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Table of Contents    
Year : 2018  |  Volume : 66  |  Issue : 5  |  Page : 1404-1406

Ossified posterior longitudinal ligament with fluorosis: Implications for the Neurosurgeon

1 Department of Neurosurgery, National Neurosciences Centre, Peerless Hospital and B.K.Roy Research Center, Kolkata, West Bengal, India
2 Department of Neuroanesthesiology, National Neurosciences Centre, Peerless Hospital and B.K.Roy Research Center, Kolkata, West Bengal, India

Date of Web Publication17-Sep-2018

Correspondence Address:
Dr. Prasad Krishnan
Department of Neurosurgery, National Neurosciences Centre, Peerless Hospital and B.K.Roy Research Center, Kolkata 360 Panchasayar, Kolkata - 700 094, West Bengal
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.241389

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How to cite this article:
Krishnan P, Ghosh N. Ossified posterior longitudinal ligament with fluorosis: Implications for the Neurosurgeon. Neurol India 2018;66:1404-6

How to cite this URL:
Krishnan P, Ghosh N. Ossified posterior longitudinal ligament with fluorosis: Implications for the Neurosurgeon. Neurol India [serial online] 2018 [cited 2019 Feb 16];66:1404-6. Available from:

Fluoride is an essential trace element and imparts stability to teeth and bone.[1] However, chronic overexposure to fluoride results in skeletal fluorosis – a toxicity affecting the bones, manifesting with deformities, spinal column involvement and diminished joint movement.[1],[2],[3] This is a public health problem in our country [1],[2] as the groundwater in several districts (potentially affecting more than 66 million people in 275 districts across 21 states)[4] is contaminated with high levels of fluorine.

Usually the neurosurgeon proceeds for surgery in a patient with symptomatic ossified posterior longitudinal ligament (OPLL) with just preoperative plain radiographs and a magnetic resonance imaging (MRI) of the cervical spine. Radiography of the forearm (where ossification of the interosseous membrane may be demonstrable) may at best buttress, but not confirm, the suspicion of background fluorosis. An awareness of pre-existing fluorosis while operating on a patient with OPLL is desirable since the neurosurgeon may encounter the following problems:

Tandem stenosis: Fluoride tends to induce periosteal new bone formation leading to creation of osteophytes [4] and also gets deposited in ligaments and fasciae inducing new bone formation [Figure 1].[5] This may occur not only in the posterior longitudinal ligament (PLL) but also in the ligamentum flavum and can cause ossified ligamentum flavum (OLF)[6],[7] with cord compression (more so in the dorsal cord). Any suspicion that fluoride ingestion may be the cause of OPLL must, therefore, prompt a full imaging study of the spine to pick up any additional compression at other levels as this may affect the outcome after surgery [Figure 2]. The comprehensive imaging will also help in planning surgery as well as prognostication.
Figure 1: Long segment OPLL in a 72--year old patient from Birbhum district (endemic for fluorosis in West Bengal) showing a high occupancy ratio, ossification of the ligamentum nuchae (green arrows) in addition to posterior longitudinal ligament (red stars) and anterior longitudinal ligament (pink stars). However, no preoperative blood investigation to confirm fluorosis could be done

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Figure 2: Sagittal MRI of a patient who presented with spastic quadriparesis showing cervical OPLL (a). He underwent a laminectomy. Postoperatively, there was no significant recovery and flexor spasms in the lower limbs worsened. A subsequent MRI revealed the ossified ligamentum flavum (b) at multiple levels in the dorsal spine. The initial tandem stenosis was not picked up

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Varying densities of the bones with propensity to fracture: Fluoride binds with and alters the chemical properties of hydroxyapatite [8] leading to sclerosis of the bones. However, radiographic osteopenia is also found commonly,[5] and the latter may be in one of the two patterns – osteoporotic (manifesting with decreased bone density) and osteomalacic (features of osteoporosis with skeletal deformity). While the sclerotic hard bone requires intensive drilling for removal, and often a high speed drill may be needed to prepare the tract for instrumentation, the porotic bone may cause the drill to “sink in” unexpectedly. The surgeon should be aware of both the possibilities co-existing in the same patient. It must be borne in mind that even sclerotic bones in fluorosis are less pliable than their normal counterparts and have an increased predisposition to fracture with trivial trauma.

Dural involvement: The dura may be involved (calcified/ossified) in patients with fluorosis who have OPLL.[9] The surgeon may often not be able to separately identify the involved dura from the OPLL; and, anterior corpectomy and decompression may inadvertently cause a dural breach with cerebrospinal fluid (CSF) leak that may be difficult to manage. An MRI scan alone is inadequate to pick up the dural ossification,[10] and in all suspicious cases of OPLL with fluorosis, it is wise to perform a computed tomography (CT) scan prior to the anterior surgery. Further, there is evidence that a higher canal occupancy ratio and a larger extent of OPLL (usually seen in the continuous type of OPLL), features that are frequently found in fluorosis, have an increased association with dural ossification.[11] If the intraoperative separation of the PLL from the dura is not possible, a thin floating plate of bone comprising of both the involved PLL and the dura may be left behind after drilling and freeing the sides. A risk of progression of the disease in the future [9] with overgrowth of the residual duro-ligamentous complex remains with this method. The alternative is the removal of involved dura as well, and for this, the surgeon must dissect meticulously and avoid an arachnoidal breech.[11] He/she must also be prepared to reconstruct the defect with fascia and fibrin glue and place a postoperative indwelling lumbar drain, if required.

Kyphotic spine: The presence of a continuous long segment OPLL is an indication for indirect decompression (laminectomy) but this procedure is often not done in a kyphotic cervical spine since the cord is left tethered to the mass anteriorly. A preoperative cervical lordosis of “at least 10 degrees” has been described as a prerequisite for successful posterior decompression [Figure 3]a and b].[12] In patients with a long segment OPLL with a large occupancy ratio (as is seen in fluorosis), the surgeon must look for the presence of preoperative kyphosis, as it is a factor causing poor postoperative results. Conversely, with an increasing cervical lordosis, the OPLL may not go behind the K-line (the line joining the midpoints of the spinal canal at C2 and C7) [Figure 3]c; and, in such patients, the posterior shift of the cord after the laminectomy will be sufficient for ensuring a good result. Also, in fluorosis, in addition to multiple ligamentous calcifications, the osteophytes cause vertebral fusion at the margins of the intervertebral discs. If this condition is associated with preserved cervical lordosis, it may obviate the need for additional instrumentation in several cases.
Figure 3: The lack of kyphosis in this patient with OPLL is shown by calculating the lordotic angle (approximately 15 degrees) on the preoperative MRI (a). An adequate dorsal shift of the cord after decompression is shown on the postoperative MRI (b). Finally, the K line (thin red line), extending from the mid--part of the canal at the C2 level to the mid--part of the canal at the C7 level, in another patient, is seen to go behind the OPLL mass and is also a predictor that the dorsal shift of the cord after a laminectomy will be adequate (a-c)

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Anaesthetic and other implications: Intubation may be problematic in patients with fluorosis due to the fixed and immobile cervical spine and may necessitate the use of a fibreoptic bronchoscope for ensuring a safe airway access.[13] Immobility of the rib cage may entail the need for postoperative ventilation, and this too must be planned for before surgery.[13] Difficulties in positioning of the patient during surgery (due to multiple joint involvement)[13] is another aspect the surgeon has to consider in advance.

Non-compressive factors causing deterioration: In patients with OPLL and fluorosis, neurological damage may be the result of direct fluoride toxicity to the anterior horn cells [4] or reduced myelinated fibre densities either due to axonal degeneration or demyelination.[4] Hence, mere decompression of the spinal pathology may not guarantee a good outcome and this phenomenon must be factored in by the surgeon while preoperatively explaining the prognosis to the patient.

As commercial tests to measure urinary and serum fluoride levels are not readily available in most parts of the country, the findings which Reddy et al.,[14] have brought to light in their paper assume importance. These may be summarised as: In an endemic belt, the patients with OPLL are more likely to have fluorosis; the continuous variant of OPLL is the commonest radiological type encountered in fluorosis; an increasing severity (high occupancy ratio) of the OPLL is seen in patients with fluorosis; and, kyphosis is rarely seen in these patients. This will serve to make the neurosurgeon consider concomitant fluorosis and be better prepared to deal with the difficulties he might encounter during and after surgery for OPLL in such patients.

  References Top

Reddy GB, Khandare AL, Reddy PY, Rao GS, Balakrishna N, Srivalli I. Antioxidant defence system and lipid peroxidation in patients with skeletal fluorosis and in fluoride-intoxicated rabbits. Toxicol Sci 2003;72:363-8.  Back to cited text no. 1
Reddy DR. Neurology of endemic skeletal fluorosis. Neurol India 2009;57:7-12.  Back to cited text no. 2
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Teotia M, Teotia SP, Kunwar KB. Endemic skeletal fluorosis. Arch Dis Child 1971;46:686-91.  Back to cited text no. 3
Reddy DR. The element fluorine and its effects on human health including its neurological manifestations. Neurol India 2017;65:238-9.  Back to cited text no. 4
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Wang Y, Yin Y, Gilula LA, Wilson AJ. Endemic fluorosis of the skeleton: Radiographic features in 127 patients. AJR Am J Roentgenol 1994;162:93-8.  Back to cited text no. 5
Muthukumar N. Ossification of the ligamentum flavum as a result of fluorosis causing myelopathy: Report of two cases. Neurosurgery 2005;56:E622.  Back to cited text no. 6
Gupta RK, Agarwal P, Kumar S, Surana PK, Lal JH, Misra UK. Compressive myelopathy in fluorosis: MRI. Neuroradiology. 1996;38:338-42.  Back to cited text no. 7
Gupta AK, Singh TP, Agrawal PK, Singh D, Sachan M, Agarwal V. Quadriparesis – A rare presentation of skeletal fluorosis. JIACM 2008;9:201-4.  Back to cited text no. 8
Kumar P, Gupta A, Sood S, Verma AK. Fluorotic cervical compressive myelopathy, 20 years after laminectomy: A rare event. Surg Neurol Int 2011;2:11.  Back to cited text no. 9
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Mizuno J, Nakagawa H, Matsuo N, Song J. Dural ossification associated with cervical ossification of the posterior longitudinal ligament: Frequency of dural ossification and comparison of neuroimaging modalities in ability to identify the disease. J Neurosurg Spine 2005;2:425-30.  Back to cited text no. 10
Chen Y, Guo Y, Chen D, Lu X, Wang X, Tian H, et al. Diagnosis and surgery of ossification of posterior longitudinal ligament associated with dural ossification in the cervical spine. Eur Spine J 2009;18:1541-7.  Back to cited text no. 11
Smith ZA, Buchanan CC, Raphael D, Khoo LT. Ossification of the posterior longitudinal ligament: Pathogenesis, management, and current surgical approaches. A review. Neurosurg Focus. 2011;30:E10.  Back to cited text no. 12
Kurdi MS. Chronic fluorosis: The disease and its anaesthetic implications. Indian J Anaes 2016;60:157-62.  Back to cited text no. 13
Reddy KVS, Mudumba VS, Tokala IM, Reddy DR. Ossification of posterior longitudinal ligament and fluorosis. Neurol India 2018;66:1394-9.  Back to cited text no. 14
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  [Figure 1], [Figure 2], [Figure 3]


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