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Scheller Delayed Facial Nerve Paresis Following Acoustic

C. Strauss
R. Fahlbusch
Neuroma Resection
J. Romstöck and Postoperative Vasoactive Treatment
Verzögerte N. facialis-Parese nach Resektion von Akustikusneurinomen

Original Article
und postoperativer vasoaktiver Therapie

Abstract Zusammenfassung

Object: Delayed facial nerve paresis is a well known clinical phe- Einleitung: Die verzögerte N. facialis-Parese ist ein bekanntes
nomenon following acoustic neuroma surgery, typically occur- klinisches Phänomen nach Resektion von Akustikusneurinomen,
ring early during the postoperative course. The clinical course of das typischerweise im frühen postoperativen Verlauf beobachtet
the delayed facial nerve paresis and intraoperative electromyo- wird. Klinischer Verlauf und intraoperative EMG-Signale wurden
graphic (EMG) signals were evaluated in a subgroup of patients bei einer Patientengruppe untersucht, bei der eine verzögerte
who underwent vasoactive treatment for preservation of hearing Parese erst nach dem Absetzen einer vasoaktiven Therapie zur
and developed secondary deterioration after termination of Erhaltung des Hörvermögens auftrat.
treatment. Patienten und Methoden: Zwischen 1990 und 2001 wurden
Methods: Between 1990 and 2001 seven patients were identi- sieben Patienten beobachtet, die über 10 Tage HAES und Nimodi-
fied who received vasoactive treatment for preservation of hear- pine zur Verbesserung der Mikrozirkulation des N. cochlearis er-
ing and developed a delayed facial nerve paresis after termina- halten hatten und die nach dem Absetzen der Medikation eine
tion of medication. Intraoperative facial nerve EMG activity was verzögerte N. facialis-Parese entwickelten. Die kontinuierlich ab-
analyzed in six patients. geleiteten intraoperativen EMG-Signale wurden bei sechs Pa- 103
Results: All patients developed a delayed facial nerve paresis be- tienten analysiert.
tween 2±5 days following termination of a 10 day treatment con- Ergebnisse: Sämtliche Patienten entwickelten zwei bis fünf Tage
sisting of HES and nimodipine. Medication was re-initiated and nach dem Absetzen der Medikation eine verzögerte N. facialis-
the facial nerve paresis improved in all patients. In two patients Parese. Es erfolgte ein erneuter Therapiezyklus mit konsekutiver
intraoperative EMG signals revealed ªA-trainsº waveform pat- Erholung der Funktion bei allen Patienten. Die Analyse der in-
terns, which are highly suggestive for an immediate postopera- traoperativen EMG-Aktivität ergab bei 2 Patienten ¹A-trainsª,
tive facial nerve paresis, whereas in four patients no pathogno- die mit einer hohen prognostischen Sicherheit auf eine unmittel-
monic EMG patterns could be recorded. bare postoperative Parese hinweisen.
Conclusions: The delayed onset of a facial paresis following ter- Schlussfolgerung: Die nach Absetzen einer vasoaktiven Thera-
mination of vasoactive treatment points to a disturbed microcir- pie verzögert auftretende N. facialis-Parese im Rahmen der oper-
culation of the nerve as the main pathophysiological feature. ativen Behandlung von Akustikusneurinomen weist auf eine ge-
Two groups could be identified on the basis of intraoperative störte Mikrozirkulation als pathophysiologische Ursache hin.
EMG activity. In one group with presence of ªA-trainsº medica- Aufgrund der intraoperativen EMG-Aktivität lieûen sich zwei Pa-
tion apparently masked the onset of an immediate postoperative tientengruppen identifizieren. Bei Patienten mit ¹Parese-spezifi-
facial nerve deficit. Four patients without ªA-trainsº did not de- scherª EMG-Aktivität (¹A-trainsª) konnte die medikamentöse
velop a typical delayed facial nerve paresis during vasoactive Therapie anscheinend das Auftreten einer unmittelbar postope-
treatment, but thereafter. The time lag between termination of rativen Parese zunächst maskieren, während sich bei den übrigen

Neurochirurgische Klinik der Universität Erlangen-Nürnberg, Germany

Prof. Dr. med. Christian Strauss ´ Neurochirurgische Klinik der Universität Erlangen-Nürnberg ´
Schwabachanlage 6 ´ 91054 Erlangen ´ Germany ´ Phone: +49/9131-8 53 43 84 ´ Fax: +49/9131-8 53 45 51 ´

Zentralbl Neurochir 2004; 65: 103±107  J. A. Barth Verlag in Georg Thieme Verlag KG
DOI 10.1055/s-2004-816268
ISSN 0044-4251
treatment and onset of a delayed palsy points to a protective ef- Patienten die Manifestation durch die Therapie zumindest ver-
fect due to improved microcirculation. zögerte. Der Zusammenhang zwischen postoperativer medika-
mentöser Therapie und verzögertem Auftreten einer N. facialis-
Key words Parese weist auf einen möglichen protektiven Effekt durch eine
Delayed facial nerve palsy ´ vasoactive treatment ´ intraoperative Verbesserung der Mikrozirkulation hin.
EMG ´ acoustic neuroma
Verzögerte N. facialis-Parese ´ vasoaktive Therapie ´ intraopera-
tives EMG ´ Akustikusneurinom

Introduction these 78 patients developed a delayed facial nerve paresis, cor-

responding to a percentage of 9 %. In patients not undergoing
Original Article

Secondary deterioration of cranial nerve function following therapy an onset later than 10 days after the surgical procedure
acoustic neuroma resection is a well known clinical phenomen- was never observed. The treatment regimen consisted of nimodi-
on [4, 5, 10, 13, 15], which usually occurs early during the post- pine (15±30 g/kg/hour; Bayer, Leverkusen, Germany) which
operative course. Experimental studies on the cochlear nerve was started at the end of the surgical procedure and hydroxye-
have focused on a disturbed microcirculation at the Oberstei- thyl starch (max. 2 ” 500 ml/d; Baxter, Unterschleiûheim, Germa-
ner-Redlich zone [20]. Patients with a reversible loss of BAEP, ny) which was started 24 hours after surgery aiming at a hema-
who account for almost half of all patients with acoustic neuro- tocrit of between 30 and 35 % [22]. Dexamethasone was given, on
mas in whom a procedure to preserve hearing is undertaken, the basis of a routine tapering scale, during the first 5 postopera-
have a 70 % risk of definite hearing loss, if postoperative medica- tive days. Mean age was 50 years, ranging from 30±61 years. All
tion is limited to routine application of dexamethasone. 40 % of patients underwent preoperative contrast enhanced magnetic
these patients suffer from a delayed hearing loss with audiome- resonance imaging (MRI). Tumor diameter was measured on ax-
trically documented hearing initially after the procedure. A re- ial T1-weighted contrast enhanced images. The extrameatal di-
cently published prospective study using intravenous nimodi- ameter ranged from 13 to 25 mm, with an average size of
pine and hydroxyethylstarch (HES) for 10 days in these patients 18 mm. The intrameatal component ranged from 0 to 9 mm
has demonstrated a statistically significant therapeutic benefit (average 5 mm). The House-Brackmann (H-B) grading system
with an increased hearing preservation rate of 66 % compared to [7] was used to determine facial nerve function (grade I in five
30 % in non-treated patients [22]. patients, grade II in two patients, Fig. 1). Based on AAO-HNS
guidelines preoperative cochlear nerve function was classified
104 Other pathophysiological factors include secondary edema [18, as ªAº in 5 patients, and as ªBº and ªDº in one patient, respective-
20] and, specifically for the facial nerve, reactivation of the ly [3]. Additional trigeminal hypesthesia was documented in one
herpes simplex virus [5, 16] has been discussed. The prognosis patient. All patients were operated upon via a lateral suboccipital
is generally considered to be excellent for spontaneous recovery approach by the senior authors (RF, CS) with intraoperative mon-
[10], although poor outcomes have been reported [13, 18]. There itoring of auditory evoked potentials (BAEP) and facial nerve
is no established definition in the literature [4], but the onset, EMG, using techniques which have been published previously
similar to delayed hearing loss, is usually within the first days [17, 22]. For EMG-monitoring non-isolated 30-mm-long needle
after the surgical procedure. Fenton [4] defined delayed facial electrodes were placed into the orbicular oculi, the nasal and
paresis as any worsening of facial function following the initial
assessment of postoperative function. Lalwani [10] considered
either deterioration of facial function from normal to abnormal
or an increased severity of the degree of facial paralysis as indic-
ative of delayed facial paresis. The incidence varies from 11.7 to
41 % [5, 10, 13, 18] and is not influenced by age, sex or tumor size
[10, 13]. Clinical and electrophysiological data in patients, who
developed a delayed facial nerve palsy after termination of va-
soactive treatment for hearing preservation, are of particular in-
terest with respect to a similar underlying pathophysiological
mechanism for both delayed hearing loss and secondary dete-
rioration of facial nerve function.

Patients and Methods

Between 1990 and 2001 78 patients out of a total number of

264 patients underwent vasoactive treatment for preservation Fig. 1 Clinical course of the facial nerve function pre- and postopera-
of hearing [22] following acoustic neuroma surgery. After termi- tive during the first course of vasoactive treatment. n/N = numbers of
nation of a 10 day treatment course 7 (4 women and 3 men) of patients.

Scheller C et al. Delayed Facial Nerve ¼ Zentralbl Neurochir 2004; 65: 103 ± 107
the orbicular oris muscle. All three channels were continuously
recorded, stored and analyzed off-line. The recording system Table 1 Intraoperative EMG activity: + = present, ± = non-pres-
consisted of a bioamplifier (Jaeger-Toennies GmbH, Hoechberg, ent
Germany), a switchboard and a personal computer with two 12-
name A-train B-train C-train spikes spikes bursts bursts
bit analog-digital conversion boards (DT2814; Data Translation; < 500 lV > 500 lV < 500 lV > 500 lV
Inc. Marlboro, MA). Analog filter settings of 2 Hz to 4 kHz were
used without a notch filter. A Modula-2 program was developed E. C. surgery was performed prior to introduction of the EMG recording
for data processing, digital antialiasing filtering, and continuous system described above
data display and storage on hard disks. Waveforms could be dis- K. E. ± ± ± + + + ±
played on the computer monitor. EMG signals were differenti- P. A. ± + + + + + +
ated into ªspikesº, ªburstsº, ªA-º, ªB-º and ªC-trainsº. ªA-trainsº R. H. ± + ± + + + ±
have been recently identified as being highly specific (89 %) and S. M. ± ± ± + + + ±
sensitive (86 %) for predicting immediate postoperative facial S. K. + + + + + + +

nerve deficits [17]. Anesthesia was maintained with propofol V. U. + ± ± + + + ±

Original Article
(6±12 mg/kg/h) and alfentanil hydrochloride (60 g/kg/h) [22].
Patients were reevaluated 6 and 12 months after the surgical
procedure, including assessment of facial and cochlear nerve one patient facial nerve function remained stable and improved
function (Department of Otorhinolaryngology) and contrast en- by two H-B grades after six months (Fig. 2). Deterioration follow-
hanced MRI. ing the termination of the second therapy cycle was not ob-

Results For analysis of intraoperative EMG the recently published classi-

fication was employed [17]. In one patient surgery was per-
Immediately after surgery six patients had no (n = 1) or moder- formed prior to introduction of the EMG recording system
ate (n = 5) deterioration of facial nerve function compared to the (Table 1). EMG activity was divided into ªspikesº, ªburstsº, ªA-º,
preoperative status. One patient showed H-B grade V initially
after the procedure. Under vasoactive treatment the H-B grade
remained stable (n = 5) or improved (n = 2). The one patient
with initial poor facial nerve function (H-B grade V) improved to
H-B grade III (Fig. 1) at the end of the treatment cycle.

All patients developed a delayed paresis between two and five

days after vasoactive treatment was terminated. Deterioration 105
varied from one (n = 1), two (n = 4) and three H-B grades
(n = 2). All patients were readmitted and underwent a second
therapy cycle with intravenous application of HES and nimodi-
pine for 10 days. Dexamethasone was not given during the sec-
ond cycle. Under medication facial nerve function did not dete-
riorate further, but improved in 6 patients by two H-B grades. In

Fig. 2 Clinical course of the facial nerve function after termination of

vasoactive treatment, discharge and reemployment of vasoactive
treatment. The patient with stable facial nerve function throughout
the second treatment course improved by two H-B grades after six Fig. 3 Intraoperative EMG patterns a ªA-trainº of various frequency
months. n/N = numbers of patients. and amplitudes, b ªB-trainº, c ªC-trainº, d Spike, e Burst.

Scheller C et al. Delayed Facial Nerve ¼ Zentralbl Neurochir 2004; 64: 103 ± 107
ªB-º and ªC-trainsº (Table 1, Fig. 3). On the basis of intraoperative Medication accelerated axonal resprouting and reduced the
EMG two different groups could be characterized. In two patients polyneuronal innervation of the target muscles in the treated
ªA-trainsº could be identified. ªA-trainsº are so far the only iden- group compared to the placebo group [2]. Mattsson et al. recent-
tified EMG pattern, which are specific and sensitive for predict- ly published their finding that nimodipine promotes regenera-
ing an immediate postoperative deterioration [17]. Four patients tion and functional recovery after intracranial facial nerve crush
showed no characteristic EMG activity suggestive for an immedi- [11]. Strauss et al. reported the benefit of vasoactive treatment
ate postoperative facial nerve deficit. In both groups spikes, for the preservation of hearing following acoustic neuroma sur-
bursts and ªnon-A-trainsº were found throughout the surgical gery as a result of improved microcirculation [22]. These findings
procedure (Table 1). point to a disturbed microcirculation as the pathophysiological
mechanism for the clinical course of delayed facial nerve paresis
Herpes serology was measured in three patients (PA, RH, VU) in this study. Therefore hemodilution, as used successfully in
without evidence for reactivation. clinical surgery [9, 22] and for treatment of acute ischemic stroke
[1], seems to be of potential benefit. It is particularly remarkable
Hearing evaluation on follow-up revealed class A in three pa- that two patients with ªA-trainsº did not show any facial nerve
Original Article

tients, class B in one and class D in three patients [3]. In one of weakness during the initial postoperative treatment cycle
the three patients some hearing remnants could be preserved. (Fig. 3), since Romstöck et al. had shown that ªA-trainsº can be
Trigeminal hypesthesia as documented before surgery in one of considered highly specific and sensitive for predicting post-
the seven patients resolved. Tumor removal was complete in all operative facial nerve deficits in acoustic neuroma surgery [17].
patients and was documented on contrast enhanced MRI. In these two cases the neuroprotective effect of nimodipine and
HES was evident. The remaining patients showed no EMG evi-
With respect to the side effects of vasoactive treatment one pa- dence for an immediate postoperative deficit (Fig. 3). These pa-
tient (PA) developed a mild transient pruritus, as a dose-related tients most likely represent the well known ªdelayed facial nerve
rare side effect [14, 19]. HES may influence coagulation dose de- paresisº phenomenon, which was masked until the 10th post-
pendently [8, 21, 23], although clinical studies have shown no operative day, when postoperative medication was terminated.
negative side effects. Because of these potential side effects, HES Its beneficial effects in this small group of patients were en-
medication was not started until 24 hours following surgery. No hanced by the second treatment course, which followed the on-
hemorrhages were observed. Hypotension as a side effect of ni- set of delayed palsy. In all patients facial nerve function im-
modipine application requiring dose reduction was not ob- proved considerably or at least remained stable as in one patient.
On the basis of clinical and electrophysiological observations in
7 patients it can certainly not be concluded whether functional
Discussion recovery occurred spontaneously or as an effect of therapy, but,
106 similar to the experiences with delayed hearing loss, a disturbed
Disturbance of microcirculation, secondary edema [18, 20] and, microcirculation seems the most important underlying patho-
more recently, reactivation of herpes simplex virus [5, 16] have physiological mechanism for delayed facial nerve palsy in acous-
been discussed as the underlying pathophysiology in delayed fa- tic neuroma surgery. The time lag between termination of va-
cial nerve paresis following acoustic neuroma surgery. The post- soactive treatment and onset of delayed palsy points to a protec-
operative course of facial nerve function in this study seemed in- tive effect of the therapeutic regimen. The value of medication
fluenced by vasoactive treatment consisting of nimodipine and needs to be clarified in a prospective study based on the presence
HES (Figs. 1, 2). Facial nerve function either improved or re- of ªA-trainº-EMG activity.
mained stable, despite the fact that EMG patterns were sugges-
tive for postoperative paresis in two patients (Fig. 3). After termi-
nation of treatment function deteriorated by an average of two
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Scheller C et al. Delayed Facial Nerve ¼ Zentralbl Neurochir 2004; 64: 103 ± 107