A 44-year-old woman with no significant medical history was referred for neck pain. Two weeks before presentation, she developed a "crick" in her neck, attributed to a sleeping position. Within 2 days, the pain intensified from 5 on a scale of 10 to 8 or 9 on a scale of 10 at night and radiated to her head, interfering with sleep. She had markedly decreased range of movement and became hypersensitive to sounds. She went repeatedly to a local emergency department, where she was given corticosteroids, diazepam, and nonsteroidal anti-inflammatory drugs for torticollis, with minimal relief. The C-reactive protein level was slightly elevated.
CT showed a calcified mass posterior to the odontoid process, which was the reason for referral. She was experiencing new pain in the right eye, ear, and jaw. She did not have arm pain, weakness, gait abnormality, dysphagia, odynophagia, bowel or bladder involvement, fever, nausea, vomiting, diarrhea, weight loss, rash, lymphadenopathy, tingling, numbness, or syncope. Neck range of motion was markedly limited. Neurologic examination was normal, including normal strength, deep tendon reflexes, and Babinski sign.
Review of the CT scan and a new MRI scan suggested a calcified intra- or extrathecal mass, possibly hemangioma, meningioma, or other tumor at the transverse ligament of the atlas. However, hydroxyapatite (HA) (calcific tendonitis) or calcium pyrophosphate (CPPD) (pseudogout), though rare in this location, were also possibilities. The location and size of the calcification raised concern for spinal cord compression.
Emergent consensus review by neurosurgery, radiology, and rheumatology concluded that the mass was not malignant and that there was no immediate neurologic threat or indication for surgery. Dissolution of part of the mass most suggested HA deposition disease (HADD), an hypothesis supported by the acute nature of pain symptoms, similar to that of calcific tendonitis occurring in other sites.
Given the inaccessibility of the site and the absence of neurologic compromise, we opted for a conservative course of anti-inflammatory therapy. Follow-up CT of the neck 2 months later, at which time the patient was asymptomatic, showed a decrease in mineralization along the transverse ligament and more dissolution, with no associated canal encroachment (Figures 1 and 2).
The clinical presentation, radiographic appearance, and evolution make HADD the most likely diagnosis. Earlier case reports have described cervical HADD anterior to the cervical vertebrae; this may be the first case of HADD inside the spinal canal. The location of the mass in a tendon area and its gradual dissolution support the identification of the deposit as HA rather than CPPD, because CPPD deposits in cartilage and does not dissipate.
CPPD at the odontoid process has been called "crowned dens syndrome." Although crystal identification was not accomplished, in such cases CPPD was assumed from its presence elsewhere in the body, as in the intervertebral disc, the ligamentum flavum, and apophyseal joints. The cases reported by Bouvet and colleagues may be HA, though not identified as such.
HADD occurs most commonly in adults of either sex who are between 30 and 60 years of age. The etiology of the deposition is unclear, but repetitive trauma, recent injury, tissue necrosis, or ischemia may play a role. Inflammatory markers, which may be slightly elevated, are nonspecific. We did not recognize an inciting event in the current case. Although we do not have crystal confirmation, we believe that the serial changes in radiographic appearance support our conclusion that this is HADD and not pseudogout.
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Cite this: Calcific Tendonitis: An Unusual Presentation of Neck Pain - Medscape - Sep 06, 2017.