Academic literature on the topic 'Tumefactive demyelinating lesions'
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Journal articles on the topic "Tumefactive demyelinating lesions"
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Barbosa, Brainner Campos, Edson Marchiori, Caio Leal Leidersnaider, Lara Brandao, and Mauricio Castillo. "Demyelinating lesions behaving like aggressive tumours on advanced MRI techniques." Neuroradiology Journal 32, no. 2 (2019): 103–7. http://dx.doi.org/10.1177/1971400919826394.
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Tumefactive demyelinating lesions are a rare disorder in which inflammatory demyelination manifests as solitary or multiple focal brain lesions (greater than 2 cm in size), which can be mistaken for glioma, lymphoma, metastasis and in some cases even brain abscess. The symptomatology of tumefactive demyelinating lesions depends on the white matter area involved and includes quickly progressing neurological deterioration of motor, sensory and visual function, praxis, language and mood impairment, as well as seizures. Recognising the key imaging features in a patient with a prior history of demyelination may expedite appropriate management. Preoperative diagnosis or at least the consideration of a demyelinating process is important to avoid unnecessary surgery. We report three patients with demyelinating lesions who presented with findings suggestive of demyelination on conventional magnetic resonance imaging studies. However, in all patients the lesions showed high perfusion and in two high permeability, which are findings generally seen with high-grade neoplasias. In rare instances, tumefactive demyelinating lesions may show increased perfusion and high permeability, imaging findings more commonly seen in high-grade gliomas. We suggest that if white matter lesions on conventional magnetic resonance imaging are compatible with tumefactive demyelinating lesions, atypical findings of high perfusion/permeability should not dissuade the radiologist from suggesting the presence of tumefactive demyelinating lesions rather than high-grade gliomas.
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Brod, Staley A., J. William Lindsey, and Flavia Nelson. "Tumefactive demyelination: Clinical outcomes, lesion evolution and treatments." Multiple Sclerosis Journal - Experimental, Translational and Clinical 5, no. 2 (2019): 205521731985575. http://dx.doi.org/10.1177/2055217319855755.
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Objective Large demyelinating lesions with possible mass effect (tumefactive multiple sclerosis or tumefactive demyelination) can be mistaken for tumour-like space-occupying lesions suggesting a malignant outcome. Methods We reviewed our own experience of multiple sclerosis subjects ( n = 28) with tumefactive demyelination to determine the relationship between clinical outcomes and lesion evolution, clinical outcomes and their relationship to different therapies. Patients with central nervous system demyelinating disease were identified from our database over the last 10 years. Results No patient increased in extended disability status scale (EDSS). Overall, lesion regression was associated with improved EDSS. Lesion regression was also associated with therapy versus no therapy. No specific therapy or corticosteroid infusions improved EDSS over the long term. The absence of enhancement on follow up on magnetic resonance imaging portended lesion regression. Conclusion Tumefactive demyelination may predict a more benign overall course and is susceptible to traditional immunomodulatory treatments.
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Weinshenker, Brian G. "Tumefactive demyelinating lesions: Characteristics of individual lesions, individual patients, or a unique disease entity?" Multiple Sclerosis Journal 21, no. 13 (2015): 1746–47. http://dx.doi.org/10.1177/1352458515603801.
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Whether or not recurrent tumefactive demyelinating lesions are a unique form of CNS demyelinating disease or part of the continuum of multiple sclerosis is a question raised by the case report on which this commentary is based. Detailed review and immunopathologic study of biopsy material may not only confirm or refute a diagnosis of demyelinating disease, but potentially uncover unique features that may assist in understanding pathophysiology and nosology of rare cases with recurrent tumefactive demyelination.
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Hudon, Mark, Richard Farb, A. P. Mitha, et al. "Tumefactive Demyelinating Lesions." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 34, no. 3 (2007): 362–64. http://dx.doi.org/10.1017/s0317167100006831.
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Dagher, A. P., and J. Smirniotopoulos. "Tumefactive demyelinating lesions." Neuroradiology 38, no. 6 (1996): 560–65. http://dx.doi.org/10.1007/s002340050308.
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Dagher, A. P., and J. Smirniotopoulos. "Tumefactive demyelinating lesions." Neuroradiology 38, no. 6 (1996): 560–65. http://dx.doi.org/10.1007/bf00626098.
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Zafar, Lubna, Obaid Ahmed Siddiqui, Shazia Durdana, and Damera Achyuth Kumar. "Tumefactive demyelination-A Rare Presentation of Multiple Sclerosis." Bangladesh Journal of Medical Science 21, no. 4 (2022): 931–34. http://dx.doi.org/10.3329/bjms.v21i4.60259.
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Background: Multiple Sclerosis is an inflammatory demyelinating disease having varied manifestations in terms of clinical featuresand radiological features. Rarely it may present as a large demyelinating lesionwith accompanying edema and mass effect, thereby simulating an intracranial tumor, known as Tumefactive Demyelination. Symptoms are usually related to the pressure of a focal mass lesion. When it manifests in a patient without pre-existing MS, it poses a diagnostic challengeas it may mimic a neoplasm, infarct or abscess. Thus, it is essential to recognize this rare clinical entity for proper patient management. Case Presentation: We report here a case of 40 years old female who presented with right sided hemiparesis. The initial brain imaging (CT) suggested left parietal lobe lesion suggestive of glioma. But MRI of the brain showed a cortical based lesion in left parietal lobe in parasaggital location which appeared hyperintense on both T2WI and FLAIR sequences. Further evaluation by MR spectroscopy suggested the lesion to be tumefactive demyelination. She was administered IV Methylprednisolone (1gm daily for 5 days) and responded well to treatment. The characteristic magnetic resonance findings of the patient, its acute onset, and its clinical improvement after corticosteroid therapy finally set the diagnosis of Tumefactive Demyelination. Conclusion: Tumefactive demyelinating lesions pose a unique diagnostic challenge in defining differential diagnosis and management and should always be considered in young patients presenting with tumour like lesions on imaging. Bangladesh Journal of Medical Science Vol. 21 No. 04 October’22 Page : 931-934
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Kalanie, Hossein, Ali Amini Harandi, Reza Bakhshandehpour, and Daryoosh Heidari. "Multiple Large Tumefactive MS Plaques in a Young Man: A Diagnostic Enigma and Therapeutic Challenge." Case Reports in Radiology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/363705.
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Tumefactive demyelinating lesion is defined as large solitary demyelinating lesion with imaging characteristics mimicking neoplasm. These atypical features include size more than 2 cm, mass effect, edema, and/or ring enhancement. Distinguishing tumefactive lesions from other etiologies of intracranial space occupying lesions is essential to avoid inadvertent surgical or toxic chemotherapeutic intervention. Symptoms are generally atypical for multiple sclerosis (MS) and usually related to the pressure of a focal mass lesion without a history of MS. The clinical presentation and MRI appearance of these lesions often lead to biopsy. Here, we present a young man with fulminating neurological symptoms and multiple large tumefactive lesions on either hemisphere. Since patient and parents were not agreed on brain biopsy, a course of steroid therapy was commenced which ended to considerable improvement and confirmed the diagnosis of tumefactive MS. Thirteen months later, he experienced another relapse when his treatment was continued by weekly intramuscular injection of interferon b1a (Avonex). Two further MRIs showed shrinkage of tumefactive plaques and resolution of edema in the periphery of lesions.
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QI, WEI, GE JIA, XINSHENG WANG, MAOZHI ZHANG, and ZHENYU MA. "Cerebral tumefactive demyelinating lesions." Oncology Letters 10, no. 3 (2015): 1763–68. http://dx.doi.org/10.3892/ol.2015.3481.
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Altintas, A., B. Petek, N. Isik, et al. "Clinical and radiological characteristics of tumefactive demyelinating lesions: follow-up study." Multiple Sclerosis Journal 18, no. 10 (2012): 1448–53. http://dx.doi.org/10.1177/1352458512438237.
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Background: Demyelinating lesions over 20 mm in size, referred to as tumefactive demyelinating lesions, can be misdiagnosed as being either a tumor or an abscess. Although some radiological characteristics can help make a differential diagnosis easier, a cerebral biopsy may still be necessary. Objective: Our objective was to assess the clinical characteristics of tumefactive lesions, with or without a diagnosis of multiple sclerosis (MS), and present follow-up data for 54 patients with tumefactive lesions. Methods: Demographic, clinical, radiological and laboratory data were gathered and treatment responses were evaluated in a total of 54 patients from five medical centers. Result: Twenty-nine patients were diagnosed with tumefactive lesions at the onset, whereas 25 patients were diagnosed with tumefactive lesions after a diagnosis of MS. Median follow-up was 38.12 months. At final examination, 19 of the patients with a tumefactive lesion diagnosis at the onset eventually developed relapsing–remitting MS, while 10 remained with the condition as a clinically isolated syndrome. The tumefactive lesions studied were mostly focal, with closed-ring enhancement. We found that oligoclonal band positivity was less frequent in the patients with tumefactive onset. Conclusion: Although our demographic data were similar to formerly collected Turkish MS data, we found that the distribution of the patients’ clinical course differed if there was an absence of primary progressive MS and that there was a lower frequency of secondary progressive MS cases in our group of patients. We believe that less frequent oligoclonal band positivity and the difference we witnessed in the clinical course of disease in our study groups suggest that there is a need for further studies to compare all the biological and immunological differences between MS and tumefactive lesion cases, in order to reveal whether there are different pathogenetic mechanisms involved.
Dissertations / Theses on the topic "Tumefactive demyelinating lesions"
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Santos, Stella de Aparecida Ederli Pinto dos. "Diagnóstico diferencial das lesões tumefativas desmielizantes do sistema nervoso central na infância e adolescência: revisão sistemática da literatura." Instituto Fernandes Figueira, 2013. https://www.arca.fiocruz.br/handle/icict/10988.
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Previous issue date: 2013<br>Fundação Oswaldo Cruz. Instituto Nacional de Saúde da Mulher, da Criança e do Adolescente Fernandes Figueira. Departamento de Ensino. Programa de Pós-Graduação em Saúde da Criança e da Mulher. Rio de Janeiro, RJ, Brasil.<br>As lesões tumefativas desmielinizantes (LTD) do SNC apresentam extrema dificuldade diagnóstica em virtude da similaridade clínica e radiológica com outras entidades nosológicas, incluindo doenças neoplásicas, inflamatórias e infecciosas. Frequentemente, o caráter indefinido das lesões aponta para a necessidade de biópsia cerebral com alto risco de morbidade. Portanto, o reconhecimento das características neurorradiológicas da LTD é fundamental para evitar a utilização de procedimentos invasivos. Na prática clínica, os exemplos das formas tumefativas não tumorais são os seguintes: esclerose múltipla (EM), neuromielite óptica (NMO), doença de Schilder e encefalomielite agudadisseminada (ADEM).Objetivo e Métodos: Analisar, através de revisão sistemática da literatura, quais ferramentas diagnósticas clínicas, radiológicas e laboratoriais são utilizadas pelos autores na investigação da etiologia das LTDs do SNC na infância.Resultados: As doenças desmielinizantes encontradas foram as seguintes: EM em 36% dos casos; LTD, sem classificação específica, em 27%; ADEM 17%;doença de Schilder 13 % e NMO 7%. De todos os casos estudados, em 45% houve recorrência de eventos desmielinizantes. Não há protocolo definido em relação aos tipos de exame solicitados nem a sequência apropriada ou oportunidade de indicá-los. Os exames mais realizados pelos autores foram os seguintes: RM de crânio, exame histopatológico, pesquisa de bandas oligoclonais e índice de IgG no líquor, RM de coluna e pesquisa de anticorpo antiaquaporina 4.
Conclusão: A análise da literatura mostra que os dados mais relevantes para se definir o diagnóstico das LTDs são obtidos através da história e evolução clínica dos pacientes, e exames de neuroimagem; é fundamental que pacientes portadores de LTD sejam acompanhados a médio/longo prazo na tentativa de aumentar as possibilidades diagnósticas; não existe protocolo universal de abordagem das LTDs; há necessidade incondicional de implementação de fluxo de procedimentos capazes de orientar o diagnóstico das LTDs na infância e adolescência.<br>Introduction: The tumefactive demyelinating lesions (TDL) of the CNS have extremely difficult diagnosis due to the clinical and radiological similarity with other nosological entities, including neoplastic, inflammatory and infectious diseases. Commonly, the undefined character of the lesions points to the need of brain biopsy with high risk of morbidity. Thus, the recognition of neuroradiological characteristics of the TDL is critical to avoid the use of invasive procedures. In the clinical practice, the examples of the non tumorous forms of tumefactive lesions are the following: multiple sclerosis (MS), optic neuromyelitis (ONM), Schilder`s disease and acute disseminated encephalomyelitis (ADEM).
Objective and Methods: Analysis, through the systematic review of the literature, which clinic, radiological and laboratorial diagnostic tools are used by the authors in the investigation of the etiology of the TDL`s of the CNS in the childhood.
Results: The following demyelinating diseases have been found: MS in 36% of the cases; TDL without a specific classification in 27%; ADEM 17%;Schilder`s disease 13 % and ONM 7%. Considering all the cases studied, in 45% had recurrence of demyelinating events. There is no defined protocol with respect to the types with medical exams requested neither the appropriate sequence or the opportunity of indicate them. The medical exams more conducted by the authors were the following: MRI of skull,histopathological exam, research of oligoclonal bands and IgGindex in the liquor, MRI of spine and research of anti-aquaporin-4 antibody.
Conclusion: The analysis of the literature shows that the most relevant data to define the diagnosis of the TDLs are obtained through the history and clinical evolution of the patients and neuroimaging tests.It is critical that the patients with TDL be accompanied over the medium/long term in an attempt of increase the diagnostic possibilities; there is not an universal protocol of approach of the TDL; there is unconditional necessity of implementation of flow of procedures able to guide the diagnosis of the TDLs in the childhood and adolescence.
Book chapters on the topic "Tumefactive demyelinating lesions"
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"Tumefactive Demyelinating Lesions (TDL)." In Neuropathology. Elsevier, 2014. http://dx.doi.org/10.1016/b978-1-4160-6220-2.00050-6.
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Kalinowska-Lyszczarz, Alicja, W. Oliver Tobin, Yong Guo, and Claudia F. Lucchinetti. "Fluctuating Vision Loss, Seizures, and Left Parieto-Occipital Mass." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0007.
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A 35-year-old man sought care for progressive visual disturbance. Magnetic resonance imaging of the brain showed a large, left-sided, parieto-occipital, contrast-enhancing lesion. He was treated with dexamethasone with brief improvement in vision. Within 5 days he had progressive vision worsening. Two weeks after the onset of his symptoms, brain magnetic resonance imaging showed a decrease in lesion size, and corticosteroids were discontinued. Two months after symptom onset he was found to have alexia without agraphia, and follow-up magnetic resonance imaging showed an increased size of the lesion. Two months after disease onset, the patient underwent a left occipital brain biopsy, which demonstrated a macrophage-enriched active demyelinating lesion with relative axonal sparing. Right arm weakness and aphasia developed, along with a fever. He was treated with dexamethasone. Electroencephalography indicated multiple seizures. Repeated cerebrospinal fluid analysis showed a slightly increased white blood cell count, increased protein level, immunoglobulin G index of 0.84, and the presence of 3 cerebrospinal fluid-unique oligoclonal bands. He was treated with 5 days of intravenous methylprednisolone and levetiracetam, with improvement. Three and a half years later, the patient came to the emergency department with weakness of the left leg associated with reduced sensation. Spinal magnetic resonance imaging showed a new demyelinating contrast-enhancing lesion from T2 to T7. He was treated with 5 days of intravenous methylprednisolone followed by 6 sessions of plasma exchange, with improvement. A diagnosis of relapsing tumefactive demyelination was made. The patient was subsequently treated with ocrelizumab. Tumefactive demyelinating lesions pose a diagnostic challenge, especially if they are the first manifestations of demyelinating disease. Typically, tumefactive demyelinating lesions are large (>2 cm) and are associated with edema, mass effect, and variable patterns of contrast enhancement.
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Litsou, Eleni. "Atypical Presentation or Variants of Multiple Sclerosis." In Multiple Sclerosis - Pathways, Diagnosis and Therapeutic Targets [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1010042.
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Multiple sclerosis (MS) is a chronic inflammatory demyelinating disorder (DD) of the central nervous system (CNS), characterized by the presence of multifocal lesions, axonal degeneration, and reactive gliosis. Remyelination may occur, particularly in the early phases of lesion development, although its extent varies among individuals. Pathological studies have highlighted significant inter-individual differences in oligodendrocyte preservation and distinct mechanisms of demyelination, including T-cell/macrophage-mediated processes, antibody/complement-mediated injury, and primary oligodendrocyte damage. Beyond classical MS, several atypical variants—such as tumefactive MS, BCS, Schilder’s diffuse sclerosis, Marburg’s acute MS and Neuromyelitis Optica Spectrum Disorder (NMOSD), share core pathological features with MS while exhibiting unique distinguishing characteristics. NMOSD, for instance, is strongly associated with aquaporin-4 (AQP4) autoantibodies and primarily involves antibody/complement-mediated demyelination, whereas BCS is marked by oligodendrocyte dystrophy and a distinct “onion-bulb” pattern of myelin loss. Acute disseminated encephalomyelitis (ADEM) represents a related inflammatory demyelinating condition but typically lacks extensive, chronic demyelination. Understanding these rare MS variants provides crucial insights into the diverse pathogenic mechanisms underlying CNS demyelination. This chapter aims to comprehensively explore these atypical forms of MS, highlighting their distinctive clinical presentations, imaging features, and pathological characteristics to improve diagnostic accuracy and therapeutic approaches.
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McKeon, Andrew. "A Woman With Headaches and a Tumefactive Brain Lesion." In Mayo Clinic Cases in Neuroimmunology, edited by Andrew McKeon, B. Mark Keegan, and W. Oliver Tobin. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780197583425.003.0065.
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A 65-year-old woman sought care for a 6-month history of confusion and emotional disturbance that was initially ascribed to stress. She then had development of headaches over several weeks, which prompted brain magnetic resonance imaging with contrast. Imaging showed a mass emanating bilaterally from the splenium of the corpus callosum with heterogeneous T1 postgadolinium enhancement. Neurologic examination indicated left homonymous hemianopia, but she was otherwise normal. She had neither alexia nor other language deficit that may appear with a splenial corpus callosum lesion. A biopsy of the brain mass was performed. Histologic analysis of the biopsy specimen revealed glioblastoma multiforme. Corticosteroid treatment was prescribed, which relieved her headache. Radiation therapy and chemotherapy (temozolomide) were recommended. No further follow-up information was available. In neurologic clinical practice, a large corpus callosum–based lesion is sometimes encountered. The localization of such lesions is not specific for any one diagnosis, but radiologic characteristics can aid clinical decision making. Although the radiologic appearance of a lesion spreading out into both hemispheres from the corpus callosum can indicate butterfly glioma, the differential diagnosis also includes tumefactive demyelinating disease and lymphoma, which can also have a callosal localization and produce mass effect.
Conference papers on the topic "Tumefactive demyelinating lesions"
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Silva, Agnes Laura, Beatriz Iolanda de Sene Ferregutti Pinheiro, Laura de Lourdes Cardoso e. Silva, et al. "Pseudotumor demyelination lesion associated with bevacizumab in oncological treatment." In XIV Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2023. http://dx.doi.org/10.5327/1516-3180.141s1.770.
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Introduction: Bevacizumab is a monoclonal antibody directed against the human isoform of vascular endothelial growth factor A (VEGF-A) and inhibits angiogenesis. Case: Female patient, 54-year-old, with a history of intestinal adenocarcinoma associated with peritoneal carcinomatosis being treated with bevacizumab. The patient started to present a deviation of the labial rhyme to the right, which showed the presence of left facial paralysis with a central pattern on the neurological physical examination, without other alterations. Magnetic resonance imaging of the brain showed a nodular lesion centered in the subcortical white matter of the right frontoparietal transition, showing T1 hyposignal, T2/FLAIR hypersignal, with areas of pronounced SWAN hyposignal, without significant post-contrast enhancement and a thin halo of diffusion. It has no significant mass effect and measures 1.4 x 2.5 x 2.0 cm. Screening for HIV, toxoplasmosis, cryptococcus and mycobacterial infection was negative. Magnetic resonance imaging of the cervical spine and cerebrospinal fluid analysis were normal. The presence of a demyelinating lesion was observed in the exteriotaxic biopsy, which confirms the hypothesis of a pseudotumoral lesion and rules out the possibility of a metastatic lesion. Over four weeks, there was resolution of neurological signs with radiological improvement in subsequent examinations. There was no evidence of new inflammatory activity, clinically and on MRI over a 2-year period. Conclusion: A definitive causal association between VEGF-A inhibition and central nervous system inflammatory demyelination could not be confirmed in this patient. However, the temporal relationship between institution of bevacizumab therapy and presentation with tumefactive demyelination is significant.