Sex Differences in Cognitive Estimation During Sleep Deprivation: Effects of Stimulant Countermeasures

Killgore, William D.S.; Muckle, Alison E; Grugle, Nancy L.; Killgore, Desiree B.; Balkin, Thomas J.

doi:10.1080/00207450802323970

Cited by 24 publications

(8 citation statements)

References 46 publications

(52 reference statements)

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“…This patient-reported amelioration was supported by the significant improvement reported by knowledgeable informants; for the other secondary cognitive end point, a performance-based computerized test of neurocognitive function, the improvement seen with LDX was not statistically superior to placebo. Overall, these findings support previous evidence of the ability of dopaminergic agents to mitigate cognitive dysfunction (Killgore et al, 2008;Schachar et al, 2008). However, because there are typically only modest correlations between BRIEF-A and performance-based measures of executive function , this finding is not surprising.…”

Section: Discussionsupporting

confidence: 78%

Lisdexamfetamine Dimesylate Augmentation in Adults With Persistent Executive Dysfunction After Partial or Full Remission of Major Depressive Disorder

Madhoo

Keefe

Roth

et al. 2013

Neuropsychopharmacol

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Evaluate lisdexamfetamine dimesylate (LDX) augmentation of antidepressant monotherapy for executive dysfunction in partially or fully remitted major depressive disorder (MDD). This randomized, placebo-controlled study (NCT00985725) enrolled 143 adults (18-55 years) with mild MDD (Montgomery-Å sberg Depression Rating Scale (MADRS) score p18) and executive dysfunction (Behavior Rating Inventory of Executive Function-Adult Version (BRIEF-A) Self-Report Global Executive Composite (GEC) T score X60) on stable antidepressant monotherapy for X8 weeks. After 2 weeks of screening, participants were randomized to 9 weeks of double-blind LDX (20-70 mg/day) or placebo augmentation, followed by 2 weeks of single-blind placebo. The primary end point was change from baseline to week 9/end of study (EOS) in BRIEF-A Self-Report GEC T score; secondary assessments included the BRIEF-A Informant Report, MADRS, and treatment-emergent adverse events (TEAEs). Of 143 randomized participants, 119 completed double-blind treatment (placebo, n ¼ 59; LDX, n ¼ 60). Mean±standard deviation (SD) BRIEF-A GEC T scores decreased from baseline (placebo, 74.2±8.88; LDX, 76.8±9.66) to week 9/EOS (placebo, 61.4±14.61; LDX, 55.2±16.15); the LS mean (95% CI) treatment difference significantly favored LDX ( À 8.0 ( À 12.7, À 3.3); P ¼ 0.0009). The LS mean (95% CI) treatment difference for MADRS total score also significantly favored LDX ( À 1.9 ( À 3.7, 0.0); P ¼ 0.0465). TEAE rates were 73.6% with placebo and 78.9% with LDX; serious TEAE rates were 4.2 and 2.8%. In this trial, LDX augmentation significantly improved executive dysfunction and depressive symptoms in participants with mild MDD. The safety profile of LDX was consistent with prior studies in adults with attention-deficit/hyperactivity disorder.

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Section: Discussionsupporting

confidence: 78%

Lisdexamfetamine Dimesylate Augmentation in Adults With Persistent Executive Dysfunction After Partial or Full Remission of Major Depressive Disorder

Madhoo

Keefe

Roth

et al. 2013

Neuropsychopharmacol

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“…Almost half of the participants generated responses indicative of sleep and wakefulness disorders (30.7% insomnia, 10.7% daytime sleepiness, 7.9% OSA). International estimates range from 9% to 36% for insomnia, 19 8.7% to 20% for daytime sleepiness, 20 and 2% to 10% for OSA. 21 It was interesting to note that the prevalence for insomnia and OSA among the participants in this study was at the higher end of the international ranges, while daytime sleepiness was comparatively lower.…”

Section: Discussionmentioning

confidence: 99%

Can a community pharmacy sleep assessment tool aid the identification of patients at risk of sleep disorders in the community: a pilot study

Kashyap¹,

Nissen²,

Smith³

et al. 2012

IPRP

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Background: When experiencing sleep problems for the first time, consumers may often approach community pharmacists for advice as they are easily accessible health care professionals in the community. In Australian community pharmacies there are no specific tools available for use by pharmacists to assist with the assessment and handling of consumers with sleep enquiries. Objective: To assess the feasibility of improving the detection of sleep disorders within the community through the pilot of a newly developed Community Pharmacy Sleep Assessment Tool (COP-SAT). Method: The COP-SAT was designed to incorporate elements from a number of existing, standardized, and validated clinical screening measures. The COP-SAT was trialed in four Australian community pharmacies over a 4-week period. Key findings: A total of 241 community pharmacy consumers were assessed using the COP-SAT. A total of 74 (30.7%) were assessed as being at risk of insomnia, 26 (10.7%) were at risk of daytime sleepiness, 19 (7.9%) were at risk of obstructive sleep apnea, and 121 (50.2%) were regular snorers. A total of 116 (48.1%) participants indicated that they consume caffeine before bedtime, of which 55 (47%) had associated symptoms of sleep onset insomnia. Moreover, 85 (35%) consumed alcohol before bedtime, of which 50 (58%) experienced fragmented sleep, 50 (58%) were regular snorers, and nine (10.6%) had apnea symptoms. The COP-SAT was feasible in the community pharmacy setting. The prevalence of sleep disorders in the sampled population was high, but generally consistent with previous studies on the general population. Conclusion: A large proportion of participants reported sleep disorder symptoms, and a link was found between the consumption of alcohol and caffeine substances at bedtime and associated symptoms. While larger studies are needed to assess the clinical properties of the tool, the results of this feasibility study have demonstrated that the COP-SAT may be a practical tool for the identification of patients at risk of developing sleep disorders in the community.

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“…In fact, there is some valuable information on the plasma pharmacokinetics of caffeine, but little is known about the dose-and time-dependent variation of caffeine levels in the relevant brain regions where it is expected to counteract neuronal (synaptic) damage. The pharmacokinetic characteristics, as well as the presence and relative importance of other ancillary factors formatting the response to caffeine, should bolster the exploitation of the different ability of caffeine to afford neuroprotection in males and females [103, [112][113][114]189,[309][310][311][312][313][314].…”

Section: Open Issues and Concluding Remarksmentioning

confidence: 99%

Chronic Caffeine Consumption Prevents Memory Disturbance in Different Animal Models of Memory Decline

Cunha

Agostinho

2010

JAD

204

141

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Caffeine, the most widely consumed psychoactive drug, enhances attention/vigilance, stabilizes mood, and might also independently enhance cognitive performance. Notably, caffeine displays clearer and more robust beneficial effects on memory performance when memory is perturbed by stressful or noxious stimuli either in human or animal studies. Thus, caffeine restores memory performance in sleep-deprived or aged human individuals, a finding replicated in rodent animal models. Likewise, in animal models of Alzheimer's disease (AD), caffeine alleviates memory dysfunction, which is in accordance with the tentative inverse correlation between caffeine intake and the incidence of AD in different (but not all) cohorts. Caffeine also affords beneficial effects in animal models of conditions expected to impair memory performance such as Parkinson's disease, chronic stress, type 2 diabetes, attention deficit and hyperactivity disorder, early life convulsions, or alcohol-induced amnesia. Thus, caffeine should not be viewed as a cognitive enhancer but instead as a cognitive normalizer. Interestingly, these beneficial effects of caffeine on stress-induced memory disturbance are mimicked by antagonists of adenosine A2A receptors. This prominent role of A2A receptors in preventing memory deterioration is probably related to the synaptic localization of this receptor in limbic areas and its ability to control glutamatergic transmission, especially NMDA receptor-dependent plasticity, and to control apoptosis, brain metabolism, and the burden of neuroinflammation. This opens the real and exciting possibility that caffeine consumption might be a prophylactic strategy and A2A receptor antagonists may be a novel therapeutic option to manage memory dysfunction both in AD and in other chronic neurodegenerative disorders where memory deficits occur.

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Sex Differences in Cognitive Estimation During Sleep Deprivation: Effects of Stimulant Countermeasures

Cited by 24 publications

References 46 publications

Lisdexamfetamine Dimesylate Augmentation in Adults With Persistent Executive Dysfunction After Partial or Full Remission of Major Depressive Disorder

Lisdexamfetamine Dimesylate Augmentation in Adults With Persistent Executive Dysfunction After Partial or Full Remission of Major Depressive Disorder

Can a community pharmacy sleep assessment tool aid the identification of patients at risk of sleep disorders in the community: a pilot study

Chronic Caffeine Consumption Prevents Memory Disturbance in Different Animal Models of Memory Decline

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