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Updated: Jun 29, 2026
Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
White Matter Alterations in Spastic Paraplegia Type 5: A Multiparametric Structural MRI Study and Correlations with
Background And Purpose:
In spastic paraplegia type 5, spinal cord atrophy and white matter signal abnormalities in the brain are the main MR imaging alterations. However, the specific mechanism remains unclear. We explored the microstructural changes occurring in spastic paraplegia type 5 and assessed the relation between MR imaging and clinical data.
Materials And Methods:
Seventeen patients with spastic paraplegia type 5 and 17 healthy controls were scanned with DTI and T1 mapping on a 3T MR imaging scanner. Fractional anisotropy, mean diffusivity, radial diffusivity, axial diffusivity, and T1 values were obtained using Tract-Based Spatial Statistics and the Spinal Cord Toolbox. Neurofilament light and myelin basic protein in the CSF were measured. The differences in MR imaging and biochemical data between patients with spastic paraplegia type 5 and healthy controls were compared using the Student t test.
Results:
A widespread reduction of fractional anisotropy values and an elevation of mean diffusivity, T1, and radial diffusivity values were found in most cervical, T4, and T5 spinal cords; corona radiata; optic radiations; and internal capsules in spastic paraplegia type 5. A variation in axial diffusivity values was shown only in C2, C6, and the corona radiata but not in the gray matter. The levels of neurofilament light and myelin basic protein were higher in those with spastic paraplegia type 5 than in healthy controls (myelin basic protein, 3507 [SD, 2291] versus 127 [SD, 219] pg/mL; neurofilament light, 617 [SD, 207] versus 265 [SD, 187] pg/mL; P < .001). No correlation was found between the clinical data and MR imaging-derived measures.
Conclusions:
Multiparametric MR imaging and biochemical indicators demonstrated that demyelination (mainly) and axonal loss led to the white matter integrity loss without gray matter injury in spastic paraplegia type 5.
Insights
Spastic paraplegia type 5 involves white matter damage, primarily demyelination and axonal loss, affecting the spinal cord and brain. This study used advanced MRI and CSF analysis to reveal these microstructural changes.
Area of Science:
- Neurology
- Radiology
- Biochemistry
Background:
- Spastic paraplegia type 5 (SPG5) is characterized by spinal cord atrophy and brain white matter abnormalities on MRI.
- The underlying microstructural mechanisms of SPG5 remain unclear.
- This study investigates microstructural changes in SPG5 and their correlation with clinical data.
Purpose of the Study:
- To explore microstructural changes in the spinal cord and brain of patients with SPG5.
- To assess the relationship between MR imaging findings and clinical data in SPG5.
- To elucidate the pathological mechanisms of white matter damage in SPG5.
Main Methods:
- Diffusion Tensor Imaging (DTI) and T1 mapping on a 3T MR scanner.
- Analysis of fractional anisotropy, diffusivity (mean, radial, axial), and T1 values using Tract-Based Spatial Statistics and Spinal Cord Toolbox.
- Measurement of neurofilament light (NfL) and myelin basic protein (MBP) in cerebrospinal fluid (CSF).
Main Results:
- Patients with SPG5 showed widespread reductions in fractional anisotropy and elevations in mean diffusivity, T1, and radial diffusivity in the spinal cord and brain white matter.
- Axial diffusivity changes were localized to specific white matter tracts.
- Elevated CSF levels of NfL and MBP were observed in SPG5 patients compared to controls (P < .001).
- No significant correlation was found between MR imaging measures and clinical data.
Conclusions:
- Multiparametric MRI and CSF biomarkers indicate that demyelination and axonal loss contribute to white matter integrity loss in SPG5.
- Gray matter appears unaffected in SPG5.
- The findings highlight the utility of advanced MRI techniques and CSF analysis in understanding the pathophysiology of SPG5.
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