Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Saturday, April 8, 2017

Sleep and Human Aging

What is your doctors sleep protocol doing to ensure you get your beauty sleep while in the hospital?  I got woken up almost every morning by the blood vampires coming for either me or my roommates at 7am.  Do they now know about needleless blood draws, only out since May 2016? Needle free blood draws or microneedles?
I only copied the abstract and the conclusion paragraphs so there is lots more at the link.
http://www.cell.com/neuron/fulltext/S0896-6273%2817%2930088-0
Older adults do not sleep as well as younger adults. Why? What alterations in sleep quantity and quality occur as we age, and are there functional consequences? What are the underlying neural mechanisms that explain age-related sleep disruption? This review tackles these questions. First, we describe canonical changes in human sleep quantity and quality in cognitively normal older adults. Second, we explore the underlying neurobiological mechanisms that may account for these human sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment as an exemplar. We conclude with a discussion of a still-debated question: do older adults simply need less sleep, or rather, are they unable to generate the sleep that they still need?

Main Text

Normative aging is associated with a reduced ability to initiate and maintain sleep. Moreover, deficits in sleep physiology, including those of non-rapid eye movement (NREM) sleep and its associated neural oscillations, are especially prominent in later life. Though sleep disruption is a common signature of “normal aging”, the underlying neural mechanisms explaining age-related sleep impairment are only now being revealed.
This review focuses on physiological changes associated with normative human aging. First, we characterize associated alterations in sleep structure and oscillatory activity in later life. Second, we describe emerging neurobiological mechanisms that may account for these sleep alterations. Third, we consider the functional consequences of age-related sleep disruption, focusing on memory impairment. We conclude with the exploration of a still-unresolved question: are older adults unable to generate the sleep that they need or do they simply need sleep less.


S

Sleep Restoration, Aging, and Memory

The vast majority of studies reporting an association between sleep, aging, and memory are correlational in nature. However, several studies have sought to enhance the sleep of older adults, and with it, memory. These studies are informative in at least two ways. First, they establish a causal contribution of sleep to memory in the elderly, as has been shown in young adults. Second, therapeutic interventions that restore sleep may deliver preventative benefits that reduce the risk and/or severity of cognitive decline in aging, or mechanisms and/or processes that lead to mild cognitive impairment or Alzheimer’s disease (Mander et al., 2016a), or body ill-health consequences, such as hypertension or chronic pain (Neikrug and Ancoli-Israel, 2010). However, it is important to note that these methods have not been investigated using longitudinal study designs, and thus the longitudinal utility of such methods remains unknown.
In young adults, transcranial direct current stimulation (tDCS) in the <1 Hz slow oscillation frequency range during slow wave sleep increases slow oscillation power and almost doubles overnight memory retention (Marshall et al., 2006). In older adults, multiple studies have shown that enhancing the slow oscillation using tDCS during an afternoon nap leads to a memory enhancement; one showing heightened SWA in the slow oscillation frequency range (<1 Hz) and word-pair performance (Westerberg et al., 2015), and another showing enhanced slow oscillation and fast sleep spindle EEG power that led to a benefit in a visual memory task (Ladenbauer et al., 2016). Auditory closed-loop stimulation during slow wave sleep has also been shown to enhance slow oscillation power and associated hippocampus-dependent memory consolidation in young adults (Ngo et al., 2013). Preliminary findings in older adults have reported increased slow oscillation power during blocks of auditory stimulation that is associated with enhanced next-day declarative memory recall (Papalambros et al., 2017). It is of note, however, that some studies implementing varied forms of brain stimulation have failed to replicate the beneficial enhancement of sleep physiology and/or memory consolidation (Eggert et al., 2013, Passmann et al., 2016, Sahlem et al., 2015). Therefore, brain stimulation methods offer potential promise as intervention tools in the context of aging, but they require further refinement and demonstration of efficacy and reproducibility before being realistic options at present.
Pharmacological methods using classic GABA-targeting hypnotics for selective NREM sleep enhancement have so far proved less promising in the context of aging and often fail to trigger any corresponding sleep-dependent memory benefit in the elderly, sometimes even causing amnestic effects (Feld et al., 2013, Hall-Porter et al., 2014, Mednick et al., 2013, Vienne et al., 2012). Little is currently known regarding the impact of more contemporary non-GABA-targeting sleep medications on enhancing sleep and/or cognition in the elderly populations at risk for dementia.
Overall, several novel, non-pharmacological approaches are emerging that may represent candidate methods for sleep restoration in the elderly and, with such restoration, improvements in those mental and physical functions that rely on sleep and are causally deficient in the elderly as a result.

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