Disconnection of Cerebellar Motor Areas and Motor Impairment in Multiple Sclerosis
Francesco Romano1, Benedetta Signoracci1, Paolo Preziosa3, Monica Margoni2, Elisabetta Pagani1, Maria Rocca3, Massimo Filippi4
1Neuroimaging Research Unit, Division of Neuroscience, 2Neuroimaging Research Unit, Division of Neuroscience; Neurology Unit; and Neurorehabilitation Unit, IRCCS San Raffaele Scientific Institute, 3Neuroimaging Research Unit, Division of Neuroscience; and Neurology Unit, 4Neuroimaging Research Unit, Division of Neuroscience; Neurology Unit; Neurorehabilitation Unit; and Neurophysiology Service, IRCCS San Raffaele Scientific Institute; Vita-Salute San Raffaele University
Objective:
To assess atrophy and T2-hyperintense lesion load in the anterior (ACMA) and posterior (PCMA) cerebellar motor areas and investigate their correlations with motor impairment in patients with multiple sclerosis (MS).
Background:
The cerebellum is susceptible to damage in patients with MS. Two motor representations have been described in cerebellar functional topography: lobules I–V (ACMA) and lobule VIII (PCMA). A primary role of the ACMA and a secondary role of the PCMA have been suggested, but their specific functions and involvement in MS are unclear.
Design/Methods:
Eighty-nine MS patients and 65 healthy controls (HC) underwent a functional assessment (gait function and hand dexterity) and structural MRI acquisition at 3.0T, used to extract cerebral and cerebellar volumes and T2-hyperintense lesion loads. Cerebellar lobules were segmented using the SUIT atlas. Between-groups comparisons and age/sex-corrected partial correlations were assessed.
Results:
Compared to HC, both ACMA and PCMA were atrophic in MS (p<0.001), with similar reductions between the two areas. More than 60% of MS patients had lesions in either motor lobule. ACMA volume was lower than PCMA in HC and MS (p<0.001), whereas T2-hyperintense lesion load was higher in the ACMA than PCMA in MS (p=0.040). Patients with lesions in both areas had worse motor performances than those without lesions in either area (p<0.001 for all). Patients with lesions only in the ACMA or PCMA had similar motor abilities. In patients, lower ACMA and PCMA volumes correlated only with worse left-hand dexterity (p<0.001), whereas higher T2-hyperintense lesion loads in both ACMA and PCMA correlated with worse performances in all motor tests (r range=-0.358;-0.445, p≤0.001 for all).
Conclusions:
The non-homogeneous distribution of lesions suggests an increased susceptibility of the ACMA to focal demyelinating lesions. Considering correlation analyses, disconnection of cerebellar motor areas, rather than localised lobular atrophy, seems to better explain motor impairment in MS.