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Peer-reviewedCC BY-NCJournal of Brown hospital medicine

Immune-Mediated Demyelinating Central Nervous System Graft-Versus-Host Disease After Allogeneic Hematopoietic Stem Cell Transplantation

  • Marie Ugo1
  • Aaliyah Shaikh1
  • Charif Sidani1,2
  • Márcio L Duarte3,4,5
  • Leonardo F Freitas2,6
6 affiliations
  1. 1Department of Radiology Florida International University/Herbert Wertheim College of Medicine
  2. 2Department of Radiology Baptist Health South Florida (Miami, Florida, USA) / Radiology Associates of South Florida (RASF)/Division of Clinical Neuroradiology
  3. 3Department of Radiology Diagnósticos da América S.A., DASA, São Paulo, Brazil
  4. 4Department of Radiology Universidade de Ribeirão Preto Campus Guarujá, Guarujá (SP)
  5. 5Instituto de Ensino e Pesquisa DASA, IEPD, São Paulo, Brazil
  6. 6Department of Radiology Florida International University (FIU)/Herbert Wertheim College of Medicine
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Abstract

Central nervous system graft-versus-host disease (CNS GVHD) is a rare and challenging complication of allogeneic hematopoietic stem cell transplantation (HSCT) that can mimic infection, malignancy, or primary demyelinating disorders. We describe a 21-year-old man with high-risk Philadelphia chromosome–like B-cell acute lymphoblastic leukemia underwent matched unrelated donor allogeneic HSCT after achieving measurable residual disease negativity. His post-transplant course was complicated by hepatic and cutaneous GVHD. Sixteen months after transplantation, he developed progressive bilateral lower-extremity weakness, gait ataxia, and blurred vision. Brain MRI demonstrated multifocal subcortical lesions, while spinal MRI revealed enhancing intramedullary lesions at multiple levels. Orbital MRI showed bilateral optic neuritis. Extensive infectious, malignant, and autoimmune evaluations were unrevealing. Given his prior GVHD, multifocal demyelinating pattern, exclusion of alternative etiologies, and response to immunosuppression, probable demyelinating CNS GVHD was diagnosed. He was treated with corticosteroids, IVIG, plasma exchange, and rituximab, followed by maintenance IVIG and prednisone, with substantial clinical and radiographic improvement. CNS GVHD should be considered in HSCT recipients with new multifocal neurologic deficits and demyelinating lesions, particularly with antecedent systemic GVHD. Early recognition and immunosuppressive treatment may improve neurologic outcomes.

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Cite

BibTeXRIS
BibTeX
@article{ugo2026immunemediated,
  title = {{Immune-Mediated Demyelinating Central Nervous System Graft-Versus-Host Disease After Allogeneic Hematopoietic Stem Cell Transplantation}},
  author = {Marie Ugo and Aaliyah Shaikh and Charif Sidani and Márcio L Duarte and Leonardo F Freitas},
  journal = {Journal of Brown hospital medicine},
  year = {2026},
  month = oct,
  doi = {10.56305/001c.168646},
  url = {https://europepmc.org/article/PMC/PMC13730617},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Immune-Mediated Demyelinating Central Nervous System Graft-Versus-Host Disease After Allogeneic Hematopoietic Stem Cell Transplantation
AU  - Marie Ugo
AU  - Aaliyah Shaikh
AU  - Charif Sidani
AU  - Márcio L Duarte
AU  - Leonardo F Freitas
PY  - 2026
DA  - 2026/10/02
JO  - Journal of Brown hospital medicine
DO  - 10.56305/001c.168646
UR  - https://europepmc.org/article/PMC/PMC13730617
AB  - Central nervous system graft-versus-host disease (CNS GVHD) is a rare and challenging complication of allogeneic hematopoietic stem cell transplantation (HSCT) that can mimic infection, malignancy, or primary demyelinating disorders. We describe a 21-year-old man with high-risk Philadelphia chromosome–like B-cell acute lymphoblastic leukemia underwent matched unrelated donor allogeneic HSCT after achieving measurable residual disease negativity. His post-transplant course was complicated by hepatic and cutaneous GVHD. Sixteen months after transplantation, he developed progressive bilateral lower-extremity weakness, gait ataxia, and blurred vision. Brain MRI demonstrated multifocal subcortical lesions, while spinal MRI revealed enhancing intramedullary lesions at multiple levels. Orbital MRI showed bilateral optic neuritis. Extensive infectious, malignant, and autoimmune evaluations were unrevealing. Given his prior GVHD, multifocal demyelinating pattern, exclusion of alternative etiologies, and response to immunosuppression, probable demyelinating CNS GVHD was diagnosed. He was treated with corticosteroids, IVIG, plasma exchange, and rituximab, followed by maintenance IVIG and prednisone, with substantial clinical and radiographic improvement. CNS GVHD should be considered in HSCT recipients with new multifocal neurologic deficits and demyelinating lesions, particularly with antecedent systemic GVHD. Early recognition and immunosuppressive treatment may improve neurologic outcomes.
SN  - 2994-5593
ER  -