Vascular cognitive impairment (VCI) — cognitive decline produced primarily or partly by cerebrovascular disease — is the second most common type of cognitive impairment after Alzheimer's disease. It often coexists with Alzheimer's pathology in mixed dementia presentations, particularly in older adults, and the vascular component is often the more responsive to intervention. Recognizing VCI is clinically important because the trajectory often responds meaningfully to vascular optimization in ways that Alzheimer's-driven decline does not.
The clinical presentation of VCI differs somewhat from Alzheimer's disease. VCI typically presents with prominent executive dysfunction (planning, multitasking, mental flexibility), processing speed slowing, gait disturbance, and mood changes (apathy, irritability, sometimes depression), with memory impairment that is less severe early on than in classical Alzheimer's. Step-wise progression is sometimes seen with discrete vascular events. Pure VCI is less common than mixed presentations; many older patients with apparent Alzheimer's disease have significant vascular contributions that respond to vascular optimization even when the underlying neurodegenerative process does not.
Imaging is central to recognition. Brain MRI showing white matter hyperintensities, lacunar infarcts, microbleeds, or clinically silent strokes establishes the vascular contribution. The Fazekas scale for white matter changes provides a semi-quantitative measure. The pattern of imaging findings often does not match the patient's reported neurological history — many patients with significant vascular brain damage have never had a recognized stroke or TIA. The disease has been silent and accumulating. CT is less sensitive than MRI for the small vessel disease that characterizes most VCI; MRI is preferred when the question is being seriously asked.
The intervention is aggressive vascular risk factor management. Blood pressure to SPRINT-MIND target. ApoB to cognitive-protection target. Glucose and insulin optimization. Smoking cessation. Atrial fibrillation management. Anticoagulation when indicated for embolic risk. Antiplatelet therapy in selected patients. Aggressive lifestyle intervention — exercise, dietary optimization, sleep, stress management. The cumulative effect of optimizing all of these factors, even after VCI is established, can slow or stabilize the trajectory; in some patients it can produce modest improvement.
The pharmacological options for VCI itself are more limited than for Alzheimer's. Cholinesterase inhibitors (donepezil, rivastigmine) have evidence for modest benefit in VCI, particularly in mixed presentations. Memantine has some evidence in moderate-to-severe VCI. Anti-amyloid antibodies (lecanemab, donanemab) are not indicated for pure VCI but may be considered in mixed presentations where Alzheimer's pathology is documented. The greatest benefit comes from the vascular work, not the pharmacological additions — though both have a place in selected patients.
The longevity-psychiatry implication of VCI is that the diagnosis often arrives after decades of suboptimal vascular care, and the intervention now is partial salvage rather than prevention. The patient with established VCI at 75 had the inflection moment somewhere in his 50s or 60s; the intervention then would have prevented much of what is now established. For the patient in front of you, the work is to slow further accumulation and address the vascular substrate that is still modifiable. For the next generation of patients, the work is to intervene earlier — in the acceleration window — so that VCI is prevented rather than diagnosed.