Development of pre-syrinx state and syringomyelia following a minor injury: a case report
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CASE REPORT
Development of pre‑syrinx state and syringomyelia following a minor injury: a case report Andrea Kleindienst1* , Tobias Engelhorn2, Verena Roeckelein1 and Michael Buchfelder1
Abstract Background: A generally accepted rule is that posttraumatic syringomyelia (PTS) results from spinal cord injury (SCI). Case presentation: Here, we report the development of syringomyelia without SCI in a 54-year-old Caucasian man following a mild motor vehicle accident. The computed tomography on admission excluded an injury of the spine. Because of neck and back pain, magnetic resonance imaging was performed on day 3 post-injury and demonstrated minimal changes from a ligamentous strain at the cervicothoracic transition. Any traumatic affection of the bone, vertebral discs, intraspinal compartment, or spinal cord were excluded. Some limb weakness and neurogenic bladder dysfunction started manifesting within the following weeks. Repeated MRIs following the accident demonstrated arachnoid adhesions at the C1–2 level and spinal cord edema equivalent to a pre-syrinx state at 12 months and syrinx formation at 24 months. Because of further deterioration, decompression was performed at 36 months. Conclusions: We conclude that even after a minor trauma PTS can occur and that medullary edema (pre-syrinx state) may precede syrinx formation. Keywords: Syringomyelia, Trauma, Pre-syrinx, Treatment, Spinal cord injury Background In the era of implementation of magnetic resonance imaging (MRI) for the diagnosis and follow-up of back pain and spinal cord injury (SCI), medullary abnormalities with a hyperintense T2 signal are increasingly detected. The attribution of these abnormalities as a prominent central canal, hydro- and syringomyelia has been classified by Milhorat [1]. Posttraumatic syringomyelia (PTS) presents with delayed progressive myelopathy often corresponding to spinal segments distant from the level of the original lesion. Experimental evidence confirms that in SCI, local ischemia, hematoma liquefaction, and/or autolytic processes trigger the development of *Correspondence: andrea.kleindienst@uk‑erlangen.de 1 Dept. of Neurosurgery, Friedrich-Alexander University ErlangenNürnberg, Schwabachanlage 6, 91054 Erlangen, Germany Full list of author information is available at the end of the article
arachnoid scars and PTS [2, 3]. Furthermore, posttraumatic kyphosis and spinal canal stenosis promote the progression of PTS [4, 5]. Mathematical modeling indicates that a phase difference between the arterial pressure pulse in the spinal subarachnoid and perivascular spaces, due to a pathologically disturbed cerebrospinal fluid (CSF) or blood flow, results in a net influx of CSF into the spinal cord [6]. As soon as the intrinsic fluid storage capacity of the spinal cord is overloaded, medullary edema may develop, presenting as a hyperintense T2 signal and referred to as the “pre-syrinx” state [7]. But neither a “pre-syrinx” nor the formation of PTS without any SCI has been reported prospectively. Here, we present t
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