Respiratory impairment in multiple sclerosis: A Single-Center Study in 371 People with MS
Ivan Murrieta-Alvarez1, Carlos A. Perez2, Andres A. Leon-Peña2, José M. Benítez-Salazar3, Moisés M. Gallardo-Pérez1, Juan C. Olivares-Gazca1, Guillermo J. Ruiz-Delgado1, Guillermo J. Ruiz-Argüelles1
1Clinica Ruiz, 2Baylor College of Medicine, 3Universidad Popular Autónoma del Estado de Puebla
Objective:
Study the association between respiratory impairment (RI) and multiple sclerosis (MS) and its relationship with
Background:
It is unclear whether RI in people with multiple sclerosis (PwMS) should be viewed as the result of muscle weakness or MS-specific structural central venous system (CNS) abnormalities as a precipitant factor for the worsening of motor impairment or cognitive symptoms. Here we present a study aimed to define the reach of RI associated with CNS damage.
Design/Methods:
Cross-sectional observational study evaluating the association between forced spirometry results with clinical and imaging features in PwM. Normative metrics of forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), and the relation FEV1/FVC were calculated. Qualitative and quantitative brain magnetic resonance imaging (MRI) examinations were conducted.
Results:
A total of 371 PwMS were included in the study. Of those 196 (53%) had RRMS, 92 (25%), and 83 (22%) PPMS. RI was present in 16 (8%), 16 (19%), and 23 (25%) of the patients in the RRMS, PPMS, and SPMS, respectively. PwMS with T2-FLAIR lesions involving the corpus callosum had a significantly higher frequency of RI (OR 3.62; 95%CI 1.33–9.83; p 0.012) than patients without lesions in that region. This relationship remained significant in the RRMS group (OR 10.1; 95%CI 1.3–67.8; p 0.031) when the model excluded PPMS and SPMS. According to our study, for every increase of 1 z-score of FVC, we observed an increase of 0.25 cm3 of hippocampal volume (β 0.25; 95%CI 0.03–0.47; p 0.023) and 0.43 cm3 of left hippocampus volume (b 0.43; 95%CI 0.16–0.71; p 0.002).
Conclusions:
We observed an incremental prevalence of RI according to the phenotype: from more early relapsing courses to long-standing progressive courses (RRMS to PPMS or SPMS). In addition, our observations shed light on the potential role of early neurodegeneration in the development of RI and vice versa.