High risk of medical morbidity and mortalityĪlthough advances in brief anesthesia and neuromuscular paralysis have improved the safety and tolerability of ECT, this modality poses numerous risks, including those associated with general anesthesia, postictal confusion, and, more rarely, short-term memory difficulties. Other components of limbic circuitry, in particular, the hippocampus and amygdala, have been implicated in depression. Vascular lesions may contribute to depression by disrupting the neural networks involved in emotion regulation-in particular, frontostriatal pathways that link the dorsolateral prefrontal cortex, orbitofrontal cortex, anterior cingulate, and dorsal cingulate. Studies suggest that seasonal affective disorder is also mediated by alterations in CNS levels of 5-HT and appears to be triggered by alterations in circadian rhythm and sunlight exposure. Seasonal affective disorder is a form of major depressive disorder that typically arises during the fall and winter and resolves during the spring and summer. Research findings imply a role for neuronal receptor regulation, intracellular signaling, and gene expression over time, in addition to enhanced neurotransmitter availability. The role of CNS 5-HT activity in the pathophysiology of major depressive disorder is suggested by the therapeutic efficacy of selective serotonin reuptake inhibitors (SSRIs). Other neurotransmitters implicated include norepinephrine (NE), dopamine (DA), glutamate, and brain-derived neurotrophic factor (BDNF). Current evidence points to a complex interaction between neurotransmitter availability and receptor regulation and sensitivity underlying the affective symptoms.Ĭlinical and preclinical trials suggest a disturbance in central nervous system serotonin (5-HT) activity as an important factor. The underlying pathophysiology of major depressive disorder has not been clearly defined. Traumatic events such as the death or loss of a loved one, lack or reduced social support, caregiver burden, financial problems, interpersonal difficulties, and conflicts are examples of stressors that can trigger depression. Life events and hassles operate as triggers for the development of depression. Neurodegenerative diseases (especially Alzheimer disease and Parkinson disease), stroke, multiple sclerosis, seizure disorders, cancer, macular degeneration, and chronic pain have been associated with higher rates of depression.
There are potential biological risk factors that have been identified for depression in the elderly. Some evidence suggests that genetic factors play a lesser role in late-onset depression than in early-onset depression. First-degree relatives of depressed individuals are about 3 times as likely to develop depression as the general population however, depression can occur in people without family histories of depression. The etiology of major depressive disorder is multifactorial with both genetic and environmental factors playing a role.
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