Burnout in nursing staff: is there a relationship between depression and burnout?

OBJECTIVE: There is evidence that burnout may be a clinical entity with pathological stress reaction features related to the inability in finding pleasure from work. The purpose of this study was to investigate the relationship between burnout and depression. METHODS: The study took place in the general hospital AHEPA of Thessaloniki. All members of the nursing staff (in total 368 subjects) took part. The protocol was self-reported and anonymous, in order to obtain as valid data as possible and included the Maslach Burnout Inventory (MBI) to assess the level of burnout, the Eysenck Personality Questionnaire (EPQ) to assess personality traits, and the Zung Self-Rating Depression Scale to assess depressive symptomatology. RESULTS: The analysis revealed a weak but significant relationship between burnout and depression. CONCLUSIONS: Depression is a pervasive disorder that affects almost every aspect of the patient's life. On the contrary, burnout is, by definition, a syndrome restricted to the patient's professional environment. However, it seems that there may be two distinct types of burnout syndromes, of which the one comprising the majority of nurses has little or no common features with depression. The second type consists of individuals with a predisposition to develop burnout. The latter is characterized by more severe symptomatology, phenotypic similarity to depression and presumably common etiological mechanisms.     

Epilepsy and autism: is there a special relationship?

Increasingly, there has been an interest in the association between epilepsy and autism. The high frequency of autism in some of the early-onset developmental encephalopathic epilepsies is frequently cited as evidence of the relationship between autism and epilepsy. While these specific forms of epilepsy carry a higher-than-expected risk of autism, most, if not all, of the association may be due to intellectual disability (ID). The high prevalence of interictal EEG discharges in children with autism is also cited as further evidence although errors in the diagnosis of epilepsy seem to account for at least part of those findings. The prevalence of ID is substantially elevated in children with either epilepsy or autism. In the absence of ID, there is little evidence of a substantial, if any, increased risk of autism in children with epilepsy. Further, although the reported prevalence of autism has increased over the last several years, much of this increase may be attributable to changes in diagnostic practices, conceptualization of autism in the presence of ID, and laws requiring provision of services for children with autism. In the context of these temporal trends, any further efforts to tease apart the relationships between epilepsy, ID, and autism will have to address head-on the accuracy of diagnosis of all three conditions before we can determine whether there is, indeed, a special relationship between autism and epilepsy.     

Worry and anxiety: is there a causal relationship?

The aim of this study was to examine the relationship between worry and anxiety and depression. Path analysis was used to estimate a nonrecursive model which describes the reciprocal causal relation between worry and anxiety. The final model fits the data well and leads to the conclusion that the association between these two constructs is not bidirectional. Indeed, we observed a significant positive effect of worry on anxiety, but no effect in the opposite direction. This result provides a supporting argument for researchers wishing to distinguish these two constructs. Moreover, depression is not directly affected by worry, but is indirectly affected through anxiety.     

Is there a relationship between depression and crying? A review

OBJECTIVE: To conduct a systematic examination of the relationship between depression and crying by reviewing all relevant theory and empirical data including the performance of crying items in measures of depression. METHOD: Review of the extant literature on depression and crying using PubMed, PsychInfo and Google Scholar databases. RESULTS: Scores on crying items of depression inventories correlate moderately with overall depression severity. Otherwise, there is surprisingly little evidence for the widespread claim that depression leads to more frequent and/or easier crying. There is also little empirical support for the competing claim that severely depressed individuals lose their capacity to cry. CONCLUSION: Current claims about the relationship between depression and crying lack a robust empirical foundation. Assessment instruments and diagnostic systems for mood disorders are inconsistent in how they handle crying as a symptom. Further work to investigate the causes and the context of crying in depressed patients is needed.     

Mental disorder and violence: is there a relationship beyond substance use?

Purpose  

A general consensus exists that severe mental illness (SMI) increases violence risk. However, a recent report claimed that SMI “alone was not statistically related to future violence in bivariate or multivariate analyses.” We reanalyze the data used to make this claim with a focus on causal relationships between SMI and violence, rather than the statistical prediction of violence.     

High altitudes,anxiety, and panic attacks: is there a relationship?

People exposed to high altitudes often experience somatic symptoms triggered by hypoxia, such as breathlessness, palpitations, dizziness, headache, and insomnia. Most of the symptoms are identical to those reported in panic attacks or severe anxiety. Potential causal links between adaptation to altitude and anxiety are apparent in all three leading models of panic, namely, hyperventilation (hypoxia leads to hypocapnia), suffocation false alarms (hypoxia counteracted to some extent by hypocapnia), and cognitive misinterpretations (symptoms from hypoxia and hypocapnia interpreted as dangerous). Furthermore, exposure to high altitudes produces respiratory disturbances during sleep in normals similar to those in panic disorder at low altitudes. In spite of these connections and their clinical importance, evidence for precipitation of panic attacks or more gradual increases in anxiety during altitude exposure is meager. We suggest some improvements that could be made in the design of future studies, possible tests of some of the theoretical causal links, and possible treatment applications, such as systematic exposure of panic patients to high altitude.     

Motor/vocal tics and compulsive behaviors on stimulant drugs: is there a common vulnerability?

The occurrence of abnormal movements or perserverative/compulsive behaviors was noted in 34 (76%) of a group of 45 hyperactive boys during a double-blind crossover treatment trial of methylphenidate and dextroamphetamine given in a wide range of doses. These adverse effects were often subtle and transient, and they usually occurred only on one drug. There was only one case where treatment was discontinued due to the severity of the tic the subject developed during his initial treatment phase. Dextroamphetamine tended to produce more compulsive behaviors, which were also more likely to resemble clinical obsessive-compulsive disorder (OCD), than did methylphenidate. Abnormal movements and compulsive behaviors tended to co-occur on methylphenidate only; no general "Tourette-OCD diathesis" was found for this population.     

The pharmacologic treatment of depression: is gender a critical factor?

BACKGROUND: In the medical literature, there is a lack of sex-specific information regarding the efficacy, metabolism, and side effects associated with psychopharmacologic treatment. In part, this lack results from the historic underinclusion of women in clinical trials during early drug development, but it also occurs because investigators of treatment and metabolic studies do not routinely analyze results according to sex. In 1993, the U.S. Food and Drug Administration (FDA) announced changes that encourage the inclusion of women in early pharmacokinetic studies and emphasize the need for subset analyses using sex and age parameters. In conjunction with advances in basic science regarding drug metabolism, these modifications have led to modest increases in information regarding sex differences in drug metabolism and efficacy. In this article, current information regarding potential sex differences in the pharmacotherapy of major depressive disorder is reviewed. DATA SOURCES: A MEDLINE search was conducted using the terms antidepressants, sex-factors, gender differences, and women for the years 1966 to 2000. DATA SYNTHESIS AND CONCLUSIONS: There are data supporting sex differences in the activity of various antidepressant-metabolizing enzymes. However, there is a paucity of investigation regarding how these differences might translate into differences in clinical efficacy. Notably, there is little work using existing databases to perform the subgroup analyses recommended by the FDA. The widespread dissemination of such work is needed, and, if conducted, investigations in this area have the potential to enhance psychopharmacologic treatment for both men and women.     

Hippocampal LTP and memory in mouse strains: is there evidence for a causal relationship?

The mechanisms underlying memory are under intense investigation. One of the most promising candidates at the cellular level is long-term potentiation (LTP). Numerous pharmacological and molecular genetic manipulations have led to alteration in both LTP and memory. However, the causal relationship between these phenotypical changes is debated. The problem of causality can be addressed in numerous ways. One suggestion is to investigate natural variation in both LTP and memory performance in mouse strains. If variation in synaptic and behavioral phenomena is found, correlation between these traits may be investigated. The advantages and disadvantages of this approach are discussed. An empirical example using four mouse strains is also presented to highlight some general problems. The following arguments are made. First, multiple electrophysiological and behavioral paradigms with idiosyncratic condition characteristics should be conducted to avoid false-positive findings due to alterations unrelated to memory and its mechanisms. Multiple stimulation and memory protocols may also allow one to study the complexity and multiplicity of processes. Second, analysis of a large number of mouse strains may be needed to avoid false interpretation of results due to spurious gene associations and/or linkage disequilibrium. Third, quantitative genetic analysis using, for example, diallele crosses, may be employed to properly investigate biologically meaningful, i.e., genetic, effects. It is concluded that with the use of additional methods (e.g., QTL analysis, gene expression arrays, and biochemical analysis) providing converging evidence, analysis of mouse strains will be instrumental in addressing the question regarding the role LTP may play in memory.     

Inflammation and depression: Is there a causal connection with dementia?

Epidemiological studies show that there is a correlation between chronic depression and the likelihood of dementia in later life. There is evidence that inflammatory changes in the brain are pathological features of both depression and dementia. This suggests that an increase in inflammation-induced apoptosis, together with a reduction in the synthesis of neurotrophic factors caused by a rise in brain glucocorticoids, may play a role in the pathology of these disorders. A reduction in the neuroprotective components of the kynurenine pathway, such as kynurenic acid, and an increase in the neurodegenerative components, 3- hydroxykynurenine and quinolinic acid, contribute to the pathological changes. Such changes are postulated to cause neuronal damage and thereby predispose chronically depressed patients to dementia.     

Obsessive-compulsive disorder and serotonin: is there a connection?

Reports of the antiobsessional efficacy of clomipramine have led to a "serotonin hypothesis" of obsessive-compulsive disorder (OCD). To test this hypothesis, 16 outpatients with DSM-III OCD were studied using several measures of serotonergic function. Platelet 3H-imipramine binding and serotonin uptake were not significantly different between the OCD patients and a normal, age-matched control group. The level of the metabolite 5-hydroxyindoleacetic acid (5-HIAA) in cerebrospinal fluid (CSF) was significantly higher in a small cohort of obsessionals compared with healthy volunteers, possibly reflecting increased brain serotonin turnover. In a direct test of the role of serotonin uptake in clomipramine's antiobsessional effects, the serotonin uptake inhibitor zimelidine was compared with the noradrenergic uptake inhibitor desipramine in a double-blind, controlled study. Zimelidine reduced CSF 5-HIAA, but was clinically ineffective in this group. Desipramine had weak but significant clinical effects. Nonresponders to zimelidine or desipramine improved significantly during a subsequent double blind trial of clomipramine. These findings demonstrate that pharmacological blockade of serotonin reuptake alone is not sufficient for an antiobsessional response.     

Cholesterol and Alzheimer's disease: is there a link?

The Abeta-amyloid peptide (Abeta), the main component of amyloid plaques, is derived by proteolytic cleavage from the amyloid precursor protein (APP). Epidemiologic and biochemical data suggest a link between cholesterol, APP processing, Abeta, and Alzheimer's disease. Two recent epidemiologic studies indicate that there is a decreased prevalence of AD associated with the use of cholesterol-lowering drugs that inhibit 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMG-CoA reductase inhibitors or statins). Experiments in cell culture and in vivo demonstrate that treatment with statins reduces production of Abeta. The authors discuss how cholesterol might modulate Abeta deposit formation. As neurons receive only small amounts of exogenous cholesterol, statins that efficiently cross the blood-brain barrier may reduce the amount of neuronal cholesterol below a critical level. Decreased neuronal cholesterol levels inhibit the Abeta-forming amyloidogenic pathway possibly by removing APP from cholesterol- and sphingolipid-enriched membrane microdomains. In addition, depletion of cellular cholesterol levels reduces the ability of Abeta to act as a seed for further fibril formation. These intriguing relationships raise the hopes that cholesterol-lowering strategies may influence the progression of AD.