Related Experiment Video
Updated: Apr 15, 2026

09:33
Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
Published on: July 28, 2013
29.5K
Diffusion tensor imaging and tract-based spatial statistics analysis in Friedreich's ataxia patients.
Simone Carreiro Vieira Karuta1, Salmo Raskin2, Arnolfo de Carvalho Neto3
1Federal University of Parana, Hospital de Clinicas, Brazil.
Parkinsonism & Related Disorders
|March 25, 2015
Summary
Diffusion tensor imaging (DTI) reveals widespread white matter damage in Friedreich's ataxia (FRDA) patients, extending beyond previously identified areas. This advanced imaging helps explain the neurological symptoms of this common hereditary ataxia.
Area of Science:
- Neuroimaging
- Neurology
- Genetics
Background:
- Friedreich's ataxia (FRDA) is the most common hereditary ataxia.
- Cervical spinal cord thinning is a consistent MRI finding in FRDA.
- Neuropathology shows neuronal loss and white matter (WM) tract degeneration in the spinal cord, brainstem, and cerebellum.
Purpose of the Study:
- To test the hypothesis that WM damage in FRDA is more extensive than previously recognized.
- To investigate if damage involves normal-appearing WM using diffusion-tensor imaging (DTI) and tract-based spatial statistics (TBSS).
Main Methods:
- A transversal study included 21 genetically confirmed FRDA patients and 17 healthy controls.
- Brain MRI on a 1.5 T scanner was performed.
- DTI data analyzed using FSL to identify Fractional Anisotropy (FA) decreases and diffusion measures (MD, RD, AD).
Main Results:
- Significant FA decreases were observed in the left superior cerebellar peduncle, left posterior thalamic radiation, major forceps, left inferior fronto-occipital fasciculus, and corpus callosum (p < 0.01).
- No significant correlation was found between diffusion measures (FA, AD, MD, RD) and clinical findings, SARA scores, or genetic expansion.
Conclusions:
- DTI and TBSS demonstrate extensive cerebral and cerebellar involvement in FRDA.
- These findings help explain the clinical phenotype of the disease.
- Larger studies are needed to correlate clinical, genetic, and ataxia scores.

