Migration of herniated intervertebral disk fragments into the dorsal epidural space is an infrequent event. Disk fragments typically follow a path of least resistance through the fissure in the posterior annulus. Due to the strength of the posterior longitudinal ligament, fragments usually remain ventral and infrequently lateral to the thecal sac. Cephalad migration is more common with lateral disk herniation, whereas caudal displacement may be more common in central disk extrusion (
4). Lateral and dorsal migration is thought to be limited by a sagittal midline septum than spans the posterior longitudinal ligament and vertebral bodies. This thin connective tissue membrane connects the posterior longitudinal ligament to the medial and lateral wall of the spinal canal (
3). The nerve roots may also act as an anatomical barrier limiting migration disk fragments to the dorsal epidural space.
Review of the literature illustrates that the clinical presentation in dorsal epidural disk herniation is variable, from low back pain without objective neurologic deficits to cauda equina syndrome. Authors have posited that due to disk fragment migration to the dorsal epidural space, several neural structures may be compromised. Hence, these patients may more often present with clinically significant neurologic deficits (
1,
5). However, a review of the published literature clearly delineates a wide spectrum of symptoms ().
Definitive diagnosis of a dorsal herniated disk fragment may be difficult. Conventional axial and sagittal magnetic resonance imaging has been the method of choice for radiologic diagnosis of lumbar degenerative conditions. However, it may not always absolutely differentiate similar processes, such as herniated disk, epidural hematoma, and abscess. Herniated disks are usually hypointense on T1-weighted images and hyperintense on 80% of T2-weighted images (
2,
3,
6). Herniated disk fragments sequestered in the dorsal epidural space may appear similar to other dorsal epidural pathologies, such as abscess, hematoma, and malignancy. As disk fragments migrate dorsally, they become surrounded by a vascular layer of epidural fat, which can induce an inflammatory response, and the formation of a granulation tissue around the disk fragment (
7,
8). The presence of circumferential contrast enhancement raises the possibility of abscess or epidural metastasis.
This patient's magnetic resonance images revealed a lesion with rim enhancement. The absence of diskitis and osteomyelitis on imaging in addition to unremarkable infectious laboratory markers (erythrocyte sedimentation rate, C-reactive protein) decreases the potential for epidural abscess; however, they do not eliminate it absolutely. Our patient also presented with a clear history of physical exertion followed promptly by onset of symptoms. Although a sequestered disk fragment was high upon our list of preoperative differential diagnoses, the severity of patient symptoms and our diagnostic uncertainty equally mandated operative exploration.
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