MR Imaging of the Spine: Urgent and Emergent Indications

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MR Imaging of the Spine: Urgent and Emergent Indications Efrat Saraf Lavi , Amit Pal , Drew Bleicher , Kyungmin Kang , Charif Sidani PII: DOI: Reference:

S0887-2171(18)30089-1 https://doi.org/10.1053/j.sult.2018.10.006 YSULT 833

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Seminars in Ultrasound CT and MRI

Please cite this article as: Efrat Saraf Lavi , Amit Pal , Drew Bleicher , Kyungmin Kang , Charif Sidani , MR Imaging of the Spine: Urgent and Emergent Indications, Seminars in Ultrasound CT and MRI (2018), doi: https://doi.org/10.1053/j.sult.2018.10.006

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MR Imaging of the Spine: Urgent and Emergent Indications Efrat Saraf Lavi1*, Amit Pal1, Drew Bleicher2, Kyungmin Kang2, Charif Sidani1 Department of radiology University of Miami Miller School of Medicine

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Department of Radiology Jackson Memorial Hospital

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*Corresponding author Efrat Saraf Lavi Associate Professor of Radiology University of Miami Miller School of Medicine 1611 NW 12th Ave. WW 279 Miami, FL 33136 Phone: 3055857500 Fax: 3055855743 [email protected]

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1.

Abstract

Spinal emergencies and urgent conditions must be recognized early so that the diagnosis can be

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quickly confirmed and treatment can be instituted to possibly prevent permanent loss of function.

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The ACR provides guidelines for recognition of patients presenting with myelopathy or acute low back pain who require further evaluation for suspicion of more serious problems and

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contribute to appropriate imaging utilization. Spinal emergencies include spinal cord compression secondary to vertebral fracture or space occupying lesion, spinal infection or

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abscess, vascular or hematologic damage, severe disc herniation and spinal stenosis.

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Introduction A wide variety of conditions can damage the spine, spinal cord tissue or nerve roots and result in perman ent paralysis or paraplegia. Urgent conditions require immediate attention, but do not always

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warrant immediate treatment. True spinal emergencies represent a potential loss of function if not treated properly and therefore prompt diagnosis is important. The American College of

Radiology (ACR) Appropriateness Criteria as well as other similar guidelines help identify

higher-risk individuals (Table 1) and aid in providing recommendations for the best imaging

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modality for patients presenting with lower back pain and myelopathy in a variety of clinical scenarios.

LOW BACK PAIN / RADICULOPATHY

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Lower back pain (LBP) without or with radiculopathy affects the majority of people over their lifetime and is a major cause of disability in the United States and the second most common

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reason for a physician visit. The Institute for Clinical Systems Improvement defines LBP as acute when duration of symptoms is from 0–6 weeks, as sub-acute from 6–12 and as chronic >12

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weeks.

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Imaging Modalities - ACR Recommendations (Table 2) Acute LBP and radiculopathy are mostly benign, self-limited conditions that do not warrant any

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imaging studies. Imaging should be reserved to those patients who have little or no improvement in their back pain after 6 weeks of medical management and physical therapy and for patients presenting with more serious underlying condition , such as cauda equina syndrome, malignancy, or infection. In these patients, magnetic resonance imaging (MRI) of the lumbar spine should be considered. Patients with recurrent low back pain and history of prior surgical intervention

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should be evaluated with contrast-enhanced MRI. Computed tomography (CT) scans with multiplanar reformatted sagittal and coronal planes is useful for revealing bone structural problems such as spondylolysis, pseudarthrosis and for postsurgical evaluation of bone graft integrity, surgical fusion, and instrumentation1.

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Acute cauda equina syndrome

Acute Cauda Equina Syndrome (ACES) is a devastating condition with classic symptoms including worsening severe low back pain, saddle anesthesia, recent onset bladder/bowel

incontinence as well as sexual dysfunction, and/or loss of reflexes in the extremities. There are

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multiple potential etiologies with the most common being disk herniation at the level of L4-L5 and L5-S1. ACES can be classified as incomplete or complete. Controversy exists regarding the timing of surgery with the general consensus that within 24 hours from symptom onset is ideal to

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prevent long-term sequelae, which is especially useful to prevent progression from an incomplete to complete syndrome. The most useful imaging modality in the evaluation of patient with ACES

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is MRI; however, depending on the institution this may not be expediently possible given the acuity of the condition and need for immediate intervention. There are multiple potential

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etiologies. In the setting of a disk herniation or metastatic disease with epidural extension,

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imaging will demonstrate severe compression of the cauda equina nerve roots and obliteration of the surrounding CSF (Fig1). Additional considerations within the spinal canal include intrinsic

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tumors such as ependymoma or astrocytoma with acute hemorrhage exacerbating symptoms2, 3. The radiographic findings should be correlated with the patient’s clinical history. An urgent neurosurgical consultation is essential to avoid delay in care and potentially catastrophic irreversible sequelae.

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Neoplasm Spinal bone metastases Bone is a common site for metastatic disease and evaluation for vertebral body metastases as a cause of lower back pain is a common indication for emergent MR imaging. Thoracic and

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lumbar vertebral bodies are most commonly affected due to the relative volume of vascularized marrow, and multiple levels of disease are often identified at the time of diagnosis. Metastatic bone lesions are usually T1-hypointense due to replacement of marrow fat with tumor, associated edema, or sclerosis and hyperintense on T2W images, although sclerotic lesions may appear

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hypointense. Fast-spin-echo (FSE) T2W images are usually unsatisfactory for the detection of vertebral metastases because both normal vertebral marrow and tumor-replaced marrow may give hyperintense signal on FSE T2W images. Hyperintensity, due to fatty marrow, can be

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suppressed by chemical shift fat saturation or STIR (short tau inversion recovery) techniques. On post contrast images, vertebral body metastases typically enhance4 (Fig 2).

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Lymphoma

Lymphomatous leptomeningitis is a rare phenomenon that more commonly occurs as a

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secondary lymphoma manifestation rather than an initial primary lymphoma presentation.

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Patients can present with spinal symptoms such as lower extremity weakness, numbness, and radicular pain. Other signs concerning for nerve root compromise may also include dermatomal

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or segmental sensory loss, which is confounding to that of cauda equina syndrome5. On MRI (Fig 3), the signal characteristics of the lymphoma on T1W, STIR and FSE T2W images nearly resemble that of cerebrospinal fluid. However diffuse enhancement along the pia, nerve roots and subarachnoid spaces helps making the diagnosis.

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Infection Infectious causes are only briefly described here and will be discussed in details in a separate manuscript. Emergent MR imaging of the spine is indicated in patients with new or worsening back pain, radiculopathy or neurologic deficits and signs or symptoms of infection. Routes of

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infection include hematogenous spread, direct and contiguous spread of disease. Infection may involve the vertebrae, discs, joint spaces, epidural space, meninges, and spinal cord. Common organisms are Staphylococcus aureus and Mycobacterium tuberculosis4. Discitis osteomyelitis

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Discitis osteomyelitis is the most common spinal infection. Vertebral segmental arteries supply the endplates on both sides of an intervertebral disc, which allows hematogenous seeding to contiguous vertebral bodies with possible extension to the disc4. Typical MR imaging findings

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are decreased vertebral body signal and loss of endplate definition on T1W images, increased disk signal intensity on T2W images and contrast enhancement of the disk and adjacent vertebral

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bodies. Treatment is with antibiotics. Epidural abscess

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Spinal epidural abscess can be primary or develop after spinal surgery.

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Primary spinal epidural abscess is rare and primarily occur in middle-aged and elderly men. Risk factors include diabetes, intravenous drug use, immunocompromised state, previous spinal

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invasive procedures, and superficial infections of the back and infections at distant sites. Staphylococcus aureus is the most common pathogen and is found in approximately 70% of cases. Patient typically present with back pain. Fever is present in about two third of patients and neurological deficit in 25-60%. MRI is the modality of choice and demonstrates peripherally enhancing fluid collection with diffusion restriction. Treatment includes surgical decompression

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with antibiotic treatment. More than 80% of patients with spinal epidural abscess have concomitant discitis osteomyelitis6. Osteoporosis Benign Compression fracture

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Patients who present with benign compression fracture are typically the elderly who are

predisposed to osteoporosis. Clinically, symptoms may be nonspecific with only a complaint of back pain. In diagnosing benign compression fractures, the challenge lies in distinguishing

between benign and malignant vertebral body fractures, which may be difficult especially if there

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is no history of malignancy as well as no history of significant trauma. Although MRI remains the modality of choice, both acute benign and malignant fracture may present with low T1W and high T2W signal. Diffusion-weighted imaging and fat-saturated post-contrast T1W images may

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help differentiate the two. Pathologic fractures may show evidence of restricted diffusion7 and diffuse vertebral body enhancement8. Chronic benign fractures marrow signal is isointense to

Chronic steroid use

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normal vertebrae on all pulse sequences in the vast majority of cases9.

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Glucocorticoids are a well-known cause of secondary osteoporosis and are associated with an

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increased risk of fracture10. Obtaining such clinical history in diagnosing vertebral compression fractures is very helpful. Finding that help support the diagnosis of vertebral compression

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fracture secondary to chronic steroid use is the identification of bands of increased T1W signal intensity along the vertebral body endplates; however this finding is nonspecific (Fig 4). Spondylolysis Patients with spondylolysis have a defect in the pars interarticularis (the portion of the neural arch that connects the superior and inferior articular facets). Spondylolysis is believed to be

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caused by repeated microtrauma resulting in stress fracture of the pars interarticularis. It is especially common in adolescents involved in certain kinds of sports. Patients with bilateral pars defects can develop spondylolisthesis of varying degree, which can progress over time. Some cases of spondylolysis and spondylolisthesis remain asymptomatic but most complain of

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symptoms ranging from low back pain to radiculopathy and neurogenic claudication11. Initial evaluation of patients with suspected spondylolysis is with plain radiography. The limitation of plain films is the inability to detect stress reactions in the pars interarticularis that have not

progressed to complete fracture. Computed tomography (CT) can demonstrate minimal anterior

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slippage and allows for direct identification of the pars defects (Fig 5) although it is not sensitive for detecting early acute stress reactions in the pars interarticularis where there is only marrow edema and microtrabecular fracture12. These findings are easily observed on MRI. Some

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investigators and practicing radiologists believe that after normal radiographs have been

MRI than with CT.

MYELOPATHY

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obtained, MRI should be next; however, identification of pars defects may be more difficult with

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The term myelopathy is used to describe any neurological deficit related to the spinal cord. The

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most common cause of myelopathy in the cervical and thoracic spine is compression of the spinal cord by osteophytes or extruded disc material. The second most common cause of

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myelopathy is spinal cord compression due to extradural masses caused by bone metastases and trauma. Intradural extramedullary tumors and a variety of cysts such as epidermoid and arachnoid cysts and cord herniation may also cause myelopathy. Other less common causes include etiologies intrinsic to the cord such as neoplastic, infectious, inflammatory, vascular and idiopathic disorders.

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Imaging Modalities - ACR Recommendations (Table 3) Imaging plays an important role in the evaluation of a patient with non-traumatic myelopathy. Because of its multiplanar capability and superior soft tissue resolution with the ability to assess the spinal cord contour and signal, MRI is the first line of imaging test. Myelopathy can be

progression (slowly progressive versus a sudden onset).

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divided into three clinical categories, based on the presence of significant trauma, pain, and

The first category is traumatic myelopathy, and will be discussed in a separate manuscript. The second category is painful myelopathy, which is most commonly caused by spinal stenosis

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secondary to spondylosis, degenerative facet disease and ligamentum flavum hypertrophy or may be secondary to congenitally short pedicles. CT is superior in the depiction of bony encroachment on the spinal canal and foraminal narrowing. Bone destruction and paravertebral

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soft issue masses are also better seen. CT myelography may be useful when MRI is contraindicated or not available. The third category is sudden onset or slowly progressive

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painless myelopathy. Differential diagnosis is broad and includes neoplastic disease of the spinal cord, extrinsic compression by epidural or intradural tumors, demyelinating diseases,

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degenerative diseases, nutrient deficiency and vascular processes. Vascular malformations,

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spinal cord infarct, and epidural hematoma account for most of the vascular lesions of the cord. If a spinal vascular malformation is considered, gadolinium-enhanced MRI and MR angiography

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(MRA) may be useful to demonstrate abnormal vasculature and guide spinal arteriography, potentially limiting the number of direct vascular injections13, 14. In particular, localization of the feeding artery and draining vein in dural arteriovenous fistula (DAVF) of the spine is useful as treatment may be achieved using endovascular techniques15.

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EXTRINSIC CAUSES Degenerative disease Cervical Spinal Canal Stenosis Myelopathy in adults is most often secondary to cervical spinal canal stenosis . Canal stenosis

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may be either congenital (secondary to short pedicles) and/or acquired secondary to disc herniation, facet degnerative change, bony spondylitic spurring, and hypertrophy of the

ligamentum flavum. (Fig 6) Ossification of the posterior longitudinal ligament (OPLL) also produces symptoms of cervical spondylotic myelopathy. (Fig 7) The pathophysiology of OPLL

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remains unclear, but there is a known association with diffuse idiopathic skeletal hyperostosis. MRI and CT are often complimentary in the diagnosis and management of cervical spinal canal stenosis16, 17.

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Extradural mass Epidural hematoma

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Spinal epidural hematoma (EDH) can compress the spinal cord or nerve roots and result in neurologic deficits. Spinal EDH occurs most commonly after spinal surgery; however, it is

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asymptomatic in the majority of cases. Risk factors associated with EDH formation include

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advanced patient age, multilevel surgery and coagulopathy. In contrast, spontaneous EDH of the spine is rare and usually occurs in patients over 50. In most cases, there is no clear source of

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hemorrhage or a causative event. The classic clinical presentation of a spinal EDH consists of the sudden onset of back or neck pain. Neurologic symptoms related to nerve root or spinal cord compression may also occur. MR imaging is excellent in the delineation of the extent of spinal hemorrhage and for determining the relationship between hemorrhage and the thecal sac and cord. Signal intensity of the collection is variable on both T1W and T2W images, although low

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signal is frequently seen on GRE images. On T1W images, acute spinal hematoma is typically isointense to cord and does not enhance while subacute hematoma is hyperintense relative to cord (Fig 8). Most hematomas occur in the cervical or the thoracic region. Treatment typically

small hematomas if there is no neurologic deficit6. Bone metastasis with epidural extension

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consists of emergent surgical decompression; however, conservative treatment is advocated with

Because of its high vascularity, bone marrow in the vertebral body is the most common site for spinal metastases. Progressive spinal metastasis may result in epidural spinal cord compression,

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and lead to paresis and paralysis if left untreated. The importance of a high index of suspicion in high-risk patients and a prompt diagnosis of metastatic spinal cord compression is crucial. Contrast enhanced MRI provides better delineation of the extent of epidural invasion. The

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contrast difference between epidural fat and enhancing tumor is further accentuated if fat suppression pulse sequences are used18. The key goal of the treatment for metastatic epidural

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spinal cord compression is prompt decompression of the spinal cord in an attempt to prevent further deterioration of neurologic function or to reverse the neurologic deficits. This can be

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accomplished by surgical decompression and/or radiation.

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Intradural extramedullary tumors The most common intradural extramedullary tumor is Schwannoma followed by meningiomas.

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Schwannomas are usually T1 hypointense and heterogenously T2 hyperintense relative to the spinal cord, with or without intralesional cysts or hemorrhage, and demonstrate peripheral or uniform enhancement (Fig 9). Meningiomas are typically eccentric in location with a broadbased dural attachment. They are usually isointense to gray matter on MRI but may be lower in signal intensity, depending on the extent of calcification. They are well circumscribed, tend to be

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located posterolaterally in the canal, and often show homogeneous enhancement (Fig 10). CT is useful in showing calcification, which helps in the differentiation from schwannomas4, 19. Cystic lesions Arachnoid Cyst

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Spinal arachnoid cysts are an uncommon and under recognized source of myelopathy. They may be asymptomatic or present with pain, ataxic gait, numbness as well as bladder incontinence. Arachnoid cysts are most commonly intradural and located in the dorsal thoracic spine, but can occur anywhere along the neural axis. MRI will demonstrate focal indentation and displacement

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of the cord with occasional thin barely perceptible margins of the cyst (Fig 11). Treatment is surgical with complete resection, marsupialization, shunting or fenestration20. Thoracic Cord Herniation

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Idiopathic spinal cord herniation (ICSH) is often confused with an arachnoid cyst, as both result in ventral displacement of the cord. Prolapse of the spinal cord through a dural defect is the

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hallmark of this entity. Although the exact etiology remains unclear, it has been proposed to be the result of clinically occult minor trauma particularly in the presence of an underlying calcified

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disc herniation. Myelopathy is generally progressive over time. MRI will demonstrate anterior

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kinking of the spinal cord with associated enlargement of the dorsal subarachnoid space (Fig 12). The angulation of the cord is usually more abrupt and acute than seen with arachnoid cysts. High

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T2 cord signal and volume loss within the cord are supportive features21, 22. INTRINSIC CAUSES Primary spinal cord neoplasms The most common intramedullary tumor in adults is ependymoma and the second most common is astrocytoma. Ependymomas typically present with neck or back pain. They are well

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circumscribed, and generally more sharply demarcated than astrocytomas. They have a propensity for intratumoral hemorrhage and may produce subarachnoid hemorrhage with leptomeningeal deposition of hemosiderin (superficial siderosis). Cystic degeneration of the tumor and extensive cyst formation rostral or caudal to the tumor may be observed (Fig 13).

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Astrocytomas are less commonly associated with cystic changes, syrinx, and intralesional

hemorrhage (Fig 14). An eccentric location is suggestive of this diagnosis. Hemangioblastomas are vascular tumors found primarily in the cerebellum and spinal cord. These tumors occur more commonly as sporadic isolated lesions; however, approximately one third of patients with spinal

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hemangioblastomas have Von Hippel-Lindau disease. Spinal hemangioblastoma is usually

intramedullary and typically located in the posterior half of the spinal cord, supplied by posterior spinal arteries. The tumor consists of a hypervascular nodular mass, usually with an associated

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cyst or syrinx and a variable degree of surrounding edema (Fig 15). Metastatic disease to the spinal cord is less common than primary tumors; however, the frequency of intramedullary

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metastases is rising because of the improvements in cancer therapy and the increased survival of patients with cancer after initial diagnosis. Lung and breast cancer are the most common primary

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tumors that metastasize to the spine. Dissemination to the spinal cord is typically hematogenous,

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although local spread of tumor from adjacent paraspinal soft tissues or bone and dissemination of disease through the CSF also can occur.

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Spinal cord infections

Infection primarily involving the spinal cord (infectious myelitis) is relatively rare, but critically important due to high associated morbidity and mortality. The diagnosis of spinal cord infection should be suspected in cases with neurologic symptoms of radiculitis and myelitis, immunosuppression state, skin rash, fever, lymphadenopathy, and recent travel to endemic areas.

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MRI is the modality of choice and typically displays hyperintense signal on T2 imaging with or without enhancement23. Inflammatory conditions Sarcoidosis

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Sarcoidosis is a systemic granulomatous disease of unknown etiology. It commonly affects middle-aged female patients of African American descent. Clinical central nervous system

(CNS) involvement is reported in up to 5% of patients. Cord involvement is much less common and may affect the cord parenchyma and or leptomeninges. Osseous involvement of the vertebral

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bodies has been also described.

The cervical and thoracic spine are more frequently involved than the lumbar spine. MRI findings include abnormal intramedullary T2W signal and cord enlargement. Cord involvement

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may be focal or extensive. Leptomeningeal disease is common and manifests as nodular enhancement. Intramedullary enhancement is variable and may be patchy, circumscribed focal

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central enhancement (purely intramedullary) or may be ill defined, extending from the leptomeninges via perivascular spaces inward. (Fig 16) Clinical signs and symptoms of neuro-

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sarcoidosis are nonspecific and depend on the level of involvement and the extent of disease.

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Treatment is with steroids with almost two thirds of cases demonstrating favorable response. Immunosuppressive therapy is used in refractory cases24, 25, and 26.

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Guillain-Barré syndrome Guillain-Barré syndrome (GBS) is an acute, typically monophasic, rapidly progressive inflammatory demyelinating polyneuropathy (AIDP). It has a distinctive clinical presentation of progressive ascending paralysis with hyporeflexia or areflexia. It is currently the most common cause of flaccid paralysis worldwide. Severe cases of GBS can progress to death from respiratory

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failure (up to 5% of cases). GBS is thought to be triggered by a post infections, immune mediated disease with nearly two thirds of cases preceded by a mild respiratory or gastrointestinal tract infection. Diagnosis is made based on the clinical presentation and CSF studies showing increased protein with pleocytosis. Imaging plays an important role in the

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diagnosis. Typically GBS demonstrates smooth pial enhancement of the cauda equina and conus medullaris with predilection to the ventral nerve roots, which explaines why most of the

symptoms are motor (Fig 17). The nerve roots may be slightly enlarged however no nodularity should be seen. Plasma exchange or intravenous immunoglobulins are the mainstay medical

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management options. Steroids alone are not very effective in GBS 27, 28. Demyelinating disease Multiple sclerosis

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Multiple Sclerosis (MS) is a progressive, idiopathic, inflammatory demyelinating autoimmune disorder of the central nervous system. It is the most common neurological disorder in young

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Caucasian adults, predominately females, and usually begins in the 2nd to 3rd decade of life. Diagnosis is made based on the McDonald criteria, revised in 2016. Although brain lesions are

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seen in vast majority of patients, up to 20% of patients can have isolated spinal disease. Most

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patients have spinal cord lesion at some point during the course of the diseases and the majority of patients have more than one cord lesion. Cord lesions are most commonly found cervical

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spine. Typical MS cord lesions are focal, extending less than two spinal segments and are hyperintense on T2W images (Fig 18). There is predominant involvement of the dorsal and lateral columns. Grey matter involvement is less common. Acute lesions can enhance. As the disease progresses, lesions may become confluent. Cord atrophy may be seen in the chronic

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stage. Treatment consists of Steroid therapy as well as immunosuppressive and immunomodulatory therapy29, 30, 31. Neuromyelitis Optica (NMO) NMO is an inflammatory and demyelinating condition, distinct from MS, characterized by

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recurrent episodes of longitudinally extensive transverse myelitis and optic neuritis. NMO

diagnosis and nomenclature has changed over time. The most recent nomenclature (2015

international consensus) defines the unifying term NMO spectrum disorders (NMOSD), which is further classified by serologic testing (NMOSD with or without AQP4-IgG). AQP4-IgG also

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known as NMO-IgG is a disease specific antibody found in the serum of affected patients32. Like multiple sclerosis, the disease is four times more common in females with a mean age of 30-40 years. On imaging, the disease has distinct features: longitudinally extensive transverse myelitis,

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optic neuritis and presence of characteristic brain lesions generally located at sites of high AQP4 expression

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including hemispheric cerebral white matter, corticospinal tracts, periependymal region surrounding the third ventricle, anterior border of the midbrain, adjacent to the forth ventricle

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and dorsal brainstem. Most patients present with a T2 hyperintense cord lesion that involves 2 or

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3 vertebral body levels. There is more involvement of the central grey matter when compared to MS and many cases involve the entire cross sectional area of the cord (Fig 19). Cord swelling

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and enhancement are seen in the acute phase and enhancement is usually solid30. Early diagnosis is extremely important to avoid relapse, which could have devastating effects. Treatment options include high dose steroids and immunosuppressive therapy. Acute disseminated encephalomyelitis (ADEM)

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ADEM is a post infections immune mediated demyelinating disease that classically follows a viral illness or vaccination. Unlike Multiple sclerosis and NMO, ADEM is typically monophasic (illness typically lasts 2 to 4 weeks), is more common in children and young adults. Brain involvement is seen in almost all patients while spine involvement is much less common. The

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clinical presentation is extremely variable and ranges from confusion, irritability and back pain to lethargy, coma and tetraparesis. Around 50-60% of patients recover completely, 30-40%

develop neurological deficit and mortality rate is 10%. On imaging, ADEM has similar features to MS and may not be distinguishable on a single study. Common spinal features include focal

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hyperintense T2W flame-shaped lesions with slight cord swelling in the dorsal white matter with variable enhancement, depending on the stage of disease; however, most lesions do not enhance (Fig 20). Intravenous steroids are the treatment of choice. Immunoglobulin therapy is sometimes

Toxic and metabolic myelopathies

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considered, while plasmapheresis is reserved for fulminant cases30.

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Toxic and metabolic myelopathies are relatively rare clinical conditions with similar clinical, neuropathologic, and imaging features. Metabolic myelopathies can be caused by nutrient

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deficiencies such as vitamin B12, folate, copper or vitamin E deficiencies. Toxic myelopathies are

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associated with drugs and chemical agents such as heroin abuse, organophosphate poisoning and chemotherapeutic agents.

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Vitamin B12 deficiency

The most common metabolic myelopathy is due to vitamin B12 deficiency. Subacute combined degeneration (SCD) is the manifestation of vitamin B12 deficiency in the spinal cord. Vitamin B12 deficiency is due to inadequate intake and malabsorption. The most common cause of vitamin B12 deficiency in the United State is pernicious anemia. Other causes include vegetarian

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diet and weight-loss surgery. Histopathologic studies demonstrate degeneration of the posterior and lateral columns. On sagittal T2W imaging, increased signal intensity in the posterior columns is noted in variable lengths. Axial images demonstrate an “inverted V” reflective of greater involvement of the lateral portions of the dorsal columns rather than the medial portions

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(Fig 21). This finding correlates with the clinical finding of relative sparing of proprioceptive sensation in the lower extremities. Restricted diffusion in the posterior columns has also been described33. Vascular process

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Vascular malformation

Spinal vascular malformations can cause neurologic symptoms by three mechanisms: hemorrhage, venous hypertension leading to reduced perfusion and ischemia and direct mass

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effect, resulting in a progressive myelopathy or radiculopathy.

The most commonly encountered spinal vascular malformation is spinal dural arteriovenous

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fistula (DAVF); however, it is still an under diagnosed entity. It is presumed to be an acquired disease though the exact etiology is unknown. Spinal DAVFs usually present in adults after the

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fifth decade and have a significant male predominance. Patients often present with vague

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complaints of back pain or radicular pain, followed by progressive lower-extremity paresis, and bowel and bladder sphincter dysfunction. Hemorrhage is extremely rare. Although most patients

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present with progressive myelopathy, acute worsening of motor or sphincter function can also occur. Because of the potential for neurologic deterioration over time, prompt treatment of the spinal DAVF is advocated. Spinal DAVF may occur anywhere from the level of the foramen magnum to the sacrum. The AV shunt is located inside the dural matter close to the spinal nerve root where the arterial blood

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flow from the radiculomedullary artery directly connects with the vein at the dorsal surface of the dural root sleeve in the neural foramen. The increased pressure in the vein leads to decreased drainage and venous congestion with intramedullary edema and progressive myelopathy. The most common finding on MR imaging in patients with DAVF is abnormal T2 signal

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hyperintensity within the cord. The presence of “flow voids” and serpentine enhancement that extend over at least three contiguous vertebral segments in the intradural space as well as

increased number, size and tortuosity of these vessels was found to be strongly associated with the presence of dural AVF. Identification of the AV shunt location may be difficult and

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challenging, especially in cases in which cord edema is extensive. Thus, the noninvasive

evaluation of the shunt location is extremely helpful to guide the invasive spinal angiography. Contrast-enhanced spinal MRA (Fig 22) has greatly contributed in diagnosing and demonstrating

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the level of the fistula and helps avoid unnecessary super selective injections of all possible arterial feeders. Two methods may be used, standard 3D time-of-flight (TOF) technique and

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dynamic bolus injected contrast enhanced MRA. While the 3D TOF technique offer good spatial resolution, only normal (large) veins are depicted while the dynamic CE technique allows the

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differentiation of normal spinal cord arteries and veins. MRA shows increased tortuosity, length

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and size of the intradural vessels. The fistula level is diagnosed by following the dominant and often tortuous draining medullary vein to the foraminal level. Selective spinal angiography is

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necessary to confirm the diagnosis and fistula level. One of the most important angiographic details to assess is the origin of the anterior spinal artery. If the anterior spinal artery shares a common origin with the supply to the DAVF, then the DAVF is not amendable to endovascular treatment. The second most common spinal vascular malformation is glomus type arteriovenous

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malformation (AVM). They tend to present in younger age compared with DAVF and usually present in young adults. They have a compact nidus that is intramedullary in location and are supplied by branches of the anterior and/or posterior spinal arteries. The intramedullary nidus drains into the coronal venous plexus on the cord surface, which in turn drains through a

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medullary vein or veins to the extradural space in an antegrade manner. In 20- 40% of cases, there is an associated arterial or venous aneurysm. Unlike the DAVF, they most commonly

presents with hemorrhage and sudden onset of neurologic symptoms. MR imaging is currently the imaging modality of choice for the initial evaluation of spinal AVMs. They are high flow

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vascular malformations capable of producing flow voids on precontrast spin-echo images.

Drainage into the coronal venous plexus on the cord surface, with engorgement of the posterior and/or anterior median vein, results in a variable appearance of perimedullary flow voids and

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cord scalloping on precontrast images, as well as serpentine enhancement on postcontrast images and MRA (Fig 23). DSA remains the definitive test for the diagnosis and treatment planning of

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spinal AVMs. Prompt recognition and treatment is warranted for preservation of neurologic function and minimization of rebleeding6.

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Cavernous venous malformation

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Spinal cavernous malformations are rare and most often found in women in the third to fifth decade of life. Spinal cord lesions have an increased frequency of bleeding compared to

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intracranial lesions. Patients may present with acute neurological compromise due to intramedullary hemorrhage or with chronic progressive myelopathy resulting from micro hemorrhages and gliosis6. Intramedullary cavernous malformation may have an exophytic component and bulge from the surface of the cord. MRI typically shows a mixed signal central core surrounded by a hypointense rim of hemosiderin giving the typical popcorn-like appearance.

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The hypointense areas show blooming on images that are heavily susceptibility-weighted (Fig 24). Cord infarct Spinal cord infarction is rare and typically affects older adults. Most patients experience pain

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before the onset of neurologic symptoms. Symptoms usually develop quickly, although some patients may experience a transient ischemic attack before the actual spinal cord infarct.

Pathophysiological mechanisms for spinal cord infarction include hypoperfusion from arterial insufficiency or hypotension, and occlusion of a supplying arterial branch. Rare spinal cord

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infarction can occur when fibrocartilagenous material enters into radicular arteries. Spinal cord infarcts occur at about equal frequency in the cervical and thoracolumbar spine, but they are extremely rare in the upper thoracic spine. The most common pattern involves the anterior spinal

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artery (unilateral or bilateral). MR imaging is the imaging modality of choice for evaluation of patients with suspected spinal cord infarct and demonstrates in the acute phase cord enlargement

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and hyperintense signal on T2-weighted images with or without contrast enhancement. Diffusion weighted imaging is particularly sensitive to the ischemic change showing marked hyperintensity

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on the DWI sequence and a reduction in the apparent diffusion coefficient.

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Abnormal signal and enhancement may demonstrate a double-dot ("owl's eyes" or “snake eyes”) pattern in the region of the anterior horns, an H-shaped pattern involving the central gray matter,

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or a more diffuse pattern involving both gray and white matter. Enhancement of the ventral part of the cauda equina, which is composed of motor fiber bundles, in association with conus enhancement have also been reported. (Fig 25) When infarction results from compromise of a segmental artery, branches supplying the ipsilateral half of the vertebral body may also be affected6, 22.

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Transverse myelitis Transverse myelitis (TM) is a clinical syndrome, which refers to band-like symptoms across a dermatomal level. Typically these symptoms include pain, abnormal sensations, extremity weakness, or autonomic dysfunction. TM is a diagnosis of exclusion and is subdivided into

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idiopathic versus disease-associated forms. Differentiation between these two forms is critical, particularly in the disease-associated form where if a specific diagnosis is obtained, such as MS or NMO, treatment options and prognosis will vary. Idiopathic TM is usually monophasic and can be diagnosed when alternative etiologies have been excluded including cord compression

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and ischemia. Importantly, evaluation with laboratory markers such as cerebrospinal fluid studies and/or autoimmune markers helps to guide therapy. MRI is the most important modality for evaluating TM. In the idiopathic form, there is usually a well-circumscribed central T2

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hyperintense/T1 hypointense lesion involving more than two thirds of the cross section of the cord with eccentric enhancement (Fig 26). There should be involvement of at least two vertebral

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body lengths, but more typically involves approximately 3-4. The most common location of the idiopathic form is within the thoracic spine. An additional radiographic distinction is

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longitudinally extensive transverse myelitis (LETM) where there is signal abnormality over three

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or more vertebral body lengths. This form typically is associated with NMO. An MRI of the brain is useful in further characterizing the disease process in the nonidioathpic form of TM.

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Follow up imaging is crucial to assess for treatment response or progression of disease29, 34. Summery

Imaging plays a critical role in the evaluation of disease of the spine and spinal cord in the urgent and emergent setting. CT is usually the preferred first test in suspected spinal trauma while MRI is usually the preferred first test in nontraumatic myelopathy. Although MR imaging is sensitive

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and specific in the detection and diagnosis of conditions such as malignancy, infection, spinal cord lesions and discogenic disease, familiarity with common features is important for prompt and accurate diagnosis. MRA and conventional spinal angiography are crucial in the evaluation of selected patients with suspected treatable causes of vascular myelopathy. MRI remains the

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first-line imaging test for the evaluation of acute back pain and myelopathy. The appropriate use of MR imaging in the emergent setting enables a higher standard of care and permits detection of spine conditions that require immediate medical or surgical intervention.

Potential Underlying Condition as Cause of Lower Back Pain

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Cancer or infection

Spinal fracture

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    

History of cancer unexplained weight loss Immunosuppression Urinary infection IV drug use Prolonged steroid use Back pain not improved with conservative management History of significant trauma Minor fall or heavy lift in a potentially osteoporotic or elderly individual or prolonged use of steroids Acute onset of urinary retention or overflow incontinence Loss of anal sphincter tone or fecal incontinence Saddle anesthesia Global or progressive motor weakness in the lower limbs

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Red Flag 

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Table 1. Red Flags in patients with back pain / radiculopathy

Cauda equina syndrome or severe neurologic compromise

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Table 2. ACR Appropriateness Criteria – Low back pain Radiology diagnostic procedure Not appropriate

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CT Lumbar spine without contrast is preferred

MRI Lumbar spine without and with IV contrast* MRI Lumbar spine without and with IV contrast*

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Clinical condition Low back pain / Radiculopathy Acute/Subacute Uncomplicated /chronic No red flags No prior management Low velocity trauma Osteoporosis Elderly individual Chronic steroid use Suspicion of cancer Infection Immunosuppression Prior surgery/intervention Persistent\progressive symptoms during or following 6 weeks of conservative therapy New or progressive symptoms / clinical findings and history of prior lumbar surgery Cauda equina syndrome/ Rapidly progressive neurologic deficit

MRI Lumbar spine without and with IV contrast** MRI Lumbar spine without contrast***

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* CT is useful if MRI is contraindicated ** CT with IV contrast is useful in postfusion patients or when MRI is contraindicated *** Use of contrast depends on clinical circumstances

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Table 3. ACR Appropriateness Criteria – Myelopathy Clinical condition Myelopathy Traumatic Painful

Radiology diagnostic procedure

Suspicion of cancer Infection Immunosuppression Extrinsic

Epidural hematoma/ Abscess

Metastasis Intradural extramedullary mass 



Meningioma Schwannoma

MRI without and with IV contrast

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Sudden onset or slowly progressive

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Spondylosis/Spinal stenosis

CT without contrast MRI without contrast CT without contrast MRI without and with IV contrast

Cystic lesions 

Intrinsic

Arachnoid cyst

MRI without contrast

Cord herniation Cord tumors  

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

Ependymoma Astrocytoma Hemangioblastoma

Demyelinating disease  

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

Multiple sclerosis ADEM NMO

MRI without and with IV contrast

Infections Inflammatory

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



Sarcoid Guillain-Barré

Nutrient deficiency 

Vitamin B12 Deficiency

Vascular process    

DAVF AVM Cavernous malformations Cord infarct

Transverse myelitis

* CT with IV contrast is useful when MRI is contraindicated

MRA of the spine with IV contrast MRI without and with IV contrast

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References 1.

ACR Appropriateness Criteria®: Low Back Pain. Available at: https://acsearch.acr.org/docs/69483/Narrative/ Accessed September 30, 2015 McNamee J, Flynn P, O’Leary S, et al: Imaging in Cauda Equina Syndrome - A Pictorial Review, Ulster Med J 82:100-108, 2013

3.

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Gardner A, Gardner E, and Tim Morley: Cauda equina syndrome: a review of the current clinical and medico-legal position: Eur Spine J 20:690-697, 2011

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emergencies. Magn Reson Imaging Clin N Am 24:325-344, 2016 5.

Chamberlain MC, Nolan C, Abrey LE: Leukemic and lymphomatous meningitis:

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incidence, prognosis and treatment. J Neurooncol 75:71-83, 2005 Wang VY, Chou D, Chin C: Spine and spinal cord emergencies: vascular and infectious

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causes. Neuroimaging Clin N Am 20:639-50, 2010 Sung JK, Jee WH, Jung JY, et al: Differentiation of acute osteoporotic and malignant

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compression fractures of the spine: use of additive qualitative and quantitative axial

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diffusion-weighted MR imaging to conventional MR imaging at 3.0 T. Radiology 271:488498, 2014

Jung HS, Jee WH, McCauley TR, et al: Discrimination of metastatic from acute

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osteoporotic compression spinal fractures with MR imaging. RadioGraphics 23:179-187, 2003

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Baker LL, Goodman SB, Perkash I, et al: Benign versus pathologic compression fractures of vertebral bodies: Assessment with conventional spin-echo, chemical-shift, and STIR MR imaging. Radiology 174:495–502,1990

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Walsh LJ, Lewis SA, Wong CA, et al: The impact of oral corticosteroid use on bone

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mineral density and vertebral fracture. Am J Respir Crit Care Med 166:691-695, 2002 Logroscino G, Mazza O, Aulisa G, et al : Spondylolysis and spondylolisthesis in the pediatric and adolescent population. Childs Nerv Syst 17:644-655, 2001 12.

Sairyo K, Katoh S, Takata Y, et al: MRI signal changes of the pedicle as an indicator for

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early diagnosis of spondylolysis in children and adolescents: a clinical and biomechanical study. Spine 31:206-211, 2006 13.

Saraf-Lavi E, Bowen BC, Quencer RM, et al: Detection of spinal dural arteriovenous

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fistula with MRI and contrast-enhanced MR angiography: Sensitivity, specificity, and prediction of vertebral level. AJNR Am J Neuroradiol 23: 858-867, 2002 Luetmer PH, Lane JI, Gilbertson JR, et al: Preangiographic evaluation of spinal dural

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arteriovenous fistulas with elliptic centric contrast-enhanced MR angiography and effect

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on radiation dose and volume of iodinated contrast material. AJNR Am J Neuroradiol

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26:711–718, 2005

Roth CJ, Angevine PD, Aulino JD, et al: ACR Appropriateness Criteria Myelopathy. J Am

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Coll Radiol 13:38-44, 2016 16.

Arce D, Sass P, Hassan A: Recognizing spinal cord emergencies. American Family Physician 64:631-638, 2001

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Choi B, Kyung-Jin S, Chang H: Ossification of the Posterior Longitudinal Ligament: A review of literature. Asian Spine Journal 4:267-276, 2011

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18.

Lo SS, Ryu S, Chang EL, et al: ACR Appropriateness Criteria® Metastatic Epidural Spinal Cord Compression and Recurrent Spinal Metastasis. J Palliat Med 18:573-584, 2015

19.

Saraf Lavi E (ed), Spine imaging: Case review series 3rd Edition, Elsevier, Saunders 2013

20.

Petridis A, Doukas A, Barth H, et al: Spinal cord compression caused by idiopathic

European Spine Journal. 19: 124-129, 2010 21.

Parmar H, Park P, Brahma B, et al: Imaging of idiopathic spinal cord herniation. Radiographics 28: 511-518, 2008

Haber M, Ngyuen D, Li S. Differentiation of idiopathic spinal cord herniation from CSF-

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intradural arachnoid cysts of the spine: review of the literature and illustrated case.

isointense intraspinal extramedullar lesions displacing the cord. Radiographics 34: 313:329, 2014

Talbott JF, Narvid J, Chazen JL, et al: An Imaging-Based Approach to Spinal Cord

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23.

Infection. Semin Ultrasound CT MR 37:411-430, 2016 Koyama T, Ueda H, Togashi K, et al: Radiologic Manifestations of Sarcoidosis in Various

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Organs. Radiographics 24:87–104, 2004 Campbell SE, Reed CM, Bui-Mansfield et al: Vertebral and Spinal Cord Sarcoidosis.

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AJR184:1686-1687, 2005

Christoforidis GA, Spickler EM: MR of CNS Sarcoidosis: Correlation of Imaging Features

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to Clinical Symptoms and Response to Treatment. AJNR 20:655-669, 1999 27.

Alkan O, Yildirim T, Tokmak N, et al: Spinal MRI Findings of Guillain-Barré Syndrome. J Radiol Case Rep 3:25-28, 2009

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Yuki N, Hartung HP: Guillain–Barré Syndrome. N Engl J Med 366:2294-2304, 2012

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29.

Rovira A, Auger C: Spinal Cord in Multiple Sclerosis: Magnetic Resonance Imaging Features and Differential Diagnosis. Semen Ultrasound CT MR 37:396-410, 2016

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Young V, Quaghebeur G: Transverse Myelitis and Neuromyelitis Optica Spectrum Disorders. Semin Ultrasound CT MR 37:384-395, 2016 Filippi M, Rocca MA, Ciccarelli O, et al: MRI criteria for the diagnosis of multiple

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sclerosis: MAGNIMS consensus guidelines. Lancet Neurol 5:292-303, 2016 32.

Wingerchuk DM, Banwell B, Bennett JL, et al: International consensus diagnostic criteria for neuromyelitis optica spectrum disorders Neurology. 85:177-189, 2015

Ramalho J, Hoffmann Nunes R, da Rocha AJ, et al: Toxic and metabolic myelopathies.

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Semin Ultrasound CT MR 37:448–65, 2016 34.

Trebst, C, Raab P, Voss EV, et al: Longitudinal extensive transverse myelitis - it's not all

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neuromyelitis optica. Nat Rev Neurol 7: 688-698, 2011

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Figures

FIGURE 1: Cauda equina syndrome. 80-year-old man with bilateral lower extremity weakness

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and urinary incontinence. (A) Sagittal STIR and (B) axial T2-weighted images show severe compression of the cauda equina nerve roots at L4-5 level (arrow) secondary to a combination a

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disk bulge, facet and ligamentum flavum hypertrophy.

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FIGURE 2: Pathological fracture. 52-year-old female with history of stage IV rectal adenocarcinoma presented with back pain. (A) Sagittal T1-weighted image (B) STIR and (C) post-contrast fat-saturated T1-weighted images show an acute compression fracture of the L4 vertebral body with posterior epidural extension (arrow) and compression of the thecal sac and cauda equina roots.

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FIGURE 3: Lymphoma. 52-year-old female with diagnosis of primary CNS lymphoma with new onset of back and lower extremity pain (A), Sagittal T2-weighted images show relatively decreased T2 signal intensity than is expected for the subarachnoid space, beginning below the

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level of the conus (Black arrow heads). (B) Sagittal postcontrast T1-weighted image show

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corresponding abnormal extensive leptomeningeal enhancement replacing the normal CSF in the

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subarachnoid space (White arrowheads).

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FIGURE 4: Chronic steroid use induced fractures in a 61-year-old female patient with history of

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systemic lupus erythematosus on chronic steroid use. Sagittal T1-weighted image show multiple chronic compression fractures with multiple bands of hyperintense signal along endplates representative of chronic focal fatty marrow accumulation (arrows).

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FIGURE 5: Spondylolysis. (A) Right parasagittal reformatted CT image of the lumbar spine shows spondylolysis at L2 (arrow), with no significant spondylolisthesis. (B) Axial CT image at

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the L2 level shows the pars defects (arrows) involving each vertebral isthmus, or pars interarticularis. Note that the pars defects have a nearly horizontal orientation. This appearance

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differs from the oblique orientation of the facet joints on axial images.

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FIGURE 6: Spinal stenosis. 47-year-old man with neck and arm pain (A) Sagittal T2- weighted images in a patient with neck pain and radiculopathy demonstrates congenital canal stenosis aggravated by multilevel cervical spondylosis. (B) Axial T2-weighed imaged demonstrates a

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superimposed left paracentral disc herniation (Arrow) at the C4-C5 level with severe cord

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compression.

FIGURE 7: Ossification of the Posterior Longitudinal Ligament with Central Canal Stenosis. 45year-old male with 6 month history of neck pain and numbness in the bilateral upper extremities. (A) Sagittal and axial CT of the cervical spine demonstrates ossification of the posterior

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longitudinal ligament (long arrow) with a classic “mushroom” type appearance (4 point star) on

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the axial images (B). Associated idiopathic skeletal hyperostosis is also noted (arrow heads).

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FIGURE 8: Spontaneous epidural hematoma. 45 year old with history of SLE who developed extremity weakness following treatment with anticoagulant. (A) Sagittal T1-weighted image

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image demonstrates an isointense posterior epidural collection compressing and anteriorly displacing the spinal cord Arrows). (B) Axial gradient-echo T2*-weighted image shows low

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signal in the left posterior epidural collection consistent with acute blood (arrow head).

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FIGURE 9: Meningioma. (A) Sagittal T2-weighted image shows an isointense mass (white

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arrow) in the posterior aspect of the upper thoracic canal compressing and anteriorly displacing the spinal cord. There is widening of the subarachnoid space indicating an intradural extramedullary location. (B) Sagittal postcontrast T1-weighted image shows the mass is homogenously enhancing with a dural tail (solid black arrows). (C) Axial CT image without

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contrast, soft tissue window, shows the mass is calcified (dotted arrow).

FIGURE 10: Schwannoma (A) Sagittal T2-weighted images show a heterogeneous mass (white arrow) widening the neural foramen. (B) Axial T2-weighted image show the mass (white arrow)

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is slightly hyperintense relative to muscle. (C) Axial postcontrast T1-weighted image shows a well-demarcated enhancing extradural mass (black arrow) in the left aspect of the canal causing

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compression and lateral displacement of the spinal cord (arrowhead).

FIGURE 11: Arachnoid cyst. 59-year-old female presented with back pain and incontinence. (A

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and B) Sagittal and axial T2-weighted images demonstrate ventral displacement of the mid thoracic cord (white arrow) with focal indentation secondary to a CSF equivalent lesion,

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compatible with an arachnoid cyst (Dotted arrow).

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FIGURE 12: Cord herniation. 55-year-old female with progressive paraparesis and rapidly progressive myelopathy. (A) Sagittal T2-weighted weighted image demonstrate abrupt angulation of the mid thoracic cord (white arrow) with a widened dorsal subarachnoid space (Black arrow). (B) Axial T2-weighted images demonstrate herniation of the cord through the

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dura with associated cord volume loss.

FIGURE 13: Ependymoma (A) Sagittal T2-weighted image show an intramedullary lesion

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expanding the cord. The lesion is hyperintense relative to the normal cord (solid arrow) with central areas of cystic changes (dotted arrows). (B) Sagittal postcontrast fat-saturated T1-

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weighted image show focal solid enhancement (star)

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Fig 14: Astrocytoma. (A) Sagittal T2-weighted image shows an ill-defined intramedullary

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hyperintense mass (arrow) associated with cord enlargement. (B) Sagittal postcontrast fat-

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saturated T1-weighted image show no appreciable enhancement.

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FIGURE 15: Hemangioblastoma. (A) Sagittal T2-weighted image show two intramedullary multiseptated cystic masses (Solid arrows) causing expansion of the thoracic cord (arrows). (B) Sagittal postcontrast fat-saturated T1-weighted images show a strongly enhancing tumor nodule (dotted arrows) and serpentine enhancement superior and dorsally to the nodule representing the feeder artery (arrowheads).

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FIGURE 16: Sarcoidosis. (A) Sagittal STIR image demonstrates long segment patchy

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abnormally increased T2W signal (arrows). (B) Sagittal post contrast fat-saturated T1-weighted

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image shows diffuse leptomeningeal disease with multiple enhancing nodular lesions along the cord surface (dotted arrows). (C) Axial postcontrast T1-weighted image shows peripheral/

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leptomeningeal enhancement extending to involve the cord parenchyma (arrowhead).

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FIGURE 17: Guillain-Barré syndrome: (A) Sagittal T2-weighted image shows no significant thickening of the nerve roots and normal appearance of the conus tip.

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(B) Axial postcontrast T1-weighted axial images at the L2 level demonstrate abnormal

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enhancement of the ventral nerve roots (arrows), with relative sparing of the dorsal roots.

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FIGURE 18: Multiple sclerosis. 20-year-old female with MS exacerbation (A) Sagittal T2-weighted image shows a focal lesion in the dorsal aspect of the cord (arrow) with associated edema and mild cord expansion. (B) Axial GRE sequence confirms the involvement of the dorsal column (arrow). (C) Sagittal postcontrast fat-saturated T1-weighted image shows

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enhancement of the lesion (arrow)

FIGURE 19: NMO. (A) Sagittal T2-weighted images show a longitudinally extensive transverse

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myelitis. Cord signal abnormality and cord expansion from C1 through C7 (Solid white arrow) (B) Axial T2-weighted image shows that more than 50% of the cord area is involved on axial

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images (solid white arrow). (C) Sagittal postcontrast fat-saturated T1-weighted image show a

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long segment patchy area of enhancement (arrow)

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FIGURE 20: ADEM. (A) Sagittal T2-weighted image show long segment of high cord signal with mild cord expansion (arrows). (B) Sagittal postcontrast fat-saturated T1-weighted image

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shows no appreciable enhancement. (C) Axial T2-weighted image shows abnormal cord signal

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involving the dorsal columns (arrow) and grey matter (arrowhead).

FIGURE 21: Vitamin B12 deficiency. 31-year-old female with no significant past medical history presenting with worsening bilateral upper and lower extremity weakness (A) Axial and

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(B) sagittal T2-weighted images demonstrate high T2 signal intensity of the dorsolateral columns

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within the cervical cord (arrows) with an “inverted V shape” configuration on the axial plane.

FIGURE 22: Dural arteriovenous fistula. (A and C) Sagittal T2-weighted image shows

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hyperintense cord signal (solid arrow) and multiple abnormal intradural “flow voids” (dotted arrows). (B) Sagittal post contrast T1-weighted image shows enhancement of the cord (black

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arrow) with serpentine enhancing structures on the cord surface. (D) MRA Coronal maximum

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intensity projection targeted to the posterior half of the spinal canal shows an enlarged tortuous vessel extending toward the left L2 foramen (solid arrow) corresponding to the posterior medullary vein. Also noted are prominent dilated draining veins of the coronal venous plexus on the cord surface (dotted arrow). (E) Posteroanterior view of spinal angiogram after injection of the dorsal ramus of the left L2 intercostal artery shows the fistula (arrow) and an enlarged and tortuous intradural vein with ascending drainage (dotted arrow).

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FIGURE 23: Glomus type AVM. 22-year-old man with lower extremity weakness. (A and B) Sagittal T1-weighted and T2-weighted image show flow voids (Solid arrows) within the spinal

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canal and cord expansion. (C) Axial T1-weighted image show intramedullary flow voids

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consistent with a nidus (dotted arrow).

FIGURE 24: Acute hemorrhage associated with Cavernous venous malformation. (A) Sagittal T2-weighted image of cervical spine shows poorly defined intramedullary lesion at C2 level

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(Solid white arrow) associated with cord edema (dotted white arrow). (B) Sagittal T1-weighted image show slightly hyperintense signal consistent with early subacute blood products (black arrow) (C) Axial GRE image show low signal intensity lesion in the left aspect of the cord

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(double white arrows).

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FIGURE 25: Cord infarct. 67-year-old man with vascular risk factors who developed sudden onset of low back pain followed by immediate weakness and sensory disturbance in the bilateral

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lower extremities. (A) Sagittal T2-weighted image shows hyperintense signal in the conus (solid arrow). (B) Sagittal DWI image shows hyperintense area in the inferior part of the spinal cord

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(dotted arrow). (C) Axial postcontrast T1-weighted image at the L1-2 level show enhancement of

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the distal conus and the ventral roots of the cauda equine (double arrows).

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FIGURE 26: Transverse myelitis. 70-year-old woman who with acute onset ataxia and

left-sided weakness. (A) Sagittal STIR image show a long segment of signal abnormality

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extending from the cervicomedullary junction inferiorly to the level of approximately C4

(arrow). (B) Axial FSE T2W image show signal abnormality (arrow) involving over two thirds

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of the cross sectional area of the cord, a finding characteristic of transverse myelitis.