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| Year : 1999 | Volume
: 47
| Issue : 4 | Page : 308-10 |
Unilateral thoracic canal stenosis.
Deogaonkar M, Goel A, Panchwagh J, Pawar V
Department of Neurosurgery, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai, 400012, India.
Correspondence Address:
Department of Neurosurgery, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai, 400012, India.
Two unusual cases of thoracic spinal canal stenosis are reported. The cord compression was a result of unilateral hypertrophy of the lamina and facet joint. Bony decompression resulted in rapid neurological recovery.
How to cite this article:
Deogaonkar M, Goel A, Panchwagh J, Pawar V. Unilateral thoracic canal stenosis. Neurol India 1999;47:308 |
Hypertrophy of the posterior spinal elements leading to compromise of the spinal canal and symptomatic compression of neural structures is a well recognised pathological entity affecting the lumbar and cervical spine.[1],[2],[3] Thoracic spinal canal stenosis is relatively rare.[4],[5],[6] In this report two rare cases of unilateral hypertrophy of bony components of the posterior spinal elements are discussed. Such a form of canal stenosis has not been reported in the literature. The radiological features, operative findings and the limited literature on thoracic canal stenosis are discussed in this short report.
A 55 year old male patient presented with a 5 days history of weakness of both legs resulting in difficulty in walking, paraesthesiae and tingling and numbness in the legs. The symptoms were worse on the right side and were progressive. At admission he could walk only with support. He was constipated and had urgency of micturation. Neurological examination revealed spasticity in both lower limbs. Power was grade 4, weakness being more on right side. Knee and ankle jerks were exaggerated with bilaterally positive Babinski's sign. All sensory modalities were affected below the 4th thoracic dermatome. Magnetic resonance imaging (MRI) showed unilateral thoracic cord compression by a hypertrophied lamina at fifth thoracic level [Figure. 1a] and [Figure. 1b]. Unilateral right sided thoracic canal stenosis was observed at surgery. The clearly hypertrophied lamina and facet joint were initially removed with the help of a rongeur and later burred away with high speed drill. The adjoining ligaments were normal. There was no abnormality of lamina or facets above or below this level. The patient showed dramatic neurological recovery after the operation. Within six days of surgery his neurological function returned to normal.
Case 2 : A 34 year old male was admitted with complaints of progressive numbness, weakness and stiffness of legs for 3 months. All complaints started on the right leg. He also complained of urgency and precipitancy of micturation and difficulty in ejaculation over the same duration. Spastic paraparesis was noted, the power being grade 2 in the right leg and grade 3 in the left leg. The sensations were depressed below the second lumbar dermatome level. Knee and ankle jerks were markedly exaggerated and were associated with well sustained clonus. MRI showed severe compression of the thoracic cord by anteriorly projecting thickened lamina at the level of disc between the tenth and eleventh thoracic vertebral bodies. Similar compression, although of lesser degree, caused by thickened laminae on the right side was seen below the sixth thoracic level [Figure. 2a],[Figure. 2b). Thoracic decompressive laminectomy (level D6-D12) was carried out. Right sided laminae were thick and tough at all these levels, the worse being the lamina of the tenth dorsal vertebra. The facet joints were normal. The laminae of the left side were normal. This patient also showed a rapid progressive post-operative recovery and regained motor power and urinary control completely within 15 days of surgery. The difficulty in ejaculation also recovered to normal. In both cases histological analysis of the bone was normal.
Descriptions of myelopathy secondary to stenosis of the thoracic spinal canal are distinctly rare.[4],[5],[6] More frequently the stenosis is a result of spondylotic changes and hypertrophy of soft tissue elements. Osseous hypertrophy of normal posterior elements causing symptomatic compression is rare.[4],[7],[8],[9] Unilateral thoracic canal stenosis as a result of osseous hypertrophy has not been reported earlier.
Marzluff[10] described four patients with thoracic spinal cord compression as a result of bilateral articular process and facetal hypertrophy. The clinical presentation was also bilateral in this series. The exact aetiopathogenesis of a unilateral hypertrophy of bony posterior elements remains unclear. Though the bone compressing the dural tube and the cord was tough and relatively vascular in both cases, its histological analysis was unremarkable. Our patient had no clinical or radiographic stigmata of any generalised disorder. The presentation was relatively acute in both cases. This feature does not adequately support the theory of a congenital origin or an unusual form and site of a degenerative change. The presentation was that of an asymmetrical motor and sensory deficit, symptoms and signs being worse on the side of compression. Sphincter disturbances were early in both the cases. A precise preoperative diagnosis of unilateral canal stenosis could be made after reviewing the MRI. Early and complete recovery following the surgical decompression was an encouraging feature in both of our patients.
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