BACKGROUND: Strategic infarct dementia (SID) is characterized by focal ischemic lesions involving specific sites that are critical for higher cortical functions. However, the mechanisms of SID are not well understood. We evaluated lesion sites, neuropsychiatric symptoms, neuroimaging and neuropsychological findings in patients with SID and have come up with suggestions of the mechanism behind SID. METHODS: Eleven patients with SID according to the NINDSAIREN criteria for vascular dementia were included. All patients were given a neurologic examination, brain MRI with MRA and brain perfusion SPECT using Tc-99m HMPAO. We evaluated neuropsychiatric symptoms and neuropsychological status using a Korean-version of the Neuropsychiatric Inventory(K-NPI) and Seoul Neuropsychological Screening Battery. RESULTS: Various sites were responsible for SID; the thalamus (n=5), genu of internal capsule (n=2), temporooccipital lobe (n=2), medial temporal lobe (n=1), medial frontal lobe (n=1). The most common neuropsychiatric symptom was apathy according to the K-NPI. Brain perfusion SPECT revealed ipsilateral cortical hypoperfusion, mainly in the frontal and temporal areas. In several cases, there were some degrees of cortical hypoperfusion in the contralateral areas of the lesion. On neuropsychological assessment, cognitive deficits on attention and frontal executive function were prominent. CONCLUSIONS: The thalamus, genu of internal capsule, and temporooccipital area were the most common sites responsible for SID. Based on the results that there were cortical hypoperfusion ipsilateral to subcortical strategic infarct and prominent cognitive deficits on attention and frontal executive function, it is suggested that disruption of the frontal-subcortical circuit may play an important role in patients with SID.