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Differentiation of Idiopathic Spinal Cord Herniation from CSF-isointense Intraspinal Extramedullary Lesions Displacing the Cord1 Marc D. Haber, MD Dustin D. Nguyen, DO Shan Li, MD, MS Abbreviations: BSS = Brown-Séquard syndrome, CSF = cerebrospinal fluid, DWI = diffusion-weighted imaging, FLAIR = fluid-attenuated inversion-recovery, FSE = fast spin-echo, ISCH = idiopathic spinal cord herniation, SEA = spinal epidural abscess RadioGraphics 2014; 34:313–329 Published online 10.1148/rg.342125136 Content Codes: From the Department of Radiology, Baystate Medical Center, Tufts University School of Medicine, 759 Chestnut Rd, Springfield, MA 01199. Recipient of a Certificate of Merit award for an education exhibit at the 2011 RSNA Annual Meeting. Received June 5, 2012; revision requested June 21; final revision received June 19, 2013; accepted June 19. For this journalbased SA-CME activity, the authors, editor, and reviewers have no financial relationships to disclose. Address correspondence to M.D.H. (e-mail: [email protected]). 1

ONLINE-ONLY SA-CME LEARNING OBJECTIVES After completing this journal-based SACME activity, participants will be able to: ■■Recognize the common diagnostic and clinical features of ISCH.

Focal spinal cord displacement can be caused by idiopathic spinal cord herniation (ISCH), in which the cord protrudes through a dural defect into the epidural space, causing cord displacement and tethering. ISCH is uncommon and often is misdiagnosed initially, which results in delayed management. ISCH can be mimicked by space-occupying cerebrospinal fluid (CSF)–isointense intraspinal extramedullary lesions, such as epidermoid cysts or teratomas, intradural arachnoid cysts, epidural hematomas or abscesses, cystic nerve sheath tumors, synovial or Tarlov cysts, meningoceles, and pseudomeningoceles. Initial computed tomography (CT) and unenhanced magnetic resonance (MR) imaging studies may depict focal cord displacement and a widened CSF space but often are not sufficient to identify the underlying cause. High-resolution thin-section MR imaging can delineate the exact location of the dural defect and the protrusion of the herniated cord through this defect into the epidural space. At imaging, unimpeded CSF pulsation artifacts seen within a widened CSF space exclude a space-occupying lesion. A filling defect seen at conventional or CT myelography can help confirm a CSFisointense space-occupying lesion; intravenous contrast agent administration can help exclude a rim-enhancing cystic extramedullary lesion. The clinical presentation usually is nonspecific, but symptom acuity, fever, and trauma can guide the imaging evaluation and help narrow the differential diagnosis. A multimodality imaging approach is essential to differentiate ISCH from spaceoccupying CSF-isointense intraspinal extramedullary lesions. ©

RSNA, 2014 • radiographics.rsna.org

■■Identify

the common diagnostic and clinical features of epidermoid cysts. ■■Discuss

how various MR imaging sequences and myelography can be used to narrow the differential diagnosis for CSF-isointense intraspinal extramedullary lesions that displace the spinal cord. See www.rsna.org/education/search/RG.

Introduction

When focal spinal cord displacement accompanied by a widened cerebrospinal fluid (CSF) space is identified at imaging, diagnosis of the underlying cause presents a challenge. Idiopathic spinal cord herniation (ISCH) is a rare cause of this finding. Other disease entities include space-occupying CSF-isointense intradural or intraspinal extramedullary lesions, such as epidermoid cysts, intradural arachnoid cysts, spinal epidural abscesses (SEAs), cystic nerve sheath tumors, meningoceles, teratomas, synovial cysts, and epidural hematomas. Often the patient’s clinical history, symptoms, and physical examination findings are nonspecific and may include back pain, weakness,

NEUROLOGIC/HEAD AND NECK IMAGING

313

Isointense

Hypo- to slightly hyperintense relative to spinal cord

Hypo- to isointense relative to spinal cord

Arachnoid cyst

SEA

Cystic schwannoma

T1WI-CE

Diffuse homogeneous or heterogeneous enhancement or peripheral enhancement Peripheral nodular enhancement

No enhance­ment

Mild to no peri­ pheral en­ hancement

No enhance­ment

T2WI

Mildly to markedly hyperintense relative to spinal cord

Hyperintense relative to spinal cord

Iso- to slightly hyperintense

Iso- to hyperintense

Anterior displacement of the spinal cord, possible kinking

CTM

Filling defect

Usually no filling defect Narrow-opening and noncom­ municating lesions can demonstrate a filling defect CTM not recommended; may seed infection into subarachnoid space

Filling defect

No filling defect

DWI

No restricted diffusion May see T2 signal shinethrough artifact

Restricted diffusion

No restricted diffusion

Restricted diffusion

No restricted diffusion

Clinical Presentation

Often asymptomatic Pain or localized findings if growth is large

Localized back pain Fever Neurologic deficit

Nonspecific; pain is the most common presenting symptom Pain may worsen with Valsalva maneuver

Nonspecific; signs and symptoms related to tumor size and location

BSS, paraparesis, isolated sensory or motor weakness Delayed diagnosis common

Comments

…

Use of T1WI and T1WI-CE is critical to detection

May see soft tissue extending through the dura on highresolution MR images Flow artifact posterior to the cord suggests the absence of a space-occupying mass Appearance at T1WI and T2WI depends on cystic protein concentration Hyperintense to CSF on FLAIR MR images May see scalloping of the posterior vertebral body or widening of the pedicles Isointense to CSF on FLAIR MR images

Note.—CTM = CT myelography, DWI = diffusion-weighted imaging, FLAIR = fluid-attenuated inversion recovery, T1WI = T1-weighted MR imaging, T1WI-CE = contrastenhanced T1-weighted MR imaging, T2WI = T2-weighted MR imaging. *Signal intensities are relative to CSF unless otherwise specified.

Iso- to hyperintense

Epidermoid cyst

T1WI

Anterior displacement of the spinal cord, possible kinking

ISCH

Disease Entity

Imaging Characteristics by Modality*

Imaging and Clinical Characteristics of ISCH and CSF-Isointense Intradural Extramedullary Lesions

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numbness, and Brown-Séquard syndrome (BSS). In some cases, the clinical presentation will help narrow the differential diagnosis, as in patients with an acute onset of symptoms, fever, bacteremia, or trauma. The use of imaging modalities such as radiography, standard or high-resolution magnetic resonance (MR) imaging, and conventional or computed tomographic (CT) myelography is required to further define the disease process and identify the underlying cause. Radiologists must understand the benefits and limitations of each imaging modality and have a general knowledge of the clinical presentation and management of these disease entities (Table).

Idiopathic Spinal Cord Herniation

First described by Wortzman et al (1) in 1974, ISCH is a relatively uncommon disease entity in which the spinal cord is displaced through a defect in the anterior or lateral dura mater. A diagnosis of ISCH should be made only after cord herniation secondary to traumatic or iatrogenic causes is excluded, although the imaging findings are similar. In the latter case, the level of the dural defect is determined by the location of the traumatic or iatrogenic insult (2,3). The exact cause of ISCH is unknown, but occult or repetitive trauma is a possible cause (4). Some investigators have proposed that dural duplication may play a significant role (5). Regardless of the cause of the defect, researchers postulate that the spinal cord becomes tethered as a result of the defect. Neurologic symptoms usually develop as spinal cord herniation and tethering worsen. Symptoms range from paresthesia and paraparesis to BSS.

Demographics Groen et al (4) have reported a clear female preponderance for ISCH, with nearly twice as many women affected as men. In the adult population, patients range in age from 21 to 78 years (mean, 51 years). Many patients exhibit symptoms for 20 years or more before diagnosis, which demonstrates the challenge of diagnosing ISCH (5–7).

Symptoms Most patients with ISCH present with symptoms of BSS, including ipsilateral upper motor neuron paralysis and loss of proprioception and contralateral loss of pain and temperature sensation. In a 2009 metaanalysis of 129 cases, Groen et al (4) reported that BSS was seen in 85 patients, paraparesis was seen in 39 patients, and isolated sensory or motor deficits were seen in four patients and one patient, respectively. Similar findings have been described in other studies reported since 2009 (8–13).

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Imaging Findings ISCH typically occurs between the levels of T3 and T7, likely because of the normal spinal thoracic curvature and anterior position of the cord at these levels. The defect most commonly occurs at the level of the intervertebral disk but may also occur at the level of the vertebral body. Rarely, the defect spans multiple vertebral segments (4). The lesion is usually solitary; however, two synchronous thoracic defects have been reported (14). Findings at MR imaging and myelography are not specific for the diagnosis of ISCH. Both imaging modalities will demonstrate obliteration of the CSF space ventral to the cord and a widened dorsal CSF space, with no solid or cystic mass posterior to the cord. ISCH can sometimes be identified at MR imaging as a small amount of soft tissue that extends from the ventral apex of the displaced cord into the epidural space (Figs 1a–1c). It may be difficult to differentiate focal spinal cord herniation from CSF flow artifact because both entities demonstrate similar hypointensities on standard T2-weighted MR images (Fig 1d). Kwong et al (13) have suggested that continuous normal CSF pulsation artifact in the widened CSF space is an important diagnostic finding that implies an unimpeded flow of CSF and argues against an obstructing lesion (Figs 1a, 1e, 1f). The use of an intravenous contrast agent during imaging is important because ISCH will not enhance; a finding of enhancement strongly supports a space-occupying lesion. At conventional myelography, a free flow of contrast material seen with fluoroscopy immediately after intrathecal contrast agent injection may support a diagnosis of ISCH but cannot completely exclude a space-occupying lesion, such as a wide-necked communicating arachnoid cyst, because space-occupying lesions can show immediate contrast agent filling. Technological advances such as phase-contrast and thin-section MR imaging techniques allow easier diagnosis and differentiation of ISCH from various mimics (15). Some authors have suggested the use of phase-contrast MR imaging to exclude the presence of a posteriorly positioned intradural arachnoid cyst (16). Highresolution MR (Figs 1e, 1f) or CT myelography can demonstrate soft tissue that extends from the apex of the cord displacement through the dural defect into the epidural space, a finding that confirms the diagnosis of ISCH (17). Axial high-resolution T2-weighted MR images can demonstrate the exact location of the herniated cord through the dural defect (Figs 1e, 1f). The degree of cord deformity or kinking seen at imaging varies from none to virtual disappearance of the cord from the bony canal.

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Figure 1.  ISCH in a 47-year-old man. (a–c) Sagittal fast spin-echo (FSE) T2-weighted (a), axial T1-weighted (b), and sagittal T1-weighted (c) MR images show ventral displacement and posterior indentation of the thoracic cord, with widening of the dorsal subarachnoid space. Focal cord herniation (arrow) is seen as a small amount of soft tissue that extends from the ventral apex of the displaced cord into the epidural space. Continuous flow artifact (arrowhead in a) within the dorsal subarachnoid space indicates unimpeded CSF flow posterior to the cord. (d) On the axial FSE T2-weighted MR image, it is difficult to differentiate focal cord herniation (arrow) from CSF flow artifact (arrowheads) because of their similar hypointensities. (e, f) Axial high-resolution maximum intensity projection MR image (e) and sagittal three-dimensional MR image obtained with T2-weighted sampling perfection with application optimized contrasts using different flip-angle evolutions (SPACE; Siemens Medical Solutions, Erlangen, Germany) (f) unequivocally demonstrate herniation of the cord (arrow) through a ventral dural defect into the right anterior epidural space. The small amount of fluid seen lateral to the herniated cord (black arrowhead in e) may represent accompanying leakage of CSF. Continuous CSF flow artifact is seen within the dorsal subarachnoid space (white arrowhead in e and f). (g, h) Intraoperative photographs show confirmed cord herniation through the dural defect (circle in g) and dural graft repair (* in h).

Imagama et al (5) have proposed three subtypes of ISCH that are based on the severity of herniation seen at sagittal MR imaging: (a) type K, described as an obvious kinking toward the ventral region; (b) type D, with the spinal cord completely disappearing at the herniated site; and (c) type P, a protrusion of the ventral aspect of the spinal cord such that the anterior subarachnoid space is fully effaced, with very little posterior cord kinking. Further classification that is based on axial MR imaging findings has been proposed, with the hiatus described as central (type C) or lateral (type L). Finally, the presence or absence of a concomitant bone defect has been noted. In a study of 12 patients, Imagama et al (5) suggested that patients with type P ISCH will have a good postoperative recovery, whereas patients with a type C hiatus and a concomitant bone defect may have severe preoperative neurologic symptoms and a poor postoperative recovery. The use of such a classification system may guide preoperative planning and help moderate the expectations of the patient and neurosurgeon. Because of the small sample size in the study by Imagama et al (5) and the variety of outcomes reported in other case studies, further evaluation is necessary to verify these findings.

Treatment A review of many case reports and the systematic reviews by Groen et al (4) and Imagama et al (5) demonstrate that even patients with long-standing neurologic symptoms can experience substantial recovery after treatment (4,5). The primary treatment goals are to resolve or improve the patient’s neurologic symptoms and avoid recurrence of spinal cord herniation or incarceration. The primary treatment involves surgical reduction and release of the spinal cord, followed by surgical widening of the dural defect or closure of the defect with an anterior patch or suture (Figs 1g, 1h). Other surgical techniques include placement of a fat graft, repair of a bone defect, and placement of a posterior dural patch (4,6,10).

The meta-analysis by Groen et al (4) reported postoperative improvement of neurologic symptoms in 88% of patients, with symptoms in 9% of patients worsening and 24% unchanged. Groen et al (4) suggest that although both dural patching and dural defect widening are associated with postoperative improvement, postoperative results are better with dural defect widening than with dural patching (postoperative improvement was seen in 81.8% of patients vs 64.3%, respectively). However, patients with BSS demonstrated better results with dural patching than with dural widening (66.2% vs 33.8%, respectively). When and how to intervene in cases of ISCH has not yet been determined with certainty and requires further investigation.

Epidermoid Cyst

Intraspinal epidermoid cysts are relatively rare benign tumors composed of a stratified squamous epithelium that lines the internal wall and collagenous tissue that forms the outer wall (18). They were originally described as “pearly tumors” by Cruveilhier in 1829 because of the waxy white substance composed of keratin, triglycerides, fatty acids, cholesterol crystals, and desquamated epithelial cells that forms the cystic contents (19,20). Because the cystic contents are derived from the desquamation and breakdown of the epithelial lining, the growth rate of the cyst is similar to that of normal skin, in contradistinction to the more rapid growth of most neoplasms (18). Spinal epidermoid cysts most commonly occur in the intradural extramedullary compartment of the lumbar spine (21). Although epidermoid cysts are generally benign, rare cases of malignant transformation into locally invasive carcinoma have been reported (22). There is a general consensus that spinal epidermoid cysts are either congenital or acquired (21). Epidermoid cysts are most commonly thought to arise congenitally from the aberrant implantation of ectoderm cells in the midst of

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Figure 2.  Epidermoid cyst in a 50-year-old woman. (a–c) Sagittal FSE T2-weighted (a), sagittal T1-weighted (b), and axial FSE T2-weighted (c) MR images show ventral displacement of the spinal cord, with focal cord compression and widening of the dorsal subarachnoid space (arrow). No continuous CSF flow artifact is seen posterior to the cord that would suggest a space-occupying lesion. (d) Lateral (left) and posteroanterior (right) images from thoracic myelography show a blockage of free-flowing contrast agent in the subarachnoid space. (e, f) Sagittal (e) and axial (f) images from CT myelography show an ovoid filling defect (white arrow) in the subarachnoid space causing ventral and leftward cord compression (black arrow). Note the CSF cleft (arrowhead) between the cord and the filling defect. (g) Intraoperative photograph shows a pearly mass (*), a finding confirmed to be an epidermoid cyst.

neural tube closure during the 3rd–5th weeks of embryonic life (23). This is a possible explanation for why the tumors are commonly seen in the lumbosacral region, which is the site for terminal closure of the neural tube (24). The second main cause of epidermoid cysts is thought to be iatrogenic and occurs when the needle used at lumbar puncture ectopically displaces epithelial tissue into the spinal canal (23). The incidence of iatrogenic epidermoid cysts has markedly decreased in the past 25 years with the introduction of needle stylets (23). Of note, the literature suggests that both lumbar and thoracic locations are common sites of intraspinal epidermoid cysts (19,24). There have been reports in the literature of epidermoid cysts that manifest with associated skin lesions, such as hairy nevi, dyschromia, angiomas, and scars, or with spinal dysraphisms, such as dermal sinus (associated with epidermoid or dermoid tumors in up to 20% of cases), spina bifida, hemivertebra, syringomyelia, tethered cord syndrome, dorsal meningocele, and diastematomyelia (19,21,24,25). Although the terms are often used interchangeably, dermoid and epidermoid cysts are different in multiple aspects. Epidermoid and dermoid cysts are both inclusion cysts composed only of ectodermal tissue, but dermoid cysts may arise earlier in the embryonic process; contain a thicker lining, which may include calcifications (versus the thin squamous lining of epidermoids); and contain sebaceous secretions, sweat glands, and hair (forming fat-fluid levels) (26). Epidermoid and dermoid cysts usually are differentiated histologically (19).

Demographics Epidermoid cysts account for an estimated 0.2%–1% of intracranial tumors and for even fewer intraspinal tumors (19). In a literature review by Roux et al (19), spinal epidermoid cysts had a male-to-female preponderance of 1.35:1. Patients ranged in age from 3 to 71 years (average, 34 years). The time from symptom onset to diagnosis ranged from 2 days to 53 years (average, 6 years), with diagnostic delays attributed to the slow growth pattern of epidermoid cysts (19).

Symptoms The symptoms of epidermoid cysts are primarily related to the size and location of the tumor and are similar to the symptoms of other spaceoccupying lesions of the spinal cord (20,23). Symptoms described in the literature are nonspecific and include weakness, back pain, paresthesia, and urinary or fecal incontinence (20,23,27). Cases of cyst rupture have been reported from incidents that suddenly increased intraabdominal or intraspinal pressure (eg, a fall, a severe cough, sneezing) and resulted in chemical meningitis or a severe inflammatory reaction (20).

Imaging Findings An epidermoid cyst typically appears as a circumscribed mass that is isointense to slightly hyperintense relative to CSF on T1- and T2weighted MR images; it may also be isointense relative to the spinal cord and CSF (Figs 2a–2c) (27,28). Rare “white epidermoids,” which are high in protein concentration, appear hyperintense on T1-weighted images and hypointense on T2-weighted images (28). An epidermoid cyst generally exerts mass effect on the surrounding structures, without evidence of peripheral edema (24,27). The variability in signal intensity is theorized to be secondary to the differing concentrations of keratin, water, and cholesterol inside the cyst (24,27,29). An epidermoid cyst is hyperintense to CSF on FLAIR MR images and hyperintense to CSF at DWI, with restricted diffusion. These imaging findings are the opposite of those for an arachnoid cyst (28,30). An epidermoid cyst may have faint to no rim enhancement, although intense enhancement has been reported in cases of malignant transformation (22,28,31). Calcifications are seen in 10%–25% of cases (28). Myelography will demonstrate an asymmetric filling defect, whereas a communicating arachnoid cyst typically opacifies (Figs 2d–2f) (32,33).

Treatment Surgical excision is the treatment of choice. The goal is extirpation of the tumor while minimizing neurologic complications. Intraoperatively, a pearly tumor is revealed in an intradural extramedullary

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Figure 3.  Intradural arachnoid cysts. (a, b) In a 52-year-old man, sagittal (a) and axial (b) FSE T2-weighted MR images show ventral cord displacement and compression, with no extruded ventral epidural soft tissue. Note the diminished CSF flow artifact (white arrow) at the widened dorsal subarachnoid space (arrowhead in a), a finding that argues against cord herniation. Focal hyperintensity (black arrow in a) in the adjacent cord may represent edema. (c, d) Sagittal (c) and axial (d) images from CT myelography in the same patient show immediate contrast agent filling in the widened subarachnoid space (arrow). An intradural arachnoid cyst with open communication to the CSF was found intraoperatively. (Figure 3 continues.)

location (Fig 2g). The surgery usually begins with emptying of the cyst contents, followed by near-complete resection of the capsule; this may prove difficult because of the tight adherence of the capsule to the dura, surrounding cord tissue, and nerve roots (20,23,27). Some surgeons may remove the sensory nerve roots involved with the tumor, while the motor nerve roots are spared, to maximize resection (34). A main surgical complication is spillage of the cyst contents into the surgical field, with possible resultant chemical meningitis and seeding of viable epidermal cells (20,21,23). Because a portion of the cyst wall may remain, the patient also is at risk for cyst recurrence (19,27). There have been reports of satisfactory treatment that consisted only of radia-

tion therapy or emptying of the cyst contents to decompress the spinal cord (20,27). After surgical treatment, patients are followed up with clinical or imaging evaluation; if there is a recurrence, a repeat operation may be performed, with favorable results reported (20,27).

Arachnoid Cyst

Arachnoid cysts, a subset of meningeal cysts, are a rare cause of spinal cord myelopathy and nerve root radiculopathy. Nabors et al (35) have classified meningeal cysts into three groups: (a) extradural arachnoid cysts without nerve root fibers (type I), (b) extradural meningeal cysts that contain neural tissue (type II, or Tarlov), and (c) intradural arachnoid cysts (type III). Type I arachnoid cysts are

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Figure 3.  (continued) (e, f) In a 76-year-old woman, axial T1-weighted (e) and FSE T2-weighted (f ) MR images show a right-sided intradural cyst (white arrow) compressing the spinal cord (black arrow) laterally to the left. Note the T2 hyperintensity seen in the compressed cord in f. (g) Axial image from CT myelography performed in the same patient immediately after intrathecal contrast agent administration shows no opacification of the cyst (white arrow). Black arrow = spinal cord, arrowhead = subarachnoid contrast agent. (h) Axial delayed image from CT myelography repeated 100 minutes after g shows contrast agent filling in the cyst (white arrow), a finding consistent with communication of the cyst with CSF through a narrow neck or one-way valve. Note the contrast agent within the subarachnoid space (arrowhead). (i) In a 46-year-old woman, sagittal FSE T2weighted MR image shows cord compression and ventral displacement. Note the diminished flow artifact (black arrow) at the widened posterior CSF space (white arrow). (j) Lateral fluoroscopic image of the thoracic spine (same patient as in i) shows needle aspiration of the cyst (arrow), which was confirmed to be a noncommunicating intradural arachnoid cyst. Note the contrast agent pooling within the cyst, with no communication with the CSF.

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further subdivided into extradural arachnoid cysts (type Ia) and sacral meningoceles (type Ib) (35). In a comprehensive literature review by Kriss and Kriss (36), 80% of intradural arachnoid cysts occurred dorsal to the neural elements in the spinal canal, and 80% occurred in the thoracic region, with only 15% in the cervical region and 5% in the lumbar region. Similarly, in a series of 31 patients reported by Kumar et al (37), roughly 71% of arachnoid cysts were in the thoracic region. Histologically, an arachnoid cyst is lined with fibrous tissue and scattered meningothelial cells (37). The mechanism of arachnoid cyst formation is incompletely understood (33,37,38). Some proposed mechanisms are arachnoid adhesions secondary to inflammation, infection, or trauma; congenital diverticula; arachnoid herniation through a dural defect; and an abnormal distribution of arachnoid trabeculations that leads to cyst formation (38,39). Arachnoid cysts may be encapsulated and completely separate from the CSF, or they may communicate with the subarachnoid space via a neck or develop a one-way valve (33,38,40). Symptoms will not occur until there is sufficient expansion of the arachnoid cyst to compress the spinal cord or nerve root (38). The cause of arachnoid cyst expansion is multifactorial. Proposed theories include the development of an osmotic gradient between the cyst and the subarachnoid space, a ball-valve mechanism that fills the cyst through a narrow stalk during surges in CSF pressure (eg, coughing or straining), and active secretions from the cyst lining (33,38). Arachnoid cysts usually manifest as solitary simple lesions. However, they may be multiple or may contain multiple septations (38). A spinal cord herniation or syrinx is sometimes associated with arachnoid cysts (38).

Demographics In 1947, Swanson and Fincher reported only four cases of acquired extradural arachnoid cysts in a series of 1700 exploratory laminectomies, a prevalence of 0.068% (41). The overall prevalence of arachnoid cysts is unknown, although their rarity is suggested in scattered case reports in the literature. Patients range in age from several months to nearly 80 years (39). In a series of 31 patients reported by Kumar et al (37), 77% of patients were aged 15–45 years, and no sex predilection was found.

Symptoms The clinical presentation usually corresponds to the location of the arachnoid cyst, with symptoms developing secondary to spinal cord or nerve root compression. Pain is the most common presenting symptom, followed by, in no particular order,

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sensory changes, urinary dysfunction, and weakness (36–39). Waxing and waning pain and progressive spastic or flaccid paresis that improves when the patient is supine and worsens during a Valsalva maneuver has been described; these symptoms may be partially explained by communication of the arachnoid cyst with the subarachnoid space (36,39). The clinical symptoms are by no means pathognomonic and must be correlated with the radiologic findings (39).

Imaging Findings Intradural arachnoid cysts can be difficult to identify because focal displacement and compression may be the only findings at MR imaging and conventional or CT myelography (Figs 3a–3d). An imaging finding of diminished CSF flow artifact (Fig 3a) in the widened dorsal subarachnoid space may suggest an intradural extramedullary space-occupying lesion. Depending on their type and location and whether they communicate with the subarachnoid space through a narrow or wide opening, arachnoid cysts will usually fill with intrathecal contrast material during myelography. Some cysts fill initially 50% of the time (Figs 3c, 3d), and others fill at delayed imaging nearly 100% of the time (Figs 3e–3h), as opposed to intraspinal epidermoid cysts, which demonstrate asymmetric filling defects (Figs 2e, 2f) (32,33,35,42,43). Some noncommunicating type III arachnoid cysts do not opacify at imaging and are difficult to differentiate from epidermoid cysts (Figs 3i, 3j) (33,40,42). MR imaging is superior to CT myelography in its sensitivity and specificity for detection of arachnoid cysts (39) and allows better characterization of the cyst’s nature and extent and associated abnormalities, such as a syrinx (40). It has been reported that constructive interference in steady-state (CISS [Siemens Medical Systems, Erlangen, Germany]) and fast imaging employing steady-state acquisition (FIESTA [General Electric Medical Systems, Milwaukee, Wis]) MR imaging sequences can demonstrate the walls of intracranial arachnoid cysts, but it is unclear whether this is applicable to the imaging of intraspinal arachnoid cysts (44). Types I and II arachnoid cysts typically are iso- to hyperintense to CSF on T1- and T2-weighted MR images, but variability in signal intensity may result from the pulsatility of the CSF or a higher protein content in the cyst (28,33). Type II arachnoid cysts contain neural elements such as nerve roots (33). Type III cysts have signal intensities similar to those of type I and II cysts but are intradural (33); mass effect may be seen, with a possible spinal cord signal intensity abnormality if the cyst is sufficiently large (39). Arachnoid cysts are nonenhancing, are isointense to CSF

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on FLAIR MR images, and do not demonstrate restricted diffusion at DWI (28). CT myelography and MR imaging are complementary modalities for detecting arachnoid cysts. CT myelography is invaluable for assessing patients with contraindications to MR imaging and for ascertaining and localizing the subarachnoid communication of a cyst (39). MR imaging allows excellent lesion characterization, and flow-sensitive MR imaging sequences may offer an alternative for pinpointing the location of communication (39). Pitfalls of CT myelography and MR imaging include misidentifying a noncommunicating arachnoid cyst as a different type of lesion because of nonopacification and failing to detect additional cysts or a small CSF-isointense arachnoid cyst that does not exert mass effect on the cord (36,45). If an extradural arachnoid cyst is large and chronic, radiographs may demonstrate scalloping of the vertebrae or widening of the pedicles (28,41–43).

Treatment Asymptomatic cysts are monitored, and symptomatic cysts are surgically removed (39). The surgical goal is complete resection of the cyst, although cyst adherence and ventral positioning may force the surgeon to perform marsupialization or fenestration of the cyst (36,39). Aspiration of the cyst contents is not recommended because the rate of cyst recurrence is high (33,36,39). Cysts refractory to fenestration may require cystoperitoneal shunt placement (38). Kumar et al (37) observed no postoperative recurrences of arachnoid cysts in 31 patients, and Bond et al (38) reported one postoperative recurrence in 31 pediatric patients. Both studies reported that most patients experienced postoperative improvement or symptom resolution (37,38).

Spinal Epidural Abscess

An SEA is a serious condition that warrants prompt diagnosis and management. The three main causes of SEAs are hematogenous (most common), contiguous, and iatrogenic (46). A hematogenous route accounts for roughly half of all SEAs and is most commonly associated with urinary tract infections, pneumonia, and previous soft-tissue or skin infections (46). A contiguous spread of infection accounts for one-third of cases and results from an infection in affected adjacent structures, most commonly osteomyelitis in the vertebral body or an abscess in the psoas muscle (46). Iatrogenic causes include invasive procedures to the spine and nearby structures (46). Staphylococcus aureus, including methicillinresistant S aureus, is the most common causative organism, comprising two-thirds of cases. Staphylococcus epidermidis (from a skin infection,

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penetrating trauma to the spine, or spinal intervention), Streptococcus pneumoniae, Escherichia coli (from urinary tract infections), and Pseudomonas aeruginosa (from intravenous drug abuse) are less common pathogens (46). Fungal, parasitic, and mycobacterial causes are rare (46). SEAs predominantly affect the dorsolateral thoracolumbar region and span multiple vertebral levels, with the thoracic region affected in 50% of cases (46,47). This may be related to the larger potential space, abundant vascularity, and epidural fat (providing relatively low resistance to infection) in the thoracic region, conditions that make it a fertile ground for infection (46). The site of intravenous drug injection correlates with the abscess location; injections in the upper extremities result in cervical abscesses, and injections in the lower extremities result in lumbar abscesses (46). Risk factors include acquired immunosuppressive or immunodeficiency disorders, drug addiction, cancer, alcoholism, systemic inflammation or infection, liver disease, diabetes, trauma, and surgical procedures that involve the spine or surrounding structures (46,48,49).

Demographics The incidence of SEA is roughly 1.8 per 100,000 people and 0.2–2.8 per 10,000 hospital admissions per year (46,49). Patients range in age from 10 days to 87 years, although patients older than 30 years are most common (46). There is a maleto-female preponderance of 1.7:1, which may be attributed to risk factors that are more common in men (46).

Symptoms The classic triad of presenting symptoms for an SEA includes localized back pain (70% of patients), fever (60%), and neurologic deficits (30%) (46,50). Patients typically present with severe back pain and fever, and symptoms may progress to radicular pain (depending on the level affected), fecal or urinary incontinence with motor or sensory deficits, and eventual rapid and irreversible neurologic deterioration (46). A study by Davis et al (48) reported that presentation with all three symptoms in the triad is uncommon (2% of patients) and by no means sensitive for diagnosis, although sensitivities of up to 100% were seen with the use of decision guidelines that incorporated risk-factor assessment with erythrocyte sedimentation rate tests (48).

Imaging Findings Sagittal MR imaging is essential to determine the craniocaudal extent of an SEA, and axial MR imaging will depict its precise location and associated findings (51). An SEA is categorized as focal if it

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affects five or fewer vertebral bodies and as diffuse if it affects more than five (51). An SEA appears hypo- to slightly hyperintense to the spinal cord on nonenhanced T1-weighted MR images and hyperintense to the spinal cord on T2-weighted MR images, rendering its differentiation from CSF difficult (Figs 4a–4c) (51). Contrast-enhanced MR images demonstrate diffuse heterogeneous or homogeneous enhancement (representing a phlegmonous infection with microabscesses) or peripheral enhancement with varying thickness around a central pus collection (Figs 4d, 4e) (51). An SEA is hyperintense at DWI, with reduced apparent diffusion coefficients (restricted diffusion) (52). Other imaging findings include linear enhancement along the compressed dura mater (in 75% of patients with a diffuse SEA only) and engorgement of the epidural or basivertebral veins that is best seen on sagittal images; these findings likely result from inflammation extending along the dura mater and inflammation or mechanical obstruction of the venous plexus (51). The epidural fat and subarachnoid space may also be effaced (51). Nonenhanced and contrast-enhanced images should be compared because an SEA may blend in with CSF on nonenhanced T1- and T2weighted MR images. Myelography is not recommended because its invasive nature may aid in seeding additional infection into the subarachnoid space (46,51). Any nearby associated pathologic imaging findings, such as osteomyelitis, discitis, and paravertebral abscess, should be noted (51). Osteomyelitis and discitis will be seen as enhancing foci in the affected or adjacent bone marrow and disk space (hypointense on T1-weighted images and hyperintense on T2-weighted images) (51). Short inversion time inversion-recovery MR imaging sequences may be used to evaluate for osteomyelitis (47).

Treatment SEAs often require urgent surgical decompression and drainage to avoid dire neurologic consequences; surgery is followed by 4–6 weeks of antibiotic therapy (46). Nonsurgical management may be pursued if the patient refuses surgery, is asymptomatic, has an extensive SEA, or has paralysis that persists for more than 48 hours (46). Successful surgical treatment is often followed by extensive physical and occupational therapy (46). Mortality is estimated at 5%–20%, with neurologic improvement observed in 45%–72% of patients (46,50).

Cystic Schwannoma

Schwannomas arise from Schwann cells and are well-encapsulated tumors that affect the peripheral nervous system (53). Wherever peripheral or cranial nerves are present, the development of a

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schwannoma is a possibility (53). Spinal schwannomas and neurofibromas account for 25%–30% of all intraspinal masses (54). Schwannomas are intradural in 70%–75% of cases, extradural in 15% of cases, both intradural and extradural in 15% of cases, and intramedullary in less than 1% of cases (54). Cystic schwannomas have been reported in the orbital region, intraventricular region, olfactory groove, and cavernous sinus (53,55). Cystic spinal schwannomas are even less common, with spinal schwannomas (cystic and noncystic) affecting the lumbar region in 48% of cases (53,55). Schwannomas are slow-growing tumors that may demonstrate variable degenerative changes such as fibrosis, cystic degeneration, calcification, and hemorrhage (53,55). If there is a constellation of such changes, the lesion is termed an ancient schwannoma (53). Purely cystic change is rare (53) and may be due to degeneration, necrosis, or tumor growth (55). Symptoms are few, if any, because of the indolent growth pattern. Uncommonly, the tumor may grow large enough to cause pain and sensory or motor changes secondary to mass effect on the cord or nerve roots (53). Schwannomas occur in men and women equally (53) and most commonly affect patients aged 40–60 years (53). Schwannomas are more common in patients with neurofibromatosis type 2 (53). The treatment goal is safe microsurgical radical excision (53,56). MR imaging demonstrates a lesion isointense to hypointense to the spinal cord on T1-weighted images, with mild to marked hyperintensity on T2-weighted images; markedly hyperintense focal areas seen on T2-weighted images likely correspond to the cystic regions, and hypointense portions likely represent dense cellularity, collagen, or hemorrhage (Figs 5a–5c) (54,57). There usually is heterogeneous and irregular nodular peripheral enhancement (Figs 5d, 5e) (54,57), and fluid-fluid levels secondary to hemorrhage may be seen (54,58). The enhancement pattern of a cystic schwannoma helps to differentiate it from an arachnoid cyst and from most epidermoid cysts, which may sometimes exhibit faint peripheral enhancement, although not with the same extent and pattern. Dermoid cysts usually can be distinguished from cystic schwannomas because they contain macroscopic fat (59).

Additional Causes

The differential diagnosis also includes pseudomeningoceles, teratomas (which can be differentiated with fat-suppressed imaging), perineural or Tarlov cysts, arachnoiditis, and epidural hematomas (Fig 6). A pseudomeningocele is a spinal cyst contiguous with the thecal sac and results

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Figure 4.  Spinal epidural abscess in a 33-yearold man. (a, b) Sagittal T1-weighted (a) and sagittal FSE T2-weighted (b) MR images show ventral cord displacement and compression by a dorsal lentiform lesion (arrow) with mixed heterogeneous hypointensity and hyperintensity. Note the increased T2 signal intensity in the marrow of an adjacent vertebral body (arrowhead in b), a finding suggestive of edema. (c–e) Axial T2-weighted MR image (c) and axial (d) and sagittal (e) contrast-enhanced T1-weighted MR images show small loculated fluid collections (arrow) with heterogeneous enhancement, findings consistent with an epidural abscess. There is also enhancement of the adjacent right psoas muscles, which contain an abscess (arrowhead in c and d). Enhancement of the vertebral body (arrowhead in e) is suggestive of osteomyelitis. Purulent liquefactive material was drained from the abscess with CT-guided percutaneous drainage.

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Figure 5.  Cystic schwannoma in a 60-yearold woman. (a–c) Sagittal (a) and axial (b) T1-weighted MR images and sagittal FSE T2-weighted MR image (c) show a lobulated cystic lesion within the subarachnoid space, causing ventral and leftward cord displacement and compression. (d, e) Sagittal (d) and axial (e) contrast-enhanced T1-weighted MR images demonstrate diffuse rim enhancement of the lesion. A cystic schwannoma was confirmed at surgery.

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Figure 6.  Epidural hematoma in a 69-yearold man with ankylosing spondylitis after a fall. Sagittal T1-weighted MR image (a) and sagittal (b) and axial (c) FSE T2-weighted MR images show a lentiform lesion (white arrow) that is isointense to the cord on the T1weighted image and heterogeneously hyperintense on the T2-weighted images. The posterior epidural space is shown compressing the lower cervical and upper thoracic cord (black arrow in c) anteriorly. An epidural hematoma was confirmed at decompression surgery.

from previous surgery or trauma. The lesion is suggested by the typical MR imaging appearance of a cyst with adjacent posttraumatic or postoperative ancillary findings (60). An intradural teratoma is a rare tumor that may contain solid and cystic components and may tether the spinal cord (61). Perineural or Tarlov cysts (type II) are cystic lesions that contain spinal tissue, most commonly nerve root fibers, and are differentiated by their extradural location (33). Postsurgical or postinflammatory arachnoiditis may be associated with intradural cysts (CSF loculations formed by adhesions) but can be differentiated by concomitant nerve clumping and enhancement (60,62,63). Spinal epidural hematomas are relatively uncommon and result from trauma, hypertension, vascular anomalies, anticoagulation, and iatrogenic causes (lumbar puncture, spinal anesthesia, or

surgery) (64,65). Spinal hematomas (epidural and subdural) have a variable MR imaging appearance depending on their acuity (Figs 6a–6c). Within the first day of injury, the hematoma is isointense to the cord on T1-weighted images and heterogeneous to the cord on T2-weighted images. Subsequently, increased signal intensity is seen on both T1- and T2-weighted images. Chronic hemorrhage appears hypointense on both T1- and T2-weighted images (64,65). Enhancement is usually not seen within the hematoma.

Conclusion

When the interpreting radiologist is confronted with imaging findings of focal cord displacement and a widened CSF space, a clear knowledge of the differential diagnoses should immediately come to mind: ISCH and the different types of CSF-isointense space-occupying intraspinal extramedullary lesions. ISCH, although rare, has been diagnosed with increasing frequency in recent years because of increased recognition in

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the literature and advances in imaging technol­ ogies. Radiologists must understand the bene­ fits and drawbacks of different imaging techniques and use them wisely to direct a thorough work­up of patients with focal cord displacement and an enlarged CSF space. Combining an assessment of the patient’s clinical symptoms with a multimodality imaging approach facilitates correct diagnosis so that prompt treatment can be provided. Acknowledgments.—The authors thank Dennis Oh,

MD, for providing the intraoperative photographs and Eugene Kang, MD, for providing additional images. The authors also thank Michael Swirsky, MD, for his assistance with the manuscript.

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TM

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Teaching Points

March-April Issue 2014

Differentiation of Idiopathic Spinal Cord Herniation from CSF-isointense Intraspinal Extramedullary Lesions Displacing the Cord Marc D. Haber, MD • Dustin D. Nguyen, DO • Shan Li, MD, MS RadioGraphics 2014; 34:313–329 • Published online 10.1148/rg.342125136 • Content Codes:

Page 315 Most patients with ISCH present with symptoms of BSS, including ipsilateral upper motor neuron paralysis and loss of proprioception and contralateral loss of pain and temperature sensation. Page 317 In a study of 12 patients, Imagama et al suggested that patients with type P ISCH will have a good postoperative recovery, whereas patients with a type C hiatus and a concomitant bone defect may have severe preoperative neurologic symptoms and a poor postoperative recovery. Page 319 An epidermoid cyst is hyperintense to CSF on FLAIR MR images and hyperintense to CSF at DWI, with restricted diffusion. These imaging findings are the opposite of those for an arachnoid cyst. Page 323 Pitfalls of CT myelography and MR imaging include misidentifying a noncommunicating arachnoid cyst as a different type of lesion because of nonopacification and failing to detect additional cysts or a small CSFisointense arachnoid cyst that does not exert mass effect on the cord. Page 324 Contrast-enhanced MR images demonstrate diffuse heterogeneous or homogeneous enhancement (representing a phlegmonous infection with microabscesses) or peripheral enhancement with varying thickness around a central pus collection. An SEA is hyperintense at DWI, with reduced apparent diffusion coefficients (restricted diffusion).