Another mechanism may involve damage of catecholamine neurons by

Another mechanism may involve selleck kinase inhibitor damage of catecholamine neurons by white matter lesions at the pons, resulting in reduction of stress responses.74 A third mechanism postulates

disruption of control exerted by the orbitofrontal cortex on the serotoninergic raphe nuclei.89 We have reported that dépressives with vascular risk factors have greater dysfunction in auditory transmission at the pons than geriatric dépressives without vascular risk factors or elderly normal controls.90 These putative mechanisms suggest that lesions at various sites may result in depression through direct disruption of the CSPTC circuits or their modulating systems. The “threshold hypothesis” postulates Inhibitors,research,lifescience,medical vulnerability that may be conferred by the lesions themselves or by a broader cerebrovascular disturbance that compromises pathways relevant to depression. Nonbiological factors may be required to trigger depression in predisposed patients. Depression developing 3 Inhibitors,research,lifescience,medical months after stroke was found to be predicted by impairment in activities of daily living, while depression occurring 12 months after

stroke was predicted by social isolation.91 Other studies have shown that reverse occipital asymmetry (right larger than left), absence of ven triculomegaly, and absence of family history of mood disorders Inhibitors,research,lifescience,medical are associated with lower frequency of poststroke Inhibitors,research,lifescience,medical depression.26 Studies of outcomes of patients with vascular disease or risk factors can identify biological

and nonbiological mechanisms that mediate or protect against depression. Prevention of vascular depression The vascular depression hypothesis provides the conceptual background for primary Inhibitors,research,lifescience,medical prevention of geriatric depression by modifying risk factors for cerebrovascular disease. Hypertension is a significant risk factor for stroke.97-94 Treatment of hypertension95 and hypercholesterolemia96 reduces cerebrovascular morbidity and mortality. Warfarin and aspirin reduce the risk of stroke in patients with atrial fibrillation.97 Ticlopidine,98 aspirin,98,99 and dipyridamole99 may prevent future stroke in patients with transient ischemic attacks or ischemic stroke. Studies are needed to ascertain whether antihypertensive, Resminostat anticholestcrolemic, and antiplatelet agents alter the course of vascular depression. Antiplatelet agents may prove to be effective in preventing further vascular damage occurring during depressive episodes, when the serotonin-mediated thrombogenic platelet response is enhanced. 100,101 In addition, longitudinal studies of patients with vascular depression can evaluate the efficacy of these agents in improving the course of illness. Drugs that reduce damage after stroke may be relevant to vascular depression.

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