Health & Medical Neurological Conditions

Neuroimaging in Dementia

Neuroimaging in Dementia

Vascular Dementia

This can result from large-vessel (cortical) or small-vessel (subcortical) vascular disease. Cognitive decline may develop as a direct result of the vascular injury (eg, multi-infarcts or a single stroke affecting a strategic location) and/or lowering the threshold for the expression of concomitant pathology, such as AD. In 1993, the National Institute of Neurological Disorders and Stroke and the Association Internationale pour la Recherche et l'Enseignement en Neurosciences reported diagnostic criteria for the diagnosis of vascular dementia for research studies. This includes CT or MR criteria (Table 4).

Lacunar Infarcts and Leukoaraiosis

Subcortical vascular dementia is the most common form of vascular dementia, and refers to cognitive impairment secondary to lacunar infarction and small-vessel disease, or leukoaraiosis. Binswanger's disease is the eponym associated with extensive white matter ischaemic change.

Lacunar infarctions result from arteriosclerosis, lipohyalinosis or embolism affecting the deep perforator arteries, such as the lenticulostriate, thalmoperforating and long medullary arterioles. Lacunar infarctions, therefore, occur in the basal ganglia, putamen, internal capsule, thalamus, corona radiata and centrum semiovale and lateral brainstem. Silent lacunes occur in 10–25% of patients aged >65 years. Patients with lacunar infarctions develop dementia 4–12 times more frequently than the normal population.

Lacunar infarctions are (radiologically) 3–15 mm in size. They are cavitating, round, oval or slit-like, and on CT are hypodense. On MRI, they often follow cerebrospinal fluid signal intensity, being hypointense on T1, and hyperintense on T2. FLAIR sequences may show hypointensity with a high signal rim.

Small-vessel disease, or leukoaraiosis, is another player in subcortical vascular dementia. White matter lesions on MRI correspond histologically to variable combinations of myelin and axonal loss and scattered microinfarctions, astrogliosis, and dilatation of periventricular spaces. These lesions are exceptionally common. White matter disease on CT shows as hypodense areas. On MR T2 and FLAIR imaging, it appears as hyperintense areas in the periventricular and deep white matter (figure 16). MRI is more sensitive than CT for detecting leukoaraiosis, although modern multislice CT may be as good. Cognitive decline relates to the severity of white matter hyperintensity and is more pronounced in patients with these changes in a periventricular location. There are rating scales to grade the severity of white matter disease in population-based studies, the most simple and commonly used being the Fazekas scale (figure 16).

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Figure 16.

White matter hyperintensities on T2-weighted MRI. Fazekas 0: none or a single punctate white matter hyperintensity lesions; Fazekas 1: multiple punctate lesions; Fazekas 2: beginning confluency of lesions (bridging); Fazekas 3: large confluent lesions. The Fazekas scale provides an overall impression of the presence of white matter hyperintensities in the entire brain. It can be scored on transverse FLAIR or T2-weighted images. As well as dementia, severe white matter hyperintensities (Fazekas 3) are associated with gait abnormalities, falls and depression, and recently, they have been shown to contribute to disability in the elderly population.


These appear as focal hypointensities on T2*-weighted or susceptibility-weighted images. Although the number of microbleeds is associated with age (occurring in 10% of the healthy elderly population), 65% of patients with vascular dementia in one series had microbleeds. In sporadic small-vessel disease, microbleeds are located centrally. The number of cerebral microbleeds is more closely associated with lacunar infarction and leukoaraiosis than it is with age. Multiple microbleeds are associated with poorer executive function and processing speed, and suggest an increased risk of vascular dementia. Mortality is increased in patients with both microbleeds and global cortical atrophy.

Volume Loss

Patients with vascular dementia also have global volume loss, perhaps due to subclinical diffuse ischaemia. The global cortical atrophy scale of Pasquier et al (figure 17) relies on assessment of sulcal opening and gyral narrowing. It was designed for MRI, but there is good agreement between MR and multidetector CT. It has good intrarater variability but poor inter-reader variability.

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Figure 17.

Cortical atrophy scale devised by Pasquier and colleagues. Scores 0–3 represent absent, mild, moderate and severe cortical atrophy respectively. Mild changes are said to be present when there is sulcal opening peripherally. Moderate changes are seen when there is widening along the length of the sulcus. Severe atrophy is present when there is gyral thinning.

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