The Cornell Scale for Depression in Dementia (CSDD) was specifically developed to assess signs and symptoms of major depression in patients with dementia. Because some of these patients may give unreliable reports, the CSDD uses a comprehensive interviewing approach that derives information from the patient and the informant. Information is elicited through two semi-structured interviews; an interview with an informant and an interview with the patient. Based on these interviews, the interviewer can score the CSDD by assigning a preliminary score to each item of the scale on the basis of the informant's report in the "Informant" column. The next step is for the rater to interview the patient using the Cornell scale items as a guide. The interviews focus on depressive symptoms and signs occurring during the week preceding the interview. Many of the items during the patient interview can be filled after direct observation of the patient. If there are discrepancies in ratings generated from the informant and the patient interviews, the rater should re-interview both the informant and the patient to resolve the discrepancies. The final ratings of the CSDD items represent the rater's clinical impression rather than the responses of the informant or the patient. The CSDD takes approximately 20 minutes to administer. Each item is rated for severity on a scale of 0-2 (0=absent, 1=mild or intermittent, 2=severe). The item scores are added. Scores above 10 indicate a probable major depression. Scores above 18 indicate a definite major depression. Scores below 6 as a rule are associated with absence of significant depressive symptoms. INTERVIEW WITH THE INFORMANT Who qualifies as an Informant? Informants should know and have frequent contact with the patient. Reliable informants can include nursing staff for patients in the hospital and nursing homes or a family member for outpatients.

Biomarkers have transformed modern medicine but remain largely elusive in psychiatry, partly because there is a weak correspondence between diagnostic labels and their neurobiological substrates. Like other neuropsychiatric disorders, depression is not a unitary disease, but rather a heterogeneous syndrome that encompasses varied, co-occurring symptoms and divergent responses to treatment. By using functional magnetic resonance imaging (fMRI) in a large multisite sample (n = 1,188), we show here that patients with depression can be subdivided into four neurophysiological subtypes (‘biotypes’) defined by distinct patterns of dysfunctional connectivity in limbic and frontostriatal networks. Clustering patients on this basis enabled the development of diagnostic classifiers (biomarkers) with high (82–93%) sensitivity and specificity for depression subtypes in multisite validation (n = 711) and out-of-sample replication (n = 477) data sets. These biotypes cannot be differentiated solely on the basis of clinical features, but they are associated with differing clinical-symptom profiles. They also predict responsiveness to transcranial magnetic stimulation therapy (n = 154). Our results define novel subtypes of depression that transcend current diagnostic boundaries and may be useful for identifying the individuals who are most likely to benefit from targeted neurostimulation therapies.

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We propose that cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive syndromes. The "vascular depression" hypothesis is supported by the comorbidity of depression, vascular disease, and vascular risk factors and the association of ischemic lesions to distinctive behavioral symptoms. Disruption of prefrontal systems or their modulating pathways by single lesions or by an accumulation of lesions exceeding a threshold are hypothesized to be central mechanisms in vascular depression. The vascular depression concept can generate studies of clinical and heuristic value. Drugs used for the prevention and treatment of cerebrovascular disease may be shown to reduce the risk for vascular depression or improve its outcomes. The choice of antidepressants in vascular depression may depend on their effect on neurologic recovery from ischemic lesions. Research can clarify the pathways to vascular depression by focusing on the site of the lesion, the resultant brain dysfunction, the presentation of depression and time of onset, and the contribution of nonbiological factors.