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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_6029_Библиотеки_им_академика_М_И_Перельмана.pdf
Degenerative Disorders
P. Suchomel and P. Barsa
21
Anatomically, atlantoaxial (AA) articulation represents a three-joint complex: the atlantodental articulation and two lateral mass joints. All three may be
involved in a degenerative osteoarthritic process that is
commonly described as osteoarthrosis. Morphology of
atlantoaxial osteoarthritis (AAOA) does not differ
from degenerative changes found elsewhere in the
spine. In clinical practice, it is commonly associated with peripheral osteoarthritis or degenerative
spine disease, predominantly in older population.
Osteoarthritis of the AA articulation, although mostly
asymptomatic, may cause severe neck pain, occipital
neuralgia, and even myelopathy. Progression of AAOA
can lead to ligamentous laxity, instability, and rarely
even to compression of the spinal cord. Degenerative
changes of the facet joints occur with radiological
prevalence of 4.8%. However, age-related progression
has been shown. While it is documented in 5.4% of
patients in their sixth decade, in ninth decade of life
18.2% of patients suffer from this problem [13]. The
prevalence of atlantodental osteoarthritis has, so far,
not been the subject of a systematic study.
21.1 History
The first reference to a neuralgic syndrome in occipital
region was made by Bruno y Lantijo and Ramosin in
1821 [9]. Since then, many authors identified cervical
arthritis as being responsible for certain suboccipital
headaches [7, 10]. Ehni and Benner in 1984 were,
however, the first to describe AAOA as a cause of pain
in the occipital region and first who attempted to treat
it surgically [2]. Ghanayem et al. published the first
large series of AAOA patients treated successfully
with posterior AA fusion [4]. The largest published
cohort of 35 patients treated for symptomatic AAOA
using transarticular screw AA fusion is that of Grob
et al. [5]. Finn et al. [3] presented a group of 26 patients
suffering from AAOA treated either with posterior
C1-2 transarticular fusion or with combined transoral
and posterior fusion procedure [3].
21.2 Etiology
Osteorthritic changes are of unknown etiology in
many of the patients. A careful history, occasionally,
points to a traumatic event years prior to presentation.
Similar to other spinal locations, degeneration of AA
joint corresponds to overload, osteophyte, and synovial cyst formation, may reflect segmental instability
and joint complex laxity with subchondral sclerosis
and may be a result of subchondral osseous healing
due to repeated (micro) trauma. Weather-sensitivity of
pain in CVJ osteoarthritis may be explained by inflammatory changes of soft tissue and involvement of the
sympathetic nervous system in the process of pain
generation.
21.3 Clinical Symptoms
P. Suchomel and P. Barsa
Department of Neurosurgery,
Neurocenter, Regional Hospital Liberec,
Husova St. 10, 46063 Liberec, Czech Republic
P. Suchomel and O. Choutka, Reconstruction of Upper Cervical Spine and Craniovertebral Junction,
DOI: 10.1007/978-3-642-13158-5_21, © Springer-Verlag Berlin Heidelberg 2011
Pain is the principal symptom in patients with AAOA.
Typically, it ascends unilaterally to the occiput, parietal
299
300
21 Degenerative Disorders
region, and may radiate frontally into ipsilateral eye.
Patients may report visual problems often leading to an
ophthalmologic workout. Painful and sometimes audible crepitation during head rotation have indeed been
described [12]. Pain quality is described as stabbing by
patients. It is of mechanical characteristics in point of
accentuation with axial rotation of the neck and in
some patients, may lead to hand support during head
movement or to prophylactic cervical collar wearing.
Dreyfuss showed that an experimental increase in lateral AA joint pressure leads to similar patterns of pain
as seen in AAOA and thus confirmed the role of lateral
AA joint as a pain generator [1]. The pain syndrome
may be weather-sensitive and low temperatures may
contribute to joint stiffness as seen in other joints
affected by arthritis. Although degenerative changes
are common in both asymptomatic and symptomatic
people, the clinical question is whether patient’s symptoms truly correspond to abnormalities seen on radiographic evaluation. Specific clinical symptom, which
could be attributed to arthritic process in CVJ does not
exist and laboratory studies (C-reactive protein, rheumatoid factor, ESR) together with clinical investigation
should be completed to rule out any systemic inflammatory disease as well as other arthropathies (psoriatic
arthropathy, Reiters syndrome, enteropathic arthropathies). There is, however, no specific laboratory marker
referring to AAOA. Atlantodental osteoarthritis may
lead to degenerative pannus (Fig. 21.1) or synovial cyst
(Fig. 21.2) formation, which may cause medial suboccipital pain and myelopathy due to spinal cord compression at the C1/C2 level [11].
21.4 Radiology
The standard radiographic investigation including transoral and lateral view represents a starting point for evaluation of arthritic changes in CVJ. The open-mouth
projection should provide an unobstructed view of the
skull base, the odontoid, as well as C1-C2 articulation.
Most often, the narrowing or obliteration of the AA joint
with or without subchondral sclerosis can be seen on
transoral films (Fig. 21.3a). Also, marked osteophytosis
of the joint can support AAOA suspicion. To exclude
Fig. 21.1 Preodontoidal degenerative pannus in the patient with ankylosing spondylitis. (a) T2 MRI sequence. (b) The same patient
T1 MRI sequence
21.4 Ra dio logy
301
Fig. 21.2 Calcified synovial cyst 14 mm in diameter protruding from right C1-2 AA joint retropharyngeally. (a) T1 MRI. (b)
Sagittal CT reconstruction. (c) Coronal CT reconstruction. (d) Axial CT in bone window
Fig. 21.3 Patient with left AAOA. (a) Transoral picture showing osteoarthritis with asymmetric left AA joint deformation. (b) CT
scan in coronal plane of the same patient
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21 Degenerative Disorders
potential AA instability, dynamic lateral radiographs
have to be obtained. It is not unusual to be able to get
only a limited information from such an evaluation due
to a slightly oblique orientation of the facet joints and the
overlap of facial bony structures in some. Coronal and/
or parasagittal reconstructions of the CT scan in bone
window will therefore provide more precise information
on the morphology of C1/C2 joint (Fig. 21.3b). A CT
scan is not only helpful in diagnostics but inevitable if
any AA-stabilizing surgery is considered. Edema of
surrounding osseous structures, possible synovial cysts,
or inflammatory reaction and the precise anatomical
picture of vertebromedullary relationship should be
assessed by an MRI (Fig. 21.4). Diagnostic bone scan
may also be added. However, presence of a “hot spot”
is not a very specific finding indicative of active
arthritic process and its presence implicates closer morphological evaluation. A typical morphologic picture of
Fig. 21.4 Another patient with AAOA. (a) Coronal CT showing left AAOA. (b) MRI of the same patient. (c, d) Dynamic lateral
pictures showing AA instability caused by AAOA
21.5 Treatment Strategy
Fig. 21.5 Accidentally found degenerative intradental cyst in a patient investigated for odontoid fracture. (a) Coronal view.
(b) Sagittal reconstruction
303
osteoarthritis located in lateral joints includes AA joint
space narrowing with subchondral sclerosis. Both cartilage and bone may become eroded, producing cyst-like
pockets in the bone, called “geodes.” Irregularities of
margins of the facet can be demonstrated on coronal or
sagittal computed tomography scan reconstructions.
Subchondral edema, fibrosis or sclerosis may be delineated on MR images. Productive changes of the bone
(osteophyte formation) are consistent with diagnosis of
osteoarthritis but they are not very typical for arthritis in
general. The atlantodental (central) osteoarthritis
involves degenerative pannus formation eventually associated with synovial or juxtafacet cysts, which may arise
from the degenerative synovial lining of the joint.
Intraodontal osseous cysts (Fig. 21.5) may also be a part
of this morphological entity [3] if other etiology is not
confirmed.
21.5 Treatment Strategy
Methods of conservative treatment include nonsteroidal anti-inflammatory medications, gentle cranial traction, and external temporary immobilization. Although,
the efficacy of such measures in reduction of AAOA
pain has not been evaluated by prospective randomized
trials, they may, nonetheless, lead to pain reduction to
a tolerable level. If these conservative therapies fail, the
patient may be referred for steroid injection into the AA
joint and a soft collar. Injection therapy may be very
successful for a limited period of time [8]. Diagnostic
facet block of C1-C2 to confirm the pain generator is
recommended by some authors in preoperative decision making. Primary conservative treatment should
be started in all AAOA patients and should continue
as long as it is effective and symptoms are tolerable.
Surgery is indicated when pain becomes intractable.
Two methods of surgical treatment have been
described in the literature. Ehni and Banner [2] performed C2 rhizotomy in three out of their seven
patients. They were influenced by the fact that pain
distribution resembled C2 dermatome and indeed their
treatment results were described as good. Other, more
commonly indicated surgical treatment is AA fusion.
As described in other chapters, it may be achieved by
various methods. The choice of a specific surgical
fusion method is a subject of each individual patient’s
anatomical situation and surgeon’s own experience
and preference. Surgical outcome is favorable regardless of the type of fusion [4]. Fusion rate of posterior
C1-C2 transarticular fixation in AAOA patients has
been reported as high as 100% with marked pain
improvement in 90% of the patients [3, 5, 12]. Transoral
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21 Degenerative Disorders
decompression of CVJ supplemented with posterior
stabilization is a method of treatment in patients who
developed myelopathy due to compression caused by
degenerative pannus formation. Similar to rheumatoid
pannus, AA stabilization may be sufficient treatment
of suboccipital pain in those patients who developed
degenerative pannus without myelopathy signs [3, 6].
21.6 Our Preference
When assessing patients with atypical headache,
occipital one in particular, we should focus also on
its concordance with head position and movement.
In situations where head rotation or axial load reproduces occipital headache, transoral and UCS dynamic
radiographs should be obtained with special attention
to the morphology of AA segment. If AA instability
is suspected, further diagnostic workup as previously
described is indicated. The majority of the patients
referred to a spine surgeon have been treated conservatively for a long time. Nevertheless, the treatment is
usually nonspecific to the AA joint. We therefore usually add at least local intra-articular injection therapy
under direct CT guidance. This minimal intervention
serves not only as a treatment modality but also as a
diagnostic tool. In cases where conservative methods
fail, surgical AA immobilization is offered. We prefer
methods that provide immediate stability. Especially in
AAOA patients, where mechanical pain is the leading
symptom, high primary stability of the construct should
be the goal as it will provide immediate pain relief for
the patient. Most of our patients are treated by Magerl or
Goel-Harms method of fusion (Fig. 21.6). The clinical
success rate is impressive.
Fig. 21.6 Patient (Fig. 21.4) treated with AA fixation according to Goel-Harms. (a) Lateral picture. (b) AP projection
References
305
21.7 Practical Conclusion
AAOA is an uncommonly diagnosed disorder of AA
junction with suboccipital, typically unilateral pain as
a leading symptom. Conservative therapy is the first
line treatment as long as myelopathy or instability is
not present. This may then be followed by facet block
or immobilization. Finally, AA fusion represents an
ultimate, highly effective therapeutic intervention in
patients who fail nonsurgical treatment.
References
1. Dreyfuss, P., Michaelsen, M., Fletcher, D.: Atlanto-occipital
and lateral atlanto-axial joint pain patterns. Spine (Phila Pa
1976) 19, 1125–1131 (1994)
2. Ehni, G., Benner, B.: Occipital neuralgia and C1-C2 arthrosis. N Engl J Med 310, 127 (1984)
3. Finn, M., Fassett, D.R., Apfelbaum, R.I.: Surgical treatment
of nonrheumatoid atlantoaxial degenerative arthritis
producing pain and myelopathy. Spine (Phila Pa 1976) 32,
3067–3073 (2007)
4. Ghanayem, A.J., Leventhal, M., Bohlman, H.H.: Osteoarthrosis
of the atlanto-axial joints. Long-term follow-up after treatment with arthrodesis. J Bone Joint Surg Am 78, 1300–1307
(1996)
5. Grob, D., Bremerich, F.H., Dvorak, J., et al.: Transarticular
screw fixation for osteoarthritis of the atlanto axial segment.
Eur Spine J 15, 283–291 (2006)
6. Grob, D., Wursch, R., Grauer, W.: Atlantoaxial fusion and
retrodental pannus in rheumatoid arthritis. Spine (Phila Pa
1976) 22, 1580–1583 (1997). discussion 1584
7. Horton, B.T., Macy Jr., D.: Treatment of headache. Med Clin
North Am 30, 811–831 (1946)
8. Chevrot, A., Cermakova, E., Vallee, C., et al.: C1-2 arthrography. Skeletal Radiol 24, 425–429 (1995)
9. Perelson, H.N.: Occipital nerve tenderness: a sign of headache. South Med J 40, 653–656 (1947)
10. Pollock, L.J.: Head pain: differential diagnosis and treatment. Med Clin North Am 25, 3–13 (1941)
11. Sato, K., Senma, S., Abe, E.: Myelopathy resulting from the
atlantodental hypertrophic osteoarthritis accompanying the
dens hypertrophy. Two case reports. Spine (Phila Pa 1976)
21, 1467–1471 (1996)
12. Schaeren, S., Jeanneret, B.: Atlantoaxial osteoarthritis: case
series and review of the literature. Eur Spine J 14, 501–506
(2005)
13. Zapletal, J., de Valois, J.C.: Radiologic prevalence of advanced
lateral C1–C2 osteoarthritis. Spine (Phila Pa 1976) 22, 2511–
2513 (1997)
Surgical failures
P. Suchomel and O. Choutka
22
No field of medicine that involves any kind of intervention is without complications. Complications can be
related to the patient, the procedure, anesthesia, or
long-term follow-up; they can be immediate, early, or
late. However, the full scope of complications related
to a patient with UCS and CVJ pathology is beyond the
scope of this chapter that focuses on some of the common and most dangerous, immediate intraoperative
complications and their solution. Reconstructions
of UCS and CVJ are no different from other fields of
medicine and all surgeons must face a certain rate of
complications related to their surgical procedure, more
so during their learning curve [2, 6]. This eloquent area
is certainly not very forgiving to complications that can
be dangerous with surgical failure being rather “expensive” in the terms of possible further solutions.
Any structural damage to neural tissue is irreversible and it, therefore, remains of utmost surgical importance to protect the spinal cord, medulla, and nerves
during any reconstructive procedure at the CVJ.
Vascular injury of large neck arteries can cause secondary brain ischemia with similar consequences, although
some protection is offered by the multi-source brain
and spinal cord vascular supply. Nevertheless, one must
not rely on this “freedom” especially if not confirmed
by angiography, preoperatively. Venous bleeding and/
or air embolism may appear insignificant but can also
P. Suchomel
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
cause harmful complications, occasionally leading to
abrupt, early termination of the procedure without execution of the planned stabilization. A misplaced screw
with incorrect anchorage or trajectory may appear as a
relatively benign error intraoperatively, especially if
only bone or extravertebral tissue is involved. However,
a poor anchorage can lead to a delayed instability
endangering the previously mentioned essential structures [1, 4, 5]. Another problem of erroneous screw
purchase is that it is very often not easy to find the alternative route for salvage screw because of limited bone
stock available in the UCS area.
An experienced surgeon must be able to recognize
an intraoperative complication early and always be
prepared to find a safe solution to the newly created
problem. In our opinion, preoperative planning is one
of the most important steps in complication avoidance.
In CVJ, this entails a thorough scrutiny of the patient’s
clinical situation and radiographic workup. A careful
assessment of all bony and vascular anatomy and morphology is essential in planning of an UCS construct.
With 3D computer modeling, the construct can be
planned virtually (Chap. 7) but should also include
alternative plans of salvage solutions to potential intraoperative events.
For example, during atlantoaxial fixation and fusion,
one has to consider that drilling, tapping, and placement of transarticular C1-2 screws may be unsuccessful and the surgeon should be prepared to alter the plan
to a construct involving pedicle or laminar screws.
Occasionally, a simple posterior wire and graft fixation
can rescue a situation when no other construct is possible due to intraoperative complications.
In general, we can divide the specific intraoperative
UCS reconstruction complications to those related to
approach, decompression, reduction, or hardware
insertion.
P. Suchomel and O. Choutka, Reconstruction of Upper Cervical Spine and Craniovertebral Junction,
DOI: 10.1007/978-3-642-13158-5_22, © Springer-Verlag Berlin Heidelberg 2011
307