MR imaging of acute non-traumatic spinal cord syndrome

Transcription

1 MR imaging of acute non-traumatic spinal cord syndrome Poster No.: C-0872 Congress: ECR 2014 Type: Educational Exhibit Authors: E. Ripoll, N. Sarbu, A. Lopez, S. Capurro, L. Oleaga Zufiría; Barcelona/ES Keywords: Neuroradiology spine, CNS, Emergency, MR, Education, Imaging sequences, Diagnostic procedure, Acute, Education and training DOI: /ecr2014/C-0872 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 60

2 Learning objectives To present the MRI features of the different causes of acute non-traumatic spinal cord syndrome To point out what clinical information must be provided To show different spine MRI protocols recommended for each diagnostic suspicion To learn the different therapeutic management of every entity Lastly, to make a comprehensive differential diagnosis between different etiologies of acute spinal cord syndrome and to present other conditions that may clinically mimic an acute non-traumatic spinal cord syndrome Background Acute non-traumatic spinal cord syndrome is a frequent and potentially disabling situation in neurological emergencies and one of the most important causes of an urgent MRI. There are many entities that may cause this syndrome: vascular, inflammatory, infectious, tumoral and metabolic. Furthermore, there are also some other illnesses that can clinically mimic this syndrome. An accurate and early MRI diagnosis will guide the different therapeutic options and will provide information about the prognosis of the patient. Findings and procedure details MAJOR NEUROANATOMICAL FEATURES: Page 2 of 60

3 Fig. 1: Left: axial T2 image at C6 level at 3-Teslas MRI. Right: Same image with coloured major neuroanatomical features. Blue: anterior horns, Brown: posterior horns, red: lateral corticospinal tract, green: dorsal columns system, violet: spinothalamic tract. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Anterior Horn: Spinal motor neurons (innervate ipsilateral muscles of their level) Posterior Horn: Spinal sensitive neurons (process sensitive input from afferent fibers) Lateral Corticospinal Tract: descending motor pathway from contralateral brain hemisphere and innervates ipsilateral anterior horn neurons Dorsal Columns System: ascending proprioception (position, pressure and vibration senses) from ipsilateral limbs. Spinothalamic Tract: ascending sense of pain and temperature from contralateral limbs SPINAL CORD SYNDROMES Page 3 of 60

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5 Fig. 2: SPINAL CORD SYNDROMES References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES CLINICAL INFORMATION AND ASSOCIATED DISEASES Page 5 of 60

6 Fig. 3: CLINICAL INFORMATION AND ASSOCIATED DISEASES References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES DIFFERENTIAL DIAGNOSIS Page 6 of 60

7 VASCULAR Spinal Cord Infarction Accounts for 5-8% of acute myelopathies. Sudden onset (minutes-hours) is the main clinical feature Anterior Spinal Artery infarction is the most frequent subtype. Aetiology: aortic pathology (atherosclerotic, aneurism, dissection), aortic surgery, aortic endovascular devices (endoprosthesis, intra-aortic balloon pump counterpulsation), vertebral dissection and systemic hypotension. It is more frequent in elderly patients with cardiovascular risk factors. Clinical presentation: as anterior spinal artery supplies blood to the anterior two thirds of cord the clinical manifestation is secondary to the bilateral involvement of anterior horns, corticospinal and spinothalamic tracts with sparing of dorsal columns. Clinical presentation consists of sudden onset (from minutes to few hours) of symmetric motor weakness and impaired pain and temperature feeling with proprioception sparing. Urinary retention and pain are usually present. As the deficit is sudden deep tendinous reflexes are usually absent. MRI findings: T2 hyperintensity involving a long segment of the anterior cord (but MRI studies show no abnormality in 45% of patients). The most frequently affected segment is the lower thoracic one. Isolated anterior involvement of grey matter (Owl-eyes sign on axial T2) or grey and white matter anterior involvement can be noticed. Concomitant vertebral body infarction can be seen if there is a proximal segmentary artery occlusion. Studies performed in subacute phase can show haemorrhagic foci or patchy gadolinium enhancement. MRI special sequences: DWI and ADC (even may be technically difficult because of vertebral bodies and aortic pulsation artifact) show a restricted diffusion area and can be useful in differentiating from inflammatory aetiologies and helping in early diagnosis. Other much less common subtypes of spinal cord infarction are: Posterior Spinal Artery infarction with involvement of one side of posterior third of the cord. Central or transverse cord infarction are seen in severe systemic hypotension, presenting as a central or a complete cord syndrome, being Page 7 of 60

8 more frequent in thoracolumbar region. They can raise diagnostic problems, mimicking acute transverse myelitis but sudden onset and clinical context support the diagnosis. DWI sequences can also help showing restricted diffusion. Treatment: increasing spinal cord perfusion pressure by improving haemodynamic situation (increasing mean blood pressure and even placement of lumbar drainage in some cases). Page 8 of 60

9 Fig. 4: Spinal Cord Infarction (Anterior Spinal Artery territory): 59 years-old woman presenting sudden paraplegia, loss of temperature and pain sense up to D10 level with preserved vibration, sphincter impairment and absence of osteotendinous reflexes. Whole cord sagittal images T1 (A), T2 (B) and STIR (C) show anterior cord hyperintensity at D10-D12 levels. Lumbar sagittal T1 + Gadolinium (D) shows patchy enhancement. Axial T2 images at D10 (E) and (F) show hyperintensity of anterior horns (owl s eye sign). Involvement of anterior two thirds of the cord is clearly seen in G (D12 axial T2 image). References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Fig. 5: Spinal Cord Infarction (Posterior Spinal Artery territory): 63 years-old patient with cardiovascular risk factors and multiple osteoporotic dorsal fractures (treated with previous vertebroplasty) that presents sudden severe paraparesis with right leg predominance and mild sensorial involvement in both legs. Sagittal T1 (A) and T2 (B) show multiple dorsal osteoporotic fractures with vertebroplasty changes and retropulsion of D10 that contacts with spinal cord but without T2 signal changes. Axial diffusion (C) and ADC (D) at D6 level show restriction in diffusion due to a recent infarct. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Page 9 of 60

10 Fig. 6: Central spinal Cord Infarction due to hypotension: 61 years-old male with acute paraparesis after cardiac surgery (pericardiectomy) complicated by cardiac arrest. Sagittal Dorsal T1 (A) and T2 (B) and sagittal dorso-lumbar T1 (C) and T2 (D) are showed. C and D show central cord hyperintensity and enlargement from D10 to conus medullaris. Axial T2 at D12 level shows hyperintensity of medullary grey and white matter. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Spinal Epidural Hematoma Aetiology: spontaneous or secondary to trauma (epidural anaesthesia), anticoagulation / antiplatelet treatments, coagulation disorders, thrombocytopenia or local lesions (AVM, tumour, cavernoma). Clinical presentation: spinal epidural hematoma causes a painful compressive myelopathy that usually manifests as a progressive motor or sensory block. MRI findings: epidural collection with different degrees of cord compression (T2WI hyperintensity within the cord). In first 24h the collection is isointense on T1WI and hyperintense-heterogeneous on T2WI. After 48h is hyperintense on both T1W1 and T2WI. MRI special sequences: T2 gradient echo sequence shows hypointensity of the collection, helping to define the haemorrhagic aetiology. Treatment: emergency surgical decompression (laminectomy) and correction of coagulation / platelet disorder if present. Page 10 of 60

11 Fig. 7: Spinal Epidural Haematoma secondary to warfarin: 85 years-old patient with chronic warfarin treatment who presents low back pain and progressive motor weakness and sensory impairment in both legs. Sagittal T1 (A), T2 (B) and STIR (C) sequences show extensive posterior epidural haematoma. Axial T1 (D) and T2 (E) better depict spinal cord compression. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Spinal AVM (Arterio-Venous Malformation) Inherited communication between a radiculomedullary artery and a medullary vein (intramedullary or superficial spinal cord vein) with secondary congestion of epidural venous plexus. Clinical presentation: usually in the third decade causing chronic symptoms due to cord oedema and mass effect or acute symptoms if bleeding (intramedullary or subarachnoid). MRI findings: serpiginous abnormal vessels within or adjacent to the spinal cord. If there is intramedullary bleeding a T2WI hyperintensity with central or peripheral hypointensity and T1WI hyperintensity (suggesting a mix of blood products) can also be seen. MRI sequences: T2 gradient echo sequences can help to detect blood products. T1WI + gadolinium better depicts abnormal vessels. 3D MRI angiography can help to define the localization, arterial supplies and can guide a further catheter angiography. Treatment: surgery or endovascular embolization, stereotactic radiosurgery Page 11 of 60

12 Fig. 8: Intramedullary Spinal AVM: 71 years-old patient with acute low back pain with severe paraparesis and sensory loss in both legs. Sagittal T1 (A) and T2 (B) show an intramedullary lesion at D8 level with tortuous vessels inside (AVM) and dilated vessels at the anterior cord surface. There is also an extensive T2 hyperintensity of the spine, better depicted on Sagittal T2 and axial T2 at D8 (D) and D10 (E) levels. Sagittal T2 gradient echo sequence (C) shows signs of intramedullary bleeding. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Spinal davf (Dural Arterio-Venous fistula) Is the most common of spine vascular malformations (70%). It is an acquired communication between a radiculomeningeal artery and a radicullary vein, causing passive congestion of perimedullary venous plexus and spinal cord oedema. Clinical presentation: usually middle-aged man with progressive subacute whole spinal cord sd. involving lower extremities which worsens with Valsalva maneuvers (as increases venous pressure) but it may present acutely. MRI findings: longitudinally extensive T2WI hyperintensity of central cord also involving the conus medullaris (which is affected in 90% of cases) with Page 12 of 60

13 spinal cord enlargement and serpiginous and dilated perimedullary veins (best depicted on T2WI). MRI sequences: T2 gradient echo sequences can help to detect blood products. T1WI + gadolinium better depicts tortuous vessels and can show patchy enhancement of the affected cord. 3D MRI angiography can also define the localization, arterial supplies and can guide a further catheter angiography. Treatment: surgery or endovascular embolization. Page 13 of 60

14 Fig. 9: Dural Arterio-Venous Fistula: 52 years-old male presenting subacute progressive paraparesis with sensitivity and sphincter impairment. Images showed are sagittal dorsal T1 (A), T2 (B), STIR (C), right parasagittal dorsal T2 (D), Sagittal dorsolumbar T1 (E), T2 (F), T1+Gadolinium (G) and axial T2 at D9 (H) and D12 (I) levels. Extensive central cord T2 hyperintensity and whole cord enlargement is seen from Page 14 of 60

15 dorsal level to conus medullaris. Serpiginous vessels are observed in posterior aspect of spinal cord. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Spinal Cavernoma Cavernomas are sinusoidal collections of abnormal vascular loops with little or no parenchyma inside, having a low risk of bleeding. Spinal cavernomas represent 5% of all CNS cavernomas and can be associated with familial multiple cavernomatosis sd. (which presents an autosomal-dominant pattern of inheritance). Cavernomas are angiographically occult. Clinical presentation: middle aged patients with progressive motor and sensitive symptoms that can show acute exacerbations due to haemorrhagic events. MRI findings: single lobulated masswith an internal heterogeneous lesion (popcorn appearance) and surrounded by a hypointense rim on T1W1 and T2WI. Surrounding T2WI cord hyperintensity can be seen if recent bleeding occurred. One third of spinal cavernomas present a venous malformation (development venous anomaly) nearby, supporting the diagnosis. MRI sequences: T2 gradient echo sequences can detect the blood products and also calcifications within the lesion. It is convenient to perform also brain imaging as cavernomas can be multiple. Treatment: surgical excision depending on symptoms and localization, usually asymptomatic or minimally symptomatic lesions are only controlled. Page 15 of 60

16 Fig. 10: Cervical Intramedullar Cavernoma: 52 years-old woman presenting as acute mild left arm paresis and sensitive impairment in both legs. Sagittal cervical T1 (A), T2 (B), STIR (C), T2 gradient-echo (D) and axial T1 (E), T2 (F) and gradient-echo (G) are showed. There is an intramedullar-left parasagittal lobulated lesion that is hyperintense on T2 and is surrounded by a hypointense halo on T2, consistent with cavernoma with chronic bleeding changes. T2 gradient-echo sequence is markedly hypointense arround the lesion due to haemorragic compounds. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES INFLAMMATORY Acute Transverse Myelitis Aetiology: Acute Transverse Myelitis is an inflammatory syndrome caused by a broad number of illnesses: Page 16 of 60

17 Demyelinating: Multiple Sclerosis: acute transverse myelitis can be the first manifestation of the illness. Neuromyelitis Optica (Devic Sd.): recurrent episodes of optic neuritis and transverse myelitis. Presence of IgG-NMO antibodies. It can be associated with other systemic autoimmune disorders. ADEM (Acute Demyelinating Encephalomyelitis): monophasic multifocal demyelinating disease that mainly occurs in children after an infectious process or a vaccine. Clinically it presents as fever, encephalopathy, multiple focal deficits, seizures or coma. Involving of spinal cord can occur in 11-28% of patients. Infectious: viral, bacterial, fungal or parasitic Parainfectious or Post-vaccination: several weeks after an infectious process / vaccine. Systemic Autoimmune Disorders: systemic lupus erythematosus, Sarcoidosis, Sjögren sd., Behçet sd. or antiphospholypid sd. Paraneoplastic: small cell lung and breast cancers. Idiopathic (15-30%) Clinical presentation: weakness, sensory loss and sphincter impairment below the lesion. It can be symmetric or asymmetric and present as various spinal cord syndromes depending on the site of the lesion. MRI findings: T2 hyperintensity inside the cord. Three different patterns of acute transverse myelitis can be seen: Complete Transverse Myelitis:lesion affecting 1-2 vertebral segments and the whole cord section or the central portion is maximally affected. Low risk of MS (Usually due to other causes) Partial Transverse Myelitis: lesion affecting 1-2 vertebral segments and does not affect the whole cord section. High risk of transition to MS. MS typical spinal cord lesions: < 1-2 vertebral segments, asymmetrical, peripheral (usually posterolateral or lateral) and involving the cervicothoracic cord. Brain study is recommended. If isolated can mimic an intramedullary tumor. Longitudinally Extensive Myelitis: involves 3 or more vertebral segments and affects the central cord or two thirds of the cord area. The different entities that cause a longitudinally extensive myelitis are: Page 17 of 60

18 Neuromyelitis Optica ADEM Systemic Autoimmune Disorders Parainfectious Paraneoplastic Mimics: Anterior Spinal cord infarction, Combined Subacute Degeneration, Radiation Myelitis, davf and intramedullary M1 can mimic a longitudinally extensive myelitis. Longitudinally extensive selective tract involvement: selective tract involvement (as bilateral involvement of corticospinal tract) also can be seen in paraneoplastic myelitis. It is seen as T2 hyperintensity and T1 + Gadolinium enhancement. MRI special sequences: T1+ gadolinium can show patchy or peripheral enhancement. In case of suspicion of MS brain study is highly recommended (MS-like brain lesions in patients with partial transverse myelitis have 80% risk of transition to a clinically defined MS in next 3-5 years). Treatment: Usually intravenouscorticosteroid therapy is used. Depending on evolution and aetiology other immunosuppressive drugs, rituximab or plasma exchange can be used. Treatment of primary tumor is needed in paraneoplastic disorders. Page 18 of 60

19 Fig. 11: Multiple foci of acute partial transverse myelitis: 18 years-old woman presenting progressive paraparesis and sensory loss in right hand. Sagittal spinal cord T1 (A), T2 (B), STIR (C) and T1+Gadolinium (D) show multiple T2 cord hyperintensities affecting less than 3 vertebral bodies with mild and patchy enhancement. Axial T2 images at medullary junction (E), C4 (F), D5 (G) and D11 (H) show partial involvement of the cord section. Brain MRI study was also performed, on axial (I) and parasagittal (J) FLAIR images we can see subcortical white matter hyperintense lesions, consistent with multiple sclerosis. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Page 19 of 60

20 Fig. 12: Acute Partial Transverse Myelitis: 19 years-old man with 7 days of progressive paresthesia and sensory loss in both legs. Sagittal cervical T1 (A), T2 (B) and T1 + gadolinium show a hyperintense and gadolinium enhancing lesion at C2 level. Axial T2 at C2 level shows a hyperintense lesion affecting the posterior region of the cord. Brain MRI was also performed, showing multiple subcortical and periventricular hyperintense lesions. The patient was later diagnosed of multiple sclerosis. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Page 20 of 60

21 Fig. 13: Neuromyelitis Optica: 56 years-old woman presenting as progressive (4 days of evolution) right leg paresis and bilateral pain and temperature loss up to D5 level. Sagittal dorsal images: T1 (A), T2 (B), T1 + Gadolinium (C) and axial images T1 (D), T2 (E), T1 + Gadolinium (F) are shown. There is T2-hyperintensity within the cord involving 4 vertebral bodies (from D4 to D8) and affecting the central and anterior regions of the cord (longitudinally extensive myelitis). This patient had positive NMOIgG antibodies. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Page 21 of 60

22 Fig. 14: Longitudinally extensive myelitis in a SLE patient: 27 years-old woman previously diagnosed of Systemic lupus erythematosus who develops acute paraparesis and sphincter dysfunction. Sagittal dorsolumbar T1 (A), T2 (B), STIR (C) and cervical T2 (D) show longitudinally extensive myelitis (whole cord length involvement) with extension to medulla, as it is showed on Axial FLAIR brain images (G). Axial T2 images at C2 (E) and C5 (F) show a wide involvement of cord section. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES TUMORAL *Primary spinal cord tumours do not often present as acute spinal cord syndrome so they are not reviewed in this differential diagnosis. Tumour Spinal Cord Compression Aetiology: tumour spinal cord compression is due to: Page 22 of 60

23 Metastatic involvement of a vertebral body that collapses, displaces posteriorly and compresses the spinal cord. This is most frequent in lung, breast and prostate cancer. Patients with myeloma and prostate cancer have the highest risk. Spreading of a paraspinal tumor that reaches the cord through the intervertebral foramen (typically caused by lymphoma, sarcoma and lung carcinoma). Clinical presentation: Tumour spinal cord compression occurs in 2-5% of cancer patients, 80% with known cancer history and in 20% being the first symptom. 30% of patients have multiple epidural involvement. Pain is the first symptom in 90% of patients, followed by motor weakness, sensitive and sphincter impairment. MRI findings: Thoracic spine is the most common site of compression (60%). As they replace the normal fat signal of the vertebral body (hyperintense on both T1 and T2 sequences), vertebral metastases are T1 hypointense and T2 and STIR hyperintense. Collapsed vertebral body and a spinal or paraspinal mass can be seen with compression and displacement of the spinal cord (with or without increased cord T2 signal). MRI special sequences: T1+ gadolinium shows enhancement of the spinal / paraspinal mass and better depicts the tumour. As metastases in vertebral bodies have a restricted diffusion, DWI can increase the detection of vertebral metastases and can be useful in differentiating tumour from osteoporotic fractures. Whole spine imaging is recommended to rule out multifocal involvement. Treatment: corticosteroids and urgent radiation therapy / decompressive laminectomy Page 23 of 60

24 Fig. 15: Spinal Cord Compression by a vertebral metastasis: 67 years-old woman previously diagnosed of a colorectal cancer with peritoneal carcinomatosis. She presents with dorsal pain, progressive paraparesis and impaired sensibility up to dorsal level. Dorso-lumbar sagittal images T1 (A), T2 (B), STIR (C) and T1 + Gadolinium (D) show an infiltration of D10 that expands the vertebral body and compresses the cord with T2 hyperintensity inside the cord. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Intramedullary Spinal Metastasis Aetiology: intramedullary spinal metastasis is rare (<1% cancer patients) and are usually metastasis from lung (small cell carcinoma), breast, melanoma, lymphoma, renal cell and colorectal cancers. Usually occur in the setting of extensive metastatic disease. They are most frequent in cervical cord (45%) and thoracic cord (35%). Concomitant brain metastases are common (57%). Clinical presentation: back pain (70%), motor weakness, sensitive and sphincter impairment. As they usually arise in the dorsolateral cord they often present as a rapidly progressive Brown-Séquard syndrome. Page 24 of 60

25 MRI findings: intramedullary lesion (usually T1 hypointense and T2 hyperintense) with mild cord expansion and surrounded by extensive T2 hyperintense signal (that extends upper and lower than the lesion) due to a prominent oedema that is disproportionately increased for the size of the lesion. MRI special sequences: T1 + gadolinium shows an intense and homogeneous enhancing mass inside the cord. T2 gradient echo sequences can be useful in depicting a haemorrhagic compound. Brain study is also recommended as one third of patients may also have brain metastasis. Treatment: radiation therapy and corticosteroids. Page 25 of 60

26 Fig. 16: Melanoma Intramedullary Metastasis: 51 years-old man with a previous diagnosis of disseminated melanoma (pulmonary M1) that presents 3 days of progressive paresis and sensitive impairment of right leg. Sagittal T1 (A) and T2 (B) show an intramedullary lesion at D12 level that enhances with contrast on C (T1 + Gadolinium). There is also a T2 hyperintensity within the cord that extends uppwards and downwards due to oedema. Axial T2 at D12 level (D) better depict the localization of the lesion (intramedullary and right parasagittal). References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Radiation Myelitis Aetiology: spinal cord damage secondary to radiation therapy of vertebral metastases or head and neck, lung, mediastinal and upper abdominal cancers. There are two types of radiation myelitis depending on the time from radiotherapy treatment and symptom onset: Early transient radiation myelopathy: first 6 months after radiation. Damage is probably due to transient demyelination. Clinical symptoms are usually sensitive and self-limiting in a few weeks or months. Late radiation myelopathy: > 6 months after radiation. Clinical setting is a chronic, painless and progressive motor weakness, sensitive and sphincter impairment, usually starting as a BrownSéquard syndrome. MRI findings: spinal cord expansion and longitudinally T2 hyperintensity of the cord in the site of treatment MRI special sequences: T1+ gadolinium can show a patchy enhancement Treatment: early transient radiation myelopathy is usually mild and selflimiting. There is no effective treatment for late onset radiation myelopathy (corticosteroids, anticoagulation and hyperbaric oxygen have been used with variable results). Page 26 of 60

27 Fig. 17: Radiation Myelitis: 60 years-old woman affected by advanced breast cancer with multiple vertebral metastases that presents mild painless paraparesis. She had been treated with local cervical radiotherapy four days before. Sagittal T1 (A), T2 (B), STIR (C) and axial T2 at C5 level are showed. Enlarged cord with central T2 hyperintensity from C3 to D1 can be seen. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES INFECTIOUS Epidural Abscess Aetiology: infectious collection within the epidural space due to haematogenous dissemination, inoculation from an invasive spinal procedure or contiguous spread from a spondylodiscitis or other local infection. S. Aureus is the most common pathogen (70%). Clinical presentation: back pain, fever and progressive spinal cord sd. Erythrocyte sedimentation rate and C-reactive protein are usually elevated. Risk factors are: diabetes mellitus, immunodeficiency, chronic renal failure, intravenous drug and alcohol abuse. MRI findings: soft tissue mass within the epidural space (usually T1 iso or hypointense and T2 hyperintense) with cord mass effect. Page 27 of 60

28 MRI special sequences: DWI: can show restriction within the collection (pus) T1 + Gadolinium: can better depict the collection and show peripheral or diffuse (homogeneous or heterogeneous) enhancement Treatment: decompressive laminectomy and antibiotic drugs. Fig. 18: Epidural Abscess: 46 years-old man HIV positive who presents acute paraparesis and sensitive loss in both legs. He previously had a bacterial otitis 15 days before. Sagittal T1 (A), T2 (B), T2 gradient-echo (C), STIR (D) and axial T2 at D5 (E) and D8 (F) levels show a posterior epidural heterogeneous mass from D4 to D9 level with mass effect over the spinal cord. The mass is T1 hypo-isointense and T2 hyperintense. T2-gradient echo does not show significant hypointensity, excluding an epidural haematoma. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Page 28 of 60

29 Pyogenic Spondylodiscitis Aetiology: infection of vertebral body from haematogenous spread of infection from a remote site (most frequent urinary tract). Usually involved pathogens are S. Aureus and E.Coli. Lumbar spine is the most frequently affected site. Clinical presentation: focal back pain and fever. A progressive spinal cord sd can also be seen. Erythrocyte sedimentation rate and C-reactive protein are usually elevated. Risk factors are: diabetes mellitus, immunodeficiency, chronic renal failure, cirrhosis, cancer and intravenous drug use. MRI findings: T1 hypo and T2 hyperintensity within the disc and adjacent vertebral bodies (inflammatory changes / edema). Loss of endplate definition at both sides of the disc. Loss of disc space height. There can also be complicated by epidural or paraspinal abscesses. MRI special sequences: Fat suppressed T2 images: help to make the distinction between vertebral body fat and inflammatory changes / edema T1 + Gadolinium: enhancement of disc and adjacent endplates. Treatment: antibiotic drugs +/- surgery. Sample extraction from the lesion (for microbiological culture) should be performed whenever is possible prior to starting empirical antibiotics. Page 29 of 60

30 Fig. 19: Pyogenic Spondylodiscitis and cord compression: 63 years-old male with previous diagnosis of diabetes mellitus, repetitive episodes of cholangitis and dorsal back pain from two months ago. He develops a 2-weeks progressive paraparesis and paresthesia of both legs. Dorso-lumbar sagittal images T1 (A), T2 (B), STIR (C), T1+gadolinium (D) and axial images at D4-D5 level T1 (E), T2 (F) and T1 + Gadolinium (G) are showed. There is an involvement of D4 and D5 vertebral bodies and disc (T1 hypointense, T2-FLAIR hyperintense and contrast enhancing), loss of endplate definition in lower D4 and upper D5, loss of disc space height and paravertebral and epidural abscess with cord compression. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES METABOLIC Subacute Combined Degeneration: Aetiology: B12 deficiency, mainly affecting patients with alcoholism, gastric surgery, pernicious anaemia and malabsorption syndromes. Page 30 of 60

31 Clinical presentation: limb paresthesia with progressive gait abnormalities, sensory ataxia and mild paresis in both legs. Peripheral blood abnormalities as megaloblastic anemia, pancytopenia or hypersegmented polymorphonuclear leukocytes can also be seen. Diagnosis is performed by B12 serum low levels or high homocysteine and methylmalonic acid raised levels (which are more sensitive) MRI findings: longitudinally extensive T2 hyperintensity in dorsal and lateral columns. MRI special sequences: T1 + gadolinium shows no enhancement of the lesion. Treatment: B12 replacement (intramuscularly) MIMICS Some entities that cause acute involvement of multiple spinal nerve roots (polyradiculopathies) can mimic an acute spinal cord syndrome as they also cause motor weakness with sensitive and sphincter impairment. In this situation osteotendinous reflexes are diminished or absent, but this feature is also common in some acute myelopathies (ie: anterior spinal cord infarction). A lumbar MRI can be helpful showing enhancement of the spinal nerve roots but it is a nonspecific finding that can be seen in: Guillain-Barré syndrome, meningeal carcinomatosis, sarcoidosis, lymphoma, AIDS-related polyradiculopathy, Lyme disease, post-operative arachnoiditis and CIDP (chronic inflammatory demyelinating polyneuropathy). Due to the illness frequency and acute-subacute setting we will comment the first two of the previously mentioned entities: Guillain-Barré Syndrome Aetiology: acute and multifocal inflammatory involvement of peripheral nerves and nerve roots (polyradiculoneuropathy) due to immunologic aetiology. In two thirds of cases a mild respiratory or gastrointestinal tract infection precedes the symptoms. Clinical presentation: rapidly progressive and ascending symmetric limb weakness with numbness and paresthesia. Usually osteotendinous reflexes are diminished or absent. During the evolution of the illness there can be Page 31 of 60

32 cranial nerve involvement (usually facial nerve palsy). Lumbar pain can also be seen. The analysis of cerebrospinal fluid usually shows increased proteins with normal cell counts (albuminocytologic dissociation). The diagnosis is based in clinical findings, cerebrospinal fluid results and nerve conduction studies. MRI is rarely needed and sometimes is used to exclude other conditions. MRI findings: enhancement of nerve roots of conus medullaris and cauda equina. Treatment: intravenous immune globulin or plasma exchange Fig. 20: Guillain-Barré syndrome: 43 years-old man presenting as 2 days progressive paraparesis and paresthesia in both legs with sphincter impairment. Osteotendinous reflexes were absent. Sagittal Lumbar T1 + gadolinium (A), axial T1 (B,D) and axial T1+gadolinium (C, E) at levels D12 and L3 show diffuse enhancement of nerve roots due to a polyradiculopathy. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Meningeal Carcinomatosis Page 32 of 60

33 Aetiology: metastatic involvement of leptomeninges occurs in 8% of cancer patients. Most common malignancies are: breast, lung, melanoma, gastrointestinal tract, non-hodgkin lymphoma and leukaemia. Diagnosis is based on cerebrospinal fluid analysis and/or MRI findings. Clinical presentation: low back pain or radicular pain, weakness and sensitive impairment in legs and sphincter involvement. Headache (due to non-absorptive hydrocephalus, 66% patients) and cranial nerve palsy (75%) are usually present. 20% of patients can also present brain metastases. MRI findings: linear or nodular enlargement of lumbar nerve roots with gadolinium enhancement. MRI special sequences: consider a brain study as brain metastases and hydrocephalus may be present. Cranial leptomeningeal involvement can also be seen as enhancement of cranial nerves, sulci and cisternal spaces. Treatment: intrathecal chemotherapy / radiation therapy Page 33 of 60

34 Fig. 21: Meningeal Carcinomatosis in a Breast Cancer: 65 years-old woman with disseminated breast cancer who develops motor weakness in both legs with gait impairment. Sagittal T2 (A,B,C) and Axial T2 at L2 (D), L5 (E) and S1 (F) show nodular enlargement of nerve roots. References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Differential Diagnosis of Acute non-traumatic Spinal Cord Syndrome Page 34 of 60

35 Fig. 22: Differential Diagnosis of Acute non-traumatic Spinal Cord Syndrome References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Fig. 23: Differential Diagnosis of Acute non-traumatic Spinal Cord Syndrome References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Page 35 of 60

36 Systematic Approach of the diagnosis of Acute Non-Traumatic Spinal Cord Syndrome Fig. 24: Systematic Approach of the diagnosis of Acute Non-Traumatic Spinal Cord Syndrome References: Radiology, CDI, Hospital Clinic de Barcelona - Barcelona/ES Images for this section: Page 36 of 60

37 Fig. 1: Left: axial T2 image at C6 level at 3-Teslas MRI. Right: Same image with coloured major neuroanatomical features. Blue: anterior horns, Brown: posterior horns, red: lateral corticospinal tract, green: dorsal columns system, violet: spinothalamic tract. Page 37 of 60

38 Page 38 of 60

39 Fig. 2: SPINAL CORD SYNDROMES Fig. 3: CLINICAL INFORMATION AND ASSOCIATED DISEASES Page 39 of 60

40 Fig. 22: Differential Diagnosis of Acute non-traumatic Spinal Cord Syndrome Fig. 23: Differential Diagnosis of Acute non-traumatic Spinal Cord Syndrome Page 40 of 60

41 Fig. 4: Spinal Cord Infarction (Anterior Spinal Artery territory): 59 years-old woman presenting sudden paraplegia, loss of temperature and pain sense up to D10 level with preserved vibration, sphincter impairment and absence of osteotendinous reflexes. Whole cord sagittal images T1 (A), T2 (B) and STIR (C) show anterior cord hyperintensity at D10-D12 levels. Lumbar sagittal T1 + Gadolinium (D) shows patchy enhancement. Axial T2 images at D10 (E) and (F) show hyperintensity of anterior horns (owl s eye sign). Involvement of anterior two thirds of the cord is clearly seen in G (D12 axial T2 image). Page 41 of 60

42 Fig. 5: Spinal Cord Infarction (Posterior Spinal Artery territory): 63 years-old patient with cardiovascular risk factors and multiple osteoporotic dorsal fractures (treated with previous vertebroplasty) that presents sudden severe paraparesis with right leg predominance and mild sensorial involvement in both legs. Sagittal T1 (A) and T2 (B) show multiple dorsal osteoporotic fractures with vertebroplasty changes and retropulsion of D10 that contacts with spinal cord but without T2 signal changes. Axial diffusion (C) and ADC (D) at D6 level show restriction in diffusion due to a recent infarct. Fig. 6: Central spinal Cord Infarction due to hypotension: 61 years-old male with acute paraparesis after cardiac surgery (pericardiectomy) complicated by cardiac arrest. Sagittal Dorsal T1 (A) and T2 (B) and sagittal dorso-lumbar T1 (C) and T2 (D) are showed. Page 42 of 60

43 C and D show central cord hyperintensity and enlargement from D10 to conus medullaris. Axial T2 at D12 level shows hyperintensity of medullary grey and white matter. Fig. 7: Spinal Epidural Haematoma secondary to warfarin: 85 years-old patient with chronic warfarin treatment who presents low back pain and progressive motor weakness and sensory impairment in both legs. Sagittal T1 (A), T2 (B) and STIR (C) sequences show extensive posterior epidural haematoma. Axial T1 (D) and T2 (E) better depict spinal cord compression. Page 43 of 60

44 Fig. 8: Intramedullary Spinal AVM: 71 years-old patient with acute low back pain with severe paraparesis and sensory loss in both legs. Sagittal T1 (A) and T2 (B) show an intramedullary lesion at D8 level with tortuous vessels inside (AVM) and dilated vessels at the anterior cord surface. There is also an extensive T2 hyperintensity of the spine, better depicted on Sagittal T2 and axial T2 at D8 (D) and D10 (E) levels. Sagittal T2 gradient echo sequence (C) shows signs of intramedullary bleeding. Page 44 of 60

45 Fig. 9: Dural Arterio-Venous Fistula: 52 years-old male presenting subacute progressive paraparesis with sensitivity and sphincter impairment. Images showed are sagittal dorsal T1 (A), T2 (B), STIR (C), right parasagittal dorsal T2 (D), Sagittal dorso-lumbar T1 (E), T2 (F), T1+Gadolinium (G) and axial T2 at D9 (H) and D12 (I) levels. Extensive central Page 45 of 60

46 cord T2 hyperintensity and whole cord enlargement is seen from dorsal level to conus medullaris. Serpiginous vessels are observed in posterior aspect of spinal cord. Fig. 10: Cervical Intramedullar Cavernoma: 52 years-old woman presenting as acute mild left arm paresis and sensitive impairment in both legs. Sagittal cervical T1 (A), T2 (B), STIR (C), T2 gradient-echo (D) and axial T1 (E), T2 (F) and gradient-echo (G) are showed. There is an intramedullar-left parasagittal lobulated lesion that is hyperintense on T2 and is surrounded by a hypointense halo on T2, consistent with cavernoma with chronic bleeding changes. T2 gradient-echo sequence is markedly hypointense arround the lesion due to haemorragic compounds. Page 46 of 60

47 Fig. 11: Multiple foci of acute partial transverse myelitis: 18 years-old woman presenting progressive paraparesis and sensory loss in right hand. Sagittal spinal cord T1 (A), T2 (B), STIR (C) and T1+Gadolinium (D) show multiple T2 cord hyperintensities affecting less than 3 vertebral bodies with mild and patchy enhancement. Axial T2 images at medullary junction (E), C4 (F), D5 (G) and D11 (H) show partial involvement of the cord section. Brain MRI study was also performed, on axial (I) and parasagittal (J) FLAIR images we can see subcortical white matter hyperintense lesions, consistent with multiple sclerosis. Page 47 of 60

48 Fig. 12: Acute Partial Transverse Myelitis: 19 years-old man with 7 days of progressive paresthesia and sensory loss in both legs. Sagittal cervical T1 (A), T2 (B) and T1 + gadolinium show a hyperintense and gadolinium enhancing lesion at C2 level. Axial T2 at C2 level shows a hyperintense lesion affecting the posterior region of the cord. Brain MRI was also performed, showing multiple subcortical and periventricular hyperintense lesions. The patient was later diagnosed of multiple sclerosis. Page 48 of 60

49 Fig. 13: Neuromyelitis Optica: 56 years-old woman presenting as progressive (4 days of evolution) right leg paresis and bilateral pain and temperature loss up to D5 level. Sagittal dorsal images: T1 (A), T2 (B), T1 + Gadolinium (C) and axial images T1 (D), T2 (E), T1 + Gadolinium (F) are shown. There is T2-hyperintensity within the cord involving 4 vertebral bodies (from D4 to D8) and affecting the central and anterior regions of the cord (longitudinally extensive myelitis). This patient had positive NMO-IgG antibodies. Page 49 of 60

50 Fig. 14: Longitudinally extensive myelitis in a SLE patient: 27 years-old woman previously diagnosed of Systemic lupus erythematosus who develops acute paraparesis and sphincter dysfunction. Sagittal dorsolumbar T1 (A), T2 (B), STIR (C) and cervical T2 (D) show longitudinally extensive myelitis (whole cord length involvement) with extension to medulla, as it is showed on Axial FLAIR brain images (G). Axial T2 images at C2 (E) and C5 (F) show a wide involvement of cord section. Page 50 of 60

51 Fig. 15: Spinal Cord Compression by a vertebral metastasis: 67 years-old woman previously diagnosed of a colorectal cancer with peritoneal carcinomatosis. She presents with dorsal pain, progressive paraparesis and impaired sensibility up to dorsal level. Dorso-lumbar sagittal images T1 (A), T2 (B), STIR (C) and T1 + Gadolinium (D) show an infiltration of D10 that expands the vertebral body and compresses the cord with T2 hyperintensity inside the cord. Page 51 of 60

52 Fig. 16: Melanoma Intramedullary Metastasis: 51 years-old man with a previous diagnosis of disseminated melanoma (pulmonary M1) that presents 3 days of progressive paresis and sensitive impairment of right leg. Sagittal T1 (A) and T2 (B) show an intramedullary lesion at D12 level that enhances with contrast on C (T1 + Gadolinium). There is also a T2 hyperintensity within the cord that extends uppwards and downwards due to oedema. Axial T2 at D12 level (D) better depict the localization of the lesion (intramedullary and right parasagittal). Page 52 of 60

53 Fig. 17: Radiation Myelitis: 60 years-old woman affected by advanced breast cancer with multiple vertebral metastases that presents mild painless paraparesis. She had been treated with local cervical radiotherapy four days before. Sagittal T1 (A), T2 (B), STIR (C) and axial T2 at C5 level are showed. Enlarged cord with central T2 hyperintensity from C3 to D1 can be seen. Page 53 of 60

54 Fig. 18: Epidural Abscess: 46 years-old man HIV positive who presents acute paraparesis and sensitive loss in both legs. He previously had a bacterial otitis 15 days before. Sagittal T1 (A), T2 (B), T2 gradient-echo (C), STIR (D) and axial T2 at D5 (E) and D8 (F) levels show a posterior epidural heterogeneous mass from D4 to D9 level with mass effect over the spinal cord. The mass is T1 hypo-isointense and T2 hyperintense. T2-gradient echo does not show significant hypointensity, excluding an epidural haematoma. Page 54 of 60

55 Fig. 19: Pyogenic Spondylodiscitis and cord compression: 63 years-old male with previous diagnosis of diabetes mellitus, repetitive episodes of cholangitis and dorsal back pain from two months ago. He develops a 2-weeks progressive paraparesis and paresthesia of both legs. Dorso-lumbar sagittal images T1 (A), T2 (B), STIR (C), T1+gadolinium (D) and axial images at D4-D5 level T1 (E), T2 (F) and T1 + Gadolinium (G) are showed. There is an involvement of D4 and D5 vertebral bodies and disc (T1 hypointense, T2-FLAIR hyperintense and contrast enhancing), loss of endplate definition in lower D4 and upper D5, loss of disc space height and paravertebral and epidural abscess with cord compression. Page 55 of 60

56 Fig. 20: Guillain-Barré syndrome: 43 years-old man presenting as 2 days progressive paraparesis and paresthesia in both legs with sphincter impairment. Osteotendinous reflexes were absent. Sagittal Lumbar T1 + gadolinium (A), axial T1 (B,D) and axial T1+gadolinium (C, E) at levels D12 and L3 show diffuse enhancement of nerve roots due to a polyradiculopathy. Page 56 of 60

57 Fig. 21: Meningeal Carcinomatosis in a Breast Cancer: 65 years-old woman with disseminated breast cancer who develops motor weakness in both legs with gait impairment. Sagittal T2 (A,B,C) and Axial T2 at L2 (D), L5 (E) and S1 (F) show nodular enlargement of nerve roots. Page 57 of 60

58 Fig. 24: Systematic Approach of the diagnosis of Acute Non-Traumatic Spinal Cord Syndrome Page 58 of 60

59 Conclusion Acute non-traumatic spinal cord syndrome is a frequent and potentially disabling entity that may be caused by multiple etiologies. Knowledge of MRI findings, clinical features and technical MRI management is crucial in order to provide an accurate and early diagnosis that will guide the therapeutic options and will provide useful data for the outcome of the patient. Personal information Enric Ripoll - Radiology Department, Hospital Clinic of Barcelona, Spain. ripoll@clinic.ub.es References Brazis PW, Masdeu JC, Biller J.Localization in Clinical Neurology, Fifth Edition. Lippincott Williams & Wilkins Bican O, Minagar A, Pruitt AA. The Spinal Cord: A Review of Functional Neuroanatomy. Neurol Clin 2013;31:1-18 Sheerin F, Collison K, Quaghebeur G. Magnetic resonance imaging of acute intramedullary myelopathy: radiological differential diagnosis for the on-call radiologist. Clinical radiology 2009; 64 (1): Rubin MN, Rabinstein AA. Vascular diseases of the spinal cord. Neurologic clinics 2013; 31: Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal Cord Ischemia: Clinical and Imaging Patterns, Pathogenesis, and Outcomes in 27 Patients. Arch Neurol. 2006; 63: Morris JM. Imaging of Dural Arteriovenous Fistula. Radiol Clin N Am 2012; 50 (4): Beh SC, Greenberg BM, Frohman T, Frohman EM. Transverse myelitis. Neurologic clinics 2013; 31(1): DeSanto J, Ross J. Spine infection/inflammation. Radiol Clin N Am 2011; 49 (1): Jacob A, Weinshenker BG. An approach to the diagnosis of acute transverse myelitis. Semin Neurol 2008; 28: Diehn, FE. Imaging of spine infection. Radiol Clin N Am 2012; 50: Page 59 of 60

60 Duarte RM, Vaccaro AR. Spinal infection: state of the art and management algorithm. Eur Spine J 2013; 22 (12): Katabathina VS, Restrepo CS, Betancourt Cuellar SL, Riascos RF, Menias CO. Imaging of Oncologic Emergencies: What Every Radiologist Should Know. RadioGraphics 2013; 33: Tanenbaum LN. Clinical Applications of Diffusion Imaging in the Spine. Magn Reson Imaging Clin N Am. 2013;21(2): Hammack, JE. Spinal Cord Disease in Patients with Cancer. Continuum Lifelong Learning Neurol 2012; 18 (2): Yuki N, Hartung H. Guillain-Barré Syndrome. N Engl J Med 2012; 366: Alkan O, Yildirim T, Tokmak N, Tan M. Spinal MRI Findings of Guillain-Barré Syndrome. Radiology Case 2009; 3 (3):25-28 Pavlidis, N. The diagnostic and therapeutic management of leptomeningeal carcinomatosis. Annals of Oncology 2004; 15 (Supplement 4): Schwendimann, RN. Metabolic, Nutritional, and Toxic Myelopathies. Neurol Clin 2013; 31: Page 60 of 60