98 research outputs found
ACUTE AND LONG-TERM MENTAL AND PHYSICAL SEQUELAE IN THE AFTERMATH OF TRAUMATIC EXPOSURE – SOME REMARKS ON “THE BODY KEEPS THE SCORE”
Traumata, by definition, refer to exterior events that expose a person to experiences of overwhelming threat and catastrophe and elicit feelings of death anxiety, panic, horror, helplessness, loss of personal control, and intractability. Most affected persons respond with at least some distressing symptoms of trauma-related memory intrusions, autonomic hyperarousal, dissociation, and depression in the acute aftermath. Fortunately, the majority of traumatized individuals succeed in coping with this major stress quite well during the following weeks and months unless the process of recovery is hampered by additional adverse psychosocial circumstances, psychological disposition or biological vulnerability. In a subgroup of persons a transition to acute and posttraumatic stress disorder or other major psychiatric disorders, e.g. depressive, anxiety, substance-related disorders may be observed. Posttraumatic stress disorders very often run a chronic course of illness
enduring for many years or even life-long. The typical course of illness in PTSD is characterized not only by major psychiatric comorbidities contributing to a dramatically reduced health-related quality of life, to many deficits of psychosocial adaptation and a heightened suicide risk. It is also associated with a lot of major somatic health problems both in acute and long-term stages. The main focus here is on this special dimension of physical comorbidities in posttraumatic disorders. Empirical evidence underscores that trauma exposure, and in particular PTSD is significantly associated with major physical health problems in
addition to well-known PTSD-related psychological, behavioural, and psychosocial impairments. Both self-report-based and objective assessments emphasized significantly increased rates of somatoform/functional syndromes and physical comorbidities,
premature all-cause and specific mortality rates, heightened medical utilization behaviours, major socioeconomic costs, and reduced
health-related quality of life in the aftermath of trauma exposure and posttraumatic stress disorders, thus defining a major challenge to any medical care system. Complex psycho-behavioural-somatic and somato-psycho-behavioural models are needed to better understand both acute and long-term effects of a perpetuating stress system on physical health
THE RELATIONSHIP BETWEEN DEPRESSION, ANXIETY AND HEART DISEASE - A PSYCHOSOMATIC CHALLENGE
Hintergrund: Depressive Störungen und Herzerkrankungen
sind auf vielfältige Weise miteinander verschränkt. Die
Analyse ihres Zusammenhangs erfolgt vorteilhaft innerhalb
eines biopsychosozialen Krankheitsmodells.
Methoden: In einer systematischen Recherche wurden in
der wissenschaftlichen Literatur der letzten 15 Jahre Studien
zu epidemiologischen, ätiopathogenetischen und therapeutischen
Dimensionen der Komorbidität von Depression, Angst
und Herzerkrankung analysiert und thematisch dargestellt.
Ergebnisse: In einer epidemiologischen Perspektive sind
rezidivierende Depressionen im Langzeitverlauf mit einer
Erhöhung des Risikos für koronare Herzerkrankungen verbunden.
Depressionen spielen eine bedeutsame Rolle in der
Auslösung kritischer kardialer Ereignisse wie z.B. Myokardinfarkt.
Für diverse kardiale Erkrankungen liegt die Querschnittsprävalenz
depressiver Störungen deutlich über der in
der körperlich gesunden Allgemeinbevölkerung erwartbaren
Rate. Depression trägt im weiteren kardialen Krankheitsverlauf
zu einer signifikanten Erhöhung der somatischen
Morbidität und Mortalität bei. Die analogen Zusammenhänge
von Angst, posttraumatischer Belastungsstörung und Herzerkrankung
bewegen sich in einem vergleichbaren Bereich.
Möglicherweise spielt Angst pathogenetisch eine bedeutsamere
Rolle hinsichtlich weiterer kardialer Komplikationen
und letaler Ausgänge als Depression. In einer ätiopathogenetischen
Perspektive sind vermutlich nicht alle symptomatologischen
Dimensionen einer Depression von gleicher
Relevanz hinsichtlich einer Kardiotoxizität. Vitale Erschöpfung,
Anhedonie und Hoffnungslosigkeit scheinen mit
einem besonderen Risiko assoziiert zu sein. Mit einer
negativen kardialen Prognose verknüpft ist eine Postmyokardinfarkt-
Depression, die sich als therapie-resistent erweist.
Auf einer psychologischen Konstruktebene wurden Typ-APersönlichkeit,
Ärger/Feindseligkeit, Typ-D-Persönlichkeit
und Alexithymie erforscht. Psychologische und psychopathologische
Variablen müssen einerseits in den Kontext
psychosozialer Stressoren gestellt, andererseits zusammen mit
Hans-Peter Kapfhammer: THE RELATIONSHIP BETWEEN DEPRESSION, ANXIETY AND HEART DISEASE -
A PSYCHOSOMATIC CHALLENGE Psychiatria Danubina, 2011; Vol. 23, No. 4, pp 412-424
413
grundlegenden psycho- und neurobiologischen Variablen
analysiert werden. Dysfunktionen der HPA-Achse und der
sympathikomedullären Aktivität, reduzierte Herzratenvariabilität,
veränderte Thrombozytenaktivität sowie erhöhte
proinflammatorische Prozesse spielen eine bedeutsame
pathophysiologische Rolle sowohl für die Depression als auch
die kardiale Erkrankung. Neurobiologische Aspekte von
Angst- und posttraumatischen Belastungsstörungen sind
hiermit zu verbinden. Differenzielle Effekte müssen für
kritische kardiale Ereignisse angenommen werden. In einer
therapeutischen Perspektive liegen mehrere randomisierte und
Plazebo-kontrollierte Studien vor, die belegen, dass SSRI
wirksam und sicher depressive Störungen bei kardiologischen
Patienten behandeln können. Sie tragen möglicherweise auch
zu einer günstigeren somatischen Prognose bei. Vor allem
kognitiv-behaviorale Psychotherapieverfahren besitzen eine
Evidenzbasierung. Es ist derzeit nicht möglich, pharmako- und
psychotherapeutische Ansätze hinsichtlich einer differentziellen
Indikation zu bewerten.
Schlussfolgerungen. Depressive und Angststörungen bei
kardialen Erkrankungen definieren paradigmatisch eine
psychosomatisch-somatopsychische Herausforderung im
medizinischen Versorgungssystem. Die pragmatische Umsetzung
dieser psychosomatischen Perspektive geschieht
vorteilhaft durch einen CL-psychiatrischen Dienst in enger
Kooperation mit der Kardiologie.Background: Depressive and cardiological disorders present
a major comorbidity. Their manifold interrelations may
be best analysed within a biopsychosocial model of disease.
Methods: A systematic research was done on empirical
studies published during the last 15 years and dealing with
epidemiological, etiopathogenetic and therapeutic dimensions
of the comorbidity of depression, anxiety and heart disease.
Results: From an epidemiological perspective recurrent
depressions are associated with a significantly increased risk
of coronary heart disease. Depressive disorders play a major
role in triggering critical cardiac events, e.g. myocardial
infarction. The prevalence rates of depressive disorders in
various cardiological conditions are significantly higher than
the frequencies that can be expected in healthy general
population. Depression shows a negative impact on the
somatic morbidity and mortality during the further course of
illness. Anxiety and posttraumatic stress disorders seem to be
interrelated with cardiological conditions in quite a similar
way, probably contributing even more negatively to critical
and lethal cardiological events than depression. From an
etiopathogenetic perspective some clusters of depressive
symptoms seem to be linked to cardiotoxicity more closely
than other, vital exhaustion, anhedonia, and hopelessness
probably mediating a special risk. In any case, postmyocardial
infarct depression that proves treatment-resistent
indicates a negative prognosis of the prevailing cardiological
condition. On a level of psychological and psychosocial
constructs type-A personality, anger/hostility, type-D
personality, and alexithymia have been explored regarding its
proper pathogenetic role. Psychological and psychopathological
variables have to be set into a context of psychosocial
stressors on the one hand, and have to be simultaneously
analysed with various underlying psycho-and neurobiological
variables on the other. Above all, HPA- and sympathicomedullary
dysfunctions, reduced heart rate variability, altered
functions of thrombocytes, and increased proinflammatory
processes have to be recognized as significantly contributing
to the pathophysiology both of depression and of heart
condition. Neurobiological aspects of anxiety and posttraumatic
stress disorders must be interlinked with these
underpinnings of depression. Differential effects on critical
cardiological events must be supposed. From a therapeutic
perspective several RCTs demonstrate that SSRIs may safely
and efficiently treat depressive disorders in cardiological
conditions, and may even improve the general somatic
prognosis. Cognitive-behavioural psychotherapies have been
empirically validated in treating depression and anxiety with
cardiological patients. So far, however, a differential
indication of psychopharmacological versus psychotherapeutic
approaches has not been proved yet.
Conclusions: Depression and anxiety disorders in patients
with heart disease paradigmatically define a psychosomaticsomatopsychic
challenge to any health delivery system. A
psychosomatic perspective may best be practised within a
Consultation-Liaison psychiatric service that cooperates
continuously and closely with cardiological departments and
experts
Psychiatric and psychosocial outcome of orthotopic liver transplantation
Background. The study aimed to explore the prevalence of psychiatric disorders among orthotopic liver transplantation (OLT) recipients, and to investigate how psychiatric morbidity was linked to health-related quality of life (HRQOL). Methods: We recruited 75 patients who had undergone OLT a median of 3.8 years previously (range = 5-129 months). Psychiatric morbidity was assessed using the Structural Clinical Interview for the IDSM-III-R. Psychometric observer-rating and self-rating scales were administered to evaluate cognitive functioning (SKT), depressive symptomatology (HAMD(17)), Posttraumatic stress symptoms (PTSS-10), social support (SSS), and HRQOL (SF-36 Health Status Questionnaire). Treatment characteristics were obtained from medical records. Results: 22.7% (n = 17) of our sample had a current or probable psychiatric diagnosis according to DSM-III-R: 2.7% full posttraumatic stress disorder (PTSD) (n = 2), 2.7% major depressive disorder (MDD) comorbid to full PTSD (n = 2), 1.3% MDD comorbid to partial PTSD (n = 1), and 16% partial PTSD (n = 12). Patients with PTSD symptoms demonstrated lower cognitive performance, higher severity of depressive symptoms and more unfavorable perception of social support. OLT-related PTSD symptomatology was associated with maximal decrements in HRQOL. The duration of intensive care treatment, the number of medical complications, and the occurrence of acute rejection were positively correlated with the risk of PTSD symptoms subsequent to OLT. Conclusion: OLT-related PTSD symptomatology impairing HRQOL is a complication for a subgroup of OLT recipients. Health-care providers should be aware of the possible presence of PTSD in OLT survivors. Copyright (C) 2002 S. KargerAG, Basel
ANGSTSTÖRUNGEN - KLINISCHE UND NEUROBIOLOGISCHE ASPEKTE
Anxiety disorders are considered among the most common psychiatric disorders in general population. They may be characterized by prominent subjective suffering, frequent chronic courses of illness, increased rates of comorbid other psychiatric disorders and somatic diseases, a distressing amount of psychosocial disabilities, in all, a challenging high burden of disease.
Anxiety disorders have principally to be conceptualized within a multifactorial biopsychosocial model. Various psychological and psychosocial approaches have contributed to a multi-layered understanding of various major predisposing, eliciting, and maintaining factors in the course of illness. Modern neurobiological research has significantly broadened and deepened the aetiopathogenetic complexity
of anxiety disorders. The main focus of this short review is on neural fear- and anxiety circuits, neurotransmitter systems, neuroendocrine and inflammatory stress systems, genetics and epigenetics that characterize the general basis of fear and anxiety regulation and their dysregulation in anxiety disorders.
Anxiety disorders may be effectively treated both by psychotherapeutic
and pharmacological approaches. Basic principles and general guidelines in the treatment of anxiety disorders are being presented.Angststörungen zählen zu den häufigsten psychischen Störungen in der Allgemeinbevölkerung. Sie bedeuten hohes subjektives Leiden und verlaufen oft chronisch. Sie sind mit zusätzlichen komorbiden psychischen und auch mit somatischen Krankheitsrisiken verbunden. Sie verursachen zahlreiche psychosozialen Beeinträchtigungen und große sozioökonomische Belastungen.
Angststörungen werden heute prinzipiell innerhalb eines
multifaktoriellen, biopsychosozialen Krankheitsmodells konzipiert.
Psychologische und psychosoziale Modelle haben zu einem sehr differenzierten ätiopathogenetischen Verständnis der Einflüsse auf Entstehung, Auslösung und Aufrechterhaltung von Angststörungen geführt, das durch moderne neurobiologische Forschungsergebnisse noch signifikant erweitert und vertieft worden ist. Angststörungen können sowohl psychopharmakologisch als auch psychotherapeutisch wirksam behandelt werden. In einer Gesamtbeurteilung kann die große Mehrheit der unkomplizierten spezifischen Phobien und Panikstörungen gut und sehr wahrscheinlich auch anhaltend mit Psychotherapie gebessert werden. Generalisierte Angststörungen und soziale Phobien benötigen hingegen häufig längerfristige störungsorientierte Psychotherapien. Schwere Angststörungen aber, vor allem bei
chronischen Verläufen, mit zusätzlichen psychischen und somatischen
Komplikationen und ausgeprägter psychosozialer Beeinträchtigung
werden in der Regel bevorzugt medikamentös und oft auch in Kombination mit Psychotherapie behandelt
Interleukin-6 Gene Expression Changes after a 4-Week Intake of a Multispecies Probiotic in Major Depressive Disorder-Preliminary Results of the PROVIT Study
Major depressive disorder (MDD) is a prevalent disease, in which one third of sufferers do not respond to antidepressants. Probiotics have the potential to be well-tolerated and cost-effcient treatment options. However, the molecular pathways of their effects are not fully elucidated yet. Based on previous literature, we assume that probiotics can positively influence inflammatory mechanisms. We aimed at analyzing the effects of probiotics on gene expression of inflammation genes as part of the randomized, placebo-controlled, multispecies probiotics PROVIT study in Graz, Austria. Fasting blood of 61 inpatients with MDD was collected before and after four weeks of probiotic intake or placebo. We analyzed the effects on gene expression of tumor necrosis factor (TNF), nuclear factor kappa B subunit 1 (NFKB1) and interleukin-6 (IL-6). In IL-6 we found no significant main effects for group (F(1,44) = 1.33, p = ns) nor time (F(1,44) = 0.00, p = ns), but interaction was significant (F(1,44) = 5.67, p < 0.05). The intervention group showed decreasing IL-6 gene expression levels while the placebo group showed increasing gene expression levels of IL-6. Probiotics could be a useful additional treatment in MDD, due to their anti-inflammatory effects. Results of the current study are promising, but further studies are required to investigate the beneficial effects of probiotic interventions in depressed individuals
Magyar Geofizika 1988
Introduction
Bipolar disorder (BD) is a chronic psychiatric disease which can take most different and unpredictable courses. It is accompanied by unspecific brainstructural changes and cognitive decline. The neurobiological underpinnings of these processes are still unclear. Emerging evidence suggests that tryptophan catabolites (TRYCATs), which involve all metabolites of tryptophan towards the kynurenine (KYN) branch, are involved in the etiology as well as in the course of BD. They are proposed to be mediators of immune-inflammation and neurodegeneration. In this study we measured the levels of KYN and its main catabolites consisting of the neurotoxic hydroxykynurenine (3-HK), the more neuroprotective kynurenic acid (KYNA) and anthranilic acid (AA) and evaluated the ratios between end-products and substrates as proxies for the specific enzymatic activity (3-HK/KYN, KYNA/KYN, AA/KYN) as well as 3-HK/KYNA as a proxy for neurotoxic vs. neuroprotective end-product relation in individuals with BD compared to healthy controls (HC).
Methods
We took peripheral TRYCAT blood levels of 143 euthymic to mild depressive BD patients and 101 HC. For statistical analyses MANCOVA's controlled for age, sex, body mass index, cardiovascular disease and smoking were performed.
Results
The levels of KYNA (F=5,579; p<.05) were reduced in BD compared to HC. The enzymatic activity of the kynurenine-3-monooxygenase (KMO) reflected by the 3-HK/KYN ratio was increased in BD individuals compared to HC (F=5,394; p<.05). Additionally the ratio of 3-HK/KYNA was increased in individuals with BD compared to healthy controls (F=11,357; p<.01).
Discussion
In conclusion our findings subserve the concept of KYN -pathway alterations in the pathophysiology of BD. We present evidence of increased breakdown towards the neurotoxic branch in KYN metabolism even in a euthymic to mild depressive state in BD. From literature we know that depression and mania are accompanied by inflammatory states which should be capable to produce an even greater imbalance due to activation of key enzymes in the neurotoxic direction of KYN -conversion. These processes could finally be involved in the development of unspecific brain structural changes and cognitive deficits which are prevalent in BD. Further research should focus on state dependent changes in TRYCATs and its relation to cognition, brain structure and staging parameters
Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study
Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation
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