Spinal compensatory mechanisms contribute to MS-related fatigue

Epub ahead of printRocca et al. Abnormal cervical cord function contributes to fatigue in multiple sclerosis. Mult Scler. 2012 Mar 2. 


Background/Objective: This group aimed to investigate whether cervical cord damage and dysfunction is associated with the presence and severity of fatigue in MS'ers using MRI.

Methods: Cervical cord functional magnetic resonance imaging (fMRI) during a tactile (light touch) stimulation of the right hand, and structural brain and cord MRI were acquired from 20 controls, 15 MS'ers without fatigue (NF) and 20 MS'ers with fatigue (F). Between-group differences in the extent of focal lesions and diffusivity abnormalities (this technique picks-up damage to axons) in the brain and cord, cord-normalized cross-sectional area (CSAn; size of the spinal cord - the smaller the cord the greater the loss of axons) and fMRI activity (cortical or gray matter activity) were assessed.  

Results: All structural MRI measures differed significantly among groups, except for cord lesion number and CSAn. Compared with controls, NF-MS patients experienced higher cord recruitment (p=0.04). Compared with F-MS, NF-MS patients had a lower brain normal-appearing white matter average fractional anisotropy (p=0.001) (this means less damage in the white matter) and increased cord recruitment (p=0.02) (this means greater compensation in the cord). In patients with MS, the extent of cord recruitment was correlated with the severity of fatigue (r=-0.34, p=0.04). Compared with the other two groups, F-MS patients had a more diffuse recruitment of cord quadrants.

Conclusions: Abnormalities of function, but not of structure, of the cervical cord are likely to contribute to the pathogenesis of fatigue in MS.

"This is an interesting study and suggests that fatigue is related to excessive compensation in the spinal cord. MS'ers who use other neuronal pathways to function get more tired. This makes sense. It also makes it difficult to treat fatigue if it is a result of compensation! Reducing the use of compensatory pathways may exacerbate neurological impairments."

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