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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular depression is, nowadays, a well-established concept in the literature. However, the possible emergence of late onset bipolar disorder in subjects with no antecedents of mood disorder or after a chronic or recurrent course of unipolar depression constitutes a poorly studied issue, despite its importance in clinical practice. Here, we present the case of a 72-year-old female patient who began to present recurrent major depressive symptoms, resistant to pharmacological treatment, from the age of 58. Three years later, she started to present phases of mania with rapid cycling features. A brain MRI scan showed prominent white matter hyperintensities (WMH). WMH are frequently found in the elderly population, but with greater burden in individuals with hypertension and cerebrovascular disease. WMH impair cortical function and damage the cerebral tissue. WMH have been associated with adult-onset bipolar disorder and late onset depression, and are linked to a worse prognosis of both conditions. The present case report highlights the possibility that vascular-related WMH may provoke late onset bipolar disorder by damaging frontolimbic circuits implicated in the pathophysiology of mania.
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PMID:Late onset bipolar disorder associated with white matter hyperintensities: a pathophysiological hypothesis. 1710 42

We evaluated the relationship between seven personality disorders listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders and coronary heart disease (CHD) in a nationally representative sample of U.S. older adults. We analyzed data on 10,573 adults aged 60 or older from the National Epidemiologic Survey on Alcohol and Related Conditions. In our results, we found that 13.30% of older adults reported a diagnosis of CHD confirmed by a health professional. Age (odds ratio or OR = 1.04), morbid obesity (OR = 1.59), hypertension (OR = 2.30), nicotine dependence (OR = 1.39), any drug use disorder (OR = 2.13), and any mood disorder (OR = 1.87) increased the odds of having CHD. Female gender (OR = 0.72) and social drinking (OR = 0.71) decreased the odds of having CHD. Controlling for these variables, we found that avoidant (OR = 1.80), schizoid (OR = 1.63), and obsessive-compulsive (OR = 1.37) personality disorders increased the odds of having CHD. Personality disorders may increase the risk of CHD in older adults. Putative mechanisms and directions for future research are proposed.
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PMID:DSM-IV personality disorders and coronary heart disease in older adults: results from The National Epidemiologic Survey on Alcohol And Related Conditions. 1790 71

Unlike depression, the relation between anxiety and the adherence to risk-reducing recommendations after myocardial infarction (MI) has not been well studied. The aim of this study was to explore the effect of anxiety on adherence after MI. Patients (n = 278) hospitalized for MI were assessed for anxiety using the Beck Anxiety Inventory during the hospitalization (baseline) and at 4 months of follow-up. The measures of adherence included following a low-sodium, low-fat diet, exercising regularly, taking medications, decreasing stress, carrying medical supplies, increasing socialization, following a diabetic diet, measuring blood glucose levels, and smoking cessation (where applicable). Baseline anxiety was associated with younger age, female gender, hypertension, tobacco use, depression, and current mood disorder. At 4 months of follow-up, anxiety was also associated with living alone, a history of coronary artery disease, and Killip class >1. An anxiety summary score was calculated to assess anxiety across both points. Summary anxiety was associated with worse adherence to exercise, reducing stress, increasing socialization, and smoking cessation but with better adherence to carrying supplies (all p <0.05). After controlling for demographic, cardiovascular, and psychological factors, summary anxiety predicted worse adherence to reducing stress (p = 0.004) and increasing socialization (p = 0.033) and was the only significant predictor of worse adherence to smoking cessation (p = 0.001) and better adherence to carrying supplies (p = 0.04). Anxiety during the initial hospitalization and 4 months later was associated with lower adherence to many important risk-reducing recommendations after MI. In conclusion, additional research is needed to evaluate whether treating anxiety can improve adherence in this setting.
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PMID:Relation of anxiety and adherence to risk-reducing recommendations following myocardial infarction. 1953 67

Recently, we encountered patients with catatonic schizophrenia who developed severe tachycardia, atrial fibrillation, and hypertension approximately 10 min after electroconvulsive therapy (ECT). Therefore, to examine whether delayed sympathetic hyperactivity occurs following ECT in patients with catatonic schizophrenia, we performed spectral analysis of heart rate variability (HRV). Nine patients with catatonic schizophrenia, 5 with noncatatonic schizophrenia, and 24 with mood disorders who received ECT consecutively were enrolled. The HRV frequency components were measured at baseline and during each 5-min time interval from the end of the ictal response to 35 min. The power spectrum of HRV was divided into 2 components: a high-frequency component (HF) and a low-frequency component (LF). The ratio of LF to HF (LF/HF) is an index of sympathetic activity. LF/HF demonstrated a transient increase between 5 and 10 min after ECT in the catatonic schizophrenia group compared to that in the mood disorder group. ECT in patients with catatonic schizophrenia is associated with delayed, transient sympathetic hyperactivity. These patients may be at an increased risk for developing tachycardia, atrial fibrillation, and hypertension following ECT.
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PMID:Delayed sympathetic hyperactivity following electroconvulsive therapy in patients with catatonic schizophrenia. 1956 46

Mood disturbances are characteristic and dominant feature of Mood disorders. Bipolar Affective Disorder (BAD) is a mood disorder which occurs equally in both sexes. BAD may occur in co morbidity with other mental diseases and disorders such as: Anorexia Nervosa, Bulimia Nervosa, Attention Deficit, Panic Disorder and Social Phobia. However, medical disorders (one or more) can also coexist with BAD. Metabolic syndrome is a combination of metabolic disorders that increase the risk of developing cardiovascular disease. A 61-year old female patient has been receiving continuous and systematic psychiatric treatment for Bipolar Affective Disorder for the last 39 years. The first episode was a depressive one and it occurred after a child delivery. Seventeen years ago the patient developed diabetes (diabetes type II), and twelve years ago arterial hypertension was diagnosed. High cholesterol and triglyceride levels as well as weight gain were objective findings. During the last nine years she has been treated for lower leg ulcer. Since metabolic syndrome includes abdominal obesity, hypertension, diabetes mellitus, increased cholesterol and serum triglyceride levels, the aforesaid patient can be diagnosed with Metabolic Syndrome. When treating Bipolar Affective Disorder, the antipsychotic drug choice should be careful and aware of its side-effects in order to avoid the development or aggravation of metabolic syndrome.
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PMID:Metabolic syndrome - the consequence of lifelong treatment of bipolar affective disorder. 2056 89

We evaluated the risks of preterm delivery and hypertensive disorders of pregnancy among pregnant women with mood and migraine disorders, using a cohort study of 3432 pregnant women. Maternal pre-pregnancy or early pregnancy (<20 weeks gestation) mood disorder and pre-pregnancy migraine diagnoses were ascertained from interview and medical record review. We fitted generalised linear models to derive risk ratios (RR) and 95% confidence intervals (CI) of preterm delivery and hypertensive disorders of pregnancy for women with isolated mood, isolated migraine and co-morbid mood-migraine disorders, respectively. Reported RR were adjusted for maternal age, race/ethnicity, marital status, parity, smoking status, chronic hypertension or pre-existing diabetes mellitus, and pre-pregnancy body mass index. Women without mood or migraine disorders were defined as the reference group. The risks for preterm delivery and hypertensive disorders of pregnancy were more consistently elevated among women with co-morbid mood-migraine disorders than among women with isolated mood or migraine disorder. Women with co-morbid disorders were almost twice as likely to deliver preterm (adjusted RR=1.87, 95% CI 1.05, 3.34) compared with the reference group. There was no clear evidence of increased risks of preterm delivery and its subtypes with isolated migraine disorder. Women with mood disorder had elevated risks of pre-eclampsia (adjusted RR=3.57, 95% CI 1.83, 6.99). Our results suggest an association between isolated migraine disorder and pregnancy-induced hypertension (adjusted RR=1.42, 95% CI 1.00, 2.01). This is the first study examining perinatal outcomes in women with co-morbid mood-migraine disorders. Pregnant women with a history of migraine may benefit from screening for depression during prenatal care and vigilant monitoring, especially for women with co-morbid mood and migraine disorders.
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PMID:Risk of preterm delivery and hypertensive disorders of pregnancy in relation to maternal co-morbid mood and migraine disorders during pregnancy. 2128 24

The aim of this study was to examine depression and anxiety disorders and their characteristic symptoms (anhedonia/low positive affect and anxious arousal, respectively), along with measures of state negative affect (NA) and Type D personality, in relation to cardiac surgery related morbidity. Patients awaiting elective coronary artery bypass graft surgery (n=158; 20.9% female; 11.4% concomitant valve surgery; age M=64.7, SD=10.6) underwent the structured MINI International Neuropsychiatric Interview to determine current affective disorders. Patients also completed the Mood and Anxiety Symptom Questionnaire and a measure of Type D personality traits. Postoperative cardiac morbidity was confirmed after surgery during the index hospitalization and included stroke,renal failure, ventilation>24 h, deep sternal wound infection, reoperation, arrhythmia and 30-day mortality at any location (n=59, 37.3% of total). After adjustment for age, recent myocardial infarction, heart failure, hypertension, urgency of surgery and time spent on cardiopulmonary bypass generalized anxiety disorder was associated with cardiac morbidity (odds ratio [OR]=3.26, 95% confidence interval [CI] 1.10-9.67, p=0.03). Adjusted analysis of personality traits revealed the NA component of Type D personality was associated with cardiac morbidity (OR=1.07, 95% CI 1.01-1.14, p=0.03). The Mood and Anxiety Symptom Questionnaire subscales were not associated with increased morbidity risk. Affective disorders, affective phenotypes, and personality traits were differentially associated with post-cardiac surgery morbidity outcomes independent of cardiac surgery morbidity risk factors. Concurrent investigation of depression and anxiety with respect to cardiac outcomes warrants further research.
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PMID:Cardiac morbidity risk and depression and anxiety: a disorder, symptom and trait analysis among cardiac surgery patients. 2149 41

Age-related neurodegeneration in the brain and retina is complicated. It comprises a series of events encompassing different modes of degeneration in neurons, as well as inflammation mediated by glial cells. Systemic inflammation and risk factors can contribute to disease progression. Age-related conditions such as Alzheimer's disease (AD), Parkinson's disease (PD) and Age-related Macular Degeneration (AMD) affect patients for 5 to 20 years and are highly associated with risk factors such as hyperhomocysteinaemia, hypercholesterolaemia, hypertension, and symptoms of mood disorder. The long duration of the degeneration and the wide array of systemic factors provide the opportunity for nutraceutical intervention to prevent or delay disease progression. Small molecules such as phenolic compounds are candidates for neuroprotection because they have anti-oxidant activities and can modulate intracellular signaling pathways. Bigger entities such as oligosaccharides and polysaccharides have often been neglected because of their complex structure. However, certain big molecules can provide neuroprotective effects. They may also have a wide spectrum of action against risk factors. In this review we use an integrative approach to the potential uses of nutraceutical products to prevent age-related neurodegeneration. These include direct effects of phenolic compounds and polysaccharides on neurons to antagonize various neurodegenerative mechanisms in AD, PD and AMD, and indirect effects of these compounds on peripheral disease-related risk factors.
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PMID:From small to big molecules: how do we prevent and delay the progression of age-related neurodegeneration? 2221 81

Remarkable proportions of individuals diagnosed with major depressive disorder (MDD) have comorbid metabolic disturbances (i.e., obesity, type 2 diabetes mellitus (T2DM), hypertension, dyslipidemia), and vice versa. Accumulating evidence suggests that common pathophysiologic pathways such as a chronic, low-grade, proinflammatory state mediate this frequent co-occurrence. However, it remains unclear what traits precede the onset and increase the risk for these pathologic states. The aim of our review was to evaluate the evidentiary base supporting the hypothesis that the increased hazard for metabolic disturbance in MDD subpopulations (and vice versa) is mediated in part by endophenotypic variations in sleep architecture. We conducted a PubMed search of all English-language literature with the following search terms: sleep disturbance, circadian rhythm, inflammation, metabolic syndrome, obesity, MDD, mood disorder, prodrome, T2DM, cytokine, interleukin, hypertension, dyslipidemia, and hypercholesterolemia. Longitudinal and meta-analysis data indicate that specific variations in sleep architecture (i.e., decreased slow-wave sleep [SWS], increased rapid eye movement [REM] density) precede the onset of depressive symptomatology for a subpopulation of individuals. The same sleep architecture variations also are associated with obesity, T2DM, and hypertension. Decreased SWS and increased REM density is correlated with an increase in proinflammatory cytokines (e.g., IL-6, tumor necrosis factor, etc.). This proinflammatory state has been independently shown to be associated with MDD and metabolic disturbances. Taken together, our review suggests that sleep architecture variation of increased REM density and decreased SWS may be an endophenotypic trait, which serves to identify a subpopulation at increased risk for depressive symptoms and metabolic disturbances. Future research is needed to discern the predictive value, sensitivity, and specificity of using sleep architecture variation as a biomarker for MDD and metabolic disturbances. Validation of this marker would have broad clinical implications, such as primary, secondary, and tertiary preventative health strategies.
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PMID:Sleep architecture variation: a mediator of metabolic disturbance in individuals with major depressive disorder. 2400 95

Background. Studies assessing the association between psychological factors and hypertension have been equivocal, which may reflect limitations in the assessment of psychological factors. Purpose. To assess the relationship between mood and anxiety disorders, measured using a psychiatric interview, and 1-year incident hypertension. Methods. 197 nonhypertensive individuals undergoing exercise stress testing at baseline provided follow-up data at 1 year. Baseline assessments included a structure psychiatric interview (PRIME-MD), physician diagnosis of hypertension, and measured blood pressure. At follow-up, hypertension status was assessed via self-reported physician diagnosis. Results. Having an anxiety disorder was associated with a 4-fold increase in the risk of developing hypertension (adjusted OR = 4.14, 95% CIs = 1.18-14.56). In contrast, having a mood disorder was not associated with incident hypertension (adjusted OR = 1.21, 95% CIs = 0.24-5.86). Conclusions. There are potential mechanisms which could explain our differential mood and anxiety findings. The impact of screening and treatment of anxiety disorders on hypertension needs to be explored.
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PMID:The impact of mood and anxiety disorders on incident hypertension at one year. 2467 13


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