Download Case report of Glossopharyngeal Neuralgia

Case report of Glossopharyngeal Neuralgia: A review
and a patient’s experience
1
Rajesh Chella Narendran , Shefali Kadambande
2
Abstract
Glossopharyngeal neuralgia is a rare neuropathic pain condition. We report the case
of a 53-year-old lady who presented to the pain clinic with features of neuropathic
pain in the sensory distribution of the glossopharyngeal nerve. The patient had
visited various specialists and undergone extensive investigations prior to
presentation to the pain clinic. In this article we would like to review the
epidemiology, clinical features, causes, and various available treatment modalities for
this condition and also present the patient’s perspective of her experience.
Keywords
Glossopharyngeal neuralgia, facial pain, clinical features, treatment outcomes, prognosis
Case History
A 53-year-old female patient was referred from ENT for persistent unilateral leftsided neck pain. Her complaints were brief episodes of severe stabbing neck pain,
each lasting a few minutes,for the past 8 years .The area was sensitive to touch and
she described an increased sensitivity to smells with retching. On questioning she did
have a history of recurrent sore throats in the past. She gave a history of sensations of
pins and needles at the back of her tongue when wearing long earrings that touched
her neck or while draping a scarf around her neck. She described syncope attacks on
turning her head or looking up while putting her clothes to dry.
She was seen by the neurologists and was discharged without a diagnosis. She also
saw ENT specialists and was investigated for tinnitus and deafness with a CT scan of
her ear. She gave a past medical history or diagnosis of Chronic Fatigue Syndrome,
(CFS), Myalgic Encephalopathy, (ME), diverticular disease and sleep disturbances.
She was a Lecturer in Computing and had to give up on health grounds. Her hobbies
were sSailing, mountaineering and rock climbing. Her anxiety and depression scores
were 0 and 7 respectively on the hospital anxiety and depression scale (HADS). Her
worst pain score was 8, least 3 and average was 6 on the brief pain inventory (BPI)
scale. Computed Tomography (CT) scan of her petrous bone and head were normal.
There were no major psychological issues. Her medications were Tramadol 50mgs
TDS, Paracetamol 500mgs TDS, Ibuprofen 200mgs PRN, Ondansetron 4-8 mgs,
Sumatriptan and Vitamin D supplements. She has also tried physiotherapy and neck
exercises. On examination allodynia to cotton wool was present over the anterior and
1
Advanced Pain Trainee,
2 Consultant in Anaesthesia and Pain Medicine, Department of Anaesthesia and Pain Medicine, University Hospital
of Wales
62
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
posterior triangle in the neck, and it caused paresthesia in the tongue and headaches.
A diagnosis of Glossopharyngeal Neuralgia was made in clinic.
The management plan included information on Glossopharyngeal Neuralgia
MRI brain to rule out other causes of the neuralgia, but it was later reported normal
Carotid Doppler - to rule out carotid sinus hypersensitivity but cardiologists reported
reflex syncope and a normal Doppler
5% Lidocaine plaster commenced over the neck 12 hours per in a day
Gabapentin at a starting dose of 100mgs TDS titrated up to 400mgs TDS
The patient reported more than 50% reduction in pain scores with the above
combination of medication. She appeared more alert on review. She reported
improvement in quality of life indicators on the BPI, including sleep, mood, and
general activity. The sense of taste improved and frequency of flare ups reduced.
She felt an increased confidence to use public transport for travel.
The patient read about Glossopharyngeal Neuralgia and that, combined with the
education and information in clinic, assisted in understanding the condition and
managing it. She was satisfied with the knowledge that Gabapentin could be titrated
to effect up to 1.2g TDS but preferred to have that as a reserve
Patient’s view point
How many doctors does it take to make a diagnosis?
In 1979 I began teaching and for the last 20 years of that career taught
CT/Computing. It was a very good job, I enjoyed it and had a clear plan for the future
- it didn't involve retiring on ill health grounds at only 49.
After an infection in 2003 problems persisted and eventually bowel issues, increasing
pain and bouts of brain-numbing exhaustion meant that being in a classroom became
impossible. During the last 7 months in work I was retching / vomiting every day and
following a lengthy sick leave I applied for Ill Health Retirement (IHR). Somewhere
along the way CFS (Chronic Fatigue Syndrome)/ME was diagnosed and CBT/GET
(Graded Exercise Therapy) was required as part of the IHR process; the final report
concluded I was physically worse than when I started.
So, in 2007, I was pensioned off but left with no real answers. The questions - Why
do I wake up at 3am and vomit? Why do I begin retching when I wash my neck or put
on a necklace? Why do I wake up every morning with a thick head, nausea and pain?
Why do even my eyeballs ache?
My route to the pain clinic was convoluted and began at gastroenterology. They were
very thorough and also tested for the less routine Whipple’s disease and Porphyria
before sending me to Dermatology. At dermatology bradycardia was picked up but
an unfortunate breakdown in communication meant that a note, suggesting a 24hour Holter and Autonomic System assessment, was not passed on, and that was
that.
Then I went deaf. Temporarily, thankfully, but it put me on a path to the
Otolaryngology head /neck clinic, thence to Audiology. As an offshoot from there I
went to Neurology - follow my finger up and down, walk in a straight line - no I am
not drunk! Discharged from clinic. Thank you to the Audiologist for persisting and
sending me to ENT and to ENT for passing me over to the pain clinic, where
Glossopharyngeal Neuralgia was diagnosed.
Having a diagnosis has its benefits but some, such as 'CFS', can prove to be a
63
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
hindrance. I have one doctor who advises no form of exercise, another who advises
be aware of your limits and a third who thinks even admitting to having limitations is
very negative. A few doctors have tried to bend my symptoms into the box that is
defined by the boundaries of their specialism, whilst one dismissed my symptoms
with a wave of the hand saying 'that doesn't happen'. The reaction now, when I say
Glossopharyngeal Neuralgia, is 'that's rare' and suddenly eyes and ears are open.
Refreshingly, at the pain clinic, everything was assessed without preconceptions and
even without my background knowledge the explanations and information I was
given were clear and full. Success and satisfaction from my point of view arise from
not only the knowledge of the doctors I meet but also from their attitude and
personability. At the pain clinic I can't fault either of those and feel happy that I could
contact the clinic if I needed to.
Throughout both my graduate and postgraduate degrees I covered a lot of anatomy
and physiology but I don't tend to tout this rusty knowledge in consultations. Perhaps
I should have, in response to the Cardiology Registrar whose reply to my request for
an explanation of Reflex Syncope was 'it's too complicated'. I have a sense of humour
but his 'get a tumble dryer' in answer to a question about persistent dizziness was
equally inappropriate. What a contrast.
The Gabapentin and Lidocaine prescribed by the pain clinic have reduced the impact
of a number of the weird symptoms I have: pins and needles in the back of my
tongue from touching the left side of my neck, retching from contact on a wide area of
my neck and left shoulder, permanent throat pain (but no sign of infection), shooting
pains into my left ear.
In combination with my other medications they act as a stimulant, which is great, but
after a few days my sleep is affected and I am up at 2-3am doing jigsaws and the like.
Conversely, I know when I am late with medication or have pushed myself too hard
as the pain in my throat returns first, followed by other symptoms such as nausea,
vomiting, vice-like headaches and increased noise hypersensitivity. Although I can
do only marginally more activity day to day, what I am doing is far more comfortable
and with fewer and less intense relapses.
If I did not have a strong sense of self-belief and self-worth I would not have been
able to adapt to long-term illness. Putting aside my loss of ability to climb or sail, it is
the inability to enjoy simple things like a short walk or a day out with friends, without
serious relapse, that are the hardest to deal with. In the last couple of years I have
found new interests. Working with glass, stained glass and fusing work is very
different but immensely enjoyable; something I would not have previously had time
to explore.
The pain consultant has done more, to reduce my symptoms and improve my day to
day living, than anyone else. I'm not 100% but hey, I can now wear a necklace and I
haven't been able to do that for 8 years.
A review of glossopharyngeal neuralgia
Introduction
Glossopharyngeal neuralgia is a chronic neuropathic pain condition characterised by
intermittent severe pain in the sensory distribution of the glossopharyngeal nerve.
Glossopharyngeal neuralgia (GPN) was first described by Weisenburg in a patient
with a tumour in the cerebellopontine angle in 1910, where he described it as part of
multiple cranial nerve palsies involving cranial nerves III, IV and VII1. GPN is a
relatively new term first coined by Harris in 19212.
The annual crude incidence rate of glossopharyngeal neuralgia per 100,000
population, is 0.2 - 0.7 for both sexes combined3, suggesting that
64
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
glossopharyngeal neuralgia is a rare disease. Bilaterality is not uncommon; it was
observed in one quarter of the patients, all of whom had mild disease3. GPN has often
been compared with trigeminal neuralgia (TN). GPN occurs much less frequently
than TN, the comparative incidence ranging from 5.9:14 to 100:15. GN is a milder
disease than TN, as indicated by the number of episodes, treatment, and
characterisation of pain4. Anecdotally left side seems to be more common than right
side, and the age at onset peaks at 40-60 years. Both sexes are affected equally.
Glossopharyngeal nerve anatomy
The glossopharyngeal nerve is the nerve of the third pharyngeal arch and ninth of the
twelve pairs of cranial nerves exiting from the upper medulla. It has both sensory and
motor components. It receives somatic sensory fibres from tonsils, pharynx, and
posterior one-third of the tongue, external ear, middle ear and mastoid process. It
receives special sensory fibres from posterior one-third of the tongue as well as
chemoreceptor and baroreceptor afferent input from carotid bodies and carotid
sinuses respectively. It also supplies parasympathetic secretomotor fibres to the
parotid gland via the otic ganglion. It supplies motor fibres to the stylopharyngeus
muscle and contributes to the pharyngeal plexus. The glossopharyngeal nerve aids in
tasting, swallowing and salivary secretions. Its superior and inferior (petrous) ganglia
contain the cell bodies of pain fibres. The
tympanic branch or Jacobson’s nerve is an
important branch which carries somatic sensory
fibres which receive pain and touch from middle
ear and mastoid, and secretomotor
parasympathetic fibres to parotid gland. It
emanates from the petrous ganglion of the
glossopharyngeal nerve at or above the level of
the jugular foramen. It leaves the base of the
skull through the jugular foramen travelling
together with the vagus and accessory nerves
and with the internal jugular vein.
Anatomy of glossopharyngeal nerve
Clinical Features
GPN is an extremely painful condition which can present not only with debilitating
pain but also with potentially life-threatening cardiovascular consequences (syncope,
bradycardia, hypotension and even asystole). GPN can present in isolation or
concurrently with other neuropathic pain conditions such as trigeminal neuralgia.
The diagnosis of this potentially debilitating condition can be challenging to the
health care professionals, probably because of the relative rarity of the condition and
some of its clinical features seen in other conditions. Patients usually describe the
pain as lancinating, stabbing, and shooting or electric shock-like pain experienced in
the neuroanatomical distribution of the glossopharyngeal nerve involving ear, throat,
soft palate, posterior part of the tongue, tonsillar area and posterior part of the
pharynx. Patients remain pain free in between the attacks. It is triggered by trivial
actions such as swallowing, speaking and rubbing the ears, disabling the patients and
resulting in severe weight loss. Onset of attack is often abrupt without any prodromal
warnings. It is characterised by clusters of attacks, with each cluster lasting from
weeks to months, with pain-free periods ranging from weeks to months or even years.
The duration of pain usually lasts from a few seconds to minutes. During the painful
attacks other features observed are swallowing movements, excessive secretion of
saliva, tinnitus, lacrimation, flushing and sweating.
65
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
Glossopharyngeal neuralgia can be classified into two types according to the
origin/distribution of pain5: otalgic type, which affects mainly the ears, and
oropharyngeal type which affects mainly the oropharyngeal area. It has been
suggested that the otalgic type may have an auricular trigger zone which may indicate
involvement of the vagus nerve. The significance of this was provided by Robson and
Bonica where pain attacks remained after section of IX nerve but were completely
abolished after the section of X nerve6.
GPN and cardiovascular manifestations
GPN is an extremely painful and disabling condition leading to severe weight loss and
psychiatric manifestations. Even worse, it can be associated with cardiac
dysrhythmias, hypotension and syncope. This could be the result of intense neuralgic
pain activating the glossopharyngeal afferent/vagal efferent reflex arc, resulting in
severe bradycardia or asystole, hypotension and syncope. Intense pain impulses from
the sensory afferents of the glossopharyngeal nerve, travelling along with the carotid
sinus nerve of hering, stimulate the dorsal motor nucleus of vagus, which represents
in the medulla oblongata, the main autonomic nucleus, whose efferents control
cardiovascular activity, either through central collateral pathways or through an
ephapse (artificial synapse). This effect is similar to that seen in carotid sinus
massage for the treatment of supraventricular arrhythmias. Reddy et al7 published a
unique condition termed “non-neuralgic glossopharyngeal neuralgia”, which is
associated with syncope precipitated by a tickling sensation in the throat (such as
swallowing) without pain. Tonic and clonic seizures have also been observed during
GPN attacks.
Aetiology
In regard to aetiology GPN can be classified as idiopathic or essential GPN when the
cause is unknown, or secondary when GPN is caused by any underlying pathology
such as trauma secondary to surgery or accidental, oropharyngeal or posterior fossa
tumours, vascular malformations, infection (e.g. parapharyngeal abscess, petrositis,
arachnoiditis), elongated styloid process and demyelination (e.g. Multiple sclerosis)8.
The most likely cause of idiopathic GPN appears to be vascular compression of the
glossopharyngeal nerve at the nerve root entry zone. The implicating vessels are
usually posterior inferior (or superior) cerebellar artery which frequently also
compress on the rootlets of vagus nerves. The other vessels that are implicated in
playing a causative role are vertebral artery and persistent hypoglossal artery, which
may frequently also compress on the rootlets of the vagus nerve9. This theory is
supported by the success of micro vascular decompression (MVD) in alleviating the
symptoms10. Opponents of the vascular compression theory refer to the fact that
vascular structures are commonly seen in contact with cranial nerves in the
cerebellopontine angle in asymptomatic individuals, and the success of MVD results
from micro traumatisation of the nerve during dissection, resembling partial
rhizotomy7. Patients suffering from the idiopathic type show no associated
neurological deficit or dysfunction and are completely pain free between attacks.
Patients in the secondary group often show neurological defect or dysfunction, may
not be pain free between attacks, and experience pain outside the ninth nerve
distribution11. Multiple sclerosis (MS) is rarely complicated by GPN, which is unlike
trigeminal neuralgia, seen in as many as 4% of MS patients.
Elongated styloid process (Eagle’s syndrome) is an underlying cause of secondary
glossopharyngeal neuralgia. It was first described by Eagle in 1937 in posttonsillectomy patients. It is characterised usually by (a) dull pharyngeal pain,
occasionally worsened by head flexion or turning, radiating to the ear (b) pain over
the internal carotid artery (c) glossopharyngeal deficit (d) occasional vertigo or
syncope on head movement which induces carotid compression by styloid process11.
66
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
These signs and symptoms can also be mimicked by ossified stylohyoid ligament.
This condition can be diagnosed by clinical examination or CT imaging.
Differential Diagnosis
Establishing the correct diagnosis and differentiating
between types of facial pain is complicated because different
Occipital neuralgia
types of facial pain share signs and symptoms and are often
Cluster headache
considered together in the differential diagnoses at first
presentation. Glossopharyngeal neuralgia shares several
Facial postherpetic neuralgia
characteristics with trigeminal neuralgia: character and
Facial neuralgia
pattern of painful episodes, triggering mechanisms, response
Atypical facial pain
to anticonvulsants and possibly pathophysiology eg:
neurovascular compression. But the distribution of pain and
triggering factors can help distinguish between the two conditions
Trigeminal neuralgia
The coincidence of these two conditions can be explained by the close anatomic
relationship of the brainstem area, peripheral connections between both nerves and
central convergence11. Cluster headache is characterised by unilateral headache
occurring in clusters, lasting for several minutes if not treated and accompanied by
various autonomic and ophthalmic features
Diagnosis
Glossopharyngeal neuralgia is an uncommon condition that can pose a serious
challenge to the pain physician, both in terms of diagnosis and treatment. It requires
diagnostic awareness, presence of trigger factors and a multidisciplinary approach to
diagnose and successfully treat the condition. The international classification of
headache disorders classifies GPN into two types, classical and symptomatic12.
Classification of Glossopharyngeal neuralgia
Classical GPN
A. Paroxysmal attacks of a facial pain lasting from a fraction of a second to 2 minutes and fulfilling criteria B and C
B. Pain has all the following characteristics
1. Unilateral location
2. Distribution within the posterior part of the tongue, tonsillar fossa, pharynx or beneath the lower angle
of jaw and /or in the ear
3. Sharp, stabbing, severe
4. Precipitated by swallowing, chewing, talking, coughing and/or yawning
C. Attacks are stereotyped in the individual patient
D. There is no clinically evident neurological deficit
E. Not attributed to another disorder
Symptomatic GPN
All features as in classical GPN, along with the criteria that the pain may persist between paroxysms and sensory
impairment may be found in the distribution of glossopharyngeal nerve.
67
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
Stepwise approach to diagnose GPN
1. The first priority is to ascertain the diagnosis of neuralgia, and to exclude other
causes of pain due to inflammation and neoplasia. The description of the pain and
the pattern of painful episodes will help to ascertain the likely cause.
2. The distribution of the pain has to be noted to ascertain if the pain is confined with
the neuroanatomical distribution of the glossopharyngeal nerve or if it involves other
cranial nerve distribution, which could be a sign of a more serious underlying
pathology.
3. What are the triggering factors, which can help in differentiating GPN from TN?
4. Is it associated with neurological deficit, which if present will warrant more
detailed investigation to determine if it is idiopathic (classical) GPN or secondary
(symptomatic) GPN
Treatment
Management of glossopharyngeal neuralgia will include pharmacological,
interventional and supportive treatment combined with patient education. The initial
approach is to offer pharmacological and supportive treatment before resorting to
more invasive procedures and also to exclude any suspected sinister causes through
appropriate investigations.
Anticonvulsants are the first line of treatment. Carbamazepine, with a proven success
in trigeminal neuralgia, has been successfully used in GPN although its long-term
benefits are limited by gradual development of tolerance with prolonged use and its
side effect profile (drowsiness, itching and, rarely, blood dyscrasias and liver
dysfunction). In addition to alleviating pain it has also been shown to improve
cardiovascular manifestations13. The recommended dose is 400 – 800mg/day.
Gabapentin has also shown to be effective in the treatment of glossopharyngeal
neuralgia14. Other anticonvulsants that have been tried and shown to be useful in the
treatment of GPN include pregabalin15, lamotrigine16 and baclofen. Other
pharmacological approaches include ketamine, topical applications and various
analgesics.
The interventional approach would include percutaneous radiofrequency thermo
coagulation of the petrous ganglion, micro vascular decompression (MVD),
intracranial sectioning of the glossopharyngeal nerve with/without the upper rootlets
of the vagus nerve.
The surgical procedures include percutaneous procedures such as micro vascular
decompression (MVD), rhizotomy of the glossopharyngeal nerve with or without the
upper rootlets of the vagus nerve, pulsed radiofrequency of the glossopharyngeal
nerve and, recently, Gamma nife radiosurgery.
Micro vascular decompression is a well-established treatment for idiopathic or
essential GPN. The likely pathology in this condition being vascular compression of
nerve roots, they respond well to MVD. Ferroli et al17 in their case series of 31 patients
68
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
with long-term follow-up (mean 7.5 years) reported that 90% of their patients were
pain free without need for medications. In another case series of 47 patients (over 10
years follow-up), Sampson et al18 reported that 98% of patients had effective pain
relief. They demonstrated the safety of this procedure with 11 patients experiencing
reversible neurological deficit and 5 with permanent neurological deficit, the majority
of these being mild hoarseness and dysphagia.
Rey-Dios et al19 in their review of neurosurgical management of GPN reported that
rhizotomy of glossopharyngeal nerve when combined with upper rootlets of vagus
gave complete pain relief in 85-100% of patients, but at the expense of increased
complications including dysphagia and vocal cord paralysis.
Pulsed radiofrequency and Gamma Knife surgery20 have been successfully used in a
few published case reports. The Gamma Knife is a type of stereotactic radiosurgery
administering high-intensity cobalt radiation therapy in a manner that concentrates
the radiation over a small volume. These techniques can be reserved for patients who
are resistant to medical therapy and not suitable for surgery.
The management would not be complete without including educating patient’s about
the condition and addressing their psychosocial issues. The patient can be given
information leaflets or referred to websites which provide support for patients
suffering from this condition and also gives them the opportunity to discuss with
other people who suffer from GPN21, 22.
The outcome of GPN depends on the underlying cause. Most often, the disease shows
relapsing and remitting pattern. The bad prognostic signs are - bilateral GPN,
constant pain, or multiple daily bouts of pain23
Conclusion
GPN is a severely debilitating painful condition with potentially life-threatening
cardiovascular consequences. The diagnosis of the condition can be challenging due
to overlapping clinical features with other facial neuralgias. GPN should be one of the
differential diagnoses in patients presenting with facial pain. Careful history taking is
the key to diagnosis. Treatment includes a multidisciplinary approach including
patient education.
Conflict of interest disclosures
Disclaimers and conflict of interest policies are found at: http://bit.ly/1wqiOcl
Article submission and acceptance
Date of Receipt: 30.05.2014
Date of Acceptance: 30.11.2014
Contact
Dr Chella Narendran Email: [email protected]
69
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800
References
1. T.H. Weisenburgh. Cerebello-pontine angle tumour diagnosed for six years as tic doulourex: The symptoms of
irritation of ninth and twelfth cranial nerves. JAMA 1910; LIV (20): 1600- 1604
2. Harris W. Persistent pain in lesions of the peripheral and central nervous system. Brain 1921; 44:557-72
3. Katusic S, Williams DB, Beard CM, Bergstralh E, Kurland LT. Incidence and clinical features of glossopharyngeal
neuralgia. Rochester, Minnesota, 1945–1984. Neuroepidemiology 1991; 10: 266-275
4. Katusic S, Williams DB, Beard CM, Bergstralh EJ,Kurland LT. Epidemiology and clinical features of idiopathic
.trigeminal neuralgia and glossopharyngeal neuralgia: similarities and differences, Rochester, Minnesota, 1945–
1984. Neuroepidemiology 1991; 10:276–281
5. Bohm E, Strang RR. Glossopharyngeal neuralgia. Brain 1962; 85:371–388
6. Robson J T, Bonica J. The vagus nerve in surgical considerations of glossopharyngeal neuralgia. J Neurosurgery
1950; 7:482-4
7. Reddy K, Hobson DE, Gomori A, Sutherland GR. Painless glossopharyngeal ‘neuralgia’ with syncope: a case
report and literature review. Neurosurgery 1987; 21:916–919
8. Konstantin V. Slavin. Glossopharyngeal Neuralgia. Seminars in Neurosurgery; 2004;15(1); 71-79
9. Sunderland S. Neurovascular relations and anomalies at the base of the brain. J Neurol Neurosurgery Psych
1948; 11:243-57
10. Atul Patel, Amin Kassam, Michael Horowitz, Yue-Fang Chang. Microvascular Decompression in the Management
of Glossopharyngeal Neuralgia: Analysis of 217 Cases. Neurosurgery, Vol. 50, No. 4, April 2002
11. Bruyn GW. Glossopharyngeal neuralgia. Cephalalgia 1983; 3: 143–157
12. Headache Classification Subcommittee of the International Headache Society (2004) the international
classification of headache disorders 2nd edn. Cephalalgia 24(Sup l1): 8–152
13. R Saviolo and G Fiasconaro. Treatment of glossopharyngeal neuralgia by carbamazepine. Br Heart J. 1987
September; 58(3): 291–292
14. Moretti R, Torre P, Antonello RM, Bava A, Cazzato G. Gabapentin treatment of glossopharyngeal neuralgia: a
follow-up of four years of a single case. Eur J Pain. 2002; 6(5):403-7.
15. Glossopharyngeal neuralgia responding to pregabalin. Guido M; Specchio LM; Headache: The Journal of Head &
Face Pain, 2006 Sep; 46(8): 1307-8
16. Use of lamotrigine in glossopharyngeal neuralgia: a case report. Titlic M; Jukic I; Tonkic A; Grani P; Jukic J;
Headache: The Journal of Head & Face Pain, 2006 Jan; 46(1): 167-9
17. Ferroli P, Fioravanti A, Schiariti M, Tringali G, Franzini A, Calbucci F, et al. Microvascular decompression for
glossopharyngeal neuralgia: A long-term retrospective review of the Milan-Bologna experience in 31 consecutive
cases. Acta Neurochir (Wien) 2009;151:1245-50
18. Sampson JH, Grossi PM, Asaoka K, Fukushima T. Microvascular decompression for glossopharyngeal neuralgia:
Long-term effectiveness and complication avoidance. Neurosurgery 2004;54: 884-9
19. Roberto Rey-Dios, Aaron A. Cohen-Gadol. Current neurosurgical management of glossopharyngeal neuralgia
and technical nuances for microvascular decompression surgery. Neurosurgical focus 2013; 34(3):1-5
20. Bruce E. Pollock, Christopher J. Boes. Stereotactic radiosurgery for glossopharyngeal neuralgia: preliminary
report of 5 cases. Journal of Neurosurgery 2011; 115; 936-939 2013
21. www.livingwithgpn.org
22. www.fpa-support.org/Pain-Symptoms
23. Singh P M, Kaur M, Trikha A. An uncommonly common: Glossopharyngeal neuralgia. Ann Indian Acad Neurol
2013;16:1-8
Intellectual property & copyright statement
We as the authors of this article retain intellectual property right on the content of this article. We as the authors of
this article assert and retain legal responsibility for this article. We fully absolve the editors and company of JoOPM of
any legal responsibility from the publication of our article on their website. Copyright 2014. This is an open-access
article distributed under the terms of the Creative Commons Attribution Licence, which permits unrestricted use,
distribution and reproduction in any medium, provided the original work is properly cited.
70
Journal of Observational Pain Medicine – Volume 1, Number 4 (2014) ISSN 2047-0800