Teaching Case

42-year-old woman attended the emergency department for a 3-day history of back and proximal lower extremities pain. It was associated with gait instability, sensory disturbances in feet and difficulty to initiate urination. Physical examination confirmed loss of strength in both lower limbs and vibratory sensation asymmetry was detected.

Initial anteroposterior radiography of the dorsal spine shows hypertrophy of the left T9/10 facet joint.
For further characterization computed tomography (CT) was performed, identifying a bony overgrowth of the superior articular process of the left facet joint in T10 and secondary bone remodelled of lower articular process of T9. Thus a significant imprint occurs in the medullary canal with occupation and extension to the left foramen, conditioning unilateral stenosis of it and of the spinal canal.
Magnetic resonance imaging (MRI) of the thoracic spine showed hypointensity on the left of the extradural sac involving the facet joint at T9/10 level with severe compression on the spinal cord.
Hemilaminectomy and exeresis was performed confirming the findings by pathology.

Hypertrophy of the cervical and lumbar facet joints associated with multisegmental spondylotic changes are common. However, these isolated findings isolated found in the dorsal spine are uncommon [1, 2]. Similarly, unlike what happens in the cervical and lumbar spine, the hypertrophy of the posterior elements of the dorsal spine is a very rare condition [3].
In view of its aetiology it is speculated that bone formation would be anomalous, rather than spondylotic changes, because it happens in relatively young patients without evidence of degenerative changes [2]. Others suspect that the facet hypertrophy is due to congenital anomalies or developmental dysplasia [4]. The theory of an old and trivial trauma that has caused myositis ossificans with pseudoarthrosis is also postulated [5].
The most common causes of spinal cord compression by posterior elements are the ossification of the yellow ligament, the hypertrophy of bilateral facet joints in the lumbar spine and the thickening of the laminar arch [6].
The ossified hypertrophy of normal posterior elements, causing compressive symptoms is rare [2], however, we must not forget it in the differential diagnosis. There are only a few case series of dorsal facet hypertrophy causing compressive symptoms. Deogaonkar has reported a case of unilateral thoracic cord compression by a hypertrophied lamina with a unilateral thoracic stenotic canal, and another case of thickened lamina at the level of the disc between two thoracic vertebral bodies [7].
Within the differential diagnosis we should include those causes that produce spinal compression at dorsal level. Among these we must assess the presence of trauma injuries, haematomas, abscesses, herniated discs, bone and neural tumours, metastases, and others.
The diagnostic key will be given by the appropriate clinical history associated with the correct sequence of imaging study.
Conventional radiology plays a role in suspicion, however, it is CT which gives us the definitive and accurate diagnosis of bone lesions. In cases where spinal and soft tissue compromise is suspected, MRI is the imaging test to be performed as soon as possible.
Treatment options depend on the grade of severity of spinal cord compression and its clinical presentation, and it may vary between conservative management to surgery. In our case with facet and spine compromise the surgery was mandatory. Thus, hemilaminectomy and exeresis was performed and the clinical and imaging findings were confirmed by pathology.
In conclusion, dorsal facet hypertrophy is a rare pathological entity with controversial aetiology that we should identify to thereby provide the best and most appropriate therapeutic option.