Does cognitive behavioural therapy for insomnia improve cognitive performance? A systematic review and narrative synthesis.

Individuals with insomnia report difficulties pertaining to their cognitive functioning. Cognitive behavioural therapy for insomnia (CBT-I) is associated with robust, long-term improvements in sleep parameters, however less is known about the impact of CBT-I on the daytime correlates of the disorder. A systematic review and narrative synthesis was conducted in order to summarise and evaluate the evidence regarding the impact of CBT-I on cognitive functioning. Reference databases were searched and studies were included if they assessed cognitive performance as an outcome of CBT-I, using either self-report questionnaires or cognitive tests. Eighteen studies met inclusion criteria, comprising 923 individuals with insomnia symptoms. The standardised mean difference was calculated at post-intervention and follow-up. We found preliminary evidence for small to moderate effects of CBT-I on subjective measures of cognitive functioning. Few of the effects were statistically significant, likely due to small sample sizes and limited statistical power. There is a lack of evidence with regards to the impact of CBT-I on objective cognitive performance, primarily due to the small number of studies that administered an objective measure (n = 4). We conclude that adequately powered randomised controlled trials, utilising both subjective and objective measures of cognitive functioning are required.

Predictors of Nightly Subjective-Objective Sleep Discrepancy in Poor Sleepers over a Seven-Day Period.

This study sought to examine predictors of subjective/objective sleep discrepancy in poor sleepers. Forty-two individuals with insomnia symptoms (mean age = 36.2 years, 81% female) were recruited to take part in a prospective study which combined seven days of actigraphy with daily assessment of sleep perceptions, self-reported arousal, sleep effort, and mood upon awakening. A high level of intra-individual variability in measures of sleep discrepancy was observed. Multilevel modelling revealed that higher levels of pre-sleep cognitive activity and lower mood upon awakening were significantly and independently predictive of the underestimation of total sleep time. Greater levels of sleep effort predicted overestimation of sleep onset latency. These results indicate that psychophysiological variables are related to subjective/objective sleep discrepancy and may be important therapeutic targets in the management of insomnia.

Depression in small-vessel disease relates to white matter ultrastructural damage, not disability.

OBJECTIVE: To determine whether cerebral small-vessel disease (SVD) is a specific risk factor for depression, whether any association is mediated via white matter damage, and to study the role of depressive symptoms and disability on quality of life (QoL) in this patient group. METHODS: Using path analyses in cross-sectional data, we modeled the relationships among depression, disability, and QoL in patients with SVD presenting with radiologically confirmed lacunar stroke (n = 100), and replicated results in a second SVD cohort (n = 100). We then compared the same model in a non-SVD stroke cohort (n = 50) and healthy older adults (n = 203). In a further study, to determine the role of white matter damage in mediating the association with depression, a subgroup of patients with SVD (n = 101) underwent diffusion tensor imaging (DTI). RESULTS: Reduced QoL was associated with depression in patients with SVD, but this association was not mediated by disability or cognition; very similar results were found in the replication SVD cohort. In contrast, the non-SVD stroke group and the healthy older adult group showed a direct relationship between disability and depression. The DTI study showed that fractional anisotropy, a marker of white matter damage, was related to depressive symptoms in patients with SVD. CONCLUSION: These results suggest that in stroke patients without SVD, disability is an important causal factor for depression, whereas in SVD stroke, other factors specific to this stroke subtype have a causal role. White matter damage detected on DTI is one factor that mediates the association between SVD and depression.

Memory processes in the development of reduced-salt foods.

Acceptance of a reduced-salt food is likely to be influenced by a mismatch between the sensory characteristics of a reformulated product and a memory for a previously-encountered formulation. In two initial pilot studies we established the reliability of a new measure of memory for saltiness, based on a method of constant stimuli. We then used this technique to explore the effects of different patterns of repeated exposure on memory for the taste of a reduced-salt soup. Participants (N = 135) were assigned to one of four exposure patterns: (1) reduced-salt, (2) no salt reduction, i.e. regular-salt, (3) reduced- and regular-salt, in an alternating pattern, and (4) gradually declining salt concentration. In the final session, all participants received an identical reduced-salt soup. Memory for the saltiness of this sample was assessed, together with its expected liking. Our results indicate that different interactions with the test soup had little effect on taste memory. Nevertheless, (1) participants remembered the final exposure soup as saltier than the reduced-salt formulation that they had received and (2) remembered salt concentrations correlated with individual ideal salt concentrations. These findings are consistent with contemporary models of reconstructive memory and they illustrate the importance of understanding 'memory for saltiness' in the acceptance of reduced-salt formulations.

Verbal fluency in cerebral small vessel disease and Alzheimer's disease.

Patterns of verbal fluency deficits have been explored across different neurodegenerative disorders. This study sought to investigate the specific pattern of verbal fluency performance in cerebral small vessel disease (SVD), which is the most common cause of vascular cognitive impairment, and compare this with Alzheimer's disease (AD). Participants with SVD (n = 45), AD (n = 24) and healthy controls (n = 80) completed assessments of semantic and phonemic fluency. Mixed-model analyses of covariance were used to compare performance on the different fluency tasks between the groups, and a discriminant function analysis was conducted to examine group differentiation. The SVD group was impaired in both fluency tasks when compared to the controls. In contrast, the AD group displayed impairment in semantic fluency only. Discriminant function analysis revealed that fluency scores correctly classified 80% of SVD patients and 92% of AD patients. The pattern of performance observed in the SVD group may reflect deficits in executive function and processing speed impacting equivalently on semantic and phonemic fluency. The differences between the SVD and AD groups highlighted in this study may be useful for distinguishing between these conditions.

Executive dysfunction, awareness deficits and quality of life in patients with cerebral small vessel disease: a structural equation model.

OBJECTIVE: To investigate the relationships between executive dysfunction, awareness deficits and perceptions of quality of life (QOL) in patients with cerebral small vessel disease (SVD). METHOD: We tested neuropsychological function with simultaneous measurement of awareness performance in 125 participants. Forty-five were carefully phenotyped patients with SVD, defined as a lacunar stroke with corresponding infarct on neuroimaging; and 80 were age-matched controls, providing a normal comparison for neuropsychological measures. Patients also completed the Stroke-Specific Quality of Life Scale. In patients with SVD, the impact of executive dysfunction on awareness and QOL was examined simultaneously using structural equation modeling. RESULTS: A simple regression indicated a positive relationship between awareness and QOL. However, when executive function was added to the model, the results showed strong relationships between executive function and awareness, and executive function and QOL, but no direct relationship between awareness and QOL. CONCLUSION: Our results show that the main neuropsychological symptom associated with SVD, namely, executive dysfunction, may predict both reductions in awareness and QOL. However, there is no direct impact of awareness deficits on QOL in patients with SVD, when executive function is included in the model.

Dopamine and food reward: effects of acute tyrosine/phenylalanine depletion on appetite.

It has been suggested that obese individuals over-eat in order to compensate for deficits in the dopaminergic reward system. The current study used acute tyrosine/phenylalanine depletion (ATPD) to investigate the effect of reduced dopamine function on appetite and the reward value of food in healthy volunteers. The compensatory-eating hypothesis would predict an increase in the reward value and consumption of food following depletion by this method. In a double-blind, counterbalanced, crossover study, 17 male participants (mean age=29.2 (SEM=2.7) years; mean body mass index=24.4 (SEM=0.6) kg/m(2)) were administered with a tyrosine/phenylalanine-free mixture (TYR/PHE-free; depletion condition) and a balanced amino acid mixture (BAL; control). Plasma amino acid levels were measured at baseline and peak depletion (300 min). Appetite, willingness to pay for food, liking, desired portion size and ad libitum food intake were also assessed. The TYR/PHE-free mixture was associated with significant decreases in tyrosine, phenylalanine, and the ratio of tyrosine+phenylalanine to the other large neutral amino acids (all p<.001). There were no effects on our measures of willingness to pay for food or liking. However, in the TYR/PHE-free condition, participants reported significantly lower levels of hunger following a fixed-test meal relative to the BAL condition. In conclusion, we found no evidence for compensatory eating following ATPD. Our results also provide support for the role of dopamine in motivational components of eating.

Serotonin and dopamine play complementary roles in gambling to recover losses.

Continued gambling to recover losses--'loss chasing'--is a prominent feature of social and pathological gambling. However, little is known about the neuromodulators that influence this behavior. In three separate experiments, we investigated the role of serotonin activity, D(2)/D(3) receptor activity, and beta-adrenoceptor activity on the loss chasing of age and IQ-matched healthy adults randomized to treatment or an appropriate control/placebo. In Experiment 1, participants consumed amino-acid drinks that did or did not contain the serotonin precursor, tryptophan. In Experiment 2, participants received a single 176 µg dose of the D(2)/D(3) receptor agonist, pramipexole, or placebo. In Experiment 3, participants received a single 80 mg dose of the beta-adrenoceptor blocker, propranolol, or placebo. Following treatment, participants completed a computerized loss-chasing game. Mood and heart rate were measured at baseline and following treatment. Tryptophan depletion significantly reduced the number of decisions made to chase losses, and the number of consecutive decisions to chase, in the absence of marked changes in mood. By contrast, pramipexole significantly increased the value of losses chased and diminished the value of losses surrendered. Propranolol markedly reduced heart rate, but produced no significant changes in loss-chasing behavior. Loss chasing can be thought of as an aversively motivated escape behavior controlled, in part, by the marginal value of continued gambling relative to the value of already accumulated losses. Serotonin and dopamine appear to play dissociable roles in the tendency of individuals to gamble to recover, or to seek to 'escape' from, previous losses. Serotonergic activity seems to promote the availability of loss chasing as a behavioral option, whereas D(2)/D(3) receptor activity produces complex changes in the value of losses judged worth chasing. Sympathetic arousal, at least as mediated by beta-adrenoceptors, does not play a major role in laboratory-based loss-chasing choices.