Using Botox for trigeminal neuralgia

46 Aesthetic Medicine • May 2017
www.aestheticmed.co.uk
Dr Patrick Treacy shares some of his most challenging cases. This month
he talks about injection of botulinum toxin type A (BOTOX) into path of
trigeminal nerve to control the pain and dysesthesia of trigeminal neuralgia
Dr Treacy’s
CASEBOOK
A
53-year-old Irish female presented with an
intractable trigeminal neuralgia pain in the
region of her left maxillary nerve (V2) who did not
respond to pharmacotherapy including pregabalin
300mgs bd and gabapentin 300mgs bd. She had
been admitted to hospital for one month for intravenous
oxycodone hydrochloride. She had also more than fifty nerve
blocks in the previous years and had undergone stereotactic
gamma knife radiosurgery which had work for five
months but later resulted in uncontrollable
dysesthesia pain in the region of her left
maxillary nerve. She defined this as a
continual unpleasant sensation of
something ‘crawling’ under her skin
in her left periorbital. There was a
sensation of intense pain in her
left external nasal area and that
ofelectricshock,burning,andpins
andneedlesandleftmentalarea.
The author evaluated pain
intensity, quality, and location
using the patient’s report. A trial
of a single dose of 165 units/ml
(Speywood) of botulinum toxin type
A (Dysport) diluted in 3.5 mL saline
was used. Fifty units of (Speywood)
botulinum toxin type A (Dysport) were
subcutaneously injected in eight points
distributed mostly along V2 in the lateral periorbital area
and in three injection points in the inferolateral area taking
care not to infiltrate too much directly under the eye to
minimise potential aesthetic side effects. Another thirty
units (Speywood) botulinum toxin type A (Dysport) was
injected in two locations into the external nasal trigger
zone taking care to remain superficial and not to inject
levator labii superiorus. Another twenty units (Speywood)
of botulinum toxin type A (Dysport) was injected into the
mental area with a view to repeating this again in ten days
to minimise the effect of upper lip paralysis
RESULT
Thepatientachievedanimmediatereductionindysesthesiain
herperiorbitalareaandthiscontinuedtocompletereduction
with48hrs.Theauthorreportedsignificantpainreliefalmost
immediately in this patient, who achieved 50% pain relief in
the external nasal region and when this remaining area was
reinjected again she achieved complete pain reduction for
4.5 months. Her mental area received another two injections
andthepainasreducedbyabout60%.Itwasdecidedtoleave
it like that due to the possibility of upper lip paralysis. When
this was injected in five more points the patient received
totalresolutionofthepain.
DISCUSSION
Trigeminal neuralgia (TN) is a
clinical condition caused by
inflammation of the trigeminal
nerve and characterised by
paroxysmal attacks of severe
and electric shock-like pain
along the distribution of one
or more its branches. It affects
approximately one person
in 25,000 people and it more
prevalent in middle or old age
group people. There is a slight
predilection for female sex. The
right side of the face is more commonly
involved than the left side of the face.1,2
Attacks of intense facial pain can occur without
warningorbetriggeredbytouchingspecificareasofthe
face.Althoughtheexactcauseoftrigeminalneuralgiaisnot
fully understood, a blood vessel is often found compressing
the nerve. Pain is unilateral and follows one or more of
the distributions of the trigeminal nerve. Mandibular and
maxillary divisions are more commonly involved than
ophthalmic division.
INFLAMMATORY PAIN
Inflammatory pain manifests as spontaneous pain and
pain hypersensitivity. Spontaneous pain reflects direct
activation of specific receptors on nociceptor terminals
by inflammatory mediators. Pain hypersensitivity is the
consequence of early posttranslational changes, both in the
peripheral terminals of the nociceptor and in dorsal horn
neurons, as well as later transcription-dependent changes
I N J E C TA B L E S
DERMAL FILLERS
Attacks of intense facial
pain can occur without
warning or be triggered by
touching specific areas of the
face. Although the exact cause of
trigeminal neuralgia is not fully
understood, a blood vessel is
often found compressing
the nerve

in effector genes, again in primary sensory and dorsal horn
neurons.4
One fundamental feature of orofacial pain is its
degree of complexity. Inflammation of the nervous system
may be involved in the alteration of the peripheral as well
as central component of sensory nervous system.5,6
Local
inflammationleadstoperipheralsensitisationofnociceptive
neurons and thus increased pain inputs. This leads to
increased release of a peptide called substance P (SP) both
centrally and peripherally by nociceptive primary afferent
C-fibers. BTX-A inhibits the release of SP, thus producing the
analgesiceffectseeninprimary headachedisorders.7
PROPOSEDMECHANISMOFBOTULINUMTOXIN(BTX)
The main effect of botulinum toxin type-A (BTX-A) is
on muscle contraction because of its binding to the
presynaptic nerve terminals, thus inhibiting the release of
the acetylcholine (Ach). A direct analgesic action has been
recognised, suggesting that BTX-A mechanism providing
pain relief may act through an alternative mode of action.
Most hypotheses assume that BTX-A inhibits the release
of Ach as well as other neurotransmitters, including
inhibition of the release of substance P or the blocking
of autonomic pathway. Inhibition of the release of these
neurotransmitters from nociceptive nerve endings can lead
to pain relief.8
It probably produces its antinociceptive effect in trigeminal
neuralgia by several mechanisms. The most likely site
for BTX-A action to produce analgesic effect could be
the postganglionic sympathetic nerve ending, which use
norepinephrine (NE) and adenosine triphosphate (ATP)
as neurotransmitters. NE is increased in chronic pain, and
ATP is involved in the stimulation of muscle nociceptors.
It has been postulated that BTX-A may inhibit the release
of these neurotransmitters and produce analgesic effect
in cases of sympathetically maintained pain involved in
complex regional pain syndrome.9
Decreased sensitisation
of peripheral sensory nerve by stimuli may contribute to
less alteration and responsiveness of peripheral and/or
principal component of sensory nervous system.10
Release of glutamate peripherally results in inflammation,
pain, and edema.11
Glutamate is a stimulant of nociceptive
neurons. It acts through the activation of receptors present
on primary afferents. BTX-A inhibits the inflammatory
pain as well as other symptoms by decreasing the release
of glutamate peripherally.12
BTX-A inhibits the release of
calcitonin gene-related peptide (CGRP), an inflammatory
neuropeptide. It reduces the pain response by inhibition of
CGRP release from afferent nerve terminals13
as well as the
trigeminal nerve.14-17
CONCLUSION
Variousmedicinalorsurgicalmodalitieshavebeenemployed
in the past with variable results as each treatment offers
benefits, but also has limitations. Botulinum toxin (BTX) has
61Aesthetic Medicine • May 2017
DERMAL FILLERS
Ophthalmic branch
Maillary branch
Mandibular branch

>> Dr Patrick Treacy is CEO of Ailesbury Clinics, chairman of the Irish Association of Cosmetic Doctors and
Irish regional representative of the British College of Aesthetic Medicine (BCAM). He is also president of
the World Trichology Association. Dr Treacy has won a number of awards for his contributions to facial
aesthetics and hair transplants including the AMEC Award in Paris in 2014. Dr Treacy also sits on the
editorial boards of three international journals and features regularly on international television and radio
programmes. He was on the scientific committee for AMWC Monaco 2015, AMWC Eastern Europe 2015,
AMWC Latin America 2015, RSM ICG7 (London) and Faculty IMCAS Paris 2015 and IMCAS China 2015.
REFERENCES
1. S. C. Bagheri, F. Farhidvash, and V. J. Perciaccante, “Diagnosis and treatment of
patients with trigeminal neuralgia,” Journal of the American Dental Association,
vol. 135, no. 12, pp. 1713–1717, 2004.
2. S. K. Dufour, “An unusual case of stabbing eye pain: a case report and review of
trigeminal neuralgia,” Optometry, vol. 73, no. 10, pp. 626–634, 2002
3. Various treatment modalities for trigeminal neuralgia include medicinal
management, peripheral nerve injection of local anesthetic or alcohol,
peripheral neurectomies, alcohol injection of trigeminal ganglion, and
intracranial neurosurgical procedures.
4. C. J. Woolf and M. Costigan, “Transcriptional and posttranslational plasticity
and the generation of inflammatory pain,” Proceedings of the National
Academy of Sciences of the United States of America, vol. 96, no. 14, pp.
7723–7730, 1999.
5. G. E. Borodic and M. A. Acquadro, “The use of botulinum toxin for the treatment
of chronic facial pain,” Journal of Pain, vol. 3, no. 1, pp. 21–27, 2002.
6. M. A. Acquadro and G. E. Borodic, “Treatment of myofascial pain with botulinum
A toxin,” Anesthesiology, vol. 80, no. 3, pp. 705–706, 1994.
7. S. Aurora, “Botulinum toxin type A for the treatment of migraine,” Expert
Opinion on Pharmacotherapy, vol. 7, no. 8, pp. 1085–1095, 2006.
8. A. W. Klein, “The therapeutic potential of botulinum toxin,” Dermatologic
Surgery, vol. 30, no. 3, pp. 452–455, 2004.
9. S. Mense, “Neurobiological basis for the use of botulinum toxin in pain therapy,”
Journal of Neurology, vol. 251, supplement 1, pp. 1–7, 2004.
10. C. J. Woolf and R. J. Mannion, “Neuropathic pain: aetiology, symptoms,
mechanisms, and management,” Lancet, vol. 353, no. 9168, pp. 1959–1964, 1999.
11. S. M. Carlton, G. L. Hargett, and R. E. Coggeshall, “Localisation and activation of
glutamate receptors in unmyelinated axons of rat glabrous skin,” Neuroscience
Letters, vol. 197, no. 1, pp. 25–28, 1995.
12. P. L. Durham, R. Cady, R. Cady, and A. J. Blumenfeld, “Regulation of
calcitonin gene-related peptide secretion from trigeminal nerve cells by
botulinum toxin type A: implications for migraine therapy,” Headache, vol.
44, no. 1, pp. 35–43, 2004.
13. D. E. Rapp, K. W. Turk, G. T. Bales, and S. P. Cook, “Botulinum toxin type a inhibits
calcitonin gene-related peptide release from isolated rat bladder,” Journal of
Urology, vol. 175, no. 3, pp. 1138–1142, 2006.
14. A. Carruthers, K. Kiene, and J. Carruthers, “Botulinum a exotoxin use in clinical
dermatology,” Journal of the American Academy of Dermatology, vol. 34, no. 5 I,
pp. 788–797, 1996.
15. J. Jankovic and M. F. Brin, “Therapeutic uses of botulinum toxin,” The New
England Journal of Medicine, vol. 324, no. 17, pp. 1186–1194, 1991.
16. C. J. Wu, Y. J. Lian, Y. K. Zheng, et al., “Botulinum toxin type A for the treatment
of trigeminal neuralgias: results from a randomised, double-blind, placebo-
controlled trial,” Cephalgia, vol. 32, no. 6, pp. 443–450, 2012.
17. E. Borodic and M. A. Acquadro, “The use of botulinum toxin for the treatment of
chronic facial pain,” Journal of Pain, vol. 3, no. 1, pp. 21–27, 2002.
18. G. E. Borodic, M. Acquadro, and E. A. Johnson, “Botulinum toxin therapy for pain
and inflammatory disorders: mechanisms and therapeutic effects,” Expert
Opinion on Investigational Drugs, vol. 10, no. 8, pp. 1531–1544, 2001.
TN BTX areas
48Aesthetic Medicine • May 2017
PREVIOUS SIMILAR STUDIES
Borodic et al. performed an open-label pilot study to
evaluate the efficacy of BTX-A in the treatment of TN. A
totalof11patientssufferingfromtrigeminalneuralgiawere
treated with BTX-A. They reported success in 8 patients
(outof11patientsofTN)foraperiodof2–4months(18).
Türk et al. performed a randomised open-ended study
to evaluate the effectiveness of botulinum toxin type-A
(BTX-A) in patients with trigeminal neuralgia refractory to
other treatment modalities. Eight patients were injected
with100unitsofbotulinumtoxinsintheregionofzygomatic
arch.Basedonpositiveoutcomesandlackofanysignificant
adverse effects, they concluded that BTX-A can be utilised
incasesofrefractorytrigeminalneuralgia(19).
Piovesan et al. reported successful outcomes with the
use of botulinum toxin type-A (BTX-A) in patients of
trigeminal neuralgia. The botulinum toxin was injected
transcutaneously among the branches of trigeminal
nerve.Outof13patientsenrolledinthestudyallpatients
showed improvement with peak effects reached in
20 days of therapy. Four patients remained pain free,
and 9 patients reported partial pain relief with >50%
reduction in medication usage. The beneficial effect
lasts for approximately 60 days (20).
Zúñiga et al. treated twelve patients of idiopathic
trigeminal neuralgia which are unresponsive to the
medicinal treatment. The cumulative mean pain score
on VAS prior to BTX-A injection was 8.83, and it reduced
to 4.08 at the 8th week. Similarly, cumulative number of
paroxysmal attacks per 24 hours reduced from 23.42 to
8.67 at the 8th week (21).
Wuetal.performedarandomised,double-blind,andplacebo-
controlled study to investigate the safety, tolerability, and
efficacyofbotulinumtoxintype-A(BTX-A)inthemanagement
of trigeminal neuralgia. A total of 42 patients were randomly
divided into experimental and placebo group (22 in
experimentaland20inplacebogroup).Theauthorsconcluded
thatbotulinumtoxintype-Amaybeasafe,novel,andefficient
strategyforthetreatmentoftrigeminalneuralgia(22).
DERMAL FILLERS
been used in the past for the treatment of regional dystonia
associated with pain or sensory disturbance. The purpose
of this paper is to establish the effect of using botulinum
toxin type-A (BTX-A) in the management of trigeminal
neuralgia. The botulinum toxin is injected subcutaneously
in divided doses at various trigger zones along the involved
branch of trigeminal nerve. BTX-A can be considered as a
safe, regional, and long-acting agent that alters the chemical
environment around the peripheral nerve involved in the
neurogenicinflammation.Theonlypotentialdisadvantageof
this technique is transient facial asymmetry during dynamic
movements, which may be either prevented or diminished
by the use of lower doses initially and by using a planned
programmeofinjectionoverathreetofour-weekperiod.
CriteriaforBTXuse:Nonresponsivenesstoatleast3drugs
wouldbeapossibleinclusioncriterionfortheuseofbotulinum
toxin in the treatment of trigeminal neuralgia (TN) AM

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