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Hypertrophic atlantoaxial ligaments: an unusual cause of compression of the upper spinal cord
  1. ALEJANDRA TERESA RABADAN
  1. Department of Neurosurgery, Instituto de Investigaciones Medicas “Alfredo Lanari”, Facultad de Medicina, Universidad de Buenos Aires, and Equipo de Neurocirugía de Buenos Aires, Argentina
  2. Department of Pathology, Clinica Bazterrica, Buenos Aires, and Equipo de Neurocirugía de Buenos Aires, Argentina
  1. Dr Alejandra T Rabadan, Billinghurst 1976 PB, 1425 Buenos Aires, Argentina. Telephone 0054 1 902 4417;fax 0054 1 903 8928;email rabadan{at}movi.com.ar
  1. GUSTAVO SEVLEVER
  1. Department of Neurosurgery, Instituto de Investigaciones Medicas “Alfredo Lanari”, Facultad de Medicina, Universidad de Buenos Aires, and Equipo de Neurocirugía de Buenos Aires, Argentina
  2. Department of Pathology, Clinica Bazterrica, Buenos Aires, and Equipo de Neurocirugía de Buenos Aires, Argentina
  1. Dr Alejandra T Rabadan, Billinghurst 1976 PB, 1425 Buenos Aires, Argentina. Telephone 0054 1 902 4417;fax 0054 1 903 8928;email rabadan{at}movi.com.ar

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The craniovertebral junction can be affected by several pseudotumorous masses extradurally located, such as rheumatoid panus, hypertrophic non-union of odontoid fracture, post-traumatic cicatrix, synovial cysts, tumorous calcium pyrophosphate dihydrate crystal deposition, tophaceous gout, calcification of the posterior longitudinal ligament, synovial disease-like pigmented villonodular synovitis, and synovial chondromatosis.1-5 Hypertrophy of the atlantoaxial ligaments as a consequence of degenerative disease was recently recognised as an individual entity. Only five previous cases have been published.1 We add another case to the short series available in the literature, emphasising that as the cause of the spinal cord compression is amenable to surgical removal, symptomatic patients should be diagnosed and treated without delay.

A 66 year old woman presented with a rapid development of progressive spastic tetraparesis and an unremarkable medical history. There was no osteolysis or instability on plain cervical radiography and CT. A bone scan with 99Tc was unremarkable. Magnetic resonance imaging showed a retro-odontoid extradural mass that was homogeneous and isointense on T1 weighted signal, demonstrated no enhancement after intravenous gadolinium contrast, and was compressing the upper cervical spinal cord (figure). The laboratory tests were normal, confirming the absence of rheumatoid arthritis, metabolic disease, or gout. Surgical removal via a transoral approach with a minimal bony resection was direct and provided sufficient space to obtain spinal cord decompression. It was followed by a posterior C1-C2 fusion. Macroscopically, the lesion had no capsule and resembled a hypertrophic ligamentum flavum. Microscopically, it was non-inflammatory, hypocellular, and ligamentary pieces found within the mass appeared fibrous and almost disintegrated. The patient regained normal neurological function. Over a 3 year follow up period there was no recurrence.

Preoperative sagittal T1 weighted MRI of the cervical spine with gadolinium enhancement. A retro-odontoid and extradural mass displacing the spinal cord is seen at the craniovertebral junction.

We focus attention on hypertrophic atlantoaxial ligamentary disease as a degenerative disease that must be considered within the possible causes of high spinal cord compression.

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