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238
Fig. 18.3 CT sagittal image
showing AA dislocation and
odontoid process destruction
caused by RA (a), CT 3D
reconstruction depicting the
AA displacement in another
patient (b)
18 Rheumatoid Arthritis
Fig. 18.4 High riding VA in RA patient. (a) Sagittal image showing the AA dislocation. (b) Left enlarged FT of C2 axial scan.
(c) Sagittal image showing lack of space for isthmic screw placement
Fig. 18.5 T2 MRI weighted
images in neurologically
intact RA patient with AA
dislocation. (a) Sagittal
image, note preodontoid
formation of inflammatory
synovial cyst. (b) Axial
image of the same patient,
note spinal cord deformity
and its posterolateral
dislocation
three-dimensional reconstructions and navigation
techniques in patients planned for posterior instrumentation in order to minimize the risk of VA injury. CT
myelography can be used if MRI is contraindicated
(pacemaker) with acceptable accuracy. However, MRI
has become the preferred modality for evaluation of
CVJ [46]. The medulla, brainstem, soft tissue destruction, ligaments, pannus formation, bone swelling or
relationship of the odontoid and/or pannus to the neural tissue and change of cervicomedullary angle (CMA)
can be directly seen (Fig. 18.5). MRI proves invaluable
in cases where soft odontoid pannus is large and
18.5 Treatment Strategy
Fig. 18.6 Dynamic MRI of
RA patient. (a) Extension
showing sufficient space for
spinal cord. (b) Flexion
causing atlantal forward
dislocation with posterior
arch compressing the cord
239
compressive while the degree of AA dislocation and/or
bone destruction is much less impressive. Recently,
dynamic (flexion-extension) MRI (Fig. 18.6) has been
shown to be able to delineate the instability and provide further information about the dynamics of CVJ, in
particular about the alarming narrowing of posterior
subarachnoid space during flexion [3, 48]. MRI is also
a very important noninvasive tool capable of monitoring disease progression during patient follow-up.
18.5 Treatment Strategy
The exact etiology of RA is not known and thus causal
treatment for the disease does not exist yet. Therapy
usually involves a combination of medications, patient
education, rehabilitation, joint protection, and surgery
focused on arthrodesis or joint replacement. It is generally accepted that early treatment of RA results in
better outcomes.
In clinically asymptomatic individuals with radiographically confirmed dangerous UCS instability or
deformity, the goal of any surgical treatment is to establish spinal stability and prevent neurological sequelae
of the disease. In symptomatic patients with radiographic compression, with or without concomitant neurological signs or symptoms, decompression with
subsequent stabilization is indicated. It is a well-known
fact that once myelopathy occurs in RA patients, prognosis is poor and can hardly be altered by intervention
[28]. Careful follow-up and early surgical intervention
is the key to prevention of neurological decline and
potential mortality as the disease is indeed progressive.
Currently, surgical treatment is clearly indicated in
RA patients with intractable pain and/or neurological
deficit with corresponding morphological background.
Even further, it is also clear that some of those without
a deficit or major pain syndrome can benefit from preventative surgery. This is especially true in cases of
AA dislocation due to the well known natural progression over time. In Smith’s series of RA patients [63],
progression of AADI occurred in 55% of patients during a 4.5 year follow-up. It advanced from an initial
average distance of 3.5–5.0 mm to 5.0–8.0 mm in 45%
and over 8.0 mm in another 10% of patients. However,
there is no single parameter capable of predicting the
future development of myelopathy and thus most
authors prefer various combinations of predicting measures [9, 10, 13, 14, 20, 67].
Schizas et al. believe that patients with AADI
greater than 6 mm in flexion should be treated surgically whereas those with cranial settling should
undergo surgery if AADI is more than 3 mm [58].
Boden reported that PADI is more correlative to eventual presence of cord compression and recommended
surgery when PADI was less than 14 mm [6]. Shen
et al. suggest surgical intervention in those with PADI
less than 14 mm measured on dynamic plain films and
SAC (space available for cord) less than 13 mm and/or
CMA less than 135° measured on MRI. If the AA dislocation is accompanied by cranial settling, they advise
to be more aggressive and to perform surgery in presence of any cord compression. However, they accept
observational strategy if there is settling without neural compression and clinical symptoms [60].
Although there is no doubt that patients with neurological deficit caused by morphological compression
have to be operated on, the questions remain if anterior, posterior or combined procedure should be performed as well as how many segments should be
included in the fixation and fusion.
240
18 Rheumatoid Arthritis
For further surgical decision, it is also necessary to
determine whether subluxation and/or deformity can
be reduced. A reducible lesion is defined as one in
which relief of compression of the cervicomedullary
neural structures could be obtained by restoring the
anatomic relationship of CVJ [41]. Generally, reduction can be accomplished by simple positioning or by
traction. Cervical skeletal traction is applied to patients
with cranial settling and/or positionally irreducible
kyphotic deformity. Depending on surgeon’s experience, traction can be used for shorter or longer periods,
preoperatively.
Simple mobile AA dislocation is most frequently
treated by posterior reduction, fixation, and fusion. The
immediately stable, fixation methods are preferred
today and thus the majority of patients are treated with
posterior C1-2 transarticular screws (Magerl), posterior
C1 lateral mass, and C2 pedicle screw construct (GoelHarms) or, in case of high-riding VA, by posterior C1
lateral mass screws connected by rods to C2 laminar
screws (Wright). Technical details of previous methods
are described in Chap. 6. Due to poor bone quality and
limited healing potential in RA, autologous bone grafts
have to be used to supplement posterior AA fixation.
Asymptomatic patients with predominantly a pannus formation can be treated by simple AA fixation and
fusion. It is known that at least part of pannus tissue is
provoked to grow by abnormal movement related to
mechanical irritation that can be eliminated by fusion.
Pannus size decreases or even disappears after AA
fusion [26, 43, 70, 72]. AA fusion can also improve the
rate of subsequent vertical odontoid migration [25].
In cases of fixed AA dislocation, posterior C1
laminectomy and fusion or transoral decompression
and fusion are recommended [41]. If AO joint is affected
by the RA process, posterior OC constructs are used to
stabilize the entire CVJ. In such cases, the extent of
fusion should not exceed the damaged segments [25].
In cases of cranial settling, with or without coincident CVJ kyphosis, it is essential to clarify if the deformity can be reduced by traction or not. If the odontoid
process can be successfully drawn out of the FM, then
posterior OC fixation and fusion is considered as sufficient [41, 60]. If sufficient reduction cannot be achieved
but neural compression is not evident the same treatment can be selected [60]. However, if brainstem is
compressed despite adequate reduction attempts, then
decompression should precede any fusion procedure.
Transoral decompression is indicated in all irreducible
dislocations with marked anterior compromise [32].
The first transoral procedure for UCS RA deformity
was performed by Sukoff et al. in 1972 [65]. Usually,
anterior decompression is followed by posterior stabilization [17, 25, 41, 60]. Alternatively, as suggested
by Harms, anterior plating between C1 lateral masses
and C2 vertebral body could be used [29]. However,
Kandziora et al. [31] proved that such construct is
not stable enough without posterior AA graft and
wire fusion. Other plating systems were subsequently
introduced that allowed for stand-alone anterior fixation and, with some, even for reduction of AA kyphosis [31, 69]. Although, the stability provided by these
anterior constructs was biomechanically comparable to
Magerl’s method [30], only a handful of patient series
treated in this manner have been reported [2, 32].
Other options include posterior reduction by forced
lordosis of C2 transpedicular screw attached to a rod
anchored in occipital plate, as described by Abumi [1];
or a direct distraction of collapsed AA joints with cage
and C1-2 plate fixation [24].
Zygmunt et al. [71] found that the majority of failures of OC fusion constructs in RA patients were the
result of a progressive subaxial instability (37 of 163
cases), particularly at C3-4 and C4-5 levels. Krause
et al. [34] described a 36% overall incidence of subaxial instability after OC fusion. This complication
can by minimized by assessment of subaxial spine
with dynamic plain films to identify any subaxial instability prior to a planned OC fusion. A more caudal
extension of OC construct would then need to be carried out if instability exists at the lower levels. The
other important key point is to respect sagittal alignment during any OC fixation to avoid undue overload
of adjacent mobile segments [47, 51].
18.6 Our Preference
There is a great variability of data evaluating the incidence of cervical spine involvement in RA patients
and its consequences. Therefore, for practical purposes, we can assume that more than half of the patients
suffering from RA would suffer from cervical spine
disease. Of those, approximately 80% would present
with UCS involvement and 20% with subaxial cervical
spine subluxations. In the UCS, AA subluxation is the
most frequently detected abnormality, with the majority
(70%) being an anterior dislocation. Lateral, posterior,
and rotational subluxations are much less frequent.
Cranial settling of AA and AO joints is seen in about
20% of those with UCS disease. Certainly, any
18.5 Treatment Strategy
241
combination of previous dislocations is possible.
Approximately 50% of RA patients with cervical spine
involvement can expect a radiographic progression of
their disease and one quarter of patients will develop
neurological compromise over 10 years.
Generally, those with radiographic evidence of disease without gross instability, neurological deficit or
intractable pain can be followed conservatively.
However, once signs of clinical and/or radiological
progression are detected, surgical intervention needs
to be considered.
At our institution, we offer surgical treatment to
those patients with AA subluxation where the AADI
is more than 6 mm and PADI less than 14mm on plain
dynamic films and/or SAC less than 13 mm with neural compression visible on MRI. We do so even in
the absence of neurologic deficit and good control of
symptoms. Patients with AA instability with intractable
pain and/or neurologic deficit are surgical candidates
without discussion. The coexistence with cranial settling makes the decision for surgical intervention more
imperative in both previously mentioned groups.
Reducible AA dislocations are treated surgically with
posterior C1-2 fusion. Majority of our patients are treated
with transarticular C1-2 fusion according to Magerl supplemented with posterior autologous H graft fixed to
arches with titanium braided wire (Fig. 18.7).
In partially reducible AA subluxations, we prefer
the use of Goel-Harms C1-2 posterior fixation as it
allows proper opening of the AA joint, C1 manipulation, and eventual C1 laminectomy (Fig. 18.8).
In cases of high-riding VA, we always prepare a virtual three-dimensional screw trajectory plan. If pedicle
or isthmic screw is not safe, we opt for a combination
construct of a laminar screw (Wright) on the affected
side and a pedicle/isthmic screw on the other.
Exceptionally bilateral high-riding VA can be found, then
C2 double-crosslaminar screw fixation can be a choice.
In positionally irreducible kyphotic deformity local-
ized predominantly to C1-2 segment, we prefer transoral odontoidectomy potentially with AA joint release
followed by immediate posterior screw and graft fusion
(Fig. 18.9). In such cases, we do not try to reduce the
deformity with traction.
Fig. 18.7 Reduced AA dislocation fixed by Magerl screws supplemented with posterior autologous Gallie-type graft fixed by
braided titanium wire. (a) Preoperative lateral plain image. (b) Preoperative MRI. (c) Postoperative lateral film
Fig. 18.8 Reduced AA dislocation due to manipulation with C1
lateral mass screws of Goel-Harms construct. (a) Preoperative
CT showing AA dislocation and embarking cranial settling.
(b) Postoperative CT depicting the reduction achieved. (c) Harms
fixator in the same patient
242
18 Rheumatoid Arthritis
Fig. 18.9 Fixed AA deformity treated with transoral odon-
toidectomy and joint release followed by posterior reduction
and transarticular C1-2 fusion. (a) Plain film in flexion. (b) Plain
film in extension. (c) Sagittal CT reconstruction. (d) Postoperative
If there is radiographic evidence of rheumatoid
pannus compressing the spinal cord/brainstem without
neurological symptoms or signs, we opt for a simple
posterior fixation and fusion only if voluntary extension of the spine reduces the dislocation without complaints. However, in presence of neurological deficit,
we would perform a transoral decompression first.
This, perhaps unusual preference of transoral decompression, stems from good long-term results with this
approach at our institution. A routine odontoidectomy
represents approximately one hour of relatively safe
surgery whereas long-term skeletal traction is not
only uncomfortable but can also be rather morbid in
patients with marked cord compression and common
RA-related systemic problems (Fig. 18.10). If any
attempt to reduce by traction is planned for AA deformity, then it is done in an anesthetized patient just prior
to the planned procedure under electrophysiological
monitoring.
sagittal CT documenting the extend of TO odontoidectomy.
(e) 3D CT showing successful reduction, note the vicinity of the
screw to C2 FT
If there is evidence of a significant AO joint involvement on CT in patients with CVJ instability, we prefer
to extend the fixation and fusion to the occiput.
Our strategy of treatment of rare complex CVJ deformities caused by RA is different. Intracranial odontoid
migration/basilar invagination often accompanied by
CVJ kyphosis can be either reducible or irreducible,
with or without neurologic deficit. In neurologically
intact patients, skeletal traction should be attempted, in
our opinion, even if longer term. If the deformity can
be reduced as evidenced by concomitant MRI-proven
neural decompression, then posterior OC fusion is
usually sufficient for those patients. If reduction is not
successful but there is no significant compression on
MRI, OC fusion can also be selected (Fig. 18.11).
In patients with irreducible deformity and with neu-
rological deficit with radiographic evidence of compression, we prefer direct decompression supplemented
by fixation and fusion. Most frequently, we use a
18.5 Treatment Strategy
243
transpalatopharyngeal anterior approach with posterior OC fusion at the same sitting.
In conclusion, it is important to emphasize that wellselected patients suffering from RA with cervical spine
involvement can benefit from surgical intervention
Fig. 18.10 Bedridden patient
with quadriparesis caused by
cord compression treated by
transoral decompression and
posterior fusion without
initial traction attempt.
(a) MRI before the surgery.
(b) MRI after surgery
with an expected improvement in two thirds of them.
Therefore, it is of utmost importance to cooperate with
referring physicians in early indication of appropriate
candidates but also in long-term evaluation of surgical
results.
Fig. 18.11 Neurologically intact patient with traction-irreducible
cranial settling treated by C1 posterior laminectomy simple OC
fixation. (a) T1 MRI sagittal image showing vertical intracranial
odontoid migration. (b) CT in the same plane. (c) Plain films of
O–C2 pedicle screw fixation. (d) Postoperative MRI
244
Fig. 18.11 (Continued)
18 Rheumatoid Arthritis
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Tumors
P. Suchomel, V. Benes, and M. Kaiser
19
The basic goal of treatment is to achieve decompression of the neural elements, ideally by complete tumor
resection, and reconstructing the spine while maintaining normal sagittal balance and minimizing loss of
motion segments. This goal is often difficult or even
impossible due to anatomical restraints and the proximity or involvement of neurovascular structures. In certain types of primary, benign bone tumors, control or
cure can be achieved by partial tumor resection. This,
however, is the exception and in most tumors, gross
total excision needs to be achieved when technically
feasible in order to prevent recurrence or progression.
Comprehensive studies of tumors in the UCS region
do not exist; however, we do know that, with a few
exceptions, the general occurrence of tumors is similar
to the subaxial spine. The occurrence of chordoma in
the C2 region is a notable exception. In general, C1 is
less commonly affected as C2 is affected by tumors
more often [60].
19.1 Extradural UCS Tumors
The most common types of extradural tumors at the
UCS are secondary tumors, at about 90%. Primary
tumors are less common but are usually difficult to
P. Suchomel, V. Benes, and M. Kaiser
Department of Neurosurgery,
Neurocenter, Regional Hospital Liberec,
Husova St. 10, 46063 Liberec, Czech Republic
treat or cure [113]. The current approach to treatment
of spinal extradural tumors is multidisciplinary. The
treatment teams are usually composed of a spine surgeon, oncologist, pathologist, and organ specialist
(urologist in renal tumors, dermatologist in melanoma,
etc.). This team must evaluate the patient’s general status, establish the diagnosis, the prognosis, and recommend the most effective treatment. This same team
theoretically should follow the patient’s course and
final outcome, all of which, unfortunately, is not common in practice.
19.1.1 Radiological Remarks
The initial evaluation of patients with suspected spinal
extradural neoplasms is plain radiographic examination. Plain radiographs require a 30% to 50% demineralization to detect a destructive process within the
vertebral body (Fig. 19.1) [32]. Plain radiographs allow
localization and determination of the extent of tumor
involvement, and with dynamic films, spinal stability
can be evaluated. For patients with a known primary
cancer, bone scintigraphy has been standard but more
recently, positron emission tomography (PET) scan is
used to screen for metastatic lesions. Although bone
scans are very sensitive in determining the presence of
a high bone metabolic turnover state and/or hyperemia,
they cannot differentiate whether the process is an
infection, a healing fracture or a tumor. CT scanning
permits direct visualization of the bone, any destruction, and allows evaluation of the anatomy for planning
for eventual stabilization procedures (Fig. 19.2). MRI
can provide information about soft tissue, including
extent of tumor involvement (Fig. 19.3), neural
P. Suchomel and O. Choutka, Reconstruction of Upper Cervical Spine and Craniovertebral Junction,
DOI: 10.1007/978-3-642-13158-5_19, © Springer-Verlag Berlin Heidelberg 2011
247