Alcohol-related problems among adolescent suicides in Finland.
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We studied 106 adolescent suicides out of a total nationwide population of 1397 suicides. Forty-four (42%) of these 13-22-year-old victims were classified as having suffered either a DSM-III-R alcohol use disorder or diagnostically subthreshold alcohol misuse according to retrospective evaluation using the Michigan Alcoholism Screening Test (MAST). These victims were found to differ from the other adolescent suicides in several characteristics: they were more likely to have comorbid categorical DSM-III-R disorders, antisocial behaviour, disturbed family backgrounds, precipitating life-events as stressors and severe psychosocial impairment. In addition, they also had a greater tendency to be alcohol-intoxicated at the time of the suicidal act, which tended to occur during weekends, suggesting that drinking in itself, and its weekly pattern, each contributed to the completion of their suicides. (+info)
Electrical stimulation of rat medial prefrontal cortex enhances forebrain serotonin output: implications for electroconvulsive therapy and transcranial magnetic stimulation in depression.
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Decreased activity of the prefrontal cortex (PFC), as well as reduced serotonergic neurotransmission, is considered as a characteristic feature of major depression. The mechanism by which electroconvulsive therapy (ECT) and transcranial magnetic stimulation (TMS) achieve their antidepressant effects may involve changes in PFC activity. It is, however, still unclear whether these changes are accompanied by increased synaptic availability of serotonin (5-HT). In the present study, 5-HT efflux in the rat ventral hippocampus and amygdala was analyzed using in vivo microdialysis during low-current electrical stimulation of PFC and other cortical regions. Electrical stimulation of the medial PFC produced current-dependent increases in limbic 5-HT output in both urethane-anesthetized and behaving rats. No effects on 5-HT levels were seen after comparable stimulation of either the lateral parts of the PFC, the medial precentral area, the primary motor cortex or the parietal cortex. This pronounced regional specificity of the effect of medial PFC stimulation on limbic 5-HT output suggests that activation of this particular area might play a crucial role in such antidepressant treatments as ECT and TMS. (+info)
Melatonin sensitivity to dim white light in affective disorders.
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Both dim and bright light has been shown to suppress the nocturnal secretion of the pineal hormone melatonin. Early reports suggests that an abnormal response to light occurs in patients with bipolar affective disorder, where as patients with major depressive disorder respond similarly to controls. It has been suggested that this abnormal sensitivity of the melatonin response to light could be a trait marker of bipolar affective disorder. However reports lack consistency. Hence, we investigated the melatonin suppression by dim light (200 lux) in patients with bipolar affective disorder, seasonal affective disorder and major depressive disorder. Results suggest that a supersensitive melatonin suppression to light in bipolar affective disorder (p < .005), and seasonal affective disorder (p < .05), whereas patients with major depressive disorder display similar suppression to controls. The supersensitivity may be a mechanism where by phase-delayed rhythms, are resynchronised to a new circadian position. Conversely, an abnormality may exist in the pathway from the retina to the suprachiamatic nucleus. (+info)
Poststroke depression correlates with cognitive impairment and neurological deficits.
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BACKGROUND AND PURPOSE: The prevalence of poststroke depression is known to be high, but the knowledge of its neuropsychological correlates is limited. This 12-month prospective study was designed to evaluate the natural history of poststroke depression and to study its neuropsychological, clinical, and functional associates. METHODS: We studied a series of 106 consecutive patients (46 women and 60 men, mean age 65.8 years) with acute first-ever ischemic stroke. The patients underwent a neurological, psychiatric, and neuropsychological examination at 3 and 12 months after the stroke. The psychiatric diagnosis of depression was based on DSM-III-R-criteria. RESULTS: Depression was diagnosed in 53% of the patients at 3 months and in 42% of the patients at 12 months after the stroke. The prevalence of major depression was 9% at 3 months and 16% at 12 months. There was an association between poststroke depression and cognitive impairment; the domains most likely to be defective in stroke-related depression were memory (P=0.022), nonverbal problem solving (P=0.039), and attention and psychomotor speed (P=0.020). The presence of dysphasia increased the risk of major depression. The depressive patients were more dependent in ADL and had more severe impairment and handicap than the nondepressive patients. CONCLUSIONS: More than half of the patients suffer from depression after stroke, and the frequency of major depression seems to increase during the first year. In addition to dysphasia, poststroke depression is correlated with other cognitive deficits. We emphasize the importance of psychiatric evaluation of stroke patients. (+info)
Depression in the workplace: effects on short-term disability.
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We analyzed data from two national surveys to estimate the short-term work disability associated with thirty-day major depression. Depressed workers were found to have between 1.5 and 3.2 more short-term work-disability days in a thirty-day period than other workers had, with a salary-equivalent productivity loss averaging between $182 and $395. These workplace costs are nearly as large as the direct costs of successful depression treatment, which suggests that encouraging depressed workers to obtain treatment might be cost-effective for some employers. (+info)
Depression without sadness: alternative presentations of depression in late life.
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Older adults often deny feeling sad while exhibiting other characteristics of depression. Elderly patients with depression who do not present with sadness often have unexplained somatic complaints and exhibit a sense of hopelessness. Anxiety and anhedonia (a general loss of ability to feel pleasure) are also encountered frequently. Other features that may indicate underlying depression include slowness of movement and lack of interest in personal care. A screening device, such as the Center for Epidemiologic Studies--Depression Scale, Revised (CES-D-R), may identify depression in suspicious cases. When this condition is identified, treatment should generally include the use of an antidepressant medication, usually a selective serotonin reuptake inhibitor. (+info)
Patterns of brain activity in patients with epilepsy and depression.
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Depression is a recognized feature of epilepsy. This study tested the hypothesis that depression arising in patients with epilepsy would be associated with decreased activity in brain regions previously demonstrated to be hypoperfused both in primary depression and in depression secondary to movement disorders. Two groups of patients with temporal lobe epilepsy were studied, one of which also met DSM IV criteria for a major depressive episode. All underwent a SPECT scan using the blood flow marker,(99m)Tc-HMPAO. An automated voxel-based analysis demonstrated no regions of relatively decreased activity in the depressed compared with the non-depressed patients. Sites of relative hyperactivity in the depressed group were concentrated in the left hemisphere, particularly in dorsolateral prefrontal cortex, striatum, thalamus and temporo-parietal regions. Comparison of these data with normal population data revealed that in the depressed epilepsy group regional activities were within the normal range whilst corresponding results from the non-depressed group were below it. Depressed patients with epilepsy have cerebral regions with greater perfusion than non-depressed people with epilepsy, although they are not hyperperfused compared with normals. Our results suggest that depression in people with epilepsy may arise from a mechanism which differs from that underlying the development of depression in patients with movement disorders. (+info)
Eosinophilic pneumonia and respiratory failure associated with venlafaxine treatment.
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Drugs are well known causes of eosinophilic lung disease. In many patients, symptoms increase slowly, pulmonary infiltrates and eosinophilia progress over weeks, and resolve upon withdrawal of the offending agent. Rarely, the disease presents like acute eosinophilic pneumonia with acute onset of symptoms and rapidly progressing infiltrates which may be associated with respiratory failure. This report describe a case of venlafaxine-induced acute eosinophilic pneumonia causing respiratory insufficiency that rapidly resolved upon institution of corticosteroid treatment. This 5-hydroxytryptamine and noradrenaline reuptake inhibitor was previously not known to cause lung or peripheral blood eosinophilia. Considering the increasing use of this class of medication physicians have to be aware of this life-threatening and fully reversible complication. (+info)