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17 Non Specific Inflammation
17.2 Clinical Symptoms and Diagnosis
Similar to other infective processes, patients can present with general symptoms of fever and fatigue as well
as symptoms and signs specific to UCS osteomyelitis.
Those may include mechanical neck pain worsening
especially in rotation, neck stiffness or swallowing difficulties, and enlargement of painful cervical lymph
nodes [8, 12, 24].
With neural compromise, patients may suffer from
cranial nerve palsies and/or signs of cord compression.
Myelopathy may range from a mild quadriparesis to a
severe bedridden status and sometimes, finally, death
of the patient [1].
Serum inflammatory markers are usually elevated,
with possible increases in ESR, CRP, and leukocytosis
with shift in differential rate to immature cells. Blood
cultures should be obtained on admission; however,
treatment usually cannot be delayed until their results
are available.
The physician should never forget to enquire about
history of diseases that compromise the immune system such as diabetes mellitus (DM), AIDS, chronic
steroid use, or immunomodulants in allergies and/or
about history of heavy smoking or other drug abuse.
17.3 Radiology
Plain radiographs will typically reveal AA subluxation
(Fig. 17.1) or osseous destruction if present (Fig. 17.2).
However, the most common finding is usually only an
Fig. 17.1 Plain lateral film showing consecutive development of
UCS inflammatory process with AA subluxation after purulent
pharyngitis (S. aureus). (a) Plain film obtained at the time of first
neck pain. Odontoid is not well outlined and retropharyngeal
Fig. 17.2 Plain lateral radiograph depicting development of
osseous C2 destruction and atlas settling within 5 months after
inflammatory process in the parotid gland (S. aureus). (a) Picture
obtained at the time of the first neck pain, only mild widening of
space widened. (b) Lateral film obtained 3 weeks after showing
marked AA dislocation. (c) Lateral fluoroscopical view at the
time of admittance to our hospital 4 weeks after the first films.
Note also development of significant kyphosis
retropharyngeal space can be detected. (b) Lost contour of odontoid process visible on lateral view 2 month later. (c) Significant
C2 destruction with AA dislocation and settling 5 months after
complaint onset
17.3 Radiology
ab
229
increase in the prevertebral space and edema of retropharyngeal tissues [8, 23]. Dynamic plain views are
absolutely necessary at the earliest convenience to
exclude a potential AA instability in primarily nondislocated cases. Similar picture but with greater detail
of bony morphology can be obtained from CT imaging
(Fig. 17.3). Contrasted CT can also demonstrate pyogenic membrane of an abscess, if already present [8,
10, 23]. The “hot spot” and also other disease foci can
Fig. 17.3 CT of purulent
destruction of odontoid
process and left C1 lateral
mass. (a) Axial scan.
(b) Coronal plane
reconstructions
be detected on bone scintigraphy in the early phases of
infection, although it is neither very specific nor
anatomically sufficient [9, 19]. The mainstay of diagnostic assessment is contrasted MRI (Fig. 17.4), possibly supplemented with dynamic positions (Fig. 17.5).
MRI is superior in demonstrating liquid abscess
(Fig. 17.6), in exclusion of spinal cord compression
(Fig. 17.7) and in determination of the extent of prevertebral tissue involvement [8, 17, 24].
Fig. 17.4 MRI in T2
sequence showing the C2
destruction with pus
spreading retropharyngeally
230
a
b
a b
Fig. 17.5 Dynamic MRI
without increased neural
compression in position
change. (a) Flexion.
(b) Extension
17 Non Specific Inflammation
Fig. 17.6 Liquid epidural pus replacing odontoid process
visible on axial MRI scan
Fig. 17.7 Destruction of
odontoid process with
inflammatory tissue
expanding posteriorly and
causing spinal cord compression (patient was quadriparetic). (a) Midsagittal MRI in
T2 sequence depicting
inflammatory retroodontoid
peg formation. (b) CT
showing the odontoid
posterior destruction
17.6 Our Preference
231
17.4 Differential Diagnosis
Occasionally, the only radiographic finding will be
a non-specific mass destroying the UCS region without any spread so typical for purulent inflammation.
The differential diagnosis then includes tuberculosis,
fungal process, and primary or secondary neoplasm –
processes where the necrotic center can mimic liquid
pus. In those situations, excisional or needle biopsy
[18] can help determine the diagnosis and identify the
infectious agent. In the vast majority of cases, the
odontoid area is affected; however, an infection involving purely the atlas has also been reported [26].
17.5 Treatment Strategy
There is a considerable risk to a delayed diagnosis with
unrecognized development of dangerous AA instability (Figs. 17.1 and 17.2). Gormley and Rock’s retrospective review of available publications found that the
late visibility of osseous destruction on plain films was
the main reason for a delay in diagnosis [8]. They recommended an assessment of possible instability as
soon as UCS involvement is suspected. Early identification of infectious agent is very important. Needle
aspiration biopsy is preferred by many [8, 23] as a first
diagnostic step after radiographic evaluation. It serves
not only as a diagnostic tool in terms of etiology of the
process but also allows for samples to be obtained for
determination of antibiotic (ATB) sensitivities. Most
authors recommend starting with external halo-vest
immobilization in patients without neurological deficit
and/or compression, and long-term antibiotic administration [8, 12, 17]. In those cases, surgical intervention
is reserved for patients who fail conservative treatment
with external immobilization. If instability or malalignment persist, posterior AA fusion is performed. On
the other hand, transoral decompression followed by
posterior fusion is recommended in patients with direct
anterior compression and/or epidural pus spread [8,
14, 28]. Posterior fixation after closed traction reduc-
tion in case of a complete inflammatory destruction of
the dens was also reported [4].
Some authors prefer an aggressive surgical approach
upfront. They argue that conservative therapy results
are questionable, especially when it comes to the eventual AA instability at the end of therapy [29].
Long-term antibiotics are always administered in
cases of osseous involvement. Once cultures and sensitivities are available, an intravenous, microbe-specific
ATB regime is instituted for 6–12 weeks followed
by long-term oral suppressive therapy for at least 6
months [24].
17.6 Our Preference
In our series of patients with infections of UCS, four
out of five patients were initially treated for pharyngitis
without any radiographic evaluation. They were referred
to our hospital late with significant UCS osseous
destruction and/or instability. This was the reason for
early surgical intervention in all of them.
We choose conservative approach only in cases
where there is no MRI-detectable pus. We respect the
old surgical rule “ubi pus ibi evacua.” The decision
whether soft collar or hard external bracing is required
should be based on the presence or absence of instability on dynamic films. We consider Philadelphia or
SOMI brace to be hard external braces and do not recommend halo-vest immobilization because of reasons
explained in Chap. 11. If either encapsulated (abscess)
or spreading (retropharyngeal or epidural empyema)
pus is detected on MRI and/or CT, it should be evacuated via the shortest and safest route, in our opinion.
Direct needle biopsy with aspiration of purulent material for microscopy, culture and sensitivity should be
done as soon as infection is suspected by MRI. The
“old fear” of possible tuberculous fistula formation is
unfounded nowadays as is documented by many
authors [2, 22, 25]. There are two approaches for UCS
needle aspiration: fluoroscopically-guided transpharyngeal route or lateral CT-guided needle aspiration.
In the absence of UCS instability or neural compromise, surgical evacuation of liquid pus collection followed by external immobilization, long-term ATB
administration, and careful radiological follow-up can
be sufficient. However, if significant bone inflammatory involvement (spondylitis) exists, we prefer to
widely debride any affected tissue (i.e., may involve
odontoidectomy) and insert antibiotics locally (gentamycin foam, spheres, etc.). In widespread bone tissue disintegration, we set up a drainage–lavage system.
Most importantly, spinal cord has to be decompressed.
As the majority of these procedures are performed
232
17 Non Specific Inflammation
transorally (Fig. 17.8) and transoral fixation possibilities are rather limited, we usually prefer to perform
posterior CVJ fixation restricted to affected motion
segment during the same procedure (Fig. 17.9).
Pyogenic inflammation in UCS region is very dan-
gerous and can culminate in patient’s death; however,
Fig. 17.8 Intraoperative picture of pus coming out immediately
after longitudinal posterior pharyngeal wall incision
if recognized early and treated properly, it can have a
relatively benign course with a very good outcome.
17.7 Remarks on Tuberculosis
in UCS Region
Spinal tuberculosis (TB) causing paraplegia was first
described by Percival Pott in 1779. Later, the old surgeons called it “Pott’s disease” or “caries in spine”.
Victor Horsley was probably the first person to perform cervical laminectomy for relief of tuberculous
compression caused by “pachymeningitis cervicalis”
in 1893 [11]. It is not clear who started to treat TB
surgically in UCS but Berchtold Hadra was probably
one of the first with his silver wire loops in the beginning of the twentieth century [11]. Nowadays, the spine
is affected in approximately 1% of all TB patients [2],
with UCS involved in 0.3–1.0% of them [3, 5]. The
incidence of newly diagnosed TB in UCS is growing in
European countries today. Although not the primary
subject of this chapter, it needs to be stressed that TB
may be finding its way back to the differential diagnosis of UCS infections with increasing frequency. There
is a large body of contemporary experience gained
from published series of patients treated in Asia [25].
Fig. 17.9 Examples of
posterior fixation performed
in single session after
transoral decompression.
(a) Transarticular screw
fixation according to Magerl.
Note the metal clip fixed to
the remnant of C1 anterior
arch (anterior tubercle
resected) as a guiding
point for Magerl screws.
(b) Occipitocervical fusion in
the case of AO and AA joint
purulent destruction
References
233
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experience. Neurosurgery 52, 331–338 (2003). discussion
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Rheumatoid Arthritis
P. Suchomel, P. Buchvald, and O. Choutka
18
Rheumatoid arthritis (RA) is defined as a sterile erosive
inflammation of the synovial membrane causing polyarthropathy and leading to destruction of ligamentous, cartilaginous, and bony structures with subsequent structural
deformity and instability. Pannus formation, articular
cartilage invasion, periarticular erosions, and destruction
of adjacent structures can all be the result of this devastating process. RA affects the cervical spine in up to 86%
of patients with majority of UCS involvement [33, 68].
Patients diagnosed as having RA must fulfill the revised
criteria of the American Rheumatism Association [4].
18.1 Etiology and UCS Pathophysiology
Although RA is a chronic auto-aggressive (autoimmune)
reaction, the exact cause of the disease is still unknown.
The era of intensive investigation of the immunologic
aspects of RA began following the initial discovery of
rheumatoid factor (RF) by Waaler in 1940 [56] and confirmation by Rose et al. in 1948 [66]. A genetic predisposition has also been identified. The combination of
genetic susceptibility with yet unidentified inciting
events can lead to disease expression [57, 64]. In the
UCS, RA process induces AA (atlanto-axial) instability
and subluxation caused by insufficiency of the transverse and alar ligaments. Subsequent morphological
destruction of AA and atlanto-occipital (AO) joints can
cause vertical instability with the atlas telescoping
downward and the odontoid process vertically migrating
into the cranial cavity – so called cranial settling.
As the odontoid process migrates cranially, it crowds
the foramen magnum (FM) and, in the worst case scenario, compresses the brainstem. Neural compromise at
this level can, however, be caused by a simple pannus
formation and/or posterior C1 arch pressure in cases of
AA subluxation [38, 41]. Subsequent progression of the
disease that occurs in the majority of cases, thus, gradually advances from relatively simple AA instability to
kyphotic deformity of the CVJ. In the final stages of the
process, what is initially a mobile deformity ultimately
becomes irreducible. Further, erosive fractures of lateral
masses and the odontoid process are also known [41].
Subaxial cervical spine RA involvement typically
includes multilevel subluxations called “stepladder
deformity” caused by destruction of ligaments, facet
joints, and discovertebral junctions (Fig. 18.1). However,
this problem is less common than the above mentioned
CVJ involvement (approx. 20% of all cervical RA).
18.2 History and Incidence
P. Suchomel and P. Buchvald
Department of Neurosurgery,
Neurocenter, Regional Hospital Liberec,
Husova St. 10, 46063 Liberec, Czech Republic
O. Choutka
University of Cincinnati, Medical Center,
Department of Neurosurgery,
Albert Sabin Way 231,
Cincinnati, OH 45267-0515, USA
P. Suchomel and O. Choutka, Reconstruction of Upper Cervical Spine and Craniovertebral Junction,
DOI: 10.1007/978-3-642-13158-5_18, © Springer-Verlag Berlin Heidelberg 2011
The first description of the disease is usually attributed to A.J. Landre-Beauvais [35], but the term rheumatoid arthritis was first used by A.B. Garrod in 1854
[22]. His son A.E. Garrod documented the RA cervical spine impact in 1890 [23]. In a group of 500
patients suffering from RA, he found 36% with
affected cervical spine. The first descriptions of the
actual destructive pathological changes in AA and
235
236
Fig. 18.1 Sagittal MRI in T2 sequence showing simultaneous
RA odontoid pannus formation and subaxial cervical “stepladder deformity”
occipitocervical (OC) regions came from Englander
[21] and Davis and Markley [19], who were also the
first to describe a case of AA subluxation causing
death in a RA patient.
The worldwide incidence of RA is around 3 cases
per 10,000 and it is two or three times more frequent in
women. The prevalence of RA is approximately 1% of
the world’s adult population when defined by either
the presence of serum rheumatoid factor (RF) or erosive changes on radiographs in a patient with a compatible clinical presentation. The onset is more frequent
during the fourth and fifth decades of life with 80% of
all patients developing the disease between 35 and 50
years of age [61].
Cervical spine is affected in 44–88% of RA patients
[5, 15, 45, 59, 63]. Based on the various studies,
between 5% and 73% of RA patients will develop AA
subluxation, about 20% will present with significant
subaxial cervical spine disease, and approximately
17% will develop neurological sequelae [15, 27, 37,
40, 50]. Mikulowski et al., Paus et al., and Hamilton
et al. estimated that 10% of patients with RA may die
from brainstem compression that is unrecognized
before their sudden death [28, 42, 49]. Oostveen et al.
reported an overall mortality rate of 17% in patients
18 Rheumatoid Arthritis
with RA and radiographic evidence of cervical subluxation [48]. The worst mortality rate was described
by Crockard and Grob who reported that half of the
RA patients presenting with myelopathy will be dead
within one year [18]. However, only 10% of patients
with juvenile RA will go on to develop destructive
polyarthropathy with the potential for cervical spine
problems. The others make a full recovery [16].
18.3 Clinical Symptoms
RA activity in the cervical spine begins early and progresses clinically and radiographically simultaneously
with the peripheral joint disease. In fact, the severity
of the peripheral erosive damage correlates with the
degree of structural damage in the cervical spine [11,
54]. Even though most patients are initially asymp-
tomatic, the signs related to cervical spinal abnormalities develop approximately in 60–80% of them [16].
The clinical manifestations can be extremely variable;
however, neck pain with radiating occipital headache
is often the leading symptom. Also, brachialgia with
“frozen shoulder” can be seen more often. Limb paresthesias, weakness, vertigo, cranial nerve palsies,
sphincter disturbance, and difficulty to walk could be
the manifestations of myelopathy/neuropathy due to
compression of spinal cord, brainstem, and cranial
nerves.
The Ranawat classification is most frequently used to
categorize patients with rheumatoid myelopathy based
on their clinical history and physical findings [52].
The Ranawat classification of neurologic deficit in RA:
Class I – No neural deficit
Class II – Subjective weakness, dysesthesias, and
hyperreflexia
Class IIIA – Objective weakness and long-tract
signs; patient remains ambulatory
Class IIIB – Objective weakness and long-tract
signs; patient no longer ambulatory
It is often difficult to distinguish which symptoms
are caused by neural compression and which ones by
the disease itself. The clinical appearance is also
frequently modified by the concomitant pharmacological treatment – corticosteroids, nonsteroidal antiinflammatory drugs (NSAIDs), disease-modifying
anti-rheumatic drugs (DMARDs), biologic medications etc. This can indirectly lead to delayed diagnosis
of neural compression and thus late surgical intervention. Marks and Sharp reported an average delay of
18.4 Radiology
237
31 weeks from the first appearance of neurologic signs
to the correct diagnosis of myelopathy [36].
18.4 Radiology
Plain radiography is still the first line of investigation
when it comes to imaging of the rheumatoid cervical
spine. Overall bony alignment, bone quality, and soft
tissue swelling should be assessed. AA instability can
be documented by flexion/extension views (Fig. 18.2).
If any suspicion of RA process is established, then CT
and MRI should be obtained to further depict the bone
and soft tissue pathologic anatomy. Depending on the
stage of the disease and subsequent surgical indication, other imaging modalities such as 3D bone CT,
CTA, dynamic MRI or scintigraphy can be added.
AA subluxation represents the most common manifestation of rheumatoid involvement of the spine [8]. In
the majority of cases, the anterior type of subluxation is
present although only 50% of these are symptomatic
[50]. Anterior atlantodental interval (AADI) of 4–6 mm
indicates early instability and implies transverse atlantal ligament damage or laxity. AADI larger than 6 mm
indicates that the alar ligaments are also damaged.
Posterior AA dislocation can occur in approximately
7% of all subluxations, if anterior C1 arch is defective
or odontoid process eroded. This is, however, usually
not accompanied by neural compression. Lateral subluxation is seen in approximately 20% of all AA
dislocations and usually is a result of lateral mass
destruction or rotational deformity. It is defined as a lateral mass shift greater than 2 mm [7, 62].
Vertical subluxation, originally defined as a protrusion of the odontoid tip by more than 7 mm above the
McGregor line [39], accounts for 22% of all dislocations. Other craniometric lines and indices obtained
from plain films were historically used to establish the
vertical odontoid migration [52, 53]. However, more
recent publications demonstrated that the accuracy of
these methods is substantially limited by the visibility
of the anatomical landmarks on plain films, especially
if their boundaries are eroded by RA process. It can be
concluded that only a combination of plain film measurements can be of some practical value [55].
Currently, CT evaluation dominates in documentation of bone destruction. Reformatted sagittal images
can precisely show the position of odontoid process
and the amount of AA dislocation (Fig. 18.3). All the
joints can be directly visualized and the actual focus
(AA or AO joint) of disease defined. The total amount
of UCS distortion can be evaluated on three-dimensional CT reconstructions. CT also plays an essential
role in showing the exact morphology and amount of
bone available for screw placement prior to any surgical fixation. According to contemporary studies of
Chen et al. [12] and Myiata et al. [44], one may need to
anticipate a high-riding vertebral artery (VA) in
31–70% of RA patients with AA instability or other
UCS RA (Fig. 18.4). This translates into an increasing
need for CTA evaluation in this situation followed by
Fig. 18.2 Dynamic
radiographs showing
atlantoaxial instability
in RA patient. (a) Flexion.
(b) Extension