The document discusses cervical ossification of the posterior longitudinal ligament (OPLL), a condition where the posterior longitudinal ligament in the neck ossifies and compresses the spinal cord. It covers the anatomy of the ligament, classification systems for OPLL, risk factors like genetics and diabetes, clinical presentation of myelopathy symptoms, diagnostic imaging tools, surgical and non-surgical treatment options, and complications. The document provides detailed information on the pathogenesis, pathophysiology, and management of cervical OPLL.

1. CERVICAL OPLL
DR SANJOG CHANDANA
(MIND)

3. • Composed of collagen fibers with elastin densely concentrated at its
centre.
• Extends from base of clivus to the sacrum
• Attached to annulus of the each intervertebral disc and the posterior
cortical surface of the vertebral body.
• Thickness 1-2 mm.

4. • Deep ventral layer, Superficial layer.
• Wider at disc level, narrow at mid body level
• Longitudinally arranged collagen and elastin – dense centrally and
thinnest at site of the most lateral attachment.
• Internal vertebral venous plexus – located in lateral PLL space.

5. History
• Ossification of Posterior longitudinal ligament was first reported in
England by CA Key in 1838.
• In 1960, Tsukimoto, Japan, reported an autopsy of a patient with
myelopathy due to OPLL.
• Hakuda S et al – on basis of study of human skeletons in Japan found
that cervical OPLL was the only ossification that increased significantly
in prevalence in people of near modern period.

6. • In INDIA – also this condition is known to cause compressive
myelopathy.
• OPLL is a distinct disease entitiy and should not be confused with
ankylosing spinal hyperosteosis, ankylosing spondylitis and DISH
• DISH – 50 % can have OPLL.

7. Incidence and prevalence
• Japan – 4.3 % of asymptomatic 60 year old man, and 2.4 % of 60 year old
women – radiographic evidence of OPLL in C –spine.
• India – 0.6 % prevalence
• OPLL – 5th and 6th decade – more common
• Male : female – 2:1
• Cervical > thoracic + lumber (10 %)

8. Aetiopathogensis
• Multifactorial
• Results of Pedigree survey, twin surveys, human leukocyte antigen
halotype analysis – Genetic
• XI – collagen (alpha ) 2 gene ( COL11A2)
• BMP -2 gene – extensive OPLL.
• HLA BW40, HLA –SA5

9. Aetiopathogensis
• BMP ( Bone Morphogenic Protein ) , Transforming growth factor –
beta
• CTGF / Hcs24 – Plays role in intiating osteogensis in spinal ligamental
cells.
• Diabetes Mellitus - Distinct risk factor.
• High glucose promotes collagen synthesis in the OPLL via endogenous
TGF – Beta 1 – resulting in hypertrophy of ligaments.

10. Aetiopathogensis
• Analysis of Blood group , Serum Group, Erythrocyte isoenzyme group,
C- reactive Protein, Erythrocyte sedimentation rate, RH factor and
HLA B27 – inclonclusive.

11. Pathophysiology
• OPLL is an ectopic ossification that causes cervical myelopathy.
• Endochondral bone formation  beginning with most superficial
layers  progressing to deep layers and this frequently involves
DURA.
• Intramembranous ossification.

12. Pathophysiology
• Genetic factors of polygenic character , anatomical stress, age and sex
– in formation of OPLL.
• Heterotopic bone formation , Fibroblast hyperplasia, and
cartilaginous proliferation with increased collagen deposition
• Followed by mineralization of thickened ligament with lamellar bone
and Haversian canal formation.

13. Pathophysiology
• The annulus fibrosus remains separate and uninvolved with
ossification at certain levels.
• The ossified ligament is not always continuous with the vertebral
body.
• OPLL grows with reported annual increase 0 .47 mm longitudinally
and 0.67 mm antereoposteriorly.

14. Pathophysiology
• Enlarging mass may have – Round , Cuboidal , Triangular or Polypoid
shape
• Base of attachment – Flat to broad, Narrow to pedunculated.
• Collagen composition- OPLL ( Type 1,2,3 ) , Normal ( Type 1,2)

15. Pathophysiology
• The encroachment of the spinal canal
causes spinal canal deformation into a
thin , crescent shaped structure.
• Neurological signs - > 60- 65 %
occlusion.
• Mechanism –
• Mechanical compression – static /
dynamic.
• Vascular compromise

16. Pathophysiology
• Extent of Gray matter changes  proportional to the anterior horn
deformity.
• Venous stasis , Oedema , Ischemic neuronal necrosis , Infarction 
cavitation and gliosis – Gray matter
• Demyelination and axonal loss – white matter.

19. Classification
• Early OPLL
• Classic OPLL.
• OPLL in evolution is an early variant and shows Focal hypertrophy and
punctate calcification and interspaces.

20. Classic OPLL
• Lateral radiographs.
• 1. Segmental
• 2.Continuous
• 3.Mixed
• 4.Localised.

21. • Hirabayshi et al. – CT based Classification
• Lateral extension

22. • Hida et al – single and
double layered OPLL on the
basis of ossification of the
superficial and deep layer
separated by hypertrophied
non ossified layer
• Mizuno et al – isolated ,
double layer and en block
type.

23. Clinical feautures
• Cervical – Radiculopathy, Myelopathy, Myeloradiculopathy
• Axial discomfort around the neck
• Limitation of cervical ROM
• 45 % motor symptoms

24. Nurick scale of myelopathy

25. Investigations
• Plain X rays – Static and
dynamic.
• Normal spinal canal Diameter –
17 mm from C3-C7 on plain X
ray taken at a distance of six
feet.
• Absolute stenosis – 10 mm or
less

26. • Occupancy ratio
• A/ B
• > 40 % . Increased risk of myelopathy

27. CT Scan
• Thin strip behind vertebral bodies
• Single / double layer sign
• Double layer - dural penetration

30. MRI
• Due to lack of MR signal from cortical bone – Inadequate for
diagnosis ossified lesions
• Provides information regarding spinal cord structure and associated
soft tissue abnormalities, CV junction
• Length of lesion, AP diameters of canal, Signal changes

32. Treatment
• Conservative
• Rest
• External spinal immobilization with collar / brace
• Analgesics
• Anti- inflammatory , antispasmodic
• Treating asymptomatic – surgically / prophylactic – Not advisable.

33. Operative
• Aim –
• Enlarging the spinal canal by decompressing bony ring.
• Maintain alignment
• Indicated:
• ACUTE / CHRONIC progression of neurological deficit
• Signal intensity changes in MRI

34. Selection of surgical procedure
• Age
• Location
• Extent of lesion
• Anterior procedure – direct access, and removal of pathology
• Posterior procedure – indirect decompression of multilevel involvement,
leaves behind the progressive anterior pathology.
• Post operative progression 2 years – 30-40 %
• More in younger age group.

35. K line
Midpoint of spinal canal at C2 – C7
K – group – sufficient decompression is
not achieved

36. • Matsunga et al
• Final functional outcome – not observed – NURICK grade 1-2
• Nurick grade 3-4 , wheelchair bound 12 % surgically treated, 89 % non
surgicall
• In effective in grade 5.

37. Anesthetic considerations
• Fiberoptic
• Can be maintained 1st post op night
( Repeated anterior surgery , >10 hrs of surgery , four or more levels,
obesity , asthma , 4 or more Blood transfusions)
Rarely - tracheostomy may require .

38. Posterior procedures
• When OPLL is continuous, involves long segment, Elderly high risk
patients, upper limit involves C2
• Laminectomy
• Laminecotmy with fusion
• Laminoplasty (modifications)
• Offer adequate decompression by LF removal .
• Mean dorsal cord shift > 3mm – good clinical outcome.

40. Anterior approach
• Overall better neurological status then posterior approach
• Segmental OPLL
• <3 levels
• ACDF / Corpectomy with removal of OPLL
• No associated dural ossifications
• Dural ossification associated

42. Complications
• CSF leak
• Temporary paraparesis
• Quadriplegia
• Graft displacement
• Infection / Bleeding
• Restenosis
• Tethering
• Epidural hematoma
• Respiratory insufficiency
• Oesophageal rupture
• Retropharyngeal abcess

43. Prognosis
• OPLL thickness
• Effective canal diameter
• Post procedure spinal cord changes ( direct or ischemic )
• Diabetes