Morphological Biomarkers in the Amygdala and Hippocampus of Children and Adults at High Familial Risk for Depression.

Major Depressive Disorder (MDD) is highly familial, and the hippocampus and amygdala are important in the pathophysiology of MDD. Whether morphological markers of risk for familial depression are present in the hippocampus or amygdala is unknown. We imaged the brains of 148 individuals, aged 6 to 54 years, who were members of a three-generation family cohort study and who were at either high or low familial risk for MDD. We compared surface morphological features of the hippocampus and amygdala across risk groups and assessed their associations with depression severity. High- compared with low-risk individuals had inward deformations of the head of both hippocampi and the medial surface of the left amygdala. The hippocampus findings persisted in analyses that included only those participants who had never had MDD, suggesting that these are true endophenotypic biomarkers for familial MDD. Posterior extension of the inward deformations was associated with more severe depressive symptoms, suggesting that a greater spatial extent of this biomarker may contribute to the transition from risk to the overt expression of symptoms. Significant associations of these biomarkers with corresponding biomarkers for cortical thickness suggest that these markers are components of a distributed cortico-limbic network of familial vulnerability to MDD.

Improvement in drug-induced parkinsonism with electroconvulsive therapy.

BACKGROUND: Drug-induced parkinsonism is a common medication side effect. OBJECTIVE: The present report describes the case of a depressed elderly woman who developed parkinsonism after receiving risperidone and who had improvement of her depression and parkinsonism after electroconvulsive therapy (ECT). CASE SUMMARY: A 67-year-old white female was admitted to a psychiatry ward for a major depressive episode with psychotic features. The patient developed pronounced parkinsonian features after taking risperidone, which did not improve with discontinuation of the drug, or with benztropine and carbidopa/levodopa. A total score of 6 was achieved using Naranjo's adverse drug reaction causality algorithm, suggesting risperidone was a probable cause of this adverse event. The patient's depression and parkinsonian symptoms did not improve until after initiation of ECT. After 19 treatments, the patient had resolution of her depression and only mild bradykinesia remained. CONCLUSIONS: This was a case of probable drug-induced parkinsonism in an elderly woman who had improvement of her depression and parkinsonism after receiving ECT.