Tuesday, 19 August 2003
This presentation is part of : Clinical Neuroscience of Late-Life Mood Disorders

S025-002 Vascular Mechanisms and Late Life Depression

K. Ranga R. Krishnan, Psychiatry and Behavioral Sciences, Psychiatry and Behavioral Sciences, Duke University Medical Center, Durham, NC, USA

Objective: To discuss data on the concept of vascular depression.

Materials and Methods: MRI studies of late life depression Diffusion Tensor studies of late life depression.

Results: Silent infarcts are common in late life depression. These lesions interrupt white matter tracts in the medial orbital frontal region

Conclusion: These changes suggest that we can classify a specific subtype of depression as secondary to vascular change. There are many ways to classify vascular depression. The first system, also known as clinically defined vascular depression, allows for classification based on conditions presumed to put the individual at risk for cerebrovascular disease coupled with cognitive tests consistent with a subcortical profile.

The latter classification requirement relies on the assumption that neuropsychological deficit is associated with subcortical brain change. In fact, there exists a substantial literature on subcortical hypertensities linking their presence with slowed speed of processing, attention and concentration problems, and frontal executive dysfunction. This approach is appealing because it does not require neuroimaging, and most clinicians can address the criteria through medical history and administration of cognitive tests. The main disadvantage is that neuropsychological performance may not correlate highly with vascular change as seen on neuroimaging.

The second classification system would retain presence of vascular risk and would expand evidence for brain change to include not only specific neuropsychological deficit, but focal neurological deficit or subcortical vascular change on neuroimaging as well.

The third classification possibilities rest largely on neuroimaging evidence. These changes on neuroimaging represent the most definitive ante-mortem evidence of subcortical ischemic pathology that exist. Thus, they should be considered the gold standard for diagnosis.

The question remains as to whether presence of vascular risk factors is important. On its face, one would think the answer would be in the affirmative. It make sense that in order for vascular disease to be present, there must be a vascular condition predisposing to development of cerebrovascular change. These associations presuppose that clinicians can readily identify the vascular risk factor. Common examples might be hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation. Yet some of these conditions may not be apparent from clinical history. Further, there may be some conditions that increase risk for cerebrovascular diseases that require specialized laboratory testing. Autoimmune disease such as Antiphospholipid Antibody Syndrome has been shown to increase risk for vascular events. The Apolipoprotein E epsilon-4 allele, known to increase risk of Alzheimer's disease, has also been associated with vascular dementia.

Back to S025 Clinical Neuroscience of Late-Life Mood Disorders
Back to The Eleventh International Congress