Although there are dozens of books on cognitive therapy of depression, a majority are edited volumes and relatively few are distinguished by the comprehensive mastery of the material and clarity of exposition apparent in this book by Clark, Beck, and Alford. This volume offers a relatively up-to-date (circa 1999) and scholarly review of the phenomenology of depressive disorders from the cognitive perspective, along with detailed evaluations of the literature pertaining to the key hypotheses of the cognitive model of depression.

The book is well written, but it is not for the cognitive therapy neophyte. It is rather lengthy and detailed. Moreover, as might be expected, the discussions of criticisms of the cognitive model are somewhat partisan, and the authors consistently present the cognitive model as dynamic and organic (as opposed to static) in response to new and at times contradictory data. Nevertheless, it provides a valuable source companion to the classic but outdated treatment manual originally published in 1979 by Dr. Beck and colleagues (Cognitive Therapy of Depression) and the excellent how-to book by Dr. Judith Beck, Cognitive Therapy: Basics and Beyond, which was published in 1995.

Subheads, periodic summaries, and statements of key points within each chapter focus the reader's attention and enhance comprehension; the authors are, after all, expert cognitive therapists. There is a minimum of redundancy across the 11 chapters, and although the copyediting is not infallible (e.g., influential early behaviorist Charles Ferster is referred to as “Fester” in both the text and the reference list), typographical errors are few.

As a treatment researcher, I was disappointed that the authors did not devote at least one chapter to reviewing the comparative outcome research studies of CT. Outcomes data has been one of the key aspects of the scientific foundation of CT for nearly 25 years.1 This is a shortcoming, particularly in view of work linking early evidence of CT's superiority (over other therapies) to strong allegiance effects2 and the increasing number of studies in which CT has not performed so well under more “neutral”3,4 or even potentially “allegiance-disadvantaged”5–7 conditions. Ultimately, the most pragmatic benefit of an elegant, scientifically strong model of psychopathology is the ability to translate such knowledge into greater or more enduring benefits for our patients. In this regard, it is not yet clear that the elaborate suprastructure of schema theory actually adds such benefits relative to simpler behavioral5 or interpersonal6 models of intervention.

Scientific Foundations of Cognitive Theory and Therapy of Depression

Abstract Background After almost 2 years of fighting against SARS-CoV-2 pandemic, the number of patients enduring persistent symptoms long after acute infection is a matter of concern. This set of symptoms was referred to as “long COVID”, and it was defined more recently as “Post COVID-19 condition” by the World health Organization (WHO). Although studies have revealed that long COVID can manifest whatever the severity of inaugural illness, the underlying pathophysiology is still enigmatic. Aim To conduct a comprehensive review to address the putative pathophysiology underlying the persisting symptoms of long COVID. Method We searched 11 bibliographic databases (Cochrane Library, JBI EBP Database, Medline, Embase, PsycInfo, CINHAL, Ovid Nursing Database, Journals@Ovid, SciLit, EuropePMC, and CoronaCentral). We selected studies that put forward hypotheses on the pathophysiology, as well as those that encompassed long COVID patients in their research investigation. Results A total of 98 articles were included in the systematic review, 54 of which exclusively addressed hypotheses on pathophysiology, while 44 involved COVID patients. Studies that included patients displayed heterogeneity with respect to the severity of initial illness, timing of analysis, or presence of a control group. Although long COVID likely results from long-term organ damage due to acute-phase infection, specific mechanisms following the initial illness could contribute to the later symptoms possibly affecting many organs. As such, autonomic nervous system damage could account for many symptoms without clear evidence of organ damage. Immune dysregulation, auto-immunity, endothelial dysfunction, occult viral persistence, as well as coagulation activation are the main underlying pathophysiological mechanisms so far. Conclusion Evidence on why persistent symptoms occur is still limited, and available studies are heterogeneous. Apart from long-term organ damage, many hints suggest that specific mechanisms following acute illness could be involved in long COVID symptoms. KEY MESSAGES Long-COVID is a multisystem disease that develops regardless of the initial disease severity. Its clinical spectrum comprises a wide range of symptoms. The mechanisms underlying its pathophysiology are still unclear. Although organ damage from the acute infection phase likely accounts for symptoms, specific long-lasting inflammatory mechanisms have been proposed, as well. Existing studies involving Long-COVID patients are highly heterogeneous, as they include patients with various COVID-19 severity levels and different time frame analysis, as well.

/pdf/pathophysiology-and-mechanism-of-long-covid-a-comprehensive-13wntrk5.pdf

Pathophysiology and mechanism of long COVID: a comprehensive review

The coronavirus disease (COVID-19), caused by severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection, is leading to unknown and unusual health conditions that are challenging to manage. Post-COVID-19 syndrome is one of those challenges, having become increasingly common as the pandemic evolves. The latest estimates suggest that 10 to 20% of the SARS-CoV-2 patients who undergo an acute symptomatic phase are experiencing effects of the disease beyond 12 weeks after diagnosis. Although research is beginning to examine this new condition, there are still serious concerns about the diagnostic identification, which limits the best therapeutic approach. Exercise programs and physical activity levels are well-known modulators of the clinical manifestations and prognosis in many chronic diseases. This narrative review summarizes the up-to-date evidence on post-COVID-19 syndrome to contribute to a better knowledge of the disease and explains how regular exercise may improve many of these symptoms and could reduce the long-term effects of COVID-19.

Post-COVID-19 Syndrome and the Potential Benefits of Exercise

Simple Summary The coronavirus can elude the immune response, potentially spreading to cells other than the respiratory tract’s epithelial cells. The neuro-invasive potential of certain coronaviruses has been observed in the severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS). Based on past outbreaks, including SARS, MERS, and current reports of neuropsychiatric complications following COVID-19, many survivors may be at risk of a number of neuropsychiatric sequelae. Mounting evidence has shown the presence of mental health implications in COVID-19 survivors. This review shows that psychological symptoms including anxiety, depression, and post-traumatic stress disorder (PTSD) have an association with post-COVID-19 infection. The exact cause of these psychiatric sequelae is yet to be determined, but it seems to involve environmental, psychological, and biological factors. Although there are variations in terms of risk factors and the prevalence rate of these psychological symptoms, risk factors including the female gender and having a history of psychiatric disorders appears to be consistent a across few studies, and there are studies showing a higher prevalence rate among post-COVID-19 survivors than among the general population. A therapeutic intervention commonly used to alleviate these psychological symptoms are psychotropic medications, but probiotics could be a safe adjunctive treatment to improve these symptoms. Abstract There is growing evidence of studies associating COVID-19 survivors with increased mental health consequences. Mental health implications related to a COVID-19 infection include both acute and long-term consequences. Here we discuss COVID-19-associated psychiatric sequelae, particularly anxiety, depression, and post-traumatic stress disorder (PTSD), drawing parallels to past coronavirus outbreaks. A literature search was completed across three databases, using keywords to search for relevant articles. The cause may directly correlate to the infection through both direct and indirect mechanisms, but the underlying etiology appears more complex and multifactorial, involving environmental, psychological, and biological factors. Although most risk factors and prevalence rates vary across various studies, being of the female gender and having a history of psychiatric disorders seem consistent. Several studies will be presented, demonstrating COVID-19 survivors presenting higher rates of mental health consequences than the general population. The possible mechanisms by which the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) enters the brain, affecting the central nervous system (CNS) and causing these psychiatric sequelae, will be discussed, particularly concerning the SARS-CoV-2 entry via the angiotensin-converting enzyme 2 (ACE-2) receptors and the implications of the immune inflammatory signaling on neuropsychiatric disorders. Some possible therapeutic options will also be considered.

https://www.mdpi.com/2079-7737/11/1/61/pdf?version=1641114300

Psychological Symptoms in COVID-19 Patients: Insights into Pathophysiology and Risk Factors of Long COVID-19

The second year of the COVID-19 (coronavirus disease) pandemic has seen the need to identify and assess the long-term consequences of a SARS-CoV-2 infection on an individual's overall wellbeing, including adequate cognitive functioning. 'Cognitive COVID' is an informal term coined to interchangeably refer to acute changes in cognition during COVID-19 and/or cognitive sequelae with various deficits following the infection. These may manifest as altered levels of consciousness, encephalopathy-like symptoms, delirium, and loss of various memory domains. Dysexecutive syndrome is a peculiar manifestation of 'Cognitive COVID' as well. In the previous major outbreaks of viruses like SARS-CoV, MERS-CoV and Influenza. There have been attempts to understand the underlying mechanisms describing the causality of similar symptoms following SARS-CoV-2 infection. This review, therefore, is attempting to highlight the current understanding of the various direct and indirect mechanisms, focusing on the role of neurotropism of SARS-CoV-2, the general pro-inflammatory state, and the pandemic-associated psychosocial stressors in the causality of 'Cognitive COVID.' Neurotropism is associated with various mechanisms including retrograde neuronal transmission via olfactory pathway, a general hematogenous spread, and the virus using immune cells as vectors. The high amounts of inflammation caused by COVID-19, compounded with potential intubation, are associated with a deleterious effect on the cognition as well. Finally, the pandemic's unique psychosocial impact has raised alarm due to its possible effect on cognition. Furthermore, with surfacing reports of post-COVID-vaccination cognitive impairments after vaccines containing mRNA encoding for spike glycoprotein of SARS-CoV-2, we hypothesize their causality and ways to mitigate the risk. The potential impact on the quality of life of an individual and the fact that even a minor proportion of COVID-19 cases developing cognitive impairment could be a significant burden on already overwhelmed healthcare systems across the world make it vital to gather further evidence regarding the prevalence, presentation, correlations, and causality of these events and reevaluate our approach to accommodate early identification, management, and rehabilitation of patients exhibiting cognitive symptoms.

https://www.mdpi.com/2077-0383/10/15/3441/pdf

SARS-CoV-2 and the Brain: What Do We Know about the Causality of 'Cognitive COVID?

Coronavirus disease 2019 (COVID-19) is likely to have long-term mental health effects on individuals who have recovered from COVID-19 Rightly, there is a global response for recognition and planning on how to deal with mental health problems for everyone impacted by the global pandemic This does not just include COVID-19 patients but the general public and health care workers as well There is also a need to understand the role of the virus itself in the pathophysiology of mental health disorders and longer-term mental health sequelae Emerging evidence suggests that COVID-19 patients develop neurological symptoms such as headache, altered consciousness, and paraesthesia Brain tissue oedema and partial neurodegeneration have also been observed in an autopsy In addition, there are reports that the virus has the potential to cause nervous system damage Together, these findings point to a possible role of the virus in the development of acute psychiatric symptoms and long-term neuropsychiatric sequelae of COVID-19 The brain pathologies associated with COVID-19 infection is likely to have a long-term impact on cognitive processes Evidence from other viral respiratory infections, such as severe acute respiratory syndrome (SARS), suggests a potential development of psychiatric disorders, long-term neuropsychiatric disorders, and cognitive problems In this paper, we will review and evaluate the available evidence of acute and possible long-term neuropsychiatric manifestations of COVID-19 We will discuss possible pathophysiological mechanisms and the implications this will have on preparing a long-term strategy to monitor and manage such patients

/pdf/neuropsychiatric-and-cognitive-sequelae-of-covid-19-1dixhubkaw.pdf

Neuropsychiatric and Cognitive Sequelae of COVID-19

We examined whether differential self-perception influences the salience of emotional stimuli in depressive disorders, using a perceptual matching task in which geometric shapes were arbitrarily assigned to the self and an unknown other. Participants associated shapes with personal labels (e.g. "self" or "other"). Each geometric shape additionally contained a happy, sad or neutral line drawing of a face. Participants then judged whether shape-label pairs were as originally shown or re-paired, whilst facial emotion was task-irrelevant. The results showed biased responses to self-relevant stimuli compared to other-relevant stimuli, regardless of facial emotion, for both control and depressed participants. This was reflected in sensitivity (d') and drift rate (v) measures, suggesting that self-bias and a bias towards emotion may reflect different underlying processes. We further computed bias scores by subtracting the "neutral" value of each measure (acting as baseline) from the "happy" and "sad" values of each measure, indexing an "emotional bias" (EB) score for "self" and "other" separately. Compared to control participants, depressed participants exhibited reduced "happy" and "sad" emotional biases, regardless of the self-relevance of stimuli. This finding indicates that depressed participants may exhibit generalised Emotion Context Insensitivity (ECI), characterised by hyopoattention to both positive and negative information, at short stimulus presentations. The implications of this are discussed.

/pdf/self-referential-processing-and-emotion-context-4cp43levgn.pdf

Tina Malhotra

Papers

Neuropsychiatric and Cognitive Sequelae of COVID-19

Self‐Referential Processing and Emotion Context Insensitivity in Major Depressive Disorder