Journal articles: 'Radiation leukoencephalopathy'

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Thiessen, Brian, and Lisa M. DeAngelis. "Hydrocephalus in Radiation Leukoencephalopathy." Archives of Neurology 55, no. 5 (May 1, 1998): 705. http://dx.doi.org/10.1001/archneur.55.5.705.

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Rauch, Philipp J., Henry S. Park, Jonathan P. S. Knisely, Veronica L. Chiang, and Alexander O. Vortmeyer. "Delayed Radiation-Induced Vasculitic Leukoencephalopathy." International Journal of Radiation Oncology*Biology*Physics 83, no. 1 (May 2012): 369–75. http://dx.doi.org/10.1016/j.ijrobp.2011.06.1982.

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Henri-Bhargava, A., and M. Freedman. "Executive dysfunction in delayed radiation-induced leukoencephalopathy." Canadian Medical Association Journal 183, no. 12 (June 20, 2011): 1401. http://dx.doi.org/10.1503/cmaj.101879.

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Cheung, Yin Ting, Noah D. Sabin, Wilburn E. Reddick, Deepa Bhojwani, Wei Liu, Tara M. Brinkman, John O. Glass, et al. "Association Between Acute Leukoencephalopathy and Long-Term Neurobehavioral and Brain Imaging Outcomes in Survivors of Childhood Acute Lymphoblastic Leukemia Treated with Chemotherapy Only." Blood 126, no. 23 (December 3, 2015): 3255. http://dx.doi.org/10.1182/blood.v126.23.3255.3255.

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Abstract Introduction: Leukoencephalopathy is observed in a subset of children undergoing chemotherapy for acute lymphoblastic leukemia (ALL), though the impact of these white matter abnormalities on long-term behavior and brain integrity are unknown. This study examines associations between acute (on-therapy) leukoencephalopathy and neurobehavioral ratings and white matter integrity in long-term survivors of ALL treated with chemotherapy only. Methods: 408 patients with newly diagnosed ALL were treated on St. Jude Total XV protocol which omitted cranial irradiation in all patients. Of the 369 patients who had prospective MRI scan of brain during active therapy, 294 were eligible for long-term follow-up and 189 (64%) participated in neurobehavioral assessment and brain imaging when ≥5 years post-diagnosis. Brain MRI's during therapy and at follow-up were systematically coded by a Board Certified Neuroradiologist (blinded to the neurobehavioral outcomes) using the Common Terminology Criteria for Adverse Events (CTCAE) 4.03. At follow-up, survivors' parents completed the Behavior Rating Inventory of Executive Function (BRIEF) to assess survivors' neurobehavioral problems. Diffusion tensor imaging (DTI) was conducted to assess white matter integrity. Fractional anisotropy (FA), axial diffusivity (AD) and radial diffusivity (RD) were extracted from DTI voxels within the frontostriatal tract, given its association with executive function. Generalized linear models were used to examine associations among leukoencephalopathy, long-term neurobehavioral and DTI outcomes, adjusting for current age. Results: Acute leukoencephalopathy was identified in 49 survivors (28.3%), 78% of whom continued to demonstrate leukoencephalopathy at follow-up. Compared to population norms, survivors had more severe problems with working memory (mean[SD] Z-score of 0.60 [1.27]), organization (0.31[1.05]), initiation (0.25[1.10]) and planning (0.33[1.19]), all p's<0.001. Survivors who developed acute leukoencephalopathy displayed more neurobehavioral problems at follow-up than those who did not, adjusting for age at diagnosis and parents' education (Table 1). Acute leukoencephalopathy was associated with reduced white matter integrity at follow-up: lower FA (p=0.03), higher AD (p=0.03) and higher RD (p=0.002). Lower FA at follow-up was associated with more neurobehavioral problems on initiation (Est -19.3, p=0.03), planning (Est -41.3, p=0.007), working memory (Est -40.6, p=0.002) and organization (Est -23.8, p=0.02). Leukoencephalopathy at follow-up was also associated with concurrent abnormalities in white matter integrity and more neurobehavioral problems on planning and organization. Conclusions: Even without cranial radiation, approximately a quarter of ALL patients developed leukoencephalopathy during active therapy, and are at risk for long-term neurobehavioral problems and reduced white matter integrity in frontal brain regions. Survivors who develop early leukoencephalopathy may benefit from preventative cognitive and/or behavioral interventions. Table 1. Survivor characteristics: Acute LeukoencephalopathyN (%) / mean [SD] No Acute LeukoencephalopathyN (%) / mean [SD] P Male (%) 27 (55) 62 (50) 0.55 Whites (%) 35 (71) 89 (72) 0.75 High risk (%) 23 (47) 48 (39) 0.32 Current age (years) 15.5 [4.8] 14.0 [4.6] 0.06 Age at diagnosis (years) 7.6 [5.0] 6.4 [4.0] 0.38 Time since diagnosis (years) 7.9 [2.0] 7.7 [1.7] 0.76 Total IV high-dose methotrexate (g/m2) 15.0 [4.4] 15.6 [7.4] 0.69 Total no. of intrathecal injections^ 15.1 [4.0] 14.1 [4.0] 0.07 Total oral dexamethasone (mg/m2) 1066.3 [343.0] 1108.1 [286.9] 0.43 BRIEF domains: Neurobehavioral problems Mean [SD]* Initiation 0.46 [1.1] 0.17 [1.1] 0.04 Organization of materials 0.65 [1.0] 0.18 [1.0] 0.004 Planning 0.57 [1.1] 0.24 [1.2] 0.04 Working memory 0.74 [1.4] 0.54 [1.2] 0.16 Emotional control 0.03 [1.0] 0.08 [1.1] 0.68 Inhibition 0.06 [1.1] 0.08 [1.2] 0.74 Shift 0.16 [1.3] -0.02 [1.1] 0.22 Monitor 0.08 [1.1] 0.02 [1.1] 0.33 *Age- and gender- adjusted scores with population mean=0 and SD=1. A higher score is indicative of more severe neurobehavioral problems. ^Inthrathecal combination of methotrexate, hydrocortisone and cytarabine Disclosures No relevant conflicts of interest to declare.

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Kim, Jaehyung, Chang-Hwan Ryu, Wonjae Sung, Hyunseung Gwak, Kyung-Pil Oh, Seong-Ho Koh, Kyu-Yong Lee, Young Joo Lee, and Hojin Choi. "Radiation-induced Leukoencephalopathy Presenting as Lower Body Parkinsonism." Journal of the Korean Neurological Association 33, no. 4 (November 1, 2015): 355–57. http://dx.doi.org/10.17340/jkna.2015.4.24.

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Eyre, J. A., D. Gardner-Medwin, and G. P. Summerfield. "Leukoencephalopathy after prophylactic radiation for leukaemia in ataxia telangiectasia." Archives of Disease in Childhood 63, no. 9 (September 1, 1988): 1079–80. http://dx.doi.org/10.1136/adc.63.9.1079.

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Pritchard, J. "Leukoencephalopathy after prophylactic radiation for leukaemia in ataxia telangiectasia." Archives of Disease in Childhood 64, no. 5 (May 1, 1989): 761–62. http://dx.doi.org/10.1136/adc.64.5.761.

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8

Cascino, Gregory D., and George L. Morris. "MULTIMODALITY EVOKED POTENTIALS IN LATE DELAYED RADIATION-INDUCED LEUKOENCEPHALOPATHY." Journal of Clinical Neurophysiology 5, no. 2 (April 1988): 199. http://dx.doi.org/10.1097/00004691-198804000-00031.

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Cummings, Michael, David W. Dougherty, Nimish A. Mohile, Kevin A. Walter, Kenneth Y. Usuki, and Michael T. Milano. "Severe radiation-induced leukoencephalopathy: Case report and literature review." Advances in Radiation Oncology 1, no. 1 (January 2016): 17–20. http://dx.doi.org/10.1016/j.adro.2016.01.002.

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Zemina, Kristen, Yolanda Piña, Patrick Malafronte, Niraja Suresh, and Rebeca Hurst. "Spongiform leukoencephalopathy: A unique case of biopsy confirmed leukoencephalopathy secondary to toxic, non-inflammatory exposure." SAGE Open Medical Case Reports 9 (January 2021): 2050313X2110429. http://dx.doi.org/10.1177/2050313x211042984.

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Toxin-induced leukoencephalopathy is a rare neurological condition that has been previously associated with intracranial radiation, chemotherapy, drugs of abuse, and environmental exposures. Herein, we present a patient with brain-biopsy proven toxin-induced leukoencephalopathy, likely secondary to multiple environmental offenders including insecticides and non-Food and Drug Administration approved anabolic steroids, opioids, and benzodiazepines. A 60-year-old man presented to our service as a direct transfer from an outside facility for evaluation of a rapidly progressive neuropsychiatric decline. Extensive workup with blood work, cerebrospinal fluid analysis, paraneoplastic panel, serial magnetic resonance imaging brain with and without contrast, and electroencephalograms were unrevealing. Magnetic resonance imaging brain showed diffuse confluent white matter disease, which was non-specific. The patient was treated with high-dose methylprednisolone and trials of intravenous immunoglobulin without any significant improvement. Finally, a brain biopsy was performed, and pathology confirmed a spongiform leukoencephalopathy, favoring a toxin-related etiology. The diagnosis of toxin-induced leukoencephalopathy should be considered in patients with steep neuropsychiatric decline and associated diffuse white matter disease. Diagnosis relies heavily on history of exposure, clinical presentation, imaging findings, and ultimately, histopathology from brain biopsy. The recognition of the clinical presentation is important to pursue the appropriate diagnostic workup and treatment.

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Ebi, J., H. Sato, and F. Shishido. "Leukoencephalopathy After Whole Brain Radiation Therapy for Metastatic Brain Tumors." International Journal of Radiation Oncology*Biology*Physics 69, no. 3 (November 2007): S255. http://dx.doi.org/10.1016/j.ijrobp.2007.07.1261.

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12

Krull, Kevin R., Noah D. Sabin, Wilburn E. Reddick, Liang Zhu, Gregory T. Armstrong, Daniel M. Green, Alejandro R. Arevalo, et al. "Neurocognitive Function and CNS Integrity in Adult Survivors of Childhood Hodgkin Lymphoma." Journal of Clinical Oncology 30, no. 29 (October 10, 2012): 3618–24. http://dx.doi.org/10.1200/jco.2012.42.6841.

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Purpose Long-term survivors of childhood Hodgkin lymphoma (HL) are at risk for cardiopulmonary complications and CNS stroke, although neurocognitive function has not been previously examined. The aim of this study was to examine neurocognitive and brain imaging outcomes in adult survivors of childhood HL. Patients and Methods In all, 62 adult survivors (mean age, 42.2 years; standard deviation [SD], 4.77; mean age at diagnosis, 15.1 years; SD, 3.30) were identified by stratified random selection from a large cohort treated with either high-dose (≥ 30 Gy) thoracic radiation (n = 38) or lower-dose (< 30 Gy) thoracic radiation combined with anthracycline (n = 24). Patients underwent neurocognitive evaluations, brain magnetic resonance imaging (MRI), echocardiograms, pulmonary function tests, and physical examinations. Results Compared with national age-adjusted norms, HL survivors demonstrated lower performance on sustained attention (P = .004), short-term memory (P = .001), long-term memory (P = .006), working memory (P < .001), naming speed (P < .001), and cognitive fluency (P = .007). MRI revealed leukoencephalopathy in 53% of survivors, and 37% had evidence of cerebrovascular injury. Higher thoracic radiation dose was associated with impaired cardiac diastolic function (E/E′; ratio of peak mitral flow velocity of early rapid filling [E] to early diastolic velocity of the mitral annulus [E′]; P = .003), impaired pulmonary function (diffusing capacity of lungs for carbon monoxide [DLcocorr; P = .04), and leukoencephalopathy (P = .02). Survivors with leukoencephalopathy demonstrated reduced cognitive fluency (P = .001). Working memory impairment was associated with E/E′, although impaired sustained attention and naming speed were associated with DLcocorr. Neurocognitive performance was associated with academic and vocational functioning. Conclusion These results suggest that adult long-term survivors of childhood HL are at risk for neurocognitive impairment, which is associated with radiologic indices suggestive of reduced brain integrity and which occurs in the presence of symptoms of cardiopulmonary dysfunction.

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Kim, Ji Yeon, Sung Tae Kim, Do-Hyun Nam, Jung-Il Lee, Kwan Park, and Doo-Sik Kong. "Leukoencephalopathy and Disseminated Necrotizing Leukoencephalopathy Following Intrathecal Methotrexate Chemotherapy and Radiation Therapy for Central Nerve System Lymphoma or Leukemia." Journal of Korean Neurosurgical Society 50, no. 4 (2011): 304. http://dx.doi.org/10.3340/jkns.2011.50.4.304.

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Kim, Byeong-suk, Jin-Hee Kim, Yun-Ha Hwang, and Taewon Kim. "Whole Brain Radiation Therapy Associated Diffuse Progressive Leukoencephalopathy and Brain Atrophy." Journal of the Korean Neurological Association 35, no. 3 (August 1, 2017): 189–90. http://dx.doi.org/10.17340/jkna.2017.3.19.

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Donker Kaat, Laura, Jacqueline C. F. van der Wielen-Jongen, Mark C. Kruit, Jacoline E. C. Bromberg, Frank Baas, and Saskia A. M. J. Lesnik Oberstein. "A case of co-occurrence of radiation-induced leukoencephalopathy and CADASIL." Neurology: Clinical Practice 10, no. 3 (August 30, 2019): e19-e21. http://dx.doi.org/10.1212/cpj.0000000000000705.

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Bompaire, Flavie, Marion Lahutte, Stephane Buffat, Carole Soussain, Anne Emmanuelle Ardisson, Robert Terziev, Magali Sallansonnet-Froment, et al. "New insights in radiation-induced leukoencephalopathy: a prospective cross-sectional study." Supportive Care in Cancer 26, no. 12 (July 7, 2018): 4217–26. http://dx.doi.org/10.1007/s00520-018-4296-9.

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Ebi, Junko, Hisashi Sato, Masaru Nakajima, and Fumio Shishido. "Incidence of Leukoencephalopathy After Whole-Brain Radiation Therapy for Brain Metastases." International Journal of Radiation Oncology*Biology*Physics 85, no. 5 (April 2013): 1212–17. http://dx.doi.org/10.1016/j.ijrobp.2012.09.025.

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Fauchon, François, Luis Davila, Gilles Chatellier, Denis Fohanno, Jacques Philippon, Alain Rey, Jacques Chiras, Michel Poisson, Jean Yves Delattre, and Jean Yves Delattre. "Treatment of Malignant Gliomas with Surgery, Intra-arterial Infusions of 1-(2-Hydroxyethyl)chloroethylnitrosourea, and Radiation Therapy: A Phase II Study." Neurosurgery 27, no. 2 (August 1, 1990): 231–34. http://dx.doi.org/10.1227/00006123-199008000-00010.

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Abstract Forty patients with malignant supratentorial gliomas were treated with surgery, intra-arterial infusions of 1-(2-hydroxyethyl) chloroethylnitrosourea, and radiation therapy. The median duration of survival was 12 months: it differed according to the histological subtype (over 30 months for patients with anaplastic astrocytomas or anaplastic oligoden-droglioma and 10.5 months for glioblastoma; P= 0.0025). Serious complications of monocular blindness and leukoencephalopathy were observed in four patients (10%).

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Trofimova, T. N., P. L. Andropova, Zh I. Savintseva, and N. A. Belyakov. "Radiology of the central nervous system of patients in the acute phase of СOVID-19." HIV Infection and Immunosuppressive Disorders 13, no. 2 (June 19, 2021): 20–32. http://dx.doi.org/10.22328/2077-9828-2021-13-2-20-32.

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This article, being based on the analysis of literature and the author’s own materials, outlines the features of the lesion of the central nervous system in a new coronavirus infection. The main idea is that despite the primary damage to the respiratory tract, SARS-CoV-2 can be attributed to a number of signs as neurotropic viruses, which is ultimately realized by the transport of the pathogen COVID-19 from the place of primary localization — the respiratory tract to the human brain. The virus is capable of hitting all possible pathways of being transferred through tissues and within a short time appears in the brain, interacting with ACE2 receptors and co-receptors, which are expressed in almost all brain cells, neurons, astrocytes, oligodendrocytes, microgliocytes, which carry out the main functional tasks of the brain. The clinical part is devoted to radiation diagnosis of lesions of the nervous system caused by the SARS-CoV-2 coronavirus. Analysis of the literature has made it possible to identify radiation variants of CNS lesions in COVID-19, illustrating the main clinical manifestations of the disease. There are several main clinical and morphological variants of CNS damage in COVID-19 1: acute ischemic stroke, acute encephalopathy, due to massive diffuse damage to the endothelium against the background of vasculitis / endotheliitis, occurring both with and without signs of cerebral artery thrombosis, hemorrhages, primarily of the type of small petechiae, polyetiologic in nature (endothelial damage, acute hypoxia, microembolism). In addition, hemorrhages can be a consequence of venous infarction against the background of sinus thrombosis. Radiological methods can diagnose multi-step lesions of the supra- and subtentorial white matter, vasculitis, in particular Susak’s syndrome, posterior reversible leukoencephalopathy — PRES, leukoencephalopathy, delayed post-hypoxic leukoencephalopathy, Miller–Fischer’s polyneuropathy (Guillain-Barre syndrome), syndrome.

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Natrusova, N. V., I. O. Shchederkina, E. V. Seliverstova, O. A. Tiganova, and K. L. Kondratchik. "Stroke-like leukopathy in children with acute lymphoblastic leukemia." Russian Journal of Pediatric Hematology and Oncology 8, no. 1 (April 7, 2021): 14–22. http://dx.doi.org/10.21682/2311-1267-2021-8-1-14-22.

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There are considerable variations in the reported incidence methotrexate-induced neurotoxicity in children with malignancies. The etiology of acute neurological deficit in pediatric patients with malignancies during polychemotherapy can be diverse: cerebrovascular disease (arterial ischemic stroke, intracranial hemorrhage, venous sinus thrombosis, or their combination), stroke-like migraine attacks after radiation therapy (SMART), posterior reversible encephalopathy syndrome (PRES), thrombotic microangiopathy, toxic leukoencephalopathy (include strokelike leukoencephalopathy). The tactics of a neurologist largely depends on the reasons that caused the neurological deficit. The doctor needs knowledge not only of the clinical picture and the characteristics of the course of the underlying disease, but also of possible complications arising both as a result of the disease itself and due to the therapy being carried out. Timely diagnosis and correct interpretation of emerging neurological events make it possible to determine rational accompanying therapy. The article presents case histories of children with acute lymphoblastic leukemias and acute neurological deficits, with an analysis of their possible causes.

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Thompson, CB, JE Sanders, N. Flournoy, CD Buckner, and ED Thomas. "The risks of central nervous system relapse and leukoencephalopathy in patients receiving marrow transplants for acute leukemia." Blood 67, no. 1 (January 1, 1986): 195–99. http://dx.doi.org/10.1182/blood.v67.1.195.195.

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Abstract The records of 415 patients who received allogeneic marrow transplants for acute leukemia were reviewed to assess the risk of central nervous system (CNS) relapse and leukoencephalopathy after marrow transplantation. The Kaplan-Meier estimates of the probability of CNS relapse posttransplant were 13% for patients with acute lymphoblastic leukemia (ALL) and 2% for patients with acute nonlymphoblastic leukemia (ANL). Previous CNS disease was significantly correlated with an increased risk of CNS relapse in patients transplanted for ALL but not for ANL. In contrast, bone marrow involvement with leukemia at the time of transplant was associated with an increased risk of CNS relapse in patients with ANL but not in patients with ALL. Seventy-one patients with ALL did not receive posttransplant intrathecal methotrexate (IT- MTX) and 127 did. The probability of CNS relapse in these two groups was 38% and 7%, respectively (P less than .02). This protective benefit from IT-MTX was present in patients both with and without a history of CNS involvement or marrow involvement at the time of transplant. In patients with ANL, 116 patients did not receive posttransplant IT-MTX and 101 patients did, but no protection from CNS relapse was observed from IT-MTX irrespective of a patient's previous CNS history or marrow status at the time of transplant. Leukoencephalopathy was seen exclusively in patients who had received radiation and/or intrathecal chemotherapy to the CNS before preparation for marrow transplantation and posttransplant IT-MTX. In such patients the risk of leukoencephalopathy was 7%. From our data, it appears that posttransplant IT-MTX is a significant benefit for ALL patients in preventing CNS relapse after marrow transplantation. A similar benefit from posttransplant IT-MTX for ANL patients cannot be established from this study. In both groups, increasing total CNS therapy was associated with an increasing risk of leukoencephalopathy.

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Thompson, CB, JE Sanders, N. Flournoy, CD Buckner, and ED Thomas. "The risks of central nervous system relapse and leukoencephalopathy in patients receiving marrow transplants for acute leukemia." Blood 67, no. 1 (January 1, 1986): 195–99. http://dx.doi.org/10.1182/blood.v67.1.195.bloodjournal671195.

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The records of 415 patients who received allogeneic marrow transplants for acute leukemia were reviewed to assess the risk of central nervous system (CNS) relapse and leukoencephalopathy after marrow transplantation. The Kaplan-Meier estimates of the probability of CNS relapse posttransplant were 13% for patients with acute lymphoblastic leukemia (ALL) and 2% for patients with acute nonlymphoblastic leukemia (ANL). Previous CNS disease was significantly correlated with an increased risk of CNS relapse in patients transplanted for ALL but not for ANL. In contrast, bone marrow involvement with leukemia at the time of transplant was associated with an increased risk of CNS relapse in patients with ANL but not in patients with ALL. Seventy-one patients with ALL did not receive posttransplant intrathecal methotrexate (IT- MTX) and 127 did. The probability of CNS relapse in these two groups was 38% and 7%, respectively (P less than .02). This protective benefit from IT-MTX was present in patients both with and without a history of CNS involvement or marrow involvement at the time of transplant. In patients with ANL, 116 patients did not receive posttransplant IT-MTX and 101 patients did, but no protection from CNS relapse was observed from IT-MTX irrespective of a patient's previous CNS history or marrow status at the time of transplant. Leukoencephalopathy was seen exclusively in patients who had received radiation and/or intrathecal chemotherapy to the CNS before preparation for marrow transplantation and posttransplant IT-MTX. In such patients the risk of leukoencephalopathy was 7%. From our data, it appears that posttransplant IT-MTX is a significant benefit for ALL patients in preventing CNS relapse after marrow transplantation. A similar benefit from posttransplant IT-MTX for ANL patients cannot be established from this study. In both groups, increasing total CNS therapy was associated with an increasing risk of leukoencephalopathy.

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Rosa Júnior, Marcos, and Antônio José da Rocha. "Late radiation therapy brain abnormalities that mimic leukoencephalopathy with anterior temporal lobe cysts." Arquivos de Neuro-Psiquiatria 75, no. 3 (March 2017): 199–200. http://dx.doi.org/10.1590/0004-282x20160196.

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Iuchi, T., K. Hatano, M. Ohira, T. Sakaida, and A. Nakagawara. "Identification of Candidate Genes which Regulate Radiation-induced Leukoencephalopathy by cDNA Microarray Analysis." International Journal of Radiation Oncology*Biology*Physics 75, no. 3 (November 2009): S233—S234. http://dx.doi.org/10.1016/j.ijrobp.2009.07.538.

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Gorgan, Mircea Radu, Andrei Giovani, Aurelia Mihaela Sandu, Felix Mircea Brehar, Narcisa Bucur, Angela Neacşu, and Catioara Fănica Cristescu. "Radio-induced brain lesions." Romanian Neurosurgery 21, no. 1 (March 1, 2014): 31–36. http://dx.doi.org/10.2478/romneu-2014-0003.

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Abstract Introduction : Radiotherapy, an important tool in multimodal oncologic treatment, can cause radio-induced brain lesion development after a long period of time following irradiation. Material and method : We report 4 cases with radio-induced brain lesions, admitted into the Fourth Department of Neurosurgery, Emergency Clinical Hospital Bagdasar-Arseni, during a 4 years period of time. Results : Two patients had meningiomas and two had unruptured cavernomas. Other side effects of radiotherapy, such as diffuse brain atrophy, leukoencephalopathy, optic atrophy, panhypopituitarism were also noted. The two patients with large meningiomas underwent surgery, with good outcome. Observation was the choice for the two asymptomatic cavernomas. Panhypopituitarism needed synthetic hormonal replacement therapy. Conclusions : Radiotherapy can cause long-term complications and can induce development of new brain lesions into previous radiation area. Meningiomas and cavernomas can be radio-induced brain lesions. Meningiomas can grow to large size, requiring surgery. Unruptured asymptomatic cavernomas can be left in place and patients are followed clinical and with serial imaging. Other findings after radiotherapy are diffuse brain atrophy, leukoencephalopathy, optic atrophy and panhypopituitarism.

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Pande, Ajaya R., Kumiko Ando, Reiichi Ishikura, Yuki Nagami, Masayo Ogawa, Norihiko Kamikonya, Yumi Kaneda, Takakuni Tanizawa, and Norio Nakao. "Disseminated necrotizing leukoencephalopathy following chemoradiation therapy for acute lymphoblastic leukemia." Radiation Medicine 24, no. 7 (September 22, 2006): 515–19. http://dx.doi.org/10.1007/s11604-006-0059-5.

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Winter, Sebastian, Joshua Klein, and Jörg Dietrich. "Neuroimaging of Brain Tumors: Pseudoprogression, Pseudoresponse, and Delayed Effects of Chemotherapy and Radiation." Seminars in Neurology 37, no. 05 (October 2017): 589–96. http://dx.doi.org/10.1055/s-0037-1608657.

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AbstractManagement of patients with brain cancer critically depends on an accurate interpretation of imaging findings that will guide treatment decisions. Treatment with chemotherapy and radiation can affect the imaging characteristics of a tumor and therefore cause misinterpretation of treatment response. Specifically, radiotherapy or chemotherapy may result in distinctive imaging abnormalities that can be challenging to differentiate from tumor itself. Moreover, cancer therapy can be associated with unique adverse effects on the brain, which need to be appropriately recognized by the treating physician to guide patient management. Specific imaging findings, such as radiation-induced tissue necrosis, leukoencephalopathy, pseudoprogression, and pseudoresponse represent treatment-related phenomena that can complicate interpretation of imaging studies and clinical decision making. The aim of this review is to describe these phenomena and improve clinician familiarity as to how these appear on structural (MRI) and functional (perfusion, spectroscopy, PET) imaging studies.

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Conill, C., J. Berenguer, M. Vargas, A. López-Soriano, I. Valduvieco, J. Marruecos, and R. Vilella. "Incidence of radiation-induced leukoencephalopathy after whole brain radiotherapy in patients with brain metastases." Clinical and Translational Oncology 9, no. 9 (September 2007): 590–95. http://dx.doi.org/10.1007/s12094-007-0108-2.

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Perrini, P., A. Scollato, F. Cioffi, H. Mouchaty, R. Conti, and N. Di Lorenzo. "Radiation leukoencephalopathy associated with moderate hydrocephalus: intracranial pressure monitoring and results of ventriculoperitoneal shunting." Neurological Sciences 23, no. 5 (December 1, 2002): 237–41. http://dx.doi.org/10.1007/s100720200048.

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Ejima, Y., R. Sasaki, A. Matsumoto, T. Soejima, T. Kawabe, H. Nishimura, and K. Sugimura. "Identification of target cells for CNS radiation injury: is apoptosis of neural stem cells a pathogenesis of radiation-induced leukoencephalopathy." International Journal of Radiation Oncology*Biology*Physics 51, no. 3 (November 2001): 127. http://dx.doi.org/10.1016/s0360-3016(01)02055-7.

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Sasaki, R., A. Matsumoto, T. Soejima, Y. Ejima, T. Kawabe, H. Nishimura, O. Fujii, and K. Sugimura. "Identification of target cells for CNS radiation injury: Is apoptosis of neural stem cells a pathogenesis of radiation-induced leukoencephalopathy?" European Journal of Cancer 37 (April 2001): S206—S207. http://dx.doi.org/10.1016/s0959-8049(01)81248-x.

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Winter, S. F., M. Gardner, M. W. Parsons, C. Grassberger, M. Bussière, D. Kaul, W. Boehmerle, M. Endres, H. A. Shih, and J. Dietrich. "P03.05.A Radiation-induced leukoencephalopathy (RIL) in glioma: unique injury dynamics following proton vs photon beam radiotherapy." Neuro-Oncology 24, Supplement_2 (September 1, 2022): ii33. http://dx.doi.org/10.1093/neuonc/noac174.109.

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Abstract Background White matter injury after brain-directed radiotherapy (RT), aka radiation-induced leukoencephalopathy (RIL), is common in brain tumor patients. Differentiation from progressive disease can be challenging. Dosimetric advantages of protons (PRT) over photons (XRT) minimize radiation to healthy brain tissue, potentially limiting radiotoxic sequelae including RIL. We characterized RIL during periods of progression-free survival (PFS) in glioma patients irradiated with either PRT or XRT, hypothesizing that PRT would result in reduced RIL outside of the target field. Material and Methods 34 patients (19 male; mean age = 40.10y) with grade 2/3 gliomas and a history of partial cranial RT were stratified by RT modality [XRT (n=17) vs PRT (n=17)] and matched on 11 criteria [age, sex, tumor type/location/laterality, mutational status (IDH; 1p19q deletion), concurrent/adjuvant chemotherapy, radiation dose/fractions] for retrospective analysis. RIL development was characterized longitudinally for up to 3 years post-RT via analysis of serial MRI T2/FLAIR sequences. A novel RIL scoring system with embedded Fazekas scale was designed to quantify injury severity at both global (whole brain) and hemispheric levels. Results Matched groups did not differ significantly on any demographic or clinical characteristics. Median PFS post-RT was 4.7 (XRT) and 5.1 (PRT) years. The novel RIL scoring system was reliable (intraclass correlation coefficient >0.9). There was a significant increase in global RIL in both XRT [F(3, 57)=8.63, p< .001] and PRT [F(3, 61)=4.69, p< .005] groups over time, relative to baseline (1-month post-RT). A majority [62% (XRT) and 72% (PRT)] developed moderate or severe RIL within 3 years, with the ipsilesional hemisphere more severely affected. Analysis of RIL injury dynamics (i.e., average % change between 1 and 3 years post-RT) at hemispheric level identified radiation modality-specific differences: XRT resulted in greater contralesional hemispheric injury than PRT [F(1, 31)=4.32, p<.05]. This effect was not observed in ipsilesional hemispheres. Conclusion RIL is common in glioma patients and quantifiable by characteristic imaging features, including early onset post-RT, greater ipsilesional injury burden, and progression over time. RIL injury dynamics appear to be radiation modality-specific, whereby XRT causes greater delayed injury in the remote, contralesional hemisphere. These findings may reflect dosimetric differences between protons and photons. The impact of such sequelae on cognitive function is subject of current investigation.

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Monaco, Edward A., Amir H. Faraji, Oren Berkowitz, Phillip V. Parry, Uri Hadelsberg, Hideyuki Kano, Ajay Niranjan, Douglas Kondziolka, and L. Dade Lunsford. "Leukoencephalopathy after whole-brain radiation therapy plus radiosurgery versus radiosurgery alone for metastatic lung cancer." Cancer 119, no. 1 (June 15, 2012): 226–32. http://dx.doi.org/10.1002/cncr.27504.

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Samotolkina, E. A., A. V. Pokrovskaya, S. V. Matosova, and E. A. Domonova. "Progressive multifocal leukoencephalopathy in HIV-infected patients: clinical features and diagnosis (literature review)." Journal Infectology 11, no. 3 (October 9, 2019): 5–12. http://dx.doi.org/10.22625/2072-6732-2019-11-3-5-12.

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Progressive multifocal leukoencephalopathy (PML) is one of the most severe opportunistic diseases of the central nervous system, which leads to multiple demyelination of brain structures, neurological symptoms and frequent death or disability of the patient. The etiological factor of this disease is Human polyomavirus 2 (JCPyV).This pathogen is widespread – antibodies are found in 80% of the world›s population. However, the clinical symptoms of this infection appear only in people with a pronounced decline in cellular immunity. Until 1980 progressive multifocal leukoencephalopathy was extremely rarely diagnosed. Now days the main cause of the clinical symptoms of PML is immunodeficiency caused by HIV infection. Clinical manifestations of PML are characterized by various non-specific neurological symptoms, similar to other lesions of the central nervous system, the symptoms progress slowly over several months, and usually lead to death. Diagnosis of PML is based on laboratory and instrumental methods, such as DNA JCPyV detection in the cerebrospinal fluid, brain biopsy, and radiation diagnostic methods. There is no effective prevention and etiotropic therapy for PML. Improved parameters of cellular immunity and antiretroviral treatment in HIV positive patients significantly increase the life expectancy of patients with PML. Despite the ability of drugs to prevent the progression of the disease, pathological changes in the brain are irreversible and lead to persistent disability of patients, therefore, it is necessary to diagnose PML in the early stages of the disease.

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Nagashima, Hiroaki, Tatsuo Hori, Hirofumi Iwahashi, Kazuhiro Tanaka, and Takashi Sasayama. "RBIO-07. HIGHER CSF IL-10 CORRELATE WITH BRAIN ATROPHY AFTER WHOLE BRAIN RADIATION THERAPY IN PRIMARY CENTRAL NERVOUS SYSTEM LYMPHOMA." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii248. http://dx.doi.org/10.1093/neuonc/noac209.959.

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Abstract Whole brain radiation therapy (WBRT) to primary central nervous system lymphoma (PCNSL) correlate with brain atrophy and leukoencephalopathy on serial computed tomography or MRI scans, negatively impacting cognitive function and quality of life. We retrospectively evaluated 53 patients with histologically proven PCNSL who underwent cerebrospinal fluid (CSF) examination including β2-MG, sIL2R, CXCL13, and IL-10 preoperatively. All patients were newly diagnosed and followed up every 3 months from the day they were discharged from the hospital. Follow up period is at least 1 year from last day of chemotherapy. Clinical data included patient demographics, radiological and characteristics; whole brain volume (mm2) calculated from BainLabTM automatically, Global Cortical Atrophy (GCA) for global brain atrophy, Medial Temporal Atrophy (MTA) for temporal atrophy, and Fazekas scale for white matter lesions. The unpaired t test and multivariable liner regression were used to examine the clinical, CSF and radiological characteristics of patients. The mean age at symptom onset was 65.2 years (47-85 years). Thirty three of 53 (62%) patients underwent WBRT with chemotherapy (WBRT group). In all patients, multivariable analysis revealed WBRT correlate with brain volume reduction (p=0.0005) and progression of temporal lobe atrophy (p=0.0056). In addition, Age correlated with increasing white matter lesions at 1 year after chemotherapy (p=0.0422). In WBRT group, multivariable analysis indicated that high CSF IL-10 level accelerated brain volume reduction (p=0.0122) and temporal lobe atrophy (p=0.0343) at 6 months after chemotherapy. However, there were no significant factor for influencing brain atrophy at 1 year. Higher IL-10 ( > 100mg/ml) level demonstrated higher brain atrophy rate (p=0.0366) and severe temporal atrophy at 1 year (p=0.0214). In elderly patients with high preoperative CSF IL-10 levels, cerebral atrophy and toxic leukoencephalopathy may progress in short period of time after WBRT. We should consider treatment strategy that avoid WBRT, such as R-MPV chemotherapy, for PCNSL patients.

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Matsubayashi, Jun, Kuniaki Tsuchiya, Takashi Matsunaga, and Kiyoshi Mukai. "Methotrexate-related leukoencephalopathy without radiation therapy: Distribution of brain lesions and pathological heterogeneity on two autopsy cases." Neuropathology 29, no. 2 (April 2009): 105–15. http://dx.doi.org/10.1111/j.1440-1789.2008.00945.x.

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Zhong, Xiaoling, Biao Huang, Jieying Feng, Wanqun Yang, and Hongjun Liu. "Delayed leukoencephalopathy of non-small cell lung cancer patients with brain metastases underwent whole brain radiation therapy." Journal of Neuro-Oncology 125, no. 1 (August 15, 2015): 177–81. http://dx.doi.org/10.1007/s11060-015-1888-9.

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Yokoyama, Tomoya, Akihiko Saida, Kenta Nagai, Megumi Ichikawa, Hiroaki Namatame, Tomoo Ohashi, and Michihiro Kohno. "A Case of Progressive Multifocal Leukoencephalopathy with Lung Cancer-related Brain Metastasis after Operation and Radiation Therapy." Japanese Journal of Neurosurgery 28, no. 4 (2019): 223–28. http://dx.doi.org/10.7887/jcns.28.223.

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Rosales, Kristofer, Ossama Maher, Maggie Fader, Natalie Gallegos, Toba Niazi, John Ragheb, and Ziad Khatib. "DDEL-14. SAFETY OF INTERVENTRICULAR METHOTREXATE ADMINISTRATION FOLLOWING RADIATION IN PEDIATRIC PATIENTS WITH MALIGNANT BRAIN TUMORS." Neuro-Oncology 22, Supplement_3 (December 1, 2020): iii286. http://dx.doi.org/10.1093/neuonc/noaa222.049.

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Abstract BACKGROUND Methotrexate has been used for intrathecal administration in leukemia as well as embryonal CNS tumors in children. Concerns about neurologic side effects including leukoencephalopathy, demyelination, and seizures have limited the use of methotrexate following exposure to focal radiation. OBJECTIVE To evaluate and determine safety of Intraventricular administration of Methotrexate in pediatric patients with recurrent malignant brain tumors along with systemic Topotecan and Cyclophosphamide after exposure to prior radiation therapy. DESIGN/METHOD: Patients with recurrent cerebellar embryonal tumors after standard treatment that included radiation were enrolled on this IRB approved phase 2 study. An Ommaya reservoir was inserted in the lateral ventricle and used to administer 4 daily doses of methotrexate (2 mg/dose) along with (Topotecan [0.75mg/m2/day] and Cyclophosphamide [250 mg/m2/day]). A neurological evaluation was performed at baseline and daily during the intraventricular administration of the Methotrexate, this evaluation was repeated prior to each subsequent cycle and at completion of the protocol. RESULTS Three patients (age range 3–20) received 2–3 cycles of intra-Ommaya Methotrexate and Topotecan/Cyclophosphamide. No MRI demyelination or white matter changes were seen after completion of the intraventricular Methotrexate therapy. None of the patients enrolled on this trial had adverse effects related to the therapy regimen received. Clinical neurological status was unchanged during the entire course of the treatment and upon completion of the scheduled therapy. CONCLUSION Intraventricular administration of daily low dose Methotrexate is well tolerated in children with recurrent embryonal CNS tumors who had prior exposure to radiation.

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Krull, Kevin R., Noah D. Sabin, Wilburn E. Reddick, Liang Zhu, Gregory T. Armstrong, Daniel M. Green, Deo Kumar Srivastava, Monika L. Metzger, Leslie L. Robison, and Melissa M. Hudson. "Central Nervous System Integrity in Adult Survivors of Childhood Hodgkin Lymphoma,." Blood 118, no. 21 (November 18, 2011): 3647. http://dx.doi.org/10.1182/blood.v118.21.3647.3647.

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Abstract Abstract 3647 Long-term survivors of childhood Hodgkin Lymphoma (HL) are at risk for cardiopulmonary complications. Although HL survivors are generally not exposed to treatments directed at the central nervous system (CNS), cardiac and pulmonary abnormalities are associated with CNS dysfunction in non-cancer populations. The aim of the current study was to examine neurocognitive and neuroanatomical outcomes in adult survivors of childhood HL. 62 adult survivors (current age mean=43.2, SD=4.79, range=34.4–55.6 years; age at diagnosis mean=15.1, SD=3.31, range=5.85–19.00 years) were identified by stratified random selection from a large cohort treated with either high dose (≥ 30 Gy) thoracic radiation (n=38) or lower dose (< 30Gy) thoracic radiation combined with anthracycline (n=24). Patients underwent neurocognitive evaluations, brain magnetic resonance imaging (MRI), echocardiograms, pulmonary function tests, and physical exams. MRI techniques included T1 and T2 weighted imaging, as well as susceptibility weighted imaging (SWI). Images were objectively processed to obtain global diffusion tensor imaging (DTI) and regional cortical thickness. Images were also reviewed and systematically coded by a board certified neuroradiologist. Compared to national age-adjusted norms, HL survivors demonstrated lower performance on attention span (p=0.01), sustained attention (p=0.01), short-term memory (p=0.001), long-term memory (p=0.006), motor dexterity (p<0.001), and cognitive fluency (p=0.007). Brain MRI revealed some degree of white matter disease (e.g. leukoencephalopathy) in 51.8% of survivors, 68.5% had at least mild cerebral atrophy, and 30.0% had SWI suggestive of cerebrovascular abnormalities. Survivors with evidence of cerebrovascular abnormalities on SWI demonstrated cortical thinning in dorsolateral frontal regions (p=0.006), those with cerebral atrophy had DTI evidence of reduced white matter integrity (p=0.04). Increased attention problems were correlated with decreased cortical thickness in frontal brain regions (p=0.03), while survivors with leukoencephalopathy demonstrated reduced cognitive fluency (p=0.001). Neurocognitive and neuroanatomical measures were associated with abnormal cardiac and pulmonary test results. Focused attention was decreased in patients with lower pulmonary forced expiratory flow (FEF; p=0.04), lower hemoglobin (p=0.02), and lower left ventricular ejection fraction (p=0.04). Long-term memory was decreased in patients with lower hemoglobin (p=0.008), and higher diastolic blood pressure (p=0.02). Survivors with SWI evidence of cerebrovascular abnormalities demonstrated reduced pulmonary FEF (p=0.03). Neurocognitive impairment was associated with dose of thoracic radiation. These results suggest that adult long-term survivors of HL are at increased risk for neurocognitive impairment, which is associated with radiological indices suggestive of reduced brain integrity and occurs in the presence of symptoms of cardiopulmonary dysfunction. Disclosures: No relevant conflicts of interest to declare.

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Focosi, Daniele, Marco Tuccori, Corrado Blandizzi, Mario Del Tacca, and Mario Petrini. "Incidence of Progressive Multifocal Leukoencephalopathy in Non-Hodgkin Lymphoma Patients Treated with Rituximab." Blood 114, no. 22 (November 20, 2009): 3675. http://dx.doi.org/10.1182/blood.v114.22.3675.3675.

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Abstract Abstract 3675 Poster Board III-611 Progressive multifocal leukoencephalopathy (PML) is a rare complication of immunesuppression due to productive reactivation of JC polyomavirus (JCV) in glial cells. In the last decades many case reports of rituximab-associated PML have raised concerns, but no systematic incidence rate analysis has been ever performed. We retrospectively reviewed our clinical records with the aim of calculating the incidence rate of PML in patients with NHL who had been treated with regimens including rituximab. Data on HIV-negative patients who received the first dose of rituximab from January 1, 2000 to June 30, 2008, were analyzed. The follow-up period was from the first rituximab dose to the last recorded visit, up to September 30, 2008. PML cases were included if symptoms occurred at least 1 month after the first dose of rituximab and the diagnosis was supported by magnetic resonance imaging and detection of JCV DNA in stereotactic brain biopsies and/or cerebrospinal fluid. We collected data from 821 consecutive patients throughout the follow-up period. All patients received chemotherapy other than rituximab, and all completed their entire treatment course at the Hematology Unit in Pisa. No radiation therapy was administered. The median time of follow-up was 20 months (range = 1-106 month), resulting in 1725 patient-years at risk. Five cases of PML (two receiving maintenance rituximab) were identified, with an incidence rate of 2.89 cases per 1000 patient-years. We found that the incidence rate of PML in our population exceeded that observed in patients who are traditionally regarded as being at high risk of PML, namely patients with B-cell chronic lymphocytic leukaemia and AIDS. Rituximab might be a potential contributing factor to the development of PML in these patients. Nevertheless, rituximab currently represents an essential therapeutic tool that can positively affect the natural history of NHL. However, because of the expanding therapeutic indications, it seems reasonable to investigate the potential contribution of rituximab to PML occurrence. Disclosures: No relevant conflicts of interest to declare.

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Bompaire, F., M. Lahutte, D. Psimaras, M. Sallansonnet-Froment, T. De Greslan, H. Taillia, J. Renard, S. Alamovitch, K. Hoang-Xuan, and D. Ricard. "O3.02 * RADIATION-INDUCED LEUKOENCEPHALOPATHY IS A DEFINITE TYPE OF SMALL VESSEL DISEASE - NEUROPSYCHOLOGICAL AND MRI DESCRIPTION IN 40 PATIENTS." Neuro-Oncology 16, suppl 2 (September 1, 2014): ii1—ii112. http://dx.doi.org/10.1093/neuonc/nou174.16.

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Beitinjaneh, Amer, Alexander McKinney, Qing Cao, and Daniel J. Weisdorf. "Fludarabine-Associated Neurotoxicity After Hematopoietic Cell Transplantation (HCT): Clinical and Radiographic Features Predict Outcome." Blood 114, no. 22 (November 20, 2009): 2270. http://dx.doi.org/10.1182/blood.v114.22.2270.2270.

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Abstract Abstract 2270 Poster Board II-247 Central nervous system (CNS) toxicity after HCT is an uncommon, but serious cause of transplant related mortality. Recently, toxic leukoencephalopathy is better defined using advanced MRI techniques. We reviewed all the medical records of HCT recipients (2000-2007) who received Flu-containing conditioning regimens in our institution and developed sever central nervous toxicity. We asked a specialized neuroradiologist to review their brain imagines blindly from patients' outcomes. From our database review, cases were excluded if neurologic symptoms were related to peripheral neuropathy, CNS infection, intracranial bleeding, stroke, CNS malignancy, sedative medication effect, or metabolic disturbance. We were able to identify 39 cases of sever leukoencephalopathy out of total1596 transplants and we described 3 distinct Flu-associated clinical syndromes with unique clinical and radiographic characteristics. Posterior reversible encephalopathy syndrome (PRES, n=17, 1.1%) presented with seizures, persistent headache, or visual changes along with varying compromise in mental status. Acute Toxic Leukoencephalopathy, (ATL, n=11, 0.7%) resulted mainly in cognitive dysfunction, decreased levels of consciousness, and some vision changes. A third distinct Leukoencephalopathy syndrome (LS, n=11, 0.7%) presented similarly to ATL but with less specific and chronic-appearing deep white matter changes on MRI. PRES favors the cortex/subcortical white matter (SCWM) in the early phases and ATL/LS favor the deep periventricular white matter (PVWM) in the early stages, these two entities can usually be distinguished from each other utilizing the combination of fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted images (DWI) MRI techniques (Typically diffusion is reduced in ATL and normal in PRES). Other associated features included: younger age in PRES (median 20 years vs. 55 in ATL and 42 in LS). ATL and LS can be reversible, but to a lesser degree than PRES. PRES developed later (median 77 days post HCT) compared to 30 and 31 days for ATL and LS. Patients who developed ATL had shorter overall survivals than patients with PRES and LS patients (Median overall survival was 6.9 month for PRES compared to 2 months in ATL). ATL/LS compared to PRES were more likely to present with cognitive dysfunction than seizure (refer to table). Flu-associated ATL/LS may be more common in older patients, those with renal dysfunction, prior CNS radiation or chemotherapy, and in patients received higher dose of Flu compared to PRES. Our review suggests Brian MRI with Diffusion-weighted imaging (DWI) can add considerable diagnostic and prognostic information. Prospective Flu pharmacokinetic and pharmacogenetic studies may be needed to determine the most appropriate Flu dosing to avoid neurotoxicity. Table: Brief summary of patients' characteristics and clinical features. Different Groups Total PRES ATL LS Number 39 17 11 11 Median Age (range) 43 (3-69) 20 55 42 Total conditioning FLU (mg/m2) 200 144 200 200 Baseline Cr CL (mg/min/1.73 m2) 92 100.6 81 85.3 Previous Flud 3 0 3 0 CNS Therapy 13 2 6 5 HCT 9 2 5 2 Presenting Symptom Seizure 8 (21%) 7 (41%) 0 1 Confusion /cognitive 12 (30%) 2(12%) 5 (46%) 5 (46%) Median survival (days) 169 208 66 204 Death Related 13 2 7 4 Disclosures: No relevant conflicts of interest to declare.

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Tsuzuki, Shunsuke, Masayuki Nitta, Taiichi Saito, Takashi Maruyama, Shunichi Koriyama, Atsushi Kuwano, Manabu Tamura, Soko Ikuta, Takakazu Kawamata, and Yoshihiro Muragaki. "RT-7 DIFFERENTIATION AND TREATMENT OF RECURRENCE AND RADIATION NECROSIS IN THE TREATMENT OF MALIGNANT GLIOMAS." Neuro-Oncology Advances 4, Supplement_3 (December 1, 2022): iii14. http://dx.doi.org/10.1093/noajnl/vdac167.051.

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Abstract Background In the course of treatment of malignant gliomas, the appearance of contrast-enhanced lesions and surrounding T2/FLAIR high-signal after treatment is often experienced. There is no modality that can reliably diagnose whether the lesion is a recurrence or a response to treatment, including radiation necrosis. Furthermore, the choice of treatment modality is often difficult, such as reexcision, stereotactic irradiation, Avastin. Very few reports have examined the relationship between the irradiation field and histology. Methods Thirty-seven lesions in 30 patients who underwent repeat resection of malignant gliomas at our institution from October 2019 to December 2021 were analyzed retrospectively. Based on postoperative pathology, the patients were classified into two groups: recurrence group and radiation necrosis group.In each group, age, gender, histology at initial surgery, IDH status, radiation and chemotherapy, TNR of Methionine-PET, and the number of days after the end of treatment until the appearance of contrast lesions were considered. Results The recurrence group consisted of 20 patients with 26 lesions, mean age 48 years, male/female = 13/7, pathology was GBM 13, DA 1, AA 3, AO 2, AE 1, TNR 3.33 (1.41-6.32), and time to contrast appearance 547 (14-2427) days. PDT in combination with initial surgery was seen in 9 patients.The necrosis group consisted of 10 patients with 11 lesions, mean age 47 years, male/female = 4/6, pathology GBM 5, AA 2, AO 1, PXA 2. TNR 2.51 (1.20-3.75), 318 (24-678) days to contrast appearance, 2 patients had PDT. Conclusions Radiation necrosis tended to have lower TNR and shorter time to lesion appearance than recurrence, but no significant difference was observed. Improvement of diagnostic accuracy with modalities is desirable, and unnecessary irradiation is highly likely to contribute to ADL deterioration such as leukoencephalopathy and higher functional impairment.

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Kraft, J., M. C. Mayinger, J. Willmann, D. H. Schanne, S. Lang, L. Willke, N. Lohaus, M. Guckenberger, and N. Andratschke. "Leukoencephalopathy after Prophylactic Whole-Brain Irradiation with or without Hippocampal Sparing: A Long-Term MRI Analysis." International Journal of Radiation Oncology*Biology*Physics 105, no. 1 (September 2019): E79. http://dx.doi.org/10.1016/j.ijrobp.2019.06.2342.

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Winter, Sebastian, Melissa Gardner, Michael Parsons, Clemens Grassberger, Marc Bussière, Felix Ehret, David Kaul, et al. "RADT-23. MODALITY-SPECIFIC CNS INJURY FOLLOWING PROTON VS PHOTON BEAM RADIOTHERAPY IN GLIOMA." Neuro-Oncology 24, Supplement_7 (November 1, 2022): vii54. http://dx.doi.org/10.1093/neuonc/noac209.213.

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Abstract BACKGROUND CNS injury following brain-directed radiotherapy (RT) is common and may mimic disease progression. Dosimetric advantages of protons (PRT) over photons (XRT) minimize radiation to healthy brain, potentially limiting radiotoxic sequelae. We characterized CNS radiotoxicity i.e., radiation-induced leukoencephalopathy (RIL), brain tissue necrosis (TN), and cerebral microbleeds (CMB), during progression-free survival (PFS) periods in glioma patients irradiated with PRT or XRT. METHODS 34 patients (19 male; mean age = 40.10y) with grade 2/3 gliomas treated by partial cranial RT were stratified by RT modality [XRT(n = 17) vs PRT(n = 17)] and matched on 11 criteria [age, sex, tumor type/location/laterality, mutational status (IDH; 1p19q deletion), concurrent/adjuvant chemotherapy, radiation dose/fractions] for retrospective analysis. Radiotoxicity was characterized longitudinally until 3 years post-RT via analysis of serial MRI T2/FLAIR- (RIL), T1+Contrast- (TN), and Susceptibility (CMB)-weighted sequences. RIL was rated using a novel scoring system with embedded Fazekas scale (intraclass correlation coefficient > 0.9), at global (whole-brain) and hemispheric levels. RESULTS Analysis of delayed radiotoxicity at 3 years post-RT identified significant modality-specific differences. While both groups developed moderate-to-severe RIL [62% (XRT) and 72% (PRT)], XRT resulted in greater RIL injury dynamics (i.e., average % change between 1 and 3 years post-RT) in the contralesional hemisphere [F(1, 31) = 4.32, p < .05]. Conversely, PRT was associated with higher TN incidence [6%(XRT) vs 18%(PRT) z = - 2.22, p < 0.03, two-tailed]. Finally, while CMB incidence [76%(XRT) vs 71%(PRT)] and burden [mean #CMB: 4.3(XRT) vs 4.2(PRT)] were comparable, lesion-to-radiation field (RF)-correlation identified preferential CMB clustering at RF margins with PRT [X2(2, N =200)= 8.8, p < .02]. CONCLUSIONS CNS radiotoxicity is common and progressive in glioma patients. Injury patterns suggest radiation modality specificity as RIL, TN, and CMB exhibit unique spatiotemporal differences following XRT vs PRT, likely reflecting dosimetric and biological differences between protons and photons. The impact of such sequelae on cognition is subject of current investigation.

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Matsumoto, Ko, Shoki Takahashi, Atsushi Sato, Masue Imaizumi, Shuichi Higano, Kiyohiko Sakamoto, Hiroshi Asakawa, and Keiya Tada. "Leukoencephalopathy in childhood hematopoietic neoplasm caused by moderate-dose methotrexate and prophylactic cranial radiotherapy—An MR analysis." International Journal of Radiation Oncology*Biology*Physics 32, no. 4 (July 1995): 913–18. http://dx.doi.org/10.1016/0360-3016(95)00565-g.

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Yu, J. S., E. Yuh, C. P. Chen, P. K. Sneed, I. J. Barani, and M. W. McDermott. "Whole Brain Radiotherapy (WBRT) Increases the Risk of and Accelerates Leukoencephalopathy (LE) in Patients with Brain Metastases." International Journal of Radiation Oncology*Biology*Physics 75, no. 3 (November 2009): S233. http://dx.doi.org/10.1016/j.ijrobp.2009.07.537.

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Asano, Kenichiro, Kiyohide Kakuta, Nozomi Fujiwara, Atsushi Saito, and Shingo Kakeda. "NI-8 LATE-DELAYED MRI FINDINGS AFTER RADIOTHERAPY: DOT-LIKE ENHANCED LESION." Neuro-Oncology Advances 4, Supplement_3 (December 1, 2022): iii17. http://dx.doi.org/10.1093/noajnl/vdac167.063.

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Abstract Introduction Late-delayed radiation reactions after radiotherapy include brain atrophy, leukoencephalopathy, radiation necrosis, and cerebrovascular disease. We will discuss the contrast-enhanced SPGR to detect dot-like enhanced lesions that are considered to be late late-delayed radiation reactions. Material and Methods One hundred eleven patients (62 males and 49 females; median age at irradiation: 49 years) who had received radiotherapy since 1994 and were alive since 2010, had dot-like lesions by contrast-enhanced SPGR, and had a PFS OS of at least 24 months were included in the study. Of these, 64 had high-grade glioma, 4 had low-grade glioma, 15 had PCNSL, 7 had metastatic brain tumors, 9 had germ cell tumors, 5 had medulloblastoma, and 7 had other tumors, with a mean follow-up of 89. Results Contrast-enhanced SPGR showed dot-like or rod-like findings in 23/111 patients (20.7%). Contrast-enhanced FIESTA and Flair-Cube were also detectable in some cases. However, it was difficult to detect by contrast SE-T1WI, SE-T2WI, or contrast SE-Flair. The lesions appeared a median of 49 months after irradiation (IQR 34, 103. Range 25-298). There were no lesions that increased in size, and multiple lesions appeared during the course of the study in 8/23 (34.8%) of the patients. All lesions occurred within the irradiated field and were seen in patients receiving a total dose of 50 Gy or more, but not in patients receiving whole-brain irradiation alone or whole-brain irradiation plus boost at 50 Gy or less. Discussion and Conclusion It is difficult to elucidate the pathogenesis without pathological evidence, but it is one of the late-delayed radiation reactions that occur more than 2 years later, and it is presumed to be vasculopathy or granulation reaction in the Virchow-Robin space. It tends to increase over time and is not considered to be a condition that causes sudden clinical manifestations.

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Rogers, Lisa R., Meredith A. Weinstein, Melinda L. Estes, J. Gregory Cairncross, and Thomas Strachan. "Diffuse bilateral cerebral astrocytomas with atypical neuroimaging studies." Journal of Neurosurgery 81, no. 6 (December 1994): 817–21. http://dx.doi.org/10.3171/jns.1994.81.6.0817.

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✓ The authors describe the clinical behavior of eight patients with cerebral astrocytomas, in whom computerized tomography (CT) or magnetic resonance (MR) imaging of the brain was characterized by diffuse bilateral cerebral hemisphere tissue density abnormalities and minimal focal mass effect. Five patients were newly diagnosed, and three others had been treated for focal low-grade astrocytoma. Histological diagnoses included anaplastic astrocytoma (three patients), low-grade astrocytoma (three patients), glioblastoma (one patient), and gliosis with later development of glioblastoma (one patient). In five patients, brain tumor was not suspected from the neuroimaging studies, the findings of which were mistaken for radiation leukoencephalopathy, vasogenic edema, or multiple sclerosis. Serial CT scans or MR images undertaken over intervals of 3 to 184 weeks showed progression of abnormal tissue densities in seven patients and multifocal contrast-enhancing masses developed on CT scan in two patients. An autopsy in each of four patients showed diffuse cerebral infiltration by astrocytoma. It is concluded that neuroimaging studies in some patients with diffusely infiltrating cerebral astrocytoma are atypical for neoplasm and can be mistaken for other diseases, especially those that predominantly affect cerebral hemisphere white matter.

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Journal articles on the topic 'Radiation leukoencephalopathy'

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