figures 4 and 5 shows thickened hyalinized barrel - shaped arterioles . figure 6 shows a focal area of lack of myelination . the myelin loss was variable with white matter reactive astrocytosis ( gfap stain ; figure 7 ) and microgliosis ( cd68 stain ; not shown ) . binswanger 's disease , also known as subcortical arteriosclerotic encephalopathy was initially recognized by otto binswanger in 1894 , and alois alzheimer first coined the term binswanger 's disease  in 1902 ( 1994 ; pantoni et al . , 1996 ) . binswanger recognized a total of eight cases in his original study , but defined the gross pathology in only one of them . later on alzheimer described the pathology and clinical characteristics of the disease and proposed it as a separate entity . an earlier review by babikian and ropper ( 1987 ) reported only 47 cases before 1987 . since then , additional cases of binswanger 's disease have been reported primarily due to the use of modern neuroimaging . vascular dementia is the second most common form of dementia in the united states , and causes an estimated 50% of dementia cases in japan . binswanger 's disease is a cause of vascular dementia ( world health organization , 1993 ) , and is most commonly observed in the fifth and sixth decades of life . slightly more common among men , it is associated with arterial hypertension and diabetes mellitus . the disease starts with mild decrease in cognitive function , referred to as vascular cognitive impairment ( bowler and hachinski , 1995 , 2003 ) . the cognitive decline is gradual in the beginning and worsens with new clinical events . as the disease progresses further decrease in the cognitive function may not be associated with new clinical events ( pohjasvaara et al . , 2003 ) . according to criteria defined by bennett et al . , binswanger 's disease is diagnosed by the presence of dementia on clinical examination or neuropsychological testing and the presence of either vascular risk factors with cerebrovascular disease or subcortical dysfunction . there should be bilateral subcortical white matter involvement , without cortical involvement on cranial computed tomography or magnetic resonance imaging ( bennett et al . , 1990).the dementia is characterized by a predominantly frontal dysexecutive syndrome with mild memory impairment . dysarthria , gait impairment , and bladder incontinence may occur early in the disease process ( baezner et al . some patients may have mania ( caplan and schoene , 1978 ) , depression ( pohjasvaara et al . , 2003 ) or mood instability with clinical fluctuations ( delong et al . , 1974 ) gross pathology is characterized by gyral atrophy and lacunar infarctions involving the basal ganglia , centrum semiovale or internal capsule . microscopically , swelling of the myelin sheath and oligodendrocytes is one of the earliest changes seen . there are microcystic areas of infarction , with relative demyelination ( pellissier and poncet , 1989 ) . the arterioles supplying the deep white matter exhibit lipohyalinosis with perivascular lymphocytes , thickened walls and basal lamina . there is increased deposition of normal collagen , disruption of the media , narrowed lumina and splitting of the internal elastic lamina , with some occluded vessels . some vessels show hypertrophy of smooth muscle cells ( akiguchi et al . , 1997 ) . the degree of cognitive decline in binswanger 's disease correlates with the progression of white matter changes . the cardiovascular health study showed a 28% increase in white matter disease among patients older than 65 years , which correlated with decline in cognitive function ( longstreth et al . the leukoaraiosis and disability study ( ladis ) , observed that 10.5% of patients with mild white matter disease progressed to death or disability as compared to 29.5% with extensive white matter disease every year ( inzitari et al . , 2007).the progress trial showed that patients with mild leukoaraiosis at the time of entry had a slower rate of progression to severe cognitive impairment as compared to patients with severe leukoaraiosis ( dufouil et al . , 2009 ) . other factors correlating with cognitive decline are microvascular retinopathy ( lesage et al . , 2009 ) and hypertension ( gottesman et al . , 2010 ) . it is important to always take into account the autoregulatory changes associated with chronic hypertension as these patients may be more likely to have hypotensive events at pressures otherwise considered as normal ( sulkava and erkinjuntti , 1987 ) . these events may be responsible for white matter changes leading to further memory impairment . lipid lowering drugs and platelet antiaggregants ( mainly aspirin ) are used in the prevention of cardiovascular and cerebrovascular disease ( sterzer et al . , 2001 ) . in one study pravastatin improved vasomotor reactivity in small vessel ischemic disease , but had no effect on volume of leukoaraiosis ( zijlmans et al . , 2004 ) . l - dopa has been used to improve gait in patients with features of vascular parkinsonism ( molnar et al . , 1998 ) . memantine , donepezil , and rivastigmine have been used to benefit vascular dementia to a modest degree ( mobius and stoffler , 2002 ; wilkinson et al . , the authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest .
a 49-year - old man presented with slurred speech , memory loss , and behavioral changes . 
 his clinical course was marked by decline in functional status and cognition . 
 he had poorly controlled hypertension and hyperlipidemia . 
 neuroimaging was remarkable for multiple subcortical white matter lesions . 
 we discuss the diagnostic and therapeutic approach of rapidly progressing cognitive decline in the given clinical setting .