Clinical neurophysiology of circadian rhythm sleep-wake disorders.

Circadian rhythms are the endogenous near-24-h oscillations in physiologic processes. In mammals the suprachiasmatic nucleus serves as the primary circadian pacemaker, and it maintains rhythmicity at a genetic level through a complex transcription-translation feedback loop of core circadian clock genes. The circadian clock is entrained to the environment through daily exposure to light and melatonin. Disruption of these endogenous rhythms or the ability to entrain to the surrounding environment results in the circadian rhythm sleep-wake disorders (CRSWDs). Patients with CRSWDs can present with either late sleep/wake times (delayed sleep-wake phase disorder), early sleep/wake times (advanced sleep-wake phase disorder), inconsistent sleep/wake times (irregular sleep-wake rhythm disorder) or sleep-wake times that move progressively later each day (non-24-h sleep-wake rhythm disorder). Diagnosis of these disorders relies on the use of sleep logs and/or actigraphy to demonstrate the daily patterns of rest and activity. Treatment of the CRSWDs focuses on sleep hygiene and strategically timed light and melatonin.

Circadian Disruption Associated with Alzheimer's Disease.

Alzheimer's disease (AD) is increasing in prevalence and has a significant impact on caregivers and the healthcare system. One of the many physiologic process affected by AD is the circadian system, with disruption reflected in abnormalities of the sleep-wake cycle. This interaction is bidirectional, with circadian and sleep disruption influencing disease progression. Understanding the bidirectional relationship between AD and circadian disruption may allow for earlier recognition of the potential to develop dementia as well as improved targeted approaches for therapy. Therapies including melatonin and bright light therapy may be advantageous in improving sleep and circadian rhythms and preventing the progression of disease. However, unfortunately, these modalities are not curative, and additional research is needed to improve treatment options for these individuals.

Streamlining door to recanalization processes in endovascular stroke therapy.

BACKGROUND: In acute stroke due to large vessel occlusion, faster reperfusion leads to better outcomes. We analyzed the effect of optimization steps aimed to reduce treatment delays at our center. METHODS: Consecutive patients with ischemic stroke treated with endovascular therapy were prospectively analyzed. We divided the patients into pre-optimization (20 April 2012 to 8 October 2013) and post-optimization (9 October 2013 to 29 July 2014) periods. The main interventions included: (1) continuous feedback; (2) standardized immediate emergency department attending to stroke attending communication with interventional team activation for all potential interventions; (3) pre-notification by the emergency medical service; (4) minimizing additional diagnostic testing; (5) direct transport to the CT scanner; (6) transport directly from the CT scanner to the angiography suite. The main metric used to measure improvement was door to groin puncture time (D2P). RESULTS: We included a total of 286 patients (178 pre-optimization, 108 post-optimization). There were no significant differences between major baseline characteristics between the groups with the exception of higher median CT Alberta Stroke Program Early CT Score in the pre-optimization group (p=0.01). Median D2P improved from 105 min pre-optimization to 67 min post-optimization (p=0.0002). Rates of good clinical outcomes (modified Rankin Scale 0-2 at 3 months) were similar in both groups, with a trend toward a better outcome in the post-optimization group in a subgroup analysis of patients with anterior circulation occlusion who received intravenous tissue plasminogen activator. CONCLUSIONS: This pilot study demonstrates that D2P times can be significantly reduced with a standardized multidisciplinary approach. There was no significant difference in the rate of 3-month good outcome, which is most likely due to the small sample size and confounding baseline patient characteristics.