Late post-traumatic spinal stenotic progressive myelo-radiculopathy.
A case of late progressive myelo-radiculopathy associated with severe canal stenosis secondary to post-traumatic hypertrophy of thoracic laminae and ossification of spinal ligaments viz. ligamentum flavum and posterior longitudinal ligament in the absence of developmental spinal stenosis or post-traumatic deformity, is presented with a brief critical review of the relevant literature.
The usual neurological complications of vertebral fractures focus on spinal cord or cauda equina injury, and rarely on radiculopathy,. The long-term clinical manifestations of stable or stabilized fractures of the thoracic and lumbar vertebrae commonly are poorly localized pain, stiffness or back weakness.
However, acquired spinal canal stenosis of traumatic origin as a cause of late progressive myelo-radiculopathy is rare,,. In most of the previously reported cases of 'traumatic stenosis', the traumatic deformities have contributed to pre-existing developmental spinal canal stenosis. In this regard, Verbiest has remarked that “to the author's knowledge, no reports of purely traumatic stenosis of the lumbar vertebral canal have been published so far; it is there fore proposed that the term 'traumatic stenosis' is ambiguous and should be replaced by the term stenosis complicated by the trauma if the patient presents with signs of the pre-existing stenosis”.
Furthermore, trauma as an etiological agent in the development of acquired spinal stenosis secondary to hypertrophic ossification of ligamentum flavum (OLF) and of posterior longitudinal ligament (OPLL) though emphasized, has never been substantiated. Unlike OPLL in the cervical spine, thoracic myelopathy due to hypertrophic ossification of spinal ligaments may be overlooked, misdiagnosed or treated inappropriately mainly because of lack of knowledge of this condition particularly outside Japan. Our case which, perhaps contradicts the first two contentions that of Verbiest 27 and Resnick and exemplifies that of Yonenobu et al is therefore considered worthy of presentation. Diligent search done by us in accessible literature failed to reveal a case similar to the one being presented here.
A 45-year-old house-wife (NS 2005/79) had suffered progressively increasing pains in mid-back and the left hip following injury due to accidental fall 10 years back. For six months prior to the admission, she had been experiencing progressively increasing neurogenic intermittent claudication impending walking for more than 10-15 minutes. For 3 months prior to the admission, she had been getting progressively increasing persistent paraesthesia and weakness in both lower limbs. She also complained of precipitancy of micturation. No significant history of other illness in the past was recorded.
General physical examination was normal including vital parameters. There was tenderness over thoraco-lumbar region and left hip joint (with mild flexion deformity), Systemic examination too was normal. Neurololical examination revealed wasted, severely spastic and weak lower limbs with occasionally evident spontaneous flexor spasms bilaterally. Motor strength in the right hip and thigh muscles was 3/5 (MRC grade) while muscles below right knee were totally paralysed (MRC grade: 0/5). Motor strength in the left lower limb was 1-2/5 (MRC grade) in all muscle groups. The left knee jerk and bilateral ankle jerks were exaggerated and the right knee jerk was depressed. Ankle clonus and Babinski's sign were present bilaterally. All sensory modalities were severely impaired below T12 level. On passive straight leg raising test, the left lower limb movements were restricted to 700 with positive Lesegue's sign. Two weeks later, the patient became paraplegic except power MRC grade 2/5 in knee extensors on the right side.
Results of the laboratory investigations were unremarkable. Roentgenographic examination demonstrated normal sacro-iliac joints, soft tissue calcification in infero-medial and posterior parts of the articular capsule of the left hip joint with an old united inter-trochanteric fracture of the neck of the femur (See [Figure - 1]). OPLL (lower one-third of T10 vertebral body to middle one-third of L3 vertebral body level, continuous variety, broad, 6 mm, at upper end and thin, 2-3 min at lower end), OLF (obliterating interlaminar spaces especially at T10-T11, T11-T12, T12-L1 levels), ossified lateral paravertebral ligaments (T11-T12, T12-L1 levels presenting as syndesmophytes), ossified inter-spinous ligaments (from T9 to L1 spinous processes, bridging them) and an oblique fracture through the T10-T11 facets and T10 laminae were evident (See [Figures:2a. b and 3]). Measurements of the interpecticular distance and anteroposterior canal diameter at all levels except at the site of post-traumatic changes were greater than 17 mm and 12 mm respectively. Myodil myclography with cisternal injection of the contrast demonstrated subtotal block at T8-T9 level and complete block at the level of middle one-third of the T10 vertebral body by posteriorly placed extradural lesion, at the adjacent levels of post-traumatic changes. (See [Figure 4a, b]).
At operation (T9 to L1 decompressive Ibminectorny) ossified interspinous ligaments and OLF (T9 to L1 levels) were confirmed. These obliterated the interlaminar spaces totally between T10-T11, and the T11-T12 levels and, also, largely between T9-T10 and tile T12 - L1 levels. Laminectomy was begun through the available small inter- laminar space between T9-T10 level. Hypertrophic (thickened) laminae and hypertrophic OLF were severely constricting and compressing the spinal cord at T10-T11 level (at the level of myelographic total block). The underlying dura mater was densely adherent to the laminae. Therefore separation between thern was practically impossible. Thus, further excision of laminae was started utilising the L1-L2 intcr-laminar space. But at T11-T12, the same phenomenon was encountered. Because of the markedly stenolic spinal canal at T10-T11-T12 levels use of electric air-drill was made to thin out the lypertrophic laminac and OLF and these could then be gradually excised. However, the dura was torn over most of this distance of 4-5 cm as it had been densely adherent to the laminae. The arachnoid too tore off but only over small area oil the right side at T10. The spinal cord was obviously constricted and compressed over this region. Post-operatively, the patient was found to be par-aplegic with retention of urine and violent flexor spasms in lower limbs. Dexamethasone therapy (Dose: 4 mg six hourly daily) did no good to her neurological status. One month later, patient remained same neurologically and then after her discharge from the hospital she was lost to follow up.
The difficulties encountered during surgical procedure were obviously due to severe grade of spinal stenosis produced by hypertrophic laminae and hypertrophic ossification of posterior spinal ligaments as well as due to the dense adhesions formed between aforementioned hyperostotic lesions and adjacent meninges (dura-arachnoid). These noteworthy adhesions were found only at the level of the severe grade of spinal stenosis near the radiologically demonstrated vertebral fracture.
Late post-traumatic progressive myelopathy is a well known entity which usually occurs due to the development of post-traumatic syringomyelia,,, less frequently due to spinal arachnoiditisti,,, and rarely due to tethering of the spinal cord or spinal stenosis complicated by trauma,,,. The term 'acquired spinal canal stenosis' signifies that the spinal stenosis per se occurring during the post-natal life has been aggravated by an acquired pathological process in one or more components constituting the walls of the spinal canal. Therefore, spinal stenoses may be produced by bony (commonest), discogenic (less common) and/or ligamentous (rare) components. As the outline of the subarachnoid spaces as delineated by the myodil column in the thoracic region elsewhere is not suggestive of congenital stenosis in the case under consideration, this case escapes the category of "developmental stenosis complicated by the trauma". Verbiest, while agreeing with Schatzker and Pennal to the rarity of traumatic spinal stenosis has stated that in his experience of four such cases, traumatic deformities have contributed, in all cases, to pre-existing developmental stenosis.
The thoracic and lumbar portions of the spinal cord are also susceptible to compression by hypertrophic ossification of the spinal ligament in the thoracic spinal canal. Such cases are well known in Japanese population,,,, less well known in Caucasians and rare in Indians.
Various etiopathological mechanisms have been incriminated in the development of hypertrophic ossification of the spinal ligaments viz. senile ankylosing hyperostosis, ankylosing spondylitis, fluorosis, vitamin A intoxication, spondylosis,,, infection, while trauma and disorders of calcium and phosphorus metabolism have rarely been incriminated in OPLL,.
Development of spinal stenosis secondary to ligamentous ossification, too, is well known. Resnick has remarked that trauma could produce ligamentous injury and reparative calcification and ossification of the paravertebral ligaments. Brish et al have stated that mild traumatic deformity leading to more widespread hypertrophic changes appears to constitute the chain of events in many cases of spinal stenosis. Fractures in vertebral elements may precede their hypertrophy. Mobility in such cases may result in continuing reparative reaction. The ineffectual callus thus formed might hypertrophy with repeated trauma and ultimately with passage of time might compress the spinal cord. Great care is, therefore, needed during surgery as meninges are frequently adherent to thick ossified ligaments, virtually leaving no space for manoeuvring during laminectomy as happened in our case. Amongst the 19 patients treated initially with posterior decompression by Yonenobu et al, four patients became paraplegic immediately following surgery because the already affected spinal cord was damaged further during surgery as in our case.
The case records, in the department of neurosurgery, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai -400 012, India, covering a period of 3 decades revealed 22 definite cases of symptomatic hypertrophic ossification of spinal ligaments of varied aetiology. However, trauma as an etio-pathogenetic agent could be justified only in the case presented here. Amongst our 22 cases, only in 3 cases was the thoraco-lumbar region, per se, affected.
In conclusion, in the face of radiological and operative evidence of trauma producing severe spinal canal stenosis with meningeal adhesions due to extradural pathological changes at the fracture site and in the absence of pre-existing spinal canal stenosis in the areas not covered by the post-traumatic bony and ligamentous changes; it is reasonable to assume that the spinal stenosis and attendant late progressive myelo-radiculopathy in this case has resulted due to the late posttraumatic, bony and ligamentous changes. Co-existence of trauma and late symptomatic bony and ligamentous stenoses cannot be excluded in the present case. However, further clinical experience is needed to confirm such a controversial co-existence.
We thank Dr. GB Parulkar, the Dean and Dr. SK Pandya, Professor and Head, Department of Neurosurgery, Seth G.S. Medical College and King Edward Memorial Hospital, Parel, Mumbai 400 012, India, for their constant encouragement, guidance and permission to use hospital records.