This document provides information on ossification of the posterior longitudinal ligament (OPLL). It describes the anatomy and function of the PLL, defines OPLL as ectopic ossification of the PLL, and discusses the epidemiology, pathogenesis, clinical presentation, diagnostic evaluation, treatment options, and prognosis of OPLL. Key points include that OPLL most commonly affects the cervical spine, causes myelopathy, and surgical treatment may involve anterior corpectomy or posterior laminoplasty depending on the location and severity of ossification.
2. Anatomy :PLL
Runs along the posterior aspect of the vertebral body inside
the vertebral canal from the body of the axis to the sacrum.
At the level of C2 , spreads out and becomes the tectorial membrane
that inserts into the base of skull.
Composed of longitudinal fibers.
Arises from sup. Margin of 1 vertebra and attach to inferior margin of
vertebra
Forms the anterior wall of vertebral canal
3.
4. Fibers wider at IVD and more adherent than vertebral body
PLL much thinner than ALL ,significant for pathophysiology of disc
herniations occurring posterolateral .
In cervical and thoracic regions has uniform width over bodies and
discs
In lumbar region widest at disc
Firmly anchored to Annulus fibrosus ,cartilage of vertebral endplates
and margins of vertebra
Cranial counterpart is Tectorial membrane
5. Comprise superficial and deep connective tissue layers
Tightens with cervical flexion
Superficial layer
More posterior
Continuation of Tectorial membrane at body of Axis
Consists of central band of fibers 8 to 10 mm wide
Described as “fan –like “giving denticulate appearance
More on thoracic and lumbar regions
Span upto 4 vertebral levels
Fibers more vertical orientation
6. Deep layer
Adherent to sup. Layer in midline
Continuation of Cruciform ligament of Atlas
Uniform diameter
2-3 mm wide at narrowest part
Also has denticulate appearance
Intersegmental
Fiber orientation can’t be established
7. Function
Proctective role than supportive role .
Sup . Layer : limit forward flexion
Deep layer :limit lateral flexion and rotation
Increased rotational and lateral flexion forces : creates more
denticulate appearance in lower thoracic and lumbar region
Elastin in PLL :role in dynamic motion of spine
8. Embryology
At 6 WOG :vertebral column appears as hypocellular light zone
forming vertebral body
Hpercellular dark zone forming IVD
At 7 WOG : light zone ad dark zone distinct but ligament unclear
At 8 WOG : longitudinal arrangement of cells and collagen fibers
appears at the adult ALL but not at PLL
At 10 WOG : Dark zone decreases in width and origin of PLL appears
( unclear at vertebral body but clear at disc )
9. Nerve supply
Primary source : meningeal branch from spinal nerve
Gives ascending and descending branches which fuses and forms
Transverse branches
Transverse branches from opposite side forms network of nerve
fibers superficially
Innervates the PLL in vertebral segments
10. Physiological variants
PLL Is narrower and weaker .
Fibers of annulus fibrosus and edge of vertebral body m/c site of
attachment
Sometimes to posterior aspect of vertebra
PLL most developed at L3 and L4 (1.4mm thickness )
Ligament in mid portion of each vertebral body covers vascular
foramina
From L2 upwards ligament thins markedly
11. Ossification of Posterior Longitudinal
Ligament (OPLL)
Chronically ,progressive disease .
Ectopic enchondral and membranous ossification
Unkown etiology
Multifactorial condition : genetic and environmental factors
Original reported from japan
12. Epidemiology
Incidence
In Japanese > 30 yrs upto 3%
In the United States and Europe , upto 1.7%
Gender
Cervical : M>F (2:1)
Dorsal :F>M
Race
More in Japanese
Age
Started in 40s and become symptomatic in 50s
13. Risk factors
Gentic locus close to HLA ,on chr. 6
DM
Obesity
Acromegaly
Hypoparathyroidism
Bone forming conditions : DISH and Fluorosis
14. PATHOGENESIS
Ligament cells from pts with OPLL have osteoblast –like
characteristics
Factors that initiate these cells to form calcification and ossification
are :
Genetic factors :COL6A1, COL11A2 and NPPS
Hormonal factors :non –insulin dependent D.M, hypoparathyroidism
Environmental factors : mechanical stress in ligaments of spine
Life style
a/w DISH and Fluorosis
15. Pathogenesis of Neural injury in OPLL
A) Mechanical
Static compression
Occupying ratio greater than 60 % indicates high risk of development of myelopathy
SAC < 6 mm
Dynamic compression
Degenerative spondylolisthesis
SAC 6-13 mm
Threshold of SAC
Normal : 13 mm
B) Vascular
20. Microscopic features
Early OPLL
Hypertrophy PLL d/to fibroblastic hyperplasia and increased collagen
deposition with punctate calcification
Immature form
Woven bone with fibrocartilaginous cell proliferation
Mature form
Lamellar bone with well developed haversian systems
Mostly endochondral ossification and sometime membranous
21. Pathological changes in cord
Demyelination and loss of axon
Always in posterior and posterolateral part of cord
22. Natural History Of OPLL
OPLL ↑in thickness 0.4mm/yr
Longitudinal expansion 0.67mm/yr
More with continuous or mixed type
Rapid progression in 4th decade and then decreases
Also occurs post –operatively
In 60-70 % after posterior decompression
In 36-64 % after anterior decompression and fusion
Matsunga et al . Demonstrated that 38 % pts presenting with myelopathy had
progressive worsening of symptoms if not operated .
23. Causes of late deterioration
Post operative progression of OPLL
Progressive deformity and instability
Thoracic myelopathy secondary to OPLL or OLF or both
Degenerative lumbar stenosis
24. Diagnostic criteria
Radiological
OPLL visible on lateral view X-ray
CT scan may be used for better assessment
Clinical
Cervical myelopathic symptoms
Radicular symptoms
Abnormality of cervical range of movement
25. Clinical picture
Accidental discovery
Onset
Usually graudual progressive but may be acute (after trauma )
Pain
Axial neck and upper limb pain
Motor abnormalities
Weakness
Incoordination
Clumsiness
Muscle wasting
Bladder –bowel dysfunction
Sensory symptoms
26. Neurological deficits
Myelopathy or myeloradiculopathy rather than radiculopathy alone
Associated co-existing conditions
DM
Hypoparathyrodism
Mytonic muscular dystrophy
Acromegaly
Obesity
35. Conservative management
Indications
Axial pain without or with subclinical myelopathy
Main insult is dynamic compression (less than 60 % stenosis or 6-13mm SAC)
Severe co morbidity
Measures
Collar
Traction
Careful life style
Analgesics and anti –inflammatory drugs
Anti depressants and anticonvulsants
Opiods
36. Surgery : Indications
Is there a rule for prophylactic surgery ?
Myelopathy or radiculo-myelopathy with predominant myelopathy
Role of prophylactic surgery in asymptomatic patient
Severe canal compromise :
•SAC <6mm or
•Occupational ratio >60 %
Presence of cord signal in MRI
SSEP is affected
Young age (< 65yrs )
37. Surgical procedures
Anterior surgery :single/ multilevel (upto 4)
Corpectomy with removal of calcified mass
Corpectomy without removal of calcified mass (ant .floating method )
Open Window Corpectomy/Skip cervical corpectomy ( removal of post ½ of body
leaving ant one )
Oblique Cervical Corpectomy
With fusion and Halo Vest or with fusion and fixation
39. Choice of approach
Factors in favor of ant .approach
Presence of facilities and expertise
Occupying ratio more than 60 %
Hill- shaped calcification
Kyphotic deformity or degenerative instability
Limited corpectomy levels (upto 4 )
Fessler et al. found pts with anterior approach t/t have improvement of
1.24 Nurick grades than laminectomy pts by 0.07.
40. Factors allowing posterior approach
Comorbidity prevent more lengthy procedures
Occupying ratio less than 60 %
Plateau – shaped calcification
Preserved lordotic spine or maximum straightening
41. Radiological signs help in choosing approach
Gwinn et al. proposed simple straight line method to effective spinal canal
lordosis
Anterior surgery :better achieve decompression in lost effective lordosis
43. Fusiyoshi et al . Proposed in K line(-) ventral approach have a better
chance of neurological outcome .
K line (-) pts have kyphosis that prohibits a dorsal approach as spinal
cord has less potential to shift following decompression .
44.
45. Anterior corpectomy and fusion
Advantages
Improved myelopathy scores
Direct removal of pathology
Disadvantages
Increased complications
Anterior approach related (dysphagia ,hoarseness ,prolonged intubation )
Graft expulsion
Pseudoarthrosis
C5 root palsy
46. Laminoplasty
Advantages
Decreased approach related complications
Better tolerated in pts >65 years
Improved stability
Disadvantages
Increased neck pain
Less improvement in myelopathy scores
Persistent ossified bar/ligament
C5 root palsy
47.
48. Prognosis
Patient’s factors :
Old age
Preoperative neurological status and duration of symptoms
H/O trauma causing acute presentations
Disease’s factors
Occupying ratio of OPLL or SAC
Saggital shape of ossification (hill –shaped ) esp. with post. Decompression
Management’s factors
Progression more with posterior decompression
Once in japan major cause of myelopathy hence Japanese disease
PERK (membrane protein kinase ) upregulated in cells
M/C AT c5
S 39 %
M 29
Con 27
Circ 5
Investigation committee on OPLL of Japanese ministry of pubic health and welfare
Circumscribed : lesion located post to disc space
Segmental : post to vertebral body
Continous : several vertebral bodies
So posterior decompression may insult the cord which is already insulted posteriorly
Do these mean prophylactic surgery indicated ??
May show double layer sign on axial ant ligamental and post dural rims of hyperdense ossification
This double layer sign to diagnose dural ossification
Hypointensity in T1 and hyperintensity on T2 image
K line positive ventral to this line
K line negative dorsal to this line