Editorial
Mechanisms of interferon-alpha-induced depressive symptoms
- M. C. Wichers, M. Maes
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- 24 June 2014, pp. 103-105
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Research Article
Assessment of borderline personality disorder: considering a diagnostic strategy
- C. K. W. Schotte
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- 24 June 2014, pp. 55-59
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Background:
Borderline personality disorder (BPD) represents a highly prevalent, severe and difficult-to-treat mental health problem.
Objective:This paper considers methods, instruments and strategies for assessing BPD as described within the frame of the DSM-IV classification.
Conclusions:Following the general diagnostic approach introduced by Van Praag in biological psychiatry, a two-tier diagnostic strategy for the descriptive diagnostic assessment of BPD is recommended. Axis one results in a DSM-IV Axis II categorical diagnosis, whereas axis two refers to a symptomatological, dimensional or functional approach, in which the psychological dysfunctions of the nosological syndrome are depicted. Moreover, in a clinical context a basic aim of the diagnostic evaluation is to obtain therapeutically valid information that leads to a constructive conceptual framework, to a case formulation in which therapeutic interventions are understood, selected and implemented. This framework should be based on a biopsychosocial theoretical model and its application in the clinical context involves feedback to the patient, in which the descriptive evaluation is integrated with etiological; and pathogenic elements using an idiographic approach. This therapeutically orientated diagnostic strategy is illustrated by the use of the ADP-IV (Assessment of DSM-IV personality disorders) questionnaire within a cognitive behavioral orientation.
Review Article
Stress, immunity, cytokines and depression
- Hymie Anisman
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- 24 June 2014, pp. 251-261
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The current issue of Acta Neuropsychiatrica presents a series of papers which together provide a broad overview relating stress, immunity, cytokine activity and depressive illness, as well as the influence of cytokines on other neurological disorders. This introduction to the issue presents a broad perspective of the impact of stressors on immune functioning in animal studies and in humans, considering the potential effects of acute, subchronic and chronic stressors, as well as the contribution of previous stressor experience in promoting neurochemical and immunological alterations. Given the supposition that cytokines may act as immunotransmitters, and immune challenge may be viewed as a stressor, a brief review is provided concerning the impact of stressors and cytokine challenges on central neurochemical functioning, with particular emphasis on the commonalties between the effects of these treatments. It is suggested that by virtue of the neurochemical changes imparted by cytokines, a depressive affect may be instigated, just as it is in response to psychogenic stressors. To this end, an overview is presented concerning the relationship between cytokines and depression, as well as the influence of cytokine treatments on behavioral changes in animal studies and among patients receiving immunotherapy. Provisionally, the data support the view that activation of the inflammatory response system may contribute to affective illness, and that cytokines may act as signaling molecules to activate central nervous system processes regulating mood states.
Original Article
Lack of effect of eicosapentaenoic acid in the Porsolt forced swimming test model of depression
- Alona Shaldubina, Boris Nemets, Yuly Bersudsky
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- 24 June 2014, pp. 203-206
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Background:
Eicosapentaenoic acid (EPA) is one of the major components of fish oils. Omega-3 fatty acids, particularly EPA, have been hypothesized to play a role in the etiology, pathogenesis and treatment of mood disorders. Clinical studies have shown beneficial effects of omega-3 fatty acids in major depression, bipolar disorder and other psychiatric disorders.
Objective:The present study design evaluates the effect of EPA in the Porsolt forced swimming test.
Results:EPA alone did not reduce the immobility time and did not enhance the anti-immobility effect of a low dose of imipramine. Contrary to the hypothesis, EPA slightly increased the immobility time, and in some experiments tended to reduce the anti-despair effect of imipramine.
Conclusion:The present results do not provide an animal model for the antidepressant effect of EPA as demonstrated in clinical experiments. The mechanism of EPA antidepressant action is unknown and the Porsolt forced swimming test could be non-sensitive for its antidepressant properties.
Review Article and Hypothesis
Considering depression as a consequence of activation of the inflammatory response system
- J. Korf, H. C. Klein, J. Versijpt, J. A. den Boer, G. J. ter Horst
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- 24 June 2014, pp. 1-10
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This paper summarizes the possible interrelation between peripheral and/or cerebral inflammation and depression. Often, depression is regarded as a consequence of life events, including disabling diseases. The question addressed here is whether activation of the inflammatory response system (IRS) can cause depression. Epidemiological studies suggest that depression can be precipitated by bacterial or viral infections. In depressed patients, peripheral markers of the IRS are often increased. There is some evidence that some forms of depression are caused by a viral infection of the limbic system. More consistent are the observations that depression in diseases with active cerebral inflammatory processes (e.g. multiple sclerosis, Alzheimer's disease) may concur. Direct evidence of a relation between depression and inflammation was found in post-mortem brain material of patients with a vascular depression. In both inflammatory brain diseases and in depression, a state-dependent increased hypothalamus–pituitary–adrenal axis activity is seen. Animals studies have shown that intact cerebral serotonin systems are required for the activation of the IRS following an endotoxin challenge and that long-term treatment with antidepressants may change such a response. Gender differences between the prevalence of depression and inflammatory diseases are similar, as more females are affected. We hypothesize that cerebral or peripheral activation of the IRS may contribute to the course of some antidepressant treatment-resistant depressions. Clinical trials combining antidepressants and drugs that reduce the activation of the IRS may provide evidence for such proposed depression subtypes.
Original Article
Stress in the brain: implications for treatment of depression
- Er de Kloet
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- 11 July 2016, pp. 155-166
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A fundamental question in stress research is when the glucocorticoid stress hormone (cortisol in man) stops being neuroprotective and becomes harmful to the brain with negative consequences for cognition and mood. To address this question Section 1 focuses on the action mechanism of glucocorticoids. These hormones act via high and low affinity nuclear receptors, which regulate gene transcription in a coordinate manner. The receptors are expressed abundantly in hippocampus, amygdala and frontal cortex involved in cognitive processes. In Section 2 hypercortisolism is considered a potential disease factor for about 50% of the patients suffering from major depression. Recent data show that these patients recover within a few days when excess cortisol action is blocked with high doses of an antiglucocorticoid. Section 3 concerns animal models with ‘depression-like’ features of hypercorticism generated by manipulation of gene X environment inputs. Using gene expression profiling technology in the hippocampal transcriptome of these animals we identified about 700 potential targets for antidepressants out of 30 000 detectable gene products. One of our models is based on early life programming of the stress system. Rats exposed as pups to maternal deprivation display at senescence an enhanced individual difference in cognitive performance. The maternally deprived senescent animals age either successfully or become senile, at the expense of the average performance of non-deprived controls. The essay is concluded with the notion that the new generation of antidepressants ameliorates specific psychic dysfunctions (e.g. cognitive performance) linked to aberrant stress hormone action in discrete brain regions.
Which depressions are related to life stress?
- E. S. Paykel
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- 24 June 2014, pp. 167-172
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This paper examines the relationship of recent life events to specific kinds of depression using published studies and the author's own work. An overall effect of life events on depression has been found consistently and is moderate in degree. In suicide attempts there are stronger and more immediate effects than in depression. Life events precede both non-melancholic and melancholic depressions. It is only in recurrent depressions that life events are less common with melancholic pictures. Life events influence bipolar disorder as well as unipolar. Mania may be preceded by life events, particularly those involving social rhythm disruption, but it is harder to rule out events which are consequences of insidious development of illness. There are strong effects of life events and social support in postpartum depressions but in postpartum psychoses these effects are absent. Events precede depression comorbid with other disorders as well as pure depression. The course of depression is also influenced by life stress with less remission where negative events occur after onset and better outcome where earlier adverse events are neutralized. Relapse is related to immediately preceding life events. However, where depressions are both severe and recurrent life stress effects weaken and as the number of episodes increases preceding life events lessen. These findings suggest that some kinds of depression are more related to psychosocial causation and some are more biological in origin.
Research Article
Event-related potentials and white matter lesions in bipolar disorder
- E. F. P. M. Vuurman, A. Honig, T. H. Lamers, J. Wiersma, L. Krabbendam, P. A. M. Hofman, W. A. Nolen, J. Jolles
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- 24 June 2014, pp. 11-16
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Objectives:
To investigate neurophysiological parameters which possibly distinguish subtypes I and II of patients with a bipolar disorder, and contrast the findings with observations from a group of schizophrenic patients and a group of healthy controls.
Methods:Sixty-six volunteers underwent a MRI scan to determine the number and location of white matter lesions (WSL). A electrophysiological registration was made while all volunteers performed a auditory ‘oddball’ task, and the amplitude of the resulting P300 wave was compared.
Results:Earlier reports of higher numbers of WSL in bipolar disorder were not replicated in this study. Subtypes I and II showed a different P300 amplitude and subtype I resembled the results of the schizophrenia group.
Conclusion:Bipolar patients in remission have a functional brain disorder that is expressed by a change in physiological response to external stimuli.
Psychobiology and treatment of borderline personality disorder
- C. Robert Cloninger
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- 24 June 2014, pp. 60-65
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Borderline personality disorder can be characterized in terms of a profile of abnormal deviations on multiple personality dimensions using the temperament and character inventory (TCI). Borderline patients show poor character development, including low TCI self-directedness (irresponsible, blaming) and low TCI cooperativeness (hostile, intolerant). Their temperament is explosive or unstable due to a combination of high TCI harm avoidance (anxious, shy), high TCI novelty seeking (impulsive, quick-tempered), and low reward dependence (cold, aloof). Consequently they are usually dysthymic with an admixture of anxiety and anger, and regulate their social problems and intense emotions in immature ways. Genetic and psychobiological studies have led to identification of biological correlates of each of the TCI dimensions of personality, including individual differences in regional brain activity, psychophysiological variables, neuroendocrine abnormalities and specific gene polymorphisms. Each dimension of personality involves complex non-linear interaction of multiple genetic and environmental factors and, in turn, each personality dimension interacts with the others in influencing the way an individual directs and adapts to his or her life experiences. Systematic clinical trials have shown that these personality variables predict the response to pharmacological and psychotherapeutic treatments. For example, high harm avoidance and low self-directedness predict slower response and more rapid relapse with both antidepressants and cognitive-behavioral therapy. Treatment with drugs and/or psychotherapy can be individually matched to the patient's profile of temperament and character traits, rather than treating a heterogeneous group of patients as if they had a discrete, homogeneous illness. Fundamental change in cognitive schemas depends on attention to all aspects of character, especially self-transcendence, which has previously been neglected in cognitive-behavioral therapy. Personality integration requires non-resistance to our natural intuitive awareness, rather than intensified intellectual and emotional defenses.
Original Article
Low IQ scores in schizophrenia: primary or secondary deficit?
- M. van Beilen, F. Withaar, A. H. van Zomeren, R. van den Bosch
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- 24 June 2014, pp. 106-110
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Background:
Schizophrenia is consistently associated with lower IQ compared to the IQ of control groups, or estimated premorbid IQ. It is not likely that the IQ scores deteriorate during the prodromal phase or first psychotic episode; they are already present before the onset of the prodromal phase and have been detected in childhood.
Methods:We investigated cognitive functioning and IQ levels in a group of 36 patients with schizophrenia or other psychotic disorders.
Results:The IQ scores in our sample were lower than average. The IQ showed a relation with attention, memory, speed of information processing and some aspects of executive functioning. However, when IQ scores were corrected for processing speed, they were no longer below average.
Conclusions:These findings are important in considering the value of intelligence levels in schizophrenia. IQ scores should be judged in combination with cognitive functioning and school career to assess a patients capabilities in society. Cognitive functions and other variables might have a considerable influence on IQ scores. This rises the question of whether the low IQ scores are a primary or secondary deficit. Schizophrenia patients may have normal IQs, but could be less capable of making an IQ-test.
Influence of cognitive reserve on neuropsychological functioning in Parkinson's disease
- Juan L Sánchez, Marina Rodríguez, Juan Carro
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- 24 June 2014, pp. 207-215
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Background:
In recent years, attention has been drawn to the association between a low level of education and dementia, an almost generalized finding in the majority of studies on the prevalence of dementia where the level of education of the population was highly diversified. The protective effect of education is not limited to Alzheimer's disease but is also seen in other types of dementia, Parkinson's disease (PD), and even in the cognitive deterioration linked to aging
Objective:To evaluate neuropsychological performance in (PD) subjects and to evaluate the influence of cognitive reserve (RC) on their neuropsychological performance.
Subjects:An extensive neuropsychological battery of tests was applied to a total of 79 subjects, 33 of whom were diagnosed with PD.
Measures:RC scores were based on a combination of years of education, a measure of occupational attainment, and an estimate of premorbid intelligence.
Results:As regards the specific disturbances found in the clinical group subjects, a lower performance in memory, attention, visuospatial, visuoconstructive, and perceptive skills was seen. With respect to our second objective, our results showed that patients diagnosed with PD who had a high RC reached a higher neuropsychological level of performance than those subjects with a low reserve.
Conclusions:Early neuropsychological impairments in PD are most evident in individuals with lower RC. As has been found in other neurological disorders, individuals with greater RC may be less sensitive to the initial clinical effects of the underlying neuropathological process.
Review Article
Brain cytokines and disease
- Carlos R Plata-Salaman
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- 24 June 2014, pp. 262-278
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Cytokines (e.g. various interleukins and subfamily members, tumor necrosis factors, interferons, chemokines and growth factors) act in the brain as immunoregulators and neuromodulators. Over a decade ago, the integrative article ‘Immunoregulators in the Nervous System’ (Neurosci Biobehav Rev 1991; 15: 185–215) provided a comprehensive framework of pivotal issues on cytokines and the nervous system that recently have been extensively studied. Cytokine profiles in the brain, including cytokine generation and action, have been studied in multiple models associated with neuropathophysiological conditions. These include: (1) acute conditions and disorders such as stroke (cerebral ischemia or infarction and intracranial hemorrhage), traumatic brain injury, spinal cord injury and acute neuropathies; (2) chronic neurodegenerative disorders and chronic conditions, including Alzheimer's disease, Parkinson's disease, neuropathic pain, epilepsy and chronic neuropathies; (3) brain infections, including bacterial meningitis and encephalitis; (4) brain tumors; (5) neuroimmunological disorders per se, such as multiple sclerosis; (5) psychiatric disorders, including schizophrenia and depression; (6) neurological and neuropsychiatric manifestations associated with non- central nervous system (CNS) disorders such as peripheral cancer, liver, kidney and metabolic compromise, and peripheral infectious and inflammatory conditions; and (7) cytokine immunotherapy, which can be accompanied by neuropsychiatric manifestations when administered either via peripheral or brain routes. Cytokine profiles have also been studied in multiple animal models challenged with inflammatory, infectious, chemical, malignant and stressor insults. Essentially data show that cytokines play a pivotal role in multiple neuropathophysiological processes associated with different types of disorders and insults. Cytokine expression and action in the brain shows a different profile across conditions, but some similarities exist. Under a defined temporal sequence, cytokine involvement in neuroprotection or the induction of a deleterious pathophysiological cascade and in resolution/healing is proposed depending on the type of cytokine. In the brain, functional interactions among cytokines, balance between pro-inflammatory and anti-inflammatory cytokines and functional interactions with neurotransmitters and neuropeptides play a pivotal role in the overall cytokine profile, pattern of neuropathophysiological cascades, and quality and magnitude of neuropsychiatric manifestations. In this brief review various selected cytokine-related issues with relevance to the brain are discussed.
Stressor-induced modulation of immune function: a review of acute, chronic effects in animals
- Alexander W. Kusnecov, Alba Rossi-George
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- 24 June 2014, pp. 279-291
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The present paper reviews recent studies on the effects of stress on immune function in laboratory animals. The emphasis is on those studies where a simultaneous comparison of acute and chronic stress regimens was determined, although additional relevant studies are also reviewed. The effects of stress on basic measurements of cellular and humoral immune measures are discussed, including the growing number of studies that have reported alterations in macrophage functions. The latter are key elements in the innate immune response, and like measurements of T cell function and antibody production, are inhibited and enhanced by stressor exposure. This review does not focus on the mechanisms by which stress alters immune function, there being little to add conceptually in terms of what was reported previously (see Kusnecov AW, Rabin BS, Int Arch Allergy Immunol 1994;105:107–121.). However, a question is raised in the conclusion as to how stressor effects on immune function should be interpreted, for it is clear that immunological processes in and of themselves elicit central nervous system responses that neurochemically and endocrinologically do not differ from those produced in response to psychological stressors. Therefore, at least in the short term stressor-induced immune changes may not necessarily reflect maladaptive adjustments, although, as demonstrated by some studies reviewed in this paper, they may pose a serious risk to health should stressor exposure be persistent and uncontrolled.
Original Article
Stress, norepinephrine and depression
- Brian E. Leonard
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- 24 June 2014, pp. 173-180
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Experimental and clinical evidence implicates stress as a major predisposing factor in depression and other severe psychiatric disorders. In this review, evidence is presented to show how the impact of stress on the central sympathetic system leads to changes in the endocrine, immune and neurotransmitter axes which underlie the main clinical symptoms of depression. Thus it can be shown that the noradrenergic system is dysfunctional in depression, a situation which reflects the chronic hypersecretion of glucocorticoids and inflammatory mediators within the brain in addition to an enhanced activity of the locus ceruleus. With regard to the actions of antidepressants in modulating the stress response and alleviating depression it is now evident that, irrespective of the presumed specificity of the antidepressants for the noradrenergic or serotonergic systems, they all normalize noradrenergic function. This action is due partly to the regulation of tyrosine hydroxylase activity in the locus ceruleus but also enhances neuronal sprouting which counteracts the neurodegenerative effects of chronic stress.
Research Article
Seasonal variation and meteotropism in suicide: clinical relevance of findings and implications for research
- A. Preti
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- 24 June 2014, pp. 17-28
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Seasonal asymmetry in yearly suicide occurrence is a long-observed phenomenon in psychiatric, suicidological and sociological research, and the effects of seasonal factors on suicidal behaviour have been the focus of a number of earlier studies. Taking into account limitations of data and methods, these studies have in general favoured interpretations based on psychosocial factors. Recent studies have challenged the widely held notion that seasonal effects on suicide are not influenced by age, gender or the circumstances of the act. The suicides committed with violent methods have been shown to follow clearer seasonal patterns than suicides by less violent methods, and differences have been found between male and female cycles of occurrence. The seasonal occurrence of suicides has also been found to differ significantly between the young and the elderly. The use of inappropriate statistics or age- and gender-biased samples may have hidden a seasonal component in some previous studies on attempted suicide. The absence of seasonality in earlier studies on attempted suicide was interpreted as depending upon the minor relevance of psychiatric and biological factors in non-fatal self-harm. However, recent studies have reported clear seasonality in attempted suicide samples, with older people showing greater seasonal effect. Recent literature after 1985 on seasonal variation and weather or climate influence in attempted and completed suicide is reviewed. Suggestions for research and the development of more effective preventative strategies are offered.
Serotonin, personality and borderline personality disorder
- M. Hansenne, W. Pitchot, M. Ansseau
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- 24 June 2014, pp. 66-70
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Serotonin is one of the neurotransmitters implicated in normal personality. Many psychobiological models of personality include some dimensions related to serotonin. For instance, the harm avoidance dimension of the biosocial model developed by Cloninger is related to serotonergic activity. Higher scores on the harm avoidance dimension should theoretically reflect increased serotonergic activity. However, correlation studies related serotonin activity to harm avoidance dimension have not yielded consistent findings. These controversial results are probably related to the complexity of the neurotransmitter systems, and the different assessment techniques used in these studies. Finally, recent genetic studies have examined the association between personality dimensions and serotonergic receptor polymorphisms with mixed results. Serotonin is not only related to some dimensions of normal personality. Several psychopathological disorders are associated with serotonergic dysfunction. More particularly, borderline personality disorder (BPD) can be defined by many of the symptoms associated with serotonergic dysregulation, including affective lability, suicidal behaviours, impulsivity and loss of impulse control. Indeed, several reports have demonstrated the efficacy of selective serotonin re-uptake drugs in treating the depressive and impulsive symptoms of patients with BPD. Moreover, some challenge studies have reported a lower serotonergic activity in BPD. Because these challenges are not specific, we have assessed the serotonergic activity in BPD with the flesinoxan challenge. Preliminary results showed that the prolactine responses to flesinoxan were significantly lower in BPD patients compared to those observed in controls.
Original Article
No allelic association between harm avoidance and the debrisoquine 4-hydroxylase gene
- Adriaan H Veefkind, Theo J M Ingenhoven, Izaäk W De Groot
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- 24 June 2014, pp. 216-218
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Background:
Several reports suggest that variance in personality traits is inherited, but little is known about the genes responsible. It has been suggested that there is a relationship between personality characteristics and the gene responsible for the activity of the enzyme debrisoquine 4-hydroxylase (CYP2D6).
Objective:To examine the proportion of poor metabolizers in a group of personality disordered patients.
Methods:Blood samples were obtained from 23 patients with a high or very high score on the dimension ‘harm avoidance’ of the Temperament and Character Inventory (TCI). The samples were genotyped for the null alleles CYP2D6*3 and*4 by performing an allele-specific polymerase chain reaction.
Results:The frequencies of genotypes in the sample were very similar to the frequencies found in a general white population.
Conclusions:The investigation produced no support for the idea that the CYP2D6 gene is related to personality by means of variations in the temperament dimension of harm avoidance.
Catatonia: the rise and fall of an intriguing psychopathological dimension
- F. M. M. A. van der Heijden, S. Tuinier, L. Pepplinkhuizen, W. M. A. Verhoeven
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- 24 June 2014, pp. 111-116
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Background:
For at least 125 years the discussion about the clinical relevance of catatonic symptoms in psychiatry continues. It started from the original description by Kahlbaum and was revived by modern factor analytical studies, that identified the catatonic dimension in about 10% of newly admitted patients.
Objective:Over a period of 2 years, four patients with an acute episodic psychosis and prominent catatonic symptoms were examined.
Methods:A clinical description is given of the psychopathology and classification is performed according to the various diagnostic instruments.
Results:All patients showed a circular fluctuation of their psychoses, with motor symptoms ranging from the excited to the inhibited pole within one episode. Their clinical pictures also comprised mood swings and anxieties as well as hallucinatory and delusional experiences, whereas the course of disease was characterized by complete recovery without residual symptoms.
Conclusions:The significance of catatonic symptoms is not recognized in the current taxonomies despite the fact that this has major pharmacological treatment implications.
Post-stroke quality of life and depression
- Krystyna Jaracz, Jan Jaracz, Wojciech Kozubski, Janusz K Rybakowski
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- 24 June 2014, pp. 219-225
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Background:
Studies on the determinants of the quality of life (QOL) after stroke bring differing results depending on the applied concept of QOL. This may lead to confusion about the contribution of various factors to the post-stroke QOL.
Objective:The aim of the study was: (i) to investigate functional and psychological QOL in the individuals after the first ischemic stroke; (ii) to identify the most important correlates of QOL; and (iii) to examine the significance of depression among the other possible predictors of QOL.
Methods:A hospital-based sample of 72 stroke patients was followed up to 6 months after stroke onset. QOL was assessed using the Polish version of the Quality of Life Index and the Sickness Impact Profile. A multiple regression procedure was performed to examine relationships between QOL and the study variables.
Results:In spite of good recovery, the psychological and functional QOL of the examined patients was impaired, although the negative impact of stroke was greater on the objective QOL than on the subjective QOL. Stroke-related impairment, depression, functional disability and marital status predicted 80% of the variance in the functional QOL. Emotional support, depression and functional disability explained 38% of the variance in psychological well-being.
Conclusions:Depression and physical disability were the most important predictors of QOL after stroke since their impact on QOL was more robust in comparison to the remaining variables. For improving QOL, a comprehensive care for patients aimed at reducing physical dependence and ameliorating depressive symptoms could be recommended.
Review Article
Early life environment: does it have implications for predisposition to disease?
- Nola Shanks
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- 24 June 2014, pp. 292-302
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Early life environmental factors have been associated with altered predisposition to a variety of pathologies. A considerable literature examines pre- and postnatal factors associated with increased risk of cardiovascular, metabolic (i.e. insulin resistance, hyperlipidemia) and psychiatric disease, and the importance of hormonal programming. The brain is exquisitely sensitive to environmental inputs during development and the stress responsiveness of the hypothalamic–pituitary–adrenal (HPA) axis has been shown to be both up- and down-regulated by early life exposure to limited nutrition, stress, altered maternal behaviors, synthetic steroids and inflammation. It has been suggested that peri-natal programming of HPA axis regulation might therefore contribute to metabolic and psychiatric disease etiology. In addition, glucocorticoids play modulatory roles regulating many aspects of immune function, notably controlling both acute and chronic inflammatory responses. Neuroendocrine–immune communication is bidirectional, and therefore it is expected that environmental factors altering HPA regulation have implications for stress effects on immune function and predisposition to inflammation. The impact of pre- and postnatal factors altering immune function, stress responsivity and predisposition to inflammatory disease are reviewed. It is also examined whether the early ‘immune environment’ might similarly influence predisposition to disease and alter neuroendocrine function. Evidence indicating a role for early life inflammation and infection as an important factor programming the neuroendocrine–immune axis and altering predisposition to disease is considered.