[Cognitive disorders and sleep disturbances in long COVID]. / Kognitive Störungen und Schlafstörungen bei Long-COVID.

BACKGROUND: During the last 2 years of the coronavirus disease 2019 (COVID-19) pandemic, knowledge about the long-term effects of the disease, the so-called long COVID, has rapidly grown; however, many questions remain unanswered, especially regarding the causes of persistent symptoms and their prognosis. Cognitive disorders and sleep disturbances are among the most frequent complaints. Both are associated with severe suffering and significant impairment in everyday functioning. OBJECTIVE: What is known about the occurrence of cognitive disorders and sleep disturbances in long COVID? What are the influencing factors and what is known about the course over time and possible underlying mechanisms? What treatment options are available? MATERIAL AND METHOD: In a narrative review, the most important findings on cognitive disorders and sleep disturbances in long COVID are presented. An overview of cohort studies with data on the prevalence and influencing factors of both symptom complexes is given. Current knowledge and hypotheses on pathophysiological mechanisms are presented and an outlook on treatment approaches is given. RESULTS: About one in five of those affected report cognitive impairment more than 3 months after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and about one third report sleep disturbances. The latter comprise symptoms of insomnia as well as hypersomnia. Cognitive impairment and sleep disturbances occur in patients with all levels of initial disease severity. There are indications of an improvement of cognitive deficits over time but further longitudinal studies are needed. CONCLUSION: In addition to the prognosis, the underlying disease mechanisms are still insufficiently understood. Furthermore, there is a great need for research on the efficacy and specific effective factors of therapeutic interventions.

Innovation in Psychotherapy, Challenges, and Opportunities: An Opinion Paper.

Psychotherapy as a field tends toward conservativism, and the rate of innovation and development of new evidence-based effective treatments has been slow. The paper explores important barriers to innovation like the dodo bird verdict and the habit of starting the development of therapeutic methods from techniques. The paper looks at the opportunities for translating basic science in psychology into psychotherapeutic techniques. Metacognitive therapy stands out from other psychotherapies by its development from basic science. The paper describes the development of the techniques detached mindfulness and attention training, how they were derived from basic science and tested for their suitability in the therapy of patients with anxiety disorders. By this process, metacognitive therapy may be an important model for the innovation process in psychotherapy.

Acute ketamine challenge increases resting state prefrontal-hippocampal connectivity in both humans and rats.

RATIONALE: Aberrant prefrontal-hippocampal (PFC-HC) connectivity is disrupted in several psychiatric and at-risk conditions. Advances in rodent functional imaging have opened the possibility that this phenotype could serve as a translational imaging marker for psychiatric research. Recent evidence from functional magnetic resonance imaging (fMRI) studies has indicated an increase in PFC-HC coupling during working-memory tasks in both schizophrenic patients and at-risk populations, in contrast to a decrease in resting-state PFC-HC connectivity. Acute ketamine challenge is widely used in both humans and rats as a pharmacological model to study the mechanisms of N-methyl-D-aspartate (NMDA) receptor hypofunction in the context of psychiatric disorders. OBJECTIVES: We aimed to establish whether acute ketamine challenge has consistent effects in rats and humans by investigating resting-state fMRI PFC-HC connectivity and thus to corroborate its potential utility as a translational probe. METHODS: Twenty-four healthy human subjects (12 females, mean age 25 years) received intravenous doses of either saline (placebo) or ketamine (0.5 mg/kg body weight). Eighteen Sprague-Dawley male rats received either saline or ketamine (25 mg/kg). Resting-state fMRI measurements took place after injections, and the data were analyzed for PFC-HC functional connectivity. RESULTS: In both species, ketamine induced a robust increase in PFC-HC coupling, in contrast to findings in chronic schizophrenia. CONCLUSIONS: This translational comparison demonstrates a cross-species consistency in pharmacological effect and elucidates ketamine-induced alterations in PFC-HC coupling, a phenotype often disrupted in pathological conditions, which may give clue to understanding of psychiatric disorders and their onset, and help in the development of new treatments.