Late-Onset Bipolar Disorder: Considerations for Diagnosis and Treatment.

Bipolar I disorder is characterized by the presence of at least one manic episode (DSM-5). Despite a decent percentage of individuals being diagnosed later in life, there currently exist no formal treatment guidelines for late-onset bipolar disorder (LOBD), which remains poorly understood. Typically, manic or manic-like episodes in elderly individuals can be thought of as arising from a secondary, physical cause. However, in the absence of a pre-existing neurological disorder - and when laboratory, imaging, and exam findings do not fully support a neurological picture - the determination of a structural versus primary etiology for LOBD becomes challenging. We present the case of Ms. S, a 79-year-old woman with a past psychiatry history of bipolar disorder diagnosed after 2012 and non-contributory past medical history who was admitted to a state mental hospital on a probate court order from local jail secondary to labile mood and physical aggression toward an officer. Initial labs were remarkable for slightly elevated low-density lipoprotein and a B12 at the lower limit of normal. She was started on a regiment oral B12 supplement, valproic acid 500 mg twice daily, haloperidol 5 mg nightly, and diphenhydramine 25 mg nightly. Despite her medication regimen, she continued to display marked mood lability, tangential thought processes, grandiose delusions, and paranoia. A CT head one week into admission revealed bilateral periventricular white-matter hyperintensities with decreased attenuation and chronic white-matter infarcts. She underwent five sessions of electroconvulsive therapy (ECT), with significantly improving Montreal Cognitive Assessment and Young Mania Rating Scale scores. At the time of discharge on day 32, the patient was fully oriented to self and surroundings with good hygiene, a normal rate of speech, euthymic mood, and congruent affect. The case of Ms. S underscores the importance of a thorough workup to rule out secondary causes of mania. In addition, it is a clarion call for revisiting and researching a comprehensive management approach to LOBD, for which serial cognitive assessments and ECTs may play an important role.

Examining educational attainment and allostatic load in non-Hispanic Black women.

BACKGROUND: Research suggests that non-Hispanic Black (henceforth, Black) women and people with lower educational attainment have higher levels of allostatic load (AL). This study sought to determine the association between educational attainment and AL among a large sample of Black women. METHODS: We analyzed data among 4177 Black women from the National Health and Nutrition Examination Survey years 1999-2018. AL score was defined as the total for abnormal measures of eight biomarkers. We further categorized participants with AL score greater than or equal to 4 as having high AL. We calculated mean estimates of total allostatic load scores using generalized linear models. We performed modified Poisson Regression models with robust variance estimation to estimate prevalence ratios (PRs) of high allostatic load and their associated 95% confidence intervals (CIs) by educational attainment. RESULTS: Black women with a college degree or higher had the lowest prevalence of high allostatic load (31.8% vs. 42.7%, 36.3%, 36.6%), and age adjusted mean allostatic load scores (mean = 1.90 vs. mean = 2.34, mean = 1.99, mean = 2.05) when compared to Black women with less than a high school diploma, high school diploma or GED, and some college or associates degree respectively. Even after accounting for age, poverty-to-income ratio, smoking, congestive heart failure, and heart attack, Black college graduates had an 14.3% lower prevalence of high allostatic load (PR = 0.857, 95% CI 0.839-0.876) when compared to Black women with lower educational attainment. CONCLUSIONS: Black women with a baccalaureate degree or higher educational attainment had lower allostatic load compared to Black women with less than a high school education. This finding further confirms higher education is a social determinant of health. Future research should explore differences in AL by more granular degree types.

Correlates of COVID-19 Vaccine Hesitancy among a Community Sample of African Americans Living in the Southern United States.

In the United States, African Americans (AAs) have been disproportionately affected by COVID-19 mortality. However, AAs are more likely to be hesitant in receiving COVID-19 vaccinations when compared to non-Hispanic Whites. We examined factors associated with vaccine hesitancy among a predominant AA community sample. We performed a cross-sectional analysis on data collected from a convenience sample of 257 community-dwelling participants in the Central Savannah River Area from 5 December 2020, through 17 April 2021. Vaccine hesitancy was categorized as resistant, hesitant, and acceptant. We estimated relative odds of vaccine resistance and vaccine hesitancy using polytomous logistic regression models. Nearly one-third of the participants were either hesitant (n = 40, 15.6%) or resistant (n = 42, 16.3%) to receiving a COVID-19 vaccination. Vaccine-resistant participants were more likely to be younger and were more likely to have experienced housing insecurity due to COVID-19 when compared to both acceptant and hesitant participants, respectively. Age accounted for nearly 25% of the variation in vaccine resistance, with 21-fold increased odds (OR: 21.93, 95% CI: 8.97-5.26-91.43) of vaccine resistance in participants aged 18 to 29 compared to 50 and older adults. Housing insecurity accounted for 8% of the variation in vaccine resistance and was associated with 7-fold increased odds of vaccine resistance (AOR: 7.35, 95% CI: 1.99-27.10). In this sample, AAs under the age of 30 and those experiencing housing insecurity because of the COVID-19 pandemic were more likely to be resistant to receiving a free COVID-19 vaccination.

Cellular reactions and compensatory tissue re-organization during spontaneous recovery after spinal cord injury in neonatal mice.

Following incomplete spinal cord injuries, neonatal mammals display a remarkable degree of behavioral recovery. Previously, we have demonstrated in neonatal mice a wholesale re-establishment and reorganization of synaptic connections from some descending axon tracts (Boulland et al.: PLoS One 8 (2013)). To assess the potential cellular mechanisms contributing to this recovery, we have here characterized a variety of cellular sequelae following thoracic compression injuries, focusing particularly on cell loss and proliferation, inflammation and reactive gliosis, and the dynamics of specific types of synaptic terminals. Early during the period of recovery, regressive events dominated. Tissue loss near the injury was severe, with about 80% loss of neurons and a similar loss of axons that later make up the white matter. There was no sign of neurogenesis, no substantial astroglial or microglial proliferation, no change in the ratio of M1 and M2 microglia and no appreciable generation of the terminal complement peptide C5a. One day after injury the number of synaptic terminals on lumbar motoneurons had dropped by a factor of 2, but normalized by 6 days. The ratio of VGLUT1/2+ to VGAT+ terminals remained similar in injured and uninjured spinal cords during this period. By 24 days after injury, when functional recovery is nearly complete, the density of 5-HT+ fibers below the injury site had increased by a factor of 2.5. Altogether this study shows that cellular reactions are diverse and dynamic. Pronounced recovery of both excitatory and inhibitory terminals and an increase in serotonergic innervation below the injury, coupled with a general lack of inflammation and reactive gliosis, are likely to contribute to the recovery. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 77: 928-946, 2017.