Showing posts with label Spine. Show all posts
Showing posts with label Spine. Show all posts

Monday, December 27, 2010

Lumbar disc extrusion with a wrapped disc







Findings

There is a left central disc extrusion at L5-S1 that causes mild to moderate left lateral recess narrowing and nerve root displacement without nerve root compression. At this level there is also contrast enhancement traversing the left laminectomy defect and encasing the disc extrusion, consistent with a wrapped disc. There is enhancement in the left lateral recess, suggesting post-operative fibrosis.

Differential diagnosis:
- Wrapped disc
- Peridural fibrosis
- Epidural abscess
- Epidural metastasis
- Nerve sheath tumor
- Disc pseudobulge
- Intervertebral disc protrusion
- Intervertebral disc extrusion
- Recurrent intervertebral disc herniation


Diagnosis: Lumbar disc extrusion with a wrapped disc


Key points: "Wrapped" disc


Disc herniation (protrusion, extrusion, or fragment) may be caused by trauma, repetitive or acute, and are a common source of pain and subsequent back surgery in the general population. In the acute phase, the herniated disc stimulates a fibrovascular response. A "wrapped disc" is the focal herniation (protrusion, extrusion, or fragment) that is encased in vascular scar tissue stimulated by this response and is evident by enhancement on contrast-enhanced T1-weighted images.

Asymptomatic or low back pain and/or radiculopathy are most common in the lumbar spine at L4-L5 and L5-S1. A wrapped disc is a post-surgical sequela, particularly following surgery for spinal stenosis in which the surgical procedure is more extensive, involving a laminectomy and a medial facetectomy.

Best imaging modality: MR (sequences: sagittal and axial T2WI and T1WI, as well as contrast-enhanced axial and sagittal T1WI)
Other imaging modalities: CT, myelography


Imaging findings

MR: Anterior extradural mass contiguous with the disc space extending into the spinal canal
*Contrast-enhanced T1WI: Peripheral enhancement surrounding the disc herniation or fragment with/without central canal, lateral recess, or foraminal stenosis and cord or nerve root impingement. (*most helpful MR sequence)
Non-enhanced T1WI: Isointense to parent disc
T2WI: Iso- to hyper intense to parent disc
General disc hypointensity and height loss at the level of the herniation, as well as postoperative changes (laminectomy defects, etc), degenerative facet disease, and osteophytes, are common associated findings.
CT:
Non-contrast CT: An anterior extradural soft tissue mass that may displace the nerve root / indent the thecal sac
Contrast-enhanced CT: Mild peripheral enhancement of the disc herniation/fragment
Myelography: An extradural mass that indents the thecal sac and nerve root sleeves
Imaging findings of other common differential diagnoses
Peridural fibrosis: Scar within epidural space after lumbar surgery that infiltrates epidural fat, causing homogeneous enhancement that diffusely surrounds the thecal sac and nerve root; increased in T2 signal relative to adjacent disc herniation
Epidural abscess: A distinct fluid collection in the epidural space with peripheral enhancement on post-contrast images, often associated with findings of diskitis
Epidural metastasis: Elongated (cranial-caudal orientation) enhancing mass with osseous involvement and may demonstrate paravertebral extension
Nerve sheath tumor: Avid enhancement surrounding the nerve root, some of which are in a "dumbbell" shape
Disc pseudobulge: Smooth generalized extension of the disc margin without a focal defect due to "uncovering" of disc related to spondylolisthesis
Intervertebral disc protrusion: Anterior extradural mass contiguous with disc space and triangular in shape with broader base than apex; no enhancement
Intervertebral disc extrusion: Anterior extradural mass contiguous with disc space by a "neck," in which this herniated disc material then widens in the epidural space
Recurrent intervertebral disc herniation: Extradural mass contiguous with intervertebral disc margin, demonstrating enhancement peripherally but without central enhancement
Treatment
Conservative: Anti-inflammatory and pain medications, avoid trauma
Surgical: Repeat surgery to remove herniated disc (protrusion, extrusion, fragment)

Thursday, December 16, 2010

Sequestered disk







Findings

There is an non- enhancing ovoid mass slightly hyper intense to muscle on both T1 and T2 sequences, in the anterior epidural space at the L3 level, measuring approximatelyl 12 x 8 x 12 mm. This is not contiguous with any adjacent disks. No signal dropout on fat-saturated sequences. The mass causes severe stenosis of the left half of the spinal canal at the L3 level, compressing the left descending nerve roots. T1 and T2 hyper intensity at the endplates abutting L2-L3 disc space representing Modic Type II changes. There is intervertebral disk space height loss at L2-L3 with severe disk desiccation changes.


Differential diagnosis:
- Sequestered disk
- Extruded disk
- Failed back surgery
- Epidermoid
- Epidural abscess
- Epidural hematoma
- Lipoma


Diagnosis: Sequestered disk


A focal disk protrusion is an extension of intervertebral disc material (nucleus pulposus) beyond the vertebral margin (AP diameter < mediolateral diameter). An extruded disk is one in which the nucleus pulposus has herniated through a rent in the annulus fibrosis. The AP diameter > ML diameter, and the disk may migrate craniocaudally, but maintains attachment to the parent disk (frequently symptomatic).
When extruded disk material loses its attachment to the parent disk, it is referred to as a sequestered disk. Sequestered discs usually lodge in the anterior epidural space (AES), just anterior to the posterior longitudinal ligament, and migrate either cephalad or caudad (with equal frequency). Because there is a midline septum associated with the PLL in the AES, the fragment is usually just off midline (to the right or left). Rarely, the sequestered fragment may migrate beyond the PLL into the posterior epidural space, through the dural ( intrathecal location), or into the paraspinal muscles.
They usually resemble the parent disk on MR, with T1 hypo intense and T2 iso- / hypo intense. There may be surrounding T2 hyper intensity and a rim of enhancement from inflammatory changes.
This is a crucial diagnosis to make, as a sequestered disk is a contraindication to limited disk procedures (e.g. Percutaneous discectomy) and may result in failed back surgery.

Tuesday, December 14, 2010

Myxopapillary ependymoma






Findings

Figure 1: Sagittal T1-weighted images reveals an isointense lobulated intradural mass at the level of the conus medullaris.
Figure 2: Sagittal T2-weighted images shows a hyperintense lobulated intradural mass extending from T11 through L2 with numerous small flow voids.
Figure 3: Sagittal T1 post-contrast images demonstrates intense enhancement of the intradural mass centered around the conus.


Diagnosis: Myxopapillary ependymoma


Myxopapillary ependymoma is a slow-growing tumor arising from the ependymal cells of the filum terminale. These tumors compromise 13% of all spinal ependymomas, and they occur almost exclusively in the conus, filum terminale, and cauda equina although extradural occurence in the sacrum and presacral region has also been reported.

The lesions tend to span two to four vertebral segments, and appear as a well-circumscribed intradural masses. In most cases the tumor is intrinsic to the conus medullaris but this is often difficult to recognize on imaging as the bulk of the mass is extramedullary. Typical MR characteristics include T1 isointensity, T2 hyperintensity, and avid enhancement on post-contrast images. As these tumors are prone to hemorrhage, a hypointensity at the tumor margin is often seen indicative of hemosiderin. Calcification and cyst formation within the mass are not infrequent.

On radiography and CT, vertebral changes can be seen which include widened interpediculate distance, thinned pedicles, posterior vertebral scalloping, and intervertebral foraminal widening due to tumor extension.

They are more common in males (M:F=2:1) with a mean age of 35 at diagnosis. Clinically, they present with back pain, paraparesis, radiculopathy, and occasionally bowel and bladder dysfunction. Because these symptoms can mimic those of disc herniation, there is often a delay in diagnosis. Treatment consists of surgical resection, and the prognosis is excellent with complete resection. Leptomeningeal seeding metastasis in myxopapillary variety is not as frequent as it is in classic spinal cord ependymomas and associated with poorer prognosis when present. Radiotheraphy after surgery improves outcome.

Friday, December 3, 2010

Basilar invagination secondary to rheumatoid arthritis








Findings

Axial and sagittal CT images demonstrate severe basilar invagination (Figure 1). The tip of the odontoid process measures 2.3 cm above Chamberlain’s line (yellow line in Figure 2). McGregor's line (red line in Figure 2) is also shown. Incidentally noted are right-sided opacified mastoid air cells (Figure 1).
Once again, severe basilar invagination is evident. On the sagittal T2 image the foramen magnum is narrowed and obliteration of the CSF space is noted at the C2-C3 level (Figure 3). On the axial T2 weighted image increased T2 signal (Figure 4) is seen within the cord at the C2-C3 level indicating edema versus myelomalacia.



Diagnosis: Basilar invagination (impression) secondary to rheumatoid arthritis.


Basilar invagination refers to a condition in which the odontoid process protrudes upward into the intracranial space. Basilar invagination may be classified as primary (congenital) or secondary (acquired). Down syndrome, Klippel-Feil syndrome and Chiari malformations are congenital causes of basilar invagination. Acquired basilar invagination, also known as basilar impression, is associated with softening of the skull base and is often due to rheumatoid arthritis, Paget disease, osteomalacia, hyperparathyroidism and osteogenesis imperfecta. Basilar invagination is probably better described as a radiologic finding rather than a diagnosis. Once the finding is identified, a cause of basilar invagination should be diligently pursued.

Plain lateral radiographs with odontoid views, although not 100% sensitive, are often the initial study used to diagnose basilar invagination. MRI is the optimal study, which also assesses the cervicomedullary junction and cervical cord. Two craniovertebral junction lines are particularly useful in defining basilar invagination. Chamberlain’s line extends between the posterior pole of the hard palate and the posterior edge of the foramen magnum (opisthion). If the dens is >3.0 mm above this line basilar invagination is present. McGregor’s line, a modification of Chamberlain’s line was developed because the opisthion could not always be seen on plain radiographs. This line extends from the posterior pole of the hard palate to the undersurface of the occiput. If the dens extends >4.5 mm above this line basilar invagination is present.

Clinical manifestations of basilar invagination include posterior skull pain, headache, signs and symptoms of brainstem and upper cervical cord compression or disturbances of CSF circulation causing obstructive hydrocephalus. The brainstem may be compressed at the level of the foramen magnum possibly resulting in compromise of the autonomic centers resulting in labile blood pressures, arrhythmias, or sudden death. Neurosurgery is recommended in patients that are symptomatic with concomitant MRI findings indicating compression. Although asymptomatic patients are often followed conservatively, many authors favor surgery even if no symptoms of cord compression are evident in rheumatoid patients.

Although often appearing together, basilar invagination or impression should not be confused with platybasia; which literally means “flattening of the base of the skull”. Platybasia, which can be seen in Klippel-Feil anomalies, cleidocranial dysplasia and achondroplasia, is present when the basal angle formed by intersecting lines from the nasion to the tuberculum sellae and from the tuberculum along the clivus to the anterior aspect of the foramen magnum (basion) is greater than 143 degrees.

Friday, November 12, 2010

Idiopathic Thoracic Cord Herniation






Findings

These MR images demonstrate focal anterior displacement of the spinal in the mid thoracic spine. The cord (Images 1,2 and 3) appears to be either tethered anteriorly or compressed from the posterior aspect. The intradural space behind the cord is widened and has signal characteristics identical to CSF (Images 1,2 and 3).


Diagnosis: Idiopathic Thoracic Cord Herniation


Spinal cord herniation occurs when the cord herniates through a defect in the dura mater. These dural defects are typically located anteriorly or laterally, and occur most often in the mid-thoracic region. They may be idiopathic, post-traumatic or iatrogenic related to prior spinal surgery. Some have suggested that a herniated and calcified disk may cause thinning, erosion, or rupture of the dura, which may also be secondary to congenital weakening of the ventral dural fibers. The presence of free flow of cerebral spinal fluid dorsal to the herniated cord is key to differentiating a spinal cord herniation from an arachnoid cyst. Spinal cord herniation occurs most commonly in the middle-aged. Symptoms of myelopathy including chronic leg pain, gait disturbance, incontinence, and leg weakness are commonly seen and may slowly worsen over time if left untreated. The most common clinical feature reported is the Brown-Séquard syndrome consisting of hemiplegia and contralateral temperature sensation deficits and pain.

Typical imaging findings are focal anterior displacement of the spinal cord with expansion of the dorsal subarachnoid space. The preferred imaging modality in the setting of myelopathy is MRI, which is often sufficient for making the correct diagnosis. Myelography with CT may be required in ambiguous cases and to demonstrate the exact location of the dural defect. With cord herniation, myelography reveals uninterrupted flow of contrast and the absence of a filling defect posterior to the herniated cord segment. An arachnoid cyst will present during myelography as an early filling defect posterior to the displaced cord. Contrast may fill the cyst with time, so rapid acquisition of CT-myelograpgy after the initial myelographic images is essential. Phase contrast cine MR imaging may provide similar CSF flow information, in addition to restricted cord motion.

Treatment consists of surgically reducing the herniation by repositioning the protruding spinal cord back into the thecal sac followed by the repair of the defect in the dural mater in order to prevent recurring herniation. After surgery, symptoms typically improve and may completely resolve, even when longstanding. Patients whose symptoms are milder and non-progressive may be eligible for less invasive therapy or conservative management with monitoring.