Abstract
BackgroundA generally accepted rule is that posttraumatic syringomyelia (PTS) results from spinal cord injury (SCI).Case presentationHere, 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.ConclusionsWe conclude that even after a minor trauma PTS can occur and that medullary edema (pre-syrinx state) may precede syrinx formation.
Highlights
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
Posttraumatic syringomyelia (PTS) presents with delayed progressive myelopathy often corresponding to spinal segments distant from the level of the original lesion
Discrete traumatic microstructural lesions of the spinal cord can be assessed with diffusion tensor imaging (DTI), T2- and T2*-weighted and shortT1 inversion recovery (STIR) sequences within the first 48 hours after the injury the clinical adoption remains elusive because of complex acquisitions, cumbersome analysis, limited reliability, and wide ranges of normal values [10]
Summary
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. Because of persistent back pain, an MRI of the spine was performed on day 3 post-injury (Fig. 1b) and evaluated as demonstrating degenerative changes and mild canal stenosis at C4/5 (10.9 mm). The neurological examination was normal besides a neurogenic bladder dysfunction lacking any explanation A neurological examination revealed a mild hemiparesis and hypesthesia on the left side, hyperreflexia in the right upper extremity, clonus, and a positive Babinski sign in the left foot. An MRI at 12 months post-injury demonstrated the development of an arachnoid cyst at the C1–2 level and medullary edema at the cervical and upper thoracic level (Fig. 2a, b).
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