Relevant bibliographies by topics / Paraneoplastic neurological syndromes

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Paraneoplastic neurological syndromes'

Author: Grafiati
Published: 21 December 2024

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Journal articles on the topic "Paraneoplastic neurological syndromes"

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Pathirana, KD. "Paraneoplastic neurological syndromes." Ceylon Medical Journal 53, no. 4 (January 26, 2009): 148. http://dx.doi.org/10.4038/cmj.v53i4.290.

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Chad, David A., and Lawrence D. Recht. "Neurological Paraneoplastic Syndromes." Cancer Investigation 6, no. 1 (January 1988): 67–82. http://dx.doi.org/10.3109/07357908809077030.

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Bashir, R., and F. Hochberg. "Paraneoplastic Neurological Syndromes." Cancer Investigation 6, no. 1 (January 1988): 117–18. http://dx.doi.org/10.3109/07357908809077035.

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Nath, U., and R. Grant. "Neurological paraneoplastic syndromes." Journal of Clinical Pathology 50, no. 12 (December 1, 1997): 975–80. http://dx.doi.org/10.1136/jcp.50.12.975.

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Sutton, Ian. "Paraneoplastic neurological syndromes." Current Opinion in Neurology 15, no. 6 (December 2002): 685–90. http://dx.doi.org/10.1097/00019052-200212000-00005.

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Sutton, Ian. "Paraneoplastic neurological syndromes." Current Opinion in Neurology 15, no. 6 (December 2002): 685–90. http://dx.doi.org/10.1097/01.wco.0000044764.39452.64.

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Leypoldt, F., and K. P. Wandinger. "Paraneoplastic neurological syndromes." Clinical & Experimental Immunology 175, no. 3 (February 4, 2014): 336–48. http://dx.doi.org/10.1111/cei.12185.

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Dalmau, Josep O., and Jerome B. Posner. "Neurological Paraneoplastic Syndromes." Neuroscientist 4, no. 6 (November 1998): 443–53. http://dx.doi.org/10.1177/107385849800400616.

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Smitt, Peter Sillevis. "Paraneoplastic neurological syndromes." Lancet Neurology 1, no. 7 (November 2002): 408. http://dx.doi.org/10.1016/s1474-4422(02)00218-1.

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Graus, Francesc, and Josep Dalmau. "Paraneoplastic neurological syndromes." Current Opinion in Neurology 25, no. 6 (December 2012): 795–801. http://dx.doi.org/10.1097/wco.0b013e328359da15.

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Dissertations / Theses on the topic "Paraneoplastic neurological syndromes"

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Villagrán-García, Macarena. "Clinical-immunological characterization and immune tolerance breakdown in paraneoplastic neurological syndromes associated with Hu antibodies." Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10259.

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Les syndromes neurologiques paranéoplasiques (SNP) associés aux anticorps Hu sont, généralement, associés à des cancers du poumon à petites cellules (CPPC). Le spectre clinique des Hu-SNP est très hétérogène, et la base immunologique de cette hétérogénéité n’est pas connue. De plus, seule une minorité de patients CPPC développent des Hu-SNP, la raison en est également inconnue. Ce projet de thèse vise à phénotyper les patients Hu-SNP et à explorer leurs caractéristiques biologiques, ainsi que les spécificités génomiques et transcriptomiques de leurs CPPC. Dans un premier temps, une classification hiérarchique a identifié trois groupes chez 466 individus Hu-SNP: atteinte du système nerveux central (SNC), neuropathie isolée et phénotypes mixtes SNC/périphériques. La survie était similaire dans les trois groupes, principalement déterminée par l’évolution du cancer, mais la dysautonomie influençait la mortalité neurologique. Les atteintes du tronc cérébral entraînaient une dysautonomie cardiovasculaire fatale ou une hypoventilation centrale, tandis que l'atteinte neurologique périphérique entraînait des troubles gastro-intestinaux ou sécrétoires, sans risque accru de mortalité. Nous avons aussi étudié des patients ayant développé des Hu-SNP après un traitement par inhibiteurs de checkpoint immunitaire (ICI). Ces patients, cliniquement indistinguables des cas spontanés, suggéraient que les ICI pourraient induire des Hu-SNP. Dans une deuxième partie, le génotypage de 100 patients a confirmé une association avec l'haplotype DR3~DQ2, essentiellement chez les patients avec neuropathie sensitive et absent chez les patients ayant une atteinte exclusive du SNC. Le séquençage par immunoprécipitation de phages a évalué la réactivité des épitopes des anticorps Hu ainsi que d'autres autoanticorps dans le sérum et/ou LCR de 210 patients. Aucune association n'a été trouvée avec l'épitote dominant Hu, mais la réactivité des épitopes différait entre le sérum et le LCR chez 75 % des échantillons appariés. Cette variation était liée au moment du prélèvement et au phénotype: les patients avec des épitopes divergents avaient des LCR prélevés plus tard, tandis que ceux avec des épitopes similaires avaient toujours une atteinte du SNC. Nous avons aussi identifié des réactivités contre d'autres protéines, certaines dans le sérum et/ou LCR, et certaines étaient corrélées à des phénotypes cliniques spécifiques. Enfin, nous avons examiné les caractéristiques moléculaires du CPPC de patients Hu-, GABAbR-SNP et témoins. Nous n’avons trouvé aucune mutation, gain, délétion ou surexpression dans les gènes Hu des patients Hu-SNP. Cependant, un profil transcriptomique distinct, avec des gènes surexprimés liés aux processus immunitaires, caractérisait les tumeurs des Hu-SNP. Nous avons aussi identifié des gènes spécifiquement surexprimés dans le CPPC des patients avec neuropathie sensitive, certains liés à l'axonogenèse et au développement de la neuropathie. Nos résultats suggèrent que plusieurs facteurs contribuent à la variabilité clinique des Hu-SNP, notamment un large spectre d'autoantigènes. Ceux-ci peuvent être liés aux profils d'expression génique dans le CPPC, certains gènes associés à l'axonogenèse étant surexprimés chez les patients ayant une neuropathie sensitive. Une prédisposition génétique pourrait également favoriser certains phénotypes, comme l'indique l'association DR3~DQ2 avec la neuropathie sensitive. La compartimentation au sein du système nerveux pourrait également contribuer: la plupart des patients ciblaient différents épitopes Hu dans leur sérum et dans leur LCR, avec certains autoantigènes plus spécifiques au LCR. Enfin, les altérations des gènes Hu dans le CPPC ne semblent pas participer à la rupture de tolérance immune, mais un profil transcriptomique distinct et les ICI pourraient y contribuer. Ce travail fait progresser la compréhension des Hu-SNP et ouvre la voie de futures recherches sur les mécanismes de l'immunité paranéoplasique
Hu antibodies, the most common in paraneoplastic neurological syndromes (PNS), strongly indicate small-cell lung cancer (SCLC). The clinical spectrum of Hu-PNS is diverse, most patients develop multifocal central, peripheral, and/or autonomic nervous system dysfunction. Despite extensive research, questions remain, namely regarding the immunological basis of clinical heterogeneity and why only a minority of SCLC patients develop Hu-PNS. Our PhD project aims to phenotype Hu-PNS patients, explore the immunogenetics and humoral responses underlying neurological phenotypes, and the genomic and transcriptomic features of their SCLC. First, we described 466 Hu-PNS patients. Hierarchical clustering identified three groups: patients with central nervous system (CNS) involvement; isolated neuropathy; and mixed CNS/peripheral phenotypes. Overall survival was similar across groups, primarily determined by cancer, but dysautonomia, present in 26% of patients, significantly influenced neurological mortality. Prominent CNS dysfunction led to fatal cardiovascular dysautonomia or central hypoventilation, while peripheral involvement was associated with gastrointestinal or secretomotor alterations, without increased mortality risk. We also characterized patients who developed neurological syndromes with Hu antibodies after immune checkpoint inhibitor (ICI) treatment. These patients were clinically indistinguishable from spontaneous cases and shared a strong association with SCLC, suggesting ICIs may induce Hu-PNS. Second, we immunologically investigated neurological phenotypes using two approaches. HLA genotyping of 100 patients confirmed an association with the DR3~DQ2 haplotype, particularly in patients with sensory neuropathy, and absent in those with only CNS involvement. Phage immunoprecipitation sequencing was used to evaluate Hu antibody epitope reactivity and other autoantibodies in serum and/or CSF of 210 patients. We found no direct clinical association with the Hu dominant epitope, but epitope reactivity differed between serum and CSF in 75% of patients with paired samples. This variation correlated with sample timing and phenotype: CSF from patients with differing serum/CSF epitopes was collected later after PNS onset, while patients with serum/CSF consistent epitope reactivity always had CNS phenotypes. In addition, we identified reactivities to other proteins, some more specific to serum or CSF, and a subset linked to specific phenotypes. Third, we examined SCLC molecular features of Hu-, GABAbR-PNS and control patients. Next-generation sequencing, copy number variation analysis, and bulk-RNA sequencing revealed no mutations, gains, deletions, or overexpression in the Hu gene family of Hu-PNS SCLC. However, a distinct transcriptomic profile with upregulated genes largely related to immune system processes characterized these tumors. We also identified specific genes upregulated in the SCLC of patients with sensory neuropathy, some of which were linked to axonogenesis and neuropathy development. Our findings suggest multiple factors contribute to Hu-PNS clinical variability, particularly a broad range of additional autoantigens. These may be partly driven by gene expression patterns in SCLC, as some upregulated genes in patients with sensory neuropathy were linked to axonogenesis. Genetic predisposition may also favor specific phenotypes, as the DR3~DQ2 haplotype was associated with sensory neuropathy. Compartmentalization within the nervous system could further contribute, as most patients targeted different Hu epitopes in serum and CSF, and some autoantigens were more specific to CSF. Finally, Hu genes alterations in SCLC are unlikely causes of neoantigenicity, while a distinct immune-related gene profile and ICIs could contribute to immune tolerance breakdown. This work advances understanding of Hu-PNS complexity and paves the way for further studies into the immunological and molecular drivers of paraneoplastic immunity
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Gebauer, Christina. "The Janus face of immunity : how anti-tumor immunity leads to autoimmunity in paraneoplastic neurological diseases." Thesis, Toulouse 3, 2016. http://www.theses.fr/2016TOU30139/document.

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Les syndromes neurologiques paranéoplasiques (SNP) sont des maladies neurologiques rares, associés à une réponse immunitaire efficace contre un cancer sous-jacent exprimant un antigène également exprimé par des cellules du système nerveux central (SNC). Le cancer déclenche alors une réponse auto-immune secondaire qui provoque la destruction des cellules du SNC. Certains travaux récents suggèrent que l'immunité à médiation cellulaire associée à des auto-anticorps reconnaissant des antigènes intracellulaires pourrait jouer un rôle majeur, bien qu'encore mal compris, dans la physiopathologie des SNP. Les exemples de SNP les plus représentatifs sont le syndrome Hu, qui conduit à la perte de diverses populations de neurones du SNC et l'ataxie cérébelleuse subaiguë (PCD en anglais, pour Paraneoplastic Cerebellar Degeneration), caractérisée par la perte sélective des cellules de Purkinje du cervelet. Alors que le syndrome Hu se développe en général chez des patients présentant des tumeurs du poumon à petites cellules qui expriment l'antigène HuD spécifique des neurones, la majorité des patients souffrant de PCD présente un cancer gynécologique qui exprime la protéine CDR2, également exprimée dans les cellules de Purkinje. Afin de mieux cerner la physiopathologie des SNP et de tester l'implication de l'immunité cellulaire, notamment des lymphocytes T, nous avons durant ma thèse développé et analysé deux modèles murins, l'un pour le syndrome Hu et l'autre pour la PCD. Ces modèles reposent sur l'utilisation de souches de souris génétiquement modifiées : la souris CamK-HA, qui exprime l'hémagglutinine (HA) du virus de la grippe dans la plupart de ses neurones du SNC et la souris L7-HA dans laquelle la protéine HA est exprimée exclusivement par les cellules de Purkinje du cervelet. Dans ces souris, une réponse anti-tumorale est provoquée par l'injection de cellules tumorales 4T1 exprimant HA (4T1-HA). Afin le faciliter le suivi des réponses cellulaires contre l'antigène HA, nous avons injecté des lymphocutes T CD4+ et/ou T CD8+ naïfs isolées à partir de souris transgéniques pour des récepteurs de lymphocytes T spécifiques de HA. Nos résultats montrent que seul le transfert in vivo des cellules tumorales 4T1-HA, et non celui des cellules 4T1 témoins, peut conduire à l'activation, la prolifération et la différentiation des deux types de lymphocytes T spécifiques pour l'antigène HA. De plus, nous avons observé que les populations de lymphocytes T CD4+ et CD8+ sont toutes deux requises, non seulement pour une réponse anti-tumorale efficace, mais aussi pour le déclenchement d'une réaction auto-immune collatérale chez la souris CamK-HA. Enfin, nous avons montré qu'il était nécessaire d'injecter en parallèle des anticorps contre le récepteur inhibiteur CTLA-4 chez la souris L7-HA, afin de permettre la migration des lymphocytes T spécifiques de HA dans le cervelet. Chez ces souris L7-HA, nous avons en outre démontré que les lymphocytes T CD8+ cytotoxiques sont les effecteurs principaux de la maladie. Ces nouveaux modèles murins représentent donc des outils précieux pour une meilleure compréhension des mécanismes moléculaires responsables du développement des SNP. De plus, ils pourraient permettre de tester et de valider de nouvelles approches thérapeutiques visant à bloquer la pénétration dans le SNC d'effecteurs immunitaires potentiellement pathogènes, tout en préservant l'efficacité de la réponse anti-tumorale en périphérie
Paraneoplastic neurological disorders (PNDs) are rare human autoimmune diseases that mostly affect the central nervous system (CNS). They are triggered by an efficient immune response against a neural self-antigen that is ectopically expressed in neoplastic tumor cells and naturally expressed in CNS cells. Due to this shared antigenic expression, the immune system reacts not only to tumor cells but also to neural cells resulting in neurological damage. Growing data point to a major role of cell-mediated immunity in PNDs associated to autoantibodies against intracellular proteins. However, its precise contribution in the pathogenesis remains unclear. Two illustrative examples of possibly cell-mediated PNDs are the Hu-syndrome, characterized by inflammation and widespread los of neurons, and paraneoplastic cerebellar degeneration (PCD), characterized by the selective loss of Purkinje cells. PCD develops mostly in patients with gynecologic carcinomas that express the Purkinje neuron-specific CDR2 protein whereas most patients with the Hu-syndrome harbor small cell lung cancer expressing the neuron-specific protein HuD. In this context, our study aimed to investigate the impact of anti-tumor cellular immune responses in the development of these PNDs. To this end, we developed two animal models mimicking the Hu-syndrome and PCD. We used a tumor cell line expressing the hemagglutinin (HA) of influenza virus to induce an anti-tumor response in CamK-HA mice, which express HA in CNS neurons and L7-HA mice, which express HA only in cerebellar Purkinje neurons. To promote and track the T cell response against the HA antigen, naïve HA-specific CD8+ and/or CD4+ T cells, originating from TCR-transgenic animals, were transferred into these mice. We demonstrate that HA-expressing tumors, but not control tumors, induce in vivo activation, proliferation and differentiation of naïve HA-specific CD4+ and CD8+ T cells into effector cells. Moreover, the collaboration between these two T cell subsets was needed to control tumor growth and induce CNS inflammation in CamK-HA mice. In L7-HA mice the additional injection of the antibody against the inhibitory receptor CTLA-4 was necessary to allow T cells to enter the cerebellum to cause inflammation and the subsequent destruction of Purkinje neurons. Furthermore, in L7-HA mice we demonstrate that cytotoxic CD8+ T cells are the main effectors driving the disease. Thus, these two new mouse models provide further insights into the cellular mechanisms of PND whereby a potent anti-tumor immunity triggers a cancer-associated autoimmune disease, and may therefore help to develop new therapeutic strategies against PND
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Sutton, Ian. "Investigation of cytotoxic T lymphocyte responses to the HuD and Yo antigens in individuals with paraneoplastic neurological syndromes." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274426.

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High titres of antibodies reactive with neuronal antigens are found within the serum of individuals with paraneoplastic encephalomyelitis/subacute sensory neuropathy (anti-Hu) and paraneopiastic cerebellar degeneration (anti-Yo). However, neither the anti-Hu nor the anti-Yo antibody response has demonstrable pathogenic effects. The work presented in this thesis examines whether cytotoxic T lymphocyte (CTL) responses to Hu and Yo antigens could mediate neuronal and tumour cell destruction. HuD and Yo genes were cloned into expression cassettes which were then cloned into replication-defective adenoviruses. Peripheral blood CTL responses in patients with paraneoplastic neurological syndromes were examined by using autologous dendritic cells infected with these recombinant adenoviruses as antigen presenting cells in an ex vivo interferon-y Elispot assay. No CD8+ CTL responses specific for epitopes derived from HuD or Yo could be detected in six patients with paraneoplastic syndromes (4 anti-Hu, 2 anti-Yo) and impaired CD8+ CTL responses to adenoviral-derived antigens were observed in this patient group. No HuD specific CTL responses could be detected in polyclonal T cell lines derived from sural nerve biopsies taken from 2 patients with subacute sensory neuropathy and immunohistochemical studies demonstrated that only 2/9 tumour sections from patients with anti-Yo antibodies contained CD8+ tumour infiltrating lymphocytes.
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Couillault, Coline. "Hétérogénéité et mécanismes d’initiation de la réponse humorale dans les tumeurs du sein et de l’ovaire." Thesis, Lyon, 2019. http://www.theses.fr/2019LYSE1051/document.

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Les lymphocytes B (LB) et les plasmocytes (PC) émergent comme des cellules importantes dans la surveillance immunitaire des tumeurs, même si leur rôle pro- ou anti-tumoral reste activement débattu. Nous avons émis l’hypothèse que cette dualité fonctionnelle de la réponse B pourrait être dictée par l'identité des sous-populations de LB infiltrant la tumeur et/ou par la nature des anticorps (Ac) qu’ils produisent. Dans ce contexte, nous avons montré que les tumeurs du sein et de l’ovaire sont souvent infiltrées par des LB mémoires et des PC exprimant/produisant principalement des IgG ou des IgA. Les IgA sont fortement enrichis dans les tumeurs mammaires in situ, plus précoces, et dans 15-20% des tumeurs invasives, suggérant un rôle différentiel des IgG et des IgA dans la progression tumorale. Les IgA, pouvant être monomériques ou dimériques dans les tumeurs, ciblent en général des antigènes (Ags) différents de ceux des IgG. Nous montrons de plus que les Ags ciblés par les IgA et les IgG sont souvent impliqués dans des fonctions de développement des tissus et d’interaction avec l’ADN, et sont parfois partagés entre patients et entre les types de tumeurs, suggérant leur importance dans la réponse anti-tumorale. En parallèle, grâce à l’étude des tumeurs de patientes souffrant d’un syndrome neurologique paranéoplasique, nous avons pu montrer que l’induction concomitante de PC à IgG et de LT CD8+ cytotoxiques dans la tumeur était liée à des amplifications et/ou des mutations dans les gènes des Ags tumoraux. Ces résultats mettent en évidence l’important des LB et des Ig dans la réponse anti-tumoral, et ouvre des pistes pour rechercher des cibles thérapeutiques en immunothérapie
B and plasma cells are rising as crucial cells in the immune surveillance of tumors, even though their pro- or anti-tumor role is still debated. We argue that this dual functionality of B cells could depend on the identity of tumor-infiltrating B cell subsets and/or by the nature of the antibodies they produce. With that knowledge, we showed that breast and ovarian tumors are usually infiltrated by memory B cells and plasma cells that express and/or produce mainly IgG or IgA. This last class of Ig in highly enriched in in situ carcinomas of the breast, corresponding to earlier tumors, and in 15-20% of invasive tumors, suggesting a differential role of IgG and IgA in tumor progression. IgA, that can be monomeric or dimeric in tumors, often target antigens that differ from those targeted by IgG. We also show that antigens targeted by IgA and IgG in the tumor are often involved in functions related to the development of tissues and DNA interactions, and can be share amongst patients and between breast and ovarian tumors, suggesting their importance in the anti-tumor immune response. In parallel, using tumors from patients suffering from a paraneoplastic neurological syndrome, we established that the concomitant induction of IgG PC and CD8+ cytotoxic T cells in the tumor is associated wth amplifications and/or mutations in the genes of tumor antigens. These results highlight the importance of B cells and Ig in the anti-tumor immune response and give leads to look for new targets in immunotherapy
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Books on the topic "Paraneoplastic neurological syndromes"

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Sutton, Ian John. Investigation of cytotoxic T lymphocyte responses to the HuD and Yo antigens in individuals with paraneoplastic neurological syndromes. Birmingham: University of Birmingham, 2003.

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Jordan, Nerissa. Non-metastatic neurological manifestations of malignancy. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0238.

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Neurological complications of systemic malignancy are frequent. They may reflect direct local effects of the tumour; CNS infection; side effects of chemotherapy or radiotherapy; nutritional or metabolic derangements; or a paraneoplastic syndrome. The paraneoplastic neurological syndromes are a group of disorders associated with a malignancy outside the nervous system. The pathophysiology is immune-mediated, with the tumour’s expression of neuronal proteins invoking antibody formation, which in turn results in neurological symptoms. This chapter will mainly focus on these syndromes.
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Caraceni, Augusto, Cinzia Martini, and Fabio Simonetti. Neurological problems in advanced cancer. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199656097.003.0141.

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Neurological complications are frequent in populations with advanced cancer. An adequate neurological assessment is always important in addressing pain, cognitive symptoms, and peripheral and central nervous system complications. This chapter discusses a variety of neurological problems found in advanced cancer together with their clinical aspects and management, including some suggested regimens for pharmacological therapy. Complications that are discussed include intracranial hypertension, seizures in patients with advanced illness (including a suggested algorithm for the management of status epilepticus), delirium, brain metastases, spinal cord compression (including an algorithm for the evaluation of back pain), leptomeningeal metastases, base of the skull and cranial nerve syndromes, and paraneoplastic neurological syndromes.
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Bielekova, Bibiana, Gary Birnbaum, and Robert P. Lisak, eds. Neuroimmunology. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190050801.001.0001.

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This book provides clinical and supporting scientific background on a diverse group of neurological disorders in an expanding field of neurology, that of neuroimmunology. It includes chapters on multiple sclerosis and related disorders in adults and children, neuromyelitis optica spectrum disorder, Guillain-Barré syndrome, chronic inflammatory deymyelinating polyradiculoneuropathy and variants, immune-mediated disorders of the neuromuscular junction, inflammatory myopathies, paraneoplastic disorders and autoimmune encephalitities, and neurologic manifestations of systemic immune-mediated diseases. In addition there is an introductory chapter dealing with basic of immunology and another on mechanisms of action of therapies used in neuroimmunologic disorders. The clinical chapters cover epidemiology, pathology, pathogenesis, and pathophysiology of the different diseases along with clinical presentation, diagnostic testing, differential diagnosis, and treatment.
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Cornblath, David R., and Richard A. C. Hughes. Peripheral neuropathy. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199658602.003.0013.

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Disorders of peripheral nerves are one of the most common neurological problems today and include the increasing number of people with diabetes worldwide and those with inherited neuropathy, toxic neuropathy, carpal tunnel syndrome, inflammatory neuropathy, radiculopathies, and, increasingly, traumatic nerve injuries. Neuropathic pain is a growing problem without solution. In this chapter, ten landmark papers in peripheral nerve disorders have been selected, covering Bell’s palsy, Charcot-Marie-Tooth disease, carpal tunnel syndrome, paraneoplastic neuropathy, neurophysiology, familial amyloid polyneuropathy, chronic inflammatory demyelinating polyradiculoneuropathy, toxic neuropathy, diabetic neuropathy, and Guillain–Barré syndrome. These important papers set the stage for many subsequent advances in the field but may be forgotten now, so they are brought to the reader’s attention.
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Book chapters on the topic "Paraneoplastic neurological syndromes"

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Vedeler, C. A., J. C. Antoine, B. Giometto, F. Graus, W. Grisold, J. Honnorat, P. A. E. Sillevis Smitt, J. J. G. M. Verschuuren, and R. Voltz. "Paraneoplastic Neurological Syndromes." In European Handbook of Neurological Management, 447–57. Oxford, UK: Wiley-Blackwell, 2010. http://dx.doi.org/10.1002/9781444328394.ch31.

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Rossiñol, Tomeu, and Francesc Graus. "Paraneoplastic Neurological Syndromes." In Diagnostic Criteria in Autoimmune Diseases, 421–26. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-60327-285-8_77.

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Muñiz-Castrillo, Sergio, and Jérôme Honnorat. "Paraneoplastic Neurological Syndromes." In Neuroimmune Diseases, 439–85. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-19515-1_14.

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Zoccarato, Marco, Luigi Zuliani, and Bruno Giometto. "Paraneoplastic Neurological Syndromes." In Prognosis of Neurological Diseases, 355–61. Milano: Springer Milan, 2015. http://dx.doi.org/10.1007/978-88-470-5755-5_27.

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Lewerenz, Jan, and Frank Leypoldt. "Paraneoplastic Neurological Syndromes." In Cerebrospinal Fluid in Clinical Neurology, 353–85. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-01225-4_21.

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Spatola, Marianna. "Paraneoplastic Neurological Syndromes." In Neuroimmunology, 243–60. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-61883-4_16.

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Dalmau, Josep, and Jerome B. Posner. "Neurological paraneoplastic syndromes." In Immunoneurology, 203–13. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61191-9_16.

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Muñiz-Castrillo, Sergio, Macarena Villagrán-García, and Jérôme Honnorat. "Paraneoplastic Neurological Syndromes." In Neuroimmune Diseases, 1–48. Cham: Springer International Publishing, 2024. http://dx.doi.org/10.1007/978-3-031-24297-7_14-1.

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Muñiz-Castrillo, Sergio, Macarena Villagrán-García, and Jérôme Honnorat. "Paraneoplastic Neurological Syndromes." In Neuroimmune Diseases, 567–614. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-60006-7_14.

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Rubin, Michael, Jason Broker, and Thomas B. Toothaker. "Paraneoplastic Neurological Syndromes, Overview." In Encyclopedia of Medical Immunology, 835–40. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_5.

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Conference papers on the topic "Paraneoplastic neurological syndromes"

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Granger, Andre, Tina Rajnauth, Divyanshu Dubey, John Mills, Michelle Mauermann, Sarah Berini, P. James B. Dyck, and Christopher Klein. "Peripheral Nerve Pathology in Antibody Positive Paraneoplastic Neurological Syndromes (P11-8.005)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000203395.

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Caiza-Zambrano, Francisco, Fabio Gonzalez, Julio Galarza, Mauricio Benetti, Claudia Uribe Roca, Pablo Bonardo, Manuel Fernández Pardal, Luciana León Cejas, and Ricardo Reisin. "Paraneoplastic Neurological Syndromes: A Single-Center Retrospective Study in Argentina (P9-13.005)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202816.

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vanDuijn, Martijn M., Peter Maat, Lennard J. Dekker, Theo M. Luider, and Peter A. Sillevis Smitt. "Abstract 1277: Antigen-specific markers for paraneoplastic neurological syndromes obtained by proteomic analysis of patient immunoglobulins." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-1277.

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Toledo, Zoe De, Sarah L. Smyth, Hooman Soleymani Majd, Zoe Traill, Kezia Gaitskell, and Sarosh Irani. "121 Paraneoplastic neurological syndromes and the importance of prompt recognition to aid the diagnosis of underlying gynaecological malignancy." In ESGO 2024 Congress Abstracts. BMJ Publishing Group Ltd, 2024. http://dx.doi.org/10.1136/ijgc-2024-esgo.487.

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Frille, A., S. Tegelkamp, M. Lerche, N. Linder, JJ Rumpf, S. Hesse, and H. Wirtz. "Paraneoplastic neurologic syndromes in lung cancer." In 21. Herbsttagung der Mitteldeutschen Gesellschaft für Pneumologie und Thoraxchirurgie. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3401412.

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Puppalwar, S., and D. Turnbull. "An unusual case of paraneoplastic neurological syndrome." In 17th Annual Conference of Indian Society of Neuroanaesthesiology and Critical Care. Thieme Medical and Scientific Publishers Private Ltd., 2016. http://dx.doi.org/10.1055/s-0038-1667598.

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Carvalho, Ana Cláudia Pires, Stella Angelis Trivellato, Guilherme Jardini Drumond Anastacio, Fernanda Rezende Dias, Luisa Crevelin Costa, Juliana Akita, and Natália de Castro Fim Nakao. "Lambert-Eaton syndrome without an identified neoplasm." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.504.

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Introduction: Lambert-Eaton syndrome occurs due to the attack of autoantibodies to voltage-gated calcium channels in the presynaptic terminal of the neuromuscular junction and is usually paraneoplastic. Objectives: Describe the case of a patient with weakness which was investigated for neoplasm. Design and setting: Case report Methods: Analysis of medical record, photographic record of the diagnostic methods and literature review. Case description: Woman, 60 years old, diabetic, hypertensive and ex-smoker, with proximal weakness in the lower limbs for 4 months with paresthesia in the extremities. In 2 months she needed a cane due to frequent falls, followed by proximal weakness of the upper limbs. She lost 8 kg in 4 months. Neurological examination showed hypotrophy in thighs, proximal tetraparesis predominantly in lower limbs and global hyporeflexia. Electroneuromyography showed decreases to repetitive low-frequency stimulation, but significant increases with repetitive high-frequency stimulation and increased amplitude of compound muscle action potentials after effort, suggesting impairment of the neuromuscular junction in the presynaptic topography. She was diagnosed with LambertEaton syndrome. An investigation of paraneoplastic syndrome was carried out, with tumor markers, tomography of the chest, abdomen and pelvis, thyroid ultrasound, mammography and oncotic colposcopy, all without findings of neoplasia. It was proposed a treatment with human immunoglobulin and followup with physiotherapy, occupational therapy and psychology. She showed a significant improvement in strength after starting treatment. Conclusion: Patients with Lambert-Eaton syndrome should be investigated for an underlying neoplasm and followed up periodically, considering the possibility of cancer diagnosis even months or years after the neurological syndrome.
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Tegelkamp, S., M. Lerche, H. Wirtz, and A. Frille. "Systematic analysis of paraneoplastic neurologic syndromes in lung cancer patients." In 60. Kongress der Deutschen Gesellschaft für Pneumologie und Beatmungsmedizin e. V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1678067.

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Canzian, Kássia Braga, Marcella Canato Toloi, David Vargas Freitas Teixeira, Vanessa de Freitas Moreira, Amanda Freitas Alves, Eric Dupont, Fernanda Maria Gonçalves de Sousa Moura, Isabela de Almeida Stella, Thiago Ivan Vilchez Santillan, and Herval Ribeiro Soares Neto. "Chronic paraneoplastic polyradiculoneuropathy during colorectal cancer: a case report." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.633.

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A 70-year-old woman, four months before admission in our Hospital started with hypoesthesia in the hands, progressing to the lower limbs, followed by sensory ataxia and decreased strength, with frequent falls, losing 8 kg in that interim. The electroneuromyography demonstrated a pattern compatible with chronic demyelinating polyradiculoneuropathy (CIDP). Pulse therapy (PT) with Methylprednisolone was administered, with remission of symptoms. She underwent neoplastic investigation, being diagnosed with moderately differentiated and invasive sigmoid adenocarcinoma (SA), with indication for colectomy (CTC). No other solid tumors (ST) more commonly related to CIDP were found. Onconeural antibodies were not evidenced by blood analysis. 5 days after treatment, she has returned to her sensory-motor clinical condition, now attacking the bulbar muscles, developing dysphagia and dyspnea, requiring orotracheal intubation (OTI) and mechanical ventilation. Submitted to drug therapy with Intravenous Human Immunoglobulin and new PT for five days, with progressive improvement in strength, being extubated 11 days after OTI. As disease-modifying therapy, Rituximab was administered, one month before CTC. The association between SA and the development of CIDP was infrequently reported in the literature, lacking data that correlate the pathophysiology of this paraneoplastic (PNP) syndrome. Immunomodulatory therapy has an impact on the functional recovery of the patient and on preventing the progression of the symptoms, but the definitive treatment is CTC. Despite the low prevalence, the search for ST of the gastrointestinal tract should be included in PNP screening in the face of a recent diagnosis of CIDP, aiming at early identification and treatment in the initial stages, with an impact on oncological and neurological prognosis.
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Morais, Gabriela Lopes de, Manoella Guerra de Albuquerque Bueno, Guilherme Otero Brum, Eder Leandro da Silva Dantas, Nathalia Rossoni Ronchi, Katharina Vieira Messias, and Vanessa Daccach Marques. "Anti-hu neuropathy as a paraneoplastic syndrome: the pursuit for the primary site." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.418.

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A 53-year-old man with a history of smoking and recent weight loss presented with progressive weakness and difficulty walking. Physical exam evidenced dysmetria on finger-to-nose test, worsened with eyes closed, pseudoathetosis, absent deep tendon reflexes and a neuropathic pattern of hypoesthesia and hypopalesthesia. He was unable to stand due to the severity of the ataxia. Initial investigation was positive for syphilis, with no history of treatment, and cerebrospinal fluid analysis showed hyperproteinrachia with normal cell count. Despite adequate treatment with penicillin, symptoms continued to progress. Electroneuromyography was remarkable for axonal sensorimotor polyneuropathy with sensitive predominance. A paraneoplastic panel was ordered and evidenced positivity to anti-Hu. The patient was then treated with high doses of methylprednisolone and plasmapheresis, with no improvement. An extensive search for malignancies was performed, and enlarged hilar lymph nodes were found on computed tomography scan. Positron Emission Tomography-scan showed pulmonary and mediastinal hypermetabolism. Tissue samples were acquired with no significant findings and tuberculosis, fungal infections and inflammatory granulomatous diseases, among other conditions, were ruled out. Due to the high suspicion for malignancy, the biopsies were reviewed by a pulmonary pathology specialist, submitted to additional immunohistochemical staining and, at last, the diagnosis of small cell lung carcinoma was made. Chemotherapy was initiated shortly after.
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