Species niches may impact population and community stability by influencing average population sizes and species richness, however, niche-based approaches are rarely applied when studying stability in natural communities. Here we utilise a niche-based approach to link niche characteristics to community stability in 140 European butterfly communities. We represent niches as hyper-volumes and generate metrics for niche overlap, mismatch, and volume. Using structural equation modelling we then test five hypotheses linking niche and community characteristics to mechanisms influencing community stability. We find that the position of a site relative to the niches of the species pool predicts species richness, and that sites with species near the centre of their niche have higher mean abundance. We then show that niche position and size influence population stability, and species richness increases asynchrony which subsequently influences community stability. Our approach demonstrates that niches metrics are useful tools for understanding the dynamics of natural communities.

The presence of neuropsychiatric disorders after stroke has been recognized for more than 100 years, but controlled systematic studies did not begin until the 1970s. The most clinically important advances, however, have been in the treatment and prevention of poststroke depression (PSD). Recent meta-analyses of randomized controlled trials (RCTs) for the treatment of PSD have demonstrated the efficacy of antidepressants. Similarly, RCTs for the prevention of PSD have shown that antidepressants significantly decrease the incidence of PSD compared with placebo. Early treatment of PSD with antidepressants also appears to enhance both physical , cognitive recovery from stroke and may increase survival up to 10 years. Genetic and epi- genetic variations, white matter disease, cerebrovascular deregulation, altered neuroplasticity , changes in glu- tamate neurotransmission may be relevant etiological factors.

OBJECTIVE Despite the high frequency of depression in the first year following stroke, few studies have predicted risk of depression after the acute and subacute stroke periods. The aim of this study was to identify, in the acute and subacute periods, measures that would predict major depression during the first year after stroke. METHODS Study subjects were inpatients with ischemic stroke aged 20-85 years within 6 weeks of onset. Patients were evaluated at baseline and at 3, 6, 9, and 12 months. Patients were diagnosed with major depression using the Structured Clinical Interview for DSM-IV. The severity of depressive symptoms was measured with the Patient Health Questionnaire-9 (PHQ-9) and the Montgomery-Åsberg Depression Rating Scale (MADRS). RESULTS Of the 152 potential patients who met inclusion criteria, 49 had follow-up evaluations; one patient with major depression in the acute and subacute periods was excluded from the analysis. Among the remaining 48 patients, the number of those with major depression during the first year of stroke onset was five (10.4%). Patients who developed major depression had significantly more depressive symptoms in the acute and subacute stroke phase as assessed by both the PHQ-9 and MADRS. Patients with PHQ-9 scores ≥9 in the acute and subacute stroke phases were significantly more likely to develop major depression in a chronic phase of stroke. CONCLUSIONS The self-administered PHQ-9 can identify patients in the acute and subacute stroke periods who are at increased risk for developing major depression during the first year after stroke.

After I completed my residency and fellowship training in 1977, I was appointed Assistant Professor at Johns Hopkins. Since then, I have been asked by many students, residents, and postdoctoral fellows whether a scientific career in psychiatry, neuroscience, geriatric psychiatry, or neuropsychiatry is feasible and whether I would advise it. I have honestly told them that an academic research career is enormously rewarding but not an easy career.

Background: To evaluate the efficacy of treatment with nefiracetam compared to placebo in poststroke apathy. Methods: A parallel group, randomized, placebo-controlled, double-blind two-center trial in patients with recent stroke and apathy was conducted in 2 tertiary teaching hospitals in Perth, Western Australia, between March 2010 and October 2014. Consenting patients hospitalized with stroke were screened for participation at the time of hospitalization and, if diagnosed with apathy 8-36 weeks later, they were randomized to 12 weeks of 900 mg/day nefiracetam or placebo. The primary efficacy parameter was change in apathy at 12 weeks defined by the 14-item Apathy Scale (AS). Results: Of 2514 patients screened, only 377 (15%) were eligible for the study after the first screening, 233 declined further participation, and 144 were assessed for apathy at 8-36 weeks post stroke to confirm eligibility. Twenty patients out of 106 with a complete psychiatric assessment had apathy (19%). Of this sample, 13 patients were randomized. Overall, the AS score decreased by a mean of 7.0 points (95% CI = -14.6 to.6), but there was no significant between-group difference at week 12 (mean paired t-tests, P > .14). Conclusions: Treatment with nefiracetam did not prove to be more efficacious than placebo in ameliorating apathy in stroke. The main limitation was the very small sample randomized, highlighting the limitations of conducting drug trials for behavioral problems among stroke patients. Pharmacological studies of apathy in stroke will require a large multicenter study and a massive sample of patients.

OBJECTIVE:This study re-examined patients from a 1-year randomized controlled double-blind trial of escitalopram, problem-solving therapy (PST), or placebo to prevent depression among patients less than 3 months after a stroke. The objective of the current study was to determine if preventive treatment would predict time to death over 8-10 years of follow-up. Based on the importance of depression in poststoke mortality and a previous study of this population at 18 months' follow-up showing that stopping escitalopram but not PST led to a significant increase in depression, the authors hypothesized that PST would be associated with the longest time to death.METHODS:Of 129 eligible patients, 122 were contacted and 7 were lost to follow-up. Families and surviving patients were interviewed to determine current health status or the date and cause of death.RESULTS:Using the Weibull model of log time (years) to death, controlled for age, severity of physical illness, gender, severity of stroke, and history of depression after study entry, there was a significant independent effect of treatment. PST significantly and independently increased the time to mortality, whereas older age and major depression significantly and independently decreased the time to death.CONCLUSION:To the authors' knowledge, this is the first time a psychological antidepressant treatment administered for 1 year has been associated with increased survival among patients who have suffered a stroke.

IMPORTANCE:Prevention is more effective than treatment to decrease the burden of significant medical conditions such as depressive disorders, a major cause of disability worldwide. Traumatic brain injury (TBI) is a candidate for selective strategies to prevent depression given the incidence, prevalence, and functional effect of depression that occurs after TBI.OBJECTIVE:To assess the efficacy of sertraline treatment in preventing depressive disorders following TBI.DESIGN, SETTING, AND PARTICIPANTS:A double-blind, placebo-controlled, parallel-group randomized clinical trial was conducted at a university hospital from July 3, 2008, to September 17, 2012, with 24 weeks of follow-up. A consecutive sample of 534 patients aged 18 to 85 years, hospitalized for mild, moderate, or severe TBI, was eligible for the study. Ninety-four patients consented to participate and were randomized (46 to placebo and 48 to sertraline), of whom 79 (84%) completed the study. Intention-to-treat data analysis was conducted from July 1, 2014, to December 31, 2015.INTERVENTIONS:Placebo or sertraline, 100 mg/d, for 24 weeks or until development of a mood disorder.MAIN OUTCOMES AND MEASURES:Time to onset of depressive disorders, as defined by the DSM-IV, associated with TBI.RESULTS:Of the 94 patients in the study (38 female and 56 male; 92 white), the number needed to treat to prevent depression after TBI at 24 weeks was 5.9 (95% CI, 3.1-71.1; χ2 = 4.6; P = .03) for sertraline treatment vs placebo. The influence of sertraline in the course of neuropsychological variables was not detected. The intervention was well tolerated, and adverse effects were mild in both the sertraline and placebo groups.CONCLUSIONS AND RELEVANCE:Sertraline appears to be efficacious to prevent the onset of depressive disorders following TBI. Future studies should replicate these findings in a large sample of patients with TBI and depict their long-term physical, cognitive, behavioral, and functional outcomes.TRIAL REGISTRATION:clinicaltrials.gov Identifier: NCT00704379.

Poststroke depression (PSD) has been recognized by psychiatrists for more than 100 years, but controlled systematic studies did not begin until the 1970s. Meta-analyses addressing almost all major clinical issues in the field have emerged because of the relatively small number of patients included in some stroke studies. In order to build large databases, these meta-analyses have merged patients with rigorously assessed mood disorders with major depressive features with patients scoring above arbitrary cutoff points on depression rating scales, thus missing important findings such as cognitive impairment associated with major but not minor depression. Nevertheless, PSD occurs in a significant number of patients and constitutes an important complication of stroke, leading to greater disability as well as increased mortality. The most clinically important advances, however, have been in the treatment and prevention of PSD. Recent meta-analyses of randomized controlled trials for the treatment of PSD have demonstrated the efficacy of antidepressants. Similarly, randomized controlled trials for prevention of PSD have shown that antidepressants significantly decrease the incidence of PSD compared with placebo. Early antidepressant treatment of PSD appears to enhance both physical and cognitive recovery from stroke and might increase survival up to 10 years following stroke. There has also been progress in understanding the pathophysiology of PSD. Inflammatory processes might be associated with the onset of at least some depressive symptoms. In addition, genetic and epigenetic variations, white matter disease, cerebrovascular deregulation, altered neuroplasticity, and changes in glutamate neurotransmission might be relevant etiological factors. Further elucidation of the mechanism of PSD may ultimately lead to specific targeted treatments.

Characteristics associated with life expectancy in Alzheimer's disease (AD) are still far from known. Here we aimed at examining the ability of baseline/longitudinal clinical variables to predict time to death. One-hundred fifty AD outpatients underwent diagnostic, neuropsychiatric, and functional assessment at baseline (when ApoE ɛ4 was also investigated) and at each subsequent annual visit. A random effects joint modeling approach was used to simultaneously model the baseline and longitudinal trajectory of each factor and predict the time to death, adjusting for demographic covariates. An ancillary analysis of ApoE ɛ4 status as a predictor was also conducted. Kaplan-Meier survival curves were constructed to elucidate the relationship between each factor and the estimated probability of death over time. Shorter survival was associated with male gender, higher education, older age, lower cognition, and worse functioning in daily life, but not ApoE ɛ4 status. Longitudinal trajectories increased predictive power over using just baseline levels highlighting apathy, and secondarily aberrant motor behaviors and sleep disorders, as a highly reliable predictor for mortality. Apathy was the strongest neuropsychiatric predictor of time to death, which supports its role in the pathogenesis of the disorder. An increased knowledge of factors modulating survival in AD is a strategic prerequisite to plan therapeutic interventions.

This study examined the efficacy of antidepressant treatment for preventing the onset of generalized anxiety disorder (GAD) among patients with recent stroke. Of 799 patients assessed, 176 were randomized, and 149 patients without evidence of GAD at the initial visit were included in this double-blind treatment with escitalopram (N=47) or placebo (N=49) or non-blinded problem-solving therapy (PST; 12 total sessions; N=53). Participants given placebo over 12 months were 4.95 times more likely to develop GAD than patients given escitalopram and 4.00 times more likely to develop GAD than patients given PST. Although these results should be considered preliminary, the authors found that both escitalopram and PST were effective in preventing new onset of post-stroke GAD.

Neuropsychiatric and cognitive symptoms are common in patients with Parkinson’s disease (PD) from the early stage of the disease but their course is still unclear. In this study we investigated prospectively the progression of affective and cognitive symptoms and disorders in de novo idiopathic PD patients. Twenty-four de novo drug naïve PD patients underwent a comprehensive neurological, psychopathological and neuropsychological evaluation at the first diagnostic visit (OFF), after 4−6 months when the antiparkinsonian therapy regimen was stabilized (ON-1), and at one year following the ON-1 follow-up visit (ON-2). Generalized least squares analysis revealed a significant improvement over time in the depressive mood, short and long term episodic verbal memory, visual memory, and the motor symptoms. Pairwise comparisons showed a significant change from OFF to ON-1 for all the aforementioned variables, except for short term episodic verbal memory which approached significance. A significant improvement from ON-1 to ON-2, however, was shown for short term episodic verbal memory. An ancillary analysis indicated that overall level and change in a number of cognitive variables, but not depression, was conditional upon age of onset, education, and sometime gender. In conclusion, early stage PD is not associated with affective and cognitive deterioration. On the contrary, very specific neuropsychiatric and cognitive symptoms may improve. This study provides Class III evidence that antiparkinsonian treatment commonly used in the clinical practice improves memory performance and depression severity in de novo patients with PD.

Lesser Black-backed Gull Larus fuscus numbers in England have fluctuated in recent decades. Both breeding and wintering populations rose sharply in the latter half of the twentieth century, mostly due to increases at a small number of colonies and changes in migratory behaviour. However, there was a decline in breeding birds between 2000 and 2013 (largely because of losses at the same key colonies) and this species is on the Birds of Conservation Concern Amber List. Although protected at various sites in the breeding season, the Lesser Black-backed Gull can be taken under three General Licences issued under the Wildlife and Countryside Act 1981, allowing population control in certain circumstances without specific permission or reporting. There are no sites where the Lesser Black-backed Gull is a protected feature outside the breeding season, although numbers surpass the relevant thresholds at certain roosts. This review paper synthesises available information on the Lesser Black-backed Gull in England to help policy makers resolve this apparent legislative contra- diction and formulate a clearer conservation policy to guide future practice.

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OBJECTIVE:This prospective study examined the course of cognitive, physical, and social impairment among patients who developed apathy during the first year after stroke.METHODS:Patients diagnosed with apathy (N = 23) were compared with patients who had no apathy (N = 33) at initial, 3, 6, 9, and 12 months after stroke for severity of global cognitive impairment as measured by Mini-Mental State Examination, severity of impairment in activities of daily living (ADLs) as measured by Functional Independence Measure, and severity of impairment in social functioning as measured by Social Functioning Exam.RESULTS:A total of 41.1% of patients met diagnostic criteria for apathy during the first year after stroke. The mean time from stroke to onset of apathy was 3.8 (3.3 SD) months and the mean duration was 5.6 (2.3 SD) months. Using a linear mixed model, after controlling for age, initial severity of impairment, and major depression, patients in the apathy group had significantly less recovery in cognition (t(149) = -2.06; p = 0.0411) and ADLs (t(104) = -3.37; p = 0.0011) during the first year after stroke compared with nonapathic patients.CONCLUSION:Apathy is common after stroke and leads to less recovery in cognition and ADLs over the first year after stroke compared with similar nonapathic patients.

The role of interleukin-6 (IL-6) as a risk factor for developing depressive symptoms, neuropsychological impairment, and related functional and neurological symptom severity during the acute phase of ischemic stroke is still underexplored. Here, the authors assessed this issue, in 48 patients without significant clinical history for major medical illnesses or other factors that promote inflammation, 72 hours after a first-ever acute ischemic stroke. In the acute phase of ischemic stroke, increased IL-6 plays a key role in the onset of depressive disorders, apathy/amotivation, somatic symptoms of depression, and neurological/functional symptoms, resulting in higher disability and poor outcome of stroke patients.

BACKGROUND:The objective of this study was to evaluate citalopram for executive functioning in Huntington's disease (HD). METHODS:The study was randomized, double-blind, and placebo-controlled. Thirty-three adults with HD, cognitive complaints, and no depression (Hamilton Depression [HAM-D] rating scale ≤ 12) were administered citalopram 20 mg or placebo (7 visits, 20 weeks), with practice and placebo run-ins. The primary outcome was change in executive functioning. RESULTS:The intent to treat analysis was controlled for practice effects, comparing visits 1 and 2 to visits 5 and 6 for citalopram versus placebo. There were no significant benefits on the executive function composite (treatment-placebo mean difference -0.167; 95% confidence interval [CI], -0.361 to 0.028; P = .092). Citalopram participants showed improved clinician-rated depression symptoms on the HAM-D (t = -2.02; P = 0.05). There were no group differences on motor ratings, self-reported executive functions, psychiatric symptoms, or functional status. CONCLUSIONS:There was no evidence that short-term treatment with citalopram improved executive functions in HD. Despite excluding patients with active depression, participants on citalopram showed improved mood, raising the possibility of efficacy for subsyndromal depression in HD.

Although stroke is a leading cause of death in the United States and around the world, many people fear this disease because of its nonfatal neurological impairments that lead to disability or dependency. Considerable research has focused on lessening the neurological effects of the acute brain injury. To date, success is limited. Despite these research efforts, only intravenous thrombolysis and endovascular interventions are accepted as effective in limiting the acute effects of ischemic stroke. Although these therapies are efficacious, only 3% to 5% of patients with stroke are receiving reperfusion-based therapies due to the very short time windows for treatment.1 No medical or surgical intervention is useful in improving outcomes after intracerebral hemorrhage.Annually, approximately 400 000 Americans need rehabilitation to help with recovery after stroke.2 Given the magnitude of the problem, effective new therapies are needed to augment the process of recovery. These therapies could be given as adjuncts to conventional rehabilitation to these patients who have potentially disabling residual neurological impairments. Because many more patients could be treated, an effective therapy that maximizes neurological recovery might have a much bigger societal impact than emergency reperfusion therapy alone.3,4 Unfortunately, relatively few clinical studies have tested interventions that might augment recovery. The basic science understandings of the process of recovery after stroke have advanced.5–10 It is now clear that the adult brain has a real capacity for physiological and anatomic modifications that lead to motor and cognitive recovery.11 This complex process is mediated by multiple mechanisms including enhanced regional metabolism and resolution of diaschisis. Cellular changes after stroke include proliferation of neural and glial cell precursors, activation of astrocytes and inflammatory cells, migration of blood vessels, increased axonal sprouting, increased branching of dendrites, and development of new synapses.12–14 …