Meta-analysis on the data from the Hamilton Rating Scale for Depression showed that cognitive therapy compared with ‘treatment as usual’ significantly reduced depressive symptoms (mean difference −2.15 (95% confidence interval −3.70 to −0.60; P<0.007, no heterogeneity)).
Full Answer
What makes cognitive rehabilitation methods effective?
In order for cognitive rehabilitation methods to be effective, patients must be adequately engaged and motivated to not only begin a rehabilitation program but also to remain involved in the intervention until a therapeutic dosage can be attained.
Does treatment as usual matter in clinical trials of cognitive-based psychotherapy?
Treatment as usual (TAU) as a control condition in trials of cognitive behavioural-based psychotherapy for self-harm: Impact of content and quality on outcomes in a systematic review TAU content and quality represents an important source of heterogeneity between trials of psychotherapeutic interventions for prevention of self-harm.
Can exercise interventions reduce cognitive impairment in dementia?
Therefore, taking exercise intervention in the early stage of MCI and healthy aging at the risk of AD could slow down the process of cognitive impairment and provide a promising cost-effective nonpharmacological therapy to dementia. 1. Introduction
Do individuals with higher levels of reserve intelligence benefit from cognitive therapy?
Individuals deemed to have greater reserves, either through education or lifelong mentally demanding professions or lifestyles, have a reduced risk of developing dementia (Stern, 2006) and may benefit more from cognitive therapies (Scarmeas and Stern, 2004).
Why is improving cognitive function important?
Cognitive function serves a critical role in everyday behavior and social behavior. For instance, when one goes shopping, it is necessary to memorize information about what to buy, how to make a proper judgment to buy, and how to have a conversation with shop assistants.
How does cognitive affect mental health?
The literature reviewed suggests that cognitive deficits are core features of mental health conditions such as schizophrenia and affective disorders, including bipolar and depression. Cognitive impairments may include problems with attention, memory recall, planning, organising, reasoning and problem solving.
What can impact cognitive function?
Factors affecting cognitive impairment that have been identified so far include age, educational period, gender [6-10], health life factors such as drinking and smoking [7], depression [11], social factors such as social activity and occupation, history of disease, and body mass index (BMI) [12].
What is the treatment of cognitive disorder?
These medications include: Benzodiazepines, used to treat conditions such as anxiety, seizures and sleep disturbances. Anticholinergics, which affect chemicals in the nervous system to treat many different types of conditions. Antihistamines, often used to manage allergy symptoms.
Why is cognitive health important?
It is important to maintain cognitive health through regular mental challenges, because cognitive capacity is associated with one's ability to perform both complex and basic activities of daily living. Cognitive decline disrupts basic abilities such as bathing, dressing, and using the phone.
How does mental illness affect cognitive development?
Many people experience memory lapses as they get older, but when some- one is depressed the forgetfulness is more severe. People with mental illness who abuse drugs and alcohol are very likely to experience cognitive problems. Drug and alcohol abuse alone can impair attention, memory and thinking skills.
How can I improve my cognitive ability?
This article outlines 22 brain exercises that may help boost memory, cognition, and creativity.Meditation. Share on Pinterest Gen Sadakane/EyeEm/Getty Images. ... Visualizing more. ... Playing games. ... Practicing crossword puzzles. ... Completing jigsaw puzzles. ... Playing sudoku. ... Playing checkers. ... Learning new skills.More items...•
How can students improve their cognitive skills?
5 Core Training Techniques to Improve Cognitive Skills:Strong Foundation. A healthy brain naturally seeks to operate as efficiently as possible. ... Repetition. With repetition, a cognitive skill can eventually become a stored routine. ... New Activities. ... Progressive Drills. ... Feedback.
What are the factors that influence cognitive development?
The risk factors and interventions influencing cognitive development in children can be divided into three domains: nutrition, environment, and maternal-child interactions.
How does cognitive impairment affect a person?
Some common signs of cognitive impairment include memory loss, frequently asking the same question or repeating the same story over and over, difficulty performing familiar tasks, trouble coming up with the right words to name objects, frequently forgetting events and appointments, not recognizing familiar people and ...
Is there treatment for mild cognitive impairment?
There currently is no standard treatment or approved medication for MCI, but there are things a person can do that may help them stay healthy and deal with changes in their thinking. Because MCI may be an early sign of more serious memory problems, it's important to see a doctor or specialist every six to 12 months.
What are some of the treatment modalities and support used with neurocognitive disorders?
Treatments for neurocognitive disorders may include:bed rest to give injuries time to heal.pain medications, such as indomethacin, to relieve headaches.antibiotics to clear remaining infections affecting the brain, such as meningitis.surgery to repair any severe brain damage.More items...
What is MCI in dementia?
Mild cognitive impairment (MCI) represents a transition stage of cognitive functioning between normal aging and dementia, which represents newly acquired cognitive deficits that are more severe than individuals with the same age and educational background [67] or emerge subjective concern regarding change in cognition while functional abilities in everyday life are preserved [68, 69]. The cognitive dysfunctions including episodic and semantic memory [3, 14], working memory, and executive function [3] are discernible in MCI, and the initial symptom of MCI is a decline in memory (amnestic MCI) [67] such as familiar names [70]. Moreover, pathological changes such as amyloid plaques and agminated tau protein in regions of entorhinal cortex, parahippocampal gyrus, and subiculum in the medial temporal lobes can be tracked in MCI as well, although it may be not that severe compared with AD [71]. MCI patients have higher risk of developing AD, 40% of individuals diagnosed with MCI progressing to AD four years later [72]. However, there is a process for the transition from normal cognition to mild cognitive impairment and to Alzheimer's disease that with typical clinical symptoms. MCI patients could own normal cognitive functioning if with effective intervention while suffer rapid decline as the progression of the disease [73] and measures need to be taken at early stage as a result. Nevertheless, the thorniest problem is that there are yet no approved drug treatments to MCI. Cholinesterase inhibitors had a negligible effect in MCI [68] while Ginkgo bilobais ineffective in primary prevention [74]. Peterson et al. conducted a RCT that discusses vitamin E and donepezil in subjects with MCI. Vitamin E did not postpone the progression to Alzheimer's disease at any time node and proved to be invalid in patients with MCI, and donepezil significantly retarded the course of Alzheimer's disease during the first 12 months of the treatment year, but the rate of progression to AD was not reduced after 3 years [74]. However, a large body of literature suggests that exercise intervention may decrease the risk of Alzheimer's disease for MCI. Studies indicate that computerized cognitive training alleviates the cognition decline during the MCI [15, 75–77]. Law et al. designed a RCT aimed at evaluating the effects of a series of functional tasks on their role in MCI; results showed that general cognitive functions, memory, executive function, and the ability of daily life improved both in postintervention and 6-month follow-up [75]. Computer-based cognitive rehabilitation (CBCR) was assessed with MCI by Galante and colleagues, suggesting that CBCR plays a role in putting off the continuous progression of cognitive decline to AD [77]. Anderson-Hanley et al. confirmed that exergaming improved executive function and clinical status of mild cognitive impairment patient [15]. In addition, other studies discuss the efficiency of exercise training in MCI and AD which show that the improvement in AD is weak and limited compared with patients of MCI [76, 78]. A 4-week cognitive multicomponent rehabilitation resulted in significant improvements on activities of daily life and episodic memory in patients with MCI and nonsignificant increase with AD patients [78].
What are the best treatments for AD?
Pharmacological and exercise therapies are the major intervention targets of AD. Cholinesterase inhibitors (donepezil, galantamine, and rivastigmine), memantine, and vitamin E have shown at least some efficacy in cognitive and functional decline [5, 6]. However, there has been no definite evidence in favor of the appropriate duration and the progression of disease when drug discontinuance. Drug treatment is always a challenge because of its great cost obviously. On the other hand, a growing base of evidence has indicated that exercise interventions enhance neuroplasticity, improve cognitive function and the ability of daily life, and reduce rates of neuropsychiatric symptoms. The mechanisms of exercise for improving cognition appear to be complex and unclear, including increased blood volume and capillarization [7, 8], decreased reactive oxygen species (ROS) and oxidative stress [9], reduced Aβload and the levels of hyperphosphorylated tau proteins [10, 11], the modulation of cholinergic system [12], and the regulation of expression of brain-derived neurotrophic factor [13]. A six-month randomized trial using resistance training and aerobic training finds functional changes in three regions of cortex and hemodynamic activity in the lingual gyrus [7]; Guiney et al. confirmed that exercise-related cognitive benefits point to cerebral blood flow (CBF) and cerebrovascular regulation [8]; Smith et al. found a significant decrease in activation intensity of eleven brain regions by fMRI after a 12-week supervised treadmill walking, which suggests exercise intervention enhances neural efficiency [14]. In addition, exergaming leads to an increase of brain-derived neurotropic factor (BDNF) after cyber cycling [15], indicating that exercise benefits cognition by modulating neuronal plasticity through the regulation of dose-dependent BDNF [16]. Exercise-induced reduction of inflammatory markers (CRP, TNF-α, and IL-6) is probably one of its molecular mechanisms as well. These trials have generally demonstrated exercise a promising treatment for AD. This review (1) highlights the importance of exercise intervention on delaying the onset or slowing the progression of cognitive decline with different stages of Alzheimer's disease, (2) compares different types of exercise intervention on their role of cognitive function, (3) expounds the underlying mechanisms of exercise intervention on cognitive improvement, and (4) provides a structured strategy of exercise for clinical benefit.
Is exercise good for Alzheimer's?
However, in most cases, drug therapy is accompanied with clinical delays when older adults have suffered from cognitive decline in episodic memory, working memory, and executive function. On the other hand, accumulating evidence suggests that exercise intervention may ameliorate the progression of cognitive impairment in aging ones while the standard strategy is lacking based on different levels of cognitive decline especially in mild cognitive impairment (MCI) and AD. MCI is the preclinical stage of AD in which neurodegeneration may be reversed via neuroplasticity. Therefore, taking exercise intervention in the early stage of MCI and healthy aging at the risk of AD could slow down the process of cognitive impairment and provide a promising cost-effective nonpharmacological therapy to dementia.
Does aerobic exercise improve cognitive function?
Aerobic exercises gain benefits by improving brain function mainly. In the early animal studies in 1995, Cotman and colleagues confirmed that a short-term wheel running for two days resulted in increased brain-derived neurotropic factor (BDNF) in the hippocampus and caudal cortex, which promotes the function of neurons [39]. Moreover, studies have demonstrated that aerobic exercises attenuate age-related myelin declines of corpus callosum [40] and remain white matter integrity [41] via better cardiorespiratory fitness. Higher levels of aerobic fitness alleviate hippocampal decay, increase hippocampal volume, and obtain better spatial memory performance as a consequence [29]. Those who participate in higher levels of physical exercises perform significantly better on global cognition and executive functioning [30–32]. On the other hand, resistance training works as an approach for cognitive enhancement as well. Twelve months of once or twice weekly resistance training benefited gait speed and decreased the risk for falls, which affects the daily life seriously [33]. However, different from aerobic-based exercise training, the mechanisms of resistance training focus on biomarkers which impact on neural functions such as insulin-like growth factor 1 (IGF-1) [34, 42] and serum homocysteine. Cassilhas et al. brought in sixty-two elderly individuals, let them participate in either moderate- or high-intensity resistance training, and found that the levels of IGF-1 which promotes neuronal growth were higher than those of the control group [34]. To the contrary, homocysteine decreases after resistance exercise training and obtains positive results because of its negative effects on neural function in the elderly [43]. Meanwhile, the relationship between Tai Chi (one of the typical modes of resistance training) and cognition was carried out in many studies. Chang and Wayne's group have gained positive results [35, 36] while Snowden et al. showed limited evidence of cognitive benefits [44]. Furthermore, a series of exercise programme comprised of resistance and balance training exercises was tested in many studies. Brown and coworkers verified that a programme composed of group-based exercise improved cognitive ability of fluid intelligence significantly [37]. Home-based strength and balance retraining was confirmed effective in executive functioning by Liu-Ambrose et al. [38]. However, different meta-analyses and systemic reviews have controversial opinions about physical intervention. A meta-analysis in 2014 found no significant cognitive benefit of aerobic training [45], and a most recent systematic review in 2017 showed no or limited effects [16], while large and specific benefits were found in 2003 [46] for the impact of physical training on executive function. Diverse and precise ways of evaluation and standardized assessment of cognition improvement in recent years may be one of the important reasons for the distinction.
Is exercise good for dementia?
Overall, exercise intervention is a promising, cost-effective treatment that benefits cognitive function and plays an important role on preventing the progression to dementia with mild cognitive impairment and older adults at risk of dementia. On the other hand, for patients with Alzheimer's disease, exercise intervention could slow down the rapid cognitive impairment and be part of comprehensive treatments. We summarized the exercise management of Alzheimer's disease (Table 1). However, to date, no standard strategy gets consistent agreement to different stages of cognitive decline. Though we have compared different types of exercise intervention, the duration of training sessions and the gender of the study participants in this review, no definite approach was gain still. Even if we have paid extensive attention to the mechanisms of exercise to cognitive improvement, including enhancing brain function, increasing cerebral blood, regulation of molecular biomarkers, balancing the oxidative challenge, reducing Aβload and the levels of hyperphosphorylated tau proteins, and modulating cholinergic system, the detailed mechanisms of neural plasticity in dementia still require further tests to confirm. More experiments are needed to break through the treatment bottleneck of Alzheimer's disease.
Does exercise affect cognition?
However, cognition will decline rapidly if one is without exercise. A RCT in JAMAsuggested that the physical function deteriorated during the year after exercise intervention regardless of group-based exercise or tailored home-based exercise while those receiving usual medicine care merely have a significantly faster decline [81]. Nascimento et al. obtained similar results that the experimental group showed a tendency for less reduction in neuropsychic disturbance and performance of instrumental activities compared to the control group who lacks exercise [84].
Is memantine a cure for Alzheimer's?
During the past decades, quite a lot of studies work on Alzheimer's disease, but no major breakthroughs seem to be forthcoming. So far, there have been no curative therapies for this terminal disease including traditional and emerging drugs as it is almost impossible to reverse the severe cognitive impairment and neurodegeneration. Cholinesterase inhibitors (donepezil, rivastigmine, and galantamine) and memantine are the major pharmacotherapy. RCTs and reviews have demonstrated cognitive benefits of drug treatments while there seems minor clinical significance. A long-term donepezil RCT in Lancet showed small but significant cognitive improvement in MMSE. However, no benefits were seen in institutionalization rates or progression of disability after 3 years [79]. Memantine is the only drug approved by the US Food and Drug Administration in 2003. Placebo-controlled, double-blind, parallel group, randomized trials of memantine in people with different stages of Alzheimer's disease were analyzed and found that memantine has a small but significant benefit effect in moderate to severe AD but those with MCI did not gain that improvement in cognition and thus provide a reasonable choice for moderate to severe AD [80]. Therefore, the treatment goal of AD has turned to delay the progression of cognition decline and maintain the ability of daily life. Research on nondrug therapies has produced promising cost-effective strategies for dementia [81, 82], which improve behavior, mood, and the quality of life for families of patients with AD [82].
Abstract
Bipolar disorder (BD) is associated with cognitive and functional difficulties, persistent beyond mood episodes. Cognitive remediation (CR) is a psychological therapy targeting cognitive and functioning difficulties.
Keywords
This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence ( http://creativecommons.org/licenses/by/4.0 ), which permits unrestricted re- use, distribution and reproduction, provided the original article is properly cited.
Introduction
Bipolar disorder (BD) is associated with significant cognitive deficits present in a substantial proportion of patients (Burdick et al., Reference Burdick, Russo, Frangou, Mahon, Braga, Shanahan and Malhotra 2014; Cullen et al., Reference Cullen, Ward, Graham, Deary, Pell, Smith and Evans 2016 ).
Methods
This is a secondary analysis of longitudinal data from the CRiB study comparing CR to treatment-as-usual (TAU) in euthymic patients with BD (Strawbridge et al., Reference Strawbridge, Tsapekos, Hodsoll, Mantingh, Yalin, McCrone and Young 2021 ). Compared to main CRiB, this study includes an extended sample (plus 20 participants).
Results
Eighty participants were equally randomized to CR ( n = 40) and TAU ( n = 40). Baseline sample characteristics are presented in Table 1. There were no missing data for participant characteristics and baseline variables, which were comparable between the two groups.
Discussion
To the best of our knowledge, this is the first study examining models of whether and how cognitive gains following CR translate into long-term functional improvements in euthymic people with BD. We considered two types of functional outcomes, a clinician-rated measure of psychosocial functioning and an idiosyncratic measure of recovery goals.
Conclusions
Our findings suggest that enhancing cognition may lead to improvements in functioning, initially supporting the theoretical model for the mechanism of action of CR.
How does cognitive rehabilitation help with Alzheimer's?
Cognitive rehabilitation therapies for Alzheimer’s disease (AD) are becoming more readily available to the geriatric population in an attempt to curb the insidious decline in cognitive and functional performance . However, people with AD may have difficulty adhering to these cognitive treatments due to denial of memory deficits, compromised brain systems, cognitive incapacity for self-awareness, general difficulty following through on daily tasks, lack of motivation, hopelessness, and apathy, all of which may be either due to the illness or be secondary to depression. Cognitive rehabilitation training exercises are also labor intensive and, unfortunately, serve as a repeated reminder about the memory impairments and attendant functional consequences. In order for cognitive rehabilitation methods to be effective, patients must be adequately engaged and motivated to not only begin a rehabilitation program but also to remain involved in the intervention until a therapeutic dosage can be attained. We review approaches to cognitive rehabilitation in AD, neuropsychological as well as psychological obstacles to effective treatment in this population, and methods that target adherence to treatment and may therefore be applicable to cognitive rehabilitation therapies for AD. The goal is to stimulate discussion among researchers and clinicians alike on how treatment effects may be mediated by engagement in treatment, and what can be done to enhance patient adherence for cognitive rehabilitation therapies in order to obtain greater cognitive and functional benefits from the treatment itself.
How does cognitive enhancement work for AD?
The core premise of cognitive enhancement therapies for AD is based on neuronal plasticity. Aging causes gradual loss in brain systems including neuromodulatory functioning. However, only recently have we learned that the nervous system has the ability to adjust its structural organization in response to the environment (Mahncke et al., 2006a). The brain has the capability for restructuring itself to adapt to changing circumstances or novel stressors. We know this happens in normal older adults with plasticity-promoting training (Ball et al., 2002, Mahncke et al., 2006b). Training can drive brain plasticity by engaging adults in stimulating cognitive, sensory, and psychomotor activities on a concentrated basis (Olesen, 2004). The training re-engages and fortifies the neuromodulatory systems that control learning, with the goal of increasing the power of cortical representations. Studies indicate that cognitive enhancement therapies can alter brain function at the molecular and synaptic levels, as well as at the neural network level. At the cellular level, this net change in neuronal activity may reflect greater activation of a minority of neurons as a result of the intervention stimulus. In a PET study of 70 patients with mild AD comparing social support, drug therapy, and/or cognitive training, a combination of cognitive training and phosphatidylserine or pyritinol drug therapy was associated with increased brain glucose metabolism in temporal–parietal brain areas during a visual recognition task (Heiss et al., 1994). In a single-blind randomized controlled trial consisting of cognitive rehabilitation (CR) and relaxation therapy versus no treatment in mild AD, Clare et al. (2010)found an increase in blood oxygen level-dependent (BOLD) signals in the CR group in areas forming part of the network for visual associative encoding and learning (right fusiform face area, right parahippocampal cortex, right temporal parietal junction, right medial prefrontal cortex) while individuals in the control condition showed reduced BOLD activity over time.
How does awareness affect CR?
Operationalizing awareness and the influences of cognitive deterioration and anosognosia plays an important role in engaging patients in a labor-intensive treatment such as CR. Earlier views did not perceive denial or unawareness as necessarily unconstructive or harmful, just as a mechanism to adapt or cope, especially in the early stages of illness (Weinstein, 1991). However, more evidence has come to light in brain injury and dementia that denial may interfere with progress in CR. The implications for CR are significant in relation to AD, as recent attempts to develop CR approaches have indicated that higher levels of awareness of difficulties appear to be associated with better outcome. For example, Koltai (2001)studied CR in 24 patients with mild to moderate AD and found that higher levels of awareness were strongly predictive of greater gains in perceived memory functioning. That is, all patients with intact awareness reported fewer memory failures following CR on the Everyday Memory Questionnaire (Sunderland et al., 1983) compared to patients without awareness (p=.028). In contrast, informants perceived greater gains among treatment subjects relative to controls independent of insight status. These results reinforce the notion that awareness may well be an important variable that moderates CR outcome.
What is cognitive training?
In contrast to cognitive stimulation, cognitive training (CT) is geared toward patients who have enough cognitive resources for a therapist or a computer program to guide them in scaffolded drill and practice of tasks designed to exercise specific cognitive functions or to work on relatively intactcognitive skills in order to support more impaired cognitive skills. CT is based on the premise of neuroplasticity--that practicing an isolated underlying cognitive skill has the potential to improve or at least maintain performance in a particular domain. There have been studies of computer-based cognitive training in AD using software packages that isolate and repeatedly train specific cognitive domains such as divided attention, spatial memory, or object discrimination. Cipriani et al. (2006)and Talassi et al. (2007)both tested a software package called Neuropsychological Training (NPT) that was originally designed for aphasia but modified for brain damage rehabilitation. The goal was to determine if NPT could be further modified for CT in AD by targeting only preserved or mildly impaired cognitive areas to improve memory in dementia. Training consisted of 30–45 minutes sessions, 4 days a week, for 3 weeks. Domain-specific exercises targeted divided attention, object identification, sequential memory, working and spatial memory, visual discrimination (for faces), phonological discrimination and recognition, and verbal comprehension. Talassi and colleagues (2007)found significant improvement in overall cognition (MMSE, p=.002), depression (Geriatric Depression Scale, p=.030), and working memory (Digit span, p=.021) in community dwelling patients with AD when compared against a control that did physical rehabilitation exercises instead of CT. Cipriani and colleagues (2006)found additional gains in executive functioning (Trailmaking Test B, p = .050; verbal fluency, p = .036) suggesting that AD patients can benefit from computer-based CT if the training targets functions that are still relatively well preserved.
What are the three types of cognitive enhancement?
Clare and Woods (2004)provided the first synthesis of cognitive enhancement in AD, and grouped the various treatments into three broad categories: cognitive stimulation, cognitive training, and cognitive rehabilitation . Below, we provide an overview of these three treatment approaches.
What is a CMI?
Another variation of CT, Cognitive-Motor Intervention (CMI) (Olazarán et al., 2004), combines practicing ADLs and cognitive exercises with cognitive stimulation techniques such as reality orientation. In an efficacy trial of CMI against a psychosocial support group, patients diagnosed with mild to moderate AD who were on cholinesterase inhibitors were randomized to receive psychosocial support plus CMI or psychosocial support alone. Compared to psychosocial support alone, which was associated with a decline in overall cognitive status, there was immediate improvement in overall cognition on the ADAS-Cog in the CMI + psychosocial support group after just 1 month of training (Z = −1.95, p = 0.050). This benefit for the CMI + psychosocial support group was maintained throughout the course of the intervention with improved quality of life reported at the end of treatment (p=.005).
What is cognitive stimulation?
As the name implies, cognitive stimulation entails engaging the patient in discussions about common everyday tasks in an effort to stimulate mental activity (Cotelli et al., 2006, Davis et al., 2001, Tárraga et al., 2006). One cognitive stimulation technique commonly employed is “reality orientation” (Spector et al., 2000). As described by Spector et al. (2003)in their version of cognitive stimulation, a “reality orientation board” is used to display both personal and orientation information (group name, location, time, etc). Specific topics included on the board consist of using money, word games, present day information, and famous faces. The therapy focuses on repeatedly reminding patients of information using themes (such as childhood and food) in order to create continuity between different bits of information (Spector et al., 2010). All sessions allow for the natural process of reminiscence, but also emphasize how the information relates to the current day (Spector et al., 2008). As one might expect, this type of therapy is predominantly geared toward more impaired AD patients who live in residential facilities. In a large, single-blind, randomized comparison in residential or adult day centers, those with moderate AD who received Spector’s CST showed better cognition on the Alzheimer’s Disease Assessment Scale-Cognition (ADAS-Cog) (Rosen et al., 1984) (F=6.18, p=.014) and MMSE (Folstein et al., 1975) (F=4.14, p=.044) and rated their quality of life more positively on the Quality of Life-Alzheimer’s Disease scale (QoL-AD)(Logsdon et al., 1999)(F=4.95, P=.028) than those in the treatment as usual control groups (Spector et al., 2010).
Who funded the study of behavior science?
The study was funded by the Behavioural Science Institute of Radboud University. The Salus Clinic Lindow provided the rooms and facilities for conducting the study. Neither funding source had any influence on the design or results of the study.
Is cognitive control training good for depression?
There is a growing body of research supporting the potential therapeutic value of the Cognitive Control Training (CCT) for depression, even though more research including a control condition is necessary to investigate its working mechanisms.
Is cognitive behavioral therapy a controlled trial?
The effect of cognitive-behavioral therapy versus treatment as usual for anxiety in children with autism spectrum disorders: a randomized, controlled trial. Relative to usual care, CBT adapted for anxious youth with high-functioning ASD demonstrates large effects in reducing anxiety symptoms. This study contributes to the growing literature ...
Does CBT help with anxiety?
Relative to usual care, CBT adapted for anxious youth with high-functioning ASD demonstrates large effects in reducing anxiety symptoms. This study contributes to the growing literature supporting adapted CBT approaches for treating anxiety in youth with ASD.