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Kyphosis One Level Above the Cervical Disc Disease

Is the Kyphosis Cause or Effect?

Özer, Ercan MD*; Yücesoy, Kemal MD*; Yurtsever, Cem MD*; Seçil, Mustafa MD

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Journal of Spinal Disorders & Techniques: February 2007 - Volume 20 - Issue 1 - p 14-19
doi: 10.1097/01.bsd.0000211274.74238.c0
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The normal cervical spine has a gentle sloping, lordotic curve from C1 to C7 and stability is afforded by bony, soft tissue, and ligamentous structures.1 Hypolordosis refers to any degree of flattening of the normal cervical lordosis. Cervical kyphosis refers to any degree of reversal of the normal cervical lordosis.2 Loss of lordosis or straightening of the cervical spine is often seen after acute cervical injury secondary to paraspinal muscle spasm.3 However, reversal of the lordotic curve into a cervical kyphosis is much less common and can be due to degenerative, inflammatory, traumatic or neoplastic conditions of the cervical spine, or due to iatrogenic damage.1,2,4 Degenerative disc disease is very common, and is a relatively common cause of kyphotic deformity. In the case of cervical disc disease (CDD), kyphosis results from the collapse of disc spaces and subsequent vertebral subluxation.1 Kyphotic angulation developing after a disc herniation usually occurs at the level of the herniated disc, if it occurs at all. Sometimes kyphosis occurs at one level above the CDD. We name this situation as kyphosis one level above (KOLA). KOLA may be a factor in the development of CDD rather than its effect.

In this study, we present a series of patients who have CDD associated with KOLA, discuss its role in postoperative problems, including adjacent level disease (ALD), and make suggestions for the surgical treatment of CDD associated with KOLA.


At our tertiary-care medical center, 147 patients having symptomatic CDD (excluding myelopathy patients) were operated upon between January 1998 and July 2003. Operative intervention was reserved for patients with radiculopathy unresponsive to conservative treatment, and radiographic evidence of cervical disc herniation (CDH) or spondylosis with matching clinical findings. Of these 147 patients, 22 had both CDD and local kyphotic angulation one level above the CDD. Patients with lordosis or kyphosis centered at the level of CDH or at any level other than one level above were not included in the study. Four patients having CDD associated with KOLA were excluded from the study because of incomplete radiologic examinations or follow-up. All of the patients' complete histories and neurologic examinations were reviewed and radiologic examinations were assessed. The radiologic evaluation of all patients included standing anteroposterior and lateral cervical x-rays (in neutral, flexion, and extension positions), and magnetic resonance imaging (MRI) of the cervical spine obtained in sagittal and axial planes. The cervical alignment was assessed by lateral x-rays and the angle of local kyphosis or lordosis was measured on lateral x-rays by using tangential lines passing on posterior borders of adjacent vertebrae of apex kyphotic level.5 The levels of disc herniations were determined on MRI. Selection criteria for the study were MRI evidence of CDH or spondylosis consistent with the clinical findings and radiographic evidence of KOLA on standing neutral plain radiography, at which level no disc herniation or spondylosis were evident by MRI.

Smith-Robinson6 and central corpectomy techniques with anterolateral approaches were used in the operations. In 1 patient, the Cloward technique7 was used. In patients having significant KOLA (greater than 11 degrees), kyphosis was also treated in addition to CDD. A 8-degree KOLA in 1 patient was also treated because of associated subluxation. Either iliac crest autograft or freeze-dried fibular allografts were used for interbody fusion. An anterior cervical plate was used in the majority of cases to confirm the stabilization and the correction of the kyphosis, and to prevent graft extrusion. In some cases, plating included KOLA without discectomy and bony fusion of that level.

Postoperatively, all patients wore a cervical collar for 2 months. Patients returned for follow-up examinations at 2, 6, 12 months, and yearly thereafter. Clinical evaluation was performed using Odom's criteria that graded the outcome from excellent to poor.8 Grading obtained at the most recent encounter was used for the study. A standing lateral cervical spine x-ray was obtained at each visit. The angle of kyphosis or lordosis was measured using the same technique, and fusion was assessed on neutral lateral cervical x-rays of the patients that were obtained in their latest visits by one radiologist.

Kyphotic corrections and clinical outcomes of patients treated versus not treated for KOLA in addition to their CDD were compared using the Mann-Whitney U test.


Of the 147 of patients operated upon for CDD during the study period, 22 of these had KOLA (14.9%). Well-documented 18 patients were included in the study with their long-term follow-up. Summary of patients are presented in Table 1. Follow-up times of patients changed between 25 and 48 months (mean: 32.11 mo). Mean age was found as 45.33 years (range: 32 to 62 y), and female/male ratio as 2 (12 females, and 6 males). All patients complained of both neck and arm pain, and all but 2 had mild to moderate neurologic deficits. Sixteen of 18 patients had soft disc herniations and 2 had spondylotic radiculopathies. CDD was localized to one level in 11 patients and to 2 levels in 7 patients. CDD was diagnosed at C4-5 in 1 patient, C5-6 in 9, C6-7 in 1, C4-5 and C5-6 in 2, and C5-6 and C6-7 in the remaining 5 patients. KOLA was localized to C3-4 in 3 (16.6%), C4-5 in 14 (77.8%), and C5-6 in 1 (5.6%) patient.

Summary of Patients

Seven patients (38.9%) having significant KOLA (6 patients greater than 11 degrees and 1 patient with 8 degrees) associated with CDD were treated also for the kyphosis in addition to the CDD. Two patients having a C5-6 herniated nucleus pulposus (HNP) and KOLA were treated with the Smith-Robinson technique and C4-6 plating. One patient with C5-6 and C6-7 spondylotic radiculopathy was treated with the Smith-Robinson technique and C4-7 plating. Another patient with C5-6 HNP and KOLA was treated initially with the Smith-Robinson technique using an iliac graft, but because of graft collapse caused by the KOLA, C5-6 fusion with a fibular allograft and C4-6 plating were performed in the second surgery (Fig. 1). One additional patient with C5-6 HNP was treated with the Cloward technique sing an iliac autograft and C4-6 plating (Fig. 2). In these 5 cases, plating included the KOLA level without any discectomy and fusion. One patient with a C4-5 and C5-6 spondylotic radiculopathy and another with a C6-7 spondylotic radiculopathy were treated with C4, C5, and C6 central corpectomies and plating, respectively. In these 2 patients, fusion and plating were also performed at the KOLA level. Of the remaining 11 patients having insignificant KOLA were treated for only HNP or spondylotic disease levels not for the KOLA. Smith-Robinson technique with a fibular allograft was used in 6, and central corpectomy and fusion with a fibular allograft in 5 of these 11 patients. In the 5 patients with multilevel disc herniation, we preferred central corpectomy because of low vertebral height, a large fragment extending behind the vertebrae, or a relatively narrow spinal canal. Plating was performed in all corpectomy cases, but in only 1 patient with discectomy and fusion.

Radiologic examinations of patient 5 with KOLA. Preoperative lateral radiography shows 14-degree local kyphosis at C4-5 level (A). Flexion and extension radiographies of patient (B and C). MRI scans (D and E) depict R C5-6 HNP. After the initial operation, graft in place (F) whereas graft collapse occurred later due to KOLA (G). Second operation involved C5-6 bony fusion and C4-6 plating. Control radiography of patient (H).
Radiologic examinations of patient 7. Preoperative neutral lateral radiography shows 15-degree segmental angulation at C4-5 level (A), MRI shows disc herniation at C5-6 (B). Patient was treated with C5-6 discectomy and fusion with Cloward technique and C4-6 plating. Postoperative lateral plain radiography shows correction of kyphosis (C).

Among all patients, the kyphotic angle at the KOLA level ranged between 3 and 18 degrees (mean: 9.56±3.61 degrees) preoperatively. The mean preoperative angle at the KOLA level on dynamic flexion radiography was 12.38±4.97 degrees, and on extension 1.38±6.66 degrees. Among patients treated for KOLA, the preoperative kyphosis angles were between 8 and 18 degrees (mean: 12.85±3.18 degrees). Postoperatively, these angles ranged between 2 and −14 degrees (mean: −7.28±4.92 degrees), thus a mean correction of 20.14±3.13 degrees was achieved in these cases. Among patients not treated for KOLA, the preoperative angles ranged from 3 to 10 degrees (mean: 7.45±1.91 degrees), postoperative angles from 7 to −2 degrees (mean: 4.45±2.94 degrees), resulting in a mean correction of 3.00±2.52 degrees. The kyphotic correction was significantly higher in patients treated for KOLA level in addition to CDD (P<0.01). Bony fusion occurred in all patients excluding the 1 patient with the graft collapse. No fusion was observed at the levels of KOLA, which included in plating without discectomy and bony fusion.

Four excellent and 3 good outcomes were obtained in the group of patients treated for KOLA. Only 2 excellent, 8 good, and 1 satisfactory results were found in the group not treated for KOLA. No poor outcome was obtained in both groups. Although not statistically significant (P<0.05), clinical outcome scores showed a trend towards improvement in the patients operated upon for kyphosis correction.


CDD is a relatively common cause of kyphosis, which generally occurs at the level of the disc degeneration.1 Sometimes, however, the kyphotic angulation is centered at one level above the level of the disc herniation. Although we found the prevalence of KOLA to be 14.9% in our patients with CDD, this has not been previously studied in the medical literature.

The normal sagittal weight-bearing axis lies posterior to the vertebral bodies of C2-C7, maintaining the normal sagittal contour and thus minimizing the demands on the posterior cervical musculature to maintain the balance of weight-bearing forces.9,10 With a loss of the normal sagittal alignment in kyphosis, the weight-bearing axis shifts anteriorly, and constant muscular contraction is required to maintain upright head posture. Eventually fatigue and pain occur, and the kyphosis progresses. The anterior shift of weight onto the vertebral bodies and degenerated discs results in a vicious cycle of disc degeneration and the formation of vertebral osteophytes.1,4,11 Thus, kyphotic sagittal alignment may provoke further degeneration at the adjacent segment.12–14 The increase in weight born by discs at lower level(s) may also cause the nucleus pulposus to herniate or degenerate. In the case of CDD associated with KOLA, instability and kyphosis may perhaps be the initiating event, which later may act as a factor in the development of disc herniation and degeneration one level below. Kyphosis and instability may occur as a result of normal degeneration process of spine.15 Spasm of cervical musculature may encourage the development of kyphotic angulation. Regarding effect of muscle spasm, in this study we found only a mean of 3 degrees of correction in patients who not treated for KOLA in addition to CDD. Although mild kyphosis was present in patients treated for CDD only, the kyphosis did not correct after CDD surgery alone, leading us to believe that structural instability is present in even mild kyphosis.

One of the aims of the cervical disc surgery is to maintain or restore normal cervical alignment.16 In the case of CDD associated with KOLA, if the kyphotic angle is greater than 11 degrees, we feel that appropriate treatment should be undertaken with plating and/or fusion. As the kyphosis progresses, the spinal cord becomes draped and flattened over the posterior aspect of the vertebral bodies and the flexion of the cervical spine diminishes the microvascular supply to the spinal cord. This produces a flattening of the small feeder vessels to the cord, and an increase in longitudinal cord tension resulting from the tethering effects of dentate ligaments and cervical roots. Thus, direct neuronal injury and myelopathy with progressive deformity may result from both spinal ischemia and increased spinal cord tension.1,4,17,18 This neurologic compromise is commonly seen in severe (80 to 90 degrees) kyphosis, but perhaps even mild kyphosis may put the spinal cord at risk for histopathologic and vascular changes. Maintaining normal cervical anatomy with its lordosis in this region of prominent movement may optimize the cord function.19,20 In kyphosis, also radicular symptoms and findings may develop secondary to foraminal narrowing from uncovertebral and/or facet joint hypertrophy.1 Secondly, ALD in the upper cervical levels may be partly due to an extension of previous KOLA and instability. Long-term follow-up studies have shown that patients who are treated surgically for CDH with anterior discectomy and fusion will have degenerative changes at adjacent levels, and approximately 10% of these patients undergo reoperation for ALD.6,12,13,21,22 The most commonly seen MRI finding in patients with ALD are spinal malalignment, disc herniation, posterior longitudinal ligament ossification, and ligamentum flavum hypertrophy.23 A high percentage of ALD after anterior discectomy and fusion may be in part due to untreated KOLA associated with previously treated CDH, because kyphotic malalignment is seen in 17% to 40% on long-term follow-up,24–26 and associated with high incidence for ALD.13,23 When adjacent levels to a fusion are considered, one should expect that the lower level should be affected more because it is bearing more weight. In contrast, in a long-term assessment of anterior cervical discectomy and fusion, dynamic radiographic examination showed that instability is mainly at the upper (13 patients) rather than lower level (2 patients).24 The incidence of ALD among patients whose KOLA was included in fusion need to be established with further and larger studies. Third, collapse of grafts placed for interbody fusion can be seen in patients with postoperative kyphotic malalignment of the cervical spine.27 In that study, 35 patients operated for failed anterior cervical discectomy and fusion, 8 (23%) (including 3 with previous laminectomy) had been operated upon due to collapse of grafts because of kyphosis. In this series of patients, we have a patient who had graft collapse due to KOLA. Fourth, if KOLA is not treated, achieving fusion at a second operation later is more difficult when anterior cervical arthrodesis is performed to a prior fusion.12 One may question that including multiple levels in a fusion will cause any problems if KOLA is treated by including its level in plating. The incidence of ALD is lower in multilevel fusion groups.12,13 We believe that some surgeons prefer to include the KOLA level when performing a fusion, but could not find any other references to this issue in the literature.

Treatment of kyphosis requires correction and stabilization of the kyphosis to neutral or normal motion segments and decompression of compression of neural elements.1 Although patients may have a flexible or fixed kyphotic deformity, our cases were mainly of the flexible type, and correction occurred with the neck extended on the operating table. Treatment of KOLA was performed in 5 with only plating. Discectomy and bony fusion was performed for CDD but not for KOLA level in these patients. Because plate could maintain sufficient stability as in pseudoarthrosis cases with plating.16 Also posterior instrument applications in cervical spine do not involve discectomy and intact disc spaces are left in constructs, this well-known application may provide some evidence to support our approach. No patient having KOLA plated without discectomy and fusion had an instrument complication. In 2 cases, central corpectomy was performed because of spondylotic changes at CDD level and bony fusion with fibular strut grafting included both kyphotic, and disc herniation levels. The KOLA level can be included in plating without any discectomy and bony fusion as in 5 of our patients. This technique is an alternative to bony fusion and plating of the kyphotic level. If the kyphotic angle of the KOLA is more than 11 degrees, we recommend surgical treatment for KOLA in addition to CDD. This angle was described by White et al28 as an instability criterion. We treated 1 patient with a KOLA of only 8 degrees, because of a coexisting subluxation of 3 mm at that level.

The effect of kyphosis on clinical outcomes is not clear.26,29 We found no statistical difference between clinical outcomes of treated or not treated KOLA patients. However, our patients treated for KOLA had higher degrees of kyphosis preoperatively. Although this, patients treated for KOLA have slightly better outcomes with excellent and good results.

Some CDD patients have kyphotic angulation one level above the level of CDD. KOLA may be a factor in the development of CDH and spondylosis, rather than its result. Perhaps upper ALD may be an extension of KOLA as well. Larger studies can further define the relationship between KOLA and CDD, indications for surgical correction of KOLA.


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kyphosis; cervical disc disease; adjacent level disease

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