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REVIEW: MANAGEMENT UPDATES (REVIEWS ON ADVANCES IN TREATMENT)
Year : 2012  |  Volume : 15  |  Issue : 1  |  Page : 6-12
 

Paraneoplastic neurologic syndrome: A practical approach


Department of Neurology, Mayo Clinic, Rochester, MN, USA,

Date of Submission05-Jul-2011
Date of Decision13-Nov-2011
Date of Acceptance12-Dec-2011
Date of Web Publication29-Feb-2012

Correspondence Address:
Sudheeran Kannoth
Puthiyadavan House, (PO) Bengalam, (Via) Nileshwar, Kasargod District, Kerala 671314, India

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DOI: 10.4103/0972-2327.93267

PMID: 22412264

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   Abstract 

Paraneoplastic neurological syndromes (PNS) are rare disorders associated with cancer, not caused by direct invasion, metastasis or consequences of treatment. They are usually autoimmune in nature. Often, PNS precedes the manifestations of cancer. Onconeural antibodies are important in the diagnosis and management of these disorders. These antibodies are specific for the malignancy rather than for a particular neurological syndrome. Often, there are different antibodies associated with the same syndrome. Multiple antibodies are also known to coexist in a given patient with malignancy. While investigating a patient for suspected PNS, the entire gamut of onconeural antibodies should be investigated so as not to miss the diagnosis. In 30-40% of the cases, PNS can occur without antibodies. Investigations for identifying the underlying cancer can be directed by the antibody panel. If conventional screening for cancer is negative, a positron emission scanning/computed tomography scan can be useful. Patients need follow-up surveillance for cancer if not detected in the first instance. Cancer detection and treatment, immunotherapy and supportive care are important components of treatment of PNS. Immunotherapy is very effective in PNS associated with cell membrane-associated antibodies like voltage-gated potassium channel complex, NMDA receptor antibodies and voltage-gated calcium channel antibodies. Immunotherapy includes steroids, IVIgG, plasmaphereis, cytotoxic medications and rituximab. Supportive therapy includes symptomatic treatment with antiepileptic and analgesic medications, physiotherapy, speech therapy and occupational therapy. PNS can mimic any neurologic syndrome. A high index of clinical suspicion is important for early diagnosis and prompt management and better outcome.


Keywords: Immunotherapy, onconeural antibodies, paraneoplastic neurological syndrome, paraneoplastic antibodies


How to cite this article:
Kannoth S. Paraneoplastic neurologic syndrome: A practical approach. Ann Indian Acad Neurol 2012;15:6-12

How to cite this URL:
Kannoth S. Paraneoplastic neurologic syndrome: A practical approach. Ann Indian Acad Neurol [serial online] 2012 [cited 2014 Jul 29];15:6-12. Available from: http://www.annalsofian.org/text.asp?2012/15/1/6/93267



   Introduction Top


Paraneoplastic neurological syndromes (PNS) are rare, but are potentially treatable. These disorders are associated with cancer, but are not caused by the direct tumor invasion, metastasis or consequences of treatment. [1] They can affect any area of the nervous system, including the central, peripheral and autonomic nervous system. Although the system involvement is often multifocal, like encephalomyelitis, it can involve a single system, e.g. cerebellar degeneration. Mainly, the PNS precede or follow the cancer diagnosis, although, in some cases, the primary cancer is not found even at autopsy. [2]

The first description of PNS was in the 19 th century by a French physician M Auche` who described the peripheral nervous system involvement in cancer patients in 1890. [3] The first antibody described was PCA-1 (Purkinje Cell Antibody 1), by Greenlee and Brashear in 1983, in two patients with ovarian carcinoma and paraneoplastic cerebellar degeneration. [4] More syndromes and antibodies have been subsequently described and the list of the syndromes and antibodies continue to increase day by day.

Pathophysiology

PNS are mainly autoimmune. [1] When the body tries to eliminate tumor cells, it launches an immune response, and this response can target normal neural tissues. [5] This could be mediated by antibodies or by T-cells. Thus, most of the PNS reflect a nervous system-specific autoimmune attack initiated by onconeural antigens released to the peripheral lymphoid tissue from an unsuspected primary or recurrent neoplasm.­ [2] Frequently, a cerebrospinal fluid (CSF) study in these patients reveals lymphocytic pleocytosis, elevated protein, increased IgG synthesis and oligoclonal bands, supporting the immunological pathology. In a recent European study, abnormal CSF was found in 93% of the cases; pleocytosis in 39%, elevated protein in 67% and oligoclonal bands (OCB) in 63%. OCBs were the only abnormality in 10%. [6] Antibodies targeted against an accessible membrane target is directly responsible for the disease, as in the case of acetyl choline receptor (AChR) antibodies in myasthenia gravis, P/Q type of voltage-gated calcium channels (VGCC) in Lambert Eaton Myasthenic syndrome (LEMS) and encephalitis associated with anti-NMDA receptor antibodies. It has been documented that tumor outcome is better among patients with paraneoplastic syndromes. [7] Often, the cancer is asymptomatic at the time of presentation with neurological syndrome. Some of the paraneoplastic antibodies are specifically associated with cancer and some are not.

Incidence and prevalence

The exact incidence and prevalence of these disorders are unknown. PNS are a rare clinical condition. The prevalence of these disorders varies from cancer to cancer. For example, PNS can occur in 2-3% of the patients with neuroblastoma or small cell lung carcinoma (SCLC) and in 30-50% of the patients with thymoma and sclerotic myeloma. Overall, it is estimated that 0.5-1% of all patients with cancer have clinically disabling PNS. [1]

Clinical features

PNS can affect any region of the nervous system. PNS can present with multiple clinical manifestations like encephalitis, autonomic failure, peripheral neuropathy, cerebellar ataxia, visual complains and many others. There can be multiple antibodies in a patient. [5] [Table 1] gives the common classical paraneoplastic syndromes with clinical features and investigations. [8] Based on the evidence accumulated over the last two decades, recognition of a classical neurologic syndrome associated with single antibody is an exception rather than a rule. [2] Usually, the onset is subacute. In approximately 60% of the cases, PNS precedes tumor [Table 1]. [1]
Table 1: Clinical syndromes[8]

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Clues to diagnosis

History or family history of cancer should alert the clinician regarding this diagnostic possibility. Medical history or family history of autoimmune diseases can be a clue to paraneoplastic neurologic autoimmunity. Subacute presentation and multiple-level involvement of neuraxis is common. The diagnosis of paraneoplastic disorder should be considered in a subacute onset and insidiously progressive neurologic condition where no clear alternate diagnosis is possible [Table 2].
Table 2: Neurological manifestations of paraneoplastic syndromes at different levels of neuraxis[2]

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Nomenclature of antibodies

Autoantibodies are classified as nuclear, cytoplasmic and cell membrane based on the predominant location of reactivity to the nervous tissue. The nomenclatures used by different groups vary. Lennon [9] proposed the generic nomenclature, which is based on immune-staining characteristics (nuclear or cytoplasmic) and chronological order of discovery (like ANNA 1, 2, 3). Similar naming was used by the groups who described the first antibody - anti-Purkinje cell and antineuronal nuclear antibody. Later, other names like Hu and Yo were introduced. [2]


   Diagnosis Top


Early diagnosis and treatment is important because any delay can result in rapid progression and irreversible neurological damage. Diagnosing PNS is often difficult. One of the reasons for the difficulty in diagnosis is presentation of the PNS before the malignancy becomes clinically overt. Other reasons are the absence of a particular clinical pattern and absence of imaging and laboratory abnormalities that are specific for PNS. Biopsies are invasive, difficult and nonspecific. A combination of clinical and laboratory evaluations has to be deployed to reach diagnosis early. Treatment of underlying cancer is important in the treatment of the neurological condition. High index of clinical suspicion is essential to achieve this goal. Past or family history of cancer is important in this regard. Presence of systemic symptoms like anorexia, weight loss, fever, fatigue and dysguesia are all important nonneurological clues. CSF often exhibit nonspecific abnormalities such as mild to moderate lymphocytic pleocytosis, elevated protein and OCBs [Table 3], [Table 4] and [Table 5].
Table 3: Oncological associations of paraneoplastic antibodies[2],[14]

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Table 4: Clinical and laboratory clues for paraneoplastic neurological syndromes (other than onconeural antibodies)

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Table 5: Magnetic resonance imaging finding in paraneoplastic neurological syndromes

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Onconeuronal antibodies are helpful for the diagnosis [Table 3]. Presence of these autoantibodies, alone or in combination, helps to detect the tumor as they are more tumor specific than for neurological syndrome. This can guide the search for the primary cancer. These antibodies establish the autoimmune nature of the disease, helping the clinician to differentiate the new neurological symptoms of PNS from treatment related-complications like toxic neuropathies, metastasis or infiltration. They are of help in detecting the recurrence of the disease in already seropositive patients.

The limitations for the paraneoplastic antibody evaluation are that only 60-70% will have detectable antibodies and that they can be seen in patients without PNS. In general, it is almost always preferable to look for the entire range of antibodies than for one or two specific ones. This is because the same clinical syndrome is associated with multiple antibodies. [5] The practice of ordering a single antibody can result in missing the potential cases. Also, there could be multiple antibodies, which predict the type of cancer better than the presence of a single antibody [Figure 1].For example, a bundle of positive antibodies - CRMP-5 IgG, antistriational muscle antibody, anti-AChR binding and modulating, voltage gated potassium channel antibodies (VGKC) in a given patient, almost always indicates presence of a thymoma while if CRMP-5 IgG alone is detected, multiple cancers have to be looked for. CSF antibody testing is encouraged along with serum testing as there are occasions where the serum is negative and CSF has been positive.
Figure 1: Algorithm for diagnosis and management of paraneoplastic neurological syndromes

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In PNS, 15% of the patients can have an unrelated additional neoplasm. [2] Therefore, if there is an obvious neoplasm, but not the one predicted by the onconeural antibodies, search should be continued for the tumor that is predicted by the antibodies. Usually, tumor is in a limited stage and needs extensive imaging for detection. Positron emission tomography (PET)/computed tomography (CT) is useful when the cancer is not detected by any other imaging modality. In 39% of the cases, tumors were detected with PET/CT when other modalities failed to detect it. [10] Mammograms are very useful, especially when PCA-1, ANNA-2 and amphiphysin antibodies are positive. Transvaginal ultrasound is an important screen for ovarian and Mullerian cancers. Even the small or suspicious abnormalities have to be pursued diligently in the presence of a positive antibody and PNS. Every attempt should be made to pursue tissue diagnosis. Even if the patient is tumor free in the initial evaluation, he/she has to be followed-up for a significant period, perhaps up to 4 years. [11] In cerebellar degeneration with PCA-1 positivity and negative mammogram, exploratory laprotomy is recommended if ovarian and Mullerian neoplasm are not otherwise detected. [12] Testicular ultrasound is an important part of the evaluation in males less than 40 years with suspected PNS, even if anti-Ma antibody is negative.

Treatment

Treatment of PNS includes treatment of the tumor, immunotherapy and supportive therapy. The best way to stabilize PNS is to treat the cancer as soon as possible. This includes surgical removal of tumor, chemotherapy and/or radiotherapy. There are no evidence-based recommendations available regarding the immunosuppressive therapy.

Immunotherapy includes steroids, intravenous immune globulins (IV IgG), plasma exchange, cyclophosphamide, azathioprine and rituximab. Those PNS mediated by antibody are more reversible; for example, PNS mediated by VGKC complex antibodies, AChR antibodies and NMDA receptor antibodies. In disorders with intracellular target antigens and a strong cellular immune reaction, damage is more severe and often irreversible. The common approach used in the autoimmune neurology clinic of Mayo Clinic is high-dose intravenous methyl prednisolone therapy. One gram of methyl prednisolone is administered intravenously for 5 days followed by weekly therapy of the same dose for 6-12 weeks. If there is response to trial therapy, medications like mycophenalate mophetyl or azathioprine can be considered for long-term immunosuppression. On the other hand, if there is no response, plasma exchange should be the next line in antibody-mediated disease. Other options include immunosuppression with cyclophosphamide. Rituximab may be useful in antibody-mediated diseases. Patient may need long-term treatment. For an individual patient, duration of treatment is usually determined by clinical response.

In anti-NMDAR encephalitis, Dalmau [13] has proposed a combined treatment as first-line -intravenous methyl prednisolone with IVIgG or plasma exchange. If there is good response to this, chronic immunosuppression with azathioprine or mycophenalate is recommended for 1 year. If there is no response, rituximab or cyclophosphamide, or both combined, should be given. If there is no response for the combined therapy of rituximab and cyclophosphamide, an alternate immunosuppressive like oral or intravenous methotrexate should be considered.

Supportive therapy includes symptomatic treatment like analgesics, antiepileptics, psychiatric medications, dysautonomia medications, physiotherapy, occupational therapy and speech and swallowing therapy. Respiratory support and nutritional support are important. 3, 4 diaminopyridine is used for symptomatic treatment of LEMS. Anticholinesterase inhibitors are used in the treatment of myasthenia gravis. Diazepam is used in Stiff Person Syndrome. Clonazepam and sodium valproate are administered in opsoclonus myoclonus. [41]

 
   References Top

1.Dalmau J, Rosenfeild MR. Paraneoplastic Neurologic syndromes. In: Harrison's Principles of Internal Medicine. 17 th ed. In: Fauci, Braunwald, Kasper, et al. editors. Vol. 1. New York: McGraw Hill Medical; 2008. p. 623-7.  Back to cited text no. 1
    
2.Lachance DH, Lennon VA. Paraneoplastic neurological autoimmunity In Neuroimmunology in Clinical Practice. In: Kalman B, Brannagan TH 3rd, editors. Oxford: Blackwell Publishing; 2008. p. 210-7.  Back to cited text no. 2
    
3.Auche M. Des nevrites peripheriques chez les cancereux. Rev Med 1890;10:785-807.  Back to cited text no. 3
    
4.Greenlee JE, Brashear HR. Autoantibodies to cerebellar Purkinje cells in patients with paraneoplastic cerebellar degeneration and ovarian carcinoma. Ann Neurol 1983;14:609.  Back to cited text no. 4
[PUBMED]    
5.Pittock SJ, Kryzer TJ, Lennon VA. Paraneoplastic antibodies coexist and predict cancer, not neurological syndrome. Ann Neurol 2004;56:715-9.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Psimaras D, Carpentier AF, Rossi C; PNS Euronetwork. Cerebrospinal fluid study in paraneoplastic syndromes. J Neurol Neurosurg Psychiatry 2010;81:42-5.  Back to cited text no. 6
[PUBMED]  [FULLTEXT]  
7.Pittock SJ, Lennon VA. Paraneoplastic autoimmunity affecting the nervous system. In Brain tumors practical guide to diagnosis and treatment. In: Baehring JM, Piepmeier JM, editors. New York NY: Informa Healthcare; 2007. p. 515-39.  Back to cited text no. 7
    
8.Gozzard P, Maddison P. Republished: Which antibody and which cancer in which paraneoplastic syndromes? Postgrad Med J 2011;87:60-70.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Lennon VA. Paraneoplastic autoantibodies: The case for a descriptive generic nomenclature. Neurology 1994;44:2236-40.  Back to cited text no. 9
[PUBMED]    
10.McKeon A, Apiwattanakul M, Lachance DH, Lennon VA, Mandrekar JN, Boeve BF, et al. Positron emission tomography-computed tomography in paraneoplastic neurologic disorders: Systematic analysis and review. Arch Neurol 2010;67:322-9.   Back to cited text no. 10
[PUBMED]  [FULLTEXT]  
11.Titulaer MJ, Soffietti R, Dalmau J, Gilhus NE, Giometto B, Graus F, et al. Screening for tumours in paraneoplastic syndromes: Report of an EFNS task force. Eur J Neurol 2011;18:19-e3.  Back to cited text no. 11
[PUBMED]  [FULLTEXT]  
12.Dalmau JO, Posner JB Paraneoplastic syndromes. Arch Neurol 1999;56:405-8.  Back to cited text no. 12
    
13.Dalmau J, Lancaster E, Martinez-Hernandez E, Rosenfeld MR, Balice-Gordon R. Clinical experience and laboratory investigations in patients with anti-NMDAR encephalitis. Lancet Neurol 2011;10:63-74.  Back to cited text no. 13
[PUBMED]  [FULLTEXT]  
14.Rosenfeld MR, Dalmau J. Update on paraneoplastic and autoimmune disorders of the central nervous system. Semin Neurol 2010;33:320-31.  Back to cited text no. 14
    
15.Lucchinetti CF, Kimmel DW, Lennon VA. Paraneoplastic and oncological profiles of patients seropositive for type 1 anti-neuronal nuclear auto antibodies. Neurology 1998;50:652-7.  Back to cited text no. 15
[PUBMED]    
16.Pittock SJ, Lucchinetti CF, Lennon VA. Anti-neuronal nuclear autoantibody type 2: Paraneoplastic accompaniments. Ann Neurol 2003;53:580-97.   Back to cited text no. 16
[PUBMED]  [FULLTEXT]  
17.Chan KH, Vernino S, Lennon VA. ANNA-3 anti-neuronal nuclear antibody: Marker of lung cancer-related autoimmunity. Ann Neurol 2001;50:301-11.  Back to cited text no. 17
[PUBMED]    
18.Graus F, Vincent A, Pozo-Rosich P, Sabater L, Saiz A, Lang B, et al. Antiglial nuclear antibody: Marker of lung cancer - related paraneoplastic neurological syndromes. J Neuroimm 2005;165:166-71.  Back to cited text no. 18
    
19.Dalmau J, Graus F, Villarejo A, Posner JB, Blumenthal D, Thiessen B, et al. Clinical analysis of anti- Ma-2associated encephalitis. Brain 2004;127:1831-44.  Back to cited text no. 19
[PUBMED]  [FULLTEXT]  
20.Bataller L, Wade DF, Graus F, Stacy HD, Rosenfeld MR, Dalmau J. Antibodies to Zic4 in paraneoplastic neurological disorders and small-cell lung cancer. Neurology 2004;62:778-82.  Back to cited text no. 20
    
21.Peterson K, Rosenblum MK, Kotanides H, Posner JB. Paraneoplastic cerebellar degeneration. I. A clinical analysis of 55 anti-Yo antibody-positive patients. Neurology 1992;42:1931-7.  Back to cited text no. 21
    
22.Vernino S, Lennon VA. New Purkinje cell antibody (PCA-2): Marker of lung cancer-related neurological autoimmunity. Ann Neurol 2000;47:297-305.  Back to cited text no. 22
[PUBMED]    
23.Bernal F, Shams'ili S, Rojas I, Sanchez-Valle R, Saiz A, Dalmau J, et al. Anti-Tr antibodies as markers of paraneoplastic cerebellar degeneration and Hodgkin's disease. Neurology 2003;60:230-4.  Back to cited text no. 23
[PUBMED]  [FULLTEXT]  
24.Pittock SJ, Lucchinetti CF, Parisi JE, Benarroch EE, Mokri B, Stephan CL, et al. Amphiphysin autoimmunity: Paraneoplastic accompaniments. Ann Neurol 2005;58:96-107.  Back to cited text no. 24
[PUBMED]  [FULLTEXT]  
25.Yu Z, Kryzer TJ, Griesmann GE, Kim K, Benarroch EE, Lennon VA. CRMP-5 neuronal autoantibody: Marker of lung cancer and thymoma-related autoimmunity. Ann Neurol 2001;49:146-54.  Back to cited text no. 25
[PUBMED]    
26.Cross SA, Salomao DR, Parisi JE, Kryzer TJ, Bradley EA, Mines JA, et al. Paraneoplastic autoimmune optic neuritis with retinitis defined by CRMP-5-IgG. Ann Neurol 2003;54:38-50.  Back to cited text no. 26
[PUBMED]  [FULLTEXT]  
27.Lennon VA, Kryzer TJ, Griesmann GE, O'Suilleabhain PE, Windebank AJ, Woppmann A, et al. Calcium-channel antibodies in the Lambert-Eaton syndrome and other paraneoplastic syndromes. N Engl J Med 1995;332:1467-74.  Back to cited text no. 27
[PUBMED]  [FULLTEXT]  
28.Vernino S, Lennon VA. Autoantibody profiles and neurological correlations of thymoma. Clin Can Res 2004;10:7270-5.  Back to cited text no. 28
    
29.Vernino S, Adamski J, Kryzer TJ, Fealey RD, Lennon VA. Neuronal nicotinic ACh receptor antibody in subacute autonomic neuropathy and cancer-related syndromes. Neurology 1998;50:1806-13.  Back to cited text no. 29
[PUBMED]    
30.Thieben MJ, Lennon VA, Boeve BF, Aksamit AJ, Keegan M, Vernino S. Potentially reversible autoimmune limbic encephalitis with neuronal potassium channel antibody. Neurology 2004;62:1177-82.  Back to cited text no. 30
[PUBMED]  [FULLTEXT]  
31.Vincent A, Buckley C, Schott JM, Baker I, Dewar BK, Detert N, et al. Potassium channel antibody-associated encephalopathy: A potentially immunotherapy-responsive form of limbic encephalitis. Brain 2004;127:701-12.  Back to cited text no. 31
[PUBMED]  [FULLTEXT]  
32.Irani SR, Alexander S, Waters P, Kleopa KA, Pettingill P, Zuliani L, et al. Antibodies to Kv1 potassium channel-complex proteins leucine-rich, glioma inactivated 1 protein and contactin-associated protein-2 in limbic encephalitis, Morvan's syndrome and acquired neuromyotonia. Brain 2010;133:2734-48.  Back to cited text no. 32
[PUBMED]  [FULLTEXT]  
33.Lai M, Huijbers MG, Lancaster E, Graus F, Bataller L, Balice-Gordon R, et al. Investigation of LGI1 as the antigen in limbic encephalitis previously attributed to potassium channels: A case series. Lancet Neurol 2010;9:776-85.   Back to cited text no. 33
[PUBMED]  [FULLTEXT]  
34.Vitiliani R, Mason W, Ances B, Zwerdling T, Jiang Z, Dalmau J. Paraneoplastic encephalitis, psychiatric symptoms, and hypoventilation in ovarian teratoma. Ann Neurol 2005;58:594-604.  Back to cited text no. 34
    
35.Irani SR, Bera K, Waters P, Zuliani L, Maxwell S, Zandi MS, et al. N-methyl-D-aspartate antibody encephalitis: Temporal progression of clinical and paraclinical observations in a predominantly non-paraneoplastic disorder of both sexes. Brain 2010;133:1655-67.  Back to cited text no. 35
[PUBMED]  [FULLTEXT]  
36.Dalmau J, Gleichman AJ, Hughes EG, Rossi JE, Peng X, Lai M, et al. Anti-NMDA-receptor encephalitis: Case series and analysis of the effects of antibodies. Lancet Neurol 2008;7:1091-8.   Back to cited text no. 36
    
37.Lai M, Hughes EG, Peng X, Zhou L, Gleichman AJ, Shu H, et al. AMPA receptor antibodies in limbic encephalitis alter synaptic receptor location. Ann Neurol 2009;65:424-34.  Back to cited text no. 37
[PUBMED]  [FULLTEXT]  
38.Lancaster E, Lai M, Peng X, Hughes E, Constantinescu R, Raizer J, et al. Antibodies to the GABA (B) receptor in limbic encephalitis with seizures: Case series and characterisation of the antigen. Lancet Neurol 2010;9:67-76.  Back to cited text no. 38
[PUBMED]  [FULLTEXT]  
39.Hutchinson M, Waters P, McHugh J, Gorman G, O'Riordan S, Connolly S, et al. Progressive encephalomyelitis, rigidity, and myoclonus: A novel glycine receptor antibody. Neurology 200871:1291-2.  Back to cited text no. 39
    
40.Sillevis Smitt P, Kinoshita A, De Leeuw B, Moll W, Coesmans M, Jaarsma D, et al. Paraneoplastic cerebellar ataxia due to autoantibodies against a glutamate receptor. N Engl J Med 2000;342:21-7.  Back to cited text no. 40
[PUBMED]  [FULLTEXT]  
41.Flanagan EP, McKeon A, Lennon VA, Kearns J, Weinshenker BG, Krecke KN, et al. Paraneoplastic isolated myelopathy: Clinical course and neuroimaging clues. Neurology 2011;76:2089-95.  Back to cited text no. 41
[PUBMED]  [FULLTEXT]  


    Figures

  [Figure 1]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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