A 56‐year‐old female presented with symptoms of flatback syndrome, including poor posture, back pain, and difficulty mobilizing. She had a lumbar epidural steroid injection several years previously for ‘sciatica’. On examination, the patient demonstrated positive sagittal imbalance despite increased pelvic retroversion, and exaggerated knee flexion. Neurological exam was normal. T1‐ and T2‐weighted magnetic resonance imaging (MRI) unexpectedly demonstrated calcification of the cauda equina, most dramatically at L4/5 (Fig. 1(a)—(d)). Computed tomography (CT) showed ankylosis resulting in reversal of normal lumbar lordosis and confirmed calcifications in the lumbar region of the spinal canal, most pronounced at L4/5 (Fig. 1(e) and (f)), likely Type III arachnoiditis ossificans (AO). 1
Fig. 1.

(a) Sagittal and (b) axial T1‐weighted magnetic resonance imaging (MRI) and (c) sagittal and (d) axial T2‐weighted MRI at the L4/5 level unexpectedly demonstrated calcification of the cauda equina. (e) Sagittal and (f) axial computed tomography (CT) confirmed calcifications in the lumbar region of the spinal canal, most pronounced at L4/5. This most likely represented Type III arachnoiditis ossificans (AO).
A three‐column osteotomy was offered as a surgical intervention. However, the patient declined after full disclosure of surgical risk. Additionally there is no evidence to support a safe osteotomy in the presence of AO and furthermore, Type III AO does not have any specific surgical treatment. 1
AO is a generally a cause of chronic, progressive myelopathy or radiculopathy and results in replacement of spinal arachnoid by bone. 1 , 2 Usually the consequence of prior trauma or procedures, 1 it is possible that the previous epidural injection was the cause in this case. The three types of AO include semi‐circular (Type I), circular (Type II), and englobing the caudal fibres (Type III). 1 AO is more common and severe in the thoracic spine where arachnoid cells are more concentrated and the spinal canal is narrower, 3 which may explain why this patient had minimal symptoms, however exceedingly few cases are found incidentally. 4 Although the patient had not reported symptoms suggestive of AO, 4 the intrathecal nature of the calcifications made the diagnosis much more likely than benign meningeal calcifications, which are common findings in post‐mortem studies. 4 , 5
Although best defined by CT, MRI is often the first choice investigation of patients with symptoms of AO. 4 Findings typically include irregular thickening and clumping of the cauda equina, and can range from hypointensity to intermediate intensity on T1 and T2 studies. 4 MRI is particularly helpful for identifying the extent of neural involvement and identify coexisting or potentially etiological pathology. 6 CT provides optimal visualization of AO due to its high sensitivity for calcification that results from the different attenuation coefficients of bone, soft tissue and cerebrospinal fluid. 1 This imaging modality further defines the characteristics of the ossifications and allows them to be classified into the three sub‐types of AO. 1 Hence, MRI and CT should be considered complementary in the diagnosis of AO and should be performed together to build a complete picture of the pathology.
CT in this case clearly complemented MRI as it provided superior detail of the calcification that would have been otherwise undetected and potentially resulted in patient morbidity should she have sought intervention. In contemporary practice, surgeons should have a low threshold for obtaining the full complement of advanced imaging when assessing spine pathology, that is CT in addition to MRI, particularly if there are atypical or unclear MRI findings.
Acknowledgement
Open access publishing facilitated by The University of Auckland, as part of the Wiley ‐ The University of Auckland agreement via the Council of Australian University Librarians.
References
- 1. Domenicucci M, Ramieri A, Passacantilli E, Russo N, Trasimeni G, Delfini R. Spinal arachnoiditis ossificans: report of three cases. Neurosurgery 2004; 55: E1011–7. [DOI] [PubMed] [Google Scholar]
- 2. Bin JK, Lee S, Kang CN, Kim TH. Arachnoid ossificans of thoracolumbosacral spine in the advanced ankylosing spondylitis: a case report. Rheumatol. Int. 2013; 33: 1623–5. [DOI] [PubMed] [Google Scholar]
- 3. Kaufman AB, Dunsmore RH. Clinicopathological considerations in spinal meningeal calcification and ossification. Neurology 1971; 21: 1243–8. [DOI] [PubMed] [Google Scholar]
- 4. Steel CJ, Abrames EL, O'Brien WT. Arachnoiditis ossificans – a rare cause of progressive myelopathy. Open Neuroimag. J. 2015; 9: 13–20. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 5. Herren Y. Occurrence and distribution of calcified plaques in the spinal arachnoid in man. Arch. Neurol. Psychiatry 1939; 41: 1180–6. [Google Scholar]
- 6. Abrams J, Li G, Mindea SA, Haynes CM, Cheng I. Arachnoid ossificans containing metaplastic hematopoietic marrow resulting in diffuse thoracic intrathecal cysts and severe myelopathy. Eur. Spine J. 2012; 21: 436–41. [DOI] [PMC free article] [PubMed] [Google Scholar]
