Post-stroke depression (PSD) is a biopsychosocial disorder that affects individuals who have suffered a stroke at any point. PSD has a 20 to 60 percent reported prevalence among stroke survivors. Its effects are usually adverse, can lead to disability, and may increase mortality if not managed or treated early. PSD is linked to several other medical conditions, including anxiety, hyper-locomotor activity, and poor functional recovery. Despite significant awareness of its adverse impacts, understanding the pathogenesis of PSD has proved challenging. The exact pathophysiology of PSD is unknown, yet its complexity has been definitively shown, involving mechanisms such as dysfunction of monoamine, the glutamatergic systems, the gut-brain axis, and neuroinflammation. The current effectiveness of PSD treatment is about 30–40 percent of all cases. In this review, we examined different pathophysiological mechanisms and current pharmacological and non-pharmacological approaches for the treatment of PSD.

Traumatic brain injury (TBI) is associated with significant cognitive and psychiatric conditions. Neuropsychiatric symptoms can persist for years following brain injury, causing major disruptions in patients’ lives. In this review, we examine the role of glutamate as an aftereffect of TBI that contributes to the development of neuropsychiatric conditions. We hypothesize that TBI causes long-term blood–brain barrier (BBB) dysfunction lasting many years and even decades. We propose that dysfunction in the BBB is the central factor that modulates increased glutamate after TBI and ultimately leads to neurodegenerative processes and subsequent manifestation of neuropsychiatric conditions. Here, we have identified factors that determine the upper and lower levels of glutamate concentration in the brain after TBI. Furthermore, we consider treatments of disruptions to BBB integrity, including repairing the BBB and controlling excess glutamate, as potential therapeutic modalities for the treatment of acute and chronic neuropsychiatric conditions and symptoms. By specifically focusing on the BBB, we hypothesize that restoring BBB integrity will alleviate neurotoxicity and related neurological sequelae.

Background: Full level 1 personal protective equipment (PPE) is used in various domains and contexts. Prior research has shown influences of such equipment on performance, comfort, and contamination levels. The coronavirus disease (COVID-19) pandemic forced a pervasive requirement of PPE, with little preparation, rushed deployment, inadequate time for training, and massive use by personnel who are inexperienced or not qualified in its effective use. Objective: This study aims to examine the key human factors (physical and ergonomic, perceptual and cognitive) that influence the use of level 1 PPE when attending to patients with suspected or confirmed COVID-19. Methods: The research approach consisted of a short survey disseminated to health care professionals in two countries, Israel and Portugal, with similar demographics and health care systems. The survey included 10 items with a 5-point Likert scale regarding the key human factors involved in level 1 PPE, as identified in prior research. Results: A total of 722 respondents from Israel and 301 respondents from Portugal were included in the analysis. All the respondents reported using level 1 PPE with patients with COVID-19 in the range of several hours daily to several hours weekly. The Cronbach α was .73 for Israel and .75 for Portugal. Responses showed high levels of difficulty, with medians of 4 for items related to discomfort (n=539/688, 78% in Israel; n=328/377, 87% in Portugal), hearing (n=236/370, 64% in Portugal; n=321/642, 50% in Israel), seeing (n=697/763, 89% in Israel; n=317/376, 84% in Portugal), and doffing (n=290/374, 77% in Portugal; n=315/713, 44% in Israel). A factor analysis showed a set of strongly related variables consisting of hearing, understanding speech, and understanding the situation. This suggests that degradation in communication was strongly associated with degradation in situational awareness. A subsequent mediation analysis showed a direct effect of PPE discomfort on situational awareness (P<.001); this was also influenced (mediated) by difficulties in communicating, namely in hearing and understanding speech. Conclusions: In 2020, the COVID-19 pandemic is paving the way for updating PPE design. The use of already deployed technology affords ample opportunities to improve, adapt, and overcome caveats. The findings here suggest that the use of level 1 PPE with patients with COVID-19 has perceptual and cognitive effects, in addition to physical and ergonomic influences. Efforts should be taken to mitigate the harmful effects of such influences, both regarding the performance of medical actions and the risk of contamination to health care workers. Such efforts involve the design of PPE; the introduction of technologies to enhance vision, hearing, and communicating during the use of PPE; and training staff in using the equipment and in effective communication and teamwork protocols.

Depression is a significant cause of disability and affects millions worldwide; however, antidepressant therapies often fail or are inadequate. Current medications for treating major depressive disorder can take weeks or months to reach efficacy, have troubling side effects, and are limited in their long-term capabilities. Recent studies have identified a new set of glutamate-based approaches, such as blood glutamate scavengers, which have the potential to provide alternatives to traditional antidepressants. In this review, we hypothesize as to the involvement of the glutamate system in the development of depression. We identify the mechanisms underlying glutamate dysregulation, offering new perspectives on the therapeutic modalities of depression with a focus on its relationship to blood–brain barrier (BBB) permeability. Ultimately, we conclude that in diseases with impaired BBB permeability, such as depression following stroke or traumatic brain injury, or in neurogenerative diseases, the glutamate system should be considered as a pathway to treatment. We propose that drugs such as blood glutamate scavengers should be further studied for treatment of these conditions.