Imaging of the Spine in Multiple Sclerosis 

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Imaging of the Spine in Multiple Sclerosis 

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Magnetic resonance imaging (MRI) was first used to visualize multiple sclerosis (MS) in the upper cervical spine in the late 1980s. [1] Spinal MS is often associated with concomitant brain lesions; however, as many as 20% of patients with spinal lesions do not have intracranial plaques. Contrary to the white and gray matter in the brain, white and gray matter can both be affected in the spine. No strong correlation has been established between the extent of the plaques and the degree of clinical disability. [2, 3, 4, 5, 6]  Spinal cord atrophy is most relevant to progressive forms of MS (primary progressive and secondary progressive), in which it closely links to physical disability. [4, 5]

MRI is currently considered to be the most sensitive diagnostic imaging modality for revealing demyelinating plaques, as recommended by the Consortium of Multiple Sclerosis Centers. [7] No specific field strength is recommended. Gadolinium is typically favored. MRI shows abnormalities in 95% of patients with clinically definitive MS. [8, 9]

On long TR sequences, MRI scans show areas of demyelination as high-signal areas. Lesions of other etiologies (eg, viral myelitis, acute disseminated encephalomyelitis [ADEM]) may resemble MS plaques and must be considered along with the clinical history and the patient’s presenting signs and symptoms. (For patient education information, see Multiple Sclerosis.)

According to an international group of neurologists and radiologists, the spinal cord MR imaging protocol for MS should include sagittal T1-weighted and proton attenuation, STIR or phase-sensitive inversion recovery, axial T2- or T2-weighted imaging through suspicious lesions, and, in some cases, postcontrast gadolinium-enhanced T1-weighted imaging. [10]

(See the image below).

Careful review of the patient’s medical history and an evaluation of the brain with MRI can prove helpful in the diagnosis, especially in young females. MS is considered to be the most common demyelinating process involving the central nervous system (CNS). [11, 12]

Imaging plays an important role in MS, as noted in the McDonald Criteria (see Table 1). It is important to note that the McDonald Criteria were largely collected from adult white European and North American populations. MRI is used to demonstrate lesion dissemination in time (DIT) and space (DIS). [13, 14, 15, 16]

 

Table 1. McDonald Criteria, Revised 2017 (Open Table in a new window)

≥1 (as well as clear-cut historical evidence of 

a previous attack involving a lesion in a distinct anatomic location)

 

If the 2017 McDonald Criteria are fulfilled and there is no better explanation for the clinical presentation, the diagnosis is multiple sclerosis. If multiple sclerosis is suspected by virtue of a clinically isolated syndrome but the 2017 McDonald Criteria are not completely met, the diagnosis is possible multiple sclerosis. If another diagnosis arises during the evaluation that better explains the clinical presentation, the diagnosis is not multiple sclerosis. 

Other key changes to the McDonald Criteria include the following:

 

Radiologically isolated syndrome (RIS) describes cases in which McDonald imaging criteria meet DIT and DIS but lack corresponding clinical symptoms. The exact significance is still a subject of debate. Some authors suggested that this could represent a stage preceding clinical isolated syndrome (CIS). In an extensive review of the RIS literature, Granberg et al [17] emphasized that approximately two thirds of cases show radiologic progression and one third develop clinical symptoms at 5-year follow-up. They also point out that clinical conversion is more likely when cervical cord lesions are present. However, further studies are needed to determine patient stratification and define the role of disease-modifying drugs in RIS.

Because computed tomography (CT) scanning has poor sensitivity, the detection, evaluation, and characterization of MS lesions and enhancement patterns are limited with this modality. As a result, with the advancement of MRI, evaluation of the spinal cord using axial CT scanning was abandoned.

On CT scans, large, masslike lesions can occasionally mimic a neoplasm, and characterizing them can be difficult. Primary and secondary neoplasms of the spinal cord (astrocytomas, ependymomas), infection, transverse myelitis, acute infarction, sarcoidosis, and systemic lupus erythematosus may mimic demyelinating MS plaques on CT scans.

MRI far exceeds CT scanning in the ability to demonstrate intramedullary pathology; MRI is currently used for the first-line investigation of spinal MS. [18] Depending on their age, MS plaques appear on unenhanced, T1-weighted images as areas of slightly low to low signal intensity. Spinal plaques may appear as nodules, rings, or arcs and generally are less than 2 vertebral bodies in length. [19] Plaques usually demonstrate prompt enhancement after the administration of a gadolinium-based contrast agent, which most often indicates active disease. [20] The enhancement may last 2-8 weeks. Classic chronic lesions do not demonstrate contrast enhancement. (See the image below.)

Most MS plaques appear hyperintense on T2-weighted images. The spinal cord may or may not be focally enlarged. Enlargement of the cord is usually seen with active disease. Larger active lesions may have extensive edema with associated cord expansion. Chronic lesions often demonstrate focal cord atrophy. Spinal lesions usually coexist with more severe concomitant brain plaques. As many as 20% of spinal MS lesions are isolated. Spinal cord narrowing due to atrophic changes is present in 10% of patients with spinal cord involvement. [21] (See the images below.)

Tumefacient MS may mimic a neoplasm; a demyelinating process should always be considered if a masslike lesion is encountered. As is the case in the brain, a ring or arc of enhancement can often be found, as opposed to a more nodular or masslike enhancement. Follow-up studies are helpful.

Although not widely implemented, newer methods may be more specific in evaluating MS plaques. [22] These methods include magnetization transfer and diffusion, as well as proton MR spectroscopy (MRS). [23, 24, 25]

Typically, fast-FLAIR (fluid-attenuated inversion recovery) sequences have been shown to have a lower sensitivity than do fast spin-echo sequences (FSE) for depicting spinal cord MS lesions. [26, 27, 28]

Studies have suggested that more cervical cord MS lesions can be revealed with magnetization transfer–prepared gradient-echo and fast-STIR (short TI inversion recovery) sequences than with FSE sequences, with fast-STIR demonstrating the greatest sensitivity. [27, 29, 30, 31, 32]

In one study, 3.5-mm axial T2-weighted images with full spinal cord coverage showed 22% more lesions in patients with MS than 3-mm sagittal scans, especially for lesions with small axial diameters. In the study, 449/509 lesions (88.2%) were detected on 3.5-mm axial scans and 337/509 (66.2%) on 3-mm sagittal scans. Only 277/449 (61.7%) axial lesions were also detected on sagittal images. [2]

Gadolinium-based contrast agents have been linked to the development of nephrogenic systemic fibrosis (NSF), also known as nephrogenic fibrosing dermopathy (NFD). The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MR angiography (MRA) scans. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble moving or straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness.

The main differentials include, but are not limited to, the following:

Primary or metastatic spinal cord neoplasms – Eg, astrocytomas, ependymomas

ADEM

Sarcoidosis

Transverse myelitis

Infarct

Vasculitis

Radiation myelitis

Arteriovenous fistula

Neoplasms

The presence of cysts and hemorrhage support the diagnosis of neoplasm

ADEM

This may show enhancement. The concomitant presence of brain lesions is the rule. ADEM typically runs a monophasic course; therefore, it does not have the relapsing course of MS. A history of viral infection within the previous 3-4 weeks should alert the radiologist.

Sarcoidosis

This involves the CNS in approximately 5% of cases. Concomitant pial involvement is frequently encountered. Enhancement is usually the rule.

Transverse myelitis

This term is usually used for idiopathic inflammatory myelopathy. Cord swelling and enhancement may be present, often involving a longer segment than does MS. MRI of the brain may be helpful for showing additional lesions in cases of MS or ADEM. Transverse myelitis usually responds to steroid therapy; therefore, a treatment trial is often considered before proceeding with biopsy. This process is typically monophasic.

Infarct

This is more common at the thoracic level. Usually, only a single lesion is present. Contrast may be present, although this is not the dominant feature. Signal alteration usually and initially involves the anterior gray matter (anterior spinal artery distribution). The patient’s clinical presentation will be acute. Particularly consider the possibility of an infarct if the patient is older and/or has a history of aortic/vascular surgery.

Vasculitis

Processes such as systemic lupus erythematosus can result in spinal lesions that mimic MS. Often, multiple lesions are present. However, the clinical history is often known and can help establish the correct diagnosis.

Radiation myelitis

Generally, doses higher than 4000 cGy are required to cause this condition. The latency period is 1-3 years. Chemotherapy may be synergistic. Images may show some peripheral enhancement.

Arteriovenous fistula

Usually, this occurs at the thoracolumbar level, and patients are usually older than 50 years, with a long history of back pain. The cord signal abnormality can involve a very long segment. Look for a serpiginous flow void along the cord surface.

Overview

What is the role of MRI in the workup of multiple sclerosis (MS)?

What are the McDonald diagnostic criteria for multiple sclerosis (MS)?

When is radiologically isolated syndrome (RIS) diagnosed following an evaluation for multiple sclerosis (MS)?

What is the role of CT scanning in the workup of multiple sclerosis (MS)?

Which findings on MRI suggest multiple sclerosis (MS)?

Which conditions are included in the differential diagnoses of multiple sclerosis?

How are spinal neoplasms differentiated from multiple sclerosis?

How is acute disseminated encephalomyelitis (ADEM) differentiated from multiple sclerosis?

How is sarcoidosis differentiated from multiple sclerosis?

How is transverse myelitis differentiated from multiple sclerosis?

How is infarct differentiated from multiple sclerosis?

How is vasculitis differentiated from multiple sclerosis?

How is radiation myelitis differentiated from multiple sclerosis?

How is arteriovenous fistula differentiated from multiple sclerosis?

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Schlaeger R, Papinutto N, Zhu AH, Lobach IV, Bevan CJ, Bucci M, et al. Association Between Thoracic Spinal Cord Gray Matter Atrophy and Disability in Multiple Sclerosis. JAMA Neurol. 2015 Aug. 72 (8):897-904. [Medline].

Lukas C, Knol DL, Sombekke MH, Bellenberg B, Hahn HK, Popescu V, et al. Cervical spinal cord volume loss is related to clinical disability progression in multiple sclerosis. J Neurol Neurosurg Psychiatry. 2015 Apr. 86 (4):410-8. [Medline].

Consortium of Multiple Sclerosis Centers. Consortium of MS Centers MRI Protocol for the Diagnosis and Follow Up of MS. Available at http://c.ymcdn.com/sites/www.mscare.org/resource/collection/9C5F19B9-3489-48B0-A54B-623A1ECEE07B/mriprotocol2009.pdf. Accessed: January 31, 2014.

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≥1 (as well as clear-cut historical evidence of 

a previous attack involving a lesion in a distinct anatomic location)

Djamil Fertikh, MD Attending Radiologist, Association of Alexandria Radiologists

Djamil Fertikh, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, American Medical Association, Radiological Society of North America

Disclosure: Nothing to disclose.

Michael L Brooks, JD, MD, FCLM Clinical Associate Professor of Radiology, Drexel University School of Medicine; Adjunct Clinical Associate Professor of Radiology, Philadelphia College of Osteopathic Medicine; Director of Neuroradiology, Mercy Diagnostic Imaging, Department of Radiology, Mercy Fitzgerald Hospital

Michael L Brooks, JD, MD, FCLM is a member of the following medical societies: American College of Legal Medicine, American College of Radiology, American Society of Neuroradiology, American Society of Pediatric Neuroradiology, American Society of Spine Radiology

Disclosure: Nothing to disclose.

James G Smirniotopoulos, MD Chief Editor, MedPix®, Lister Hill National Center for Biomedical Communications, US National Library of Medicine; Professorial Lecturer, Department of Radiology, George Washington University School of Medicine and Health Sciences

James G Smirniotopoulos, MD is a member of the following medical societies: American College of Radiology, American Society of Neuroradiology, Radiological Society of North America

Disclosure: Nothing to disclose.

Mahesh R Patel, MD Chief of MRI, Department of Diagnostic Imaging, Santa Clara Valley Medical Center

Mahesh R Patel, MD is a member of the following medical societies: American Roentgen Ray Society, American Society of Neuroradiology, and Radiological Society of North America

Disclosure: Nothing to disclose.

Imaging of the Spine in Multiple Sclerosis 

Research & References of Imaging of the Spine in Multiple Sclerosis |A&C Accounting And Tax Services
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Imaging of the Spine in Multiple Sclerosis 

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