Timothy C. Hain, MD. • Page last modified: November 30, 2017
Cerebral atrophy means brain shrinkage. A synonym for this term is "cerebral volume loss".
Brain atrophy occurs normally in aging. Of course, it is better not to have shrinkage of one's brain.
Imbalance also occurs normally in aging. As both brain atrophy and imbalance occur in aging, it is tempting to conclude that atrophy causes imbalance. However, while it seems likely that there is some connection, we do not have literature to prove this.
This page attempts to review some of the recent literature about brain shrinkage.
A general problem is determining whether a particular disease or observation causes brain atrophy, whether brain atrophy causes that observation, or whether there is a shared underlying cause. In other words, all we have is association studies. We do not have any studies where (for example), a group of 1000 patients are randomized into one group getting drug A and another no drug, and comparing their MRI scans 10 years later. This is what it would take to draw a stronger inference that any particular intervention affects brain atrophy.
Akiyama et al (1997) reported on 94 of their patients and reported that "(1) after age 60, cerebral atrophy, polio- and leuko-araiosis doubled and cerebral perfusion decreased, with marked individual variations; (2) risk factors independently accelerating cerebral atrophy and cortico-subcortical perfusional declines included TIAs, hypertension, smoking, hyperlipidemia, excessive alcohol consumption and male gender; " They stated then that "accelerated cerebral atrophic and degenerative changes identified by neuroimaging should be considered as markers for depleted neuronal synaptic reserves, which predispose to cognitive declines. Interventions available for controlling some of these risk factors include control of TIAs, hypertension, and hyperlipidemia, as well as tobacco and alcohol withdrawal." I would call this the "common sense" type advice type paper -- avoid things that damage your brain, and your brain will be better.
Zonneveled et al (2015), using data from the 3011 patients in the Rotterdam study, noted that reduced cerebral blood flow was correlated with brain atrophy. They stated that "Our results indicate that brain atrophy causes CBF to decrease over time, rather than vice versa". So this would suggest that circulation is an effect rather than a cause of brain atrophy.
Vleck et al (2009) also agreed that "Progression of cerebral atrophy in this population may be associated with advanced physiological aging, but is probably not caused by elevated BP.", suggesting in essence that brain atrophy is not caused by hypertension.
Avdibegovic, E., et al. (2007). found brain atrophy frequently in psychiatric patients with cognitive dysfunction. "Cerebral atrophy is frequent in patients with PTSD, whereas in patients with depression, besides cerebral atrophy, silent brain infarct is also frequently present." This is a "horse-cart" type paper -- which came first -- brain atrophy or psychiatric disturbances ?
Reitz et al (2006) reported that patients with parkinsonism had more severe symptoms when there was also more brain atrophy. Another horse-cart type report.
Knopman et al (2005) reported that increased levels of blood glucose in diabetes was associated with greater brain atrophy. Another horse-cart report.
Gustafson noted an association between body mass index (BMI) and cerbral atrophy. They looked at atrophy of several places in the brain, and suggested that atrophy of the temporal lobe alone was associated with a greater BMI. We think this is probably just a statistical anomaly that comes about with testing for multiple things without a clear reason for a finding. In other words, we don't think that BMI causes brain shrinkage.
Zanardi et al(2001) suggested that systemic steroids were associated with cerebral atrophy. They stated that " Chronic glucocorticoid therapy was responsible for cerebral atrophy, with a comparable incidence in both lupus and non-lupus patients compared to age and gender-matched normal subjects untreated with glucocorticoids. " Again, they noted an association here, and did not establish causality.]
Palson et al (2001) stated that "Brain atrophy on CT is not associated with depression in the general population, despite the fact that individuals with depression have a worse cognitive performance. The finding that cognitive performance was not decreased in individuals with previous depression suggests that cognitive dysfunction is a state phenomenon in depression. "
Luoto, R., et al. (2000) reported on Estrogen replacement therapoy users. They stated that "Bifrontal distance, the largest distance between frontal horns, and the size of ventricles were larger among current ERT users compared to past users or nonusers (P (trend) = .01), adjusted for all other covariates, but no dose-response relationship to current or past ERT use was found. Duration of estrogen use was not associated with any atrophy measure. Cortical atrophy measure, sulcal widening, or white matter disease did not differ significantly by ERT use or duration of use. Central measures of atrophy, bifrontal distance, and ventricular size were significantly associated with cognition as measured by MMSE". So in essence, persons using Estrogen replacement have more brain atrophy and poorer thinking. Again, this is an association, not a cause.
The studies reviewed above show that brain atrophy is correlated with many medical issues including poorer thinking, as well as a variety of lifestyle choices (e.g. excessive alcohol, smoking). It would seem prudent to pursue a more healthy lifestyle. The papers reviewed above do not put these risks into context or help doctors give evidence driven advice about what to do about particular medications or potentially damaging behaviors.