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Clinical Anatomy 28:101108 (2015)

REVIEW

Occipital Neuralgia:
Anatomic Considerations
ALPER CESMEBASI,1,2 MITCHEL A. MUHLEMAN,2,3 PAUL HULSBERG,2 JERZY GIELECKI,4
PETRU MATUSZ,5 R. SHANE TUBBS,2,6 AND MARIOS LOUKAS2,4*
1

Department of Neurologic Surgery, Mayo Clinic, Rochester, Minnesota


Department of Anatomical Sciences, School of Medicine, St. Georges University, Grenada, West Indies
3
Department of Surgery, St Joseph Mercy Oakland Hospital, Pontiac, Michigan
4
Department of Anatomy, Medical School Varmia and Mazuria, Olsztyn, Poland
5
Department of Anatomy, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania
6
Pediatric Neurosurgery, Childrens Hospital, Birmingham, Alabama

Occipital neuralgia is a debilitating disorder rst described in 1821 as recurrent


headaches localized in the occipital region. Other symptoms that have been
associated with this condition include paroxysmal burning and aching pain in
the distribution of the greater, lesser, or third occipital nerves. Several etiologies have been identied in the cause of occipital neuralgia and include, but
are not limited to, trauma, brositis, myositis, fracture of the atlas, and compression of the C-2 nerve root, C1-2 arthrosis syndrome, atlantoaxial lateral
mass osteoarthritis, hypertrophic cervical pachymeningitis, cervical cord tumor,
Chiari malformation, and neurosyphilis. The management of occipital neuralgia
can include conservative approaches and/or surgical interventions. Occipital
neuralgia is a multifactorial problem where multiple anatomic areas/structures
may be involved with this pathology. A review of these etiologies may provide
guidance in better understanding occipital neuralgia. Clin. Anat. 28:101108,
2015. VC 2014 Wiley Periodicals, Inc.
Key words: Arnolds neuralgia; migraine; cervicogenic headache; greater occipital nerve; lesser occipital nerve; third occipital nerve; Chiari
malformation

INTRODUCTION
First described in 1821 by J. Beruto y Lentijo and
M.M. Ramos, occipital neuralgia can be a debilitating
disorder characterized by recurrent headaches localized in the occipital region (Perelson, 1947). The
symptoms of occipital neuralgia are often described as
paroxysmal burning, aching pain in the distribution of
the greater, lesser or third occipital nerves (Graff-Radford et al., 1986; Horowitz and Yonas, 1993; Sulfaro
and Gobetti, 1995). The International Headache Society (2013) denes these headaches as consisting of
paroxysms of jabbing pain in the distribution of the
greater, lesser, or third occipital nerves.
Of the 180 types of headache recognized by the
International Headache Society, occipital neuralgia is
classied as a subset including post traumatic pain,
whiplash, cervical spine abnormality, tension head-

C
V

2014 Wiley Periodicals, Inc.

ache, chronic daily headache, and migraine (Hecht,


2004; Ducic et al., 2009). Many appellations are
referred to in the literature, including Arnolds neuralgia and occipital neuritis (Bovim et al., 1991; Pantaloni and Sullivan, 2000; Ballasteros-Del Rio et al.,
2003; Slavin et al., 2006; Ducic et al., 2009).
Although pain in the occipital region may result from
other forms of cephalgia, the standard for diagnosis is

*Correspondence to: Marios Loukas, Department of Anatomical


Sciences, St Georges University, School of Medicine, Grenada,
West Indies. E-mail: mloukas@sgu.edu
Received 12 September 2011; Revised 20 August 2014;
Accepted 27 August 2014
Published online 22 September 2014 in Wiley Online Library
(wileyonlinelibrary.com). DOI: 10.1002/ca.22468

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Cesmebasi et al.

TABLE 1. Reported Etiologies of Occipital Neuralgia


Etiology
Trauma
Fractures and subsequent nerve root compression
Hematoma
Iatrogenic
C1 lateral mass screw-induced
C1-C2 xation with Harms construct
Anatomical
Trigger point compression
Chiari malformation
Entrapment by the atlanto-epistrophic ligament
Fibromyalgia
Tumors
Osteochondroma of cervical vertebra
Neuromas (secondary to neurobromatosis type 1)
Multiple myeloma (causing vertebral relapse)
Atlantoaxial lateral masses
Infection
Pyomyositis
Neurosyphilis
Hypertrophic cervical pachymeningitis
Degenerative changes
Atlantoaxial lateral mass osteoarthritis
C1-C2 arthrosis syndrome

dened as tenderness of the skin overlying the occiput


and elimination of pain following anesthetic block of
the affected nerve(s) (Ducic et al., 2009; International
Headache Society, 2013).
Occipital neuralgia can be conservatively managed
in several ways, including antiepileptic drugs, antidepressants, neural blockade, nonsteroidal analgesics,
opioids, neuromodulators, transcutaneous electrical
nerve stimulation, and external orthosis (Anthony,
1992; Merskey, 1986; Oh et al., 2004; SahaiSrivastava and Subhani, 2010). While pharmacotherapy and non-invasive procedures can help manage the
symptoms of mild occipital neuralgia, refractory pain
usually warrants surgery as a last resort treatment. The
procedures used to correct occipital neuralgia include
neurolysis and decompression, neurectomy, rhizotomy
and ganglionectomy, C1-C2 fusion, radio frequency
ablation, and peripheral nerve stimulation (Lozano,
1972; Onofrio and Campa, 1972; Blume, 1976; Picaza
et al., 1977; Merskey, 1986; Horowitz and Yonas,
1993; Joseph and Kumar, 1994; Steechison and Mullin,
1994; Dubuisson, 1995; Oh et al., 2004).
There are several etiologies that have been implicated in the incidence of occipital neuralgia, which
may be summarized in Table 1. With the variety in
reported etiologies, the aim of this study was to
review the various anatomical features that have been
implicated in the etiology of occipital neuralgia, with
specic reference to the greater, lesser and third occipital nerves, whose courses and distributions are
responsible for the painful sensations associated with
the condition (Figs. 1 and 2).

The Greater Occipital Nerve


General anatomy of the greater occipital nerve.
The second cervical nerve gives rise to the largest
dorsal ramus among all cervical nerves (Schaeffer,

Reporting authors
Various authors

Conroy et al. 2010


Rhee et al. 2008
Brown, 1996; Dash et al., 2005
Various authors
Poletti and Sweet, 1990; Anthony, 1992
Various authors
Baer-Henney et al., 2001
Skaribas et al., 2011
Sierra-Hidalgo et al., 2011
Clavel and Clavel, 1996
Sierra-Hidalgo et al., 2011
Various authors
Star et al., 1992
Ehni and Benner, 1984

1953). The greater occipital nerve (GON) splits from


the lateral branch of the second dorsal ramus and
runs medially around the lower border of the obliquus
capitis inferior muscle (Schaeffer, 1953; Standring,
2008). After crossing the suboccipital triangle
obliquely, the GON runs rostrally along the rectus capitis posterior major muscle and then receives a communicating branch from the third occipital nerve

Fig. 1. Gross image of the greater, lesser and third


occipital nerve and possible compression points as they
exist through the attachment of the trapezius muscle and
between the sternocleidomastoid, semispinalis capitis,
splenius capitis, rectus capitis and oblique capitis
muscles. [Color gure can be viewed in the online issue,
which is available at wileyonlinelibrary.com.]

Occipital Neuralgia

103

Fig. 2. Drawing of the nerves of the occiput. Surrounding images depict potential compression sites of
these nerves along their course. 1: Origin of the third
occipital nerve and proximal connection with the greater
occipital nerve. 2: Greater occipital nerve as it courses
inferior to the inferior oblique muscle. 3: Greater occipital
nerve coursing through the semispinalis capitis muscle.
4: Greater occipital nerve exiting the aponeurosis of the
trapezius muscle. 5: Greater occipital nerve traveling

with the occipital artery. 6: Origin of the greater occipital


nerve and relationship to the descending branch of the
occipital artery. 7: Suboccipital nerve relation to the vertebral artery and the descending branch of the occipital
artery and this nerves interconnection to the greater occipital nerve. 8: Relationship between the third occipital
nerve and the C2-C3 joint complex. [Color gure can be
viewed in the online issue, which is available at wileyonlinelibrary.com.]

before innervating and piercing the semispinalis capitis muscle (Standring, 2008). The GON then pierces
the tendon of the trapezius muscle along with the
deep cervical fascia just below the superior nuchal line
of the occipital bone (Schaeffer, 1953). While traversing the supercial fascia along with the occipital
artery, the GON splits into many terminal branches
that connect with the third and lesser occipital nerves
to supply the skin of the scalp as far forward as the
coronal suture (Schaeffer, 1953; Standring, 2008).
Tubbs et al. (2007) found that the GON pierced the
semispinalis capitis muscle on average 2 cm superior
to the intermastoid line. The mean diameter of this
nerve was 3.5 mm and it was found to branch into
medial and lateral branches on average 0.5 cm superior to the inion.
Emerging from the C2 dorsal ramus. With such
a meandering path through the posterior head and
neck, it is not surprising that the GON is at high risk
for compression and entrapment. The rst area where
the GON may be irritated is just as the nerve emerges
from the C2 dorsal ramus between the atlas and the
axis (Hunter and Mayeld, 1949; Steechison and Mullin, 1994; Loukas et al., 2006; Hoppenfeld, 2012).
Hunter and Mayeld (1949) have described the anatomical basis for this compression, particularly when

the head is rotated, causing excursion of the articular


facets of the atlanto-axial articulations.
When the head is turned to the left, for example,
the lower left atlantal facet slides posteriorly and
medially until it is almost completely displaced from
the axial facet. This places the lower atlantal facet in a
position at which it directly impinges on the superior
margin of the posterior arch of the axis (Hunter and
Mayeld, 1949). Either an extraordinary force in this
position or an aberrant course of the GON can lead to
a crush injury at the point where the atlantal facet
strikes the axial lamina (Hunter and Mayeld, 1949).
During this same rotation, the arches of the contralateral atlas and axis are actually in contact and can
compress the emerging C2 dorsal ramus (Hunter and
Mayeld, 1949).
Hunter and Mayeld proposed that while the GON
is not typically vulnerable during normal range of
motion, added force applied at the limit of the normal
range might permanently damage the nerve, leading
to the painful sensations experienced while the neck
is in a limited range of motion or even at rest (Hunter
and Mayeld, 1949). In correlation with this anatomical basis of occipital neuralgia, Hunter and Mayeld
proposed treating 11 patients suffering from the condition with neurotomy of the GON (Hunter and

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Cesmebasi et al.

Mayeld, 1949; Gille et al., 2004). Eight of these


patients had favorable results; however, neurotomy
has since been criticized for sometimes producing
dense anesthesia of the scalp or even worsening the
condition through early pain recurrence, extreme
scalp hypersensitivity, dysesthesias, or formation of
painful neuroma beneath the scalp (Murphy, 1969;
Gille et al., 2004).
Crossing the inferior oblique muscle. Another
anatomical landmark that may result in irritation of
the GON is the point at which the nerve courses
between the obliquus capitis inferior and semispinalis
capitis muscles (Fig. 2) (Loukas et al., 2006). Vital
et al. (1989) described the relationship of the GON to
the inferior oblique along with two other points of
compression in an anatomical study of occipital neuralgia. The researchers separated the path of the GON
into three portions and two bends. The rst portion
(P1) was dened as the lateral-posterior path and
traveled from the nerve root to reach to inferior
oblique, followed by the bend (A1) around the inferior
border of the muscle and the second portion (P2)
travelling superiorly and medially toward the nuchal
ligament. This second portion, of which the present
discussion pertains, is bordered supercially by the
semispinalis capitis muscle and deeply by the inferior
oblique, rectus capitis posterior and rectus capitis
anterior muscles.
Vital et al. (1989) discussed how exion of the
neck, by increasing the atlanto-occipital and atlantoaxial intervals, causes P2 to stretch in a vertical
direction, while extension allows P2 to relax in the
horizontal plane. During exion-extension movements, the inferior oblique is immobile, and acts as a
pivot point, keeping A1 at a xed angle and allowing
P2 to stretch and relax (Vital et al., 1989). This feature can thus be used to localize the point of compression in occipital neuralgia. Patients whose pain is
exacerbated by exion of the neck and alleviated by
extension could be experiencing a stretching of P2
over the inferior oblique muscle. Furthermore, the clinician can help rule in this localization by applying
deep pressure 2 cm lateral to and 1 cm below the spinous process of the axis, and testing for exacerbation
of pain (Vital et al., 1989).
This anatomical relationship has recently been used
by to alleviate occipital neuralgia through sectioning
of the inferior oblique muscle (Gille et al., 2004). By
detaching the inferior oblique muscle from the lateral
aspect of the spinous process of the axis, orthopedists
and neurosurgeons can release the GON, thus allowing relaxation even while in the exed position (Gille
et al., 2004).
Piercing the semispinalis muscle. Vital et al.
(1989) dened the second bend (A2) as the point at
which the GON passes through the bers of the semispinalis capitis muscle to emerge at the surface of the
muscle approximately 1 cm lateral to the nuchal ligament. It has been postulated by Bogduk that contraction of the semispinalis capitis muscle can cause
compression, although Vital et al. were unable to verify this claim in their study (Bogduk, 1980; Vital et al.,
1989). Moreover, Bogduk (1981) himself later discussed the unlikelihood of an anatomical compression

at this point being a tenable etiology of occipital


neuralgia.
Exiting the tendinous aponeurosis of the trapezius muscle. After emerging from the semispinalis
muscle at A2, the third portion (P3) of the GON travels
superiorly and laterally between the dorsal aspect of
the semispinalis capitis muscle and the deep aspect of
the trapezius muscle (Fig. 2) (Vital et al., 1989). The
nerve then divides into terminal subcutaneous
branches either before or (more commonly) after traversing through the narrow aperture of the trapezius
tendon (Vital et al., 1989). Bogduk (1981) discussed
how the nerve does not actually perforate the muscle,
but passes above the aponeurotic sling between the
sternocleidomastoid and the trapezius muscles. For
this reason, this author stated that spasm of the trapezius muscle would draw the sling downwards, giving
the nerve more room rather than compressing it.
There have been reports of chronic inammation at
the trapezius leading to occipital headache, but the
pathological evidence of such an etiology is lacking
(Haden, 1940; Schultz, 1977; Hammond and Danta,
1978; Bogduk, 1981). Lastly, in this more supercial
region, the nerve may be compressed by the occipital
artery. Cornely et al. (2011) have reported a patient
with severe occipital neuralgia who was refractory to
medical treatment. Intraoperative ndings noted a
close contact relationship between the occipital artery
and greater occipital nerve. Long-distance decompression and neurolysis were done along with excision and
ligature of the occipital artery, which resulted in complete resolution of the patients symptoms (Cornely
et al., 2011).

The Lesser Occipital Nerve


General anatomy of the lesser occipital nerve.
Although less commonly presented and frequently in
conjunction with the neuralgia of the GON, damage or
irritation of the lesser occipital nerve (LON) can also
lead to the painful symptoms of occipital neuralgia
(Vaneldren et al., 2010). The nerve is mainly derived
from the ventral ramus of the second cervical nerve,
although the third cervical nerve (or the loop between
the two) sometimes contributes (Schaeffer, 1953;
Standring, 2008). Traversing rostrally and dorsally,
the LON winds around the inferior border of the spinal
accessory nerve and then ascends along the posterior
border of the sternocleidomastoid muscle toward the
mastoid process (Schaeffer, 1953). At the level of the
cranium, the LON pierces the deep cervical fascia and
runs across the posterior edge of the sternocleidomastoid insertion into the supercial fascia of the
scalp (Schaeffer, 1953). The nerve then splits into the
auricular, mastoid, and occipital branches. The auricular branch runs anteriorly and superiorly to supply the
upper medial aspect of the auricle and communicates
with the posterior branch of the great auricular nerve
(Schaeffer, 1953; Standring, 2008). Occasionally the
auricular branch arises from the GON rather than the
LON (Standring, 2008). The mastoid branch is somewhat smaller and simply supplies the skin over the
mastoid process, while the occipital branches ramify

Occipital Neuralgia
above the mastoid process to supply the skin of the
scalp along with the GON (Schaeffer, 1953). Tubbs
et al. (2007) found that the LON branched into a
medial and lateral component at approximately the
midpoint between a horizontal line drawn through the
inion and the intermastoid line. The main LON trunk
was found on average 7 cm lateral to the inion.
Stretching of the LON by the inferior oblique
muscle. Compared with the vast amount of studies
on the contributions of the GON to occipital neuralgia,
there is a somewhat limited amount of literature concerning the anatomical etiology of lesser occipital neuralgia. Lucas et al. (1994) published a comprehensive
review concerning the LON and the etiology of cervicogenic headaches. They described the details of the
C2 ventral ramus, noting that either the levator scapulae or the middle scalene can be encircled anteriorly
by one of the loops of this nerve (Lucas et al., 1994).
When forceful movements are made, the inferior
oblique muscle can stretch the C2 ventral ramus,
which can result in neuralgia of the LON (Lucas et al.,
1994).
Crossing the atlantoaxial junction. Another
point of compression for the C2 ventral ramus is present as the nerve crosses the lateral atlantoaxial articulation on the posterosuperior articular process of the
axis, rather than the facet of the axis (Lucas et al.,
1994). Hunter and Mayeld (1949) described this site
in their discussion of rotary movements of the head.
While the dorsal ramus (GON) is compressed at the
point where the atlantal facet strikes the lamina of the
axis, the ventral ramus is also at risk because of the
increased distance that the nerve must traverse in
order to leave the spine. When a force is applied in
this position, a stretch injury of the LON may occur
(Hunter and Mayeld, 1949).
Compression by the vertebral artery. The proximity of the C2 ventral ramus to the vertebral artery
can lead to a form of vascular compression, particularly when the nerve crosses the posterolateral surface of the artery (Lucas et al., 1994). The path of the
ventral ramus is known to express anatomical variations as Bogduk (1981) stated that the nerve crosses
anteriorly to the vessel, while Lucas et al. (1994)
were only able to nd one example of this aberration
in 16 dissections.
Clinical features of LON compression. Neuralgia
of the LON can sometimes be confused with that of
the GON, leading to an under-representation of LON
neuralgia in the literature. Sjaastad et al. (1983), in a
hypothesis of cervicogenic headaches, stated that
anesthetic blockade of the GON stopped the pain of
occipital neuralgia and led to sensory decit in the
area above and behind the ear. According to the anatomical study performed by Lucas et al. (1994), this
area is actually innervated by the LON rather than the
GON. The authors of the latter study suggest that
Sjaastad et al. (1983) were actually treating lesser
occipital neuralgia, most likely in conjunction with that
of the GON due to their overlap in cutaneous distribution (Lucas et al., 1994).
In another study on cervicogenic headaches, Fredriksen et al. (1987) reported the clinical manifestations of 11 patients. Ten of these patients experienced

105

pain in the distribution of the LON, while only three


patients had symptoms involving the GON (Fredriksen
et al., 1987; Lucas et al., 1994). The authors used the
median point between the external occipital protuberance and the mastoid process as well as the area
behind and slightly caudal to the mastoid process as
trigger points for precipitation of pain. Lucas et al.
(1994) cite this as evidence of lesser occipital neuralgia, since both points lie along the path of the LON.

The Third Occipital Nerve


General anatomy of the third occipital nerve.
Of the three nerves resulting in occipital neuralgia, the
third occipital nerve (TON) (Figs. 1 and 2) is by far the
least referenced, and the symptoms of TON neuralgia
commonly mimic that of the greater occipital nerve.
The third cervical dorsal ramus has a complex branching pattern, which starts at the articular pillar of the
third cervical vertebra (Standring, 2008). The nerve
then divides into lateral and medial branches, the latter of which ramies into deep and supercial divisions. The supercial medial branch formally referred
to as the third (or dorsal/posterior) occipital nerve,
curves around the dorsolateral surfaces of the C2-C3
facet joint, which it innervates. The TON then supplies
the semispinalis capitis muscle and travels deeply
along the muscle before sending a communicating
branch to the GON. At the level of the superior surface
of the second cervical spinal process, the TON turns
dorsally and pierces the semispinalis capitis, splenius
capitis, and trapezius muscles. After exiting the
muscles, the nerve becomes cutaneous and supplies a
small area just below the superior nuchal line (Standring, 2008). The TON sends many communicating
branches to the terminal branches of the greater and
LON, so it can sometimes be difcult to determine
which nerve is primarily responsible for a specic
areas painful symptoms.
Tubbs et al. (2007) found that the TON was, on
average, 3 mm lateral to the external occipital protuberance and small branches were found to cross the
midline and communicate with the contralateral TON
inferior to the external occipital protuberance (EOP) in
the majority of sides. The mean diameter of the main
TON trunk was 1.3 mm. This trunk became subcutaneous at a mean of 6 cm inferior to the EOP (Tubbs
et al., 2007).
The C2-3 facet joint. Perhaps the most heavily
implicated area in third occipital neuralgia results from
the nerves innervation of the C2-3 facet joint. While
the atlanto-occipital and atlanto-axial joints lie ventral
to the emerging spinal nerves, the C2-3 facet joints
are positioned behind the intervertebral joints at the
level of the intervertebral disc (Bogduk and Marsland,
1986). This biomechanical vulnerability when compared with the other upper cervical synovial joints has
been well documented in the literature concerning
third occipital nerve entrapment (Trevor-Jones, 1964;
Maigne, 1981; Bogduk and Marsland, 1986).
The only structures innervated by the third occipital
nerve include a small area of skin in the occipital
region, part of the semispinalis capitis muscle, and

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Cesmebasi et al.

the C2-3 facet joint (Bogduk, 1982; Bogduk and


Marsland, 1986). Since there exist neither any occult
conditions of the skin and nor selective conditions
affecting only the TON-innervated portion of semispinalis, Bogduk and Marsland (1986) reasoned that the
only structure possible of causing chronic third occipital neuralgia was the C2-3 facet joint. An epidemiological analysis by Lord et al. (1994) revealed that a
combination of headache and tenderness over the
C2-3 zygapophysial joint yields a positive likelihood
ration of 2.1 for third occipital neuralgia.
Other theories have been suggested that account
for the pain distribution of TON headaches. Dash et al.
(2005) have suggested that the TON could be constricted peripherally by its muscular investment, but
data on this etiology are lacking.

it is Valsalva-induced. Rapoport et al. (1999) presented two similar cases, each representing one of
the conditions in present discussion, and discussed
the similarities and distinctive presentations of each.
The most commonly presenting symptom of the
Chiari I malformation is headache, head pain, and
pressure in the occipital region (Cesmebasi et al.,
2014). If a patients occipital pain is worsened by
coughing, yawning, or Valsalva maneuvers, this is typically indicative of Chiari I malformation. Such maneuvers may result in descent of the herniated cerebellar
tonsils with subsequent intradural irritation of the
upper cervical nerve roots and thus radiating pain in
the distribution of the occipital nerves.

Clinical features of TON compression. Although


restricted neck movements and facet tenderness are
cited as putative diagnostic signs of third occipital
neuralgia, the only true diagnostic feature of TON
headache is a positive response to TON blocks (Bogduk and Marsland, 1986). Due to the low risk of this
diagnostic procedure, Bogduk and Marsland (1986)
recommend performing a TON block whenever third
occipital neuralgia can be suspected as a cause of
occipital pain. The authors also suggested causative
pathology in their seven patients with TON headaches.
The most likely causes of third occipital neuralgia are
traumatic arthropathy or degenerative joint disease of
the C2-3 facet joint (Bogduk and Marsland, 1986).
Lord et al. (1994) stated that the prevalence of TON
headache among patients in whom headache is the
predominant complaint after whiplash was as high as
53%. This suggests that third occipital neuralgia is the
most common cause of headache in patients who
experienced whiplash (Lord et al., 1994). Various
therapies for the treatment of third occipital neuralgia
exist giving clinicians a variety of nonsurgical options
to treat their patients (Ashkenazi and Levin, 2004;
Tobin and Flitman, 2009). Ashkenazi and Levin (2004)
state occipital nerve block holds both a diagnostic and
therapeutic value with regards to third occipital neuralgia. Other authors have reported successful treatment of TON neuralgia with implantable pacemakers
providing neurostimulation (Chaiban et al., 2014;
Hong et al., 2014). Radiofrequency ablation has also
been a viable option for the treatment of TON neuralgia (Vanderhoek et al., 2013; Hamer and Purath,
2014). In cases of several TON neuralgia refractory to
nerve decompression, surgical excision of the third
occipital nerve may done as a last resort (Ashkenazi
and Levin, 2004; Gille et al., 2004; Ducic et al., 2009,
2014).

CONCLUSIONS

Chiari Malformation: An Important


Diagnostic Consideration
Although Chiari malformations do not typically
compress the occipital nerves directly, the symptoms
of this congenital anomaly are often confused with
occipital neuralgia (Cesmebasi et al., 2014). Therefore
it is important to consider this possibility whenever
patients present with occipital headache especially, if

Occipital neuralgia is a common and sometimes


debilitating condition caused by compression, entrapment, or stretching of the occipital nerves. Its primary
symptom of paroxysmal burning pain is usually present along the cutaneous distribution of the nerve
being compromised. It is important for clinicians to be
familiar with the anatomical points of compression
and with the distributions of each nerve in order to
identify the etiology of pain. Furthermore, as variations of these nerves are common and there are often
interneural connections (Fig. 2), multiple anatomic
etiologies should be considered.

ACKNOWLEDGMENTS
The authors thank the individuals who donated their
bodies to the Department of Anatomy. This article was
made possible by the seless gift from donor cadaver
patients.

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