Transverse myelitis revisited

Transcription

1 Transverse myelitis revisited Poster No.: C-0341 Congress: ECR 2012 Type: Educational Exhibit Authors: V. Lolli, D. Balériaux; Brussels/BE Keywords: Inflammation, Diagnostic procedure, MR, Neuroradiology spine, Education DOI: /ecr2012/C-0341 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 29

2 Learning objectives To review the relevant imaging features of transverse myelitis. To outline the key role of magnetic resonance imaging (MRI) in differential diagnosis and follow-up. Background Diagnostic criteria for transverse myelitis have been established by the Transverse Myelitis Consortium Working Group in 2002 and include the following: (a) bilateral weakness, sensory disturbance, and autonomic dysfunction that typically progress to maximal clinical severity between 4 hours and 21 days from onset; (b) inflammation of the spinal cord demonstrated by CSF pleocytosis, elevated IgG, or gadolinium enhancement on MRI. [1] The main causes of acute non-compressive transverse myelitis can be broadly classified into primary and secondary demyelinating (see Fig. 1). Page 2 of 29

3 Fig. 1: Nosology of acute transverse myelitis. Primary and secondary demyelinating disorders of the spinal cord. References: V. Lolli; Radiology, Brussels, BELGIUM MR is the imaging modality of choice for the diagnosis of transverse myelitis. Sagittal and axial T1-weigthed (W), fast spin echo (FSE) T2W and post-gadolinium T1W sequences are the most frequently used. The extent and pattern of demyelination are demonstrated based on signal abnormalities, most of the lesions featuring high signal intensity on T2weighted images (WI). Cord abnormalities with prolonged T2 relaxion times need to be analyzed for lesion length, cross-sectional area, axial distribution, and pattern of gadolinium enhancement. The main MS differentials are reviewed and illustrated. Neurosarcoidosis and primary CNS vasculitis, as well as vitamin and trace metal deficiencies, though predominantly subacute or chronic, can result in similar imaging findings and are therefore also discussed in this exhibit. Page 3 of 29

4 Imaging findings OR Procedure details Multiple Sclerosis (MS) Transverse myelitis can be a presenting feature of MS. Patients who are ultimately diagnosed with MS are more likely to have short-segment, wedge-shaped asymmetric lesions. The cervical spinal cord is the most frequent site of involvement (see Fig. 2 on page 11). Imaging findings MS plaques are classically less than two vertebral segments in lenght. On axial sections, lesions tend to involve less than half of the cross-sectional cord area and to be eccentrically located, preferentially involving the lateral and dorsal spinal cord columns. Swelling and ring-like enhancement are common in acute plaques and may mimic an intramedullary tumor. In patiens with a single demyelinating episode, definite MS diagnosis requires clinical or imaging evidence of new lesions on follow-up examinations, that fulfill the "dissemination in space and time" criteria. [2,3] Neuromyelitis Optica (NMO) and the NMO spectrum NMO, also referred to as Devic's disease, is a demyelinating disorder of the CNS preferentially involving the optic nerves and the spinal cord, with limited brain parenchymal involvement (see Fig. 3 on page 11). Proposed diagnostic criteria for NMO include: a) optic neuritis (ON) b) acute myelitis c) at least two of three supportive criteria: 1. contiguous spinal cord MRI lesion extending over three or more vertebral segments Page 4 of 29

5 2. brain MRI not meeting diagnostic criteria for MS 3. NMO-IgG seropositive status. [4,5] Limited forms of NMO (either single or recurrent ON or myelitis in the setting of a positive NMO-IgG status) are not uncommon and are classified as part of the NMO spectrum. [6] Imaging findings Imaging features classically include longitudinally extensive transverse myelitis extending over three or more cervical segments in lenght. NMO lesions tend to symmetric and centrally located, involving both gray and white matter. Swelling and associated patchy central enhancement are common in the acute phase. Brain involvement commonly occurs in later stages of the disease. Lesions are usually clinically silent and do not meet neuroimaging criteria for the diagnosis of MS. [7] NMO carries a poorer prognosis than MS, with greater residual disability and neurological impairment. [8] Systemic autoimmune and connective tissue disorders Systemic autoimmune or connective tissue disorders such as systemic lupus erythematosus, Sjogren's syndrome, and sarcoidosis account for approximately 20% of all cases of transverse myelitis. Neurosarcoidosis Sarcoidosis affects the CNS in 5% to 10% of all cases. Spinal cord involvement is uncommon and has been reported in 6% to 8% of patients with CNS disease. [9] Neurological symptoms are usually subacute or chronic according to the pseudotumoral features of the underlying granulomatous inflammation. Imaging findings The cervical spinal cord is the most common site of involvement. Page 5 of 29

6 Lesions are often longitudinally extensive and may mimic those of an intramedullary mass as well as those of cervical spondylotic myelopathy in the elderly patients. Cord enlargement and associated patchy parenchymal and leptomeningeal enhancement are common findings. Definitive diagnosis requires pathological evidence of noncaseating granulomas in tissue specimens. Spinal cord biopsy may be required when the spinal cord is the only site of involvement. MRI findings, though non-specific, are of the utmost importance, allowing the neurosurgeon a limited myelotomy, centered on the enhancing areas (see Fig. 4 on page 12 and Fig. 5 on page 13). Acute disseminated encephalopathy (ADEM) ADEM is an immune-mediated inflammatory disorder of the CNS associated with widespread demyelinating white matter lesions of the brain and the spinal cord, classically diagnosed in children and young adults in the setting of a viral illness or vaccination (see Fig. 6 on page 14). Imaging findings ADEM lesions are most frequently identified as poorly marginated, asymmetric areas of increased signal intensity on T2WI diffusely involving the cerebral white matter. Deep gray matter structures such as the thalami and the basal ganglia are frequently involved. Spinal cord involvement has been reported in up to 28% of cases. The typical spinal cord lesion is large, swollen, and predominantly affects the thoracic region. The incidence and pattern of Gadolinium enhancement may vary according to the stage of the lesions. Meningeal enhancement is unusual. Complete resolution of the white matter abnormalities on follow-up imaging studies has been reported in up to 75% of ADEM patients after treatment with high-dose intravenous steroids or plasmapheresis. Recurrent (RDEM) and multiphasic (MDEM) variants of the disorder have been described, with new or relapsing demyelinating events occurring at least three months after the initial attack. [10] Infectious myelitis Rarely, evidence of CNS infection is demonstrated by CSF-Polymerase-Chain Reaction (PCR) positivity or by the presence of specific serum IgM antibodies. Page 6 of 29

7 Viral myelitis Viral infections of the CNS are uncommon but have to be considered in the differential diagnosis of acute myelopathies. MRI may reveal a swollen cord with patchy gadolinium enhancement usually more posteriorly (see Fig. 7 on page 15). [11] Tuberculous (TB) myelitis CNS TB infection is thought to spread by hematogenous dissemination from a primary source. TB myelitis usually occurs as a secondary event in the course of common forms of TB meningitis. Less frequently, it may develop following downward extension from intracranial TB meningitis, or from adjacent foci of vertebral TB (see Fig. 8 on page 16 and Fig. 9 on page 17). Imaging findings Gadolinium-enhanced MR sequences typically show nodular enhancement of the surface of the spinal cord and nerve roots. T1 and T2 WI may reveal prominent cord edema and swelling, which may be related to granulomatous vasculitis changes and subsequent ischemia. Cavitation of the cord, central or eccentric, may develop secondarily. Parenchymal TB granulomas or abscesses may be seen in the spinal cord. Diagnosis is usually based on the clinical manifestations and on laboratory findings. PCR of the CSF for Mycobacteriam tuberculosis is faster and more sensitive than culture, which often takes up to six weeks for positive identification. [11] Neuroborreliosis Lyme neuroborreliosis is secondary to systemic infection by the tick-transmitted spirochete Borrelia burgdorferi and is reported in up to 15% of patients with untreated Lyme disease. The involvement of the spinal cord is rare, and is described in approximately 5% of patients diagnosed with neuroborreliosis. Imaging findings include diffuse or multifocal tumefactive tumor-like white matter lesions and nerve root enhancement on post contrast T1WI. Page 7 of 29

8 The diagnosis is based on a history of tick exposure and on laboratory findings, including serum and CSF presence of anti-borrelia burgdorferi IgM antibodies (see Fig. 10 on page 18). [12] Idiopatic Transverse Myelitis (ITM) ITM accounts for approximately 15% of cases of acute transverse myelitis. According to the Transverse Myelitis Consortium Working Group criteria, the term ITM is referred to cases of transverse myelitis in which connective tissue disorders, CNS infection, MS and optic neuritis have been excluded. [1] Imaging findings ITM lesions are typically focal and well-marginated, centrally located, and usually involve more than 2/3 of the cross sectional cord area. The thoracic cord is the most frequent site of involvement. Enhancement has been reported in up to 75% of cases, and is usually described as patchy or eccentric. Clinical course is classically described as monophasic. Follow-up data on large series show that outcome is variable, with one third of patients recovering completely after highdose intravenous steroids treatment, one third improving at slower rates and one third experiencing residual moderate to severe disability. Recurrence has been reported in up to 25% of cases, with relapsing cases having an increased tendency to be longitudinally extensive (see Fig. 11 on page 19). Cobalamin and copper deficiency Vitamin B12 deficiency is responsible for impairment of DNA synthesis and can affect the central or peripheral nervous system, causing subacute combined degeneration (SCD) with demyelination and vacuolation of the spinal cord, often associated with megaloblastic anemia. Clinical features typically include sensory ataxia due to marked dorsal columns deficit. Imaging findings On T2 MR images, symmetric increased signal intensity involving the posterior and lateral white matter columns is seen, with the cervical and upper thoracic cord most severely Page 8 of 29

9 affected, and with a typical rabbit-ear appearance on axial images. The spinal cord usually does not enhance. Copper is an essential trace element, which acts as a prosthetic group in several key enzymes. Acquired copper deficiency, most commonly due to reduced absorption after gastric surgery, may result in similar severe hematological and neurological effects. Imaging features closely mimic SCD of the spinal cord due to vitamin B12 deficit (see Fig. 12 on page 20). Malabsorption syndromes, the use of copper chelating agents, and zinc or iron overload are also recognized risk factors. [13,14] Posterior Reversible Encephalopathy Syndrome (PRES) PRES is a neurotoxic state recognized in the setting of eclampsia, organ transplantation, and severe hypertension. Imaging findings include either focal either confluent regions of symmetric brain vasogenic edema due to failed autoregulation and hyperperfusion. The parietal and occipital lobes are most frequently affected. Focal areas of vasogenic edema may also be seen in the basal ganglia, brain stem, and cerebellum. [15] Involvement of the spinal cord is exceedingly rare and only a few cases have been published in the literature. We report the case of a severely hypertensive 46-year-old male presenting with typical cerebral PRES lesions and associated extensive cervical spinal cord involvement (see Fig. 13 on page 21 ). Spinal cord ischemia Spinal cord infarction accounts for approximately 1% of all strokes. It has been related to aortic pathology and surgery, spine compression fractures, spondylolisthesis, and chronic cervical disk protrusion. The anterior spinal artery supplies the corticospinal tracts and all gray matter except for the posterior horns, and is the most frequent site of occlusion. Imaging findings In most cases, MR shows a well-defined lesion corresponding to the involved arterial territory (see Fig. 14 on page 22). Characteristic spinal cord stroke syndromes include the following patterns: anterior spinal artery; anterior and posterior unilateral; posterior spinal artery; transverse syndromes. Page 9 of 29

10 Transverse syndromes are commonly related to prolonged hypotension and systemic atherosclerosis. [16] Radiation myelitis Myelitis is an uncommon but well-recognized complication of radiotherapy, characterized by delayed development of symptoms, due to microvascular damage and subsequent medullary infarction or bleeding (see Fig. 15 on page 23). Imaging findings Imaging findings are non-specific and include increased T2 signal intensity and swelling of the spinal cord, with patchy or ring-like areas of enhancement. Spinal cord lesions lie within the radiation field and appear at least 6 to 24 months after radiation exposure. Associated fatty marrow changes within the adjacent vertebral bodies may help narrow the differential diagnosis. [8] Other conditions to be considered in the differential diagnosis of transverse myelitis Primary CNS vasculitis Primary CNS vasculitis is an uncommon disorder characterized by primary inflammation of blood vessels in the brain or spinal cord. Involvement of the spinal cord has been reported in approximately 5-14% of patients, and is most frequently associated with cerebral manifestations. [17,18] Imaging findings are non-specific and may mimic intramedullary tumors. Biopsy is necessary to provide the definite diagnosis (see Fig. 16 on page 24). Vascular malformations Dural arteriovenous fistula (AVF) is the most common subtype and accounts for approximately 70% of all spinal vascular malformations. [19] Page 10 of 29

11 Dural AVFs are most commonly found in the thoracolumbar region. Imaging findings classically include vascular flow voids and increased T2 signal intensity due to venous congestion, hypoxia, and edema of the spinal cord (see Fig. 17 on page 25). The diagnosis is confirmed by spinal angiography. Images for this section: Fig. 2: Multiple Sclerosis - 40-year-old male with recurrent episodes of weakness and dysesthesia of the right upper and lower extremities and urinary incontinence. Sagittal and axial MR images demonstrate short-segment T2 hyperintensity and swelling of the spinal cord at the C3-C4 level. The lesion is eccentrically located and shows peripheral enhancement after Gadolinium administration. Multiple PD hyperintense lesions are demonstrated in the cerebral white matter. Page 11 of 29

12 Fig. 3: Neuromyelitis Optica. 36-year-old female with complaints of throbbing pain in the left gluteal region and progressive left lower and right upper limbs paresthesia. Sagittal and axial MR images of the spinal cord demonstrate longitudinally extensive transverse myelitis extending from the C2 to the D2 level, enlargement of the spinal cord and patchy central enhancement at the C6-C7 level after Gadolinium administration. Page 12 of 29

13 Fig. 4: Neurosarcoidosis (1). 46 year-old female with a 4-month history of progressive upper limbs paresthesia and neck pain. Sagittal T2WI of the spinal cord demonstrate mildly increased signal intensity of the anterior cord at the C6-C7 level, and associated longitudinally extensive hyperintensity consistent with surrounding vasogenic edema. Axial T2WI at the C6-C7 level show conspicuous enlargement of the spinal cord. Page 13 of 29

14 Fig. 5: Neurosarcoidosis (2). Sagittal and axial post-gd T1WI show parenchymal enhancement in the anterior cord at the C6-C7 level, eccentric on the right side and protruding outside the contour of the spinal cord along the dural sheaths. Histologic examination shows noncaseating granulomas surrounded by a rim of lymphocytes, consistent with sarcoidosis. Page 14 of 29

15 Fig. 6: ADEM. 14 year-old female with new-onset generalized seizures, acute paraparesis and urinary retention. Axial T2 FLAIR WI of the brain show hyperintense lesions in the left thalamus and right dentate nucleus. Sagittal and axial T2WI of the spinal cord demonstrate longitudinally extensive hyperintensity of the anterior spinal cord most pronounced at the D9-D11 level, with involvement of the central gray matter. In this case there is no evidence of contrast enhancement. Page 15 of 29

16 Fig. 7: Viral myelitis. 40-year-old male complaining of inferior limbs dysesthesia and shooting electric-like sensations in the lower extremities when the head was flexed (Lhermitte's sign). T2 MR images show multiple, short segment hyperintense lesions in the dorsal midline cervical and thoracic spinal cord. Post-Gadolinium T1WI show multiple enhancing nodules in the posterior midline cord. Symptoms occurred in the setting of a genital Herpes Simplex infection, and the patient had positive anti-hsv IgM antibodies. Page 16 of 29

17 Fig. 8: Tuberculous myelitis (1). 59-year-old female presenting with a 2-week history of progressive lower limbs paresthesia and bladder dysfunction. Sagittal and axial T2 WI demonstrate longitudinally extensive T2 hyperintensity of the spinal cord. The lower cervical (C5-C7) and midthoracic (D4-D8) cord is moderately enlarged. Page 17 of 29

18 Fig. 9: Tubercolous myelitis (2). Post-Gadoliniumd T1WI show multiple foci of nodular enhancement predominantly involving the midline posterior spinal cord surface and contrast enhancement around the conus medullaris. Whole body FDG PET scan revealed pathologically increased FDG uptake in the inguinal and abdominal lymph nodes. Histopathologic examination demonstrated granulomatous inflammation with central caseous necrosis, consistent with tuberculosis. CSF PCR for Mycobacterium tuberculosis positive. Page 18 of 29

19 Fig. 10: Neuroborreliosis - 24-year-old male presenting with a four-week history of bilateral lower limb paresthesia, neck pain, stiffness, and fatigue. No history of tick bite or erythema migrans was reported. Sagittal MR images depict extensive T2 central hyperintensities and swelling of the spinal cord extending from the C2 to the T1 level. Post-contrast axial T1WI show thickened, abnormally enhancing anterior and posterior roots, and eccentric enhancing nodules located within the spinal cord. CSF examination revealed marked CSF mononuclear pleocytosis, an elevated protein content, and a decreased glucose profile. IgM antibodies to Borrelia Burgdorferi were positive on Western blotting in both serum and CSF. Page 19 of 29

20 Fig. 11: Idiopatic Transverse Myelitis - 53-year-old female with bilateral lower limb and trunk dysesthesia, bladder dysfunction and gait difficulty. Sagittal and axial MR images demonstrate focal enlargement of the spinal cord at the T4-T5 level, with a central T2 hyperintensity occupying more than two thirds of the cross-sectional cord area. The lesion is hypointense on T1WI and shows eccentric enhancement after intravenous Gadolinium administration. Page 20 of 29

21 Fig. 12: Copper deficiency - 73-year-old female with a past history of subtotal Billroth II gastrectomy presenting with progressive tetraparesis and sensory disturbance. Laboratory abnormalities included macrocytic anemia and leukopenia. A bone marrow aspiration revealed a markedly hypocellular marrow with dysplastic myelopoiesis and vacuolisation of the myeloid precursors. Sagittal T2W MR images demonstrate abnormally increased signal intensity involving the posterior cervical cord at the C4-C5 level. Axial T2 WI at these levels depict symmetric hyperintensity within the posterior spinal cord corresponding to the dorsal columns. Trace metal tests were performed and demonstrated low serum copper and caeruloplasmin levels associated with low urinary copper excretion and increased serum and urinary zinc levels, providing the diagnosis of copper deficiency due to excess zinc. In this patient, the excess zinc was related to excessive consumption of denture adhesive paste containing zinc. Page 21 of 29

22 Fig. 13: Posterior Reversible Encephalopathy Syndrome - 46-year-old male presenting with worsening headache, visual disturbances, nausea and vomiting, and who then progressed to coma. On physical examination, systolic blood pressure was as high as 210 mmhg. Fundoscopic examination of the eye revealed grade IV hypertensive retinopathy. Axial T2 FLAIR WI of the brain demonstrate focal regions of symmetric vasogenic edema in the occipital lobes, without contrast enhancement. Focal patchy areas of vasogenic edema are seen in the left thalamus, in the cerebellum and in the medulla oblongata. Sagittal T2 WI show longitudinally extensive hyperintensity and mild expansion of the upper cervical cord. The patient was intubated and treated with antihypertensive drugs upon which his blood pressure normalized within one day. Two days after admission, MRI of the brain showed almost complete resolution of the previously seen abnormalities. Page 22 of 29

23 Fig. 14: Spinal cord ischemia - 37-year-old female known for cystic fibrosis with abrupt onset upper limbs paresis following bronchial artery embolization for recurrent haemottisis. Sagittal and axial T2WI of the spinal cord show a well-demarcated area of increased signal intensity involving the anterior horns and the surrounding white matter consistent with an anterior spinal artery infarct at the C5-C7 level. Page 23 of 29

24 Fig. 15: Radiation myelitis. 21-year-old female with a recent history of posterior fossa radiation following surgical resection of a cerebellopontine angle ependymoma, complaining of sensory loss in both hands and trunk. MR images show extensive T2 hyperintensity and swelling of the upper cervical spinal cord and medulla oblongata with pacthy peripheral enhancement after Gadolinium administration. Histologic photomicrographs of the biopsy specimen show extensive hemorrhagic necrosis with no evidence of viable tumor cells. Page 24 of 29

25 Fig. 16: Primary CNS vasculitis - 32-year-old male with progressive left inferior limb weakness and paresthesia. Sagittal and axial MR images show increased T2 signal intensity and enlargement of the spinal cord from C5 to C7, and focal patchy enhancement after Gadolinium injection. Photomicorgraphs of the surgical specimen show prominent vascular endothelial proliferation, perivascular lymphocytic and plasmacytic infiltrates with reactive gliosis, providing the diagnosis of primary CNS granulomatous vasculitis. Page 25 of 29

26 Fig. 17: Dural AV fistula - 32-year-old male complaining of low back pain and gait difficulty. Sagittal T2W and myelographic MR images show increased signal intensity of the lower thoracic cord consistent with vasogenic edema and perimedullary dilated vessels. Page 26 of 29

27 Conclusion Transverse myelitis is an acute inflammatory process associated with bilateral motor, sensory and autonomic dysfunction, requiring urgent medical evaluation. Key concepts in MR imaging of transverse myelitis: Exclusion of acute compressive causes In patients with recent onset symptoms, MRI is required to exclude the need of neurosurgical cord decompression. Assessment of disease extension Examination of the enire spine is mandatory, and so is brain imaging, in order to assess intracranial involvement. Lesion characterization As illustrated, imaging of the spinal cord may reveal distinctive patterns of signal abnormality that help narrow the differential diagnosis. Follow-up Sequential MRI plays a key role in defining the monophasic course of a disorder and for therapy response assessment. Biopsy guidance MRI may provide useful information to guide the procedure when a spinal cord biopsy is needed. Personal Information The authors greatly acknowledge: - the staff of the "Clinique de Neuroradiologie", Hopital Erasme, ULB - and especially Dr. I. Delpierre - Prof. J. Brotchi (Department of Neurosurgery, Hopital Erasme, ULB) - Prof. I. Salmon, Dr. C. Maris and Dr. A-L. Trépant (Department of Pathology, Hopital Erasme, ULB) - Dr. B. Vandersmissen (Department of Neurology, Hopital Erasme, ULB) - Dr. A. Cornil (RHEMS-Ath) for their help and contribution. Dr Lolli would like to acknowledge the financial support from the ESOR/ESNR Exchange Programme for Fellowships Page 27 of 29

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29 [15] Bartynski WS, Boardman. Distinct imaging patterns and lesion distribution in posterior reversible encephalopathy syndrome. Am J Neuroradiol 2007; 28: [16] Novy J, Carruzzo A, Maeder P et al. Spinal cord ischemia. Arch Neurol 2006; 63: [17] Calabrese LH, Duna GF, Lie JT. Vasculitis in the central nervous system. Arthritis Rheum 1997; 40(7): [18] Salvarani C, Brown RD JR, Calamia KT et al. Primary central nervous system vasculitis: comparison of patients with and without cerebral amyloid angiopathy. Rheumatology 2008; 47(11): [19] Patsalides A, Santillan A, Knopman J et al. Endovascular management of spinal dural arteriovenous fistulas. J NeuroIntervent Surg. 2010; 3(1): Page 29 of 29