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Vol No. 1 Issue No. 1

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■ Incidence

The cervical segment is the most mobile portion of thespine and it is no wonder that 44% 14,22 of the injuries occurin the cervical spine. In terms of functional utility this is themost important segment of the spine and the spinal cord.Besides lower extremities and the autonomic functions, theupper extremities and the respiratory centers are involvedmaking the patient completely disabled and bed ridden.

The next vulnerable portion is the unstable dorso lumbarjunction and accounts for 41% of the injuries but upper

limbs are not involved. Less frequently the injuries occurin the lumbar and sacral spine (15%).

Most of the time besides injury to the bony spine the spinalcord is contused or transected and these findings can bedemonstrated on MRI studies. Intramedullaryhaemorrhage, oedema and compression from outside alsocontribute to the damage in the cord.

■ Sequelae of injury

Once the cord is damaged there is primary cell death.18

There is breakage of axons and there is progressive tissueloss. Following trauma haemorrhagic necrosis in the cordcan occur within 2 to 3 hours. Within the same time thewhite matter blood flow falls by 50% and normalmetabolism is compromised resulting in accumulation ofhigh levels of lactic acid.1,2,5,6,8,9,20

Calcium quickly enters the cells causing its swelling anddisruption and activates proteases and phospholipidaseswhich break proteins and lipids. Calcium itself binds tomitochondria and releases free radicals. Free radicals areunpaired electrons and they cause further neuronal damage.The peak of destruction of cellular activity is at 48 hoursand 10 to 14 days for destruction of white matter tracts.

Once the blood–neuronal barrier is broken down theprocess of inflammation in the cord begins and its activityis at its peak at 6 hours. The process of inflammationactivates macrophages and reactive astrocytes causinggliosis and forming scar in the injured cord.

From these sequelae it is clear that secondary changesdeveloping in the cord following trauma plays an importantrole in worsening the damage sustained primarily to thecord at the time of accident. Most of the secondary damageoccurs within three hours and this period seems crucial toattempt to prevent further insult to the already damagedspinal cord. Unfortunately the period is too short for anymeaningful interference in the majority of cases in ourcountry.

Where do we stand with acute spinal cord injured patients?

P. S. Ramani, MDDepartment of Neurosurgery, Lilavati Hospital & Research Center, Mumbai

AbstractOccurrence of acute spinal cord injury isuniversally recognized as a major cause ofmortality and morbidity with many left behindwith permanent disability.1,14,22 Road trafficaccidents is a common cause of spinal cordinjury and of the 36% injuries due to roadaccidents, two wheelers are most frequentlyinvolved. Two wheelers are usually driven bythe young who are full of vigour and enthusiasmbut their vigour is noted to be misdirected onseveral occasions. Many times he is the onlybread winner of the family. Knowing these direconsequences efforts have been made in twodirections. 1: To prevent occurrence of injury tothe spinal cord and 2: Effective managementof the injured spinal cord and the spine as it isestimated that between 14.5 to 57.8 injuriesper million occur round the world in any givenyear. In India it is estimated that around 26,000injuries occur per year accounting for 30 injuriesper million per year. This is indeed a very largenumber producing tremendous pressure onmeager rehabilitation facilities in our country.

Key Words❉ L5-S1 disc Acute spinal cord injury❉ Methylprednisolone

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■ Management

Following are the aims of management of acute spinal cordinjury in broad principles once the patient is admitted tothe hospital.1. To start treatment to immediately prevent secondary

damage occurring to the spinal cord2. To stabilize and realign the spine and remove external

compression on the spinal cord3. To maintain normal levels of blood pressure to maintain

spinal cord perfusion4. Prevent complications5. Possibly help in regeneration of nervous tissue by

suppressing glial proliferation and promoting axonalregeneration

1. Prevention of secondary damage

If secondary damage is prevented, better axonalregeneration can be expected. National Acute Spinal CordInjury Studies (NASCIS) II and NASCIS III studies haveshown some functional benefit of Methyl prednisolonewhen administered soon after spinal cordinjury.4,5,6,7,8,9,10,20,21 It has proved to be a safe drug andcan be administered intravenously no sooner the patientarrives in the hospital and currently it is the most widelyaccepted pharmacological treatment. It is a treatment optionbut all over the world, today, it is accepted as the standardof care.

Several reports on Cochrane Database RandomisedSystematic Reviews have been published5 on the drugmethyl predisolone and its use in acute spinal cord injury.It is accepted as a neuroprotective agent whenadministered in time. Evidence shows that it protects theneural tissue and helps in regeneration.

Following benefits have been attributed to the use ofmethylprednisolone.1. Antioxidation: High doses prevents lipid peroxidation

and reduces calcium mediated necrosis in the cord2. Anti-inflammation: 3,4,6

It reduces inflammation producing cytokines (IL-1b,IL-6, TNF-a)It also reduces apoptosis

3. Antisprouting: Regulates neurotropic gene expressionand prevents development of neuropathic pain.12,13

4. Suppresses T-cell mediated hypersensitivity:3,9

Decreases post traumatic expression of pro-inflammatory mediatorsActivator protein-1 (AP-1), Nuclear factor (NFKB),Matrix metalloproteinase 1 and 9

5. It also helps to counteract spinal shock19

■ Other options for management[pharmacological]7

1. Non glucocorticoid 21-aminosteroid – tirilazad isknown to duplicate the anti-oxidant, neuroprotectiveefficacy of methyl prednisolone

2. Opiate receptor antagonist – naloxone demonstratesbeneficial effects

3. GM1 or mono sialo ganglioside is also known toimprove neurological recovery

4. Ganglioside, Thyrotropin releasing hormone,Galyclidine, Nimodipine, etc. also showpharmacological properties to pretect the injuredspinal cord

5. Carnosine is a neuroprotective dipeptide found in brainand musclesBut these pharmacological agents have not foundmuch favour with clinicians and certainly they are notpopular in India

2. Decompression of cord, realignment of spineand stabilization

Timing of surgery

The concept of timing of surgery has changed with theintroduction of methyl prednisolone.5 It is believed that it isnot necessary to wait for patient to come out of spinalshock before undertaking any surgical intervention. Afteradministering a bolus of methyl prednisolone the patientcan be safely taken for surgery. Spinal shock is neurogenicand has motor, sensory, reflex and autonomic components.Higher the lesion, greater is the severity of shock and longeris the duration. It is possibly caused by temporaryelectrolytic or neurotransmitter effect on impulseconduction (Figure 1).

Figure 1Combined anterior and posterior one stage reconstruction ofburst DL fracture. There is no definite dictate regarding timing ofsurgery


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NASCIS II5,20 has reported that mortality is much higherin conservatively treated group at 15.2% as against 6.1%in surgically treated group. This is in spite of the fact theincidence of thromboembolism is much higher in the surgicalgroup.

Having cleared the gate for early surgical intervention amulti-centric retrospective study in US of 585 patientsshowed that only 23.5% of the patients were operatedearly within 24 hours. On analysing the results of this studythey had following observations to make.14,18

1. Prospective case series

Surgical decompression before 24 hours or after 200 hoursdid help to improve neurological recovery than treatingconservatively.

Early surgery (within 24 hours) did not improve neurologicalrecovery.

2. Retrospective case series

Surgery did help to improve neurological deficit but onlyin cases with incomplete spinal cord injury. There was norelationship between improvement and timing of surgery.

3. Experimental studies in animal models12,13,15,16

If compression was severe, the vascular damage causedirreversible injury to the cord. But if the canal compromisewas minimum in partially damaged cord then early surgerypromoted neurological recovery.

4. Reduction of dislocation and neurologicalrecovery

This is one type of injury where there has been uniform

consensus that dislocation should be reduced early. Earlyreduction either close or open caused improvement in 67%of the cases including improvement in root palsies. Rapidalignment improves neurological recovery.

A representative case treated by the author.

A 61-year-old male fell from a height of 10 feet and becamequadruparetic. He was given immediate first aid treatmentat the place of accident and immediately solumedrolaccording to the NASCIS regime was started.

He had sustained dislocation with bilateral facet lock inthe cervical spine. His left side of the body including upperand lower extremities was totally paralysed but on the rightside he was partially paralysed (Figures 2 & 3).

The facet lock did not get unlocked even under generalanaesthesia by applying close reduction. The facets werethen surgically unlocked and the spine was stabilised bothanteriorly and posteriorly (Figure 4).

It is now universally believed that facet lock should bereduced as quickly as possible.

During the postoperative period he has been showing

Figure 2Cervical spine dislocation at C4/C5 with bilateral facet lock

Figure 3MRI pictures of the same patient showing dislocation and facetlock

Figure 4Postoperative X rays showing unlocking of the facets andreduction of dislocation followed by stabilization of the spineboth anteriorly and posteriorly

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significant improvement in the right side of body. Thedeductions as mentioned here are in line with the thinkingof STASCIS (Surgical treatment of acute spinal cord injurystudy) as expressed in the annual conference of AmericanAssociation of Neurological Surgeons (AANS) in April2008. However this study was more in favour of earlysurgery than late.

5. Central spinal cord injury

In cervical region acute disc herniation is very common.Early surgery in all patients showed rapid improvement.

The outcome remained poor with injuries like fracturedislocations.

75% of patients with acute central cord primary injury whentreated conservatively, regained ambulatory skills.

6. Retrospective clinical studies of improvementafter late decompression12

Uniformly there was improvement in neurological statussignificantly only in incomplete spinal cord damage.

The pattern of acute injury to the spinal cord is extremelyvariegated depending on number of factors involved inproducing the final picture that the clinician is seeing. Inthese circumstances the observations mentioned above areextremely useful as guidelines in day to day clinicalmanagement of patients who have sustained acute spineand spinal cord injury. It will be injudicious to irrationallyrush the patient to operation theatre particularly in patientswith complete spinal cord injury.

■ Stem cell therapy in spinal cord injury 3,11,15,16,18,21

In recent years there has been much talk, much hype andat times ill founded faith in stem cell therapy. As said earlierthe spine injured patient is young and family members getemotional and want to give him everything that is availablejust to see him walk again. They do not know whoChristopher Reeves was although they might have seenhis movies.

How to tamper the emotions without hurting deep routedrelations is a challenge which clinicians must accept. Infact there is, as of now, limited evidence from animalexperiments that stem cells improve the functional outcomein spinal cord injured animals. Uncontrolled trials in clinicalpractice have proved unconvincing. When I personally

talked to Dr. Almeida Lima in Lisbon, he said that patientmust be under his supervision for at least one year beforeassessment can be made. His selection of patients andkeeping them under his personal observation for threemonths before stem cell therapy to know if there is anynatural improvement is quite rigid.

It is indeed interesting that there are plenty of areas in thebrain and the cranial nerves like dentate gyrus andhippocampus, subventricular zone and along ependymaupto 4th ventricle, hypothalamus, susbstantia nigra andalfactory nerves which are full of stem cells. So there arestem cells in the brain which have potential to proliferateand there are naturally occurring factors in the body whichcan induce stem cell proliferation and guide the cells alongglial and neuronal lineages. Steroids and imuno modulatingdrugs given at this time systemically suppresses formationof gliosis which impairs attempts of axons to regrow.

Naturally found cells proliferate along glial lineages andless along neuronal lineages. The effort of stem cells isessentially to provide a substrate for axonal regenerationand and remyelination of axons.

The naturally found cells are insufficient and at times ininappropriate locations. They are not sufficient to achievefunctional restoration. That is where exogenous neural stemcells have achieved importance. They are multiplied in thelaboratory.

Commonly used cells are 1: alfactory ensheathing cells(OEC), 2: Schwann cells, 3: Neural stem cells, 4:Embryonic stem cells, 5: bone marrow stromal cells(BMSC) or 6: genetically engineered cells. The recoveryis essentially through remyelination by oligodendrocytelineage cells. Stem cells transplantation in animals withASCI has produced functional recovery.

The structural involvement in spinal cord injury is asfollows:

1. The long tracts particularly the cortico spinal tracts ormotor tracts

2. Neurons at the site of injury particularly motor neurons3. Vascular disruptions

Conventional pharmacological immuno modulatory drugsincluding much used methyl prednisolone and as confirmedby NASCIS shows an improvement in functional status ofthe patient but the neurological level of damage remainsthe same.


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The reason being the drugs are aimed at facilitating axonalregrowth and their re-myelination.

The neurons and for that matter even the cortico spinaltracts are not targeted by these agents.

The target of therapy with stem cells is the long tracts.Their disruption produces motor, sensory and autonomicloss below the level of injury. Neurons involved areessentially sensory at the root entry zone.

Stem cells provoked into neural differentiation in thelaboratory are being extensively used. But they must becorrectly placed at the site of injury after excising the scaror along the tracts of normal neuronal migration. Then onlythey can be expected to be useful.

There is lot to be thought of than what catches the innocenteye. Even certain cells like mononuclear or lymphocyticlineage can be used as immunomodulators so that axonalgrowth can be promoted.

Many clinicians use auto marrow aspirate mesenchymalstromal cells (purified from a bone marrow aspirate— needat least 40 to 50 mls of marrow aspirate to centrifuge andseparate 1.5 to 2mls of stromal cells) but they are justinjected through lumbar puncture into the spinalsubarachnoid space. Some clinicians are using alfactoryensheathing glial cells, harvested from uppermost tonefourth of nasal mucosa which is rich in alfactory stem cells.Usually alfactory cells are directly placed at the site of injuryafter cleaning the debris and any scar tissue during surgery.

Cells can also be delivered as near as is possible to theinjury by doing selective angiography. Cells injected intothe subarachnoid space, which according to the clinicianshas shown neurological improvement, possibly act asmacrophages and remove inflammatory debris and thuspromote axonal regeneration.

■ Conclusion

The aim of treatment in acute spinal cord injury is toimmediately remove all external pressure which iscompressing the spinal cord, prevent cascade of secondarydamage and then help is regeneration of axons and promoteremyelination. Spinal cord injury is very common all overthe world as it is in India but treatment options are limited.All attempts should be made by clinicians backed by agood rehabilitation centre to provide a more dignified lifefor these unfortunate victims.

■ References

1. Ackery A, Tator C, Krassioukov A. A global perspective on spinalcord injury epidemiology. J Neurotrauma 21(10);1355-70, 2004.

2. Anderson DK, Means ED, Waters TR, Green ES. Microvascularperfusion and metabolism in injured spinal cord aftermethylprednisolone treatment. J Neurosurg 56(1);106-13, 1982.

3. Ankey DP, Mctique DM, Jakeman LB. Bone marrow transplantsprovide tissue protection and direction guidance for axons aftercontusive spinal cord injury in rats. Exp Neurol 190;17-31, 2004

4. Bracken MB. Administration of Methylprednisolone for 24 or 48hours or tirilazad mesylate for 48 hours in the treatment of acutespinal cord injury: Results of the third national acute spinal cordinjury randomized controlled trial. JAMA 277(20);1597, 1997.

5. Bracken MB. Steroids for acute spinal cord injury (Review).Cochrane Database of Systematic Reviews, Issue 2, 2009.

6. Celik JB, Gormus N, Okesli S, Gormus ZI, Solak H.Methylprednisolone prevents inflammatory reaction occurring duringcardiopulmonary bypass: effects on TNF-alpha, IL-6, IL-8, IL-10.Perfusion 19(3);185-91, 2004.

7. Chikawa T, Ikata T, Katoh S, Hamada Y, Kogure K, Fukuzawa K.Preventive effects of lecithinized superoxide dismutase andmethylprednisolone on spinal cord injury in rats: transcriptionalregulation of inflammatory and neurotrophic genes. J Neurotrauma18(1);93-103, 2001.

8. Diem R, Hobom M, Maier K et al. Methylprednisolone increasesneuronal apoptosis during autoimmune CNS inflammation byinhibition of an endogenous neuroprotective pathway. J Neurosci23(18);6993-7000, 2003.

9. Faludi G, Mills LC, Chayes ZW. Effects of steroids on muscle. ActaEndocrinologica 45;68-78, 1964.

10. Hirano T. Differential respiratory effects of glucocorticoids. Update2004: clinical perspectives on acute asthma therapy 12-16, 2004.

11. Horner PJ, Power AE, Kemperonon G, et al. Proliferation anddifferentiation of progenitor cells throughout the intact adult spinalcord. J Neurosci 20;2218-28,2004.

12. Houle JD, Tessler A. Repair of chronic spinal cord injury. Exp Neurol182(2);247-60, 2003.

13. Johansson A, Bennett GJ. Effect of local methylprednisolone onpain in a nerve injury model. A pilot study. Reg Anesth 22(1);59-65,1997.

14. Kraus JF, Terry AS, McArtha DL. Epidemiology of spinal cord injury.In: principles of spinal surgery. Eds, Menezes and Sonntag; McGrawHill Vol 1; Chapter 3:41-58, 1996.

15. Lu D, Li Y, Mahmood M, et al. Neural and marrow derived stromalcell transplantation in rat model of traumatic brain injury. J Neurosurg94;765-74, 2001.

16. Picard Riera N, Nait-Oumermar B. Endogenous adult stem cells:Limit and potential to repair the injured CNS. J Neurosci Res 76:223-31, 2004

17. Schimmer BP, Parker KL. Adrenocorticotropic hormone;adrenocortical steroids and their synthetic analogs; inhibitors ofthe synthesis and actions of adrenocortical hormones. In: BruntonLL, Lazo JS, Parker KL, eds. Goodman and Gilman’s ThePharmacological Basis of Therapeutics. 11th ed. New York: Mac-Graw Hill companies, Inc. 1587-612, 2006.

18. Tator CH. Spinal cord syndromes, physiological and anatomicalcorrelations. In: principles of spinal surgery. Eds, Menezes andSonntag; McGraw Hill. Vol 2; Chapter 50:785-800, 1996.

19. Vecchiarelli A, Siracusa A, Cenci E, Puliti M, Abbritti G. Effect ofcorticosteroid treatment on interleukin-1 and tumor necrosis factorsecretion by monocytes from subjects with asthma. Clin Exp Allergy22:365-370, 1992.

20. Young W, Bracken MB. The second national acute spinal cordinjury study. J Neurotrauma 9(Suppl 1), 1992.

21. Xu J, Gingras KM, Bengston L, Di Marco A, Forger NG. Blockade ofendogenous neurotrophic factors prevents the androgenic rescueof rat spinal motoneurons. J Neurosci 15;21(12):4366-72, 2001.

22. Zhao YD, Wang W. Neurosurgical trauma in People’s Republic ofChina. World J Surg 25:1202-4, 2001.

Address for correspondenceDr. P. S. Ramani : Email : [email protected]

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■ Introduction

The fifth lumbar is one of the most common lumbar discsto require interbody fusion for pain relief in degenerativedisorder. Several surgical approaches like posterior (ortransforaminal), anterior, and lateral have been describedto approach the lumbar discs. In the lateral root the disc isencountered between the great vessels and the neural canal.It is relatively a safer approach and prevents damage to

adjacent structures. It is also considered less traumatic.3

However, several authors using this approach by open orendoscopic surgery to fifth lumbar disc have expressedconcern because of overhanging iliac crest obstructing thelateral trajectory.2,3,4,5,6 Till today lateral approach to thefifth lumbar disc has not been described.

The purpose of this study is to report our surgical methodof lateral retroperitoneal approach to the L5-S1 disc in 42patients using mini-open surgery, and to discuss theanatomical variations affecting accessibility and relatedtechnical issues.

■ Material and methods

A total of 42 patients with pathologies of the L5-S1 discwho underwent lateral retroperitoneal approach forinterbody fusion over a 3 year period from January 2005till December 2007 were retrospectively reviewed. Themean follow-up period was 32.6 months (range, 21 to 44months). There were 14 males and 28 females with a meanage 61.7 years (range, 35 to 82 years). Among them, 30patients (71.4%) underwent fusion at one level (L5-S1),12 patients (28.6%) at two-levels (L4-5 and L5-S1), anda total of 54 levels were fused. The medical charts, surgicalnotes and pre- and postoperative images were reviewedand analyzed.

The indications for surgery were degenerative disorders(n=39, 92.8%), pyogenic discitis (n=1, 2.4%), andpseudarthrosis of L5-S1 level (n=2, 4.8%; failed anteriorinterbody and posterior interbody fusions). Two patientshad grade-one L5-S1 isthmic spondylolisthesis. Sixteenpatients (38.1%) required posterior decompression forstenosis (n=14) or herniated disc (n=2). Single stand alone,either cylindrical or rectangular titanium cage (HELIX 26-mm long, and LATERO 35-mm long, respectively, A-SpineCo., Taipei, Taiwan) was used in 53 levels (graft only inthe case of discitis). A mean of 6.5 c.c. bone graft (range,5-16 c.c.) was used for one disc level. Autograft was usedin 36 patients (85.7%) and allograft was used in 6 patients

The lateral retroperitoneal approach to the fifth lumbar disc(Applied anatomy, surgical technique for anterior interbody fusion and personal experiences of 42 cases)

Jin Fu Lin, MD,* Myung-Sang Moon, MD*Department of Spinal Surgery, Taipei Hospital, D.O.H. Taipei, TaiwanDepartment of Spinal Surgery, Halla General Hospital, Cheju, Korea

AbstractLateral retroperitoneal approach to the L5-S1disc is difficult due to obstruction of the iliaccrest. We reviewed 42 patients who underwentone (L5-S1) and two-level lateral fusion (L5-S1and L4-5). We categorized the cases into twomain anatomical variations which influence theaccessibility: 1. variations of the iliolumbar vein:present or absent, location, and diameter.2. locations of the L5-S1 disc in the pelvis,relative to the intercristal line: shallow or high-riding, middle, deep or low-seated. Lateralaccessibility varies from easy to cumbersomeor challenging, rather than impossible. It mostlydepends upon handling of adjacent venoussystem to avoid vascular injury; and the iliaccrest is annoying at best. The key surgical pointis to dissect the psoas muscle backward, findand divide the iliolumbar vein and then mobilizethe tethered common iliac vein from theanterolateral aspect of the L5-S1 disc in orderto do lateral fusion.

Key Words❉ L5-S1 disc❉ Lateral retroperitoneal approach❉ Iliolumbar vein❉ Common iliac vein❉ Psoas muscle❉ Iliac crest❉ Intercristal line


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(14.3%). Left flank approach was used in 38 patients(90.5%) and right flank approach in 4 patients (9.5%).

■ Surgical technique

Positioning of the patient

All patients were operated without the assistance of avascular surgeon. Long-handle blunt tipped tools wereused; and the suction pressure was reduced to a minimumworking level. Following induction with general anesthesia,the patient was first placed prone and when necessary thedecompression laminectomy was performed. Autograft wasthen harvested from the posterior iliac crest and the woundwas closed. The patient was then turned to lateral decubitusposition and the trunk was kept perpendicular to the floor.

The trunk and the pelvis were firmly fixed. The ipsialteralthigh was flexed to relax the psoas muscle and the tablewas bent at the lumbopelvic junction to open the lateralspace. Using lateral fluoroscopy and opaque flexible stillwires as markers, the L4-5 and L5-S1 disc spaces wereidentified and marked with marking pencil for the line ofthe incision (Figure 1).

After preparing and draping, an oblique incision, about 6to 10-cm long, centered at the skin marking starting in theanterior axilla line and moving forward to the pubis aboutone-inch anterior to the iliac crest, was marked along theline of marker at the operation site (Figure 2).

Entering the retroperitoneal cavity

The skin and subcutaneous fat were incised. After dissectingthe abdominal muscles, the retroperitoneal cavity was

entered by penetrating the posterior end of the transversusabdominis muscle using a long-handle curved hemostat.The psoas muscle was identified by sweeping away theretroperitoneal fat.

The L4-5 disc was palpated along the anterior margin ofthe psoas muscle. A malleable retractor placed against theanterior longitudinal ligament (ALL) separates the softorgans (ureter, great vessels) from the disc. A 2-mmKirschner wire (K-wire) is hammered into the proximalportion of the L5 vertebra, and a lateral C-arm image isobtained to check the disc level (Figure 3).

Figure 1The trunk is placed absolute vertically; the operating table isbended to open up the lateral space, and the hip is flexed. Beforedraping, the skin over the index disc levels is marked with an oilpen

Figure 2The entry point to the retroperitoneal cavity is at the posterior endof the transverse muscle (arrow); if penetrating the muscle tooanterior, the peritoneal cavity will be entered

Figure 3The common iliac vein (arrow A) runs at the anterolateral cornerof the L5-S1 disc. Before mobilizing the tethered CIV from thedisc, the iliolumbar vein (arrow B) has to be divided. The ILV isusually at the waist of the L5 vertebra. The ILV is exposed bydissecting the psoas muscle backward and fixed in situ usingK-wires (not shown) above and below the vein. The engorgedILV is shrunk by using the retracted muscle pressure to stopfeeding blood from entering the lumen. To shrink the ILV furtherand stretch it a little longer, a sucker head (arrow C) is gentlypressing at the junction of the CIV and ILV. The ILV is coagulatedat its mid-portion and leave a safe length of stump connectingthe CIV

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Identifying and handling the iliolumar vein

The psoas muscle covering the L5 vertebra was identifiedand carefully dissected away going above downwards tolook for the iliolumbar vein (ILV). The ILV is usually locatedat the waist of the L5 vertebra and runs the same courseas the segmental vessels.

After the ILV was identified, the psoas muscle above andbelow the vein was dissected backward maximally toexpose the ILV fully, and the dissected muscle was fixedin situ using two K-wires hammered into the L5 vertebraabove and below the vein. This maneuver helps to shrinkthe size of ILV. The dissected psoas muscle overlying theILV exerts pressure on the vein and reduces afferent bloodfrom entering the ILV lumen. The shrunk ILV was stretcheda little longer and shrunk further by a sucker head gentlypressing at the junction of ILV and common iliac vein (CIV).The sucker head was also used to protect the CIV duringbipolar diathermy. The mid-portion of the exposed ILVwas then coagulated with bipolar coagulation and dividedafter leaving a safe length of ILV stump connecting theCIV.

Protecting the common iliac vein and discectomy

After division of the ILV, the CIV was carefully mobilizedaway from the anterolateral aspects of the L5 vertebraand the L5-S1 disc and protected by placing a malleableretractor against the ALL. The lateral annulus of the L5-S1 disc was then exposed by fixing the dissected psoasmuscle by retracting the deissected psoas muscle usingtwo K-wires hammered in the L5 vertebra and the sacrum.The disc space was then prepared for fusion (Figure 4).

L5 lateral wedge osteotomy and preparation of bedfor fusion

At first lateral distal L5 wedge osteotomy was performedto improve the working field in cases with obliquetrajectory and narrowed disc space. The disc tissue andthe cartilaginous end plates were excised and space forfusion was prepared by doing decortication. Bone graftswere packed inside the space prepared and then a cagewas hammered into the disc space behind the ALL underC-arm control. The K-wires were removed and the woundwas closed without drainage tube.

In simultaneous two-level fusion (L4-5 and L5-S1), theL4-5 level was prepared thereafter. The fusion procedureof the L4-5 level was substantially easier since there wasno need to handle the venous system. The sympatheticchain running along at the anterolateral aspect of the lumbarcolumn had to be severed in order to do discectomy.

■ Results

The mean blood loss and operating time are listed in Table1. The mean hospital stay was 6.8 days (range, 4 to 10days).

■ Anatomical variations

The main anatomical variations encountered and relatedto surgical approach are as follows:1. The iliolumbar vein, and2. The variable distance of the intercristal line (ICL) to

the L5-S1 disc.

1. Variations of the ILV and tethering of the CIV

In 32 patients (76.2%) the CIV was tethered by the ILV.The CIV coursed over the anterolateral aspect of the L5-S1 disc, and the ILV had to be divided before mobilizingthe CIV away from L5-S1 disc for discectomy. In the rest

Figure 4The trajectory is oblique in the middle and low-seated L5-S1discs. Lateral wedge osteotomy (arrow) of the L5 vertebraimproves the working field

Table 1: Mean blood loss and operating time(excluding decompression and graft harvesting)

1-level 2-level

Mean Blood loss 120 ml 250 mlRange 50-250 150-800

Mean operating time 75 min 110 minRange 60-120 90-300


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of the patients (23.8%) the ILV was absent and that theCIV was not tethered. It could be mobilized easily andprotected.

The courses of the 32 ILVs were: at the waist of L5 vertebra(n=24, 75%), near the L4-5 disc (n=3, 9.4%), near theL5-S1 disc (n=4, 12.5 %), and one ILV was just sittingon the L5-S1 disc (3.1%). The diameters of the ILV wereestimated from 5 to 12-mm (Figure 5A, B & C).

2. Distance of the ICL to the L5-S1 disc

This was referred to the position of the L5-S1 disc in thepelvis7. There were three varieties: shallow, middle, anddeep; and the influence of iliac crest upon accessibility weredescribed:

1. Shallow, or high-riding L5-S1 discs (n=8, 19%)

In high-riding L5-S1 disc, the ICL was parallel to or slightlyabove the L5-S1 disc level. Lateral approach to theshallow L5-S1 discs was straightforward with littlehindrance of the iliac crest, and not unlike approaching tothe L4-5 disc. The visual and working fields were excellent.

2. Middle, the ICL crossing the L4-5 disc (n=30, 71%)

In the most common type of middle ICL, the iliac crestslightly hindered the maneuverability of the tools fordiscectomy. Maneuverability and visibility wereconsiderably improved by L5 lateral wedge osteotomy.Osteotomy was also necessary in narrow discs withosteophytes.

3. Deep, or low-seated L5-S1 disc (n=4, 10%)

In the least common type of low-seated L5-S1 disc (the

ICL crossing in the middle of L4 vertebra), maneuverabilityof the tools and visibility of the disc were moderatelyhindered by the iliac crest due to more obliquity oftrajectory than the middle ICL; they were also improvedby L5 osteotomy. The long-handled tools were pressedagainst the crest with some force to open up the disc spaceslightly to facilitate maneuvering the tools inside the disc.

■ Left and right approach (Figure 6)

There was no technical difference between left and rightapproach to the L5-S1 disc, except that in right approach,the vena cava was nearer to the lumbar column than theaorta of left approach.

Perioperative complications

One incidence of ILV injury occurred during the attempt

Figure 5A. High-riding L5-S1 disc. The intercristal line (ICL) is near the L5-S1 level, lateral access is easy. B. Middle. The ICL traverses the L4-5 disc, and this is the most common type. C. In low-seated L5-S1 disc, the ICL traverses the L4 vertebra. Note that the cylindrical cage(arrow) at the L5-S1 level is in transverse direction

Figure 6The patient (57 years old female) was diagnosed of discogenicpain with degenerative scoliosis of right lumbar curve. In orderto jack up the tilted discs, right approach was used to fuse theL4-5 and L5-S1 levels (left, arrows). At 12 months follow-up, CTimage shows solid union (right)

L5

L5L5

L4

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of ligating the engorged ILV and the resulted profusebleeding (700 cc) was stopped by tamponade with massivegauze padding for 30 minutes. Fusion procedure wascompleted after hemostasis. In the other case, the venouswall of CIV was found impinged with the cylindrical cagein the disc space after cage insertion, it was left alone andno sequel occurred.

One patient suffered from left L5 nerve incomplete injuryfor revision of failed ALIF and the cause was unknown.Three possibilities were postulated: injured by the K-wire,compressed by the bone graft, or excessive traction of thepsoas muscle.

There was no retrograde ejaculation in male patients, deepvein thrombosis, deep infection, and no death. There wasno graft protrusion into the spinal canal or cage migration.The sympathetic chain was severed in 40 patients (95.2%)and resulted in postoperative ipsilateral warm leg due tounopposed parasympathetic effect of vasodilatation. Thesymptom was resolved within 6 months.

The major perioperative complication rate was 4.8% (n=2,one vascular and one nerve), and there was no lateapproach-related complication at the final follow-up.

■ Discussion

The inaccessibility of the L5-S1 disc using lateralretroperitoneal approach has been imputed to the hindranceof the iliac crest. However, it is felt that the major obstacleis not the iliac crest itself, even in the deep-seated L5-S1discs. Instead, it is the venous system, especially, theiliolumbar vein and the tethered common iliac vein, thatmakes lateral approach challenging.

Peretti in 1996 using laparoscopy in 4 patients could notreach the L5-S1 disc due to obstruction by the iliac crest.10

McAfee in 1998 also used endoscopic surgery in 18patients and the lowest accessible was 4th lumbar disc. Hestated that endoscopic lateral approach to the L5-S1 discis usually not possible.8 Wolfla in 2002 reported opensurgery in 15 patients, and also stated that true lateraltrajectory is not possible for the L5-S1 disc and instead,they used 45-degrees of oblique trajectory and inserted ashort, 12 or 14-mm long of cylindrical cage for interbodyfusion.11 Bergey in 2004 also used endoscopic lateral trans-psoas approach in 21 cases but none of the L5-S1 dischad been fused and he stated that in order to access theL5-S1 disc, part of the iliac crest might have to be excised.2

In the recently introduced trans-psoas or so called extreme

lateral interbody fusion or XLIF technique in 13 patientsin 2006 by Ozgur and Pimenta, likewise the L4-5 discwas the lower limit.9

The inaccessibility of the L5-S1 disc by lateral approachbecause of the anatomical barrier is known. We feel thatthe iliac crest makes lateral access cumbersome, but not atrue obstacle. In the high-riding L5-S1 disc, the ICL isnearly parallel to the disc and the iliac crest does not poseany obstacle. In the middle ICL and low-seated settings,the iliac crest renders lateral access cumbersome. Thesolution suggested by us is to perform an L5 lateral wedgeosteotomy and press the long-handled tools against theiliac crest to improve the surgical field. All of the insertedcages in this series are of standard length and in transversedirection (Figure 5C and Figure 6), and there is no needto use a short cage in oblique trajectory as one author hassuggested.8

The vital issue to approach the fifth disc by the lateral rootis not the iliac crest but the adjacent venous system thatinadvertent injury may be fatal. It is known that the CIV isusually tethered by the ILV. Without division of the ILV, itis not possible to mobilize the CIV and perform lateralL5-S1 fusion. The high incidence of variations of the ILVis also well documented.4,6 We have also observedvariations of presence (in 76.2% of patients) or absence,location (high, at the waist of L5, or low) and its diameter.The absence rate (23.8%) of the ILV in this series isinconsistent with 100% presence rate in the literature.4,6

Due to variations in location, it is perceivable that in thisseries a certain percentage of the ILVs are outside of theconfined surgical field which is dissimilar to the cadavericsetting. Whether the ILV is present or not is unpredictable.Preoperatively we presume this vein is present in everycase.

We suggest searching for the ILV first, beginning from theL4-5 disc level downward rather than aiming the L5-S1disc directly because the ILV may be located at the waistof the L5 vertebra, near the L4-5 disc, or even sitting onthe L5-S1 disc (n=1). When the diameter of ILV is largethe method described by us is helpful (Figure 3). Beforethe ILV has been shrunk, the engorged vein is difficult tobe ligated and easily injured. But when it is shrunk andgently stretched, it can be handled easily and the ligatedeither by using a ligature or vascular clips or low-voltagebipolar diathermy. We have always preferred to use bipolarcoagulation for convenience. It should be noted that whenthe CIV has been mobilized and protected using a malleableretractor, a portion of the retracted CIV may protrude


17

into the surgical field and can be mistaken for a fibrousband and easily injured.5

The only case of ILV injury in our series occurred duringligation of an engorged ILV. In this case we had not utilizedour method of shrinking the vein. However, the bleedingwas stopped by the tamponade method effectively. Thesame method was used by us in three other incidences ofCIV injury. The CIV was penetrated by a 2.5-mm K-wire (n=2), or the venous wall was cut by a scalpel (n=1),resulting in massive bleeding. No attempt was made tosuture the tears. It was speculated that these four venousinjuries were all minor tears, and the tears werespontaneously sealed off given enough time and pressure.Tamponade method seems to be a viable strategy whenencountering massive venous bleeding by a small tearbefore considering formal repair.

Trans-psoas lateral approach has the advantage ofeliminating the process of muscle dissection and has beenadvocated by some authors for the L4-5 level and above.2,9

This method had been used only in one case of L5-S1pyogenic discitis that the surrounding anatomy wasobscured by the inflammatory tissue. Trans-psoas approachto the L5-S1 disc without knowing the actual location ofthe vessels in the vicinity of the disc may put the CIV andILV at risk. Even the easier of lateral access to the L4-5disc cannot be taken lightly since the ILV may be near theL4-5 disc and covered by the psoas. In addition, acadaveric study shows that, the risk of the lumbar plexusinjury is also increased in the lower lumbar column by trans-psoas approach, because the lumbar plexus is running moreanteriorly inside the psoas muscle at the lower lumbarlevels.1 We prefer to use the dissected psoas muscle massto protect the lumbar plexus and leave the psoas as intactas possible. In older patients with atrophied psoas muscle,the muscle is easy to dissect. In younger patients with strongand bulky psoas muscle, the muscle can be dissectedbackward gradually. The tension of the psoas muscle canalso be relieved by incising the psoas fascia without adverseeffect. The K-wire fixation technique is versatile and canbe used to fix the retracted muscle or to protect the greatveins. When the K-wires are properly placed there is littlebone bleeding after removal or rare risk of endangeringthe adjacent structure.

In accessing the L5-S1 disc, we advocate lateral approachover anterior trajectory for several reasons. There is noneed to displace the abdominal contents since there areonly two veins (ILV and CIV) which need to be takencare of. There is no risk of retrograde ejaculation; movingtools transversely inside the disc seems safer than inanteroposterior direction; and there are two sides to choosebased on the pathology.

In conclusion, degree of ease of lateral accessibility of theL5-S1 disc varies from easy (high-riding disc and absenceof the ILV) to cumbersome or challenging (low-seated discand presence of the ILV) and is not impossible. The degreeof difficulty heavily depends upon handling of the venoussystem to avoid vascular injury. Lateral access provides auseful alternative trajectory for various disc pathologiesand for simultaneous multi-level fusion, and great attentionshould be paid to the adjacent venous structure.

■ References

1. Benglis DM, Vanni S, Levi AD. An anatomical study of thelumbosacral plexus as related to the minimally invasive transpsoasapproach to the lumbar spine. J Neurosurg: Spine 10(2):139-44,2009.

2. Bergey DL, Villavicencio AT, Goldstein, et al. Endoscopic lateraltranspsoas approach to the lumbar spine. Spine 29(15):1681-8,2004.

3. Heth JA, Hitchon PW, Goel VK, et al. A biomechanical comparisonbetween anterior and transverse interbody fusion cages. Spine26(12):E261-7, 2001.

4. Jasani V, Jaffray D. The anatomy of the iliolumbar vein. A cadaverstudy. J Bone Joint Surg Br 84(7):1046-9, 2002.

5. Khoo LT, Rhim SC, Fessler RG. Complications during anterior surgeryof the lumbar spine: an anatomically based study and review.Neurosurg Focus 7(6):e9, 1999.

6. Kiray A, Akcali O, Guvencer M, Tetik S, et al. Iliolumbar veins havea high frequency of variations. Clin Orthop Relat Res 425:252-7,2004.

7. MacGibbon, Farfan HF. A radiologic survey of various configurationsof the lumbar spine. Spine 4(3):258-66, 1979.

8. McAfee PC, Regan JJ, Geis WP, et al. Minimally invasive anteriorretroperitoneal approach to the lumbar spine. Emphasis on thelateral BAK. Spine 23(13):1476-84, 1998.

9. Ozgur BM, Aryan HE, Pimenta L, et al. Extreme Lateral InterbodyFusion (XLIF): a novel surgical technique for anterior lumbarinterbody fusion. Spine J 6(4):435-43, 2006.

10. Peretti F. Hovorka I, Fabiani P, et al. New possibilities in L2-L5lumbar arthrodesis using a lateral retroperitoneal approach assistedby laparoscopy: preliminary results. Eur Spine J 5(3):210-6, 1996.

11. Wolfla CE, Maiman DJ, Coufal FJ, et al. Retroperitoneal lateral lumbarinterbody fusion with titanium threaded fusion cages. J Neurosurg96:50-5, 2002.

Address for correspondenceDr. Jin Fu Lin : Email : [email protected]

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Ossified yellow ligament causing thoracic myelopathy:The management dilemmas

Sandeep Mohindra, MD, Rahul Gupta,* MD, Rajesh Chhabra, MD,Sunil K. Gupta, MD, Virender K. Khosla, MDDepartment of Neurosurgery, Postgraduate Institute of Medical Education and Research, Chandigarh*Department of Neurosurgery, G. B. Pant Hospital, New Delhi

AbstractThirteen cases of ossified yellow ligamentscausing thoracic myelo-radiculopathy aredescribed. The clinical presentation,associated other findings along with differentialdiagnoses are discussed. The detailed neuro-radiological findings, including CT scans andMRI scans are presented. The surgicaltechnique of drilling and yellow ligamentexcision is described in detail. Even when poorsurgical outcome is accepted world-wide, wepresent a relatively favourable neurologicaloutcome at follow-up.

Key Words❉ Ossified yellow ligament

■ Introduction

Ossification of ligamentum flavum or yellow ligament (OYL)leading on to thoracic myelopathy is a rare entity.5 As lowerthoracic spine is the usual site of pathology, the spasticparaparesis is the common presentation.4 Till the presenttimes, the pathogenesis of this entity remains far fromestablished. Initially thought to involve Japanese race, thisdisease is being increasingly reported from other parts ofworld, including Indian subcontinent. 5

In the present communication we describe a short seriesof 13 patients, harboring OYL as a cause of thoracicmyelopathy.


Since January 2003, a total of 13 patients harboring OYLwere managed in our Department of Neurosurgery. Theclinical presentation and epidemiological features of thesepatients are described in Table 1. Men were afflicted more

often than women.6,1 The patients’ age ranged from 32 to67 years, but the majority were in 4th or 5th decades oflife. There was predominant involvement of lower thoracicspine, 4 whereas cervical spine was spared in all (Table 1).

■ Clinical presentation

Spastic paraparesis was the commonest presentation evenwhen sensory loss was noted in almost all patients. Bowel-bladder involvement was noted in 6 of 13 patients. Clinicalgrading was allocated to all patients pre-operatively basedon Nurik’s Scale. All the patients were bed-ridden pre-operatively.

■ Diagnostic procedures

After detailed neurological assessment and findings,radiological evaluation was carried out. Plain radiographsare hardly of any utility, but we continue to ask for theseso as to rule out other causes of compressive myelopathylike Pott’s spine or osteoporotic vertebral body collapse.MRI (Figures 1 to 4A & B) was performed for all patients,which showed sharp beak- like projections from behind,compressing the cord and significantly obliterating the spinalcanal. Only one patient had single level OYL (Figure 3),while rest 12 had widespread involvement of thoracic spinewith multiple beak-like projections (Figure 2). CT scans,along with 2D-reconstruction of involved spinal regionswere performed to delineate the extent of calcification/ossification (Figure 5A, B & Figure 6).


All patients underwent decompressive laminectomies atinvolved levels. High-speed drills were used and the drillingwas commenced “outside in” under operating microscope.Laterally, identification of dura was commenced and thedural surface was followed medially, detaching ossifiedplates all around, leading to floating islands of bony plates.


19

Table 1: Summary of clinical manifestations of the ossification of ligamentum flavum

Age/ Level Symptomatology-Duration Bowel/Bladder Reflexes Nurik’s Associated Surgery Follow- Nurik’sSex grade pathology up grade

pre- post-operative operative

50/F D11-12 lumbago-5 years involved brisk III nil D11-12 4 years VLaminectomy

45/M C7-D3 gait disturbance-2 months uninvolved brisk III CCS C7-D2 1 year IILaminectomy

36/F D8-D12 spastic paraparesis- uninvolved brisk V nil D7-12 9 months V6 months Laminectomy

39/M D3-4, 9-12 spastic paraparesis- involved brisk V LCS D3-12 10 years III6 months Laminectomy

67/F D2-4 lower limb numbness- uninvolved brisk IV nil D2-4 3 years II1.5 years Laminectomy

45/M D10-12 spastic paraparesis- involved brisk III nil D9-12 1.5 years III9 months Laminectomy

40/M D7-11 spastic paraparesis- involved brisk V nil D7-12 15 IV3 years Laminectomy months

54/M D5-9 gait disturbance-1 months uninvolved brisk IV nil D5-10 5 years IILaminectomy

57/M D7-11 lumbago-3 years involved brisk IV nil D6-12 6 months IILaminectomy

47/F D8-12 spastic paraparesis- uninvolved brisk IV nil D7-12 9 months I11 months Laminectomy

42/F D7-11 gait disturbance- uninvolved brisk III nil D7-12 18 II6 months Laminectomy months

36/M D8-11 lumbago- involved brisk V nil D7-12 3 years III8 years Laminectomy

32/M D10-L3 spastic paraparesis- uninvolved brisk III LCS D10-L5 2 years I4 months Laminectomy

Figure 3Sagittal section (T2-weighted MRI)showing single level involvement ofthoracic spine

Figure 2Sagittal section (T2-weighted MRI)showing multiple level involvement oflower thoracic spine by the beak-likeprojections, which are shining againsthyper-intense CSF

Figure 1Sagittal section (T1-weighted MRI)showing hypo-intense masscompressing thoracic cord from behind

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Figure 5A & BAxial section (CT scan) showing ossified yellow ligamentencroaching intra-spinal space

Figure 6Sagittal section (2D reconstruction) showing multiple level spineinvolvement

In all cases, we excised all ossified ligaments anddecompression was achieved laterally till the exiting rootsalong with dural sheaths were noted. Dura remained intactin all patients. The usage of roungers was kept to minimum,while bone nibblers were not used at all.

All patients had worsening of neurological statusimmediately after surgery, which improved after 48 hourspost-operatively. Spasticity and backache improvedminimally, while motor power recovered to near-normallevels in almost all cases.

■ Discussion

“Thoracic Spinal Stenosis,” hypertrophic ossification ofligamentum flavum, ossified ligamntum flavum or OYL arefew names given to the same clinical entity.2 Classicallydescribed among Japanese,2,5 the disease probably isspread out worldwide and has been reported from Indiansubcontinent also. Most of the patients present with severeunrelenting dysasthesias, along with severe lower limb

Figure 4A & BAxial section (T2-weighted MRI) showing completely obliteratedCSF space

A

B

A

B


21

spasticity and bowel-bladder involvement.5

That the involvement of lower thoracic spine is morecommon as compared to upper is a well established andaccepted fact.8 However, the etio-pathogenesis remainsunclear.7 As there is transition from the stable thoracic spineto the mobile lumbar region, the thoraco-lumbar junctionis particularly more vulnerable to micro-trauma.7,8

Extra-dural thoracic compressive myelopathy calls forvarious differential diagnoses. Infectious cause includestuberculosis, which is of significant importance in Indiansub-continent, while developmental anomalies likeMorquio-Brailsford disease or Maroteaux –Lamysyndrome (with gibbus) or achondroplasia associatedthoracic spinal stenosis (without gibbus) may occur. Rarely,thoracic disc herniations may cause thoracic myelo-radiculopathy.2 Metabolic imbalance like Paget’s diseaseor rheumatoid granulomata may lead on to thoracicmyelopathy. Skeletal fluorosis, as an association with OYLhas also been reported.3

Such exhaustive varied reasons behind thoracicmyelopathy ask for thought provoking radiological,neurological, and bio-chemical examination of a patient.

As tuberculosis is endemic in Indian sub-continent, plainradiographs are usually performed for all patients presentingwith backache.2,3 Further, OPLL is another entity whichmay be detectable on plain radiographs. Myelography isusually not required in the present era. CT scan remainsan important investigative tool.1 It may determine the exactlocation and extent of OYL. Axial sections of CT scandetermine the extent of lateral spread of OYL and foraminainvolvement. Also, 2-Dimentional reconstruction canprovide the exact location and extent of spine involvement(Figure 6). For a given case of thoracic myelopathy, MRIremains the radiological investigation of choice.1 OYLpresent as beak-like projections from behind, protrudinginto and obliterating the spinal canal. On T1-weightedscans, these are hypo-intense lesions like candle droppingsinvolving spine in a widespread fashion (Figure 1). On T2-weighted scans, these are hypo-intense lesions, which shineagainst hyper-intense signals of CSF (Figures 2, 3). Axialsections of T2-weighted scans show completely obliteratedspinal canal and CSF spaces due to crowded intra-spinalstructures (Figure 4A & B). MRI is also required so as todescribe any T2-weighted signal changes within the cordsubstance.6,9 Often, CT scan is performed, even when MRIhas been done, so as to better delineate the anatomical

intra-spinal structures (Figures 6 to 8). Hence, bothinvestigations should supplement each other for betterunderstanding of the pathology.6

Even when various surgical techniques like laminoplasty,foraminotomy, extended partial laminectomy have beendescribed, decompressive laminectomy along withcomplete excision of ligamentum flavum remains the surgicalprocedure of choice.2,3,9

Among the first 5 patients, the results remained equivocaland spasticity failed to respond to surgical treatment, evenat a follow up of more than 3 years.

However, last 8 patients were managed surgically usinghigh speed drills (Midas Rex AM8, AM8D, Classic G8-130, G8-130D). Intra-operatively, the dura was identifiedat normal regions first and was then followed cranially andcaudally. The drilling was commenced strictly from lateralto medial and outside in. The medial most ossified fragmentwas left adhered to dura till the end of surgical procedureand was detached from all around making it an island offree floating papery-bone, which was gradually peeled offfrom the dura under microscope.

Lateral extent of bony decompression was carried till allexiting roots from thecal sac were visible bilaterally. Durawas handled with great caution to prevent problems likeCSF leak, wound infection, and intra-operative corddamage. We operated all patients in prone position, onarch bar. Bone nibblers were forbidden during entiresurgery, whereas roungers of 1mm were used minimallyand at the lateral edges of lamina (Figure 7A, B & Figure8). Decompression was carried cranially and caudally onelevel more than the involved levels. Muscle layer was closed

Figure 7A & BSagittal section (2D reconstruction) post-operatively showingmultiple level spine involvement

A B

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in single layer while skin and subcutaneous layers wereclosed separately.

Even when poor long-term outcome has been described,we believe that sufficiently good neurological status maybe achieved. Spasticity tends to respond the worst whereas power improves to near-normal state in most of thepatients. Bowel- bladder problems also respond well tosurgery. Dyasesthesis continue to be problematic for mostof the patients and various pain modulators are put to use.

■ Conclusion

OYL remains an important cause of thoracic myelopathyin Indian subcontinent and the entity remains under-estimated and under-reported due to scarcity ofradiological investigations in less-privileged parts of India.MRI and CT scans are the investigations of choice andthe classical radiological findings should be easilyrecognizable by the clinicians treating the spinal disorders.

The surgical intervention should be carried on at highercenters, where high-speed drills and operating microscopesare available, so as to have good surgical outcome.

■ References

1. Hanakita J, Suwa H, Nagayasu S, Nishi S, Ohta F, Sakaida H.Clinical analysis of ossified thoracic ligaments and thoracic dischernia. Neurol Med Chir (Tokyo) 31:936-42,1991.

2. Mohindra S, Chhabra R, Mukherjee KK, Gupta SK, Vaiphei K, KhoslaVK. Spinal compression due to ossified yellow ligament: a shortseries of 5 patients and literature review. Surg Neurol 65:377-84,discussion 384, 2006.

3. Muthukumar N. Ossification of the ligamentum flavum as a result offluorosis causing myelopathy: report of two cases. Neurosurgery56:E622; discussion E622, 2005.

4. Pantazis G, Tsitsopoulos P, Bibis A, Mihas C, Chatzistamou I, KouzelisC. Symptomatic ossification of the ligamentum flavum at the lumbarspine: a retrospective study. Spine 33:306-11, 2008.

5. Park BC, Min WK, Oh CW, Jeon IH, Kim SY, Kyung HS, Oh SH.Surgical outcome of thoracic myelopathy secondary to ossificationof ligamentum flavum. Joint Bone Spine 74:600-5, 2007.

6. Pascal-Moussellard H, Cabre P, Smadja D, Catonné Y. Symptomaticossification of the ligamentum flavum: a clinical series from theFrench Antilles. Spine 30:E400-5, 2005.

7. Payer M, Bruder E, Fischer JA, Benini A. Thoracic myelopathy dueto enlarged ossified yellow ligaments. Case report and review ofthe literature. J Neurosurg 92 (Suppl):105-8. Review, 2000.

8. Yano T, Doita M, Iguchi T, Kurihara A, Kasahara K, Nishida K, YoshiyaS. Radiculopathy due to ossification of the yellow ligament at thelower lumbar spine. Spine 28:E401-4, 2003.

9. Yatsuzuka H, Kitajima T, Taguchi Y, Sakai H, Nakamura N. A case ofossified yellow ligaments (ossified ligamenta flava) of the thoraco-lumbar region and magnetic resonance imaging. No Shinkei Geka14:1121-5. Japanese, 1986.

Address for correspondenceDr. Sandeep Mohindra : Email : [email protected]

Figure 8Post-operative axial section (CT scan) showing extensive laminectomy and decompressed lateral gutters


23

Lumbar canal stenosis due to ossification in the ligamentumflavum: A rare entity: Case reports with review of literature

Shradha Maheshwari, Paresh Sodhiya, Manish Mair, Meenal S. Hastak,* MDP. S. Ramani, MDDepartment of Neurosurgery, Lilavati Hospital and Research Center, Mumbai*Department of Histopathology, Lilavati Hospital and Research Center, Mumbai

AbstractOssification of the ligamentum flavum is thedisease predominantly reported to affect thethoracic region and rarely lumbar or cervicalregion. Only 47 cases have been found in worldliterature reporting its incidence in the lumbarregion.5 We report two cases of a middle-agedfemale who presented to us with the complaintsof persistent low backache and progressiveneurogenic claudication over a period of morethan 5 years. A positive history of traumapreceded in one case. The patients hadexcellent surgical outcome followingdecompressive laminectomy. Both cases didnot have sciatic pain. We discuss these caseswith a possible role of trauma in itspathogenesis and highlight the importance ofthis such underreported disease worldwide.

Key Words❉ Ossified ligamentum flavum❉ Lumber canal stenosis❉ Laminectomy❉ Neurogenic claudication

■ Introduction

Symptomatic ossification of the ligamentum flavum is a raredisorder. Ossified ligamentum flavum was first described

by Poglar in 1920.12 This condition was reported in Asia,mostly in Japanese people, and therefore it has been termedas “Japanese disease.” It mostly involves the thoracic spineand rarely the lumbar or the cervical spine.1,5 Its exactetiopathogenesis is still not well established and subjectedto debate. It is widely accepted that ossification ofligamentum flavum is a slowly progressive disease and earlydiagnosis is difficult.5

Though all reported cases have been subjected to operativemanagement with excellent outcome4,5,7,8 nothing isconvincingly stated regarding its long term outcome andrecurrences considering the rarity of the cases. In our caseswe propose a correlation of a direct mechanical traumainitiating a hyperostotic tissue response which culminatedinto ossification of ligamentum flavum in one case and inthe other case positive history of trauma was notforthcoming. In view of long history and village life shemight have injured her spine.

■ Case reports

Case 1

A 39-year-old female presented with complaints of low backpain for 5 years. Her symptoms had begun followingaccidental fall on the back from the staircase (Figure 1 A , BC, D & E). It caused no immediate consequences other

Figure 1A , B, C, D & EA & B: T2WI & T1WI images showing no evidence of ossification in the ligamentum flavumC, D & E: Axial cuts showing prolapsed discs

A B C D E

L3-L4 L5-S1L1

L3

L5

L1

L3

L5

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than a dull backache lasting for a few days. Subsequentlypatient started getting episodes of back pain which wereworse with exertional activities and she felt relief with restand pain killers. The X-rays of the lumbar spine were normaland MRI showed presence of prolapsed discs.

A few years later she started having claudication pain inboth her legs which kept on worsening. She presented tous with rapid progression of symptoms over past twomonths characterized by pain and numbness on standingor walking for a few steps. Symptoms were more severeon right side than on left. There was no associated bowelor bladder dysfunction. She did not have any other medicalillnesses. Family history was insignificant. Her brother hasbeen operated upon for a lumbar disc prolapse.

She was slightly overweight, weighing 62 kgs with a heightof 152 cms. Neurological examination revealed bilaterallyabsent ankle jerks. Straight Leg Raise test was negative.Pulsations in the limbs were normal. There was no wastingin the muscles and there was no sensory loss. There wasloss of lumbar lordosis. Her back was stiff and movementswere restricted and painful. A clinical diagnosis ofneurogenic claudication because of lumbar canal stenosiswas made.

X-rays of the lumbar spine showed early spondyloticchanges and loss of lumbar lordosis. A faint nodularcalcification was appreciable on lateral view of the lumberspine in the L3-4, L4-5 neural foramen (Figure 2). Thefacet at L3/4 and L4/5 looked hypertrophic. The discspaces were normal and there was no spondylolithesis.

MRI of the lumbar spine confirmed early spondyloticchanges. At the level of L3-4 and L4-5 interspaces thecanal was compromised and the thecal sac wascompressed by soft tissue and incurling of the ligamentumflavum which was hypointense on T1WI and T2WI

sequences. Narrow bony canal was evident. In axial cutsthe subarachnoid space was obliterated by the pathology.Screening MRI of whole spine suggested early spondyloticchanges in the cervical region and absence of any otherlesion (Figure 3A, B & C).

As compared to an earlier MRI done 4 years back thelumbar canal stenosis had increased significantly. A CT scanof the lumbar region confirmed presence of calcification inthe ligamentum flavum in the L3-4 and L4-5 interspaces.

Case 2

A 65-year-old female presented to us with low back painand progressive history of neurogenic claudication of morethan 5 years duration. There was no definitive history ofsciatica. Being in the village, she was accustomed to hardwork but no definitive history of trauma to the spine wasforthcoming. She felt relief on lying down and withpainkillers. There was no bladder or bowel dysfunction.

Figure 2X-ray showing ossification of the facet joint

Figure 3A, B & CDense ossification in the ligamentum flavum causing compression on the thecal sac and obliteration of the subarachnoid space

A B C

L3

L4

L2 L3-4L4-5

L5


25

Very recently within the last one year, she has beendiagnosed of diabetes and hypertension. Her family historywas insignificant.

She was slightly overweight with a weight of 66 kgs andheight was 148 cms. Neurological examination revealedbilaterally absent ankle and knee jerks. SLR was negativebilaterally. Pulsations were normal in the limbs. There wassignificant wasting in the left calf muscles and lumbarlordosis was obliterated. A clinical diagnosis of neurogenicclaudication due to lumbar canal stenosis was entertained.

X-rays of the lumbar spine showed less of lumbar lordosisand early spondylotic changes. Facet joints werehypertrophied and disc spaces in the lower lumbar spinewere slightly reduced. MRI of the lumbar spine showedsevere compression of the theca from L

3 to S

1 by soft tissue

compression and incurling of the ligamentum flavum whichwas hypointense on both T1 and T2 weighted images. Inaxial cuts, the subarachnoid space was obliterated.

We are describing here operative findings in detail of case1 (Figure 4A, B, C & D).

■ Operative findings

A planned decompressive laminectomy at L4 and part L3was done. Use of high speed drill greatly simplified thelaminectomy which was otherwise very difficult. Lumbarcanal was severely stenosed and there was no apparentspace between the lamina, calcified ligamentum and the dura.The lateral recess was filled with hard ligamentum flavum.There was thick compact bony ligamentum flavum betweenthe laminae and dura posteriorly and laterally. The dura,though severely compressed, was neither infiltrated northinned out. The calcified plaques were inseparably adheringto it at places. It was very carefully excised after separating

it from the dura using micro techniques (Figure 5).

■ Ossified ligamentum flavum being lifted of thedura with microdissection

The dura was decompressed. The lateral recesses wereopened out and the nerve roots were followed up to theexit foramina and decompressed (Figure 6A & B).

There was no disc prolapse or evidence of ossification ofthe posterior longitudinal ligament. A small rent in the durawas sealed with fibrin glue and muscle patch.

■ Post operative course

An uneventful hospital course was characterized by relieffrom claudication pain and backache. She was quicklymobilized. Post operative MRI showed gooddecompression of the thecal sac. There was still ossificationin the facet joints. She was discharged from the hospitalon the third day with a home plan for physiotherapy (Figure7A, B, C, D & E).

Figure 5Ossified ligamentum flavum being lifted of the dura

Figure 4A, B, C & DExtensive ossification in the ligamentum flavum causing compression of the cauda equine in the lower lumbar spine

A B C D

L3 L4 L5

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B

Figure 7A , B, C, D & EPostoperative MRI showing good decompression of the thecal sac but presence of ossification in the facet joints

A B C D E

Figure 6A & BDecompressed dural sac after excision of ossified ligamentum flavum

■ Histopathology

Histopathological examination of the specimen confirmedthe presence of ossification with lamellar bone formationin the ligamentum flavum. There was thick bone formationand the transition zone between the ligament and the bonecould be distinctly identified with osteoblastic rimming ofthe osteoid tissue. Few osteoclastic giant cell were alsoseen in the transition zone (Figure 8A & B).

■ Discussion

Symptomatic ossification of the ligamentum flavum is a rare

disorder affecting mostly the thoracic spine.1,5 Only fewauthors have published surgically treated cases thatinvolved patients with ossification of ligamentum flavum inthe lumbar spine.4,5,7,8,15,16 So far only 47 cases having beenmanaged surgically are reported in the literature.5 Of the47 reported cases 26 were females suggesting a slightfemale preponderance. The age range had been between27 years – 78 years. Our patients were of 39 and 65 yearold females.

The entity of ossification in the ossification of ligamentumflavum is mainly reported in the literature coming fromJapan.1,7,8,16 There are only a few sporadic case reports

Figure 8BHistopathology showing osteoblastic rimming of osteoid tissuewith few osteoclastic Giant cells

Figure 8AHistopathology examination showing yellow ligament, transitionzone and abundant ossification in the yellow ligament

A

L3L4 L5


27

from Europe, N. America, Africa, and other Asian countriesshowing the occurrence of ossification of ligamentumflavum in the thoracic or cervical spine.1,5 Reports fromIndia are scanty. Kurihara et al have reported an incidenceof 8.4% of ossification of ligamentum flavum in the lumberspine in the Japanese population on the basis ofroentgenological analysis.8 He found frequent involvementof the upper and middle lumbar spine. Coulier,3 in an articlein French, had analyzed CT scans of lumber region. Hereported a prevalence of 5.44% of ossification inligamentum flavum. In more than 96% of cases, theossifications remained confined to the lateral articularportion of the ligament; the central ossifications were veryrare. The radiological appearances of the ossification ofligamentum flavum in thoracic spine has been classified as– hook, beak, linear and nodular types.13 The radiologicalappearances of ossification of ligamentum flavum dependson the site at which calcification occurs. In most cases,ossification of ligamentum flavum occurs at the attachmentof the ligamentum to the inferior facet, the superior facet,or both, and most commonly has the appearance of a hookor beak.

Epstein et al,4 in a retrospective analysis of cases operatedfor spinal stenosis, had reported that 2.3% of patients hadossification of ligamentum flavum or OPLL or both. UsingOdom’s criteria, good to excellent outcomes were achievedin 73% of OPLL and 83% of ossification of ligamentumflavum patients with laminectomy alone.

The pathogenesis of ossification of ligamentum flavum isstill debatable.5 An increase in the concentration offibronectin or in the concentration of bone morphogenicproteins are proposed to cause both OPLL and ossificationof ligamentum flavum.6,9 An occupation-associatedrepeated mechanical stress and lumbar trauma in thepathogenesis of OLF is another possible mechanism.5,16 Itis known that incidence of ossification of ligamentum flavumis higher in patients with diffuse idiopathic skeletalhyperostosis, flurosis, ankylosing spondylitis, systemicdiseases such as diabetes mellitus, obesity, hyperinsulinism,hemochromatosis and calcium metabolic disorders.5,11

Okada et al10 found that ossification of ligamentum flavumis preceded by calcification and hypertrophy. Theossification initiates on the capsular side of the ligament infront of the facet joints and expands later on the outersurface of the ligament towards the dura. This capsularoutgrowth rarely impinges on an existing nerve root causingradiculopathy or foraminal stenosis.

According to Epstein NE et al.,4 ossification of ligamentum

flavum originates as ingrowths of fibrocartilage due toproliferation of type II collagen. Ligamentous hypertrophythen follows and deposition of calcium crystals lead toprogressive ossification which begins laterally at the enthesisand extends medially.2 Crystals consists of calciumpyrophosphate dehydrate with occasional hydroxyappetiteand calcium orthophosphate.

Apparently ossification of ligamentum flavum alone mayremain asymptomatic and neurologic symptoms do notappear unless other factors, such as trauma, OPLL, orsevere degeneration, occurs. In our case, a welldocumented history of direct trauma initialized thesymptoms of low backache which progressed to featuresof lumbar canal stenosis in case 1. It is likely that an initialinflammatory response perpetuated the process ofossification of the ligamentum flavum. A pre-existing canalstenosis has further contributed causing the patient tobecome symptomatic and present much earlier. There wasno evidence of OPLL or diffuse idiopathic skeletalhyperostosis in our cases. The clinical presentation is non-specific and the presenting symptoms are indistinguishablefrom those seen in degenerative lumbar stenosis.Ossification of ligamentum flavum may lead to more severecauda equine and /or spinal nerve damage than other causesof lumbar stenosis.5 A MRI and a CT scan is reliablysuggestive of the pathology which can be confirmed onlyby intra operative findings and histopathological study.

A screening MRI of whole spine is mandatory in all suchcases to rule out other lesions. Any doubtful lesion shouldbe comfirmed with a CT scan. A CT scan can differentiateossification of ligamentum flavum from hypertrophy ofligamentum flavum.14 However, a preoperativedifferentiation between these two entities is not alwayspossible.5

Once the diagnosis is established, medical screening shouldbe done to rule out associated metabolic disorders. Thesuggested surgical techniques are laminectomy,4,7,8

laminoplasty,7,10 partial laminectomy, or fenestration1

depending on the extent of compression of the caudaequina. Early surgery prevents neurological deteriorationand is associated with significant clinical improvement. CSFleakage is the most common reported complication inpatients with hyperostotic lumbar canal stenosis.7

■ Conclusion

Ossification of the ligamentum flavum of the lumbar regionis a rare entity. Clinical presentation is indistinguishable from

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those of degenerative lumbar canal stenosis. A preoperativediagnosis is supported by MRI and CT scan and can onlybe confirmed intraoperatively and on histopathologicalevaluation. Meticulous microdissection and use of highspeed drill can avoid the potential complication of duraltear and CSF leakage. The whole spine should be screenedfor the presence of lesions in other parts. Associatedmetabolic disorders should be ruled out. Early surgery isassociated with excellent recovery.

■ References

1. Aizawa T, Sato T, Sasaki H, et al. Thoracic myelopathy caused byossification of the ligamentum flavum: clinical features and surgicalresults in the Japanese population. J Neurosurg Spine.5;514-9,2006.

2. Baba H, Maezawa Y, Furusava N, et al. The role of calcium depositionin the ligamentum flavum causing a cauda equine syndrome andlumber radiculopathy. Paraplegia 33:219-23, 1995.

3. Coulier B. Prevelence, morphology, and pathological implications ofossification of lumber ligamenta flavum: a large prospective CTstudy. JBR-BTR 82(2):53-6, 1992.

4. Epstein NE. Ossification of the yellow ligament and spondylosisand/ or ossification of the posterior longitudinal ligament of thethoracic and lumber spine. J Spinal Disord 12:250-6, 1999.

5. Georgios Pantazis, Parmenion Tsitsopoulos, Alexios Bibis, et al.Symptomatic ossification of the ligamentum flavum at the Lumberspine. Spine volume 33(3);306-11, 2008.

6. Hayashi K, Ishidou Y, Yonemori K, et al. Expression and localizationof bone morphogenic p[roteinsand BMP receptorsin the ossificationof the ligamentum flavum. Bone 21:23-30, 1997.

7. Kawaguchi Y, Oya T, Abe Y, et al. Spinal stenosis due to ossifiedlumber lesions. J Neurosurg Spine 4:262-70, 2005.

8. Kurihara A, Tanaka Y, Tsumura N et al. Hyperostotic lumber spinalstenosis. A review of 12 surgically treated cases withroentgenographic survey of ossification of the yellow ligament atthe lumbar spine. Spine 3:1308-16, 1988.

9. Miyamoto S, Yonenobu Ono K. Elevated Plasma fibronectinconcentration in patients with ossification of the posteriorlongitudinal ligament and ossification of the ligamentum flavum. Spine18:2267-70, 1993.

10. Okada K, Oka S, Tohge K, et al. Thoracic myelopathy caused byossification of the ligamentum flavum. Clinicopathologic study andsurgical treatment. Spine 16:280-7, 1991.

11. Philip V, Theodosopoulos, Phlip R. Weinstein. Ossification ofposterior longitudinal ligament and other enthesiopathies. YoumansNeurological Surgery; 5th edition, Saunders 4475-87, 2004.

12. Polgar F. Uber interakuelle wirbelverkalkung. Fortschr GebRontgenstr Nuklearmed Erganzungsbd. 40:292-8, 1920.

13. Sho Kudo, Minoro Ono, Walter J Russell. Ossification of thoracicligamenta flavum. AJR 141:117-21, 1983.

14. Sushil P, Anant K. Ossified- calcified ligamentum flavum causingdorsal cord compression with computed tomography-magneticresonance imaging features. Surg Neurol 41:441-2, 1994.

15. Weiss MH, Spencer GE. Ossification of a lumbar interspinousligament with compression of the cauda equine. J Bone Joint Surg(Am) 52:165-7, 1970.

16. Yano T, Doita M, Iguchi T et al. Radiculopathy due to ossification ofthe yellow ligament at the lower lumbar spine. Spine 28;E401-E404,2003.



29

■ Introduction

Herniation of the intervertebral disc with compression ofthe nerve root in the spinal canal is the most common causeof the low back pain in clinical practices. MRI is now thefirst modality of choice in all cases of spinal pathologies.Routine MRI protocols include T1 and T2 W images insagittal and axial planes.4 The routine imaging may beequivocal in many cases and may not explain the patientssymptomatology. This is especially true in cases of foraminaland extraforaminal discs. The new 3D heavily T2W gradientsequence (Constructive interference in steady state - CISSin Siemens, 3D FIESTA in GE) gives a millimeter slicethickness which improves the visualization of the spinalnerve roots and its relation with the herniated disc.5 It givesmyelographic images and may be important in lumbar spinalimaging when conventional T1 and T2 W images areequivocal.


During the last one year we have utilized this investigationin 3 cases where standard MRI could not explain the

patients’ symptoms. Having done these investigations wecould then established the relation between patients’symptoms, the herniated lumbar intervertebral disc and theoutgoing nerve root.

■ Case Reports

Case 1

This 42-year-old obese female CEO was travelling toAmsterdam from Mumbai. There was turbulence and theplane was jerking. She got acute pain in the back and theright sciatica. By the time she reached the airport her rightleg was like a log of wood. She had to take help of theAirport medical facility. She was told that she has developedacute disc syndrome and required admission to the hospital.However, she had an urgent meeting to attend so she tookstrong injections and returned to Mumbai after two days.She was immediately taken to the hospital. MRI study didnot obviously show a disc prolapse (Figure 1A & B) andshe was treated conservatively.

Over the next 2 months she received a variety of treatmentwithout much relief and in fact she developed right footdrop. EMG and nerve conduction studies confirmed rightL5 radiculopathy. When seen by us she had backache andright sciatica and she could not take weight on the rightleg. She was linking. Clinically, her back was stiff withrestricted and painful ROM. Right SLR was restricted.

MR neurography in lumbar discovertebral disease

Makarand Kulkarni, MD, Manoj Deshmukh, MD, Rashmi Siraslewala,Kajal Mehta,Sumer ShikareDepartment of Neuroradiology, Lilavati Hospital & Research Center, Mumbai

AbstractHigh spatial resolution is one of the majorproblems in spinal nerve imaging. Constructiveinterference in steady state (CISS- siemens/FIESTAC- GE) is a robust sequence in imagingthe spinal nerve pathologies.5 This report ofthree cases shows importance of thissequence in demonstrating the compressionof spinal nerve roots by herniated discsespecially in cases of foraminal disc herniationwhen the routine T1 and T2W sequences areequivocal.

Key Words❉ Neurography❉ Prolapsed disc❉ Foraminal disc❉ Extraforaminal disc

Figure 1 A & BThe standard MRI did not show significant disc prolapse at thelevel of L4-5

A B

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The power in right EHL was 0/5 and right TA 2/5. Therewas dense hypoaesthesia in the distribution of right L5 rootand particularly over right great toe. MR neurography wasdone and it clearly showed laterally placed disc compressingthe right L5 nerve root (Figure 2A & B).

She was expeditiously operated upon. Right L4-5 microlumbar exploration was done and the laterally prolapseddisc was excised after doing foraminetomy. She is relievedof pain and is now receiving physiotherapy for the rightfoot drop.

Case 2

A 54-year-old obese female patient presented with a historyof 2 months of backache in left sciatica. Gradually the sciaticpain had become more severe and she could not walk orkeep the left leg down on the floor. During the last 2 weeksshe was virtually bedridden.

On clinical examination the SLR on the left side wasrestricted to 30 degrees and she had developed weaknessin the left EHL. There was no wasting in the muscles andthe pulsations were normal. The back muscles were inspasm with painfully restricted spinal movements.

An MRI of the lumbar spine was performed on siemens1.5 T machine using routine T1, T2 sagittal and axialsections, showing diffuse posterior disc bulge with smallleft paracentral disc herniation on T2W sequence (Figure3A). The image morphology was not significant enough toexplain the patient’s symptomatology. An additional CISS

sequence was performed in sagittal plane and the imageswere reconstructed in coronal and axial planes. There wasa large left paracentral disc herniation compressing the leftsided traversing nerve root and clearly depicting thedeflection of traversing nerve roots (Figure 3B & C).

Figure 2 A & BMR neurography in the same patient clerarly demonstratedlaterally placed prolapsed disc at L4-5 on the right sidecompressing the right L5 nerve root

A B

Figure 3ARoutine T2 W image showing small left paracentral discherniation with compression of thecal sac but the patient’ssymptoms were disproportionate to the disc herniation

Figure 3B & 3CB: Axial sections with CISS sequence showing a large extrudedfragment (white arrow) of disc in the left lateral recess

C: CISS sequence with coronal reformation showing large leftparacentral disc herniation (black arrow) compressing anddeflecting the left sided traversing nerve root (white arrow)

B

C

A

disc

nerve rootnerve rootdisc


31

With these findings the patient was immediately operatedupon. Under general anesthesia in prone position a lumbarlaminectomy was performed followed by fourth lumbardiscoidectomy on the left side. With the informationobtained, the foramen was explored, foraminectomy wasdone, the root was decompressed and mobilized and thelarge protrusion of the disc was excised with completerelief of symptoms.

Case 3

A 52-year-old female patient had complained of backachefor more than 1 year. Recently over a period of 6 weeksshe had developed left sciatic pain and she had difficulty inwalking. On examination clinically her SLR was restrictedto 20 degrees and there was marked weakness in left TAand DHR. Ankle jerks were present. There was no wastingin the muscles and the pulsation was normal. Her backwas stiff and there was list of the spine with concavity tothe left side. She has been a known person of hypertensionfor several years.

An MRI of the lumbar spine with routine T1 and T2 Wsequence could not satisfactorily explain the patient’ssymptoms. Far lateral sections showed a foraminalcomponent compromising the left-sided neural foramen.CISS sequence was performed and it showed clearcompression of left L5 root in the foramen (Figure 4A, B& C). The path of the nerve root was deflected.

She was operated upon under general anesthesia, leftmicrolumbar discectomy was done. The root wasdecompressed by doing a foraminectomy. The foraminalportion of the disc was sequestrated and was outside thePLL fibers. It was excised. Patient obtained complete reliefof symptoms and received physiotherapy for improvement

in weakness of TA and EHL.

Case 4

A 49-year-old female, obese but nonhypertensive andnondiabetic had complained of backache of and on for along time. For the last few months she had complained ofleft-sided sciatic pain. However, 6 days back she was seenby a specialist consultant spinal surgeon. She hadcomplained of very severe left sciatic pain. She could notperform any of her day to day activities and she wasvirtually bedridden.

On examination clinically her left SLR was restricted to 40degrees but there was no obvious weakness in left DA orEHL but there was hypoesthesia over left great toe.Pulsations were normal and left ankle jerks were absent.Her back was straightened and stiff with painful restrictedspinal movements and obliterated lumbar lordosis.

An MRI of the lumbar spine showed interesting findings.She had a large 4th lumbar posterolateral disc prolapse whichwas clearly visible in a standard MRI. It also gave impressionthat there could be component of the disc in the foremenalso which was compressing the outgoing nerve root. Todemonstrate this pathology better CISS sequence wasperformed which showed clear deflection of the nerve rootin the foramen by a disc component (Figure 5A, B & C).

She was operated upon successfully by doing amicrolumbar discectomy. The disc was so large that theforaminal component could have been missed by the spinalsurgeon being satisfied on finding a large disc in theposterolateral compartment. Her recovery could have beenincomplete since the foraminal component was not excisedby doing a foraminetomy and mobilizing the nerve root.

Figure 4 A, B & C

A: T1W sagittal image showing a foraminal disc herniation(white arrow) which appears away from exiting L5 nerve root

B: Axial T1W sequence which shows left foraminal disc herniation (grey arrow) abutting the left sided exiting nerve root

C: Oblique axial reconstructed image with CISS sequence showing clear compression of left nerve root by the herniated disc (grey arrow)

A B C

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Although not reported in the literature, all the 3 cases inthis series had following common pictures.

1. All of them were females2. All of them were around 50 years old and3. All 3 of them have 4th lumbar disc prolapsed

These are just coincidental findings.

■ Discussion

Nerve root compression by the herniated intervertebraldisc is the commonest cause of low back pain. The nerveroot compression can occur within the spinal canal, in thelateral recess, within the neural foramen or just outside theneural foramen.2 There are various imaging modalities inthe imaging of degenerative disc disease which includesconventional myelography, CT scan, CT myelography andMRI. The MRI is the imaging modality of choice indegenerative spinal diseases. It is superior to CT scanbecause of its better soft tissue resolution. The CTmyelography is invasive investigation which needsintrathecal injection of contrast.

Routine MR imaging include T1 and T2 W sagittal andaxial imaging. The conventional imaging sequences maysometimes not able to demonstrate the nerve rootcompression by the herniated intervertebral disc. This ismainly seen in cases of foraminal disc herniation.2 The 3DCISS is a robust sequence in imaging of the spinal nerves.It gives millimeter thin sections with high spatial resolutionand clear delineation of spinal nerve root. It givesmyelographic images without injection of intrathecalcontrast. Being a volume sequence all the three planes canbe reconstructed after acquiring the data in a singleplane.1,2,3,5

In all our three cases the CISS sequence has givenadditional information than the conventional sequences andclearly demonstrated the relationship of nerve roots withherniated disc which was not clear with routine T1 and T2W TSE sequences. In third case apart from left paracentraldisc herniation additional information of left foraminal disccompressing the exiting nerve root was obtained on CISSimages.

The disadvantage of this sequence is a long acquisitiontime. It cannot differentiate an acute and a chronic discherniation, osteophyte from herniated disc.4

■ Conclusion

The CISS sequence should be taken in all the equivocalcases where the symptomatology of the patient isdisproportionate to disc herniation on conventional imagingsequence. It gives a high spatial resolution neurographicimages with clear delineation of nerve root in relation withherniated disc specially in foraminal disc herniation.

■ References

1. Eberhardt KEW, Hollenbach HP, Tomandl B, Huk WJ. Three-dimensional MR myelography of the lumbar spine: comparative casestudy to X-ray myelography. Eur Radiol 7:737-42, 1997.

2. Filler AG, Maravilla KR, Tsuruda JS. MR neurography and muscleMR imaging for image diagnosis of disorders affecting the peripheralnerves and musculature. Neurol Clin 22:643-82, 2004.

3. Georgy BA and Hesselink JR. MR Imaging of the Spine: RecentAdvances in Pulse Sequences and Special Techniques. AJRi62:923-34, 1994.

4. Georgy BA, Snow RD, Hesselink JR. MR Imaging of Spinal NerveRoots: Techniques, Enhancement Patterns, and Imaging Findings.AJR 166, 1996.

5. Ramila N, Cooper A, and Jaspan A. Pictorial review. High resolutionCISS imaging of the spine. The British Journal of Radiology 74:862-73, 2001.

Address for correspondenceDr. Makarand Kulkarni : Email : [email protected]

Figures 5A, B & C

A & B: T2W axial images showing a large left paracentral disc herniation with compression of left sided traversing nerve root .There wasa left foraminal component abutting the left sided exiting nerve root

C: CISS coronal reconstruction images showing compression of left sided exiting nerve root (white arrow)by the extraforaminal discherniation (grey arrow) at L4-L5 level


33

Use of titanium implants for reconstruction of anterior column ofspine: A review of 167 cases

Ram Chaddha, MDSpinal Surgeon, Lilavati Hospital & Research Center, Mumbai

IntroductionAutograft for mechanical and biologicalreasons has been the gold standard to fillanterior vertebral discal or corporal defects. Themethod of reconstruction of the anterior spinalcolumn is often dictated by surgeon familiarityand/or resources available at a particularinstitution and/or financial affordability of thepatient in a given country. Structural autograftalone or supported by anterior or posteriorinstrumentation, or both, have conventionallybeen used.

Last decade of last century saw emergence of implantsand very soon the market was flooded with titaniumimplants. They are convenient to use, provide betterreconstruction and offer good stability to the spine.3,4,11


Over a period of six years reconstruction of the anteriorcolumn of the spine was done using titanium implants in167 patients. The implants used came from surgicalcompanies Medtronics-Sofamor Danek; Depuy-Johnson& Johnson and Sushrut-Adler.

The cages:The titanium mesh cylindrical cage is a prostheticreplacement that represents one option for anterior columnreconstruction. It is implanted in the vertical orientation,singly or as a pair, between vertebral endplates, followingresection of disc or body with adjacent discs.

The cage is versatile with respect to diameter, length and

Key Words❉ Titanium implants❉ Cages; Pedicle screws and rods❉ Reconstruction of anterior column❉ Fusion

shape allowing the surgeon to place it in optimal sagittalalignment abutting against the endplates. It is expected toprovide immediate structural support to the anteriorcolumn.

The pedicle screws and rods (plates):The cages are always used in conjunction with the anteriorand posterior screws with rods and/or plates to stabilizethe motion segment.6

The autograft:Morselized, non- structural healthy autograft is obtainedfrom the local area or from the patient’s iliac crest. It isloaded and packed into and around the cage to promotesolid osseous union and eventually long-term stability.11

The goal of this paper is to evaluate the ability of the implantsto maintain the sagittal plane alignment and preventsubsidence when used for reconstruction of anterior discalor corporal defects of varied aetiologies. The scope andlimitations of the operative technique have been described.Suggestions have been made to avoid failures in feature.

Clinico-radiological evaluation has been done with immediateand delayed post-operative radiographs and feedbackinformation from the patients. CT scan in conjunction withX-rays has been used to evaluate bony union.

Over a period of six years 200 titanium mesh cylindricalcages were implanted in 167 patients. The follow-up hasbeen for a minimum period of one year and maximum sixyears. The indications for surgeries are outlined in Table 1.

Table 1: Indications for surgeryIndications No. of cases Percentage

Degenerative 62 37

Infective 54 32

Traumatic 47 28

Neoplastic 02 2

Deformity 02 2

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1. Included in the degenerative group are cases of cervicaland lumbosacral instability and discogenic noninfectiveiatrogenic failed back syndromes. In this group in thecervical spine 1 cage was used in 9 patients, and inthe lumbosacral spine 2 cages were used at one levelin 28 patients and 1 cage in 3 patients. In 2 patients, 1cage each was used 2 levels.

2. In the infective group 48 reconstructions were carriedout at various levels for tuberculosis of the spine. Thereconstruction was carried out in 6 cases for pyogenicinfection including 4 cases of failed back surgery(Figure 1A & B).

3. In the traumatic group the cervical and dorsolumbarspine predominated for reconstruction (Figure 2A, B& Figure 3 ).

The distribution of reconstruction for trauma to thespine is shown in the following Table 2.

Figure 1A & BTrauma to the cervical spine at the level of C3 vertebral body treated with corpectomy and reconstruction

Figure 2 A & BTrauma to the DL spine treated withA: anterior and posterior approachB: anterior approach

Figure 3Trauma to the DL spine treated bycombined anterior and posteriorapproach

Table 2: Reconstruction of spine for traumaRegion No. of Cases Percentage

Cervical 17 36

Dorsal 6 13

Dorsolumbar 21 45

Lumbar 3 6

4. In the neoplastic group there were only 2 patients.One patient of treated multiple myeloma in the dorsalspine and one patient of metastasis from Ca- breastin the lumbar spine were treated with a single cage atone level (Figures 4 & 5).

5. In the deformity group both patients were treated withtwo cages each for correction of localized scolioticdeformity in the dorso-lumbar region.


Approach was anterior, posterior or combined. The disc

A B

A B


35

and/or the vertebral body was ressected to achievedecompression of the spinal cord. The bony end plateswere preserved.

All patients treated for burst fractures had autograftobtained from fractured vertebral body. Rib was used forgrafting when it was ressected for transthoracic approachand when posterior approach was used the spinousprocesses and laminae excised were used for grafting. Localbone was not used when reconstruction was done ininfective or neoplastic patient. In these cases the graft wasobtained from the iliac crest.

The bone chips were tightly packed within the cylindricalcages. Additional graft was placed anterior or lateral tothe cage. This graft helped to achieve bony fusion.

In all cases, the insertion of cage was supplemented withpedicle screws and the rods / plates. The cages are notdesigned to be stable without supplemental fixation. Theapproach, degree of deformity and instability encountereddetermined the construct configuration. Gentle distractionof the bed created for the cage followed by optimalcompression as a technical step allowed safe cage insertionand achieving adequate stability and restoration of sagittalalignment.

■ Radiographic analysis

The ability of the titanium construct to provide immediateand long-term anterior column support was assessed.

The sagittal alignment on pre-operative, post-operative andone-year follow-up X-rays was observed. The vertebralbodies above and below the reconstruction were included

in the measurement of the Cobb angle. All radiographicassessments were done by an independent observer (spinesurgeon) not involved with the care of the patients.

The extent of cage subsidence into the end plates wasdetermined as a factor, loss of sagittal alignment. Subsidencewas measured in relation to the rhomboid-shapedfenestrations on the cages. The number or fraction of theserhomboid-shaped fenestrations that had penetrated thecephalad or caudad end plate were evaluated on serialradiographs.

The evaluation of osseous fusion was done on X-rays andCT scan.

The Bridwell et el criteria were used.2

Grade I – complete union with remodeling andtrabeculae

Grade II – intact graft with no lucencies, withoutremodeling or incorporation

Grade III – definite lucency at top or bottom of graftGrade IV – inadequate fusion or implant failure despite

fusion

■ Patient clinical outcome

The patient’s clinical outcome was measured by askingthem to rank their overall quality of life on a scale of 1(poor)to 5(excellent). They were also asked to indicate theirsymptom satisfaction on a scale of 1(very dissatisfied) to5(very satisfied).

■ Results

Evaluation for five years with a minimum follow-up of one

Figure 4Malignancy in the body of L3 treated by anterior approach withexcision and reconstruction

Figure 5Recurrent desmoid tumour of the lower thoracic spine treatedwith excision and the posterior stabilization. Anteriorreconstruction was done during the first surgery

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36

year was done.95% satisfactory (good + excellent) & 5% unsatisfactoryresults were noted in the series of the patients who hadfollowed up for at least one year (110 out of 167 patients).3 patients died following surgery, 1 within a week (MDRtuberculosis of DL junction), 1 within three months (fractureL2) and 1 within nine months (metastasis from Ca-breast).

Radiographically 12 had Grade I fusion, 76 had Grade IIfusion, 16 had Grade III fusion and 6 had Grade IV fusionas per Bridwell et el criteria. There were no cage fracturesbut significant loosening and displacement in the 6 patientswith Grade IV fusion. No incidence of significant migrationof cage intra/extra osseous was noted.

Patient’s outcome was uniformly satisfactory in the series.

❖ 3 patients had stormy post-operative period for threedays to a week, with increase in radicular symptomsfollowing transforaminal stabilization for listhesis

❖ 2 settled completely on analgesics while one had are-exploration with debridement and wound irrigation,removal of additional non-structural graft outside cagehave caused neural irritation and redirection of the S1screw, which was in close proximity to the root. Thispatient had no neurological deterioration at any time

❖ 2 patients had post-operative L5 root neurologicaldeficits, one unilateral on the side of the transforaminaldecompression and stabilization and the other bilateralin a case of posterior lumbar interbody fusion (PLIF).The bilateral deficit completely recovered at one year.The unilateral deficit incompletely recovered at oneyear

❖ 1 patient developed delayed infection at three monthswith sudden onset bilateral L5S1 deficit. She was re-explored and the pus pocket was drained. It waspossibly due to foreign body reaction as the culturewas negative. Implants were not removed. Patient wastreated with broad spectrum antibiotics for six weeks.She settled down and progressed to a final good result

❖ 1 patient had cage loosening with anterior screw backout for tuberculosis of lumbar spine. Re-explorationat six weeks was considered but patient’s clinicalcomfort and the addition of fifth drug (Ofloxacin) tothe four-drug therapy with review at three months sawthe patient progressing satisfactorily to Grade IV fusion

■ Discussion

There is no effect of smoking on fusion in our series.

Subsidence however, is higher in the smokers andtobacco chewers. Junctional areas and upper lumbarspine are more prone to post-operative instabilitypatterns as compared to dorsal and cervical regions ifstabilized by a monosegmental mono rod construct toneutralize the cage.

The cylindrical mesh cage is effective at maintaining sagittalalignment over a post-operative period of at least one year.2,4,7,9,10 The primary function of the device is to providestructural support to the anterior spinal column, which isknown to transmit 80% of the axial load applied to thespine. An ideal anterior support provides a mechanicallystable construct between vertebral end plates whilefacilitating the development of a biologically stable fusionmass.1,4,5,7

The cut edges of the cage leave sharp edges with a smallsurface area of contact, even when used with rings andmay contribute to some early subsidence.

Satisfactory osseous fusion despite subsidence may be themore important factor in good patient outcome.1,2 Fusionwas easier to assess anterior or by the side of the cagethan within it. It is a practice to pack grafts within andbeside the cage. Posterolateral fusion is not added in casesound anterior fusion is anticipated. In most cases wherepostero-lateral graft was added besides facet fusion forinter-transverse fusion in addition to the cage, the graftshave progressively disappeared.

While allograft bone may provide more flexibility in termsof graft length and configuration, the limited availability andrisk (albeit small) of disease transmission impose aconstraint. Cages have been evaluated for their mechanicalstrength, radiological evaluation, pull out strength, adjacentdegeneration, mechanical strength of fused spine and havebeen found to be comparable.7,9

■ Conclusion

The titanium implants, supplemented with non-structuralautograft, is an effective option for the reconstruction ofthe anterior column of the spine. Radiographic analysisreveals that there may be a loss of an average of < 5degrees of sagittal alignment in association with some cagesubsidence into adjacent endplates. Despite re-explorationsmost patients had solid osseous union suggesting that aftera period of settling the cage achieves sufficient stability tofacilitate bony healing.


37

■ References

1. Bradford DS. Treatment of severe spondylolisthesis: a combinedapproach for reduction and stabilization. Spine 4:423-9: 1979.

2. Bridwell KH, De Wald RL, eds. The Textbook of Spinal Surgery, 2nd

ed. Philadelphia: Lippincott- Raven 1211-54: 1997.3. Chen PQ, Lin SJ, Wu SS, et al. Mechanical performance of the new

posterior spinal implant: effect of materials, connecting plate, andpedicle screw design. Spine 28(9):881-6; discussion 887:2003

4. Goel VK, Panjabi MM, Patwardhan AG, et al. Test Protocols forEvaluation of Spinal Implants. J Bone Joint Surg Am 88:103-9: 2006.

5. Kirkaldy Willis WH, Farfan HF, Instability of the lumbar spine. ClinOrthop 165:110-23:1982.

6. Lehmar Steffee AD, Gaines RW Jr. Treatment of L5-S1spondyloptosis by staged L5 resection with reduction and fusion

of L4 onto S1 (Gaines procedure). Spine 19:1916-25:1994.7. Liu CL, Chen HH, Cheng CK, et al. Biomechanical evaluation of a

new anterior spinal implant. Clin Biomech (Bristol, Avon) 13(1 Suppl1);S40-S45:1988.

8. Pope MH, Panjabi M. Biomechanical definitions of spinal instability.Spine 10:255-6:1985

9. Steinhauser E, Bader R, Rechl H, et al. Mechanical study of spinalinterbody implants—characteristics and limits of standardizedtesting. Biomed Tech (Berl) 46(11):325-32:2001

10. Tsantrizos T, Andreou A, Steffen T. Primary stability of anteriorinterbody fusion implants. A comparative study. Mcgill universityorthopaedic research laboratory.

11. Ullrich PF, Interbody fusion spinal implants and bone grafts. In:Spine Health Jan 2004.

Address for correspondenceDr. Ram Chaddha : Email : [email protected]

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Posterior migration of sequestered lumbar disc presenting ascauda equina syndrome

Harjinder Singh Bhatoe, MD, Prakash SinghDepartment of Neurosurgery Command Hospital (SC) & Armed Forces Medical College, Pune

ABSTRACTMigration of a sequestered lumbarintervertebral disc is a common event, mostoften occurring in the subligamentous plane.Dorsal epidural migration with compression ofcauda equina is rare. We report four suchpatients who had acute onset of neurogenicbladder dysfunction and weakness of ankles.All were adult males. Imaging revealed epiduralcompression of cauda equina with discprolapse at L3/4 level in two and L4/5 twopatients. All patients underwent emergencylaminectomy and disc excision, withneurological recovery. Posterior longitudinalligament, peridural membrane and the nerveroot for important barriers to dorsal migration.

Key Words❉ Cauda equina syndrome❉ Disc migration❉ Intervertebral disc prolapse❉ Sequestered disc

■ Introduction

Sequestered disc is completely separated from the parentdisc and lies free in the epidural space. The usual site oflodgment of sequestered discs is the anterior epidural space,wherefrom they can migrate in the spinal canal in the superior(cranial), inferior (caudal) or lateral direction. Posteriorepidural migration of sequestered disc is rare.


We present four cases with features of cauda equinasyndrome due to epidural compression by a dorsally lodgedsequestered lumbar disc. Relevant literature and thepreviously reported cases are briefly reviewed.

■ Case reports

Case 1

A 41-year-old male was admitted with history of bilateralfoot drop, and inability to pass urine for last 24 hours. Forabout two weeks prior to onset of present illness, he hadright sided sciatica. Clinical examination revealed restrictionof lumbar spine movements, spasm of sacrospinalis,bilateral foot drop and calf weakness (motor power grade0/5) and perianal anesthesia. Ankle jerks and anal reflexwere absent. MRI lumbar spine revealed an isointenseextradural lesion at L3/L4 compressing the dura and nerveroots contained therein, with loss of signal intensity at L3/L4 intervertebral disc (Figure 1).

Intravenous contrast administration revealed mild contrastenhancement in the dorsal epidural lesion. He wascatherised and underwent emergency laminectomy of L3.A large, sequestered fragment of prolapsed disc was seenlying free under the lamina dorsal to the dura. The fragmentwas removed, and a rent in the annulus was seen in theL3/L4 intervertebral disc on the left side. Residual discwas curetted out. He showed gradual neurological

Figure 1MRI showing extradural lesion compressing dura and nerveroots showing mild enhancement on contrast administration


39

recovery over the next three months and when reviewedeighteen months later, was continent and had grade 5/5power. Perianal anesthesia had recovered.

Case 2

A 62-year-old male was admitted with sudden ‘catch inthe back’ following unaccustomed physical exertion (liftingof a heavy weight), and inability to pass urine. He did nothave any preceding illness. Rectal examination for prostatichypertrophy was negative. Power in both ankle dorsiflexorsand calves was grade 3/5 with absent ankle jerks.Hypoesthesia was detected over the back of thighs andthe perianal region. MRI spine revealed an extradural lesionlying posterolaterally causing compression of the nerveroots at L3/L4 (Figure 2). No intravenous contrast couldbe administered. He underwent emergency laminectomyof L3, which revealed a sequestered disc fragment lyingdorsal to the dura. Disc fragment was excised and left L4nerve root was retracted, which revealed a small rent inthe annulus and slight disc bulge. Residual disc was curettedout and wound closed. He showed slow recovery overthe next twelve months. When last reviewed two yearsafter surgery, he was continent, and had grade 5/5 powerin the lower limbs.

Case 3

A 35-year-old male was admitted with two-day history ofweakness and numbness of both feet and inability to passurine. There was no preceding illness. Clinically, lumbarspine movements were restricted. Power in ankledorsiflexors and calves was grade 0/5 with hypoesthesiaover S1-S4 distribution. Anal sphincter was lax. CT lumbarspine with intravenous iopamidol showed epidural lesionat L4/L5 with mild contrast enhancement (Figure 3).

Figure 2Extradural lesion lying posterolaterally and compressing thenerve roots

Figure 3CT lumbar spine with IV contrast shows epidural lesion at L4-5level with mild contrast enhancement

He underwent emergency laminectomy of L4. A largesequestered disc fragment was seen lying dorsal to thedura, compressing the nerve roots. Disc fragment wasremoved and a rent was demonstrated in the annulus onthe left side. Residual disc was curetted out. He showedprotracted recovery and after three months, power in ankledorsiflexors and calves was grade 3/5. Bladder washypotonic and he had to carry out clean intermittentcatheterisation for complete bladder evacuation. Perianalhypoesthesia had persisted.

Case 4

A 47-year-old male was admitted with acute cauda equinasyndrome of nearly 72 hours duration. There was norelevant previous illness. Clinically, he had bilateral footweakness with sensory impairment over S2-S4dermatome, and absent ankle jerks, along with neurogenicbladder dysfunction. Lumbar spine radiograph was normal,and lumbar myelogram revealed total extradural cutoff atL4/L5. He underwent emergency laminectomy L4 and alarge sequestered disc lying posteriorly under L4 laminaand pressing the dura. A portion of the sequestered discwas seen leading towards the nerve root and l4/L5 discon the left side. He underwent L4/L5 discectomy afterremoval of the sequestered fragment. Postoperatively, heshowed gradual neurological recovery, and when reviewedsix months later, had regained full motor power and bladdercontrol.

■ Discussion

The prolapsed intervertebral discs are known to migratesuperiorly, inferiorly or laterally. PLL, ligaments, dura,epidural vessels, fat and the root itself act as anatomicalbarriers against movement of the fragment posteriorly. The

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most common path of migration of extruded disc is in aposterior and posterolateral direction to the anterior epiduralspace. Posterior migration, circumventing the thecal sac isexceptionally rare, and only sixteen well-documented caseshave been reported in world literature (Table 1).

A lateral membrane (peridural membrane) is attachedbetween the posterior longitudinal ligament (PLL) andthe lateral wall of the spinal canal. A disc fragment gettingsequestered through the annulus generally lies free in theanterior epidural space, limited by the components of theposterior longitudinal ligament and the lateralmembranes.1 Although the L4/L5 and L5/S1 discs arethe ones most commonly afflicted by degeneration andprolapse, posterior migration is reported almostexclusively in discs cranial to L4. In a literature survey ofpatients prior to the present report, posterior migration

below L4 was seen only in four out of sixteen patientsreported. Whereas the other anatomical factors areconstant, the take-off angle of the root moving caudallymay have some bearing on the incidence of posteriormigration of extruded disc: the take-off angle decreasesfrom L1 to S.3,5 However, one study showed the take-off angle to be constant at 40 degrees.2 There is probablya strong relation between the position of the nerve rootand migration of a sequestered disc fragment: when thedisc space is cranial or caudal to the intervertebralforamen, the nerve root cannot be an effective barrier tosuch migration.8 Nevertheless, further studies are neededto analyse the pathoanatomy of relationship of extrathecalsegment of nerve roots to the intervertebral disc levels,especially in the setting of disc prolapse. A pressuregradient in the epidural space too has been described asbeing responsible for disc migration.4

Table 1: Documented cases of posterior migration, circumventing the thecal sac

Author Age/gender Preceding Precipitating Presentation Imaging Levelhistory event

Bonaroti & Welch1 51/M CES MRI L3/L4 (RI)

Dosoglu et al4 47/M LBA, sciatica Chiropactic CES Myelo, MRI L2/L3manipulation

Hirabayashi et al6 58/M LBA CES CT myelo, MRI L2/L3

Hodges et al7 NA Ac groin &thigh pain MRI L4/L5

Kuzeyli et al8 49/M Lifting of load Ac sciatica MRI L4/L5

62/F Lifting of load Ac lumbago MRI L1/L2

47/F LBA Paresthesiae MRI L2/L3 (RI)

Lichtor9 61/M LBA Ac lumbago CT Myelo, MRI L2/L3

Lutz et al10 30/M LBA Martial arts CES CT Myelo L4/L5

Neugroschl et al12 57/M LBA Ac sciatica Myelo, MRI L2/L3

64/M LBA Ac sciatica Myelo, MRI L2/L3 (RI)

Pillai et al13 35/M LBA CES MRI L3/L4

Robe et al14 68/M Lifting of load, CES MRI L3/L4 (RI)chiropacticmanipulation

41/F LBA, sciatica CES MRI L3/L4 (RI)

Sakas et al15 70/M LBA CES CT L4/L5

Sekerci et al16 58/M LBA CES Myelo L3/L4

Present series 41/M Sciatica CES MRI L3/L4

62/M Lifting of load CES MRI L3/L4

35/M CES CT L4/L5

47/M CES Myelo L4/L5

Abbreviations: Ac, acute; CES, cauda equina syndrome; LBA, low backache; Myelo, myelography; NA, information not available; RI, rimenhancement


41

Posterior migration of extruded disc is described almostexclusively in males: there were only three females in theentire survey.8,14 Mean age was 51.73 years with a rangeof 30 years(Lutz et al 1990)10 to 70 years.15 Three patientswere below 40 years, six between 41 and 50, four between51 and 60 and six patients were between 61 and 70 years.A definite history of unaccustomed physical exertion orisometric activity though expected, is generally notforthcoming. Only six out of twenty cases reported hadsevere physical exertion prior to onset of cauda equinasyndrome due to posterior migration of sequestered disc;one of these patients, a martial arts enthusiast, continuedstrenuous activities after onset of pain and developed caudaequina syndrome.10 Two of the patients had undergonechiropractic manipulation for backache,4 while two hadhistory of lifting of heavy load prior to onset of symptoms.8

Most of the cases have a history of backache, which hadaggravated recently. Often there is an acute onset of sciaticawith urinary symptoms and weakness of ankle dorsiflexion.Cauda equina syndrome is seen in almost fifty percent ofcases. Rest of the patients may have features of incompletecauda equina syndrome, or only backache and sciaticawith absent ankle jerks.

A patient presenting with cauda equina syndrome needsimmediate evaluation by MRI. Posterior sequestered discsare of soft-tissue intensity on T1-weighted images. Eightypercent cases show T2-hyperintensity.11 Despite high T2signal in the sequestered discs, loss of T2 signal is seen inthe disc space of origin of the sequestered fragment. Rimenhancement of the sequestered fragment has been reportedconsistently, and is attributed to inflammatory process andwrapping of the fragment in vascularised fat.8,14 Fragmentshave demonstrated neo-vascularisation and this too canbe responsible for contrast enhancement.8,17 A dorsallymigrated disc needs to be differentiated from infectivelesions like epidural abscess, tumors like metastases,lymphomas, and other lesions like synovial cysts of facetjoints.

Patients with dorsally migrated lumbar discs presenting withcauda equina syndrome require to be operated uponwithout any delay. Disc fragment removal is accomplishedwithout any difficulty by an appropriately placedlaminectomy. A portion of the sequestered disc may beseen lead to the interspace of origin. The disc space oforigin should also be emptied of its contents. Long-termresults following surgery are gratifying, and none of thepatients reported required any other procedure after firstsurgery.

■ Conclusion

Sequestration and migration of prolapsed lumbar disc iscommon; however, posterior migration is rare, and occurspreferentially in discs cranial to L4. Exact aetiology is yetunsettled, and it is likely that the nerve root is an importantbarrier against dorsal migration. Presentation usually is inthe form of cauda equina syndrome. MRI demonstrates adorsally placed contrast enhancing epidural compressivelesion in the lumbar spine, and the offending disc is excisedby an appropriately placed laminectomy. Reports showexcellent postoperative neurological recovery.

■ References

1. Bonaroti EA, Welch WC. Posterior epidural migration of an extrudedlumbar disc fragment causing cauda equina syndrome. Spine23:378-81, 1998.

2. Cohen MS, Wall EJ, Brown RA, Rydevik B, Garfin SR. Cauda equinaanatomy II. Extrathecal nerve roots and dorsal root ganglia. Spine15:1248-5, 1990.

3. Crock HV. Normal and pathological anatomy of the lumbar spinalnerve root canals. J Bone Jt Surg 63B:487-90, 1981.

4. Dosoglu M, Is M, Gezen F, Ziyal MI. Posterior epidural migration of alumbar disc fragment causing cauda equina syndrome: Case reportand review of the relevant literature. Eur Spine J 10:348-51, 2001.

5. Hilel N, Feuerstein M. Angulated course of spinal nerve roots. JNeurosurg 32:349-52, 1970.

6. Hirabayashi S, Kumano K, Tsuiki T, Eguchi M, Ikeda S. A dorsallydisplaced free fragment of lumbar disc herniation and its interestinghistologic findings. Spine 15:1231-3, 1990.

7. Hodges SD, Humphrey SC, Eck JC, Covington LA. Posteriorextradural lumbar disc fragment. J South Orthop Assoc 8:222-8,1999

8. Kuzeyli K, Cakir E, Usul H, et al. Posterior epidural migration oflumbar disc fragments: report of three cases. Spine 28:E64-7, 2003

9. Lichtor T. Posterior epidural migration of extruded lumbar disc. SurgNeurol 32:311-2, 1989.

10. Lutz JD, Smith RR, Jones HM. CT myelography of a fragment ofalumbar disc sequestered posterior to the thecal sac. AJNR 11:610-11, 1990.

11. Masaryk TJ, Ross JS, Modic MT, Boumphrey F, Bohlman H, WilberG. High resolution MR imaging of sequestered lumbar intervertebraldiscs. Am J Roentgenol. 150:1155-62, 1988.

12. Neugroschl P, Kehrli P, Gigaud M, et al. Posterior extradural migrationof extruded thoracic and lumbar disc fragments: role of MRI.Neuroradiology 41:630-5, 1999.

13. Pillai RPK, Sampath S, Chandramouli BA, Kolluri VRS. Posteriorepidural migration of sequestered lumbar disc. Neurology India49(Supplement 1): P40, 1999.

14. Robe P, Martin D, Lenelle J, Stevenaert A. Posterior epidural migrationof sequestered lumbar disc fragments. Report of two cases. JNeurosurg (Spine) 90:264-6, 1999.

15. Sakas DE, Farrell MA, Young S, Toland J. Posterior thecal lumbardisc herniation mimicking synovial cyst. Neuroradiology 37:192-4,1995.

16. Sekerci Z, Ildan F, Yuksel M, Gul B, Kilik C. Cauda equina compressiondue to posterior epidural migration of extruded lumbar disc.Neurosurg Rev 15:311-3, 1992.

17. Virri J, Sikk S, Gronblad M, et al. Concomitant immunocytochemicalstudy of macrophage cells and blood vessels in disk herniation.Eur Spine J 3:336-41, 1994.

Address for correspondenceDr. Bhatoe : Email : [email protected]

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Posterior epidural migration of extruded lumbar disc fragment:Report of two cases with review of literature

Antonio Figueiredo, Shradha Maheshwari, Chandralekha Tampi,* P. S. Ramani, MD***Department of Histopathology, Lilavati Hospital and Research Centre, Mumbai**Department of Neurosurgery, Lilavati Hospital and Research Centre, Mumbai

AbstractMajority of symptomatic lumbar disc herniationsare noted to be in a postero-lateral position withresultant nerve root irritation.1,3,6,9 Althoughcaudal, rostral, and lateral migration of discfragments is possible, extruded disc fragmentsare commonly located at the ventral aspect ofdural sac and nerve root. Posterior migrationof disc is rare due to anatomic barriers. Wepresent two cases that had posterior migrationof sequestrated disc fragment and review therelevant literature.

Key Words❉ Posterior disc migration❉ Rent at the junction of

annulus with the loweredge of the vertebra

■ Introduction

The lumbar segment of spine, being the weight bearingsegment is most often affected by degenerative changes.The last two segments are most frequently affected andtherefore, disc herniations are most common at L4/5 andL5/ S1 levels. Due to the anatomical situation, herniationsof the nucleus pulposus commonly result in an anteriorcompression of the neural structure, the posterolateraldirection being most common path for disc migration.Migration of a sequestrated disc fragment in the posteriorepidural space is rare. A combination of longstandingdegeneration and a subsequent change in the ability of thedisc to resist applied forceful stress have been suggestedto cause posterior migration of the disc.

■ Case reports

Case 1

A 32-year-old male patient came to our clinic with

complaints of severe back pain and right sciatica since thelast three months. His job consisted of frequent travellingby road. The pain had started after a jerky travel and hadincreased to become very severe. He was unable to walkdue to the pain. He also complained of paraesthesia in theright leg. On examination, his right SLR was severelyrestricted to 20o and his right ankle jerk was absent. Hehad decreased sensation in the right S1 dermatome. Therewas no motor deficit or sphincter involvement.

He had been taking pain killers for the last 3 months whichgave him temporary relief and subsequently MRI was donewhich showed a large postero inferior disc extrusiondisplacing the thecal sac and compressing the right S1 nerveroot (Figure 1).

He was then operated by a microlumbar approach on theright side. After removing the thinned out ligamentumflavum, an abnormal, soft material was identified lyingpoteriorly over the cord. It was carefully dissected andproved to be a dorsally migrated extruded disc which waspartially connected with the main disc with a thin threadbare disc tissue. The connection was going through theaxilla of the root to the main disc. The root itself was pushedlaterally into the narrow rescess. The pathologic examinationconfirmed that the specimen was an intervetebral disc.

Figure 1Posterior migration of fifth lumbar disc prolapsed

S1


43

Postoperatively, he had complete relief of pain and couldwalk comfortably within hours of surgery.

Case 2

A 41-year-old mechanical engineer came with a history ofgradually increasing pain in the left leg over the past oneyear. His complaints had started after lifting some heavyweight machinery at his work. The pain had graduallybecome worse and when he came to our clinic, he waslimping while walking and needed support to walk. Hegave a history of similar episode of left leg pain four yearsback. He complained of intermittent episodes ofradiculopathy in the left leg which were not very severeand relieved with rest.

Clinically, he had restricted left SLR at 40o, there wasweakness in left TA and EHL muscles and his left anklejerk was diminished. He walked with a limp and the trunkwas tilted on the left side. He did not have any sensoryloss and his bladder and bowel functions were normal.

MRI showed decreased L4/5 disc space with a largeepidural mass located postero laterally on left aspect ofleft L4/5 disc space compressing the left L5 nerve root. Aleft-sided microlumbar surgery was done and on removingthe flavum a large sequestrated disc fragment was identifiedon the left lateral and posterior aspect to the thecal sac(Figure 2).

The fragment had an attachment which was going upto themain disc lateral to the nerve root. The attachment was cutand the posterior fragment was removed. It contained apiece of hard tissue, presumably a piece of cartilage. Thecanal was broad and the left L5 nerve root was clearlyseen without doing IDSS. Carefully retracting the rootmedially, we could identify a rent in the annulus at itsjunction with the lower edge of the vertebra located rightunder the root (Figures 3 & 4)

Figure 2Posteriorly migrated disc having pedicle with the parent discand a piece of cartilage from the lower vertebra

Figure 3Rent in the annulus at its junction with lower vertebra under theroot

Figure 4Schematic diagram showing a rent in the annulus at its junctionwith the lower edge of the vertebra

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Microscopic examination of the posteriorly migrated discrevealed a piece of hyaline cartilage along with prolapseddisc. The piece removed from the main disc showed normaldisc with annulus and the nucleus. It also showedneovascularisation suggestive of acute trauma (Figures 5& 6).

Patient was completely relieved of pain following thesurgery and showed improvement in his motor power.

■ Discussion

Of all the discs, the lumbar ones are most often affectedby degeneration as they are located at the maximum loadbearing region of the spine. The most commonly affectedlevels are L4/5 and L5/S1. A combination of longstandingdegeneration and a subsequent change in the ability of thedisc to resist applied forceful stress lead to disc herniation.Normally, when intradiscal pressure is increased,

Figure 5Posteriorly migrated disc fragment contained a piece of hyalinecartilage

degenerated disc herniates through a point of lowerresistance in the PLL.6, 7

The herniated parts of a nucleus pulposus usually remainsin a subligamentous location. They may retain continuitywith the parent disc or may become free fragments. Discsequestration is defined as a herniated disc with perforationof the fibrous annulus and the posterior longitudinal ligamentwith migration of the disc fragment to the epidural space.1

These fragments are free to migrate in any direction.However the most common path of disc fragment migrationis in posterior and posterolateral direction in the anteriorepidural space i. e. ventral to the cord.1, 3, 7

Some anatomical configurations of the spine have beensuggested as the cause of normal disc prolapsed in thepostero-lateral direction.1

1. A sagittal midline septum spans the space betweenthe vertebral body and the posterior longitudinalligament. This septum directs the fragment laterally tothe midline and into the lateral recess, and influenceslateral subligamentous migration

2. The peridural or lateral membrane attaches to the freeedge of the posterior longitudinal ligament mediallyand laterally to the wall of the spinal canal thusrestricting the disc movement

3. Once a fragment transgresses the peridural membrane,the epidural fat and the epidural venous plexuspresumably act as obstacles to migration.

4. Some reports have suggested that the root itself maybe a very potent anatomical barrier10

The disc fragment migration usually occurs cranially,caudally or laterally but seldom posterior to the anteriorepidural space. Migration of a sequestrated disc fragmentin this manner has been reported only rarely.1, 3,9,11,12

Several mechanisms explaining the dorsal migration of thedisc material have been proposed.8

1. Slight adhesion between the annulus fibrous and thedural sac caused by previous asymptomatic discherniation may accelerate the dorsal migration of thesequestrated disc material. This can also lead tomigration of the disc dorsally through the axilla of theroot

2. Remarkably, acute strong pressure may push the discmaterial to the dorsal site of the dural sac

3. If the laceration of the annulus fibrous is situated in thelateral point near the pedicle, the sequestrated disc

Figure 6Normal disc tissue containing nucleus pulposus and annulusfibrosus. It shows neovascularisation suggestive of recenttrauma


45

material may migrate along the medial site of thepedicle to the lateral and dorsal sides of the dural sac

It is our opinion that the size of the canal has an importantrole to play in the dorsal migration of the disc. In our case1 the canal was narrow and the nerve was displacedlaterally into the narrow lateral rescess. There was amplespace in the axilla of the root and the disc migrated throughthe axilla.

In the second case the canal was broad, the nerve rootwas clearly visible and there was ample space lateral tothe nerve root.

In the second case, we have clearly demonstrated the rentat the lower end of the disc, at its junction with the lowersurface of the vertebral body. The rent was located rightunder the root. The location of the rent and uprooting of apiece of cartilage from the vertebral body suggestsapplication of violent force causing dorsal migration of thedisc and the path taken depending on the size of the bonylumbar spinal canal.

Histological examination has confirmed the presence ofhyaline cartilage in the posteriorly migrated disc andneovascularisation within the disc space suggesting trauma.

Diagnosis is difficult prior to surgery without radiologicstudy. MR imaging, especially with gadoliniumadministration, appears to be the method of choice fordiagnosis. Sequestrated fragments usually show low signalintensity on T1-weighted images, and 80% of cases exhibithigh signal intensity on T2-weighted images relative to thedegenerated disc of origin. The high signal intensity on T2-weighted images can be explained as either the herniatedmaterial still having high water content or a reparativeprocess leading to a transient water gain. The remaining20% had isointense signal intensity relative to thedegenerated disc on T2-weighted image.2 Most of the disc

fragments show peripheral contrast enhancement attributedto an inflammatory response with granulation tissue andnewly formed vessels around the sequestrated tissue.2, 5, 13

Posterior extrusion of the disc although rare can occur.Repeated trauma seems to push a possibly sequestratedfragment posteriorly to reach the dorsal aspect of the cord.The clinical presentation is usual but radiology may beconfusing occasionally.

■ References

1. Bonaroti EA, Welch WC. Posterior epidural migration of an extrudedlumbar disc fragment causing cauda equina syndrome: clinical andmagnetic resonance imaging evaluation. Spine 23:378-81, 1997.

2. Chen CY, Chuang YL, Yao MS. Posterior Epidural Migration of aSequestrated Lumbar Disk Fragment: MR Imaging Findings AmericanJournal of Neuroradiology 27:1592-4, 2006.

3. Dosoglu M, Is M, Gezen F, et al. Posterior epidural migration of alumbar disc fragment causing cauda equina syndrome: case reportand review of the relevant literature. Eur Spine J 10:348-51, 2001.

4. Gordon SJ, Yang KH, Mayer PJ, et al: Mechanism of disc rupture. Apreliminary report. Spine 16:450-6, 1991.

5. Hwang GJ, Suh JS, Na JB, et al. Contrast enhancement pattern andfrequency of previously unoperated lumbar discs on MRI. J MagnReson Imaging 7:575-8, 1997.

6. Iencean SM: Lumbar intervertebral disc herniation followingexperimental intradiscal pressure increase. Acta Neurochir 142:669-76, 2000.

7. Martin MD, Boxell CM. Pathophysiology of lumbar disc degeneration:a review of the literature. Neurosurg Focus 13, 2002.

8. Morizane A, Hanakita J, Suwa H, Ohshita N, Gotoh K, Matsuoka T.Dorsally sequestrated thoracic disc herniation-case report. NeurolMed Chir (Tokyo) 39:769-72, 1999.

9. Neugroschl C, Kehrli P, Gigaud M, et al. Posterior extradural migrationof extruded thoracic and lumbar disc fragments: role of MRI.Neuroradiol 41:630-5, 1999.

10. Robe P, Martin D, Lenelle J, Stevenaert A. Posterior epidural migrationof sequestered lumbar disc fragments. Report of two cases. JNeurosurg (Spine 2) 90:264-6, 1999.

11. Sarlieve P, Delabrousse E, Clair C, et al. Intradural disc herniationwith cranial migration of an excluded fragment. Clin Imaging 28:170-2, 2004.

12. Schellinger D, Manz HJ, Vidic B, et al. Disc fragment migration.Radiology 175:831-6, 1990.

13. Tsuji H, Hirano N, Ohshima H, et al: Structural variation of the anteriorand posterior anulus fibrosus in the development of human lumbarintervertebral disc. A risk factor for intervertebral disc rupture.Spine 18:204-10, 1993.

14. Wasserstrom R, Mamourian AC, Black JF, et al. Intradural lumbardisk fragment with ring enhancement on MR. AJNR Am J Neuroradiol14:401-4, 1993.

Address for correspondenceDr. Antonio Figueiredo : Email : [email protected]

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Iatrogenic cervical vertebral artery pseudoaneurysm successfullytreated by an endovascular approach: Case report

Mehmet Zileli, MD,* Sedat Cagli, MD,* Ismail Oran, MD,** Murat Kalayci, MD,***Sertac Islekel, MD**Departments of Neurosurgery and **Radiology, Ege University Faculty of Medicine, Izmir, Department of Neurosurgery,***Karaelmas University, Zonguldak, Turkey

AbstractVertebral artery injury during anterior surgeryof the cervical spine is a rare complication andits treatment is challenging. This reportdescribes a case of an 80-year-old man withvertebral artery injury occurred during anteriorcervical spine surgery for cervical spondyloticmyelopathy. The bleeding was initially controlledby packing with bone wax, but recurred sevendays later. Emergency angiographydemonstrated a pseudoaneurysm of the rightvertebral artery that was occluded by anendovascular approach using coils in the samesetting, with persistent elimination of thepseudoaneurysm in the long term clinical follow-up.

■ Introduction

Anterior surgical approach to the cervical spine has becomea commonly used procedure for treatment of a number ofconditions, including degenerative disc disease,spondylosis, fractures, neoplasm and infections. Whileremoving the cervical disc or drilling the spurs narrowing a

neuroforamen, vertebral artery may be injured. Vertebralartery injuries during anterior cervical spine surgery areinfrequent, but can be catastrophic, due to exceesivebleeding and ischemic neurological complications. Casesof vascular complications are rare incidents and aretherefore only occasionally found in the literature. Daentzeret al3 recently reviewed the vertebral artery injuries duringanterior cervical spine surgery and reported a very lowincidence. The reported cases in the literature is 32.

This paper reports a patient with vertebral artery injuryduring anterior cervical spine surgery. A pertinent reviewof the literature about vascular complications of thevertebral artery in anterior approaches to the cervical spineis presented.

■ Case report

An 80-year-old man has suffered from tetraparesis anddifficulty in walking for four months. He had a history ofsurgery (laryngectomy) for larynx carcinoma 15 years ago.On examination, he had clinical signs of a severe cervicalmyelopathy. Diagnostic workup disclosed a severe stenosisof the cervical spinal canal at the levels of C3-4, C4-5,C5-6 (Figure 1A, B, C, D & E).

Figure 1Sagittal T1 (A) and T2 (B) wieghted sagittal and axial (C,D,E) images taken before first surgery on January 2000

A B C D E


47

On February 2000, a C4-C5 corpectomy was performed.An autologous tricortical iliac crest graft and an anteriorcervical plate with screws on C3 and C6 were placed(Figure 2A & B).

Because of lack of symptomatic relief, MR images obtainedfive months later showed the lack of decompression andongoing kyphosis (Figure 3A & B).

We decided a second surgery and decompression fromC3-4 to C6-7 disc levels. He was operated again in June2002, and a three level corpectomy was done. While drillingfusioned bone graft on the right side at C3-C4 disc level, amassive arterial bleeding occurred due to right vertebralartery injury. The bleeding was controlled by packing withsurgicel and bone wax. A fibular allograft was used toestablish a fusion and an anterior cervical plate was placedwith screws on C3 and C7 vertebral bodies (Figure 4A &B). Since bleeding was controlled completely, direct repair

of the injured vessel was not performed. Postoperativelythe patient was well, and no new neurological deficits wasobserved.

On the seventh postoperative day, a massive bleeding onthe surgical wound was observed. It was a 1200 mlhemorrhage that did not cause any subcutaneous hematomaand airway obstruction because of previous laryngectomyscar. An immediate angiography was performed whichdemonstrated a pseudoaneurysm of the right vertebralartery. It was occluded by coils in the same setting. Controlangiography at the end of this procedure confirmed totalocclusion of the aneurysm (Figure 5A & B).

Follow-up of the patient was uneventful. An outpatientexamination three months later demonstrated significantimprovement of tetraparesis and his walking ability was

Figure 2A & BAfter C4 and C5 corpectomy, lateral (A) and AP (B) radiographsshowing anterior cervical plate with screws on C3 and C6vertebral bodies

Figure 3A & BPostoperative MR images (A,B) showing inappropriatedecompression and residual kyphosis

Figure 4A & BLateral (A) and AP (B) radiographs after second surgery with C4,C5, C6 corpectomy and anterior cervical plate with screws onC3 and C7 vertebral bodies

Figure 5A & BOn 7th postoperative day after a new bleeding on surgical site, avertebral angiography was performed which showed apseudoaneurysm on right vertebral artery (A). Detachable coilocclusion was performed at the same setting resulting in totalocclusion of the pseudoaneurysm (B)

A B

A B

A B

A B

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significantly better than before surgery. The patient wasfree of signs and symptoms related to the previous vertebralartery injury for more than 2.5 years.

■ Discussion

The rate of complications of anterior cervical spine surgeryis about 5%. 1 The most frequent complications are linkedfrom the use of grafts and hardware placement, recurrentlaryngeal nerve lesions, neurological complications (whichare rare), infections, esophageal complications and vascularcomplications. Apart from the carotid artery, the vertebralartery may be injured during anterior cervical spine surgery.Vertebral artery injury occurs in 0.3-2.1% of all anteriorcervical spine surgeries.1,5,6 Possible complications after avertebral artery injury includes arteriovenous fistulas, late-onset haemorrhages, pseudoaneurysms, thrombosis, andemboli.3

Many treatment options of vertebral artery injuries havebeen recommended. Most authors favour primary repairof the vessel whenever possible to avoid placing the patientat risk of ischemic complications.4,6,8,10 The clinical resultsafter direct surgical repair of an injured vertebral arteryare excellent. If the vertebral artery is occluded by eitherdirect ligation or coils, neurological sequela may occur whena hypoplastic contralateral artery is not able to maintaincerebral perfusion. This risk can be avoided byintraoperative angiography, if direct vessel repair is notpossible and proximal and distal ligation is intended.3

Whenever an injured vertebral artery cannot be directlyrepaired intraoperatively, and the bleeding is controlled bytamponade only, angiography should be performedimmediately after operation. In this setting, the lesion shouldbe treated endovascularly, if possible. Some types ofvertebral artery injuries were treated endovascularly in theliterature.7,9 Daentzer et al3 have reported a patient withvertebral artery pseudoaneurysm following anterior cervicalspine surgery, in whom they treated the aneurysmsuccessfully with preservation of the parent artery. Ourcase is the second such case in the English literature. Wethink that this treatment is a good alternative because ofthe advances in endovascular techniques in recent years.The favourable results in these two cases support thistheory.

Sometimes, the vertebral artery injury may be so complexthat the lesion cannot be repaired endovascularly withoutsacrificing the parent artery. In such conditions, checkingthe contralateral vertebral artery flow and collateral flow

through the circle of Willis is crucial to prevent ischemiccomplications.2,4,6 If a conventional angiography is notavailable, less invasive techniques such as magneticresonance imaging or CT angiography are alternatives.Although they are useful tools for follow-up examinations,they can not provide an interventional treatment.3

The best measurement against iatrogenic vertebral arteryinjury is its prevention. Preoperatively, the surgeon shouldnote the position of the vertebral arteries on CT or magneticresonance images to detect any ectatic arteries orinvolvement in a tumor or infection. Preoperative magneticresonance angiography or conventional angiography shouldbe considered in special cases. For example, if the arteryis displaced, tortuous, or dilated, surgery should be changedaccording to these abnormalities. During surgery, meticulousattention to identify the midline anatomic structures ismandatory. The surgeon should keep in mind that thevertebral artery may be injured while microsurgicallyremoving the cervical disc or drilling the spurs narrowingthe neuroforamen for decompression. The risk of arterialinjury is higher, if a corpectomy is performed. Corpectomyusually requires extensive use of motorized burrs in tightconfines.5 The removal of bone and disc material must beperformed in the midline and should not be excessivelywide. Lateral extension of the decompression to theuncovertebral joints and removal of the disc material shouldbe performed using small diamond drills, fine curettes, andKerrison punches as needed.3,10 The risk is seeminglyhigher in case of reoperations as in this presentation.

■ Conclusion

Iatrogenic vertebral artery injury during anterior cervicalspine procedures is an infrequent, yet potentiallycatastrophic complication. In this surgery, distinctpreoperative planning and a detailed knowledge of thesurgical anatomy are mandatory to prevent vascular injury.The surgeon should be aware of vascular(pseudoaneurysm, arteriovenous fistula, occlusion etc.) andclinical (late hemorrhage, ischemia etc.) consequences ofthe injury. If direct surgical repair is not appropriate, thevascular lesions can be treated with endovasculartechniques as in the presented case.

■ References

1. Burke JP, Gerszten PC, Welch WC. Iatrogenic vertebral artery injuryduring anterior cervical spine surgery. Porc 16th Annual MeetingNorth Am Spine Soc, The Spine Journal 2:2S, 2002 (Abstract).

2. Cosgrove GR, Theron J. Vertebral arteriovenous fistula followinganterior cervical spine surgery: report of two cases. J Neurosurg66:297-9, 1987.


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3. Daentzer D, Deinsberger W, Boker DK. Vertebral arterycomplications in anterior approaches to the cervical spine. Reportof two cases and review of the literature. Surg Neurol 59:300-9,2003.

4. De los Reyes RA, Moser FG, Sachs DP, Boehm FH. Direct repair ofan extracranial vertebral artery pseudoaneurysm: case report andreview of the literature. Neurosurgery 26:528-33, 1990.

5. Eleraky MA, Llanos C, Sonntag VKH. Cervical corporectomy: reportof 185 cases and review of the literature. J Neurosurg Spine 90:35-41, 1999.

6. Golfinos JG, Dickman CA, Zabramski JM, et al. Repair of vertebralartery injury during anterior cervical decompression. Spine 19:2552-2556, 1994.

7. Mwipatayi BP, Jeffery P, Beningfield SJ, et al. Management of extra-cranial vertebral artery injuries. Eur J Vasc Endovasc Surg 27:157-62, 2004.

8. Pfeifer BA, Freidberg SR, Jewell ER. Repair of injured vertebralartery in anterior cervical procedures. Spine 19:1471-4, 1994.

9. Prabhu VC, France JC, Voelker JL, Zoarski GH. Vertebral arterypseudoaneurysm complicating posterior C1-2 transarticular screwfixation. Surg Neurol 55:29-34, 2001.

10. Smith MD, Emery SE, Dudley A, et al. Vertebral artery injury duringanterior decompression of the cervical spine. J Bone Joint Surg75-B:410-5, 1993.

Address for correspondenceDr. Mehmet Zileli : Email : [email protected]

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Rare presentation of spinal chondrosarcoma withboth intraspinal and intrathoracic extension

Tarak Patel, Sameer Kalkotwar, Gautam Prasad, Prasad Karpe, R. K. Deshpande,MDShekhar Bhojraj, MDSpinal Surgery and Thoracic Surgery, Breach Candy Hospital, Mumbai

AbstractChondrosarcomas are malignant tumors that rarely grow in-side the spinal canal. Prognosis depends on histological grad-ing, tumor staging, patient’s age and surgical margins freefrom tumor. This tumor is usually chemo and radio resistant.Ideal treatment consists of total “en-block” resection, if notobtainable due to location, compromise of stability and risk ofneurological damage, adjuvant radio and/or chemotherapyshould be added. Case of spinal Chondrosarcomas with rarepresentation of both intra spinal and bilateral intra thoracicextension is reported. Pre operative CT guided biopsy re-ported as? chordoma, which proved to be chondrasarcomagrade II after histopathological examination of tumor mass.Surgical technique consisted of initial debulking by bilateralthoracotomy followed by removal of intra spinal tumour mass.Total resection was accomplished without spinal stabilization.Although “en-block” resection of a chondrosarcoma shouldbe tried whenever possible, piecemeal tumour excision shouldbe considered in difficult cases, as in the present case reportalong with adjuvant chemo and/or radio therapy. Immediatepost operative imaging showed good debulking without anyresidual tumor mass with adequate spinal decompression.For disease free interval and survival rate long term followup will be important.

Key Words❉ Spinal chondrosarcoma❉ Intra spinal❉ Intra thoracic❉ Mediastinal tumor

■ Introduction

Chondrosarcoma (CHS) constitutes a family of malignanttumors in which cells tends to differentiate into cartilage.3,15

Chondrosarcoma are classified as central, peripheral, orperiostal. Two rare varieties are mesenchymal (CHS) andclear-cell Chondrosarcomas (CHS).3 Thompson andTurner-Warwick had classified chondrosarcomas into 3histological grading:26 Grade I is a low grade, well-defferentiated tumor containing increased numbers ofcartilaginous cell with well-formed matrices. Grade II isand average grade tumor with less metrix and increased

cellularity. The cells vary in size and shape with nuclearirregularities. Grade III represents a high grade tumor withanaplasia, mitosis and only rare islands of cartilage.Chondrosarcoms represent the second most commonprimary tumor of the skeleton.19,28 However, presentationas primary tumor of the spine is extremely rare.1 Lumbarspine is the most common site in the spine.3 Maximumincidence is found in patients 30 to 70 year of age. It rarelyoccurs before 20 year of age, and only exceptionally foundbefore puberty.3 Primary malignant tumors should beresected with wide safety margins. However, limitationsto total resection may involve risk of causing spinal instabilityand/or inflicting new deficits. Isolated cases of spinalChondrosarcomas have been reported1,2,5-11,13,14,17,18,20,23

as well as a few series with limited number of patients.3,24,28

■ Case report

A 52-year-old man presented with mid back pain since 3months. He had no history of any constitutional symptoms.On examination deep tenderness was present at D5-D6vertebral level. Neurological examination showed no motoror sensory deficit. Reflexes were normal and bilaterallyequal with absent babinski sign.

Pre operative X-rays showed mediastinal widening.Preoperative CT scan was done which also showed dumbbellshaped intrathoracic mass. Mass was measuring 11.7 X7.3 cm in maximum transverse diameter and 13.4 insupero-inferior extent in posterior mediastinum. The massextended superiorly from the level of D1-D2 disc to theinferior endplate of D8 vertebra. It also showed destructionof posterior part of left 5th and 6th rib and transverseprocess and pedicle of 5th thoracic vertebra.

MRI showed a huge soft tissue mass in both thoracic cavitiesconnected through posterior mediastinum. Mass wasextending into the spinal canal through left T5-6 intervertebralforamina causing widening of foramen. Tumour mass wascausing thecal sac compression from left side.


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Pre operative CT guided biopsy was done to have preoperative histological diagnosis which was reported as ?chordoma.

Considering the tumor to be chordoma, complete tumormass excision was planned. A right posterolateralthoracotomy along the upper border of the sixth rib wasdone first. Bosselated tumor mass was found extendingfrom the 2nd to the 8th thoracic vertebra pushing themedaistinal contents including esophagus anteriorly. Tumorhad engulfed azygose vein, which was ligated and

sacrificed. Mass was freed from mediastinal structures andremoved by sectioning vertically from its continuation intothe left chest. This was followed by a similar left thoracotomyand total tumor mass excision in fragmentation. The tumorwas originating from an area around the 5th Intervertebralforamen on the left and the adjoing part of the left 5th and6th rib. Part of tumor mass compressing thecal sac wasremoved through the widened foremen and space createdby removing 5th rib, transverse process and pedicle.Posterior part of left 5th and 6th rib, left transverse processand pedicle were removed. The mass was completelyresected in a piece-meal fashion until margins free of tumorwere obtained. Spinal stabilization was not consideredbecause out of three anatomical columns two werepreserved, right sided structures were intact and becauseof inherent stability of thoracic spine provided by rib cage.Post-operative period was uneventful. Post operative CTscan showed no residual tumour mass.

Histopathological examination showed the tumour to beGrade II chondrosarcoma. The tumour is resistant to chemoand the readio therapy. “En-block” resection could not bedone in this case and hence adjuvant chemo and radiotherapy is planned 3 months after surgery (Figures 1 to 5).

Figure 1Preoperative X-ray showing widening of the mediastinum

Figure 2Preoperative CT Scan showing dumble shaped tumour passing into the spinal canal from the left side to the intervertebral foramen atthe D5-D6. The pedicle of D5 is destroyed on the left side. Left D5 and D6 ribs and transverse processes are also destroyed

Figure 3Preoperative MRI showing the large dumbel shaped tumour going into the spinal canal from the left side

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■ Discussion

Surgical treatment of spinal chondrosarcoma is wide “enblock” excision, which is often not obtainable in spinemaking its treatment difficult and requires piecemealexcision. Prognosis depends mainly on tumor removal,whereas the peculiar anatomical feature of the spinepractically avoids an ideal “en-block” resection. When alllocations are considered, survival from chondrosarcomavaries between 55% and 75% With median length ofsurvival being 16 months to 6 years.19,24,28 Most importantprognostic factors are histological grading, tumour staging,patient’s age and surgical margins free from tumor.3,15,19,20

There are only a few series in the literature concerningspinal chondrosarcomas.3,24,28 Lumbar spine is the mostcommon location and the male sex is predominant.3

Total “en-block” excision whenever possible is thetreatment of choice for chondrosarcoma.13,14,27 Adjuvantchemo and/or radio therapy is recommended when thisgoal of total en block excision is not obtained.

Spinal stabilization should be considered in all cases whenspinal stability is in doubt following excision of the

tumour.4,27 Tomita et al has reported new technique of totalen bloc spondylectomy, consisting of en bloc laminectomyand en bloc corpectomy followed by anteriorinstrumentation with spacer grafting and posterior spinalinstrumentation.27 All seven patients in his series exceptone, attained significant clinical improvement after surgerywith no major complications. Author concluded that the“total en bloc spondylectomy” which include resection ofthe involved vertabra(e) in two major blocs, rather than ina piecemeal pattern, offers one of the most aggressivemodes of therapy for primary spinal malignancy. Few othercases are also reported in literature with an “en-bloc”resection of the lesions with spinal instrumentation.4

There are no studies in the literature which have provedthe effectiveness of radiotherapy, as well as ofchemotherapy, in spinal chondrosarcoma. Many authorshave shown significant increase in survival after adjuvanttherapy,15,28 some have suggested adjuvant chemo and/orradio therapy considering its probable extraspinalmesenchymal origin,16,21,22,23,25,28 as in this case.

Boriani et al evaluated 22 patients, with mean age of 37years (30-70yrs). Out of 22 patients intralesional excisionwas done in 10 patients while enblock excision wasperformed in 12 patients. Recurrence rate was 100 % (10patients) in first group and 20 %( 3 patients) in secondgroup with overall rate was 59 % (13 patients). Theyconcluded that “enblock” excision (wide or even marginal)found to give the pt best chance of survival and lowestrecurrence rate.3

According to York et al.28 who studied 21 patients withspinal chondrosarcoma, during a period of 43 years,demonstrating a longer disease free interval in patients withtotal rather than subtotal resection. The tumor recurred in64% of the patients and the median disease free intervalwas 16 months without adjuvant therapy.

Shives et al.24 studied 20 patients with chondrosarcomaof the spine and found 100% recurrence in patientssubmitted to tumor debulking only, half of the casesrecurring among the six patients with inappropriate surgicalmargins and no recurrences in two patients with radicalresection.

■ Conclusion

“En block” surgical resection is the best therapeutic optionfor chondrosarcomas, considering its resistance toradiotherapy and chemotherapy.3,16,21,24,27,28 Piece-meal

Figure 4Preoperative MRI showing huge mass in both thoracic cavitiesconnected by growth in the posterior mediastinum

Figure 5Postoperative CT Scan showing total removal of the tumour bybilateral thoracotomy


53

removal should be attempted when “en-block” resectionis not feasible, but assurance of margins free from tumormust be obtained along with adjuvant radio and/orchemotherapy.

■ References

1. Bartalena T, Rimondi E, Rossi G, Bianchi G, Alberghini M. Low gradecentral chondrosarcoma of the fifth costotransverse joint. AustralasRadiol Oct;51 Spec No.:B122-5, 2007.

2. Belhachmi A, Akhaddar A, Gazzaz M, Elasri C, Elmostarchid B,Boucetta M, Albouzidi A. Primary spinal intradural mesenchymalchondrosarcoma. A pediatric case report. Neuroradiol Jul;35(3):189-91, 2008.

3. Boriani S, De Iure F, Bandiera S, Campanacci L, Biagini R, Di FioreM, Bandello L, Picci P, Bacchini P. Chondrosarcoma of the mobilespine: report on 22 cases. Spine 2000 Apr 1;25(7):804-12.Chondrosarcoma of bone: does the size of the tumor, the presenceof a pathologic fracture, or prior intervention have an impact onlocal control and survival? J Cancer Res Ther 2009 Jan-Mar;5(1):14-9.

4. Domínguez CJ, Martín-Ferrer S, Rimbau J, Joly C. [Upper cervicalchondrosarcoma]Neurocirugia (Astur) 2005 Jun;16(3):261-5;discussion 265.

5. Gelabert-González M, Reyes-Santías RM, García-Pravos A. [Dorsalmedullary compression due to a primary vertebralchondrosarcomaRev Neurol 2000 Feb 16-29;30(4):322-4.

6. He XL, Pan D, Zhou Y, Gan YL, Zhang HB. [Mesenchymalchondrosarcoma of thoracic spine: report of a case]ZhonghuaBing Li Xue Za Zhi 2006 Dec;35(12):766-7.

7. Huang KF, Tzaan WC, Lin CY. Primary intraspinal mesenchymalchondrosarcoma: a case report and literature review. Chang GungMed J 2003 May;26(5):370-6.

8. Kotil K, Bilge T, Olagac V. Primary intradural myxoid chondrosarcoma:a case report and review in the literature. J Neurooncol 2005 Nov;75(2):169-72.

9. Kruse R, Simon RG, Stanton R, Grissom LE, Conard K. Mesenchymalchondrosarcoma of the cervical spine in a child. Am J Orthop 1997Apr;26(4):279-82. Erratum in: Am J Orthop 1997 May;26(5):334.

10. Li YH, Yao XH. Primary intradural mesenchymal chondrosarcomaof the spine in a child. Pediatr Radiol 2007 Nov;37(11):1155-8.

11. Lloret I, Server A, Bjerkehegen B primary spinal chondrosarcoma:radiological findings with pathological correlation. Acta radiology2006 Feb; 47(1):77-84.

12. Mandelli C, Bernucci C, Mortini P, Tartara F, Scomazzoni F, GiovanelliM. Chondrosarcoma of the thoracic spine: total en bloc sagittalresection. A case report. J Neurosurg Sci 2001 Jun;45(2):114-9.

13. Matsuda Y, Sakayama K, Sugawara Y, Miyawaki J, Kidani T,Miyazaki T, Tanji N, Yamamoto H. Mesenchymal chondrosarcoma

treated with total en bloc spondylectomy for 2 consecutive lumbarvertebrae resulted in continuous disease-free survival for morethan 5 years: case report. Spine 2006 Apr 15;31(8):E231-6.

14. McLoughlin GS, Sciubba DM, Wolinsky JP.Chondroma/Chondrosarcoma of the spine. Neurosurg Clin N Am 2008Jan;19(1):57-63.

15. Mody MG, Rao G, Rhines LD. Surgical management of spinalmesenchymal tumors. Curr Oncol Rep 2006 Jul;8(4):297-304.

16. Pennekamp PH, Falkenhausen M, Zhou H, Stütz A, Kraft CN, DiedrichO. [Invasive chondrosarcoma of the thoracic spine as a rare causeof acute paraplegia] Z Orthop Ihre Grenzgeb 2005 Mar-Apr;143(2):219-21.

17. Platania N, Nicoletti G, Lanzafame S, Albanese V.J Spinal meningealmesenchymal chondrosarcoma. Report of a new case and reviewof the literature. Neurosurg Sci 2003 Jun;47(2):107-10.

18. Puri A, Shah M, Agarwal MG, Jambhekar NA, BasappaP,Chondrosarcoma of bone: does size of tumour, the presence ofa pathological fracture, or prior intervention have an impact onlocal control and survival. Cancer Res Thes 2009 Jan-Mar;5(1):14-9

19. Quiriny M, Gebhart M. Chondrosarcoma of the spine: a report ofthree cases and literature review. Acta Orthop Belg 2008Dec;74(6):885-90.

20. Riedel RF, Larrier N, Dodd L, Kirsch D, Martinez S, Brigman BE. TheClinical Management of Chondrosarcoma.Curr Treat Options Oncol2009 Feb 24.

21. Rutz HP, Weber DC, Goitein G, Ares C, Bolsi A, Lomax AJ, PedroniE, Coray A, Hug EB, Timmermann B. Postoperative spot-scanningproton radiation therapy for chordoma and chondrosarcoma inchildren and adolescents: initial experience at paul scherrerinstitute.Int J Radiat Oncol Biol Phys 2008 May 1;71(1):220-5.

22. Sakayama K, Kawatani Y, Kidani T, Sugawara Y, Miyazaki T,Fujibuchi T, Yamamoto H. Dumbbell-shaped chondrosarcoma thatprimarily developed in the cervical spine: a case report. J OrthopSci 2004;9(2):166-70.

23. Shives TC, McLeod RA, Unni KK, et al. Chondrosarcoma of thespine. J Bone Joint Surg 1989;71:1158-65.

24. Sundaresan N, Rosen G, Boriani S. Primary malignant tumors of thespine: Orthop Clin North Am 2009 Jan;40(1):21-36.

25. York JE, Berk RH, Fuller GN, et al. Chondrosarcoma of the spine:1954 to 1997. J Neurosurg (Spine 1) 1999;90:73-78.

26. Thomson AD, Turner-Warwick RT. Skeletal sarcomat and geant-cell tumor JBJS 1955, 37-B:266-33.

27. Doh JW, Halliday AL, Baldwin NG, Benzel EC. Spinal stabilization byusing crossed-swrew anterior-posterior fixation aftermultisegmental total spondylectomy for thoracic chondrosarcoa.Case report. J neurosurg 2001 Apr;04 (2 suppl):279-83.

28. Tomita K, Kawahara N, Baba H, Tsuchiya H, Fujita T, Toribatake Y.A new surgical technique for primary malignant vertebral tumors.Spine 1997 Feb 1;2(3):324-33.

Address for correspondenceDr. Shekhar Bhojraj : Email : [email protected]

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Unusual low back pain: A micro view

Chandralekha Tampi, MD (Path), Leera Gonsalves, DPBDepartment of Histopathology, Lilavati Hospital and Research Centre, Mumbai

Clinical PresentationA 15 year old boy complained of discomfort,lower back radiating to buttocks and thighssince 6 months. The pain increased whengetting up from lying down position. He alsohad constipation since 3 weeks. Onexamination there was tenderness over lowerback and movements of the hip wererestricted.

No neurological deficit was observed.

■ Radiology

MRI of LS spine with contrast was suggestive of a welldefined intradural extramedullary space occupying lesionbelow the level of the conus with intermediate signals onT1 & T2 and enhancement on post contrast. Cordexpansion (Figure 1) was seen.

■ Pathology

The mass was excised and small creamish coloured pieces

aggregating to 2 cms were received for histopathology.

The microscopic features (Figure 2A & B) showed smallcuboidal cells with bland nuclei, aligned around basophilicmucinous material which collared stromal blood vesselsand also collected in microcystic spaces.

No nuclear pleomorphism, mitosis or necrosis were seen.What was the lesion? (Answer on page no. 55).

The post operative period was uneventful and the patientis now symptom free.

Figure 1Cord expansion seen

Figure 2A: & B: Microscopic features of excised mass. Can you guessthe lesion? Answer on page no. 55

A

B


55

■ Discussion

Myxopapillary Ependymoma is a morphologically distinctvariant of ependymoma virtually restricted to the region ofconus medullaris and filum terminale. Thoughependymomas are seen in adults in the third to fifth decadesof life, nearly 1/5th of Myxopapillary Ependymomas involveyoung children less than 20 years of age.1

Nearly all produce low back pain, sciatica, some also showurinary and faecal incontinence, impotence andsensorineural deficit. The ependymal cells form the internallining of the neural tube and later line the cavities of thebrain and spinal cord. They possess motile cilia that helpto produce movement of the CSF. They have lowregenerative potential but can show neoplastictransformation to form tumorous masses. They are thecommonest intramedullary spinal tumors and differ fromastrocytomas in being better demarcated, thus lendingthemselves to better surgical eradication.

Ependymomas of the spinal cord usually arise within cervicothoracic segments and usually in the 4th & 5th decades.Rarely these tumors also erode neighbouring bonystructures and infiltrate paraspinal soft tissue. Myxopapillaryependymoma occasionally spread to higher neuroaxialregions through the cerebrospinal fluid. Multifocality maybeseen in ependyomas complicating Type 2 neurofibromatosis(NF-2).2

Neuroimaging studies show a sharply delineated enhancingmass. The tumor is highly vascularised, ovoid to sausageshaped and can have a fibrous pseudocapsule.Schwannomas which can have a similar appearance onimaging are solitary, benign, truly encapsulated, wellvascularised lesions composed of proliferating S-100positive, bland spindle cells arranged in Antoni ‘A’ and

Antoni ‘B’ patterns of high and low cellularity.

Microscopically, in a conventional ependymoma, smallcuboidal cells are seen, within a dense meshwork of fibrillaryprocesses often arranged collar like around stromal bloodvessels (pseudo rosettes) Sometimes canals and tubuleslined by these cells are seen within the tumor, recapitulatingthe original nature of the ependymal cells. As a glial tumorit shows positivity for Glial fibrillary acidic protein (GFAP).

More aggressive tumors show dense cellularity, conspiciousmitosis, necrosis and microvascular proliferation (WHOGrade III). The extensive myxomatous appearance of themyxopapillary ependymoma can be mistaken for aChordoma which however involves the vertebral body andis not glial in origin. Gross total resection is the treatmentof choice and extent of resection is the single most importantprognostic factor. Post operative imaging should be doneto detect unsuspected residual tumor. Spinal cord tumorshave the best prognosis as complete resection is nearlyalways possible. Total resection carries a 10 yr. survival of85 – 90%, subtotal resection of 80% and biopsy of 25%.3

In the WHO classification myxopapillary Ependymomasare Grade I tumors, while conventional Ependymomas areGrade II & anaplastic Ependymomas are Grade III tumors.

■■■■■ References

1. Sonneland PR, Scheithauer BW, Onofrio BM. MyxopapillaryEpendymoma. A clinicopathologic and immunocytochemical studyof 77 cases. Cancer 56:883-93, 1985.

2. Weistler OD, Schiffer D, Coons SW, Prayson RA, Rosenblum MK.Ependymal tumors. In Klrihues P, Cavenee WK (eds):World HealthOrganization classification of tumours. Pathology and Genetics-Tumours of the nervous system. Lyon, IARC press: pp 71-81,2000.

3. Fehlings M.G and Rao, S.C.2000: Spinal cord and spinal columntumours. In.Bernstein M, and Berger,M.s (eds), Neurooncology.The essentials. New York, Thieme Medical Publishers, pp 372-3.

Address for correspondenceDr. Chandralekha Tampi : Email : [email protected]

Answer : The tumor represents a Myxopapillary Ependymoma

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Unusual presentation of acute cervical disc prolapse as spinalcord injury: A case report

Paresh Sodhiya MD, Sushil Patkar, MDDepartment of Neurosurgery, Poona Hospital, Pune

AbstractThe degenerative diseases of the cervicalspine are a common occurrence. However,majority of these are either asymptomatic orrespond to conservative management. Acutecervical disc prolapse causing myelopathy isquite rare8. Only 7 cases with severeneurological deterioration following acutecervical disc prolapsed have been reported.10

We report another interesting case of acutecervical myelopathy who, after an initial goodresponse to anterior cervical discectomy andfusion, failed to improve further. A new onset ofposterior compression of the cord by thebuckling of the ligamentum flavum wasidentified in the early post operative period.Patient underwent cervical laminoplastyfollowing which he recovered rapidly asexpected. The purpose of this case report is tohighlight the importance of strong clinicalsuspicion and early surgical intervention incases of acute cervical myelopathy in olderpatients.

Key Words❉ Acute cervical myelopathy❉ Cervical disc prolapse❉ Anterior cervical discectomy and fusion❉ Laminoplasty

■ Introduction

Acute cervical disc prolapse causing radiculopathycommonly occurs in younger age. On the other hand,cervical spondylosis causing myelopathy is more commonlyseen in older age group.7 Presentation of cervical disc withacute neurological deterioration is rare.8,11 Only 7 caseshave been reported so far mentioning the cervical disc asa non traumatic cause for acute neurological deterioration.10

In most cases, acute symptoms were precipitated by disc

prolapse in the presence of pre-existing spinal canalstenosis. However, soft cervical disc herniation presentingwith myelopathy have not been investigated sufficientlybecause of low clinical attention and small case volume.11

We review the literature and present this case demonstratingthat acute quadriparesis secondary to cervical discherniation may occur without a history of myelopathy orspinal canal stenosis.

■ Case report

A 65-year-old man presented to us with sudden onset ofweakness of all four limbs, numbness below nipples,breathlessness and urinary retention. Symptoms were ofless than 24 hours duration. There was neither history ofany episode of similar nature previously nor the history ofany trauma or fever. He was a known asthmatic for manyyears and had been on steroids off and on for symptomaticcontrol. Before he was seen by us he had already receiveda bolus dosed of intravenous steroids (Solumedrol) afterthe onset of quadriparesis.

Examination revealed hypotonia of all four limbs. Therewas no wasting or fasciculation. Power in both shouldersand elbows was grade 5/5. Power in both the hands wasgrade 1/5 and in both the lower limbs was grade 0/5. Therewas sensory hypoesthesia below the level of nipples. Poorchest expansion was causing breathlessness. He wascatheterized for urinary retention.

A clinical diagnosis of acute lower cervical cordcompression of uncertain etiology was made. X-rays ofthe cervical spine showed spondylotic changes with adecreased dick space at C6-7 level.

MRI of the cervical spine showed spondylotic spine withobliteration of subarachnoid space in the subaxial spine.The lordotic curve was maintained. A prominent centraldisc prolapse at C6-7 level was compressing the cord(Figure 1). There were no signal changes in the cord in T2


57

weighted sequences suggestive of injury to the cord.

Expeditiously the patient was operated upon. Theprocedure of anterior cervical discectomy at the level ofC6-7 was performed to decompress the spinal cord. Thespine was stabilized maintaining the disc height byperforming interbody fusion using autologous iliac crestgraft.

■ Post operative progress of the patient

Patient started improving immediately and hisneurological status on the 4th post operative day wasas follows: His power had improved from a grade of 1/5 to grade 4/5 in the hands and grade of 0/5 to grade of1-2 /5 in both lower limbs. MRI scan was done on 4th

post operative day. It showed good anteriordecompression and acceptable position of the graft.

There was straightening of the cervical spine and T2weighted signal changes in the cord at C6-7 levelsuggesting oedema of the spinal cord. The subarachnoidspace anterior and posterior to the cord was bettervisualized than before surgery. Patient was kept in thehospital and was started with limb physiotherapyprogram and a short course of steroids (Solumedrol)(Figure 2).

Further progress

By the end of third week no further improvement wasnoticed, particularly in the lower limbs, as was expectedby the surgeon. MRI was repeated on the 21st postoperative day. It showed subsidence of the cord oedemabut there was a buckling of the ligamentum flavum in theC6-7 interlaminar space causing significant posteriorcompression of the cord (Figure 3). The anterior surfaceof the cord was free with no anterior compression.

A satisfactory early recovery in patient’s neurologicalstatus was followed by a lack of further improvementas expected. It was thus presumed that the compressionof the cord posteriorly by the buckled ligamentum flavumwas preventing further recovery in the neurologicalstatus. It was decided to decompress the cord frombehind. This was explained to the patient and with hisconsent a laminoplasty from C3-7 was done undergeneral anesthesia in next few days.

An immediate improvement in neurological status wasseen by the second day of surgery. The power in theright lower limb improved to grade 4/5 and the powerin the left lower limb improved to grade 3/5. Follow upMRI three weeks later showed opening of all

Figure 1Acute cervical disc prolapse at C6-7 level giving rise topresentation of acute spinal cord injury. The spinal cord itselfdoes not show any changes suggestive of primary damage

Figure 2Postop. MRI on the 4th day shows edema in the spinal cord

Figure 3MRI done 3 weeks later doess not show any compressionanteriorly but posteriorly there is significant compression bybuckling in of the ligamentum flavum

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subarachnoid spaces and resolution of spinal cordoedema as suggested by resolution of cord signalchanges (Figure 4).

■ Discussion

Cervical myelopathy can be caused by numerous diseasessuch as cervical spondylosis, soft cervical disc prolapse,ossification of posterior longitudinal ligament (OPLL),tumor, infection (spondylitis), and bony architecturalabnormalities (fracture, dislocation).11 Cervical spondylosisis the most common cause of myelopathy in patients olderthan 55 years.3 Radiographic evidence of cervicalspondylosis is present in 75-85% of population by the ageof 65 years.8 In our country most of the patients have longstanding history with well established neurodeficits.7

Soft cervical disc herniation accounts for 64 to 89% ofruptured cervical disc.3 It exhibits a distinct predilectionfor males in the fourth decade of life and C5-6 and C6-7level are the most frequently involved sites.4 Acute cervicalmyelopathy may result from a sizable central soft discprolapse or following minor cervical trauma in a patientwith spondylosis or a preexisting compromise of the spinalcanal.11The incidence of soft cervical disc prolapse causingcervical myelopathy is not known clearly. According toone study, soft cervical disc herniation accounts forapproximately 23% of cause for cervical myelopathy.5,11

Incomplete spinal cord compression causing central spinalcord syndrome, Brown Sequard syndrome and anteriorcord syndrome occur more frequently. These syndromesfollowing incomplete acute spinal cord compression mayoccur with some variation or in combination. Spinal cordcompression with loss of all motor and sensory modalities

below the level of functional compression as a result ofacute soft disc prolapse is rare.8 According to one recentstudy, only 7 cases have been reported so far mentioningthe cervical disc as a non traumatic cause for severe acuteneurological deterioration.10 In most of these cases, anassociated congenitally narrow canal or ligamenthypertrophy causing posterior compromise of the spinalcanal is contributory.5

The acute compressive myelopathy caused by soft discprolapse is dealt by anterior decompression of the cordby excising the offending disc in majority of the patients.The outcome in these patients is related to the durationand severity of neurological dysfunction beforedecompression and the level of neurological function inthe first few days after treatment.8 In the literature, thesurgical outcome of cervical discogenic myelopathy is betterthan that of the cervical spondylotic myelopathy.11

A chronic compression of the cord leading to irreversibleneuronal injury explains the poor results in spondyloticmyelopathy. However, an acutely ruptured soft disc causingvascular compromise and severe ischemia resulting inedema of the cord explains for the dramatic onset ofsymptoms and also better response to timely surgery incases of discogenic acute cervical myelopathy10,11 The spinalcord is most subject to compression in the lower cervicalregion and thus, represent the region of the greatest vascularvulnerability on an anatomic basis.6

Different studies have established a complete or nearcomplete relief of preopereative symptomatology ofcervical myelopathy from soft disc prolapse in more than80% of the patients following timely done conventionalanterior cervical discectomy and fusion.1,11

In our case the patient presented within 24 hours of onsetof acute disc prolapse causing quadriparesis. He wasexpeditiously operated upon to remove anteriorcompressing disc and doing reconstruction of spine withinterbody fusion. As there was no history or clinical featuresto suggest a pre existing spondylotic myelopathy, a rapidand sustained recovery was genuinely expected. However,the ongoing improvement had ceased after preliminaryimprovement in upper limbs. There was no further progressduring the next three weeks. This was puzzling and raisedthe suspicion of a missed pathology or a failed surgery. Ahigh clinical suspicion and timely imaging studies identifieda significant compression from behind by buckledligamentum flavum as the cause of persistent weakness inboth lower limbs. Our patient was already operated upon

Figure 4MRI 3 weeks after second operation shows that the spinal cordis now free without any compression either anteriorly orposteriorly


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anteriorly and hence we preferred to do laminoplasty toremove posterior compression with gratifying results. Alaminoplasty was done well in time to relieve posteriorcompression. This was followed by an immediate expectedimprovement in the neurological status of the patient.Laminaplasty may reduce the incidence of post operativekyphosis. Neurological outcome however is same as withlaminectomy.8

■ Conclusion

Successful treatment in this patient lay in keeping the patientin the hospital longer than necessary and observing hisprogress continuously and then doing surgical interventionwhen it was felt necessary. This part of management couldhave been overlooked in case the patient was dischargedhome.

■ References

1. Bucciero A, Visioli L, Cerillo A. Soft cervical disc herniation. Ananalysis of 187 cases. J Neurosurg Sci 42 : 125-30, 1998.

2. Collias JC, Roberts MP. Posterior operations for cervical discherniation and spondylotic myelopathy in Schmidek HH, SweetWH(eds): Operative neurosurgical techniques. Indication, methods,and results, Pheladelphia : W.B. Saunders Company,1988 Vol 2,pp1347-58.

3. Cooper PR. Cervical spondylotic myelopathy. Contemp Neurosurg19:1-8, 1997

4. Dubisson A, Lenelle J, Stevenaert A. Soft cervical disc herniation:A retrospective study of 100 cases. Acta Neurochir (Wein) 125:115-9, 1993.

5. Lestini WF, Weisel SW. Pathogenesis of cervical spondylosis. ClinOrthop Relat Res 239:69-93, 1989.

6. Parke WW. Correlative anatomy of cervical spondylotic myelopathy.Spine 13:831-7,1988.

7. P.S. Ramani, Anant S Kamat. Cervical Spondylotic Myelopathy. Textbook of Spinal Surgery- A comprehensive guide to the managementof spinal problems. 1st edition, Jaypee Brothers, 2005. pp 3219-25.

8. Robert J Jackson, Ziya L Gokaslan. Treatment of disc andligamentous diseases of the cervical spine. Youman’s NeurologicalSurgery:5th edition, Saunders, 2004; pp 4395-407.

9. Rovira M, Torrent O, Ruscalleda J. Some aspects of the spinal cordcirculation in cervical myelopathy. Neuroradiology 9: 209-14, 1975.

10. Venkatraman Sadanand, Michael Kelly, George Varughese, DarylR. Fourney. Sudden Quadriplegia after Acute Cervical DiscHerniation. The Canadian Journal of Neurological Sciences Volume32, Number 3: August 2005; Pp 356-58.

11. Young-Jin Kim, Seong-Hoon Oh, Hyeong-Joong Yi, Young-Soo Kim,Yong Ko, Suck Jun Oh. Myelopathy Caused by Soft Cervical DiscHerniation: Surgical Results and Prognostic Factors J KoreanNeurosurg Soc 42:441-5, 2007.

Address for correspondenceDr. Sushil Patkar : Email : [email protected]

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“Floating” posterior tubercle of atlas as a cause of cord contusion:Case report and review of the literature

K. Sridhar, MD, B. JoseDepartment of Neurosurgery, Malar Hospital, Chennai

AbstractWe report a 25 year old female patient whoafter an incident of trivial trauma to the back ofthe head experienced severe neck pain andquadriparesis. Investigations showed that therewas a congenital absence of the posterior archof the atlas with persistence of posteriortubercle, with a contusion of the upper cervicalcord. An occipito-cervical fusion was performedafter excision of the posterior tubercle. Thepathogenesis and clinical implications of thecongenital “floating” posterior tubercle of C1and other anomalies of the posterior arch ofthe atlas are discussed and the literature isreviewed.

Key Words❉ Atlas❉ Congenital defects❉ Floating posterior tubercle❉ Spinal cord contusion

■ Introduction

Congenital anomalies of the atlas are relatively uncommon

with the incidence varying from 0.87% to 5% in differentanatomic and radiologic studies.4 It is essential to recognizethe condition in order to distinguish it from traumaticabnormalities of the atlas. Among the various aplasias ofthe atlas, the commonest is a median defect of the posteriorarch which is asymptomatic on most occasions. Aplasia ofthe posterior arch of C1 with persistence of the posteriortubercle is a distinct and very rare entity, which couldpredispose to neurological deficits following trivial trauma(Figure 1A, B & C).3

■ Case report

A 25-year-old female presented with history of severe neckpain and paresthesias below the level of the nipple thatdeveloped following a trivial trauma, when she hit herforehead against roof of the car while getting out. Therewas no radicular pain, nor loss of consciousness, vertigoor difficulty in speech. Neurological examination revealednormal cranial nerves including the spinal accessory. Thepower in all four limbs was normal. There was hypertoniain all four limbs, with a bilateral extensor plantar. All deeptendon reflexes were exaggerated. There was hypoesthesiain the C2 and C3 dermatomes. Sensations includingposterior column were normal, though she complained of

Figure 1A, B & CA: Plain x-ray lateral view showing a ‘floating’ posterior tubercle of the atlasB: 3D CT scan showing floating tubercle (1) and absence of posterior arch (2)C: MRI showing contusion in the cord following trivial trauma

A B


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spontaneous paresthesia below D5 dermatome. Therewere no appendicular cerebellar signs. The neck muscleswere in severe spasm. The X-ray cervical spine lateralview showed a defect of posterior arch of atlas.

There was no obvious instability. 3D spiral CT scan showedcongenital absence of the part of posterior arch of C1 oneither side. The odontoid was in normal position. MRI ofthe cervical spine showed hyperintense signal changes inthe posterior aspect of the cord in the T2 weighted imageopposite C2- C3. The Transverse ligament was foundintact.

At surgery, the posterior elements of the atlas and axiswere exposed. The posterior tubercle of atlas was floatingwith a fibrous band extending beyond the bone margin onthe left and thick ligamentous structure on the right. Theposterior tubercle was freely mobile. This was excised andan occipito cervical fusion was performed using a Y- platefixed between occiput and C2. Postoperatively sheremained neurologically stationary and was mobilized withmodified Philadelphia collar on the second postoperativeday. At follow-up after 1 month she had total relief ofhyperaesthesia and 80 % reduction of parasthesia belowthe level of nipple. Radiological fusion was confirmed at 6months. At follow-up of over 50 months she has remainedasymptomatic and with no neurological deficit (Figure 2).

■ Discussion

Congenital anomalies of the posterior arch of the atlas arerare and occur during development. They are presentlythough to be a defect of ‘chondrogenesis’.5,7 The atlas hasthree primary ossification centers that form during theembryonic period. During the seventh week of intrauterinelife, the two lateral centers located at the lateral masses

extend dorsally to form the posterior arch. The anteriorossification center forms the anterior tubercle and theanterior arch, which usually unites with the two lateralcenters by the 6th to 8th year. The two posterior halvesare nearly fused at birth, except for several millimeters ofcartilage, and in approximately 2% of the population, afourth posterior ossification center forms the posteriortubercle between the two neural arches. The latter processusually occurs around the 2nd year of life (Table 1).

Curriano G et al 1 have classified anomalies of the posteriorarch of atlas into five types (Table 1). Median clefts of theposterior arch (Type A) have been estimated to occur in4% of the population and represent 97% of all posteriorarch defects. Type B through Type E congenital defectshave been reported to occur in 0.69% of the populationand consist of varying degrees of unilateral cleft defects(Type B), bilateral cleft defects (Type C), absence ofposterior arch with persistent posterior tubercle (Type D),and total agenesis of the posterior arch (Type E). Senogluet al8 evaluated 1104 patients with medical problems, 166dried C1 specimens and 84 fresh cadaveric specimens forcongenital defects of the anterior and posterior arches ofatlas. They found posterior arch defects in 3.35% of the1104 patients evaluated with a CT Scan. Significantly, noType C or Type D abnormalities were found.

The clinical presentation of reported cases in the literaturehas been variable. In their review of the literature, Currianoet al1 divided patients into five groups depending on theirclinical presentation and found that almost one third (Group1) are asymptomatic. Other patients present with neck painor spasm (Group 2), chronic neck symptoms (Group 3)or chronic neurological problems (Group 4). Group 5patients, such as the case reported above, present withacute neurological symptoms following minor trauma andare seen with Type C and D anomalies.3 Saiguchi et al7

found 18 such cases reported in literature. The presenceof an isolated posterior bony fragment predisposes thesepatients to neurologic morbidity secondary to cordcompression, and caused by the mobility of the isolatedposterior bony fragment during extension of the cervical

Figure 2Plain x-ray lateral view taken at 1 month post-operative follow upshowing the occipito-axial fusion and graft in place

Table 1: Classification of Anomalies of theposterior arch of atlas

Type Description

A Failure of posterior midline fusion of the two hemiarches

B Unilateral defect

C Bilateral defects

D Absence of posterior arch with persistent posterior tubercle

E Absence of entire arch ,including the tubercle

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spine.6,9 The posterior isolated bony fragment movesseparate from the anterior arch. The presence of fibroustissue in place of the posterior arch of atlas, which wasalso seen in our patient, predisposes towards the potentialinstability.5 Compression of the cord occurs duringextension, when, with inward buckling of the attachedligaments, and anterior displacement of the bony fragmentinto the spinal canal, there is a gross reduction in the distancebetween the occiput and the spinous process of the axis,causing neurological deficit.7,9 Dynamic radiographs whendone occasionally demonstrate the abnormal movement.CT scan show the rounded edges of the bone with acortex, differentiating the defect from traumatic in origin.2,5

MRI shows signal change in the cord in patients withneurological symptoms or deficit. In most, the signal changein the cord is seen at a level just below the posterior tubercleof atlas, indicating that the injury to the cord occurs duringextention of the spine.7 We do not think that it is prudentto do dynamic x-rays in a patient with clinical signs of cranio-cervical instability. The presence of the signal change inthe MRI is proof enough that the cord has been damagedduring some movement.

Type C and Type D defects need surgical intervention,while the others, which are most often asymptomatic, canbe treated symptomatically. Excision of the posteriortubercle or the bony remnant of the arch and the fibrousligaments with a occipito cervical or atlanto-axial fusion isindicated.

■ Conclusion

Congenital anomalies of the posterior arch of atlas are rare.

“Floating” remnants of the posterior arch, which are theType C and D defects, are a potential cause of injury tothe cervico-medullary junction after trivial trauma.Physicians should be aware that these anomalies may notbe apparent on lateral screening x-rays alone, and mayneed furthur imaging for delineation. Suspicious C1fractures after a minor trauma may actually be a congenitalposterior arch defect. Type C and Type D defects needsurgery and a fusion procedure to prevent a catastrophicneurological morbidity.

■ References

1. Curriano G, Rollings N, Diehl JT. Congenital defects of the posteriorarch of the atlas: a report of seven cases including an affectedmother and son. AJNR 15:249-54, 1994.

2. Dorne HL, Just N, Lander PH. CT recognition of anomalies of theposterior arch of the atlas vertebra: differentiation from fractures.AJNR 7:176-7, 1986.

3. Gangopadhyay S, Aslam M. Posterior arch defects of the atlas:significance in trauma and literature review. European Journal ofEmergency Medicine 10:238-40, 2003.

4. Mcrae DL. The significance of abnormalities of the cervical spineAJR 84:3-25, 1960.

5. Panagopoulos A, Zouboulis P, Athanaselis E, Papadopoulos AX,Dimakopoulos P. Aplasia of the posterior arch of atlas with persistentposterior tubercle: a case report. Eur Spine Journal 14:205-7, 2005.

6. Richardson EG, Boon SC, Reid RL. Intermittent quadriparesisassociated with a congenital anomaly of the posterior arch of theatlas. J Bone Joint Surg (Am) 57:853-4, 1975.

7. Saiguchi T, Tachibana S, Sato K, Shimizu S, Kobayashi I, Oka H,Fujii K, Kan S. Lhermitte sign during yawning associated withcongenital partial aplasia of the posterior arch of atlas. AJNR 27:258-60, 2006.

8. Senoglu M, Safavi-Abbasi S, Theodore N, Bambakidis NC, CrawfordNR, Sonntag VKH. The frequency and clinical significance ofcongenital defects of the anterior and posterior arch of atlas. JNeurourg Spine 7:300-402, 2007.

9. Sharma A, Gaikwad SB, Doel PS, Mishra NK, Kale SS. Partial aplasiaof the posterior arch of atlas with an isolated posterior arch remnant:findings in three cases. AJNR 21:1167-71, 2000.

Address for correspondenceDr. K. Sridhar : Email : [email protected]


63

A rare case of lumbarspine osteochondroma causingcauda equina syndrome

Prakash Modha, MD,* Ajay Rajyaguru MD,** Kartik Modha, MD,*** Vishal Modha****Department of Neurosurgery & General Surgery, PDU Medical College, Rajkot, Gujarat* Honorary Prof. of Department of Neurosurgery, PDU Medical College, Rajkot** Assistant Prof. of General Surgery, PDU Medical College, Rajkot*** Associate Prof. of Neurosurgery, PDU Medical College, Rajkot**** Intern Department of General Surgery, PDU Medical College, Rajkot

AbstractOsteochondroma or so called exostosis iscommon in the bones of the limbs. It is rare inthe lumbar spine. We encountered one suchcase which was reported here. The tumour wasbenign and it had caused cauda equinasyndrome. Surgery which was necessary wascarried out successfully to decompress theneural elements. He did not require furtherfollow-up treatment as histopathologicalstudies revealed the tumour to be benignosteochondroma.

Key Words❉ Spinal osteeochondroma❉ Cauda equina compression❉ IGN tumour

■ Introduction

Osteochondroma or exostosis are common in the longbones particularly femur and tibia. It is rare in the spine.Recently we encountered one case of lumbar spinalosteochodroma which had caused cauda equina syndromenecessitating surgical intervention with successful outcome.The diagnosis was confirmed with histopathologicalexamination.

■ Case report

A 35-year-old male patient presented to us with backacheand difficulty in walking since 6 months. Starting withbackpain, over a period of six months the symptomsgradually progressed necessitating the patient to seekmedical advice. For the last two months he was also

constipated and had difficulty in passing urine. Every timehe had to force and apply pressure to pass urine. Recentlyhe has complained of numbness in the perianal region onthe left side. The pain in the back had become excruciating.

On clinical examination he was walking slowly and limpingin the left leg. He was averagely built. He had developedweakness in both lower limbs below knee joint andpowering the muscles was grade 3. Power in the hips wasnormal. There was no wasting in the muscles. There waspatchy sensory loss in the distribution of L4, L5 and S1roots. S2, S3 and S4 roots were also involved and therewas hypoesthesia on the left side in the perianal region.

In the lumbar region a mass could be felt in the paramedianregion on the left side under the skin and paraspinal muscles.The spine itself had developed scoliosis with concavity tothe left. Clinical examination also showed asymptomaticexostosis in both tibial bones.

Investigations including X-rays, CT scan and MRI of thelumbar spine showed a large bony growth arising from L2vertebra on the left side and involving the body, thetransverse process, the pedicle, the facet joint and thelamina on the left side (Figures 1 & 2). The growth hadencroached into the canal and had caused cauda equinecompression. Survey x-rays of the limbs showed exostosisin both tibial bones (Figure 3).

In view of cauda equine compression, severe pain andneurological deficit, it was decided to decompress thecauda equine. This was done under general anesthesia inprone position through a midline incision. The paraspinalmuscles on the left side were incised horizontally to exposethe tumour. It was grayish yellow in colour and relativelyavascular. It was removed piecemeal by using high speeddrill bone roungers and osteotomes. The tumour from the

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Figure 1MRI sagittal cut showing a large tumour arising from the L2vertebra and encroaching into the canal as shown by arrow

Figure 2CT scan axial cut of the lumbar spine at L2 level shows thetumour (shown by arrow) arising as described above andencroaching into the spinal canal

Figure 3X-rays of lower limbs confirms the presence of exostosis in both tibial bones

canal was completely excised. As much as possible thetumour was excised from the body, pedicel and thetransverse process on the left side. The spine did not lookunstable obviously and hence no stabilization procedurewas carried out at this time.

Patient stood the procedure well and he was quicklymobilized on the second day with frame type LS belt andwas given vigorous physiotherapy to improve the powerin the lower limbs. In consultation with urology specialisthe was given Urispass tablets and the catheter wasremoved on the 4th day. He is able to pass urine morecomfortably but he remains constipated. The power in thelower limbers is improving gradually.

Histopathological examination of the tissue showed acartilaginous cap resembling normal hyaline cartilage withbenign chondrocytes. At the interface active endochondralossification was amplysing. After the interface bonytrabeculae of the osteochondroma were seen without anymalignant transformation in any part (Figure 4).

Figure 4Histopathological examinaition of the tissue shows it to be benignosteochondroma

Interface between the cartilage andthe bony trabaculae of the bony partof the tumour showing activeendochondral ossification.

Bony trabaculae of theosteoma part of theosteochondroma.

Hyaline cartilagecap of the tumour


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The diagnosis of benign osteochondroma was made andno further treatment was carried out for the tumour. Sincethe exostosis on the tibia was asymptomatic, they havenot been treated.

■ Discussion

Between 1-4% of osteochondroma arise in spine. Solomonreported an incidence of 9% of spinal osteochondromasin a series of 52 patients with hereditary multipleexostoses.3,4 Compression of spinal cord is an uncommonmanifestation of osteochondroma. The neurological deficitis invariably the result of compression caused by anexpanding lesion arising from the posterior element of thevertebra. Pain & palpable mass were the commonestsymptoms. Males are more frequently affected thenfemales. Patient with multiple exostosis presenting with aspinal lesion are usually in there second or third decade.Lumbar osteochondroma is uncommon in comparision withcervical & thoracic osteochondroma.1 Both CT & MRIscan is extremely effective for assessment of the size &extent of the bony stock as well as of the cartilaginouscap. T2 weighted images show well-defined bone, cartilage& marrow signal intensities. MRI of spinal osteochondromashows an outer osteochondral layer & an ossified controlmass.2,5 An osteochondroma of the spine should beexcluded in all patients with hereditary multiple exostosiswho have spinal pain with neurological deficit.

Osteochondroma is thought to be associated with a genecalled EXT-1. Alterations in the gene are thought to be thecause of this disease. It can be passed along in families.There is no other known risk factor or cause. There areincrease chances of benign tumors turning malignant.7

■ Conclusion

In benign osteochondromas, decompression of the caudaequina has given good results. The patient is being keptunder observation. In case he gets continuous pain in theback or develops instability a spinal stabilization procedurewill be carried out in future.

■ References

1. Carmel PW, Camer FJ. Cervical cord compression due to exostosisin a patient with hereditary multiple exostoses: case report. JNeurosurg. 28:500-3, 1968.

2. Moriwaka F, Hozen H, Nakane K, Sasaki H, Tashiro K, Abe H.myelopathy due to osteochondroma : MR & CT studies. J Computassist tomogr. 14(1):128-30, 1990.

3. Solomon C. Hereditary multiple exotoses. Am J Hum Genet 16:351-63,1964.

4. Solomon L. Hereditary multiple exostosis. J Bone Joint Surg [Br].45-B: 292-304, 1963.

5. Wold Le, Mcleod Ra, Si FH, Unni KK. Atlas of orthopaedic pathology.Philadelphia: W. B. Saunders 50-5, 1992.

6. Van Der Sluis R, Gurr K, Joseph MG. osteochondroma of the lumbarspine: an unusual case of sciatica. Spine 17:1519-21, 1992.

7. www.aaos.org

Address for correspondenceDr. Prakash Modha : Email : [email protected]

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Operative technique : Micro lumbar discectomy

P. S. Ramani, MDDepartment of Neurosurgery, Lilavati Hospital & Research Center, Mumbai, India

IntroductionThe treatment options for prolapsed lumbarintervertebral disc include various surgicalprocedures. When the conservative treatmentfails to treat source of nerve root compressionsurgical procedure is advocated.

In 1934, Mixter and Barr treated prolapsedlumbar intervertebral disc surgically for the firsttime by doing hemilaminectomy and excisionof the prolapsed disc. Laminectomy anddiscoidectomy then became the standardprocedure for a long time.Since 1977, whenmicrolumbar discectomy for herniated disc wasfirst reported by Yasargil and Caspar, manyresearchers have described its usefulness. Itis less invasive than some other operativemethods because the small skin incisioncauses little damage to the musculature andbecause the nervous structures can be safelymobilized in the clear and magnified viewunder the microscope.

Microlumbar discectomy today is the goldstandard with which other procedures can becompared. Smaller skin incision, less intra-operative bleeding, shorter length of stay inhospital and early return to work makesmicrolumbar discectomy – a minimally invasiveprocedure – suitable for surgical treatment ofa given case of prolapsed lumbar intervertebraldisc in modern times.

■ Occurrence of prolapsed lumbar intervertebraldisc

Prolapsed lumbar intervertebral disc is most commonbetween the ages of 30 and 50 years. It is frequently foundbetween 20 and 30 years of age. It is more common in the

males and 95% patients suffer from 4th or 5th lumbar discprolapse (Figure 1A, B & C).

Figure 1A: X-rays B: & C: MRI show a very large prolapsed disc

A

B

C


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■ Advantages of microlumbar discectomy

❖ Very short incision (23mm)❖ Paramedian incision is less painful❖ Least morbidity❖ Integrity of the motion segment is preserved❖ Direct magnified and bright illumination of the

prolapsed disc and its visualization in 3-dimensionsmakes it a gold standard procedure

❖ Even medially placed disc can be effectively excised❖ Less than 1 day stay in the hospital❖ Early return to work❖ Resumption of heavy manual work

■ Contraindications

❖ Not a suitable procedure for multiple level lateralrescess stenosis

❖ In elderly patients with associated degenerativechanges in the spine

■ Alternative choices

❖ This procedure can be done at one or multiple levelon the same side by extending the incision

❖ Bilateral microlumbar can be done through a midlineincision

❖ Skip prolapse can be done through separate incision.Skip prolapse may be on the same side or the oppositeside

■ Ideal cases for microlumbar discectomy

❖ Posteriolateral disc prolapse (Figure 2)❖ Foraminal disc prolapse❖ Posteriomedial disc prolapse❖ Sequestrated disc prolapse

■ Anesthesia

❖ The procedure is performed under general anesthesia❖ The blood pressure is maintained at normal levels❖ The peak airway pressure has to be maintained at

around 20 to prevent epidural congestion

■ Position of the patient

❖ Patient lies prone on two bolsters on the operationtable

❖ The table is slightly bent at the level of the disc prolapseto open the spine

❖ Small bolsters kept under the iliac crest helps furtherto open the spine

❖ The legs are bent upwards to prevent stasis of blood(Figure 3)

■ Identifying the level of surgery

❖ Image intensifier is used to correctly identify the levelof disc prolapse

❖ With short incision it is possible to miss the level❖ A number 18 needle is pierced through the skin at the

anticipated level of disc prolapse❖ C-arm image confirms the level (Figure 4)

■ Preparation of skin and prophylacticantibiotics

❖ Shaving of back❖ Scrubbing with an antiseptic soap solution e.g.

Povidone iodine❖ Cleaning with sterilium❖ Painting with betadine solution❖ Prophylactic antibiotics – cefotaxime 1g

Figure 2Suitable cases for microlumbar discectomy

Bulge Sequestration

Figure 3Patient on the operation table for microlumbar discectomy

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■ Skin incision and facial flap

❖ Skin incision is 1-inch (25mm) long taken paramediallyin curvilinear fashion 1.5 cm away from midline

❖ With C-arm facilities the correct level is easily identified❖ In absence of C-arm following guidelines can be

followed❖ For 5th lumbar disc prolapsed the center of the incision

should be exactly in the space between the spinousprocesses of L5 and S1

❖ For 4th lumbar disc prolapse the incision should be 1/3rd below and 2/3rd above the center between thespinous processes of L4 and L5

❖ For 3rd lumbar disc prolapsed the incision should be1/4th below and 3/4th above the center between thespinous processes of L3 and L4

❖ The variable placement of the incision is in keepingwith the obliquity of the laminae of the lumbar spinefrom below upwards (Figure 5 A & B)

Superficial exposure

❖ Skin and subcutaneous tissues are incised❖ The flap is turned medially and held in place with two

subcutaneous sutures❖ Hemostasis achieved with bipolar coagulation❖ The paravertebral fascia is then incised along the line

of incision and reflected medially and held in placewith two sutures

❖ The paravertebral muscles are separatedsubperiosteally from spinous processes and the laminaeusing electrocautery

■ Exposure of interlaminar space

Dr Ramani’s microlumbar retractor consists of two typesof blades. The medial blade is a hook which is anchoredagainst the spinous process or the interspinous ligament.The lateral one is a blade and it is positioned against thereflected paraspinal muscles. In a given set the blades comein different lengths so that the blades of correct depth for agiven patient can be selected. The retractor has a ratchetand once it is engaged in the blades it can retract the musclesforcefully (Figure 6A & B).

The interspinous space and the ligamentum flavum isexposed.

Further retraction laterally should be carried out until facetjoints are exposed.

■ Use of microscope

Now the microscope is introduced. It uses magnification

Figure 4Needle showing the correct level of prolapsed disc

Figure 5A & BMarking the incision and turning the flap medially

A B


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of 300 (Figure 7A & B).

■ Excision of ligamentum flavum

Using no. 11 blade and cutting upwards, the ligamentumflavum is incised vertically into medial and lateral hives.The lateral half of the ligamentum flavum is excised in onepiece and preserved to be replaced in the window afterdiscoidectomy. It forms a good protecting barrier betweenthe nerve root below and muscles above. It is a barrier ofliving tissue although there is no vascular pedicle. Anyportion of lamina is not removed in this procedure.

However at L3/4 level the undersurface of the junction oflamina with facet may need to be undercut to expose theprolapsed disc.

Using image intensifier, the level is confirmed (Figures 8 to10).

■ Exploration of epidural space

❖ The epidural fat is exposed. The root is lying underthe epidural fat

Figure 6A & BA: Microlumbar retractor B: Retractor in position exposing the interlaminar space

A B

Figure 7A & B(Pentaro – fully automatic with Carl Zeiss lens)

Figure 8Only the lateral half of the ligamentum flavum is excised in onepiece

A B

❖ The epidural fat is excised using bipolar coagulationand microscissors

❖ The root is exposed. It is a tubular structure andappears glistening white under the microscope withblood vessels of the root running over it

❖ Usually the root is displaced medially by the prolapseddisc. The root is gently retracted medially using no. 4

Figure 9Black line divides the ligamentum flavum into lateral and medialhalf. The lateral half is excised

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Figure 10Micro instruments

dissector exposing the epidural blood vessels❖ Meticulous hemostasis under vision is obtained by

carefully coagulating the vessels with bipolarcoagulation and cutting them with microscissors

❖ If necessary foraminotomy is done to decompress thenerve root in the foramen

❖ The prolapsed intervertebral disc is clearly exposed

■ Retraction of nerve root

Two small cottonoids are placed on either side of the discto retract the root.

The left hand of the surgeon is free.

However, if felt necessary, intermittently no. 4 can be usedas retractor.

Under magnification the prolapsed disc looks glisteningwhite and fibrous, if the posterior longitudinal ligament isintact.

If it is sequestrated then it looks white but not fibrous andmay not be glistening.

■ Incision of post long ligament

A 5mm long horizontal incision is made in the posteriorlongitudinal ligament parallel to rims of the vertebral bodies(Figure 11).

The prolapsed disc is then removed using microlumbardiscoidectomy forceps.

The disc is removed piecemeal meticulously with patience.A little more disc tissue from the disc space is then removed.

All loose fragments are removed.

The disc space is not curetted.

Once the discoidectomy is completed the root is checkedto be lying free (Figure 12A, B & C & Figure 13).

■ Closure

Hemostasis is achieved and the piece of ligamentum flavumexcised is replaced back in the window.

Figure 11The sequestrated disc prolapse

Figure 12A, B & CThe sequestrated disc is pulled out with disc rougeurs

A B C


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Figure 13Inconspicuous scar of surgery

Muscles are allowed to fall back.

The fascia is approximated with three interrupted suturesof fine 3/0 vicryl.

Using the same suture material four interruptedsubcutaneous sutures are taken.

The skin edges are approximated with subcuticular nylon.The nylon is pulled out on the sixth day. (In fatty persons itis advisable to keep a minivac drain).

■ Post operative management

❖ Bed is kept in normal position❖ Steroids either locally or systemically are not used

❖ Four doses of antibiotics (Inj. Cefotaxime sodium 1gm IV) are administered. One dose is given prior tosurgery and three doses after surgery at 12 hourlyintervals

❖ Oral medications, a combination of ibuprofen andparacetamol tablets (3 times a day) is administeredfor two weeks

❖ The patient may need one pain killing injection (Inj.Voveran) during the immediate postoperative period

■ Mobilization and discharge

❖ Patient is allowed to get out of bed and walk up to thetoilet on the day of the operation

❖ He is discharged home on the next day❖ The patient is taught a set of exercises to carry out at

home with the intention to keep the back strong andmobile

❖ Lumbosacral belt is not used

■ Limitations

❖ He is not allowed to drive a two wheeler for 3 weeks❖ He is not allowed to drive a car for 2 weeks❖ He is not allowed to lift weights or twist his back

■ Resumption of duties

❖ Light office work within 3 weeks❖ Normal work and the traveling within 4 weeks❖ Heavy manual work after 2 months

Complications

Intra Op Wrong level Use of image intensifier after position and after exposure of lamina can avoid thiscomplication

Dural tear & CSF leak Microscope gave better visualization of all structures and micro instrument better controlof hands. CSF leak and neural damage is rare

Post Op Wound infection Small incision, sterile techniques, less muscle handling. Usually infection is not aproblem with this procedure

Wound haematoma Less blood loss, Bipolar cauterization, tight closure, small exposure. Haematomaformation is rare

Follow Up Recurrence There is upto 6% chance of recurrence at the same disc level

Residual Pain This is a distinct possibility in some cases due to degeneration in the spine or formationof fibrosis or lack of postoperative exercises

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■ Conclusion

Microlumbar discectomy preserves better the integrity ofnormal spinal architecture. The trauma inflicted is minimaland tissue damage is very little. The procedure representsa significant refinement with no morbidity and earlyassurance to return to work in comparison to standardlaminectomy.

■ References

1. Ramani PS. Textbook of Spinal Surgery. A comprehensive guide

to the management of spinal problems. 1st edition: 348-410,2005.

2. Yasargil MG. Microsurgical operation of herniated lumbar disc. AdvNeurosurgery 4:81, 1977.

3. Ramani PS, Chagla A. Microlumbar disectomy state of art treatmentfor prolapsed lumbar intervertebral disc. Neurology India 44:102-7,1996.

4. Henriksen I, Schmidt K, Eskesen V, Jantzen E. A controlled study ofmicrosurgical versus standard lumbar disectomy. British Journal ofNeurosurgery 10(3):289-93, 1996.

5. Goald HJ. Microlumbar disectomy. Follow up of 147 patients. Spine3(2):183-5, 1978.

6. Carragee EJ. Clinical outcomes after lumbar disectomy for sciatica.The effects of fragment types and competence. J Bone Joint SurgAm 85(1):102-8, 2003.


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