Eur Arch Otorhinolaryngol (2012) 269:9–16
DOI 10.1007/s00405-011-1746-0
REVIEW ARTICLE
Less known non-infectious and neuromusculoskeletal systemoriginated anterolateral neck and craniofacial pain disorders
Utku Aydil • Yusuf Kizil • Ahmet Köybaşioğlu
Received: 27 May 2011 / Accepted: 1 August 2011 / Published online: 13 August 2011
Ó Springer-Verlag 2011
Abstract Pain syndromes of neuromusculoskeletal origin
are not well-known by most of the clinicians working on
head and neck area. As a result, most of the patients with
these syndromes are either overlooked without having any
treatment or they inappropriately have antibiotic treatments
or surgical interventions such as dental extractions and
tonsillectomies. Better recognition of the pain syndromes of
the neck and face region or entities related to neuromusculoskeletal system may result in more appropriate and
effective management of such conditions while avoiding
unnecessary medical and surgical treatments. In this review,
causes, clinical characteristics, diagnostic and treatment
modalities of relatively less known craniofacial and neck
pain entities including Eagle syndrome, carotidynia, glossopharyngeal neuralgia, superior laryngeal neuralgia, hyoid
bone syndrome, acute calcific retropharyngeal tendinitis,
temporal tendinitis, thyroid and cricoid cartilage syndromes, and mastoid process syndrome are summarized.
Keywords Anterior neck pain Eagle syndrome Tendinitis Glossopharyngeal neuralgia Craniofacial pain syndromes
Introduction
Anterior/anterolateral neck pain is a common complaint of
patients who admit to ENT outpatient clinics. Many of
U. Aydil (&) Y. Kizil A. Köybaşioğlu
Department of Otorhinolaryngology,
Gazi University School of Medicine,
Gazi Ün. Tıp. Fak. KBB A.D., Beşevler,
06500 Ankara, Turkey
e-mail: utkuaydil@yahoo.com
these patients have diagnosis related to odontogenic
and infectious disorders. Although relatively rare, noninfectious, non-odontogenic and neuromusculoskeletaloriginated pain syndromes are not well known by most of
the clinicians working on head and neck area. ENT and
Head and Neck surgeons, dentists, oral and maxillofacial
surgeons, neurologists, physical therapy specialists, and
neurosurgeons are among the clinicians who encounter this
group of patients. In clinical practice, we experience that
many of patients with these problems have several ampiric
antibiotic treatments, dental extractions, and undergo surgeries (i.e. tonsillectomy) inappropriately. Better recognition of the neck and face region pain syndromes or entities
related to neuromusculoskeletal system may result in more
appropriate and effective management of such conditions.
Also by this way, unnecessary operations, invasive procedures, investigations and medications could be avoided.
In this review, some of relatively less known craniofacial and neck pain entities including Eagle syndrome,
carotidynia, glossopharyngeal neuralgia, superior laryngeal
neuralgia (SLN), hyoid bone syndrome, acute calcific retropharyngeal tendinitis, temporal tendinitis (TT), thyroid
and cricoid cartilage syndromes, and mastoid process
syndrome will be summarized. Prominent clinical features
of these entities are also summarized in Table 1.
Common and well-known causes of neck and craniofacial pain such as vertebral problems, infectious
causes, thyroid diseases, odontogenic causes, temporomandibular joint problems and trigeminal neuralgia are
not discussed here. Some of the other rare entities which
we do not discuss in this paper are occipital neuralgia,
neuralgia inducing cavitational osteonecrosis (NICO),
trigeminal deafferentation pain (TDP), atypical facial
pain (AFP), geniculate neuralgia, and postradical neck
pain syndrome.
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Behind angle of
mandible
Carotid bifurcation
Throat and base of
tongue
Thyrohyoid membrane/
pyriform sinus wall
Greater horn of hyoid
bone
Throat/central upper
neck
Temporal region
Lateral portion of
thyroid or cricoid
cartilage
Mastoid tip
Eagle syndrome
Carotidynia
Glossopharyngeal
neuralgia
Superior laryngeal
neuralgia
Hyoid bone syndrome
Calcific retropharyngeal
tendinitis
Temporal tendinitis
Thyroid/cricoid
cartilage syndromes
–
–
–
Confirm the diagnosis
–
Rule out organic pathologies
such as tumors
Rule out organic pathologies such
as tumors and vascular
compression at the CPA
Rule out serious comorbid
situations like aneurism and
thrombosis
Determine styloid process length
or ossification of the ligaments
Imaging rationale
–
–
–
Lateral films, CT, MRI
–
CT, MRI
CT, MRI
Lateral cephalogram,
panoramic radiograms,
CT, 3D CT
Ultrasonography,
doppler, CT, MRI
Imaging modality
–
–
–
Calcification anterior to C1
and C2, swelling in the
retropharyngeal space
–
–
Vascular compression at the
CPA
Styloid process length
[25 mm or stylohyoid
ligament ossification
Carotid artery wall
thickening
Imaging findings
NSAIDs
NSAIDs, SI, LAI
NSAIDs, SI, LAI
NSAIDs
NSAIDs, LAI, SI
Carbamazepine
Carbamazepine,
cardiac
pacemakers,
LAI
NSAIDs
NSAIDs, SI, LAI
First line
treatment
–
–
RFA, excision of
temporal muscle
tendon
–
Excision of greater
cornu
LAI, resection of the
nerve
RFA, microvascular
decompression, GN
resection
İntraoral or external
styloid process
excision
–
Surgical treatment
CPA cerebellopontine angle, 3D three-dimensional, CT computed tomography, MRI magnetic resonance imaging, NSAIDs non-steroid anti-inflammatory drugs, SI steroid injection, LAI local
anesthetic injection, RFA radiofrequency ablation, GN glossopharyngeal nerve)
Mastoid process
syndrome
Pain localization
Entity
Table 1 Management of the anterolateral neck pain entities
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Eur Arch Otorhinolaryngol (2012) 269:9–16
Eur Arch Otorhinolaryngol (2012) 269:9–16
Fig. 1 Left styloid process (asterisk and arrow) from left posterolateral view on 3D CT image
Eagle syndrome/styloid pain
One of the numerous causes of cervical and facial pain is
elongated styloid process. Since this situation is first
described by W.W. Eagle, elongated styloid process pain
syndrome is also known as Eagle’s or Eagle syndrome,
however various names were used to describe this entity [1].
These are styloid/stylohyoid syndrome, stylalgia, elongated
styloid process syndrome, stylohyoid syndrome, styloid
syndrome, and styloid process neuralgia. Symptoms of
Eagle syndrome are throat pain, foreign body sensation in
the throat, dysphagia, painful swallowing, facial pain, jaw
pain and ear pain. In our series, pain on swallowing and ear
pain are the most common ones [2]. Rarely an elongated
styloid process may be the cause of transient ischemic
attacks or glossopharyngeal neuralgia [3, 4]. External palpation of the styloid process or palpation of the tonsillar
fossa can trigger pain. Bilateral occurrence of Eagle syndrome is very high and can be more frequent than 50% [2, 5].
To confirm the diagnosis, radiological studies are
helpful. On lateral cephalograms, panaromic radiograms
and computed tomography (CT) images, length of the styloid process can be measured; however, three-dimensional
(3D) CT is the gold standard in evaluation of these patients.
In 3D CT images, dimension, localization and topography
of the styloid process can be perfectly visualised (Fig. 1).
Most authors reported that mean length of the styloid process is between 20 and 30 mm and the length increases with
age [6–9]. In case of existence of characteristic symptoms
and findings, if the styloid process is longer than 30 mm,
Eagle syndrome should be considered but isolated elongation of the styloid process is not a pathological situation.
11
Exact cause or triggering factor for the onset of this
clinical situation is unknown despite some theories.
Degenerative and inflammatory changes of muscular
attachments to the styloid process like in other insertion
tendinitis entities, calcification of the tendons and ligaments, tonsillectomy and other traumas may be among
etiologic factors. We have also observed styloid pain after
neck dissections in some patients so that we suggest routine
palpation of the styloid process during neck dissection and
excision if it is elongated.
Frequency of elongated styloid process and stylohyoid
ligament is not very low according to the literature [10–12].
However symptomatic cases are relatively low. Frequency
of elongated styloid process is 4% in general population
according to Eagle [10]. Kaufman et al. [11] reported
incidence of isolated styloid process elongation as 7.3%,
and 28% if stylohyoid ligament calcification is taken into
account. Correll et al. [12] reported styloid process elongation or stylohyoid and stylomandibular ligament calcification in 18.2% of 1,771 panaromic radiograms. However
only eight patients were symptomatic in Correll’s study.
Certainly all patients with an elongated styloid process do
not need treatment. In case of a patient with characteristic
symptoms, treatment is initially medical. Non-steroidal antiinflammatory drugs (NSAIDs), transpharyngeal steroid and
local anesthetic injections may alleviate symptoms in some
patients [13]. If conservative options fail, surgical shortening
of the styloid process is an effective solution. There are two
approaches for surgical shortening procedure: intraoral and
external. The main advantage of intraoral approach is the
absence of a postoperative scar in the neck. However intraoral approach brings some potential complications. The
potential risks with intraoral approach is deep cervical
infection due to bacterial contamination from oral cavity and
increased risk of trauma to the external carotid artery and IX–
XII cranial nerves due to poor exposure of the surgical field.
Despite these potential complications, Ghosh and Dubey [5]
did not report any serious complication by intraoral approach
in their series and advocated intraoral approach as a safe
procedure. However, our choice is external approach. We
think that external approach is safer and postoperative scar
formation is acceptable. In our cases, serious complications
or damage to major neurovascular structures had not
observed in 88 external styloid process excision from 61
patients [2]. Operative time in external approach is approximately 15–20 min and postoperative period is uneventful.
Carotidynia
Some authors describe carotidynia as a ‘myth’ [14].
Despite doubts on reality or existance of such an entity,
Upton et al. [15] reported macroscopic and histological
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clues of carotidynia in a patient who had undergone an
elective carotid endarterectomy procedure. The authors
reported edematous, gray and abnormally appearing carotid
artery intraoperatively with vascular proliferation of small
blood vessels, fibroblast proliferation and low grade
chronic active inflammation on adventitial biopsy.
The pain in carotidynia is characteristically located
unilaterally on the carotid bifurcation, and sometimes
radiates upwards to the ear, teeth, mandible and eye. The
pain may be aggrevated by head movements, coughing and
swallowing. Accompanying dysphonia and atypical
migraine is also reported [16]. The most prominent physical sign is tenderness on palpation of the carotid artery
bifurcation. In 1988, acute idiopathic carotidyna was
classified by the International Headache Society (IHS)
Classification Committee with four diagnostic criteria:
(a) at least one of the following overlying the carotid
artery: (1) tenderness, (2) swelling, (3) increased pulsations. (b) Appropriate investigations do not reveal structural abnormality. (c) Pain over the affected side of the
neck. May project to the ipsilateral side of the head. (d) A
self-limiting syndrome of \2 weeks duration [17]. However, carotidynia was removed from the following classification in 2004 [18]. In the latter classification, carotidynia
was not validated as an independent entity but a form of
unilateral neck pain. Although one of the diagnostic criteria
determined in 1988 was ‘self-limiting syndrome of
\2 weeks duration’, in our clinical practice we have seen
many carotidynia patients suffering from pain for several
weeks.
There are controversies about definition, aetiology, and
characteristics of this rare entity. Most of the carotidynia
cases are believed to be idiopathic but it is also suggested
that it may be a subset of vasculitis [19]. Reported elevated
levels of high-sensitivity C-reactive protein (CRP),
Fig. 2 Enlargement of posterior carotid artery wall on ultrasound
imaging in a 38-year-old male patient
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erythrocyte sedimentation rate (ESR) and serum amyloid A
protein levels support inflammation theory in or around the
carotid artery wall [20, 21]. Arning reported six consecutive carotidynia patients in which hypoechoic wall thickening of the bulb was seen exactly in the region of
tenderness and resolution of the findings in follow-up
ultrasound [22]. This is also what we have seen in some
carotidynia patients (Fig. 2). Some other reports have
demonstrated the presence of amorphous enhancing soft
tissue surrounding the carotid bifurcation and wall thickening on magnetic resonance, ultrasonography, and doppler
in patients with carotidynia, suggesting the presence of an
inflammatory process recently [22–24]. Positron emission
tomography evaluation of a carotidynia patient demonstrated a short segment of increased [18F] fluorodeoxyglucose activity corresponding to the region of soft tissue
thickening within the carotid sheath [21]. These findings
also support the existance of an inflammation.
We suggest that the term ‘carotidynia’ would better
represent a clinical situation which is not related to any
other organic pathology or disease process. In this clinical
entity, some imaging findings isolated to the carotid artery
may be present as pointed out. Other conditions mimicking
idiopathic carotidynia should be evaluated separately.
Some of these potentially mortal conditions are plaque
formation in the carotid artery lumen, carotid artery dissection, Takayusu arteritis, nasopharyngeal carcinoma,
total carotid artery occlusion, and septic embolisation to
the carotid bulb [25–31]. In the absence of fever, chills,
confusion, vision change or other positive neurological
symptoms or signs, our suggestion is to obtain only a
carotid ultrasound and doppler imaging studies routinly.
Presence of such signs and symptoms necessiates investigation of an arteritis or a cerebrovascular event. Routinely,
there is no need for any blood test such as ESR or CRP for
diagnosis or monitoring. A very rare entity in differential
diagnosis is idiopathic inflammatory pseudotumor of the
carotid sheath. In this entity, a mass lesion of unknown
etiology encasing the carotid bifurcation is detected on
imaging studies [32, 33]. Carotid involvement in this
situation is extremely rare however, these patients may
represent with carotidynia symptomatology.
NSAIDs are highly effective in carotidynia and we had
perfect responses to etodolac in our carotidynia patients.
Cannon [34] and Orfei and Meienberg [35] also reported
satisfactory results with NSAIDs like ibuprofen, ketoprofen, indomethacin and flurbiprofen and in case of failure
methysergide and steroids may benefit patients. Sporadic
good results with almotriptan and dihydroergotamine are
also reported [16, 36]. De Vries et al. [37] reported
immediate relief of symptoms in a severe carotidynia
patient who is refractory to medical therapy after surgical
denervation of the carotid bulb.
Eur Arch Otorhinolaryngol (2012) 269:9–16
Glossopharyngeal/vagoglossopharyngeal neuralgia
This rare craniofacial syndrome is generally known as
glossopharyngeal neuralgia (GN) and can be denominated
as vagoglossopharyngeal neuralgia (VGN) when cardiac
symptoms arise [38, 39]. This entity is not only a painful
condition and may result in fear of swallowing, weight loss
and death in case of vagal involvement. In this syndrome,
patients generally suffer from a unilateral paroxysmal and
stabbing throat and base of the tongue pain which may
occur spontaneously or precipitated by coughing, swallowing (particularly with cold, salty, acidic and bitter),
talking or head movements [40, 41]. Patients may also
suffer from dysphagia. Rarely, a trigger zone located on the
tonsillar fossa may be present [41]. Pain may radiate to the
neck, ear, and angle of the jaw. However, involvement of
glossopharyngeal nerve may be painless rarely[39]. When
vagal nerve is involved, bradicardia, asystole, syncope and
seizures may accompany cervicofacial pain [39–41].
Drinking carbonated water can initiate an attack and can be
used as a diagnostic test [40]. GN may be idiopathic or
secondary to another medical condition. It is postulated
that idiopathic cases may be secondary to vascular
compression of the nerve(s) in cerebellopontine angle
(CPA) [38, 39]. Reported causes of secondary GN are CPA
tumors, parapharyngeal lesions, multiple sclerosis, Eagle
syndrome, trauma, cranial base tumors and head and neck
tumors [4, 41–47].
Treatment of this entity includes several medical and
surgical options. These are carbamazepine, temporary or
permanent pacemakers, local anesthetic injections and
spraying pharynx for temporary relief, atropine and isoprenaline for emergency situations, percutaneous radiofrequency ablation of the nerve, surgical removal of styloid
process, microvascular decompression of the nerve(s) in
the CPA, dissection and avulsion of glossopharyngeal
nerve in the neck, in the tonsillary bed or in the CPA (with
upper vagal rootlets) [4, 38–41, 48]. Initial treatment
should be carbamazepine however effectivity of carbamazepine therapy may gradually decline with time and best
results are achieved with dissection or decompression of
the nerves by CPA approaches [38, 39, 48].
Superior laryngeal neuralgia
Patients with SLN present with a lancinating neck pain
with localized tenderness at one of the lateral edges of the
thyrohyoid membrane. The pain comes paroxysmally, and
can be triggered by swallowing, with shouting, and head
turning. Paroxysmal pain may last minutes to hours. In
almost every patient, a trigger point can be found on
digital palpation [49]. Trigger points may be either on
13
pyriform sinus wall where the nerve stands superficially
or the point where the internal branch pierces the thyrohyoid membrane. The pain may extend to ipsilateral jaw
and ear. Bilateral occurance is rare [50]. Several etiological factors have been reported to precipitate SLN.
Tumors of the larynx are among them so that imaging
studies such as computed tomography and magnetic resonance imaging should be performed if suspicion arises.
Spraying larynx with local anesthetic may improve pain
and superior laryngeal nerve block can be used for
diagnosis [51, 52]. In the past, laryngeal tuberculosis was
also one of the common causes before eradication in the
modern era. Upper airway tract infections such as influenza or laryngitis, previous throat/larynx operations or
trauma, entrapment after carotid endarterectomy operation, compression due to a deviated hyoid bone, and lateral pharyngeal diverticulum are other reported causes of
SLN [38, 49, 51, 53, 54]. Treatment of SLN is largely
medical. Carbamazepine is reported to be successful in
the treatment of SLN [50, 52, 55]. Superior laryngeal
nerve block is also reported to be effective and even a
single local anesthetic injection may be sufficient for
treatment [51, 56]. In intractable cases, resection of the
nerve may be indicated.
Hyoid bone syndrome
Hyoid bone is the only bone in the body that does not form
any joint. Hyoid muscles attach to the bone without any
relation to the periosteum and their constant movement
during swallowing, respiration and articulation makes them
prone to degenerative and inflammatory changes. Hyoid
bone syndrome is a form of insertion tendinitis as a result
of inflammation and degeneration of these hyoid muscles.
Hyoid bone syndrome is first described by Brown [57].
Steinmann reported this situation as a form of tendinitis
and suggested steroid and anesthetic injections for therapy
[58]. In 1975, Kopstein [59] offered resection of the greater
cornu. Histopathological evidence for hyoid bone syndrome was reported by Ernest and Salter [60] and Aydil
et al. [61].
Hyoid bone syndrome is a complex of symptoms comprising tenderness on greater cornu of hyoid on palpation,
pain in the neck and throat during swallowing and neck
movement [62]. Sharp or dull pain spreading to temporal
region, sternocleidomastoid muscle, posterior pharyngeal
wall, ear or supraclavicular region is the main symptom
[62]. Swallowing or head movement can trigger or increase
the pain. Systemic and topical NSAIDs, steroid and local
anesthetic injections to the greater cornu of hyoid bone are
treatment choices that were reported to be highly successful [63–66]. Nir et al. [63] reported symptomatic relief
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in 2/3 of 38 patients with NSAIDs. If all conservative
treatment options fail, excision of greater cornu of hyoid
bone is an effective surgical option. Lim [62] reported rate
of 90% immediate relief after operation in a series
including 50 patients.
Acute calcific retropharyngeal tendinitis
This is also known as acute aseptic tendinitis of the longus
colli muscle. Retropharyngeal tendinitis is a rare condition
presented with acute upper neck pain and stiffness,
restriction of neck movements and difficulty and pain on
swallowing [67]. Mild fever, elevation of eryrthrocyte
sedimentation rate, and leukocytosis may be present
[67, 68]. There may be a history of mild trauma. To confirm the diagnosis and exclude some other serious disease
processes such as retropharyngeal abscess/sellulitis, traumatic disc herniation, cervical osteomyelitis, and arterial
dissection, radiological studies are mandatory. Conventional radiographs, CT images and MRI studies are helpful
in diagnosis. We recommend to obtain a lateral neck film
as an initial imaging study. Calcification anterior to C1 and
C2 vertebra with soft tissue swelling in the retropharyngeal
space on direct films; amorphous calcification anterior to
C1 and C2 with asymmetric soft tissue swelling on CT
images; prominent high signal in the prevertebral region on
T2-weighted MRI images are characteristic [67–69].
Absence of calcification on imaging studies does not definitely exclude the diagnosis.
This condition is benign and self limited, resolves in a
couple of weeks. NSAIDs are promptly effective and sufficient for the treatment. In case of unresponsiveness to
NSAIDs in 24–48 h, accompanying toxic appearance,
existance of moderate to severe trauma history, diagnosis
should be revised.
Temporal tendinitis
The condition ‘‘temporal tendinitis’’ refers to inflammation and tenderness of the tendon of temporal muscle.
Temporal tendinitis (TT) is also called ‘migraine mimic’
because its presentation is similar to migraine headache. It
can be also accepted as a part of temporomandibular joint
disorders (TMD) and naming it separately from TMD is
arguable. Temporal muscle is one of the masticator
muscles and can be affected by the causes of TMD so that
differentiating it from TMD group and evaluating separately can be confusing. Histological evidences of this
entity was reported by Ernest et al. [70]. Etiology is not
clear but whiplash injuries from car accidents may be one
of the reasons. Patients with TT may suffer from temple
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pain, molar toothache, aching behind eye, and referred pain
to neck and shoulder regions. Most prominent symptoms
are jaw joint pain, restriction in jaw opening, temple sensitivity from sun hats and glasses, ear pain and pressure and
cheek pain. In physical examination, tenderness and pain
stimulation occurs on oral palpation of coronoid process
where temporal muscle attaches. For diagnosis of temporal
tendinitis, imaging studies are not helpful. Treatment is like
in other tendinitis clinics. Firstly, conservative treatment
options like anti-inflammatory drugs, muscle relaxants,
heat application, soft diet are employed. Second line
therapy is consisted of steroid and local anesthetic injections and if these fail, surgery is the last choice. Surgical
treatment options include radiofrequency thermal ablation/
thermolysis and excision of temporal muscle tendon and
may be necessary for patients who have longer symptom
duration [71].
Thyroid cartilage and cricoid cartilage syndromes
Thyroid and cricoid cartilages may also be the origins of
anterior cervical discomfort. The pathophysiology of the
hyoid bone syndrome is probably valid in these syndromes.
Thyroid ala and cricoid cartilage are attached by strong
muscles and inflammation and tendinitis at these insertion
points are responsible from the pain syndromes. These
clinical pictures were first described by Kunachak [72]. In
this article, the author presented 16 patients with thyroid
cartilage syndrome and eight patients with cricoid cartilage
syndrome. In 1997, Hefer et al. [73] contributed with seven
patients with thyroid cartilage syndromes. Since then, any
other case has not been reported to our knowledge but we
had experience on a few patients in our practice. In all
reported cases, the only positive finding is localized point
of tenderness corresponding to the site of discomfort. The
duration of symptoms were missing in the first report and
reported between 12 days and 3 months in the second one.
There were strong female predominance in both reports.
Kunachak reported the pain occurring almost always unilateral (only one midline pain), however in the second case
series, the pain was localized on the right thyroid ala in
four patients and in the midline in three patients. Triamcinolone acetonide injection to the affected site was the
treatment of choice by Kunachak in all of the cases. Eight
of the patients with thyroid cartilage syndrome were
reported to be cured following one injection, and a second
injection was necessary for three patients. In the remaining
five patients, migration of the pain to the hyoid bone and
cricoid cartilage has been reported. The author reported
complete cure of five of the eight cricoid cartilage syndrome patients after one injection. The pain was migrated
to the thyroid cartilages in the two and to the carotid bulb
Eur Arch Otorhinolaryngol (2012) 269:9–16
in the one of the remaining patients according to the author.
In all cases of pain migration, complete relief of symptoms
were reported by subsequent injections. In all cases, any
recurrence has not been reported by the mean 30-months
follow-up. Hefer et al. achieved complete relief in six of
the patients and partial improvement in one of the patients
with oral and topical diclofenac treatment for 10 days. No
recurrences were reported with a follow-up period of
5–30 months.
Mastoid process syndrome
To date, only one case has been reported and called as
‘mastoid process syndrome’ in the English medical literature [73]. The clinical picture is similar to those of other
cervical pain syndromes except for the localization of the
pain. The pain is located at the region of the sternocleidomastoid muscle insertion to the mastoid process and
aggravated by the head movements. The only positive
physical examination finding is tenderness over the muscle’s
attachment zone without swelling, erythema or fluctuation.
The case is reported to be treated by oral and topical diclofenac successfully and did not recur during the 10-month
follow-up period. In our clinical practice, we have rarely
encountered patients who are suffering from pain at the
mastoid tip. In these patients, positive physical examination
findings are limited to tenderness on the mastoid tip only. To
our experience, oral NSAIDs are effective in the short term
but we do not have long term follow-up data.
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