Vascular Dementia MCQ — NEET PG Practice Question | NEETPGAI
Vascular Dementia
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stethoscope Medicine
A 75-year-old man with hypertension, diabetes, and atrial fibrillation presents with cognitive decline that has worsened ABRUPTLY twice over 3 years, each time following a clinical stroke. He complains of difficulty planning and organizing tasks, and his family notes a shuffling gait. Examination reveals pyramidal signs and frontal release signs. MMSE is 21/30, with preserved recall after cueing but impaired attention and executive function. MRI shows bilateral cortical infarcts, multiple subcortical lacunes, and confluent periventricular white-matter hyperintensities (Fazekas 3) on FLAIR. The hippocampi are relatively preserved (MTA 1).
The imaging pattern marked **B** in the diagram is most consistent with which of the following subtypes of vascular dementia?
A. Hypoperfusion dementia secondary to chronic global cerebral hypoperfusion
B. Subcortical ischemic vascular dementia (Binswanger disease) with small-vessel disease and confluent white-matter change
C. Strategic infarct dementia affecting the thalamus and angular gyrus
D. Multi-infarct dementia with stepwise decline from large-vessel cortical strokes and subcortical lacunes
Explanation
Why "Multi-infarct dementia with stepwise decline from large-vessel cortical strokes and subcortical lacunes" is right
The clinical presentation—ABRUPT WORSENING after each stroke, BILATERAL CORTICAL INFARCTS in MCA and ACA territories, MULTIPLE SUBCORTICAL LACUNES in basal ganglia and thalami, and STEPWISE COGNITIVE DECLINE—is the hallmark of multi-infarct dementia (MID), a subtype of vascular dementia. The NINDS-AIREN and VASCOG criteria require cognitive impairment, cerebrovascular disease on imaging, and a reasonable temporal and anatomic relationship between infarcts and cognitive decline. The pattern marked B (multi-infarct burden with confluent leukoaraiosis) captures both the large-vessel cortical component and the subcortical lacunar component characteristic of MID. Executive dysfunction and preserved cued recall are the cognitive signature of vascular dementia, distinguishing it from Alzheimer disease.
Why each distractor is wrong
Strategic infarct dementia affecting the thalamus and angular gyrus: While the patient does have subcortical lacunes, the presence of BILATERAL CORTICAL INFARCTS in MCA and ACA territories is the dominant imaging finding. Strategic infarct dementia typically presents with cognitive decline from a single strategically placed infarct (e.g., medial thalamus or angular gyrus), not multiple cortical and subcortical lesions. This patient's pattern is multi-infarct, not strategic.
Subcortical ischemic vascular dementia (Binswanger disease) with small-vessel disease and confluent white-matter change: Although the patient does have confluent periventricular white-matter hyperintensities (Fazekas 3), Binswanger disease is characterized by GRADUAL cognitive decline and EXECUTIVE/GAIT DEFICITS in the absence of large cortical infarcts. The presence of BILATERAL CORTICAL INFARCTS and ABRUPT WORSENING after each stroke indicates large-vessel disease, not pure small-vessel disease. Binswanger disease is a subtype of subcortical ischemic VaD, not the primary diagnosis here.
Hypoperfusion dementia secondary to chronic global cerebrovascular hypoperfusion: This subtype presents with diffuse cognitive impairment in the setting of chronic global hypoperfusion (e.g., from severe carotid stenosis or cardiac pump failure) without discrete infarcts. The presence of multiple DISCRETE CORTICAL AND SUBCORTICAL INFARCTS rules out pure hypoperfusion dementia.
