The cognitive deficits in VaD and VCI are characterized by disturbance of frontal functions, with less verbal memory impairment. VaD and VCI differ in severity but not pattern of disturbance. The brain lesions that best account for these deficits are noninfarct subcortical white matter and gray matter changes due to ischemia. The picture of VaD/VCI presented shows subcortical deficits embellished by cognitive deficits from cortical infarctions.

The neuropsychological differentiation of VaD from AD was consistent with the different neuroimaging findings in the two disorders, and argues for differential criteria for the definition of the syndromes. The simple application of Alzheimer's dementia criteria to VaD, with the inclusion of cerebrovascular disease etiology, may not be sufficient to capture the uniqueness of VaD.

Background: Dementia following stroke is common but its determinants are still incompletely understood. Methods: In the Sydney Stroke Study, we performed detailed neuropsychological and medical-psychiatric assessments on 169 patients aged 50–85 years, 3–6 months after a stroke, and 103 controls with a majority of both groups undergoing MRI brain scans. Stroke subjects were diagnosed as having vascular mild cognitive impairment (VaMCI) or vascular dementia (VaD) or no cognitive impairment by consensus. Demographic, functional, cerebrovascular risk factors and neuroimaging parameters were examined as determinants of dementia using planned logistic regression. Results: 21.3% of subjects were diagnosed with VaD, with one case in those aged 50–59 years, 24% in those aged 60–69 years and 23% in those 70–79 years. There was no difference by sex. The prevalence of VaMCI was 36.7%. VaD subjects had lower premorbid intellectual functioning and had 0.9 years less education than controls. The VaD and VaMCI groups did not differ from the no cognitive impairment group on any specific cerebrovascular risk factor, however overall those with impairment had a greater number of risk factors. They did not differ consistently on depression severity, homocysteine levels and neuroimaging parameters (atrophy, infarct volume and number of infarcts) except for an excess of white matter lesions on MRI and greater number of infarcts in the VaD and VaMCI groups. On a series of logistic regression analyses, stroke volume and premorbid function were significant determinants of cognitive impairment in stroke patients. Conclusion: Post-stroke dementia and MCI are common, especially in older individuals. Cerebrovascular risk factors are not independent risk factors for VaD, but stroke volume is a significant determinant of dementia. Premorbid functioning is a determinant of post- stroke impairment.

Objective: To provide a rapid clinical update on the evidence for telehealth in mental healthcare in the context of the COVID-19 pandemic public health measures. Conclusions: Telehealth has been rapidly implemented in metropolitan and rural settings and the existing evidence base demonstrates that it represents an effective mode of service delivery.

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Psychiatrists can apply their skills and training in the diagnosis of AD, which is based upon a comprehensive assessment comprising history, investigations, and cognitive and functional assessment, guided by accepted diagnostic criteria.

Hippocampal pathology is central to Alzheimer’s disease (AD) and other forms of dementia such as frontotemporal lobar degeneration (FTLD). Autopsy studies have shown that certain hippocampal subfields are more vulnerable than others to AD and FTLD pathology, in particular the subiculum and cornu ammonis 1 (CA1). We conducted shape analysis of hippocampi segmented from structural T1 MRI images on clinically diagnosed dementia patients and controls. The subjects included 19 AD and 35 FTLD patients (13 frontotemporal dementia [FTD], 13 semantic dementia [SD] and 9 progressive nonfluent aphasia [PNFA]) and 21 controls. Compared to controls, SD displayed severe atrophy of the whole left hippocampus. PNFA and FTD also displayed atrophy on the left side, restricted to the hippocampal head in FTD. AD finally displayed most atrophy in left hippocampal body with relative sparing of the hippocampal head. Consistent with pathological studies most deformation was found in CA1 and subiculum areas in FTLD and AD.

BACKGROUND AND PURPOSE:Frontostriatal circuits involving the caudate nucleus have been implicated in frontotemporal lobar degeneration (FTLD). We assessed caudate nucleus volumetrics in FTLD and subtypes: frontotemporal dementia (FTD, n ϭ 12), semantic dementia (SD, n ϭ 13), and progressive nonfluent aphasia (PNFA, n ϭ 9) in comparison with healthy controls (n ϭ 27) and subjects with Alzheimer disease (AD, n ϭ 19).