Prevalence of posttraumatic stress disorder after stroke: A systematic literature review.

BACKGROUND: Posttraumatic stress disorder (PTSD) has shown to be related to worse functional outcome in individuals with stroke. This systematic literature review aimed to 1) provide a comprehensive overview of the evidence of prevalence of PTSD after stroke; 2) explore possible differences in prevalence between pathogenic origin of stroke and location of lesion; and 3) explore possible differences in prevalence between method of assessment of PTSD. METHODS: A systematic literature search was performed on studies reporting on PTSD post-stroke. Risk of bias was assessed using an adapted version of the Joanna Briggs Institute's critical appraisal tool. RESULTS: Thirty studies, reporting on 4320 individuals, were included. The weighted median PTSD prevalence overall was 17.5 % (2.9 %-71.4 %), in ischemic stroke 13.8 %, in transient ischemic attack 4.6 %, in intracerebral hemorrhage 6.5 %, and in subarachnoid hemorrhage 37.1 %. The weighted median prevalence based on self-report questionnaires was 17.8 % (3.7 %-71.4 %,) and based on PTSD interviews 4.0 % (2.9 %-32.8 %). At three and ≥ 12 months post-stroke the weighted median prevalence was respectively 24.7 % (0.0 %-37.1 %) and 17.8 % (6.5 %-71.4 %). CONCLUSION: Results suggest that PTSD is common after stroke, and even more so after subarachnoid hemorrhage. This underlines the importance of awareness of and screening for PTSD post-stroke, even after the first year post-stroke.

[Perspectives and practices of speech therapists regarding friendships after brain injury]. / Visie en werkzaamheden van logopedisten aangaande vriendschappen na hersen­letsel.

BACKGROUND: Acquired brain injury (ABI) is a common comorbidity in the psychiatric population. Consequences of ABI, including social communication problems, negatively affect friendships. However, current speech pathology practices regarding friendships after ABI remain unknown. AIM: To monitor perspectives, practices and facilitating as well as limiting factors with regard to these practices of Dutch speech therapists regarding friendships after ABI. METHOD: Survey study on whether, why, and how speech therapists do (not) perform work on friendships after ABI. RESULTS: Up to 90% of the 36 participating speech therapists believed that work related to friendships after ABI falls within the scope of their responsibilities. 78% of the speech therapists actually performed such activities. The most frequently mentioned facilitating factor in activities regarding friendship was the presence of supporting material, e.g. educational modules. The most frequently reported barrier was the very limited existence of social networks of persons with ABI. CONCLUSIONS: Work activities by speech therapists regarding friendships after ABI are numerous. Speech therapists are in need of material that can be used to support their work on friendships.

[Prevalence and manifestations of aggression in adult patients with acquired brain injury: a review]. / Prevalentie en uitingsvormen van agressie bij volwassen patiënten met niet-aangeboren hersenletsel: een literatuuroverzicht.

BACKGROUND: Aggression after acquired brain injury has a major impact on daily functioning for the patient, their family, and caregivers.
AIM: To present the prevalence and manifestations of aggression in patients with different types of brain injury.
METHOD: Systematic search of the literature in PubMed, Psycinfo and Embase.
RESULTS: Fourty-one studies were included in which 15 different outcome measures for aggression were used. The prevalence of agitation ranged between 4.0%-93.9% (median 35.8%), of aggression between 3.7%-88.0% (median 35.3%) and of hostility between 4.0%-45.7% (median 9.1%). Prevalence rates were highest in patients with traumatic brain injury. Verbal aggression occurred more frequently (median 33.0%, 14.0%-70.0%) than physical aggression (median 11.5%, 1.5%-33.8%), but manifestations of aggression were only examined in ten studies.
CONCLUSION: Aggression is a common behavioral problem after brain injury. The prevalence varies and depends on the type of brain injury, the specific target behavior and the outcome measure. It is recommended to reach consensus on definitions and outcome measures.

[Cognitive communication disorder due to right hemispheric brain injury]. / Cognitieve communicatiestoornis ten gevolge van niet-aangeboren hersenletsel in de rechter hemisfeer.

Communication disorders can arise as a consequence of right hemispheric brain injury due to, for example, stroke. These disorders can comprise language comprehension, language production and pragmatic language use. If these problems are not recognised in time, treatment will probably focus on behavioural problems, which would lead to further deterioration of the patient due to an escalation in interaction. We present a patient in whom this situation occured. However, by addressing her underlying communication problem, we were able to improve her quality of life.

[The neurotrophic hypothesis of depression]. / De neurotrofe hypothese van depressie.

BACKGROUND: The neurotrophic hypothesis of depression postulates that neuronal plasticity is a key factor in the development of depression and in the clinical response to antidepressants. Brain-derived neurotrophic factor (BDNF) is an important protein in this process. AIM: To provide a survey of the current scientific view regarding the neurotrophic hypothesis of depression. METHOD: We studied the literature using PubMed. RESULTS: The serum bdnf level was found to be consistently lower in depressed patients compared to healthy controls. In short open-label antidepressant treatment trials the bdnf levels were found to be higher post-treatment than pre-treatment. Longitudinal analysis of a large naturalistic cohort study revealed that it was more likely that bdnf serum levels were lower as a result of depression than that they represented an etiological factor for the illness. CONCLUSION: These findings show that the neurotrophic hypothesis of depression is more complex than previously assumed. Animal studies have shown a correlation between stress, diminished bdnf expression in the brain and depressive-like behavior. Studies in humans, on the other hand, particularly those with a longitudinal design, suggest that the decrease in serum bdnf is a consequence of the depression rather than vice versa. This is in sharp contrast to the original assumptions of the neurotrophic hypothesis.

Chronic depression is associated with a pronounced decrease in serum brain-derived neurotrophic factor over time.

One of the leading neurobiological hypotheses on depression states that decreased expression of brain-derived neurotrophic factor (BDNF) contributes to depression. This is supported by consistent findings of low serum BDNF levels in depressed patients compared with non-depressed controls. Whereas it has been generally assumed that this is a state characteristic of depression, strong inferences about state or trait effects require a longitudinal study design. To investigate the longitudinal association between serum BDNF and depression, we measured serum BDNF, (current and past) depression status, use of antidepressants, and all potential covariates at baseline and after 2 years in 1751 individuals, consisting of patients with an incident (n=153), remitted (n=420) and persistent depression (n=310) and non-depressed controls (n=868). We analyzed change/differences in serum BDNF across these four groups with analyses of covariance adjusted for covariates and baseline BDNF value, together with the effects of starting and stopping antidepressant treatment. Our analyses revealed a significant difference for the depression course groups (P=0.007). Compared with non-depressed controls, persistently depressed and remitted patients had a steeper decrease of BDNF levels over time (-1.33 (P=0.001) and -0.97 ng ml(-1) (P=0.011), respectively), whereas BDNF reductions in patients with incident depression were similar to those in healthy controls. Initiation or discontinuation of antidepressants was not associated with BDNF change (P=0.72). These findings suggest that BDNF not only contributes to depression, but that depression in turn may also contribute to low BDNF.

Low serum BDNF levels in depressed patients cannot be attributed to individual depressive symptoms or symptom cluster.

OBJECTIVES: Low serum BDNF levels have been found in depressed patients. No study has systematically investigated whether individual symptoms or symptom profiles within a depressed population contribute to low BDNF levels found in depressed subjects. METHODS: All 1070 patients with a past 6-month diagnosis of major depressive disorder from the Netherlands Study of Depression and Anxiety (NESDA) were included. Composite International Diagnostic Interview (CIDI) and Inventory of Depressive Symptoms (IDS) items were tested individually in separate multiple regression analyses with serum BDNF level as the dependent and the CIDI or IDS item as independent variable. Subsequently, we compared BDNF levels between patients with seasonal affective disorder (based on the Seasonal Pattern Assessment Questionnaire) and melancholic depression, atypical depression and moderate depression (based on a latent class analysis). All analyses were adjusted for confounders. RESULTS: Only one item was significantly associated with serum BDNF levels, namely the CIDI item "loss of interest" (ß = 0.14; P < 0.01). Counterintuitively the presence of this symptom was associated with higher BDNF levels. Other items and the comparison between different types of depression did not reveal significant differences. CONCLUSIONS: Decreased serum BDNF levels in depression cannot be attributed to a specific symptom or symptom cluster.

Serum BDNF concentrations as peripheral manifestations of depression: evidence from a systematic review and meta-analyses on 179 associations (N=9484).

Meta-analyses, published in 2008-2010, have confirmed abnormally low serum brain-derived neurotrophic factor (BDNF) concentrations in depressed patients and normalization of this by antidepressant treatment. These findings are believed to reflect peripheral manifestations of the neurotrophin hypothesis, which states that depression is secondary to an altered expression of BDNF in the brain. Since the publication of these meta-analyses, the field has seen a huge increase in studies on these topics. This motivated us to update the evidence on the aforementioned associations and, in addition, to compile the data on serum BDNF concentrations in relation to the symptom severity of depression. Using a manifold of data as compared with earlier meta-analyses, we find low serum BDNF concentrations in 2384 antidepressant-free depressed patients relative to 2982 healthy controls and to 1249 antidepressant-treated depressed patients (Cohen's d=-0.71 and -0.56, P-values <0.0000001). When publication bias is accounted for, these effect-sizes become substantially smaller (d=-0.47 and -0.34, respectively, P-values<0.0001). We detect between-study heterogeneity in outcomes for which only year of publication and sample size are significant moderators, with more recent papers and larger samples sizes in general being associated with smaller between-group differences. Finally, the aggregated data negate consistent associations between serum BDNF concentrations and the symptom severity of depression. Our findings corroborate the claim that altered serum BDNF concentrations are peripheral manifestations of depression. However, here we highlight that the evidence for this claim is slimmer as was initially thought and amidst a lot of noise.

Serum levels of brain-derived neurotrophic factor in major depressive disorder: state-trait issues, clinical features and pharmacological treatment.

Recent evidence supports 'the neurotrophin hypothesis of depression' in its prediction that brain-derived neurotrophic factor (BDNF) is involved in depression. However, some key questions remain unanswered, including whether abnormalities in BDNF persist beyond the clinical state of depression, whether BDNF levels are related to the clinical features of depression and whether distinct antidepressants affect BDNF levels equally. We addressed these questions and investigated serum BDNF levels in 962 depressed patients, 700 fully remitted persons (≥6 months) and 382 healthy controls. We found serum BDNF levels to be low in antidepressant-free depressed patients relative to controls (P=0.007) and to depressed patients who were treated with an antidepressant (P=0.001). BDNF levels of fully remitted persons (whether unmedicated or treated with an antidepressant) were comparable to those of controls. Analyzing the sample of antidepressant-free depressed patients showed that BDNF levels were unrelated to the core clinical features of depression such as its severity or first versus a recurrent episode. The antidepressant associated upregulation of serum BDNF in depressed patients was confined to selective serotonin reuptake inhibitors (SSRIs) (P=0.003) and St John's wort (P=0.03). Our results suggest that low serum levels of BDNF are a state abnormality that is evident during depression and normalizes during remission. Increases in serum levels of BDNF during antidepressant treatment appear to be confined to some antidepressants and do not parallel clinical characteristics, such as the severity of depressive symptoms.

Depressive symptom clusters are differentially associated with atherosclerotic disease.

BACKGROUND: Depression increases the risk of subsequent vascular events in both cardiac and non-cardiac patients. Atherosclerosis, the underlying process leading to vascular events, has been associated with depression. This association, however, may be confounded by the somatic-affective symptoms being a consequence of cardiovascular disease. While taking into account the differentiation between somatic-affective and cognitive-affective symptoms of depression, we examined the association between depression and atherosclerosis in a community-based sample. METHOD: In 1261 participants of the Nijmegen Biomedical Study (NBS), aged 50-70 years and free of stroke and dementia, we measured the intima-media thickness (IMT) of the carotid artery as a measure of atherosclerosis and we assessed depressive symptoms using the Beck Depression Inventory (BDI). Principal components analysis (PCA) of the BDI items yielded two factors, representing a cognitive-affective and a somatic-affective symptom cluster. While correcting for confounders, we used separate multiple regression analyses to test the BDI sum score and both depression symptom clusters. RESULTS: We found a significant correlation between the BDI sum score and the IMT. Cognitive-affective, but not somatic-affective, symptoms were also associated with the IMT. When we stratified for coronary artery disease (CAD), the somatic-affective symptom cluster correlated significantly with depression in both patients with and patients without CAD. CONCLUSIONS: The association between depressive symptoms and atherosclerosis is explained by the somatic-affective symptom cluster of depression. Subclinical vascular disease thus may inflate depressive symptom scores and may explain why treatment of depression in cardiac patients hardly affects vascular outcome.

Determinants of serum brain-derived neurotrophic factor.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) belongs to the neurotrophin family of growth factors and affects the survival and plasticity of neurons in the adult central nervous system. The high correlation between cortical and serum BDNF levels has led to many human studies on BDNF levels in various populations, however knowledge about determinants that influence BDNF is lacking. AIMS: To gain insight into the factors that influence BDNF levels in humans. METHODS: In 1168 people aged 18 through 65, free of antidepressants and current psychiatric disease, from the Netherlands study of depression and anxiety four categories of determinants (sampling, sociodemographics, lifestyle indicators and diseases) were measured as well as BDNF level. We used univariate analyses as well as multivariate linear regression analyses in particular to determine which of the possible determinants significantly influenced serum BDNF levels. RESULTS: The mean BDNF level was 8.98ng/ml (SD 3.1ng/ml) with a range from 1.56ng/ml through 18.50ng/ml. Our final multivariate regression analysis revealed that a non-fasting state of blood draw (ß=-.067; p=.019), later measurement (ß=-.065; p=.022), longer sample storage (ß=-.082; p=.004) and being a binge drinker (ß=-.063; p=.035) all resulted in attenuated BDNF levels. This was in contrast to smoking (ß=.098; p=.001) and living in an urban area (ß=.109; p<.001), which resulted in increased BDNF levels. Moreover we found that older subjects also had higher BDNF levels, but this only applied to women (ß=.226; p<.001). CONCLUSIONS: Future studies on serum levels of BDNF in humans should correct for the time of blood withdrawal, storage, urbanicity, age, sex, smoking status and food and alcohol intake.