Table 11.
VaD subtypes related to | Newcastle subtype |
---|---|
Large infarct or several infarcts
|
I |
Multiple small or microinfarcts
|
II |
White matter lesions/leukoaraiosis/Binswanger disease | |
Strategic infarcts (e.g., thalamus, hippocampus, basal forebrain) | III |
Cerebral hypoperfusion (hippocampal sclerosis, ischemic–anoxic damage, cortical laminar necrosis, borderzone infarcts involving three different coronal levels) | IV |
Cerebral hemorrhages (lobar, intracerebral, subarachnoidal) | V |
Cerebrovascular changes with Alzheimer pathology (above Braak stage III); mixed dementia (according to the author's experience stage IV would be appropriate) | VI |
Combined cerebrovascular lesions |
The age of the vascular lesion(s) should correspond with the time when disease began. Post-stroke cases are usually included in subtypes I–III.
Subtype I may result from large vessel occlusion (atherothromboembolism), artery-to-artery embolism or cardioembolism. Subtype II usually involves descriptions of arteriosclerosis, lipohyalinosis, hypertensive, arteriosclerotic, amyloid or collagen angiopathy. Subtypes I, II, and V may result from aneurysms, arterial dissections, arteriovenous malformations and various forms of vasculitis.