Paraneoplastic Myelopathy Research Articles

Anti‐Ri‐antibodies associated paraneoplastic myelopathy revealing a woman's breast cancer: A case report

Anti‐Ri‐antibodies associated paraneoplastic myelopathy revealing a woman's breast cancer: A case report

Imaging-negative CV2/collapsin response mediator protein 5 antibody-related paraneoplastic myelopathy: a rare and challenging diagnosis.

Imaging-negative CV2/collapsin response mediator protein 5 antibody-related paraneoplastic myelopathy: a rare and challenging diagnosis.

Isolated Myelopathy in Occult Breast Carcinoma with Negative Paraneoplastic Antibodies: A Case Report of a Rare Condition

Isolated paraneoplastic myelopathy (IPM) is a rare neurological manifestation of systemic cancer and represents an intermediate-risk phenotype of disease according to the diagnostic criteria for Paraneoplastic Neurologic Syndromes (PNS). Here, we present the case of a 47-year-old woman who developed subacute cervical myelopathy and was then diagnosed with breast cancer. Through this lens, we provide a discussion of current literature on IPM. Over four months, our patient developed progressive tetraparesis, hypoesthesia with C3 level, and urinary retention. The first MRI was negative, but a four-month-control MRI showed a T2-hyperintense spinal lesion (C2–C7 and T2–T4). Cerebrospinal fluid (CSF) analysis was normal. Infective and autoimmune screening, including onconeural, anti-MOG, and aquaporin-4 antibodies, was unremarkable. The total-body CT scan was negative, but total-body PET-CT scan evidenced an enlarged axillary lymph node, with the detection of breast cancer cells at fine-needle aspiration. Despite negative mammography, a breast MRI confirmed a mammary nodule, which was removed, and a ductal infiltrating breast carcinoma diagnosis was made. Her neurological condition partially improved after steroid therapy. Our final diagnosis was probable IPM, according to PNS criteria. This rare condition affects most frequently middle-aged women and is often associated with breast and lung cancer, even if two-thirds of patients’ cancer diagnosis is subsequent to the onset of neurological deficits. Clinical presentation is often subtle, and CSF analysis, neuroimaging, and onconeural autoantibodies could be negative or non-specific. However, if the suspect of paraneoplastic disease is strong, cancer should be searched thoroughly since early diagnosis and treatment are associated with a better outcome.

MOG Antibody-Positive Myelopathy as a Paraneoplastic Manifestation of Lymphoma

Although myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an autoimmune demyelinating disease, it may occur as a paraneoplastic syndrome in rare instances. A 80-year-old woman presented with paresthesia and weakness of four extremities for 10 days. Spine magnetic resonance imaging showed longitudinally extensive transverse myelitis. Laboratory tests revealed positive MOG antibodies. Both high-dose intravenous methylprednisolone and plasma exchange were not effective and further evaluation showed lymphoma. Herein, we reported a case of MOG-positive paraneoplastic myelopathy with lymphoma.

Neuroimaging of Spinal Cord and Cauda Equina Disorders.

This article reviews the neuroimaging of disorders of the spinal cord and cauda equina, with a focus on MRI. An anatomic approach is used; diseases of the extradural, intradural-extramedullary, and intramedullary (parenchymal) compartments are considered, and both neoplastic and non-neoplastic conditions are covered. Differentiating imaging features are highlighted. Although T2-hyperintense signal abnormality of the spinal cord can have myriad etiologies, neuroimaging can provide specific diagnoses or considerably narrow the differential diagnosis in many cases. Intradural-extramedullary lesions compressing the spinal cord have a limited differential diagnosis and are usually benign; meningiomas and schwannomas are most common. Extradural lesions can often be specifically diagnosed. Disk herniations are the most commonly encountered mass of the epidural space. Cervical spondylotic myelopathy can cause a characteristic pattern of enhancement, which may be mistaken for an intrinsic myelopathy. A do-not-miss diagnosis of the extradural compartment is idiopathic spinal cord herniation, the appearance of which can overlap with arachnoid cysts and webs. Regarding intrinsic causes of myelopathy, the lesions of multiple sclerosis are characteristically short segment but can be confluent when multiple. Postcontrast MRI can be particularly helpful, including when attempting to differentiate the long-segment myelopathy of neurosarcoidosis and aquaporin-4 (AQP4)-IgG-seropositive neuromyelitis optica spectrum disorder (NMOSD) and when characterizing spinal cord tumors such as primary neoplasms and metastases. Spinal dural arteriovenous fistula is another do-not-miss diagnosis, with characteristic MRI features both precontrast and postcontrast. Tract-specific white matter involvement can be a clue for diseases such as subacute combined degeneration, paraneoplastic myelopathy, and radiation myelitis, whereas gray matter-specific involvement can suggest conditions such as cord infarct, viral myelitis, or myelin oligodendrocyte glycoprotein (MOG)-IgG associated disorder. Knowledge of the neuroimaging findings of the many causes of spinal cord and cauda equina dysfunction is critical for both neurologists and neuroradiologists. A structured approach to lesion compartmental location and imaging feature characterization is recommended.

Myelopathy associated with acute leukemia. Multidisciplinary view on the problem

Leukemia-associated myelitis is a rare but underestimated complication. It has a different etiology associated with both, the main disease and its treatment methods. It requires differential diagnosis with funicular myelosis, polyradiculoneuropathy, tumor and hemorrhagic formation, stroke, dysmetabolic manifestations, as well as with the consequences of treatment of the underlying disease using radiation, cytostatic, targeted therapy.It should also be differentiated from paraneoplastic myelopathy and progression of the underlying disease. However,with the help of neuroimaging methods, it can be detected more recently than a detailed clinical picture appears. A case report of myelopathy in a 31 year old patient with acute lymphoblastic leukemia is presented. Treatment of the underlying disease was carried out with the use of chemotherapy, radiation therapy, allogeneic hematopoietic stem cell transplantation and targeted therapy. The nature of the disease,i.e. recurrent course of acute lymphoblastic leukemia, the variety of treatment methods, and the absence of focal changes in neuroimaging in the zone that determines clinical manifestations, made it necessary to consider a wide range of possible etiological factors for the development of myelopathy. Myelopathy was confirmed by MRI 2.5 months after the debut of neurological symptoms, which corresponds to modern concepts and time criteria for visualization in neurooncology. The article presents the criteria for diagnosing myelopathy, a complication of acute lymphoblastic leukemia. It should also be differentiated from However, with the help of neuroimaging methods, it can be detected more recently than a detailed clinical picture appears.

Myelitis Presenting Anti-Yo Antibody in a Patient with Prostatic Adenocarcinoma

Antineuronal antibody-associated paraneoplastic neurologic syndromes result from tumor-stimulated autoimmune attacks against components of the nervous system. Paraneoplastic myelopathy associated with Purkinje-cell cytoplasmic autoantibody type 1 (anti-Yo) is extremely rare disorder. It is almost exclusively reported in women with gynecological tumors. Even though few cases of anti-Yo-associated paraneoplastic neurologic syndrome related to other cancers are reported, it is a very uncommon condition, especially in males. The author report here the first case of anti-Yo myelopathy with prostatic adenocarcinoma.

Clinical characteristics of patients with paraneoplastic myelopathy

Paraneoplastic myelopathy is rare paraneoplastic neurological syndromes. We reviewed patients through medical records system and screened patients who presented with myelopathy, and/or coexisting cancer, and/or onconeural antibodies. Nine patients were identified as paraneoplastic myelopathy presenting with progressive subacute (2/9) or insidious (7/9) myelopathy. CSF abnormalities included elevated protein, 5; pleocytosis, 4; excess oligoclonal bands, 6. Seven patients had onconeural antibody. Cancer was confirmed histopathologically in 6 and diagnosed by PET-CT in 1. Four patients had symmetric, longitudinally extensive grey matter or tract-specific changes on spinal cord MRI. It was associated with significant morbidity and had poor response to treatment.

An interesting and rare association of paraneoplastic myelopathy with Hurthle cell neoplasm

An interesting and rare association of paraneoplastic myelopathy with Hurthle cell neoplasm

Paraneoplastic myelopathy and ophthalmoplegia secondary to gray zone lymphoma with excellent response to immuno-chemotherapy: Case report

Paraneoplastic myelopathy and ophthalmoplegia secondary to gray zone lymphoma with excellent response to immuno-chemotherapy: Case report

Amphiphysin-positive paraneoplastic myelitis and stiff-person syndrome.

Finding the underlying etiology of transverse myelitis (TM) can be challenging, as several disorders, including multiple sclerosis (MS), neuromyelitis optica, acute disseminated encephalomyelitis, postvaccine myelitis, Sjogren disease, neurosarcoidosis, infectious myelopathies, or idiopathic TM, may be causative.1 Paraneoplastic myelopathy, another differential diagnosis, is associated with a broad range of neoplasms and bears a severe risk to develop disability.2 Stiff-person syndrome (SPS) can occur as a result of some neoplasms and is characterized by skeletal muscle rigidity and spasms.

A Rare Cause of Myelopathy: Anti-Ri (ANNA-2) Associated Paraneoplastic Myelopathy (P6.148)

A Rare Cause of Myelopathy: Anti-Ri (ANNA-2) Associated Paraneoplastic Myelopathy (P6.148)

Longitudinally extensive spinal cord lesion: etiology and imaging features

To explore the etiologies and imaging features of longitudinally extensive spinal cord lesion (LESCL). The etiologies and magnetic resonance (MR) imaging features of 51 hospitalized LESCL patients from January 2011 to August 2013 were reviewed and retrospectively analyzed. Among them, the causes were neuromyelitis optica spectrum disorder (NMOSD, n = 25), isolated longitudinally extensive transverse myelitis (n = 6), subacute combined degeneration (n = 4), multiple sclerosis (MS, n = 3), paraneoplastic myelopathy (n = 3), anterior spinal artery syndrome (n = 3), acute disseminated encephalomyelitis (n = 2), spinal dural arteriovenous fistula (n = 2), intramedullary spinal cord metastasis (n = 1), myelopathic leukemia (n = 1) and syringomyelus (n = 1). For MR imaging, at least one lesion of each patient presented continuously longitudinal profile and whole-length spinal cord was involved in 11 patients. LESCL may be caused by various diseases. And the imaging features may aid its diagnosis despite a lack of specificity.

Poster 307 Paraneoplastic Myelopathy as an Opportunity for Collaborative Palliative Rehabilitation: A Case Report

PM&RVolume 6, Issue 9S p. S291-S291 Saturday Poster Presentations - Poster Hall Poster 307 Paraneoplastic Myelopathy as an Opportunity for Collaborative Palliative Rehabilitation: A Case Report Erin M. Grimsby MD, Erin M. Grimsby MD Medical College of Wisconsin, Milwaukee, WI, United StatesSearch for more papers by this authorAnn Catlett MD, Ann Catlett MD Medical College of Wisconsin, Milwaukee, WI, United StatesSearch for more papers by this authorWilliam Waring MD, William Waring MD Medical College of Wisconsin, Milwaukee, WI, United StatesSearch for more papers by this author Erin M. Grimsby MD, Erin M. Grimsby MD Medical College of Wisconsin, Milwaukee, WI, United StatesSearch for more papers by this authorAnn Catlett MD, Ann Catlett MD Medical College of Wisconsin, Milwaukee, WI, United StatesSearch for more papers by this authorWilliam Waring MD, William Waring MD Medical College of Wisconsin, Milwaukee, WI, United StatesSearch for more papers by this author First published: 29 September 2014 https://doi.org/10.1016/j.pmrj.2014.08.687Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume6, Issue9SSeptember 2014Pages S291-S291 RelatedInformation

Answer to the letter to the editor of R. Nardone et al. concerning “Hepatic myelopathy with spastic paraparesis: report of two cases and review of the literature” (by Sana Ben Amor et al. (2013), Eur Spine J; DOI 10.1007/s00586-013-2828-z)

We would like to thank Drs. R. Nardone et al. for their comments. We are in agreement that the motor evoked potentials (MEP) elicited by transcranial magnetic stimulation may be helpful in the diagnosis of hepatic myelopathy especially in patients with chronic liver disease associated with a portosystemic shunt [1]. But we think that MEP is not specific for this pathology. MEP is a sensitive method to detect abnormalities of corticospinal pathways even in the absence of radiological changes [2]. In the event, myelopathy was the presenting manifestation we think that in such situation MEP could not be helpful for diagnosis of hepatic myelopathy. So, the diagnosis of hepatic myelopathy should be considered when all the other possible diagnoses were ruled out such as infectious or paraneoplastic myelopathy and degenerative diseases [3]. On the other hand, MEP could be abnormal in cirrhotic patients before hepatic encephalopathy is clinically manifesting [4]. This complication is more frequent than hepatic myelopathy in patients with chronic liver disease [1].

First, the flow stopped, then the hair grew and finally, the legs gave away: A case of adrenal carcinoma with paraneoplastic myelopathy

Adrenocortical carcinoma is a rare neoplasm with an incidence of about one case per million population. We present a rare case of an adrenal cortical tumor with paraneoplastic myelopathy and features of virilization and Cushing's disease.

Paraneoplastic isolated myelopathy

To report the clinical phenotype and outcome of isolated paraneoplastic myelopathy. We systematically reviewed clinical, serologic, and MRI data for 31 patients (20 female) who presented with an isolated myelopathy and coexisting cancer: carcinoma (lung, 9; breast, 7; kidney, 2; thyroid, 2; ovary/endometrium, 2), melanoma (2), or other cancer (3), or a paraneoplastic autoantibody with strong cancer association (amphiphysin-immunoglobulin G [IgG], 9; collapsin response-mediator protein 5-IgG, 9; Purkinje-cell cytoplasmic autoantibody type 1, 2; antineuronal nuclear autoantibody [ANNA]-1, 1; ANNA-3, 1). Of 31 patients who presented with a progressive myelopathy, symptom onset was subacute in 16 (52%). The median age was 62 years. CSF abnormalities included elevated protein (>45 mg/dL), 22; pleocytosis, 15; excess oligoclonal bands (normal <4), 7. MRI cord abnormalities identified in 20 patients were longitudinally extensive (>3 vertebral segments), 14; symmetric tract or gray matter-specific signal abnormality, 15 (enhancing in 13). Myelopathy preceded cancer diagnosis in 18 patients (median interval 12 months; range 2-44). After myelopathy onset, 26 patients underwent oncologic treatment, immunosuppressive treatment (median delay to commencing immunotherapy 9.5 months [range 1-54]), or both; only 8 improved (31%). At last neurologic evaluation (median interval after onset 17 months; range 1-165 months), 16 patients (52%) were wheelchair-dependent (median time from onset to wheelchair 9 months [range 1-21]). Ten patients died after a median of 38 months from symptom onset (range 7-152). Symmetric, longitudinally extensive tract or gray matter-specific changes on spinal MRI should raise suspicion for a paraneoplastic myelopathy. Resulting disability is often severe. Only a minority of patients improve with treatment.

Lymphoma-related resolving paraneoplastic myelopathy with MRI correlation

We present here a case of paraneoplastic myelopathy with significant cord abnormality documented on MRI. Following treatment of the patient's underlying haematological malignancy, there was marked improvement both symptomatically and on follow-up MR imaging. This has rarely been described in the literature in relation to lymphoma or with imaging correlation.

A case of paraneoplastic myelopathy associated with the neuromyelitis optica antibody

A 63-year-old woman with a history of metastatic breast cancer presented to the emergency department with chest pain in a band-like distribution. Within 1 day of presentation the patient developed bilateral lower-extremity weakness and urinary retention. The emergence of these symptoms coincided with the recurrence of her metastatic breast cancer. Fifteen months before presentation the patient had experienced a similar episode of myelopathy in the setting of recurrence of her breast cancer, from which she recovered completely following treatment with steroids. General and neurological examination, routine laboratory testing, MRI of the brain and spine, tests for serum autoimmune antibodies, infectious serology testing, lumbar puncture, paraneoplastic panel, neuromyelitis optica antibody testing, evaluation for celiac disease, CT scans of the chest, abdomen and pelvis, whole-body [(18)F]fluoro-2-deoxyglucose PET scan, lymph node biopsy, electroencephalography observing visual and brainstem auditory evoked potentials, and neuro-ophthalmological examination. Myelopathy, possibly paraneoplastic, associated with the neuromyelitis optica antibody in the setting of metastatic breast cancer. Corticosteroids to treat the myelopathy and chemotherapy for the breast cancer.