San Raffaele Scientific Institute and University Hospital
Department of Neurology

Author Of 2 Presentations

Clinical Outcome Measures Poster Presentation

P0095 - Intracortical motor conduction is associated with dexterity in progressive multiple sclerosis (ID 1841)

Speakers
Presentation Number
P0095
Presentation Topic
Clinical Outcome Measures

Abstract

Background

Hand dexterity dysfunction is a key feature of disability in people with progressive multiple sclerosis (PMS). It underlies corticospinal tract (CST) and cerebellar integrity but also disruption of cortical networks, which are hardly assessed by standard techniques. Transcranial magnetic stimulation is a promising tool for evaluating the integrity of intracortical motor pathways.

Objectives

to investigate neurophysiological correlates of motor hand impairment in PMS and assess intracortical motor conduction through the use of a innovative TMS protocol.

Methods

Antero-posterior (AP) stimulation of the primary motor cortex activates the CST indirectly through polysynaptic pathways, while a direct CST activation occurs with latero-medial (LM) directed current. 30 PMS and 15 healthy controls underwent dominant hand motor evoked potentials (MEP) using AP and LM-directed stimulation, and a clinical assessment of dexterity (nine-hole peg test) and strength (MRC scale, grip and pinch).

Results

PMS with AP-LM latency difference 2.5 standard deviation above the mean of controls (33%) showed worse dexterity but no difference in upper limb strength. Accordingly, AP-LM latency shortening predicted dexterity (R2 0.538, p<0.001), but not strength impairment. On the contrary, absolute MEP latencies only correlated with strength (grip: R2 0.381, p=0.014; MRC: R2 0.184, p=0.041).

Conclusions

AP-LM latency shortening may be used to assess the integrity polysynaptic intracortical networks implicated in dexterity impairment.

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Rehabilitation and Comprehensive Care Poster Presentation

P1091 - Effect of BDNF Val66Met polymorphism on motor recovery after rehabilitation in progressive MS (ID 1676)

Speakers
Presentation Number
P1091
Presentation Topic
Rehabilitation and Comprehensive Care

Abstract

Background

It is known that a single-nucleotide polymorphism mapping to the Brain-Derived Neurotrophic Factor (BDNF) gene and resulting in the valine to methionine change (Val66Met or V66M), impacts memory, cognition and motor learning. Previous studies have shown that V66M polymorphism may exert a protective effect on grey matter atrophy in multiple sclerosis (MS) patients; however, its influence on motor recovery after rehabilitation is not known.

Objectives

To explore the possible influence of BDNF V66M polymorphism on motor recovery after rehabilitation in progressive MS subjects and to investigate the effect of two SNPs (rs2289656 and rs1212171) in NTRK2 gene, which encodes for BDNF receptor.

Methods

We retrospectively included in the study patients with primary progressive (PP) and secondary progressive (SP) MS, who were admitted to the Neurorehabilitation Unit and who had already available genetic data. The results of tests for gait (Six-minutes Walking Test, 6MWT; 10-Meters Test, 10MT) and hand dexterity (Nine-Hole Peg Test, 9HPT) were collected at baseline and after a 4-week inpatient rehabilitation program. We used ANCOVA models to explore the effects of the selected SNPs on the change of such clinical outcomes after rehabilitation, expressed as ratio values.

Results

100 patients (79 SP, 21 PP) with available clinical and genetic data were included in the study. Female:Male ratio was 1.27, mean age was 51±10 years and median EDSS score was 6.0 (range: 5.5-6.5). Sixty-eight patients were carriers of the more common genotype (GG), while the remaining were heterozygote (n=28) or homozygote (n=4) carriers of the V66M polymorphism (Met-carriers). Among 89 subjects with available data on 6MWT, Met-carriers showed greater improvement after rehabilitation if compared to GG patients (p=0.024; mean variation=0.16 [CI: 0.02-0.29]). SNPs in NTRK2 did not show any association with 6MWT change after rehabilitation neither alone, nor in interaction with V66M. As regards data on 10MT (n=42) and 9HPT (n=45), no associations were found for V66M or SNPs in NTRK2.

Conclusions

In the present pilot study, progressive MS patients carrying V66M polymorphism seem to have a greater improvement in walking performance at 6MWT after rehabilitation. These data need to be confirmed in larger and independent datasets, in order to better explore the effect of this polymorphism in MS patients undergoing intense rehabilitation program.

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