[18F]-Fluorodeoxyglucose–Positron Emission Tomography in Patients With Active Myelopathy

doi:10.1016/j.mayocp.2013.07.019

Mayo Clinic Proceedings

Volume 88, Issue 11, November 2013, Pages 1204-1212

https://doi.org/10.1016/j.mayocp.2013.07.019 Get rights and content

Abstract

Objective

To report and compare spinal cord [¹⁸F]-fluorodeoxyglucose–positron emission tomography (FDG-PET) metabolism in 51 patients with active myelopathy.

Patients and Methods

We retrospectively identified patients from January 1, 2001, through December 31, 2011, with active myelopathy in whom FDG-PET was performed. Inclusion criteria were (1) intramedullary myelopathy, (2) neoplastic/inflammatory etiology, and (3) FDG-PET performed after myelopathy onset. Exclusion criteria were (1) extramedullary myelopathy, (2) radiation-associated myelopathy, (3) no pathological confirmation of neoplasm, and (4) inactive myelopathy. Diagnostic categories of nonsarcoid inflammatory, neoplastic, and neurosarcoid were based on their final myelopathic diagnosis. Two radiologists who independently assessed FDG-PET for spinal cord hypermetabolism and maximum standardized uptake value (SUVmax) were blinded to the underlying etiology.

Results

Fifty-one patients (53% women) with a median age of 60 years (range, 20-82 years) were included. Inflammatory myelopathic diagnoses (n=24) were as follows: paraneoplastic (n=13), autoimmune/other (n=5), inflammatory demyelinating (n=4), and transverse myelitis (n=2). Neoplastic diagnoses (n=21) were as follows: intramedullary metastases (n=12), intramedullary lymphoma/leukemia (n=7), and primary intramedullary neoplasm (n=2). Six patients had neurosarcoid myelopathy. Spinal cord hypermetabolism was more common with neoplastic myelopathy than with nonsarcoid inflammatory myelopathy (17 of 21 [81%] vs 6 of 24 [25%]; P<.001). Agreement between radiologist’s assessments was excellent (κ=0.88). Median SUVmax was greater in neoplastic than in nonsarcoid inflammatory causes of myelopathy (3.3 g/mL vs 1.9 g/mL; P<.001). The FDG-PET hypermetabolism was seen in 3 of the 6 patients (50%) with neurosarcoid myelopathy (median SUVmax, 2.6 g/mL; range, 1.8-12.2 g/mL).

Conclusion

Spinal cord FDG-PET hypermetabolism in patients with active myelopathy may be reliably detected and was more common in neoplastic than in inflammatory myelopathies in this study. Future investigation of spinal cord FDG-PET is indicated to assess its potential contributions in evaluating active myelopathies.

Section snippets

Patients and Methods

The Mayo Foundation Institutional Review Board approved the study. Patients were identified retrospectively by searching the Mayo Clinic patient database from January 1, 1996, through July 31, 2011 (Figure 1). The FDG-PET technology was introduced at our institution in 2001, and so all patients were recruited from that date. Inclusion criteria were (1) myelopathy due to an intramedullary spinal cord process, (2) a neoplastic or inflammatory etiology, and (3) FDG-PET performed after myelopathy

Patient Characteristics

Fifty-one patients were included (Table 2), and their median age was 60 years (range, 20-82 years). The patients were divided into 3 groups on the basis of their final myelopathic diagnosis (Table 2): inflammatory, 24 (47%); neoplastic, 21 (41%); and neurosarcoidosis, 6 (12%). Inflammatory myelopathies were paraneoplastic, 13 (diagnosed by the presence of cancer and a neural autoantibody, 7; myelopathy in the setting of cancer without neural autoantibody detected, 3; and myelopathy with

Discussion

This study describes spinal cord FDG-PET in 51 patients with active inflammatory or neoplastic myelopathies. We found that spinal cord FDG-PET hypermetabolism is reliably detected by experienced radiologists and that hypermetabolism is seen more commonly in neoplastic than in inflammatory myelopathies. Further studies investigating spinal cord FDG-PET may assess its potential clinical utility in distinguishing myelopathic etiologies.

Clinical presentation, CSF examination, and both brain and

Conclusion

The FDG-PET may be performed for various reasons in patients with myelopathy, and clinicians and radiologists should be alerted to direct attention to the metabolic features within the spinal cord. Spinal cord FDG-PET hypermetabolism in patients with active myelopathy may be reliably detected and was more common in patients with neoplastic myelopathies than in patients with inflammatory myelopathies in this study. Further investigations of spinal cord FDG-PET are warranted to assess its utility

References (28)

M. Iacoboni et al.
Emission tomography contribution to clinical neurology
Clin Neurophysiol
(1999)
M.V. Jayasundera et al.
Intramedullary spinal cord metastasis from carcinoma of the lung: detection by positron emission tomography
Eur J Cancer
(1997)
B.J. Stern et al.
Neurologic presentations of sarcoidosis
Neurol Clin
(2010)
S.B. Knight et al.
Evaluation of pulmonary lesions with FDG-PET: comparison of findings in patients with and without a history of prior malignancy
Chest
(1996)
P. Seam et al.
The role of FDG-PET scans in patients with lymphoma
Blood
(2007)
A.A. Cohen-Gadol et al.
Spinal cord biopsy: a review of 38 cases
Neurosurgery
(2003)
M.E. Juweid et al.
Positron-emission tomography and assessment of cancer therapy
N Engl J Med
(2006)
K. Ota et al.
18F-FDG PET successfully detects spinal cord sarcoidosis
J Neurol
(2009)
K. Sakushima et al.
FDG-PET SUV can distinguish between spinal sarcoidosis and myelopathy with canal stenosis
J Neurol
(2011)
W. Chamroonrat et al.
Radiation myelopathy visualized as increased FDG uptake on positron emission tomography
Clin Nucl Med
(2005)

E.P. Flanagan et al.

Secondary intramedullary spinal cord non-Hodgkin’s lymphoma

J Neurooncol

(2012)

E.P. Flanagan et al.

Primary intramedullary spinal cord lymphoma

Neurology

(2011)

D. Karantanis et al.

18F-FDG PET/CT in primary central nervous system lymphoma in HIV-negative patients

Nucl Med Commun

(2007)

J.M. Wilmshurst et al.

Positron emission tomography in imaging spinal cord tumors

J Child Neurol

(2000)

Cited by (37)

Distinguishing CNS neurosarcoidosis from multiple sclerosis and an approach to “overlap” cases
2022, Journal of Neuroimmunology
Citation Excerpt :
The granulomatous lesions of sarcoidosis are FDG-PET avid and as many as 60–70% of neurosarcoidosis patients will have a positive whole body FDG-PET (Arun et al., 2020). CNS granulomatous lesions are usually beneath the resolution of PET scanning with the exception being when CNS sarcoidosis presents as a mass lesion (Chan and Hsiao, 2017), or when there is transverse myelitis (Flanagan et al., 2013), when increased glucose uptake may be seen. In MS, brain and whole body FDG-PET scanning should be normal.
Neurosarcoidosis is an important diagnosis to exclude in the work-up for suspected multiple sclerosis (MS). The distinction between the two conditions is usually possible due to characteristic clinical manifestations, magnetic resonance imaging (MRI) findings, and the results of other supportive investigations such as CT-PET. Definitive diagnosis can be made by histopathological examination, but this is not always practical. Misdiagnosis can occur when the clinical characteristics and MRI findings of both conditions overlap. Those patients with characteristic findings of MS but extraneural histopathological evidence of sarcoidosis are a particularly difficult diagnostic group. Diagnostic clarity is essential to inform treatment, especially as certain treatments for one disorder can exacerbate the other. This article summarises the clinical, laboratory and radiological findings that aid the clinician in distinguishing between the two conditions. It also discusses the literature on the potential for sarcoidosis and MS to co-exist in some patients, and how to approach the treatment of these “overlap” patients.
Neuroimaging in paraneoplastic syndromes
2022, Handbook of Neuro-Oncology Neuroimaging
Imaging the central nervous system is an important facet of diagnosing paraneoplastic neurological disorders. Many such disorders have characteristic imaging findings. However, even in syndromes without corollary imaging abnormalities, exclusion of additional or alternative diagnoses by neuraxis imaging is prudent. Here, we discuss the most commonly associated imaging abnormalities in such cases, as well as information on differentiation from common mimicking disorders. We also discuss imaging of the body for identification of a primary tumour in patients with suspected paraneoplastic disorders, including data for the most sensitive imaging modality.
Diagnosis and management of spinal cord emergencies
2017, Handbook of Clinical Neurology
Citation Excerpt :
18F-fluorodeoxyglucose positron emission tomography (PET) is often used to assess for an underlying malignancy or to stage a known cancer. In such cases, the spinal cord glucose metabolism should also be assessed, as intramedullary hypermetabolic lesions are more common with neoplastic (Fig. 17.4A1 and B2–3) than nonsarcoid inflammatory causes (Flanagan et al., 2013); spinal cord sarcoid is frequently hypermetabolic within the cord and lungs (Fig. 17.4C2), although use of corticosteroids prior to imaging can reduce the metabolic activity. CSF cytology or flow cytometry may be diagnostic in intramedullary spinal cord lymphoma and repeated studies may increase the yield, but spinal cord biopsy may be needed (Flanagan et al., 2011c).
Most spinal cord injury is seen with trauma. Nontraumatic spinal cord emergencies are discussed in this chapter. These myelopathies are rare but potentially devastating neurologic disorders. In some situations prior comorbidity (e.g., advanced cancer) provides a clue, but in others (e.g., autoimmune myelopathies) it may come with little warning. Neurologic examination helps distinguish spinal cord emergencies from peripheral nervous system emergencies (e.g., Guillain–Barré), although some features overlap. Neurologic deficits are often severe and may quickly become irreversible, highlighting the importance of early diagnosis and treatment. Emergent magnetic resonance imaging (MRI) of the entire spine is the imaging modality of choice for nontraumatic spinal cord emergencies and helps differentiate extramedullary compressive causes (e.g., epidural abscess, metastatic compression, epidural hematoma) from intramedullary etiologies (e.g., transverse myelitis, infectious myelitis, or spinal cord infarct). The MRI characteristics may give a clue to the diagnosis (e.g., flow voids dorsal to the cord in dural arteriovenous fistula). However, additional investigations (e.g., aquaporin-4-IgG) are often necessary to diagnose intramedullary etiologies and guide treatment. Emergency decompressive surgery is necessary for many extramedullary compressive causes, either alone or in combination with other treatments (e.g., radiation) and preoperative neurologic deficit is the best predictor of outcome.
Neuroimaging in Paraneoplastic Syndromes
2016, Handbook of Neuro-Oncology Neuroimaging: Second Edition
Imaging the central nervous system is an important facet of diagnosing paraneoplastic neurological disorders. Many such disorders have characteristic imaging findings. However, even in syndromes without corollary imaging abnormalities, exclusion of additional or alternative diagnoses by neuraxis imaging is prudent. Here, we discuss the most commonly associated imaging abnormalities in such cases, as well as information on differentiation from common mimicking disorders. We also discuss imaging of the body for identification of a primary tumor in patients with suspected paraneoplastic disorders, including data for the most sensitive imaging modality.
Autoimmune myelopathies
2016, Handbook of Clinical Neurology
Citation Excerpt :
Patchy enhancement of a longitudinally extensive lesion in the thoracic cord, although nonspecific, may be seen with dural arteriovenous fistulas (Fig. 19.5C). Patients with myelopathy may undergo FDG-PET scans for a variety of reasons (e.g., concern for paraneoplastic disease; suspicion of sarcoidosis or lymphoma) and the neurologist and neuroradiologist should assess the degree of glucose uptake within the spinal cord as it may give additional helpful information (Flanagan et al., 2013). While limited somewhat by the poor spatial resolution, marked FDG-PET hypermetabolism with high standardized uptake values (Fig. 19.7) are more suggestive of a neoplastic cause or spinal cord sarcoidosis than other nonsarcoid inflammatory causes (e.g., paraneoplastic myelopathy or demyelinating disease) (Fig. 19.8) (Flanagan et al., 2013).
Autoimmune myelopathies are a heterogeneous group of immune-mediated spinal cord disorders with a broad differential diagnosis. They encompass myelopathies with an immune attack on the spinal cord (e.g., aquaporin-4-IgG (AQP4-IgG) seropositive neuromyelitis optica (NMO) and its spectrum disorders (NMOSD)), myelopathies occurring with systemic autoimmune disorders (which may also be due to coexisting NMO/NMOSD), paraneoplastic autoimmune myelopathies, postinfectious autoimmune myelopathies (e.g., acute disseminated encephalomyelitis), and myelopathies thought to be immune-related (e.g., multiple sclerosis and spinal cord sarcoidosis). Spine magnetic resonance imaging is extremely useful in the evaluation of autoimmune myelopathies as the location of signal change, length of the lesion, gadolinium enhancement pattern, and evolution over time narrow the differential diagnosis considerably. The recent discovery of multiple novel neural-specific autoantibodies accompanying autoimmune myelopathies has improved their classification. These autoantibodies may be pathogenic (e.g., AQP4-IgG) or nonpathogenic and more reflective of a cytotoxic T-cell-mediated autoimmune response (collapsin response mediator protein-5(CRMP5)-IgG). The presence of an autoantibody may help guide cancer search, assist treatment decisions, and predict outcome/relapse. With paraneoplastic myelopathies the initial goal is detection and treatment of the underlying cancer. The aim of immunotherapy in all autoimmune myelopathies is to maximize reversibility, maintain benefits (while preventing relapse), and minimize side effects.
Paraneoplastic Syndromes from Head to Toe: Pathophysiology, Imaging Features, and Workup
2023, Radiographics

View all citing articles on Scopus

: For editorial comment, see page 1188

: Potential Competing Interests: Dr O’Neill serves on scientific advisory committees of the V Foundation, Accelerate Brain Cancer Cure (ABC2), and the Sontag Foundation. He receives research support from the Mayo Foundation, ABC2, the National Cancer Institute, and the National Institute of Neurologic Disorders and Stroke. Dr Lowe serves on the scientific advisory board for Bayer Schering Pharma and receives research support from GE Healthcare, Siemens Molecular Imaging, AVID Radiopharmaceuticals, the National Institutes of Health (National Institute on Aging, National Cancer Institute), the MN Partnership for Biotechnology and Medical Genomics, and the Leukemia & Lymphoma Society. Dr Pittock is a named inventor on patents (no. 12/678,350 filed 2010 and no. 12/573,942 filed 2008) that relate to functional AQP4/NMO-IgG assays and NMO-IgG as a cancer marker; receives research support from Alexion Pharmaceuticals, Inc, the Guthy Jackson Charitable Foundation, and the National Institutes of Health. Dr Keegan has served as a consultant to Novartis, Bionest, and Bristol Meyers Squibb and has research funded by Terumo BCT.

View full text

Original article[18F]-Fluorodeoxyglucose–Positron Emission Tomography in Patients With Active Myelopathy

Abstract

Objective

Patients and Methods

Results

Conclusion

Section snippets

Patients and Methods

Patient Characteristics

Discussion

Conclusion

Clin Neurophysiol

Eur J Cancer

Neurol Clin

Chest

Blood

Spinal cord biopsy: a review of 38 cases

Neurosurgery

Positron-emission tomography and assessment of cancer therapy

N Engl J Med

18F-FDG PET successfully detects spinal cord sarcoidosis

J Neurol

FDG-PET SUV can distinguish between spinal sarcoidosis and myelopathy with canal stenosis

J Neurol

Radiation myelopathy visualized as increased FDG uptake on positron emission tomography

Clin Nucl Med

Secondary intramedullary spinal cord non-Hodgkin’s lymphoma

J Neurooncol

Primary intramedullary spinal cord lymphoma

Neurology

18F-FDG PET/CT in primary central nervous system lymphoma in HIV-negative patients

Nucl Med Commun

Positron emission tomography in imaging spinal cord tumors

J Child Neurol

Original article
[¹⁸F]-Fluorodeoxyglucose–Positron Emission Tomography in Patients With Active Myelopathy