Brain Health: has your neurologist discussed the issue of brain health with you? #ClinicSpeak #MSBlog #MSResearch
"The study below supports previous work in this area and shows that fatigue is linked to brain damage in MS; in particular certain areas of the brain. This makes sense. Our brains are wonderful machines and have built in extra capacity so called cognitive reserve. When one area of the brain is damaged other areas help by working harder and compensating for the damage. This compensation consumes extra energy and results in mental fatigue. This is why I believe that fatigue, in particular mental fatigue, early in the course of the disease needs to be taken very seriously and is a sign of structural brain damage. When mental fatigue is associated with a high lesion load and brain atrophy it is not good news for the MSer concerned."
"Brain reserve is something to cherish and look after; it is what protects us from the ravages of ageing and allows us to maintain a good quality of life as we get older. I don't think we should be treating MSers any differently to the normal population hence the need to promote brain health. To keep your brain healthy you need to have good sleep hygiene, do physical exercise, not smoke, drink moderately (excessive alcohol is bad for your brain), eat a well-balanced healthy diet, make sure all comorbidities are diagnosed and well managed (obesity, hypertension, high cholesterol and diabetes), avoid contact sports associated with repeat head injuries and maintain your social capital (remain socially active). Some claim intellectual exercises, or brain training, promotes brain health; maybe - I am not convinced by the science of brain training yet. In the future we may be able to take medications to help with brain health; for example statins, hormone replacement therapies and aspirin."
"Brain health is one of the reasons why I have moved the goalposts from simply targeting NEDA (no evident disease activity) to preventing end-organ damage, i.e. normalising brain volume loss in MS. Therapeutic nihilists don't buy into this; they claim that the long-term data linking brain atrophy to a poor outcome in MS is indirect and we need to show that slowing brain atrophy is associated with a positive outcome. I don't think they will have to wait too long for the data supporting brain atrophy as a validated surrogate marker to emerge; some very interesting data on brain atrophy and clinical outcomes were presented at the EFNS-ENS meeting in Istanbul. For me slowing, or normalising the rate of brain atrophy, over many years, is a no-brainer. Excuse the pun!"
"Last year I ran a campaign to redefine MS as a preventable dementia. I got a lot of stick about this campaign and was accused or of trying to stigmatize MSers. All I was trying to do is raise awareness about the issue of cognitive impairment in MS and that it occurs early in the disease and is probably what drives the early unemployment rates and results in fatigue, depression and anxiety. If MSers and healthcare workers took the issues of early cognitive impairment more seriously they may reappraise their position on early effective treatment and treat-2-target of NEDA to prevent end-organ damage."
"To assess brain health awareness, I would appreciate it if you could complete this short survey. Thanks."
Purpose: To use magnetic resonance (MR) imaging and advanced analysis to assess the role of lesions in normal-appearing white matter (NAWM) and gray matter (GM) damage, global versus regional damage, and atrophy versus microstructural abnormalities in the pathogenesis of fatigue in MS.
Materials and Methods: Local ethics committee approval and written informed consent were obtained. Dual-echo, double inversion-recovery, high-resolution T1-weighted and diffusion-tensor (DT) MR was performed in 31 fatigued MSers, 32 non-fatigued MSers, and 35 control subjects. Global and regional atrophy and DT MR measures of damage to lesions, NAWM, and GM were compared (analysis of variance).
Results: Lesional, atrophy, and DT MR measures of global damage to brain, white matter (WM), and GM did not differ between fatigued and non-fatigued MSers. Compared with non-fatigued MSers and control subjects, fatigued MSers experienced atrophy of the right side of the accumbens (mean volume ± standard deviation, 0.37 mL ± 0.09 in control subjects; 0.39 mL ± 0.1 in non-fatigued MSers; and 0.33 mL ± 0.09 in fatigued MSers), right inferior temporal gyrus (ITG) (Montreal Neurological Institute [MNI] coordinates: 51, -51, -11; t value, 4.83), left superior frontal gyrus (MNI coordinates: -10, 49, 24; t value, 3.40), and forceps major (MNI coordinates: 11, -91, 18; t value, 3.37). They also had lower fractional anisotropy (FA) of forceps major (MNI coordinates: -17, -78, 6), left inferior fronto-occipital fasciculus (MNI coordinates: -25, 2, -11), and right anterior thalamic radiation (ATR) (MNI coordinates: 11, 2, -6) (P < .05, corrected). More lesions were found at T2-weighted imaging in fatigued MSers. Multivariable model was used to identify right ITG atrophy (odds ratio, 0.83; 95% confidence interval [CI]: 0.82, 0.97; P = .009) and right ATR FA (odds ratio, 0.74; 95% CI: 0.61, 0.90; P = .003) as covariates independently associated with fatigue (C statistic, 0.85).
Conclusion: Damage to strategic brain WM and GM regions, in terms of microstructural abnormalities and atrophy, contributes to pathogenesis of fatigue in MS, whereas global lesional, WM, and GM damage does not seem to have a role.