Does MS grey matter atrophy progress faster in regions with more damage in connected white matter?

Does MS grey matter atrophy progress faster in regions with more damage in connected white matter? - Rate of GM atrophy in MS

Status

Active, not recruiting

Phases

Unknown

Study type

Observational

Source

NL-OMON

Registry ID

NL-OMON43307

Enrollment

Registered

2016-09-07

Start date

2016-11-17

Completion date

Unknown

Last updated

2024-04-23

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

multiple sclerosis

Interventions

None listed

Eligibility

Age

18 Years to 99 Years

Inclusion criteria

Inclusion criteria: Patient group: 1. Minimum age 18 years 2. Clinical definite relapsing remitting MS for

Exclusion criteria

Exclusion criteria: 1. Past or current clinical relevant non-MS neurological or psychiatric disorder(s) 2. Past or current clinical relevant (auto)immune disorder(s) 3. Treatment with first line therapy for less than 6 months 4. Treatment with second line therapy 5. Relapse and/or steroid treatment in past 3 months 6. Pregnancy 7. MRI incompatibility, e.g. metal objects in or around the body, claustrophobia or inability to lie still in the scanner

Design outcomes

Primary

Measure	Time frame
Three measures for WM damage will be assessed, i.e. lesion volume, lesion fractional anisotropy (FA) and NAWM FA, from which a composite WM damage score will be computed. High versus low WM damage scores will then be compared to the atrophy rates in the GM, based on subcortical volume and cortical thickness measures. From this, we can compare atrophy rates of each GM structure from baseline to follow-up 1 between the group of patients with higher damage in the WM tracts connected to that GM structure on the one hand, and the group of patients with lower damage in those WM tracts on the other. Similar calculations will be performed between follow-up 1 and follow-up 2 in order to determine whether a larger increase of WM damage over the first study year is predictive of faster subsequent GM atrophy in the second year.	—

Measure

Time frame

Three measures for WM damage will be assessed, i.e. lesion volume, lesion fractional anisotropy (FA) and NAWM FA, from which a composite WM damage score will be computed. High versus low WM damage scores will then be compared to the atrophy rates in the GM, based on subcortical volume and cortical thickness measures. From this, we can compare atrophy rates of each GM structure from baseline to follow-up 1 between the group of patients with higher damage in the WM tracts connected to that GM structure on the one hand, and the group of patients with lower damage in those WM tracts on the other. Similar calculations will be performed between follow-up 1 and follow-up 2 in order to determine whether a larger increase of WM damage over the first study year is predictive of faster subsequent GM atrophy in the second year.

—

Secondary

Measure	Time frame
Next to the measures for GM and WM damage, resting state functional connectivity measurements will be used to assess whether GM and WM damage patterns effect the functional organization of the brain at rest, either prior to GM/WM damage, or following the damage patterns observed. Furthermore, clinical measurements will be taken into account, in order to link the structural data to functionality of the brain in the RRMS patients.	—

Measure

Time frame

Next to the measures for GM and WM damage, resting state functional connectivity measurements will be used to assess whether GM and WM damage patterns effect the functional organization of the brain at rest, either prior to GM/WM damage, or following the damage patterns observed. Furthermore, clinical measurements will be taken into account, in order to link the structural data to functionality of the brain in the RRMS patients.

—

Countries

Netherlands

Outcome results