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British Journal of Neurosurgery 2000; 14(1): 33-39

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ORIGINAL ARTICLE

Bilateral trigeminal neuralgia: a therapeutic dilemma


L.TACCONI & J. B. MILES
Department of Neurosurgery,Walton Centre for Neurology and Neurosurgery, Liverpool, UK

Abstract
In order to illustrate the inherent problems of managing bilateral trigeminal neuralgia a retrospective study of the 16 cases
of bilateral trigeminal neuralgia, out of just over 300 cases of trigeminal neuralgia, treated over a 14-year period, has been
performed. All the patients, presented with a typical history of trigeminal neuralgia and underwent surgical exploration. Pain
relief was initially achieved in all cases; however, only four remained cured, three have become pain free after additional
rhizotomy, a further one after peripheral cryotherapy and four with medical treatment. Four patients have had bilateral
operations for trigeminal neuralgia, but in two cases the pain was relieved on one side only. Bilateral trigeminal neuralgia
presents special problems of management with respect to underlying neuropathology (e.g. multiple sclerosis), the need for
the limitation of the use of ablative techniques in order to minimise the disability of bilateral sensory and motor dysfunction,
and the relatively poor response to microvascular decompression. These factors emphasize the multifactorial nature of the
cause of trigeminal neuralgia. Magnetic resonance tomographic angiography is now available and is important in determining
the range of therapeutic options for this group of patients.
Key words: bilateral, evoked potential, facial pain, microvascular decompression, trigeminal neuralgia.

Introduction
Idiopathic trigeminal neuralgia (TGN) is usually a
unilateral disease and bilateral cases are quite rare.^
Bilateral TGN (BTGN) has been reported to have an
incidence which varies between 0.3 and 6%.^"'
While the treatment of idiopathic TGN has become
relatively standarized, there remains a major
therapeutic dilemma in how to treat bilateral cases.
Ablative techniques carry the obligatory risk of
sensory and/or motor trigeminal deficits which, if
bilateral, may cause the patient to have serious
problems with speaking and eating, and therefore the
use of non-ablative methods must be considered.
To illustrate the magnitude of the problem, we
have retrospectively reviewed 16 cases of BTGN from
a total of 302 patients (5.2%) operated on for TGN
in our centre over the last 14 years.
Patients and methods
A total of 16 patients with BTGN presented to the
Walton Centre for Neurology and Neurosurgery in
Liverpool (UK) between 1983 and 1997, and have
been analysed. All presented as clinically typical of
TGN according to Rasmussen's classification.^
The ages ranged between 24 and 78 years (mean

age 54.9) and the duration of symptoms from 1 to 28


years (mean 6.9). There was no difference in the sex
distribution. In one patient, the initial presentation
was with bilateral pain. In six cases (37.5%) the pain
had started on the lefr side, while in the remaining
cases it began on the right side. The second and third
branches were the most commonly involved. Involvement of a single branch was present in six patients.
Generally, the pain was more severe on the side of
the initial presentation.
Two patients (12%) were first degree relatives
(father and son) suffering from Charcot-MarieTooth disease; two had multiple sclerosis (MS) and
another one had probable inclusion body myositis.
Magnetic resonance tomographic angiography
(MRTA)^ was performed in all cases and was useful
in showing a vascular compression in 81 % (13 cases).
In nine cases it was bilaterally positive including the
two patients with MS.
The median interval between the appearance of
the first symptom on one side and the onset on the
opposite side was 5.1 years (range between 7 days
and 19 years). Six patients had previously received
other forms of treatment such as percutaneous radiofrequency coagulation or peripheral nerve cryotherapy. All of them presented with established mild

Correspondence to. Professor J. Miles, Department of Neurological Sciences, Walton Centre for Neurology and Neurosurgery, Lower Lane,
Fazakerley, Liverpool L97 LJ, UK. Fax: 0151 529 5509. E-mail: MILES-J@WCNN.CO.UK
Received for publication 9 March 1999. Accepted 5 August 1999.
ISSN 0268-8697 print/ISSN 1360-046X online/00/010033-07 The Neurosurgical Foundation

34

L. Tacconi &J. B. Miles

to severe sensory impairment on the treated side.


One of them had undergone microvascular
decompression (MVD) elsewhere. All patients
underwent surgical exploration. MVD was performed
in 14 patients, in four (25%) this was done bilaterally
and two underwent posterior fossa rhizotomy.
Vascular compression of the trigeminal nerve by
an artery at the root entry zone on the symptomatic
side was confirmed in 12 cases (seven left side); a
vein was found in two cases and in two patients there
was a combination of artery and vein. In those who
underwent bilateral exploration neurovascular
compression (artery and/or vein) was identified in all
cases confirming the preoperative MRTA findings.
Immediate surgical outcome was successful, in
terms of pain control, in all patients. At a median
follow-up of 36 months (range between 1 and 120
months) only four patients had been cured by MVD.
The others (75%) had recurrence of their pain (two
bilaterally). Four of these (one bilateral) have achieved
pain control with medication (three with
carbamazepine, one with lamotrigine), three after
additional posterior fossa rhizotomy and one by
further cryotherapy (short follow-up). In total, seven
patients (44%) have been cured by surgery alone and
four (25%) controlled by surgery and medication.
Two patients with unilateral pain recurrence are
considering posterior fossa rhizotomy.
Complications were: one patient had a cerebrospinal fiuid leak cured by lumbar puncture; one a
temporary paresis of the IV cranial nerve; and one,
an elderly quadriplegic patient with MS, died of
pneumonia 3 weeks after the operation. Table I
summarizes the clinical and surgical features.
Illustrative cases
Case 2

Idiopathic BTGN. A 33-year-old woman, presented


with typical BTGN. The pain had started 18 months
previously on the left side involving the second and
third divisions of the trigeminal nerve. The third
branch on the right side had been involved for 12
months. Initially, the pain was controlled with a daily
gram of carbamazepine, however, owing to the onset
of side effects, the drug had to be reduced and eventually discontinued.
The patient's neurological examination was
unremarkable with no clinical or radiographic
evidence of MS.
MRTA clearly showed trigeminal vascular compression at the root entry zone bilaterally and the patient
opted for a simultaneous surgical decompression of
both trigeminal nerves. The surgicalfindingscoincided
with the MRTA appearance. The superior cerebellar
artery was dissected and pushed away on the left
side, while on the right, an artery and two veins were
separated from the nerve and the veins divided. The
surgical recovery was quick and uncomplicated.

Unfortunately, she remained totally free from pain


for only a matter of weeks. MRTA confirmed satisfactory bilateral decompression. At 24 months follow-up,
she has recurrent BTGN that is satisfactorily relieved
by 1 g of carbamazepine daily in conjunction with
clonazepam 1 mg nocte.
Case 13

Idiopathic BTGN. This 71-year-old woman


presented after 15 years of bilateral facial pain
involving the second and third division on each side.
Carbamazepine gave some relief, but it had to be
discontinued because of severe side effects. Phenytoin and baclofen gave no relief. Radiofrequency
coagulation on the right side (the worse side) gave
only a temporary improvement with sensory impairment. MRTA showed typical bilateral vascular
compression. Bilateral MVD was performed at the
same procedure. A vein was found on the right side,
while an artery was the source of compression on the
left hand side. The postoperative recovery was
unremarkable and the pain disappeared. At 5 years
follow-up she is still pain free.
Case 3

BTGN and MS. A 71-year-old man had suffered 8


years' typical left-sided TGN involving the second
division. In the last 2 years he also experienced pain
in the same distribution on the opposite side. He had
suffered with MS for the past 30 years, resulting in
such a severe quadriparesis that he was chair bound
and could not feed himself. The pain was either so
severe as to preclude eating or with even moderate
doses of carbamazepine and apparent pain suppression, he was rendered too sedated to be fed. He had
been treated with repeated radiofrequency coagulation, eight times on one side and 10 times on the
other, with recent periods of relief limited to only
weeks. Neurological examination showed unilateral
masseter weakness and bilateral patchy trigeminal
sensory loss in addition to the profound quadriparesis.
MRTA was positive bilaterally. As the right-sided
pain was so much more severe then the left and the
latter having had the more effective recent radiofrequency coagulation, it was decided to proceed with a
right-sided MVD. At surgery, an artery was found
and easily dissected away from the nerve. The first
few postoperative days were unremarkable with disappearance of the pain but unfortunately he died from
pneumonia 3 weeks after the operation.
Case 6

BTGN and MS. A 47-year-old woman had suffered


with typical left-sided TGN involving the second
branch, for 1 year. In the last month she also
experienced right-sided pain involving the same

Bilateral trigeminal neuralgia

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36

L. Tacconi &J. B. Miles

distribution. She had been diagnosed with MS 10


years previously, when she had presented with optic
neuritis. MRTA was bilaterally positive. As she could
not tolerate carbamazepine, she underwent MVD on
the left side which was the more affected side. At
operation, an ectatic superior cerebellar artery was
identified and displaced with a non-absorbable
sponge. At 2 years follow-up she had no pain on the
left side and has approximately monthly fiashes of
pain on the right side.
Cases 5 and 7
BTGN and Charcot-Marie-Tooth disease (familial
cases). Case 7 was a 48-year-old man who presented
with a 24-year history of right-sided TGN involving
the second and third division, and a 10-year history
of left-sided pain involving mainly the second branch.
He, like his son, suffered from Charcot-Marie-Tooth
Disease. At another hospital he underwent alcohol
injection and radioftequency coagulation on the right
side, which gave him only short-term relief from the
pain, but left him with sensory impairment on this
side of the face. A gram of carbamazepine per day
ceased being effective so in 1987 he underwent a rightsided MVD. The finding at operation was that of a
typical arterial compression. This procedure stopped
the pain for only 4 months. A MRTA, performed in our
unit, showed vascular compression only on the left side
and the patient opted for a MVD on this side. At
surgery, two veins were found, coagulated and divided
at the root entry zone. The procedure has stopped his
pain and at 5 years follow-up he only suffers occasional
right-sided twitches of pain, well controlled by a small
dose of medication.
His 24-year-old son (case 5) presented with a 4-year
history of right-sided 2nd and 3rd division TGN and
1 year history of left sided 3rd division TGN. MRTA
showed bilateral neurovascular compression of the
trigeminal nerves at the root entry zone. He
underwent bilateral simultaneous MVD with the findings of a single vein compression on the right side
and an arterial compression on the left side.
Unfortunately, he remained totally free from pain for
only 2 weeks then the pain recurred bilaterally, initially
mild in form. Repeat MRTA showed satisfactory
decompression on the left side, but a suspect vessel
was present on the opposite side. He opted for repeat
exploration on the right side. A small vein of suspect
dimensions was the only finding and so a partial
rhizotomy was undertaken. Two years postoperatively, he is pain free on the right side, but he suffers
mild TGN on the opposite side, controlled by
intermittent moderate doses of carbamazepine.
Discussion
Epidemiology

The first few cases of BTGN^'^ were reported more


than 200 years after the first description of TGN by
Locke in 1677.''"

From an epidemiological point of view, BTGN is


somewhat different from the unilateral condition.
Pollack et al., in a review of 30 cases of BTGN out of
a total of 664 cases found in the first group a higher
percentage of females, a higher rate of familial cases
and an increased occurrence of additional cranial
nerve dysfunction. ^'^ The familial incidence found in
this study reached a very high statistical significance
(p<0.001) when compared with the control group.^
In our series the ratio female/male was equal. One
patient, only, presented with additional VII cranial
nerve dysfunction (case 12) and only two had a history
of familial incidence (cases 5 and 7).
We noticed, as did others,' a lapse of many years
between the onset of pain on one side and the development of the pain on the other. In our series, however,
the pain began simultaneously bilaterally in only one
of our 16 patients.
Incidence

A large review of 14,692 cases of TGN in 1969 by


White and Sweet, found a 3.3% incidence of
BTGN,'^ while 32 out of 269 consecutive patients in
Brisman's series (11.9%), were affected.'^The difference in incidence can, probably, be explained on the
basis of the prevalence of MS in the series''' or
because of the different length of the follow-up. The
longer the history, the more likely it is that there will
be an appearance of BTGN. Peet and Schneider
reported that the incidence of bilaterality in their
patients increased firom 2.7% when they were first
seen to 4.9% at their latest follow-up." However, the
incidence of pure idiopathic bilateral TGN seems to
be 1-5%.''5
Concomitant illness

Approximately 1% of patients with MS develop TGN


and 2-4% of patients with TGN have evidence of
MS."*-'^ In 10-20% of cases TGN can be the
presenting symptoms in otherwise asymptomatic
patients with MS.'^ MS should be considered in any
young patient who develops TGN, particularly if it is
bilateral." In Jensen's et al. series seven out of 22
patients (32%) with MS had bilateral TGN and this
high incidence was significant (p<0.01).''' It seems
that in patients with MS and TGN, BTGN can
develop twice as often.'^ In a series of seven patients
with trigeminal neuralgia and MS a vascular compression of the nerve was seen in 5 of the cases^ versus
an incidence of 85-95% of cases in the so called
idiopathic trigeminal neuralgia group.^
Trigeminal neuralgia has been reported to be
associated, although very rarely, with various connective tissue disorders, especially systemic sclerosis.^'"^^
The reason for this tendency is not clear, but it does
not seem to be due to vasculitis.
In our series, we have two patients with established
MS (cases 3 and 6), one with atypical myositis disease

Bilateral trigeminal neuralgia

(case 12) and two with Charcot-Marie-Tooth disease


(cases 5 and 7). The remainder did not have any
clinical or radiographic evidence of MS. However, it
is possible that they may later develop this disease,
although their mean age of 52.7 years, seems to be
well above the age when MS normally presents itself.
Aetiology

Vascular compression at the nerve root entry zone is


the main causative factor in TGN^'^'^^ with about
10% of cases due to cerebellopontine masses such as
tumour^^ and aneurysm.^^ Demyelinating plaques,
syringobulbia and brain stem infarct have an incidence
of 1%.25'3
The aetiology of BTGN is undoubtedly too
complex to be explained only on the bases of a
mechanical compression at the root entry zone. Most
likely, a multifactorial mechanism plays an important
role with, possible, central and peripheral influences.
Likewise the position of the MS plaque in the
central part of the root entry zone and the efficacy of
central acting anticonvulsant therapy again, seems to
validate this hypothesis.This might explain the surgical
failure of pain control, even, in patients with positive
intraoperative findings of neurovascular compression.
Treatment

The aim of treatment for TGN is suppression of


pain, but with due consideration to the quality of life
on prolonged treatment. Optimally, MRI of the brain
should always be performed to exclude the presence
of a structural pathology, before starting medical treatment with carbamazepine.^''^^ Approximately 50%
of patients do not achieve long-term relief with
medical therapy either because of drug tolerance or
toxic side effects.^^ When medical treatment fails,
then different surgical options must be considered.
There is no doubt that interrupting the pathway at
any location along the trigeminal nerve can relieve
the pain;^*"^^ however, the duration of pain relief
and the specific side efifects will be different depending
upon which technique is used and particularly where
it is applied anatomically.
Percutaneous ablations (peripheral neurectomy,
glycerol injection, radiofrequency or balloon microcompression) are easily performed, but the relief is
temporary and results in varying degrees of deficits
in terms of sensory impairment and motor dysfunction. Percutaneous radiofrequency coagulation (RFC)
can suppress the pain but it is associated with obligatory sensory loss,^^ with up to 19% risk of postoperative dysaesthetic complication^ and 4% incidence of
corneal anaesthesia.^^ This procedure should not be
used in patients with pain involving the first distribution of the trigeminal nerve.
Percutaneous glycerol injection (PGI) was said to
be, rarely, associated with dysaesthesias or anaesthesia

37

dolorosa,^"'*' but recent publications do not support


this belief.*^ Its success rate is also lower when
compared with the other techniques.^^
Percutaneous microcompression (PM) can be suitable also for patients with first division pain and seems
to carry less sensory impairment;*^ however, the
predictable duration of pain relief has yet to be
established.
The morbidity associated with all these procedures
(RFC, PGI, PM), when used bilaterally, must be
bourne in mind. The patient may end up being unable
to eat, either because of total loss of sensation or
masticatory paralysis.'^
Microvascular decompression (MVD) for
trigeminal neuralgia seems to be the most physiological way to deal with this problem.^^ The success
rate with unilateral cases is very high 80-90% at 1
year follow-up, with a very low rate in term of
permanent neurological sequelae^^'*"* and a mortality
rate less than 0.5%.^"^ All patients with TGN should
have MRTA. We have demonstrated, in a previous
publication, the utility, the extreme sensitivity and
specificity of this technique in demonstrating neurovascular compression in patients with TGN.*^ As a
result, open surgical procedures can be recommended with confidence in any case where MRTA is
positive. A long-term analysis substantiates that MVD
carries the highest rate of long-term cure, the lowest
recurrence rate, and the least trigeminal sensory and
motor loss,*''"*^ which is vitally important when
applied to bilateral disease. Careful quantitative
sensory neurology has shown that in fact, MVD
restores to normal the subtle sensory deficits found
in TGN.'*^''*^ The electrophysiological restitution of
normal conduction can also be demonstrated at the
time of surgery."*^
MVD offers the option of cure and is, in our
opinion, the treatment of choice, particularly in
patients with involvement of the ophthalmic division.
It can be recommended for all patients considered fit
enough for surgery, regardless of their age. While the
success rate of MVD alone in BTGN in our series is
only four out of 16 cases, the quality of pain relief
with normal neurological function, the extremely low
mortality, 0.3% and morbidity rate (if we consider all
the cases of TGN operated on by MVD in our Unit)
makes it an essential consideration for treatment, in
presence of a positive MRTA.
When neurovascular compression is not
demonstrated by MRTA, decompressive surgery may
be excluded but partial root section of the trigeminal
nerve in the root entry zone can still be considered.
The advantages of partial root section by open operation at the root entry zone (REZ) are that it assures
protection of motor function, it provides longer or
permanent pain relief, while, in a manner as yet
unexplained, virtually always leaves some light touch
sensation (authors' observation). This makes it safer
when used to treat TGN in the first division; it also

38

L. Tacconi & J. B. Miles

has a much lower risk of provoking anaesthesia doloSimultaneously bilateral MVD is a feasible and
reasonable option' if MRTA is positive bilaterally
and the pains of equal significance, such that removal
of one would not allow reduction in medication. This
would not only save the patients from two operations
with their attendant risks and complication, but also
save them from bearing the pain for an unnecessary
length of time.
More recently gamma knife radiosurgery has been
used, especially for patients in poor medical condition, with encouraging initial results. ^^ Some of the
problems of this technique are, however, that the
treatment will take several weeks to show some effect,
the follow-up available is still quite short and the
recurrence rate seems to be higher than with the
traditional treatment. Delayed radionecrosis may also
prove to be a risk, especially if the targeting involves
the pontine REZ region.
The problem of evolving pathology such as may be
expected in MS, also infiuences therapeutic decisions. We believe, as do Broggi et al.^^ that in cases
where the neurological condition is stable, perhaps,
for more than 2 years and particularly in the absence
of overt brain stem demyelination on MRI, neurovascular decompression should be considered. The
preoperative validation of vascular compression by
MRTA is again essential in these cases.
We believe that it is now possible to establish real
time intraoperative neurophysiological evidence of
improvement in nerve conduction in the trigeminal
nerve by MVD.*^ If this facility becomes routine it
might well play a major role in the surgical management of BTGN.
Conclusions
BTGN presents a definite therapeutic dilemma
compared with unilateral TGN. The pathophysiological mechanism responsible for the pain may be
more complex than that of unilateral cases.
The success rate of MVD for bilateral pain is far
less satisfactory than for the unilateral condition.
However, the quality of pain relief without
neurological deficit, still makes MVD a definite option
for treatment of this condition. Great consideration
must be given to the whole range of surgical options,
directed particularly, to minimizing denervating
morbidity.
In all cases where MVD will not work or will fail
with time (the median follow-up of our patients is
quite short), then a partial rhizotomy at the REZ
must be considered. However, if a percutaneous
procedure is to be used, then percutaneous microcompression seems to be, at the present time, the best
available option in terms of pain control and sensorymotor deficits.
Intraoperative trigeminal evoked potentials may

help in establishing the efficacy of MVD, which is,


when possible, be the best physiological option.
Acknowledgements
We thank Professor H. B. Coakham, Frenchay
Hospital, Bristol (UK), for allowing us to include a
case of his whom we investigated.
References
1 Frazier CH. Bilateral trigeminal neuralgia. Ann Surg
1934;100:770-8.
2 Cushing H. The role of deep alcohol injections in the
treatment
of
trigeminal
neuralgia.
JAMA
1920;75:441-3.
3 Harris W. An analysis of 1,433 cases of paroxysmal
trigeminal neuralgia (trigeminal tic) and the end-results
of gasserian alcohol injection. Brain 1940;63:209-24.
4 Velasco Siles JM, Ouaknine GE, Mohr G, Molina Negro
P, Hardy J. Bilateral trigeminal neuralgia. Surg Neurol
1981;16:106-8.
5 Pollack IF, Jannetta JP, Bissonette DJ. Bilateral
trigeminal neuralgia: a 14 year experience with microvascular decompression. J Neurosurg 1988568:559-65.
6 Rasmussen P. Facial pain. A Clinical Study with Special
Reference to Symptomatology, Ftiology and Surgical
Therapy. Copenhagen: Munksgaard, 1965.
7 Meaney JFM, Miles JB, Nixon TE, Whitehouse GH,
Ballantyne ES, Eldridge PR. Vascular contact with the
fifth cranial nerve at the pons in patients with trigeminal
neuralgia: detection with 3 D FISP imaging. Am J
Roentgenol 1994; 163:1447-52.
8 Winslow CH. Bilateral trigeminal neuralgia. Ann Surg
1896;24:748.
9 Krause F. Resection des trigeminus. Innerhalb der
Schadelhole. Verh Dtsch Ges Chir 1892;21:199-210.
10 Locke J. The celebrate Locke as a physician. Lancet
1829;ii:367.
11 Locke J. Letters to Dr Mapletoft: Letter VII, Paris, 9
Aug. 1677; Letter IX, X, Paris, 4 Dec. 1677, The
European Magazine, pp. 89-90, February, 1789; pp
185-186, March, 1789.
12 White JC, Sweet WH. Pain and the Neurosurgeon. A
Forty-year Experience Springfield: Charles C Thomas,
1969.
13 Brisman R. Bilateral trigeminal neuralgia. J Neurosurg
1987;67:44-8.
14 Jensen ST, Rasmussen P, Reske-Nielsen E. Association
of trigeminal neuralgia with multiple sclerosis: clinical
and pathological features. Acta Neurol Scand
1982;65:182-9.
15 Peet MM, Schneider RC.Trigeminal neuralgia. A review
of six hundred and eighty-nine cases with a follow-up
study on sixty-five percent of the group. J Neurosurg
1952;9:367-77.
16 Lazar ML, Kirkpatrick JB. Trigeminal neuralgia and
multiple sclerosis: demonstration of the plaque in an
operative case. Neurosurgery 1979;5:711-12.
17 Rushton JG, Olafson RA. Trigeminal neuralgia associated with multiple sclerosis. Report of 35 cases. Arch
iVewro/1965; 13:383-6.
18 De Marco JK, Hesselink JR. Trigeminal neuropathy.
Neurosurgical perspectives on trigeminal neuralgia.
Neurosurg Glin NAm, 1997;8(l):103-30.
19 Taha J, Tew JM. Treatment of trigeminal neuralgia by
percutaneous radiofrequency rhizotomy. Neurosurgical
perspectives on trigeminal neuralgia. Neurosurg Clin N
Am 1997;8(l):31-40.

Bilateral trigeminal neuralgia


20 Meaney JFM, Watt JWG, Eldridge PR, Whitehouse GH,
Wells JCD, Miles JB. Association between trigeminal
neuralgia and multiple sclerosis: role of magnetic
resonance imaging. J Neurol Neurosurg Psychiatry
1995;59:253-9.
21 Senecal UJL. Polymyositis presenting as bilateral
trigeminal neuropathy BrJ Rheumatol 1994;33:1191-2.
22 Farrell DA, Medsger TA. Trigeminal neuropathy in
progressive systemic sclerosis. Am J Med
1982;73:57-62.
23 Ashworth B, Tait GBW. Trigeminal neuropathy in
connective tissue disease. Neurology 1971j21:609-14.
24 Heald A. Progressive systemic sclerosis presenting as a
case of trigeminal neuropathy (letter). J Neurol Neurosurg Psychiatry 1989;52:918-20.
25 Hagen NA, Stevens JC, Michet CJ. Trigeminal sensory
neuropathy associated with connettive tissue disease.
Neurology 1990;40:891.
26 Jannetta PJ. Neurovascular compression in cranial nerve
and systemic disease. Ann Surg 1980;192:518-25.
27 Cheng TMW, Cascino TL, Onofrio BM.
Comprehensive study of diagnosis and treatment of
trigeminal neuralgia secondary to tumours. Neurology
1993;43: 2298-302.
28 Rosa A, Mizon JP, Sevestre H. Aneurisme geant
vertebro-basilaire. Syndrome frontal. Rev Neurol (Paris)
1991;147:827-9.
29 Olafson RA, Rushton JG, Sayre GP. Trigeminal
neuralgia in a patient with multiple sclerosis. J Neurosurg 1966;24J 55-9.
30 Brisman R. Trigeminal neuralgia and multiple sclerosis.
Arch Neurol 1987;44: 379-81.
31 Cherrick HM.Trigeminal neuralgia. Report of a bilateral
case. Oral Surg, OralMed, OralPathol 1972;34:714-26.
32 Nicol CR A four year double-blind study of tegretol in
facial pain. Headache 1961;9:54.
33 Taylor JC, Brauer S, Espir ML. Long-term treatment
of trigeminal neuralgia with carbamazepine. Postgrad
34 Brett DC, Ferguson GG, Ebers GC, Patty DW. Percutaneous trigeminal rhyzotomy. Treatment of trigeminal
neuralgia secondary to multiple sclerosis. Arch Neurol
1982;39:219-21.
35 Linderoth B,' Hakanson S. Paroxysmal facial pain in
disseminated sclerosis treated by retrogasserian glycerol
injection. Acta Neurol Scand 1989;80:341-6.
36 Fromm GH. Medical treatment of patients with
trigeminal neuralgia. In Fromm GH, Sessle BJ, eds,
Trigeminal Neuralgia. Stoneham: Butterworth, 1991:
131-44.
37 Lovely T, Jannetta PJ. Microvascular decompression
for trigeminal neuralgia. Neurosurgical perspectives on
trigeminal neuralgia. Neurosurg Clin N Am
1997;8(l):ll-29.
38 Taha JM,Tew JM Jr, A prospective 15-year follow-up of
154 consecutive patients with trigeminal neuralgia

39

40

41

42
43
44

45

46

47
48

49
50

51

52

39

treated by percutaneous stereotactic radiofrequency


rhyzotomy. J NewrosMrg^ 1995;83:989-93.
Rovit RL. Percutaneous radiofrequency thermal
coagulation of the gasserian ganglion. In: Brown C-L.,
ed., Trigeminal Neuralgia. Baltimore: William & Wilkins,
1990.
Nugent GR. Radiofrequency treatment of trigeminal
neuralgia using a cordotomy-type electrode.
Neurosurgical perspectives on trigeminal neuralgia.
Neurosurg Clin NAm, 1997;8(l):41-52.
Jho HD and Lunsford LD. Percutaneous retrogasserian glycerol rhizotomy. Neurosurgical perspectives on
trigeminal neuralgia, Neurosurg Clin N Am
1997;8(l):63-74.
Taha JM, Tew JM Jr. Comparison of surgical treatments for trigeminal Neuralgia: reevaluation of radiofrequency rhizotomy. Neurosurgery 1996;38:865-71.
Mullan S. Percutaneous microcompression of the
trigeminal ganglion. In Brown C-L, ed., Trigeminal
Neuralgia. Baltimore:William &Wilkins, 1990;137.
Sindou M, Mertens P. Microsurgical vascular
decompression (MVD) in trigeminal and glosso-vagopharyngcal neuralgias. A twenty year experience. Acta
Neurochir [Suppl] (Wien) 1993^58:168-72.
Meaney JFM, Eldridge PR, Dunn LT, Nixon TE,
Whitehouse GH, Miles JB. Demonstration of neurovascular compression in trigeminal neuralgia with
magnetic resonance imazmg.JNeurosurg 1995;83:799805.
Barker FG II, Jannetta PJ, Bissonette DJ, Larkins MV,
Jho HD. Long term outcome after microvascular
decompression for typical trigeminal neuralgia. N Engl
JMed 1996;334:1077-83.
Miles JB, Eldridge PR, Haggett CE, Bowsher D. Sensory
effects of microvascular decompression in trigeminal
neuralgia. J Neurosurg 1997;86:193-6.
Bowsher D, Miles JB, Haggett CE, Eldridge PR.
Trigeminal neuralgia: a quantitative sensory perception
threshold study in patients who had not undergone
previous invasive procedures. J Neurosurg
1997;86:190-2.
Leandri M, Eldridge PR, Miles JB. Recovery of nerve
conduction following microvascular decompression for
trigeminal neuralgia. Neurology 1999;51:1641-6.
Jannetta PJ. Microvascular decompression of the
trigeminal nerve root entry zone. In: Brown C-L, ed.,
Trigeminal Neuralgia. Baltimore: William & Wilkins,
1990:201.
Kondziolka D, Lunsford LD, Habeck M, Flickinger
JC. Gamma knife radiosurgery for trigeminal neuralgia.
Neurosurgical perspectives on trigeminal neuralgia.
Neurosurg Clin NAm 1997;8(l):79-86.
Broggi G, Franzini D, Servello D, Dones I. Microvascular decompression in patients with trigeminal
neuralgia and multiple sclerosis. Abstract (0-28-410),
Clin Neurol Neurosurg 1999(Suppl. 1):S 210.

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