Please forgive my my layperson's ignorance, but did you mean WMH are CSF/fluid spaces? In the radiologist's report on my MRI, he stated that my WMH were what he thought would be consistent with sequalae of chronic migraines or the beginning of chronic small vessel ischemic disease
Definitely listen to your doctors' advice on this one. I'm trying to discuss generally and point out where there are things we would like to understand better. I'm also far from expert in adult neuro-imaging, so I may have misunderstandings of what we
do know.
(When reading the following, T2-weighted sequences show fluid such as water, CSF as
hyperintense/bright as well as non-fluid effects such as cytotoxic oedema eg ischaemia/infarction, vasogenic oedema eg around tumours/abscesses, gliosis from 'repaired' damage, loss of myelin, blood products;
FLAIR generally makes fluids hypointense/dark, but tends to leave the non-fluid causes as hyperintense/bright. Things can show as FLAIR-bright for unusual reasons other than the above, including
slow flow in vessels, as a
transient post-seizure effect and we sometimes see it under
general anaesthesia with supplemental oxygen.)
If the WMH are defined as purely FLAIR-hyperintense (bright) — excluding FLAIR-dark — then yes I think most interpretations would weight toward them being a marker of small-vessel ischaemic change. If they allow to include T2-hyperintense (bright) but FLAIR-hypointense (dark), then they could also include perivascular spaces where the T2 signal is following closest to CSF. Probably the definitions for WMH over recent years are tightening up to refer
only to FLAIR-bright / T2 dark lesions and I probably need to brush up on the more recent literature. But FLAIR suppression doesn't always follow the rules if the fluid content is not simple CSF eg high protein content might stay high; so there are caveats, which is why I'm keen for us to learn more about these small abnormalities on the 7T research magnets.
With all that said, for clinical imaging, it's difficult to know what they might mean for any individual patient. There was an
editorial in Mayo Proceedings in 2019 that is reasonably readable, that tries to answer what a neurologist might do in terms of advice for referred patients. The summary is probably: assume they represent a marker of vascular pathology and look for reversible factors to try and prevent progression. However, caveat being it's hard to know with certainty what they represent for that individual patient, so this advice is generally sensible and safe, even while playing the odds —
What are WMHs and what causes them? Are they the same as a stroke? Are they a marker for impending stroke, dementia, or death?
Changes in the white matter of presumed vascular origin were first identified as hypo-attenuation of the white matter on computed tomography but now are more often seen as patchy areas of signal hyperintensity in deep and periventricular white matter areas on T2-weighted sequences, particularly fluid- attenuated inversion recovery.
Aging and hypertension are the main predictors of WMHs, and genome-wide association studies have identified associations with genes involved in blood pressure regulation. Other risk factors associated with WMHs include diabetes, hypercholesterolemia, smoking, carotid artery disease, atrial fibrillation, and heart failure.
(From your earlier comment those risk factors don't seem to apply in your case
@Michelle)
The observed associations with adverse outcomes suggest that these lesions are a surrogate marker for the burden of vascular risk factors and a marker of diffuse vascular pathology involving different cerebral, cardiac, and systemic vasculatures.
I wonder if they're more indirectly correlated.
Similar to small subcortical infarcts, lacunes, cerebral microbleeds, and enlarged perivascular spaces, WMHs are a manifestation of small vessel disease.
Stated, but I don't think we know this for certain. Eg, continuing with —
In addition, other processes that may be involved in the genesis of WMHs include dysfunction of oligodendrocyte precursor cells, failure of the glymphatic system, venous collagenosis, and alterations in RNA transcription.
Studies using serial imaging have shown that WMH can increase in size, shrink, or, in rare instances, disappear and, thus, raise the possibility that the process may be reversible before axonal damage and demyelination have occurred.
Although we have learned a great deal about the etiology, associations, and implications of WMHs in the past 2 decades, there is still much uncertainty about what to do when they are identified. Because they are a manifestation of small vessel disease and have been associated with several vascular risk factors, it makes sense to screen patients who harbor WMHs in their scans for these risk factors.
I have baseline MRIs of my brain from a few years ago, but I'm a bit reluctant to see what it looks like now! Especially as there's not much I can do about it at the moment.
