Update on cerebral small vessel disease: a dynamic whole-brain disease

Abstract

Cerebral small vessel disease (CSVD) is a very common neurological disease in older people. It causes stroke and dementia, mood disturbance and gait problems. Since it is difficult to visualise CSVD pathologies in vivo, the diagnosis of CSVD has relied on imaging findings including white matter hyperintensities, lacunar ischaemic stroke, lacunes, microbleeds, visible perivascular spaces and many haemorrhagic strokes. However, variations in the use of definition and terms of these features have probably caused confusion and difficulties in interpreting results of previous studies. A standardised use of terms should be encouraged in CSVD research. These CSVD features have long been regarded as different lesions, but emerging evidence has indicated that they might share some common intrinsic microvascular pathologies and therefore, owing to its diffuse nature, CSVD should be regarded as a ‘whole-brain disease’. Single antiplatelet (for acute lacunar ischaemic stroke) and management of traditional risk factors still remain the most important therapeutic and preventive approach, due to limited understanding of pathophysiology in CSVD. Increasing evidence suggests that new studies should consider drugs that target endothelium and blood–brain barrier to prevent and treat CSVD. Epidemiology of CSVD might differ in Asian compared with Western populations (where most results and guidelines about CSVD and stroke originate), but more community-based data and clear stratification of stroke types are required to address this.

BOLD‐based cerebrovascular reactivity vascular transfer function isolates amplitude and timing responses to better characterize cerebral small vessel disease

“…VTF‐AUC at follow‐up was lower in GM and WM in WMH groups. These results likely reflect dynamic changes associated with sporadic CSVD, such as size and location of WMH, not detected by change in WMH volume. Previous studies confirm the association between CVR decline over one year in CSVD by showing both reduced baseline conventional CVR and reduced speed and magnitude CVR measures in normal‐appearing WM prior to the progression of WMH.…”

Visceral obesity relates to deep white matter hyperintensities via inflammation

“…10 Longitudinal cohort data indicate that WMH load is associated with higher risk of cognitive decline, dementia, and stroke. 16 Interestingly, variations in location and configuration of WMH may differentially relate to pathomechanisms and risk factors. 14 These vascular pathologies eventually lead to tissue damage that can impact brain function, histologically evident as (incomplete or complete) infarcts, demyelination, loss of oligodendrocytes, and/or axonal damage.…”

“…This issue is of highest relevance given that, so far, modification of vascular risk factors has shown only limited effects to slow the progression of WMH. 16 Interestingly, variations in location and configuration of WMH may differentially relate to pathomechanisms and risk factors. Particularly, the distinction between patchy WMH around the ventricles (periventricular, pvWMH) versus more confluent WMH in the deep white matter (dWMH) may be of relevance.…”

An atypical subacute presentation of posterior reversible encephalopathy syndrome

“…The subcortical white matter hyperintensities that persisted after treatment are nonspecific and may represent non-pathological age-related white matter changes or white matter hyperintensities of presumed vascular origin (WMHPV) [29,30], chronic changes unrelated to the acute event. WMHPV are not uncommon in the general population and have hypertension and chronic kidney disease among their significant risk factors [29].…”

“…WMHPV are not uncommon in the general population and have hypertension and chronic kidney disease among their significant risk factors [29]. …”