You are in: eMedicine Specialties > Radiology > BRAIN/SPINE Multiple Sclerosis, SpineArticle Last Updated: May 24, 2008AUTHOR AND EDITOR INFORMATIONSection 1 of 8
  Author: Djamil Fertikh, MD, Attending Physician, Division of Radiology, Association of Alexandria Radiologists Djamil Fertikh is a member of the following medical societies: American College of Radiology, American Medical Association, and Radiological Society of North America Coauthor(s): Michael L Brooks, MD, JD, FCLM, Clinical Associate Professor of Radiology, Philadelphia College of Osteopathic Medicine; Director of Neuroradiology, Mercy Diagnostic Imaging, Department of Radiology, Mercy Fitzgerald Hospital Editors: Mahesh R Patel, MD, Chief of MRI, Department of Radiology, Santa Clara Valley Medical Center; Bernard D Coombs, MB, ChB, PhD, Consulting Staff, Department of Specialist Rehabilitation Services, Hutt Valley District Health Board, New Zealand; Val Runge, MD, Robert and Alma Moreton Centennial Chair in Radiology, Professor, Editor-in-Chief of Investigative Radiology, Department of Radiology, Scott and White Clinic and Hospital; Robert M Krasny, MD, Consulting Staff, Department of Radiology, The Angeles Clinic and Research Institute; James G Smirniotopoulos, MD, Professor of Radiology, Neurology, and Biomedical Informatics, Chairman, Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences Author and Editor Disclosure Synonyms and related keywords: MS, demyelinating process, brain lesions, spine lesions, perivenular inflammation, plaques, fibrillary gliosis, oligodendroglia, spinal MS, spinal multiple sclerosis, Devic neuromyelitis optica, optic neuritis INTRODUCTIONSection 2 of 8
  BackgroundMultiple sclerosis (MS) is considered the most common demyelinating process involving the central nervous system (CNS).1 In 1988, MS was first described in the upper cervical spine using magnetic resonance imaging (MRI). Spinal MS is often associated with concomitant brain lesions; however, as many as 20% of patients with spinal lesions do not have intracranial plaques. No strong correlation has been established between the extent of the plaques and the degree of clinical disability. For excellent patient education resources, visit eMedicine's Muscle Disorders Center. Also, see eMedicine's patient education article Multiple Sclerosis. PathophysiologyThe exact cause of MS remains unclear; however, hypotheses include viral and autoimmune etiologies. In the acute stage, perivenular inflammation with hypercellularity (macrophages and/or lymphocytes) is encountered in typically well-demarcated areas of demyelination. In the chronic stages of the disease, fibrillary gliosis occurs with a breakdown of myelin. The axonal structure is conserved, with a reduction or absence of oligodendroglia. Occasionally, lesions resolve incompletely, but most progress to demyelination. FrequencyUnited StatesThere are an estimated 250,000-350,000 patients in the United States with MS. InternationalMS occurs worldwide.2 Its prevalence varies depending on the geographic location, rising as the northerly or southerly distance from the equator increases. Depending on the country or the specific population, the prevalence of MS ranges from 2 cases per 100,000 population to 150 cases per 100,000 population. Mortality/Morbidity
Related Medscape topics: RaceEpidemiologic series have shown that western Europeans living in temperate zones have a higher risk for MS than do other groups. SexThe male-to-female ratio is 2:3. AgeMS frequently occurs in persons aged 10-50 years. However, MS has also been described in the pediatric population and in individuals older than 50 years. AnatomySpinal MS has a predilection for the cervical spinal cord (67% of cases), with preferential, eccentric involvement of the dorsal and lateral areas of the spinal cord abutting the subarachnoid space around the cord. The gray matter may be involved. Approximately 55-75% of patients with MS have spinal lesions at some point during the course of the disease. Clinical DetailsThe clinical signs vary depending on the spinal cord segment affected and the degree of involvement. MS is characterized by a typical relapsing-remitting clinical course. Spastic paraparesis/paraplegia with neurogenic bowel and bladder, as well as with sexual dysfunction, can be encountered. Dysesthetic pain syndromes may result from spinal or cranial nerve root involvement. Heredity is suggested to be involved in the etiology of the disease because affected relatives occasionally are identified. A concomitant presence of optic neuritis (unilateral, bilateral, or chiasm) constitutes Devic neuromyelitis optica. The brain is usually normal, but the condition is associated with a poor prognosis. Preferred ExaminationAlthough nonspecific, MRI is presently considered to be the most sensitive diagnostic imaging modality for revealing demyelinating plaques. MRI shows abnormalities in 95% of patients with clinically definitive MS.4, 5 Limitations of TechniquesMRI is sensitive to areas of demyelination, which appear as high signal areas on long TR sequences. 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. DIFFERENTIALSSection 3 of 8
Sarcoidosis Systemic Lupus Erythematosus Other Problems to Be ConsideredSpinal cord tumors (primary or metastasis) CT SCANSection 4 of 8
FindingsWith the advancement of MRI, evaluation of the spinal cord using axial computed tomography (CT) scanning was abandoned because of its poor sensitivity. Large, masslike lesions can occasionally mimic a neoplasm, and characterizing them can be difficult. Degree of ConfidenceAs a result of CT scanning's poor sensitivity, the detection, evaluation, and characterization of MS lesions and enhancement patterns are limited with this modality. False Positives/NegativesPrimary and secondary neoplasms of the spinal cord (astrocytomas, ependymomas), infection, transverse myelitis, acute infarction, sarcoidosis, and systemic lupus erythematosus may mimic demyelinating MS plaques. MRISection 5 of 8
FindingsMRI far exceeds CT scanning in the ability to demonstrate intramedullary pathology; MRI is currently used for the first-line investigation.6 Depending on their age, MS plaques appear on unenhanced, T1-weighted images as areas of slightly low to low signal intensity. Plaques may appear as nodules, rings, or arcs and generally are less than 2 vertebral bodies in length.7 Plaques usually demonstrate prompt enhancement after the administration of a gadolinium-based contrast agent, which most often indicates active disease.8 The enhancement may last 2-8 weeks. Steroids typically do not suppress the enhancement of the active plaques. Classic chronic lesions do not demonstrate contrast enhancement. 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. 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.9 These methods include magnetization transfer and diffusion, as well as proton magnetic resonance spectroscopy (MRS).10, 11 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.12, 13, 14 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.13, 15, 16, 17, 18 Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. 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 magnetic resonance angiography (MRA) scans. Degree of ConfidenceAlthough MRI is not specific, it is considered the most sensitive imaging modality for diagnosing spinal cord MS, for evaluating its extent, and for following up the response to treatment. MRI is more sensitive for identifying active plaques than is double-dose CT scanning or clinical examination. False Positives/NegativesThe main differentials include, but are not limited to, the following:
INTERVENTIONSection 6 of 8
Medical/Legal Pitfalls
MULTIMEDIASection 7 of 8
REFERENCESSection 8 of 8
Multiple Sclerosis, Spine excerpt Article Last Updated: May 24, 2008 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
