European Journal of Cardiovascular Medicine

The ligamentum flavum extends from C2-S1. The ligamentum flavum is composed of elastic fibres (80%) and collagen fibres (20%). It is attached to the under surface of the lamina above and the upper part of the lamina below. It has a capsular portion and inter laminar portion.^1,2 Ossified yellow ligament (OYL) is a representation of ageing of the vertebral ligaments and is linked to the systemic ossification trait. Usually, it occurs at the lower thoracic levels. It may occur in combination with ossified posterior longitudinal ligament (OPLL).

The cause of ossification of the yellow ligament is multifactorial ranging from heredity, abnormal glucose metabolism, abnormal calcium metabolism, abnormalities in the gender hormones, degeneration of the ligament etc.³ In degenerative conditions, the mechanical stress to the ligament especially at the capsular position, lead to OYL. Chondrocytes are activated by the stress of the ligament, this will lead to production of type- 2 collagen, which in turn gets transformed to type-1 collagen in the course of endochondral ossification of the yellow ligament. People with collagen 11 A2gene and 6A1 gene are shown to be predisposed for this development. Growth factors and transcription factors like cartilage derived morphogenic protein- 1, promyelocytic leukaemia zinc finger and tumour necrosis factor alpha stimulated gene 6 are related to the transformation of the undifferentiated mesenchymal cell to the osteoblastic cell.^4,5

In the lower thoracic spine, the kyphotic alignment with strong traction force and rotational movements, act on the ligamentum flavum and influence the ossification mechanism.^6,7 In the lordotic lumbar and cervical spines, the traction force doesn’t act strongly, so calcification tend to develop rather than ossification of trabecular structure.

All the cases of ossified yellow ligaments operated by the 1^st author from 2003 onwards till 2024 May are reviewed. 18 cases of OYL of different neurological status were operated. 11 of them were males and 7 were females. Age group ranged from 44 years to 91 years. OYL was seen more within 50-70 years age group.

8 patients were diabetic (3 males and 5 females), 4 patients were hypertensive, one had hypothyroidism, two among them had both hypertension and diabetes. 5 patients (3 males and 2 females) had associated ossified posterior longitudinal ligament (OPLL) at the same level as OYL or at different locations: mostly in the cervical spine.

One of the patients developed OYL and paraplegia 5 years after sustaining a traumatic disc prolapse with quadriplegia and recovery after surgery. The patients at admission were assessed neurologically and JOA scoring was applied. 6 patients out of 18 had bladder and bowel involvement.

The patients were evaluated with plain Xray of the spine and MRI. Once the diagnosis was made, CT scan of the level of interest was taken to look for the bony extent of the lesion and the presence of dural ossification. MRI depicted the extent of myelomalacia and thinning of the cord. Further evaluation was done to ensure the surgical fitness of these patients.

All patients had OYL in the thoracic spine. Some patients had OYL at multiple levels. 7 patients had OYL at D10-11 and 6 patients had OYL at D9-D10. Two patients had OYL at D8 to D10.

Associated OPLL was present in 4 patients at the cervical levels and thoracic levels. One had OPLL at C5-C6/C6-C7 and D12-L1, 2^nd patient had OPLL at C4-7 and D8-10, 3^rd patient had OPLL at C3-6 only and the 4^th patient had OPLL at D8-D10 and C4-C7: One patient had isolated OPLL in the thoracic spine along with thoracic OYL and the rest 3 patients had combination of thoracic and cervical OPLL along with thoracic OYL.

The neurological status was assessed using JOA scoring system.

Surgery

All patients underwent laminectomy and instrumented fusion. Wide laminectomy was done. Dural calcifications were addressed by floating technique. Diamond burr was used to thin out the calcified mass and left as such.  No dural tear was encountered. No neurological deterioration was noticed in the post operative period.

6 out of 18 patients had bowel/bladder dysfunction at admission. 5 of them recovered the bowel bladder dysfunction. One patient had no improvement of bladder function at 1 year post-surgery. 8 patients had JOA score zero at admission; 5 patients had score of one at admission. Another set of 5 patients had JOA score of 2 at admission. 4 patients with ‘0’ JOA score at admission were JOA score of 4 (completely recovered) at 1 year after surgery. 2 patients had JOA score ‘0’ at admission and improved to JOA score of 3 at 1 year post surgery. Another 2 patients had JOA score of ‘0” at admission and improved to JOA score 2. All patients with JA score 1 and 2 at admission improved to normalcy at 1 year (JOA score – 4).

So, out of the 18 patients, all patients with JOA score one and two (total 10 patients) recovered completely at 1 year post surgery. Of the 8 patients who presented with JOA score of zero, 4 of them recovered completely at 1 year (50%), two of them to JOA score of 3 and another 2 to JOA score of 2.

The overall complete neurological improvement in our scores were 77.77%. JOA scores one and above at admission recovered completely at 1 year (100%). This is in agreement with Joji Inamasu et al, who stated that preoperative neurological status is a predictor of neurological recovery after surgery.⁸