Psychological and behavioral treatments for medical disorders. An annotated bibliography. Volume 2: Disorders of the immune system

1987 ◽  
Vol 31 (4) ◽  
pp. 532
Author(s):  
David F. Peck
2021 ◽  
Vol 12 ◽  
Author(s):  
Salma Sultan ◽  
Mohammed El-Mowafy ◽  
Abdelaziz Elgaml ◽  
Tamer A. E. Ahmed ◽  
Hebatoallah Hassan ◽  
...  

Inflammatory bowel diseases (IBD) are chronic medical disorders characterized by recurrent gastrointestinal inflammation. While the etiology of IBD is still unknown, the pathogenesis of the disease results from perturbations in both gut microbiota and the host immune system. Gut microbiota dysbiosis in IBD is characterized by depleted diversity, reduced abundance of short chain fatty acids (SCFAs) producers and enriched proinflammatory microbes such as adherent/invasive E. coli and H2S producers. This dysbiosis may contribute to the inflammation through affecting either the immune system or a metabolic pathway. The immune responses to gut microbiota in IBD are extensively discussed. In this review, we highlight the main metabolic pathways that regulate the host-microbiota interaction. We also discuss the reported findings indicating that the microbial dysbiosis during IBD has a potential metabolic impact on colonocytes and this may underlie the disease progression. Moreover, we present the host metabolic defectiveness that adds to the impact of symbiont dysbiosis on the disease progression. This will raise the possibility that gut microbiota dysbiosis associated with IBD results in functional perturbations of host-microbiota interactions, and consequently modulates the disease development. Finally, we shed light on the possible therapeutic approaches of IBD through targeting gut microbiome.


Author(s):  
Maya Henry

Abstract Primary progressive aphasia (PPA) is a relatively new diagnostic entity, for which few behavioral treatments have been investigated. Recent work has helped to clarify the nature of distinct PPA variants, including a nonfluent variant (NFV-PPA), a logopenic variant (LV-PPA), and a semantic variant (SV-PPA). This paper reviews treatment research to date in each subtype of PPA, including restitutive, augmentative, and functional approaches. The evidence suggests that restitutive behavioral treatment can result in improved or stabilized language performance within treated domains. Specifically, sentence production and lexical retrieval have been addressed in NFV-PPA, whereas lexical retrieval has been the primary object of treatment in LV and SV-PPA. Use of augmentative communication techniques, as well as implementation of functional communication approaches, also may result in improved communication skills in individuals with PPA. The ideal treatment approach may be one that combines restitutive, augmentative, and functional approaches to treatment, in order to maximize residual cognitive-linguistic skills in patients. Additional research is warranted to determine which modes of treatment are most beneficial in each type of PPA at various stages of severity.


2014 ◽  
Vol 222 (3) ◽  
pp. 148-153 ◽  
Author(s):  
Sabine Vits ◽  
Manfred Schedlowski

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.


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