mobilized, and shredded
Teflon® felt implants were placed between the artery and
nerve. During the MVD, BAEP were stable and latency increases
were less than 1 millisecond. However, during closure of the
dura, there was spontaneous loss of BAEP (Figure
1).
The
dura was reopened and no hemorrhage or swelling was encountered.
The cerebellum was gently elevated and the flocculus sharply
dissected away from the vestibular-cochlear nerve. The AICA
was found to be compressing the cochlear nerve and its root
entry zone, before coursing up between the seventh and eighth
cranial nerves towards the trigeminal nerve where it was previously
decompressed (Figure 2).
A MVD of the cochlear nerve was performed. The BAEP then rapidly
returned towards baseline (Figure
1). The dura was then closed and the procedure completed.
Postoperatively the patient awoke neurologically intact and
demonstrated no evidence of hearing loss, as compared to pre-operative
assessment (Table).
|
Table:
Pre- and Post-operative audiology; PTA = pure tone average
(dB); SDS = speech discrimination score (%@ dB) Tests
performed within one week perioperatively.
|
|
Patient
|
Test
|
Side
|
Pre-Op
|
Post-Op
|
|
1
|
PTA
|
R
|
8
|
7
|
|
|
SDS
|
R
|
96@
58
|
96@
47
|
|
|
PTA
|
L
|
12
|
7
|
|
|
SDS
|
L
|
96@
52
|
96@
47
|
|
2
|
PTA
|
R
|
17
|
20
|
|
|
SDS
|
R
|
80@
65
|
86@
60
|
|
|
PTA
|
L
|
10
|
17
|
|
|
SDS
|
L
|
84@
55
|
86@
57
|
Patient
2
A
55-year-old man presented with a ten-year history of typical
trigeminal neuralgia (V2,3), refractory to medical
treatment. Preoperative audiometry and BAEP disclosed a mild
hearing deficit (Table). At surgery, a large arterial loop
was incidentally noted caudal to the eighth nerve, although
this was not approached or manipulated. The trigeminal nerve
was compressed by a loop of the superior cerebellar artery,
and a MVD was performed. BAEP were variable with latency delays
of up to 1.25 milliseconds that corrected with adjustment
of cerebellar retraction. No significant amplitude reduction
occurred. While the dura was being closed, the BAEP suddenly
decreased and disappeared.
The
dura was reopened and no swelling or hemorrhage was encountered.
Vascular compression of the cochlear nerve was suspected as
the cause of cochlear nerve dysfunction. The cerebellum was
mobilized and retracted from the lower cranial nerves with
additional arachnoid dissection. The rostral knuckle of the
vertebral artery was found to be severely compressing the
cochlear nerve at the brainstem. The BAEP improved somewhat
with initial retraction of the cerebellum and then dramatically
improved with MVD of the cochlear nerve, returning to preoperative
baseline by the completion of closure. In the recovery room
hearing was grossly intact, and postoperative audiometry performed
one week later demonstrated no significant change in the patient's
pre-established baseline mild hearing deficit (Table).
Discussion
BAEP
have been consistently used at the University of Pittsburgh
Medical Center for all microvascular decompression cases since
1984. The well described technique involves placement of scalp
needle electrodes and a bilateral earphone to deliver alternating
95 dB auditory clicks at 17.5 Hz. The observational interval
is 10 msec, with 1024 target trials, and a sample rate of
10,000 Hz.(12) Prior to the initiation of routine intraoperative
monitoring, the risk of hearing loss during MVD procedures
was 2.6%, and thereafter decreased to 0.6%.(1) Other centers
have reported similar reliance upon this technology.(10,11,14,16,17)
Despite these observations, it has been difficult to prove
the actual efficacy of BAEP in preventing hearing loss during
microvascular decompression procedures.(10,14,18) Nevertheless,
we have made efforts to respond to changes of BAEP with adjustment
of retraction, further arachnoid dissection, or mobilization
of vessels causing apparent cochlear nerve compression. These
interventions are made for any increased latency approaching
1 millisecond, as prolonged delays between 1.5 and 2.5 milliseconds
carry a significant risk of hearing loss.(14,19)
The
complete intraoperative loss of BAEP is strongly, although
not absolutely, predictive of hearing loss if not immediately
reversed.10,14 Figure 3
presents selected BAEP tracings at key times during the surgical
procedure in Patient 1, and clearly demonstrates loss of all
waves. While wave V is typically followed during intraoperative
monitoring, all preceding waves were also lost in the two
presented patients, while contralateral responses remained
unchanged. This supports the concept that the ipsilateral
signal loss was related to cochlear nerve compression, since
waves I and II are generated by the distal and proximal portions
of the cochlear nerve.(12) Unfortunately, computerized records
of BAEP in Patient 2 were lost. However, the intraoperative
events and BAEP changes in both cases were alike. The immediate
recovery of BAEP following cochlear nerve MVD is highly suggestive
that such vascular compression may produce physiologic loss
of auditory function.
In
the patients presented, the intraoperative loss of auditory
function apparently due to vascular compression of the cochlear
nerve. In Patient 1, the direct manipulation of the AICA loop
during trigeminal nerve MVD may have produced compression
upon the cochlear nerve. In Patient 2, shift of the ectatic
vertebral artery following arachnoid dissection and cerebellar
retraction may have aggravated the degree of compression upon
the cochlear nerve. It is not clear whether the loss of BAEP
during dural closure was due to sudden compression of the
cochlear nerve precipitated by re-accumulation of cerebrospinal
fluid or related to vascular compression caused during arachnoid
or vascular manipulations during the trigeminal nerve MVD.
Nevertheless, we found that in this setting of the dramatic
BAEP loss, predictive of post-operative deafness, surgical
intervention to alleviate vascular compression upon the cochlear
nerve may be effective to normalize neurophysiologic cochlear
nerve function.
Summary
Intraoperative
monitoring of BAEP effectively identifies physiological dysfunction
of the cochlear nerve, and thereby alerts the neurosurgeon
to take corrective measures. The two cases presented illustrate
intraoperative loss of auditory function apparently due to
exacerbation of vascular compression of the cochlear nerve.
Appropriately directed cochlear nerve MVD effectively alleviated
this potential cause of hearing loss.
References
