ABSTRACT
The importance of vascular factors in the aetiology of cognitive impairment was recognised over a century ago1, but there was debate regarding the mechanisms by which this occurred. Alzheimer2 described “arteriosclerotic cerebral atrophy” as a cause of senility around the same time as Binswanger’s3 paper on “encephalitis subcorticalis chronica progressiva” was published in 1884. A close examination of Binswanger’s report suggests that the diagnosis was not certain. The patient, a man in his mid-fifties with a history of syphilis, presented with a progressive decline in speech and memory, as well as depression and personality change. On post-mortem examination, there was minimal atherosclerosis, enlargement of lateral ventricles, marked atrophy of the cerebral white matter, granular deposits on basal dura mater, and multiple ependymal thickenings.3 It was Alzheimer4 who attributed this white matter change to atherosclerosis when he described an analogous case in 1902. Modern reviewers consider Binswanger’s case to have been one of neurosyphilis,5,6 but the concept of extensive atherosclerotic white matter disease associated with cognitive decline became known as Binswanger’s disease. Alzheimer’s7 description of plaques and tangles as a basis of dementia in the first decade of this century did not greatly reduce the emphasis on vascular factors that were still considered to be the more common cause of dementia. Half a century later, the idea that critical atherosclerotic narrowing of cerebral arteries commonly led to progressive ischaemia, neuronal loss and dementia still held sway although Alzheimer’s disease (AD) had by now found its way into most neurological texts. A number of developments in the last three decades have led to a radical rethinking of the association between cerebrovascular disease (CVD) and dementia, and set the stage for a reconceptualisation of vascular dementia.
