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A process similar to Binswanger leukoencephalopathy, but without hypertension, has been identi ed as an autosomal dominant familial trait linked in several families to a mutation on chromosome 19 It had been described previously under a number of names, including hereditary multi-infarct dementia The acronym CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) is now applied In these patients, recurrent small strokes, often beginning in early adulthood, culminate in a subcortical dementia Migraine headaches, often with neurologic accompaniments, may precede the strokes by several years, as may numerous and varied TIAs that are attributed, probably incorrectly, to the migraine Some individuals display few clinical changes; others are demented or have strokes that simulate lacunes We are unable to comment on the encephalopathy and coma, in some cases accompanied by fever, described by Schon and colleagues It seems to represent another very rare condition The familial nature of the process may not be appreciated because genetic penetrance is not complete until after 60 years of age On MRI scans, clinically unaffected family members may show substantial changes in the white matter well before strokes or dementia arises In some cases, particularly in Japan, early alopecia and lumbar spondylosis have been associated with CADASIL The MRI and CT appearance of multiple con uent white matter lesions of various sizes, many quite small and concentrated around the basal ganglia and periventricular areas, is similar to that in Binswanger disease When these are asymmetrical and periventricular, they are dif cult to distinguish from the lesions of multiple sclerosis In the autopsy cases studied by Jung and colleagues, numerous partially cavitated infarctions were found in the white matter and basal ganglia In the regions of these infarctions were small vessels, 100 to 200 mm diameter, in which the media contained basophilic granular deposits with degeneration of the smooth muscle bers Attribution of the white matter degeneration to these vascular changes presents the same problems as in Binswanger disease, particularly in view of patency of most of the many small vessels in the material Again, the relation of the vascular changes to lesions in the brain has not been studied in serial sections Nevertheless, CADASIL is probably the main cause of sporadic instances of what otherwise passes for Binswanger disease but without the obligate hypertension of the latter Also, migraine headaches are not a component of Binswanger disease.

Binswanger disease has been mentioned brie y in the discussion of the course and prognosis of atherothrombotic infarction and as a cause of dementia in Chaps 21 and 39 The term has come to denote a widespread degeneration of cerebral white matter having a vascular causation and observed in the context of hypertension, atherosclerosis of the small blood vessels, and multiple strokes (see page 909) Hemiparesis, dysarthria, TIAs, and typical lacunar or cortical strokes are admixed in many cases The process has been associated with a particular radiologic appearance that re ects the con uence of areas of white matter changes The term leukoareosis, meant to describe the less intense appearance of periventricular tissues in imaging studies, complicates the matter, since this condition is also assumed to have a vascular basis, and the term has been used indiscriminately, particularly by some radiologists, as equivalent to Binswanger disease Whether multiple discrete lacunes in the deep white matter constitutes Binswanger disease may be a semantic issue, but we adhere to the notion that the former is characterized by a more con uent and widespread ischemic and gliotic change in the deep white matter Dementia, a pseudobulbar state, and a gait disorder, alone or in combination, are the main features of Binswanger cases They have been attributed to the cumulative effects of the ischemic changes and speci cally to the white matter degeneration The pathologic basis of such a clinical entity has not been well delineated More importantly, the gliosis that is found in white matter has been assumed to represent a special type of ischemic change,

The responsible mutation on chromosome 19 of the Notch 3 gene, in the same locus as the gene for familial hemiplegic migraine, has been characterized by Joutel and colleagues; this provides a diagnostic test that can be performed on the blood or skin However, the mechanism by which this leads to the vasculopathy or white matter changes is not clear The diagnosis can also be con rmed by nding eosinophilic inclusions in the arterioles of a skin biopsy (osmophilic with electron microscopy) Awareness of this apparently vascular form of white matter degeneration adds to the list of inherited leukoencephalopathies, the others being inherited metabolic disturbances, as discussed in Chap 38

TABLE 2-2

This process is discussed further on in relation to lobar cerebral hemorrhages in the elderly The angiopathy consists of the deposition of amyloid in the media and adventitia of small vessels, predominantly in the meninges, cortex, and cortical penetrating vessels The incidence at autopsy of vascular amyloid deposition in the brain is related to the age of the population studied; rates of 12 percent are cited in patients above 85 years of age (the same changes are present in over 25 percent of individuals with Alzheimer disease, but the nature of the amyloid is different in the two conditions) Over the last few years, however, our colleague Greenberg has emphasized certain clinical features associated solely with cerebrovascular amyloidosis Of interest here are multiple TIAs, some with migrainous features such as spreading sensory symptoms, and fairly rapid progression to dementia Telltale signs of small hemorrhages that are more characteristic of diffuse cerebrovascular amyloid are often present in these cases These old hemorrhages are seen to advantage with gradient echo sequences on the MRI The frequency of this interesting condition in the elderly is unclear There is a separate familial amyloidotic condition of diffuse white matter degeneration with dementia, associated in some families with calci cation in the occipital lobes