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Published on: July 28, 2013
Association between Brain White Matter Lesions and Disease Activity in HAM/TSP Patients
Keiko Tamaki1, Shinji Ouma1, Nobutaka Takahashi1
1Department of Neurology, Fukuoka University School of Medicine, Fukuoka 814-0180, Japan.
Abstract:
Human T-cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) patients may have brain white matter (WM) lesions, but the association of these lesions with disease activity is poorly understood. We retrospectively evaluated the brain WM lesions of 22 HAM/TSP patients (male 4: female 18) including 5 rapid progressors, 16 slow progressors, and 1 very slow progressor. The severity of WM brain lesions on axial Fluid Attenuated Inversion Recovery images was evaluated utilizing the Fazekas scale, cerebrospinal fluid biomarkers, and proviral load in peripheral blood mononuclear cells. Imaging and biological data were compared at the first visit and a subsequent visit more than 4 years later. Patients with comorbidities including adult T-cell leukemia-lymphoma and cerebrovascular disease were excluded. The results revealed that brain WM lesions in the rapid progressors group were more pronounced than those in slow progressors. In patients with HAM/TSP, severe and persistent inflammation of the spinal cord may cause brain WM lesions.
Insights
Brain white matter lesions are more pronounced in rapid progressors with Human T-cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). Spinal cord inflammation may contribute to these brain lesions in HAM/TSP patients.
Area of Science:
- Neurology
- Virology
- Radiology
Background:
- Human T-cell leukemia virus type 1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) can affect brain white matter (WM).
- The relationship between brain WM lesions and HAM/TSP disease activity is not well understood.
Purpose of the Study:
- To evaluate brain WM lesions in HAM/TSP patients.
- To correlate lesion severity with disease progression and inflammatory markers.
Main Methods:
- Retrospective analysis of 22 HAM/TSP patients.
- Assessment of WM lesions using Fazekas scale on FLAIR MRI.
- Analysis of cerebrospinal fluid biomarkers and proviral load.
Main Results:
- Rapid progressors showed more pronounced brain WM lesions compared to slow progressors.
- Severe and persistent spinal cord inflammation may be linked to brain WM lesions in HAM/TSP.
Conclusions:
- Brain WM lesions are associated with disease severity in HAM/TSP.
- Spinal cord inflammation is a potential cause of brain WM lesions in HAM/TSP.
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