Management of Ossification of the Posterior Longitudinal Ligament

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Chapter 221 Management of Ossification of the Posterior Longitudinal Ligament

Cervical Laminoplasty: Open Door

Ossification of the posterior longitudinal ligament (OPLL) is a pathologic condition in which ectopic bone formation within the posterior longitudinal ligament (PLL) causes progressive narrowing of the spinal canal. First described by Key in 1838,1 an autopsy report by Tsukimoto2 in 1960 in a Japanese patient is credited with redirecting attention on this pathologic process as a cause of cervical myelopathy in this population.3 Since then, there has been a growing body of evidence that has helped to define its pathogenesis, underlying genetics, and natural history. A clear understanding of these processes is critical to provide the best neurosurgical management for these patients.

Etiology and Epidemiology

Evidence suggests that OPLL is a multifactorial disease with underlying genetic, environmental, and biomechanical contributions.4 Early epidemiologic and more recent genetic studies, for example, have identified numerous genes that may have causal associations with OPLL, including the genes for collagen 11,5,6 nucleotide pyrophosphate,7 and transforming growth factor-β.8 Likewise, histochemical studies of OPLL show possible involvement of a number of cytokines and growth factors, such as bone morphogenetic proteins9,10 and transforming growth factor-β.8,11 It is proposed that these proteins may function by inducing osteogenesis in the PLL of patients with this condition.12

Other factors, such as diet and comorbidities, may also be related to the induction or progression of OPLL in individual patients. Vegetarian diets and diets high in salt and vitamin A have all been reported to be associated with OPLL,1317 although data are limited and further studies are necessary to clarify these associations. In addition, a higher incidence of OPLL has been reported in patients with endocrinologic comorbidities such as glucose metabolism disturbances, hypoparathyroidism, and acromegaly.1821

Epidemiologic studies have identified a modest radiographic frequency (1.9–4.3%) of OPLL in the Japanese population.22 Although similar ranges have been reported in other Asian populations, the incidence in the European and North America populations remains much lower (0.1–1.3%).22 Proportionally, however, patients with OPLL may represent up to one fourth of those presenting with signs and symptoms of myelopathy, regardless of their ethnic background.23,24 Most studies also support a sex difference in the prevalence of OPLL, with a reported male-to-female ratio of 2 to 3:1.22,25

Radiographic and Clinical Presentation

The diagnosis of OPLL is established by its pathognomonic radiographic characteristics. Most commonly, but not exclusively, identified in the cervical spine, a dense calcified strip of variable thickness (1–5 mm) can be found along the dorsal margins of the vertebral bodies and the intervertebral discs. The intervertebral discs in the involved area usually are well preserved, without evidence of disc space narrowing. The shape and volume of OPLL can be quite varied, compromising anywhere from a small fraction to greater than 50% of the spinal canal. Radiographically, OPLL has been classified into four groups: segmental (one or more separate lesions behind the vertebral body); continuous (a continuous lesion spanning several vertebral bodies); mixed (a combination of the two aforementioned types); and circumscribed (located primarily behind the intervertebral disc spaces).23

Anatomically, the PLL consists of two layers, a deep and a superficial one. The deep layer fuses with the periosteum of the dorsal corner of the vertebral body.26 This point of attachment is believed to be the site of initiation of OPLL in the segmental subtype. In the continuous form, the development is less clear. Although some authors advocate that it represents a continuous extension of the segmental subtype, others maintain that it results from progression of multiple scattered OPLLs.26

The clinical presentation of patients with OPLL can be varied, largely because of the differing forms and extent of the pathologic process, as described previously. Approximately half the patients are asymptomatic when the diagnosis is made.23 Typically, it presents in the fourth and fifth decades of life with an insidious onset of symptoms of cervical radiculopathy or myelopathy.24 More commonly, up to two thirds of patients complain of neck pain or stiffness and/or pain or numbness in the upper extremities, with fewer (40%) complaining of motor symptoms in the arms.27 Motor and sensory changes in the lower extremities are less common (40%), although the majority of patients (57%) are found to be hyper-reflexic. Less than 20% have bowel or bladder symptoms on presentation.27

Natural History

An understanding of the natural history of OPLL is essential in managing patients, particularly in the subset of patients for whom the diagnosis was found incidentally. Not unexpectedly, reviewing recent studies on OPLL patients demonstrates a natural radiographic progression of the disease in the majority of patients regardless of treatment approach.4 In one recent study, Matsunaga et al.28 observed an increase in PLL thickness in 70 (42%) of 167 patients managed conservatively; in 32 of these patients (19%) this increase was greater than 2 mm (marked development) over a mean follow-up of 11.2 years. There was a longitudinal increase in 144 (86%) in this same group, with 59 patients (35%) demonstrating ossification behind more than one vertebral level (marked development).

More recent studies by this same group examined the symptomatic progression of patients with OPLL in an effort to better delineate the clinical course of the disease as well as the radiographic predictors that might correlate to this course.29,30 Following a small group of patients (N = 36) who presented with myelopathy, Matsunaga et al.30 reported that 64% progressed over the study’s more than 10-year follow-up. Of the 323 patients who were not myelopathic on presentation, myelopathy developed in only 55 (17%). The Kaplan-Meier estimate of the myelopathy-free rate in the latter group was 71% at 30-year follow-up.

A severely narrowed spinal canal has been identified as a risk factor in the development of myelopathy in this condition, with 100% of patients with a canal diameter of less than 6 mm28 or greater than 60% stenosis30 experiencing this neurologic debility. In patients with canal diameters reduced by OPLL but not to such critical levels, presence of myelopathy does not appear to be correlated with diameter size per se.28 Such findings have led authors to consider other factors that may contribute to the development of neurologic symptomatology in these patients. Instead, the pathology of cervical myelopathy in patients with OPLL can be explained in two different ways. In patients with significant canal compromise (>60%), the ossified ligament acts as a source of ongoing mechanical or static compression. In others with more moderate compression, cervical motion between adjacent ossified segments plays a role in the development of symptoms as a form of dynamic compression.29,31,32

Management Strategies

The primary indication for surgical management in a patient with OPLL is cervical myelopathy. Variable combinations of motor, sensory, and reflex changes are usually present. Prophylactic surgery in mildly symptomatic or asymptomatic patients is controversial. As indicated previously, only a small proportion of these patients have been found to progress clinically,30 suggesting that in the absence of known risk factors such as extreme canal compromise or evidence of increased cervical motion, conservative treatment may be preferable. And although trauma is a known risk factor for development of neurologic symptomatology in this patient population, this risk appears to be relatively low; in a recent prospective study only 6 of 368 asymptomatic patients with OPLL (2%) went on to develop trauma-induced myelopathy during a minimum 10-year follow-up period.33 As a result, most authors do not recommend prophylactic surgery in this group, although a frank discussion with patients is warranted to involve them in the decision-making process.

Conservative management of OPLL is largely empirical. There exist no well-designed clinical studies systematically evaluating the efficacy of common treatment modalities. The mainstay of conservative therapy is immobilization together with anti-inflammatory medications, in an attempt to address modifiable sources of static and dynamic cord compression. Cervical traction has also been suggested by some based on their overall experience with patients with cervical spondylitic myelopathy.34 In theory, immobilization of the grossly or microscopically unstable spine prevents ongoing dynamic compression and may facilitate resorption of degenerative osteophytes.

The goal of surgical intervention in patients with OPLL is to decompress the neural structures while stabilizing the spine: in effect, to eliminate the static and dynamic factors that are thought to be responsible for the clinical disease. Once the decision for surgical intervention is taken, the principal decision regarding surgical management is whether a ventral or dorsal approach should be used because comparable results have been achieved with both.35,36 In general, a ventral decompressive procedure and fusion is the most appropriate surgical procedure in the presence of ventral compressive factors, such as OPLL, limited to three or fewer vertebral bodies. This procedure, combined with resectioning or floating of the ossified PLL, directly addresses the pathologic process and facilitates fusion with the use of bone graft. For many, it is the procedure of choice in patients with OPLL with significant canal stenosis (>60%), particularly if the lesion is focal or kyphotic angulation of the cervical spine is present. Compared with a dorsal approach, it may carry increased risk of surgical complications, including risk of cerebrospinal fluid leak as well as adjacent-segment disease due to progression of OPLL.35,37 At 5-year follow-up, good to excellent clinical results have been achieved in as much as 80% of patients who underwent a ventral procedure, although 8% of these patients ultimately required further dorsal surgery.35

Sir Victor Horsley is the neurosurgeon first credited with decompressing the cervical spine of a patient with progressive cervical spondylotic myelopathy using a dorsal approach.38 This was once the procedure of choice for patients with cervical OPLL.39 Although this procedure effectively enlarges the functional spinal canal area, thus allowing the spinal cord to move away from compressive elements and expand, it does so at the expense of dorsal stabilizing structures. Depending on preoperative spinal alignment and time since surgery, up to 50% of patients with OPLL who undergo a laminectomy for treatment develop spinal instability and a gradual kyphotic deformity.39 Given these concerns, together with a considerable population suffering from a multilevel compressive pathologic process necessitating dorsal decompression, Asian surgeons developed the laminoplasty as a “tissue-sparing” procedure in the late 1970s to effectively remodel the spinal canal.40,41 In theory, one can successfully enlarge the spinal canal while largely preserving dorsal stabilizing structures, thus reducing postoperative deformity or instability and alleviating the need to perform additional fusions.

Initial laminoplasty procedures were cumbersome and lengthy, requiring complex reconstruction of the dorsal arch.41 Numerous subsequent modifications have resulted in simplified, faster procedures with improved stability.40,4246 In particular, preservation of posterior elements was recognized significantly to increase the closing force on the elevated laminae, resulting in a “sinkage” effect with associated restenosis of the spinal canal.47 To combat this problem, a variety of techniques have been used. These primarily involve the use of spacers to buttress the created gap or the use of sutures or titanium plates to “attach” the remaining spinous process(es) to the facet or soft tissue structures of the hinge side.40,46,4850 We prefer the former, using fibular allograft, with the “closing forces” maintaining firm positioning of the graft and facilitating fusion. Further stability may be obtained, in addition to or in lieu of the aforementioned techniques, using onlay bone grafting at the hinge site(s).51

Animal studies have supported the presumed benefits of laminoplasty over laminectomy. In one study, laminectomies or laminoplasties were performed from C3-5 in goats, with monthly radiographic follow-up for 6 months. Radiographic results were compared with control animals, confirming that laminoplasties were biomechanically superior in maintaining alignment.52 An additional study in rabbits found that although postoperative range of motion was similar between groups, laminectomy was associated with increased angle deformity and poorer outcome.53 Similarly, a biomechanical advantage of laminoplasty has been found in a retrospective study comparing different cohorts of patients.54

Surgical Technique

Perioperative Considerations

Cervical laminoplasty is usually recommended in patients with OPLL who have multilevel cervical disease typically extending over three to four levels. Patients usually have a normal cervical lordosis or a relatively straight cervical spine. A dorsal decompressive procedure is avoided in the presence of significant kyphosis. For the majority of patients, the recommendation is to undergo decompression with an open-door cervical laminoplasty from C3 to C7, with partial laminectomies of C2 and T1 and fusion with rib allograft at C3, C5, and C7 supplemented by vertebral autograft. The decompression extends somewhat rostral and caudal to the maximum levels of compression so that the spinal cord does not migrate back and become entrapped or kinked at the rostral or caudal levels (lamina) of the decompression.

With the patient in the supine position and the neck minimally extended, endotracheal intubation is performed after administration of a general anesthetic. In selected cases, the surgeon may be especially concerned about the risk for spinal cord injury with any extension of the cervical spine because of the severity of the stenosis and spinal cord compression. An awake fiberoptic intubation with the aid of a bronchoscope can then be performed to reduce the risk of neck hyperextension and permit the surgeon to repeat the neurologic examination after placement of the endotracheal tube. In certain rare cases, the surgeon may prefer to turn the patient to the prone position while still awake, because this represents yet another instance in which inadvertent movements of the neck may occur and result in neurologic deterioration. Some neurosurgeons advocate the routine use of methylprednisolone prophylaxis as a neuroprotective agent before the start of surgery, the rationale being that provision of this drug in the setting of potential spinal cord injury may reduce the severity of injury. Because no data have been presented to suggest that it is effective as a neuroprotective agent in cervical decompressive surgery, its routine use cannot be recommended. We do, however, routinely give patients preoperative antibiotics within 30 minutes of starting the procedure.

Neurophysiologic monitoring options include somatosensory evoked potentials, motor evoked potentials, and electromyography. The value of routine neurophysiologic monitoring is often questioned because it has been difficult to demonstrate that the information provided can actually change what the surgeon does during the surgery, making it safer. However, some retrospective studies have demonstrated the positive predictive value of such tests in determining outcome.55,56 The stimulating and recording electrodes are placed and secured and baseline recordings are obtained before turning the patient. A number of options exist for holding the head during surgery in the prone position. We use the Mayfield three-pin head holder, which allows the surgeon to easily control the degree of cervical spine flexion and extension and reduces the possibility of pressure being exerted on the patient’s eyes. The patient is then transferred onto the operating table in the prone position, with the head secured in a slightly flexed position. Tape can be applied to the superior and dorsolateral aspects of both shoulders and secured to the caudal region of the operating table to assist with intraoperative radiographic visualization of the lower cervical levels.

Open-Door Expansile Cervical Laminoplasty

After the operative field is prepared and draped, the midline is infiltrated with commercially available 1% lidocaine with epinephrine to minimize skin bleeding. A midline incision is made and monopolar or bipolar electrocautery is used to control soft tissue bleeding. The midline fascia is then incised with monopolar electrocautery, and subperiosteal dissection is used to reflect the extensor cervical muscle groups, exposing the cervical lamina and mesial facets from the caudal portion of C2 to the rostral limit of T1, taking care to preserve the facet capsules (Fig. 221-1). The caudal one third of the C2 lamina and the rostral one third of the T1 lamina are removed, using a combination of a high-speed air drill and a 2-mm Kerrison punch, to visualize the underlying dura at this level. We also remove the spinous processes of C3 to C7 inclusively with Stille-Horsley bone-cutting forceps and morselize the bone for subsequent autografting.

The next phase of the procedure involves performing osteotomies of the C3-7 laminae. In so doing, one creates an “open” side and a “hinged” side of these laminae (Figs. 221-2 and 221-3). In general, the side with the greatest compression or the most clinically symptomatic side is the open side. If one is planning to perform foraminotomies in addition to the laminoplasty, the open side is best placed on the side of the intended foraminotomies. A high-speed air drill with a small bit is used to create troughs at the level of the laminofacet junction from C3 to C7. Drilling proceeds through the outer and inner cortical margins of the lamina on the side to be opened. On the hinge side, drilling proceeds through the outer cortical margin and cancellous bone; however, the inner cortex is not violated.

After the drilling is complete, bone allografts are prepared to stabilize the canal expansion. We prefer to use rib allografts for this purpose. Again using the drill, three separate grafts are cut, each approximately 10 to 18 mm long. Grooves are then made transversely along the cut surfaces of the rib grafts, approximating the thickness of the cut laminae.

After the grafts have been prepared, attention is turned to “opening the door.” Initially, two small curettes are introduced into the gap produced by drilling the laminae and advanced just deep to the outer cortex. By pulling the curettes upward, the laminar facet gap on the open side is slowly enlarged, and this creates a greenstick fracture along the previously created trough on the hinged side. Minimal advances are made before moving to other laminae in an effort to open all the involved laminae as a functional unit. The goal is to expand the anteroposterior diameter of the canal by approximately 4 mm (see Fig. 221-3). Great care must be taken to achieve this goal without fracturing the inner cortex of the hinge side.

Once this is accomplished, the rib allografts are placed in the gap that has been created at the C3, C5, and C7 levels, with the cut edges of the laminae resting in the cut grooves of the rib grafts (Fig. 221-4). If done properly, the grafts should fit snugly in the gap, there should be a slight “closing” force securing the grafts in position, and the inner cortex of the hinge side should be intact. We then use the morselized spinous process autograft and place it over the decorticated bone surfaces of the facet and lamina on the hinged side to promote intersegment fusion.

Should the patient have radiculopathy as well as myelopathy, one can add one or several foraminotomies to the laminoplasty procedure. Typically, the foraminotomy is initiated once the lamina has been elevated and the ligamentum flavum excised. The mesial one third to one half of the facet over the exiting nerve root is drilled with a high-speed drill. The opening can be widened with 1- or 2-mm angled Kerrison punches.

Should rigid stabilization be required, facet cables with or without rib allograft can be inserted. Lateral mass screws attached to a plate or a rod can also be applied. It is sometimes difficult to position the rib allografts to hold open the laminae once additional hardware is placed, but it can be done. In this case, we perform the drilling and “opening the door” first, but no graft is inserted until the instrumentation is in place. Variations to the approach include use of the spinous process autograft instead of the rib allograft to hold open the lamina. Some surgeons prefer to use miniplates or sutures to stabilize the rib allograft to the adjacent lamina and facet on the open side.50 The lamina can be split in the midline with a T-handled “Gigli-like” saw and the allograft spacers positioned between the greenstick-fractured hemi-lamina.57

In our experience, an open-door expansile cervical laminoplasty (without additional stabilization procedures) takes approximately 90 minutes to complete, with an average blood loss of 200 mL. In general, the complication rate is low (see next section), particularly compared with decompressive procedures that attempt to achieve the same number of levels of decompression and stabilization from a ventral approach.58


The surgical complication rate for dorsal decompressive procedures is low,48 and includes but is not limited to infection, cerebrospinal fluid leak, hemorrhage, spinal cord injury, nerve root injury, and the risk associated with the general anesthetic. Among them, long-tract paralysis, although rare, can often be attributed to definite causes such as traumatic surgical technique, reclosure of the opened laminae, or postoperative hematoma, all of which are theoretically preventable.59

Specific longer-term complications historically associated with laminoplasty itself include postoperative neck pain, reduced range of motion (ROM), canal restenosis, loss of cervical lordosis, and segmental motor paralysis/nerve root palsy.49,6063 Axial neck and shoulder girdle pain can be problematic and several papers have highlighted an increased incidence of neck pain when comparing dorsal (40–60%) and ventral (15–19%) surgery groups.64,65 Neck pain usually responds to an aggressive course of physical therapy.

Both clinically and radiographically, limited ROM is frequently observed after laminoplasty. Studies suggest that approximately 50% of ROM is lost after laminoplasty, particularly in extension.36,57,61,66 This correlates well with radiographic evidence of spontaneous bony fusion.67 It has been proposed that this is actually beneficial in that it ameliorates ongoing mechanical stress or injury without being “rigid” and inducing stress and degeneration in adjacent levels. Numerous studies have shown no correlation between limited ROM and recovery rates or outcome, including neck pain.36,66 However, it is important to remember that most of the literature pertains to patients undergoing decompression for OPLL, which is itself associated with increased rigidity, and thus may overestimate the restricted ROM attributable to the laminoplasty procedure.

Despite the theoretical biomechanical advantage conferred by laminoplasty, up to 50% of patients experience deteriorating cervical alignment after the procedure, with 2% to 15% developing new-onset kyphosis.66 The clinical implication of these radiographic changes remains unclear because both axial neck pain and malalignment have little impact on the ultimate outcome and Japanese Orthopaedic Association (JOA) scores,49,68,69 unless associated with a decrease of greater than 10 in the cervical curvature index.44

Segmental motor paralysis involving primarily C5 is another neurologic complication occasionally seen in patients undergoing laminoplasty. Delayed C5 nerve root weakness occurs at a reported rate of 4.6% to 13.3%.44,68 Although it is transient in most cases, recovery may require up to 6 years.44 Traditionally, it has been attributed to either direct damage to exiting nerve roots by suboptimal surgical techniques, or a tethering effect on the nerve root secondary to posterior shift of the spinal cord after decompression.44,47,61 The prevalence of C5 injury in particular was thought to result from the most significant “migration” of the cord at this level because it frequently represents the apex of the lordotic curve. However, more recent studies with improved imaging quality suggest that it may, in fact, represent intrinsic perioperative damage to the spinal cord itself at that level.70,71

An additional concern that stems from the laminectomy literature is the development of the “postlaminectomy membrane.”72 This entity has been implicated in arachnoiditis and restenosis, and may theoretically result in clinical deterioration.50 To date, these findings have not been reported after laminoplasty.

Neurologic Outcomes

Overall, the recovery rate in patients with OPLL after cervical laminoplasty, typically assessed by the JOA scoring system, has been reported to be approximately 60% at 5-year follow-up.44,7375 In these series, a subsequent decline in patient scores appears to develop between the 5- and 10-year follow-ups. The cause for this late deterioration is not well understood. Although radiographic progression of OPLL was cited as a cause of deterioration in at least one study,75 it was not found to correlate with clinical deterioration among the 53 patients followed by Chiba et al.73 Several factors have been implicated as predictors of poor outcome in these patients, including severity of preoperative myelopathy, increasing age, history of trauma, and duration of symptoms.36,39,44,69,74 Likewise, a recent study highlights the need properly to assess patients’ preoperative imaging before deciding on surgical approach. Based on both the degree of stenosis secondary to OPLL and the spinal curvature, Fujiyoshi et al.76 proposed an index to predict if the amount of posterior shift of the spinal cord after laminoplasty would be adequate for improvement in neurologic status.

Studies have shown that clinical improvement directly correlates with the degree of canal expansion. However, excessive expansion as well as an irregular canal area may be associated with additional problems.77,78 It appears that the optimal canal expansion approximates 4 to 5 mm in the sagittal anteroposterior diameter,40 correlating with approximately a 50% increase in canal area79,80 and facilitating a 3-mm dorsal shift of the spinal cord.81 However, decreased lordosis correlates with decreased volume expansion after laminoplasty, as well as with decreased dorsal migration of the cord.80 Far more critical than canal expansion is subsequent cord expansion, with studies showing a direct correlation between JOA scores and spinal cord area.82


Management decisions in patients with OPLL must take into account a number of factors and are highly individualized. Although conservative management is warranted in asymptomatic patients with OPLL or those with only the mildest symptoms, surgical treatment is indicated in those patients with significant neurologic deficit or evidence of increased cervical motion; it has been shown to be effective in improving the neurologic status in the majority of patients. Dorsal decompression for patients with OPLL is specifically indicated when multisegment disease needs to be addressed, but should be undertaken with caution in individuals with marked loss of normal cervical lordosis or marked canal stenosis. It is particularly advantageous in that it avoids the additional risk of dural laceration associated with a ventral approach. Although laminectomy has traditionally been used for decompression of the spinal canal in North America, this is done at the expense of the dorsal stabilizing structures, and the resulting loss of cervical lordosis or the development of kyphosis may result in secondary cord compression and is associated with poorer outcomes. By leaving the dorsal stabilizing structures in situ, laminoplasty is believed to mitigate the development of kyphosis and, with subsequent bone fusion, stabilize the cervical spine, leading to improved outcomes. Although numerous variations on laminoplasty have been described, there is little comparative literature to support the advantage of one type over another.

Decisions regarding when to treat patients with OPLL and which approach to use should always be made in consultation with the patients themselves, such that reasonable expectations regarding outcomes as well as a proper understanding of the risks involved are achieved. This is particularly important in managing patients with OPLL, given the natural history of disease progression even in the face of aggressive surgical management.


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5. Koga H., Hayashi K., Taketomi E., et al. Restriction fragment length polymorphism of genes of the alpha 2(XI) collagen, bone morphogenetic protein-2, alkaline phosphatase, and tumor necrosis factor-alpha among patients with ossification of posterior longitudinal ligament and controls from the Japanese population. Spine (Phila Pa 1976). 1996;21:469-473.

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34. Fukui K., Kataoka O., Sho T., et al. Pathomechanism, pathogenesis, and results of treatment in cervical spondylotic myelopathy caused by dynamic canal stenosis. Spine (Phila Pa 1976). 1990;15:1148-1152.

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36. Iwasaki M., Kawaguchi Y., Kimura T., et al. Long-term results of expansive laminoplasty for ossification of the posterior longitudinal ligament of the cervical spine: more than 10 years follow up. J Neurosurg. 2002;96(Suppl 2):180-189.

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