Diffuse tibiofemoral cartilage change prior to the development of accelerated knee osteoarthritis: Data from the osteoarthritis initiative

We compared the spatial distribution of tibiofemoral cartilage change between individuals who will develop accelerated knee osteoarthritis (KOA) versus typical onset of KOA prior to the development of radiographic KOA. We conducted a longitudinal case–control analysis of 129 individuals from the Osteoarthritis Initiative. We assessed the percent change in tibiofemoral cartilage on magnetic resonance images at 36 informative locations from 2 to 1 year prior to the development of accelerated (n = 44) versus typical KOA (n = 40). We defined cartilage change in the accelerated and typical KOA groups at 36 informative locations based on thresholds of cartilage percent change in a no KOA group (n = 45). We described the spatial patterns of cartilage change in the accelerated KOA and typical KOA groups and performed a logistic regression to determine if diffuse cartilage change (predictor; at least half of the tibiofemoral regions demonstrating change in multiple informative locations) was associated with KOA group (outcome). There was a non‐significant trend that individuals with diffuse tibiofemoral cartilage change were 2.2 times more likely to develop accelerated knee OA when compared with individuals who develop typical knee OA (OR [95% CI] = 2.2 [0.90–5.14]. Adults with accelerated or typical KOA demonstrate heterogeneity in spatial distribution of cartilage thinning and thickening. These results provide preliminary evidence of a different spatial pattern of cartilage change between individuals who will develop accelerated versus typical KOA. These data suggest there may be different mechanisms driving the early structural disease progression between accelerated versus typical KOA. Clin. Anat. 32:369–378, 2019. © 2018 Wiley Periodicals, Inc.     

Socially oriented thinking and the biological stress response: Thinking of friends and family predicts trajectories of salivary cortisol decline

The cortisol stress response has been related to perceived social support, but previous studies rely on self‐reported social support variables. The cortisol recovery phase in particular has been theorized to serve a social coping function, but individual differences in recovery slope have not yet been examined in relation to social coping‐relevant indices. This study addressed these gaps by examining the relationship of cortisol trajectories after a socioevaluative task to individual differences in covertly assessed cognitions related to close social relationships. We examined trajectories of cortisol change related to socially oriented thinking, the semi‐implicit activation of cognitive representations of friends or family. Young adults (N = 64) gave salivary cortisol samples before and for 45 min after a speech task. Participants' thoughts were sampled repeatedly; the frequency of words related to friends or family was assessed to index socially oriented thinking. A free curve slope intercept latent growth curve model showed excellent fit with the cortisol data. Socially oriented thinking was unrelated to overall magnitude of cortisol response to the task (latent intercept) but predicted the latent cortisol trajectory, independently of cortisol intercept and baseline cortisol levels. Socially oriented thinkers showed more gradual cortisol declines, whereas nonsocially oriented thinkers showed a steeper downslope driven primarily by cortisol changes 45 min after the task. Individual differences in socially oriented thinking may manifest in different rates of biological changes following a performance task.     

Twin pregnancy with a chimeric androgenetic and biparental placenta in one twin displaying placental mesenchymal dysplasia phenotype

OBJECTIVES: The aim was to report an unusual trizygotic pregnancy that resulted in live-born twins. The placenta of one twin had placental mesenchymal dysplasia (PMD), which resulted from a chimeric fusion of an androgenetic zygote and a normal biparental zygote. The literature review was summarized. METHODS: The case was first detected by prenatal ultrasound, and was then followed by a histologic and detailed genetic investigation. The literature on PMD, complete hydatidiform moles (CHMs), and placental mosaicism and chimerism was also reviewed. RESULTS: One placenta of a twin pregnancy was noted to be diffusely cystic and enlarged. The macroscopic and microscopic findings were consistent with the diagnosis of PMD; however, genetic findings confirmed confined placental chimerism involving a normal biparental 46,XY male conceptus and an androgenetic 46,XX complete hydatidiform mole. CONCLUSIONS: This case represents a rare placental abnormality, PMD, which may have a diverse etiology. Therefore, detailed histologic and genetic analysis were performed for an accurate diagnosis.     

Internet-Based Behavioral Activation Program for Depression and Problem Gambling: Lessons Learned from Stakeholder Interviews

International Journal of Mental Health and Addiction - Behavioral activation (BA) is a well-established treatment for depression, often used as an adjuvant for gambling disorder. Internet-based BA...     

Heightened Hippocampal β-Adrenergic Receptor Function Drives Synaptic Potentiation and Supports Learning and Memory in the TgF344-AD Rat Model during Prodromal Alzheimer's Disease

The central noradrenergic (NA) system is critical for the maintenance of attention, behavioral flexibility, spatial navigation, and learning and memory, those cognitive functions lost first in early Alzheimer''s disease (AD). In fact, the locus coeruleus (LC), the sole source of norepinephrine (NE) for >90% of the brain, is the first site of pathologic tau accumulation in human AD with axon loss throughout forebrain, including hippocampus. The dentate gyrus is heavily innervated by LC–NA axons, where released NE acts on β-adrenergic receptors (ARs) at excitatory synapses from entorhinal cortex to facilitate long-term synaptic plasticity and memory formation. These synapses experience dysfunction in early AD before cognitive impairment. In the TgF344-AD rat model of AD, degeneration of LC–NA axons in hippocampus recapitulates human AD, providing a preclinical model to investigate synaptic and behavioral consequences. Using immunohistochemistry, Western blot analysis, and brain slice electrophysiology in 6- to 9-month-old wild-type and TgF344-AD rats, we discovered that the loss of LC–NA axons coincides with the heightened β-AR function at medial perforant path–dentate granule cell synapses that is responsible for the increase in LTP magnitude at these synapses. Furthermore, novel object recognition is facilitated in TgF344-AD rats that requires β-ARs, and pharmacological blockade of β-ARs unmasks a deficit in extinction learning only in TgF344-AD rats, indicating a greater reliance on β-ARs in both behaviors. Thus, a compensatory increase in β-AR function during prodromal AD in TgF344-AD rats heightens synaptic plasticity and preserves some forms of learning and memory.SIGNIFICANCE STATEMENT The locus coeruleus (LC), a brain region located in the brainstem which is responsible for attention and arousal, is damaged first by Alzheimer''s disease (AD) pathology. The LC sends axons to hippocampus where released norepinephrine (NE) modulates synaptic function required for learning and memory. How degeneration of LC axons and loss of NE in hippocampus in early AD impacts synaptic function and learning and memory is not well understood despite the importance of LC in cognitive function. We used a transgenic AD rat model with LC axon degeneration mimicking human AD and found that heightened function of β-adrenergic receptors in the dentate gyrus increased synaptic plasticity and preserved learning and memory in early stages of the disease.     

Brain activation in response to overt and covert fear and happy faces in women with borderline personality disorder

Borderline personality disorder (BPD) is a serious condition involving emotion dysregulation. Past research has identified BPD-associated differences within fronto-limbic circuitry during conditions of processing negative emotion. Functional magnetic resonance imaging (fMRI) paradigms that incorporate overt and covert (masked) presentations of emotional stimuli can provide complementary information about neural systems underlying emotion processing (e.g., both slow [overt] and fast [covert; automatic] processing pathways). This study examined brain activation during processing of overt and covert presentations of emotional faces in 12 women with BPD and 12 age-matched healthy controls. To assess a range of emotional valence and arousal, we examined responses to fear, happy and neutral expressions. All participants underwent an fMRI scanning session in which participants passively viewed emotional faces. Scanning sessions consisted of 5 runs including: (1) Overt Fear (OF) versus Neutral (N), (2) Covert Fear (CF) versus Covert Neutral (CN), (3) Overt Happy (OH) versus N, (4) Covert Happy (CH) versus CN, and (5) N versus fixation. We compared whole-brain activation between groups for each run. In response to overt fear, BPD patients showed greater activation both in left amygdala and in several frontal cortical regions. There were no significant differences in brain activation in response to overt happy faces. In response to covert fear and covert happy stimuli, the BPD group also showed greater activation than controls in several regions including frontal and temporal cortical regions, as well as cerebellum and thalamus. These findings add to prior reports suggesting increased amygdala activation in BPD, but we found this only in the overt fear versus fixation condition. In this sample, BPD patients showed hyper-activation, rather than hypo-activation, of cortical regulatory regions during overt fear. Enhanced cortical recruitment in response to covert fear and happy faces in BPD could reflect a more extended response system in which stimuli that typically only activate automatic pathways are additionally tapping into cortical regulatory systems. The observation of this pattern both in response to fear and in response to happy presentations suggests that the effect of arousal may be as or more impactful than the effect of emotional valence.     

Understanding the relationship between co-occurring PTSD and MDD: symptom severity and affect

How to best understand theoretically the nature of the relationship between co-occurring PTSD and MDD (PTSD + MDD) is unclear. In a sample of 173 individuals with chronic PTSD, we examined whether the data were more consistent with current co-occurring MDD as a separate construct or as a marker of posttraumatic stress severity, and whether the relationship between PTSD and MDD is a function of shared symptom clusters and affect components. Results showed that the more severe depressive symptoms found in PTSD + MDD as compared to PTSD remained after controlling for PTSD symptom severity. Additionally, depressive symptom severity significantly predicted co-occurring MDD even when controlling for PTSD severity. In comparison to PTSD, PTSD + MDD had elevated dysphoria and re-experiencing – but not avoidance and hyperarousal – PTSD symptom cluster scores, higher levels of negative affect, and lower levels of positive affect. These findings provide support for PTSD and MDD as two distinct constructs with overlapping distress components.     

The impact of neurocognitive impairment on occupational recovery of clinically stable patients with bipolar disorder: a prospective study

Bearden CE, Shih VH, Green MF, Gitlin M, Sokolski KN, Levander E, Marusak S, Hammen C, Sugar CA, Altshuler LL. The impact of neurocognitive impairment on occupational recovery of clinically stable patients with bipolar disorder: a prospective study.
Bipolar Disord 2011: 13: 323–333. © 2011 The Authors.
Journal compilation © 2011 John Wiley & Sons A/S. Objective: Many patients with bipolar disorder do not regain their premorbid level of occupational functioning even after mood episodes have resolved. The reasons for this are not well understood. We evaluated the relationship between neurocognition and occupational function in bipolar disorder patients, following symptomatic recovery. Methods: A total of 79 previously employed adults with bipolar I disorder who achieved symptomatic recovery (i.e., at least six weeks clinically euthymic) following a manic episode underwent a neurocognitive evaluation and assessment of occupational functioning. Study participants were evaluated every three months thereafter for up to nine months. Factor analysis was applied to reduce the initial set of neurocognitive variables to five domains: episodic memory, working memory/attention, executive function, visual scanning, and speed of processing. Multiple logistic regression models were used to examine the joint predictive values of these domains for determining occupational recovery. Results: At the time of symptomatic recovery, four of five neurocognitive factors were significant predictors of concomitant occupational recovery and the fifth, executive function, showed a trend in the same direction. For those not occupationally recovered at baseline, longitudinal analyses revealed that changes between baseline and the three‐month follow‐up timepoint in most cognitive domains were robust and highly significant predictors of occupational recovery at three months. Conclusions: These findings indicate that better neurocognitive function in multiple domains and improvement in these domains over time are strongly predictive of subsequent occupational recovery. Treatments that target cognitive deficit may therefore have potential for improving long‐term vocational functioning in bipolar illness.     

Group-Based Trajectory Modeling of Suppression Ratio After Cardiac Arrest

Background

Existing studies of quantitative electroencephalography (qEEG) as a prognostic tool after cardiac arrest (CA) use methods that ignore the longitudinal pattern of qEEG data, resulting in significant information loss and precluding analysis of clinically important temporal trends. We tested the utility of group-based trajectory modeling (GBTM) for qEEG classification, focusing on the specific example of suppression ratio (SR).

Methods

We included comatose CA patients hospitalized from April 2010 to October 2014, excluding CA from trauma or neurological catastrophe. We used Persyst^®v12 to generate SR trends and used semi-quantitative methods to choose appropriate sampling and averaging strategies. We used GBTM to partition SR data into different trajectories and regression associate trajectories with outcome. We derived a multivariate logistic model using clinical variables without qEEG to predict survival, then added trajectories and/or non-longitudinal SR estimates, and assessed changes in model performance.

Results

Overall, 289 CA patients had ≥36 h of EEG yielding 10,404 h of data (mean age 57 years, 81 % arrested out-of-hospital, 33 % shockable rhythms, 31 % overall survival, 17 % discharged to home or acute rehabilitation). We identified 4 distinct SR trajectories associated with survival (62, 26, 12, and 0 %, P < 0.0001 across groups) and CPC (35, 10, 4, and 0 %, P < 0.0001 across groups). Adding trajectories significantly improved model performance compared to adding non-longitudinal data.

Conclusions

Longitudinal analysis of continuous qEEG data using GBTM provides more predictive information than analysis of qEEG at single time-points after CA.