Intradural Disk Herniation Mimicking a Spinal Tumor: Radiologic Imaging, Pathogenesis, and Operative Management

Intradural disk herniation (IDH) is a rare condition, occurring more often at the L4-5 level. We examined a case of an IDH at the L1-2 level mimicking an intradural spinal tumor. A 71-year-old woman with a long history of backache and pain radiating down the left leg was admitted to our hospital with the worsening of these symptoms. Magnetic resonance imaging and computed tomographic myelography demonstrated an intradural mass at the L1-2 level. Given the radiologic findings and the location of the mass, the preoperative differential diagnosis centered on intradural spinal tumors. Dural incision was performed using a surgical microscope to resect the mass. Contrary to our expectation, the diagnosis made during the surgery was IDH. Despite advances in imaging techniques, IDH could not be definitively diagnosed preoperatively. The pathogenesis of IDH remains unclear. In our patient, the ventral dural defect was smooth and round, and the dural tissue around the defect was thickened. These intraoperative findings suggested that the patient’s IDH resulted not from an acute new event but from a chronic process. We recommend dural incision using a surgical microscope for treating IDH because it provides a clear visual field.

Vanishing calcification associated with a spontaneous ventral spinal cerebrospinal fluid leak

Background Some patients with spontaneous intracranial hypotension have a ventral spinal cerebrospinal fluid (CSF) leak and these CSF leaks may be associated with calcified disk herniations. Identifying these calcifications is helpful in directing treatment. We report here the unusual case of a patient with a ventral CSF leak in whom the associated calcification absorbed over a five-month period. Case report A 42-year-old woman developed orthostatic headaches and bilateral abducens nerve palsies. Magnetic resonance imaging of her brain showed typical findings of spontaneous intracranial hypotension. Magnetic resonance imaging of her spine showed an extensive cervicothoracic CSF leak. Computed tomographic myelography showed calcification at the Th1–2 disk space. Three epidural blood patches were performed, but her symptoms persisted. Digital subtraction myelography performed five months later showed an upper thoracic ventral CSF, but the calcification was no longer present. A dural tear, found at surgery at the Th1–2 level, was repaired and the patient made an uneventful recovery. Discussion The resorption of calcifications at the level of a ventral spinal CSF leak could explain the absence of any calcifications in at least some patients with such leaks and demonstrates the usefulness of reviewing previous imaging in patients with ventral CSF leaks if the exact site of the leak remains unknown.

Surgical Management of a Patient With Thoracic Spinal Cord Herniation

BACKGROUND AND IMPORTANCE: Thoracic spinal cord herniation (TSCH) is rare and likely underdiagnosed. It is characterized by ventral herniation of the spinal cord through a dural defect, effacement of the anterior subarachnoid space, and increased posterior subarachnoid space. We present here a case of TSCH diagnosed and surgically treated at Barrow Neurological Institute, along with supplemental intraoperative video. CLINICAL PRESENTATION: A 61-year-old man with a history of progressive myelopathy causing left lower-extremity weakness with associated numbness, impaired gait, foot drop, incontinence, and sexual impotence was referred without any previous treatment. Computed tomographic myelography and magnetic resonance imaging of the thoracic spine showed ventral spinal cord herniation at T3-T4. Neurological monitoring was recorded preoperatively and intraoperatively. The patient underwent left-sided posterolateral exploration via T3-T4 laminectomies and costotransversectomy for intradural cord release/detethering of the spinal cord with additional superior and inferior extension and repair of the dural defect. Arthrodesis was not considered necessary. After cord release, motor evoked potentials showed immediate improvement from baseline. Dural duplication was considered the cause of TSCH in this case. Total reduction of herniation was evident in postoperative images. The postoperative course was uneventful, and at the last follow-up, the patient had regained ambulation and sphincter control. CONCLUSION: Anterior displacement of the thoracic spinal cord should elicit consideration of herniation to prevent misdiagnosis and inadequate surgery. Surgical cord release and enlargement of the dural defect are safe and associated with good clinical outcomes.

Ventral “Spinal Epidural Meningeal Cysts”—Not Epidural and Not Cysts? Case Series and Review of the Literature

BACKGROUND: Ventral spinal epidural meningeal cysts are rare entities for which the pathogenesis is poorly understood. OBJECTIVE: We present the clinical, radiographic, surgical, and pathologic findings of 4 patients with extensive ventral spinal epidural meningeal cysts and review the relevant literature. In addition, we discuss a suspected mechanism for pathogenesis. METHODS: Four patients with anterior spinal epidural meningeal cysts are retrospectively reviewed. RESULTS: Ventral spinal epidural meningeal cysts are often large, extending on average from C2 to L1 in our series. Patients typically present with a prolonged course of symptoms and signs, including segmental muscle weakness and atrophy, subtle myelopathy, mild to moderate spinal pain, and headache. Histopathologic analysis of the cyst wall demonstrates collagenous tissue consistent with dura but without arachnoid features. Dynamic computed tomographic myelography is the study of choice for localization of the primary dural defect. Patient symptoms and neurological deficits routinely improve after appropriate surgical intervention. CONCLUSION: Diverse signs and symptoms herald the presentation of ventral spinal meningoceles. Intraoperative, radiographic, and pathological findings are all suggestive of an intradural dissection as the etiology. Hence, they may be more appropriately named “ventral spinal intradural dissecting meningoceles.” Definitive treatment involves identification and obliteration of the dural defect.