Biomedical subjects

Y Harrison

Publications and source records attributed to Y Harrison.

13 recordsLinked to original sources

PubMed2001

Frontal lobe function, sleep loss and fragmented sleep.

Recent experimental studies involving total sleep loss, sleep reduction and clinically related sleep fragmentation report impaired performance on tasks of frontal lobe or executive function, including measures of verbal fluency, creativity and planning skills. Severity of sleep disturbance in obstructive sleep apnoea syndrome (OSAS) is correlated with level of executive impairment, with some residual impairment despite treatment (continuous positive airway pressure - CPAP). Executive impairment appears to be more closely related to hypoxaemic events rather than daytime sleepiness. Studies of electroencephalographic (EEG) changes throughout the course of sleep and following sleep deprivation as well as functional neuroimaging and psychophysiological changes (event-related potentials - ERPs) following sleep deprivation provide further indication of the relative importance of the frontal regions of the brain to sleep. However, neurocognitive studies present many inconsistencies, task classification is often ambiguous and, in the absence of any unifying explanation at the level of cognitive mechanisms, the overall picture is one of a disparate range of impairment following sleep loss and sleep fragmentation. Poorly defined concepts of frontal lobe function, executive function, memory and attention, using tasks largely developed with more severe deficit levels in mind, create further difficulties in interpreting current findings.

Journal Article↗

PubMed2000

Prefrontal neuropsychological effects of sleep deprivation in young adults--a model for healthy aging?

Neuropsychological testing and brain imaging show that healthy aging leads to a preferential impairment of the prefrontal cortex (PFC). Interestingly, in young adults sleep deprivation (SD) has similar effects. Psychological tasks not so oriented to the PFC are less sensitive both to SD and aging. The PFC is a cortical region working particularly hard during wakefulness, which may make it more vulnerable to "deterioration," whether this is through aging or SD. In these respects SD in young adults may offer a model for aging. No study has directly compared aging with SD. We compared groups comprising (equal sexes): YOUNG (av. 23y), MIDDLE AGED (av. 60y) and OLD (av. 73y). Young were subdivided into SD and non-sleep deprived groups. All participants were carefully screened, were healthy, good sleepers and with a similar educational background. A battery of PFC-oriented, short and straightforward neuropsychological tests was used to compare the effects of 36h of SD in the young group, with findings from the healthy, alert, non-sleep deprived groups. Tests relied on accuracy rather than speed (which took into account the problem of "global slowing" in the older participants), and were administered once (i.e., were novel). Test outcomes were significantly affected by: (1) SD in the young groups, and (2) by age. A non-PFC component of one test was not affected by SD or by age. It was concluded that 36h SD in young adults produces effects on the PFC similar to those found in normal, alert people aged about 60 years. However, it can not be concluded that an aged brain is a sleep-deprived brain.

Adult↗

PubMed2000

The impact of sleep deprivation on decision making: a review.

Few sleep deprivation (SD) studies involve realism or high-level decision making, factors relevant to managers, military commanders, and so forth, who are undergoing prolonged work during crises. Instead, research has favored simple tasks sensitive to SD mostly because of their dull monotony. In contrast, complex rule-based, convergent, and logical tasks are unaffected by short-term SD, seemingly because of heightened participant interest and compensatory effort. However, recent findings show that despite this effort, SD still impairs decision making involving the unexpected, innovation, revising plans, competing distraction, and effective communication. Decision-making models developed outside SD provide useful perspectives on these latter effects, as does a neuropsychological explanation of sleep function. SD presents particular difficulties for sleep-deprived decision makers who require these latter skills during emergency situations.

Decision Making↗

PubMed2000

Sleep loss and temporal memory.

Historical evidence suggests that sleep deprivation affects temporal memory, but this has not been studied systematically. We explored the effects of 36 hr of sleep deprivation on a neuropsychological test of temporal memory. To promote optimal performance, the test was short, novel, and interesting, and caffeine was used to reduce "sleepiness". A total of 40 young adults were randomized into four groups: control + caffeine (Cc), control + placebo (Cp), sleep deprived + caffeine (SDc), and sleep deprived + placebo (SDp). Controls slept normally. Caffeine (350 mg) or placebo were given just prior to testing. The task comprised colour photographs of unknown faces and had two components: recognition memory (distinction between previously presented and novel faces), and recency discrimination (temporal memory), when a previously shown face was presented. An interpolated task, self-ordered pointing, acted as a distraction. Caffeine had no effects within control conditions, but significantly reduced subjective sleepiness in SDc. Recognition was unaffected by sleep deprivation, whereas for recency, sleep deprivation groups scored significantly lower than controls. There was no significant improvement of recency with caffeine in the SDc group. Both sleep deprivation groups had poorer insight into their performance with recency. Self-ordered pointing remained unchanged. In conclusion, sleep deprivation impairs temporal memory (i.e. recency) despite other conditions promoting optimal performance.

Adolescent↗

PubMed1999

One night of sleep loss impairs innovative thinking and flexible decision making.

Recent findings with clinically oriented neuropsychological tests suggest that one night without sleep causes particular impairment to tasks requiring flexible thinking and the updating of plans in the light of new information. This relatively little investigated field of sleep deprivation research has real-world implications for decision makers having lost a night's sleep. To explore this latter perspective further, we adapted a dynamic and realistic marketing decision making "game" embodying the need for these skills, and whereby such performance could be measured. As the task relied on the comprehension of a large amount of written information, a critical reasoning test was also administered to ascertain whether any failure at the marketing game might lie with information acquisition rather than with failures in decision making. Ten healthy highly motivated and trained participants underwent two counterbalanced 36 h trials, sleep vs no sleep. The critical reasoning task was unaffected by sleep loss, whereas performance at the game significantly deteri orated after 32-36 h of sleep loss, when sleep deprivation led to more rigid thinking, increased perseverative errors, and marked difficulty in appreciating an updated situation. At this point, and despite the sleep-deprived participants' best efforts to do well, their play collapsed, unlike that of the nonsleep-deprived participants. Copyright 1999 Academic Press.

Journal Article↗

PubMed1998

Sleep loss impairs short and novel language tasks having a prefrontal focus.

Most cognitive tests administered during sleep loss are well rehearsed to remove practice effects. This can introduce tedium and a loss of novelty, which may be the key to the test's subsequent sensitivity to sleep loss, and why it may need only a few minutes administration before sleep loss effects are apparent. There is little evidence to show that any of these tests are actually affected by sleep loss is given de novo, without practice, but using a non-sleep deprived control group. Although the sleep deprivation literature advocates that short, novel and stimulating tests would not be expected to be sensitive to sleep loss, recent sleep loss findings using neuropsychological tests focussing on the prefrontal cortex, indicate that such tests may challenge this maxim. Twenty healthy young adults were randomly assigned to two groups: nil sleep deprivation (control). and 36h continuous sleep deprivation (SD). Two, novel, interesting and short (6 min) language tests, known (by brain imaging) to have predominantly a PFC focus, were given, once, towards the end of SD: (i) the Haylings test--which measures the capacity to inhibit strong associations in favour of novel responses, and (ii) a variant of the word fluency test--innovation in a verb-to-noun association. Subjects were exhorted to do their best. Compared with control subjects both tasks were significantly impaired by SD. As a check on the effects on the Haylings test, a repeat study was undertaken with 30 more subjects randomly divided as before. The outcome was similar. Linguistically, sleep loss appears to interfere with novel responses and the ability to suppress routine answers.

Adolescent↗

PubMed1997

Sleep deprivation affects speech.

Historical accounts of sleep loss studies have described changes in the content and patterns of speech, although to date these claims have not been systematically studied. We examined the effects of sleep loss on the spontaneous generation of words during a verbal word fluency task and the articulation of speech during a vocalized reading task. Nine subjects underwent two counterbalanced 36-hour trials involving sleep deprivation (SD) and no sleep deprivation (NSD). After SD, there was a significant deterioration in word generation and a tendency for subjects to become fixated within a semantic category. There was a significant reduction in the subjects' use of appropriate intonation in the voice after SD, with subjects displaying more monotonic or flattened voices. These findings are discussed in light of neuropsychological evidence concerning the functions of sleep in relation to the frontal cortex and in light of the implications for interpersonal communication in the event of sleep loss.

Adult↗

PubMed1996

Occurrence of "microsleeps' during daytime sleep onset in normal subjects.

The main aim of this study was to explore whether the multiple sleep latency test (MSLT) could be made more sensitive to low daytime sleepiness in normal, healthy subjects by adopting a shorter period of sleep (microsleep) as a sleep onset criterion. Subjects underwent MSLTs under two conditions: after normal (baseline) nighttime sleep, and after nighttime sleep extension (creating a "floor effect' of minimal daytime sleepiness). MSLT sleep onset thresholds of 5 s (microsleeps), 30 s (the norm) and 90 s of sustained sleep gave 3 separate sleep latency scores for 240 MSLT trials derived from 10 subjects. With low daytime sleepiness, whether this be in the morning after baseline sleep or throughout the day after sleep extension, the 5 s sleep onset criterion was a more sensitive measure of sleepiness than the established 30 s criterion. This was the case both for sleep onset latency and for the frequency of sleep onsets. Spectral analyses of the EEG indicated that successive microsleep episodes generally became more substantial, and, depending on the level of sleepiness, culminated in more overt signs of sleep. There was little difference between the 30 s and 90 s criteria for sleep onset latency scores, although there was a small but significant difference between them in the frequency of sleep onsets. As daytime sleepiness increased, particularly in the afternoon and under baseline, the 5 s criterion reached a ceiling, with the 30 s criterion becoming more sensitive.

Adolescent↗

PubMed1996

"High sleepability without sleepiness". The ability to fall asleep rapidly without other signs of sleepiness.

We find by the (polygraphic) multiple sleep latency test (MSLT) of daytime sleepiness that some normal, healthy subjects seem to be pathologically sleepy, but by equally discerning psychological tests of vigilance and sleepiness, this is not the case. They show no other symptoms of excessive daytime sleepiness, are good sleepers, and do not complain of daytime sleepiness. When they are given ad libitum sleep at night, the low MSLT scores persist; ie, when there is no underlying sleep debt. Such subjects are not unusual in the scientific literature, but unrecognised as such by many sleep researchers who maintain that they must be sleepy and "chronically sleep deprived'. We find that these "high sleepability no sleepiness' subjects can relax and "switch off' very efficiently, and if they wish, can simply go to sleep in the daytime, seemingly with little real need to sleep then.

Adult↗

PubMed1996

Can normal subjects be motivated to fall asleep faster?

The Multiple Sleep Latency Test (MSLT) is widely believed to offer an objective, physiological measure of sleepiness. The speed with which a person falls asleep throughout the day is understood to be related systematically to sleep need and circadian phase. This study examined whether normal subjects (n = 14 young female adults) could achieve faster MSLT sleep onsets if they were given the incentive to do so. During week 1 baseline MSLTs were determined over 1 day for all subjects. In week 2 they were randomly assigned to two groups. Control subjects underwent a second MSLT testing day identical to that of week 1, whereas Incentive subjects had an additional financial incentive to sleep. There was a significant reduction in sleep onset latency (indicating increased sleepiness) during the 1500 h trial following the incentive, when subjects also reported a significantly greater increase in sleepiness over the trial. These findings suggest that when coupled with a mid-afternoon increase in sleepiness, increased motivation to sleep can reduce sleep onset latency.

Adolescent↗

PubMed1996

Long-term extension to sleep--are we really chronically sleep deprived?

During 26 consecutive nights, electroencephalographic recordings and/or actigraphs were used to monitor the nighttime sleep of 10 asymptomatic healthy sleepers (mean age = 23.6 years). The schedule comprised: 7 nights of baseline sleep, 14 nights of extended sleep (up to 10 hr/night), and 5 nights of recovery sleep. During extended sleep, subjects slept significantly longer (approximately 1 hr), but sleep latency and interim wakefulness deteriorated. Extended sleep produced no improvements to self-rated mood or subjective sleepiness. Vigilance tests showed a small but significant reduction in reaction time following extended compared with both baseline and recovery nights. Ability to detect target tones did not change significantly. Multiple Sleep Latency Test scores during extended sleep showed small (about 1 min) reductions. These findings give little support to the view of chronic sleep deprivation in the average 7.5-hr sleeper.

Adolescent↗

PubMed1995

Should we be taking more sleep?

Reports of reduced daytime sleepiness following extended nighttime sleep in normal, regular sleepers suggest that they (and perhaps much of the general population) are chronically sleep deprived. However, 1) the social and environmental contexts of sleep allow for much intraindividual variation in sleep duration and structure; 2) animal studies show that when there is opportunity for sleep and few incentives to remain awake, sleep occurs for reasons other than in response to a physiological requirement, i.e. sleep satiation may precede actual awakening, 3) accounts of increased sleep duration earlier this century are flawed and 4) because increased sleep onset latency and wake after sleep onset are features of extended sleep, it would be difficult to persuade people to sleep longer for the small benefits to daytime alertness. Laboratory studies show that 1) following extended sleep the improvements in daytime alertness are minor, even by the Multiple Sleep Latency Test (MSLT), and could be achieved equally successfully and with less disruption to habitual daily patterns by taking a short nap; 2) normal subjects extend sleep at night not necessarily because they are chronically sleepy, because there may be no prior MSLT signs of daytime sleepiness; 3) mood effects of extended sleep are confounded by earlier bedtimes; and 4) extended sleep does not necessarily make subjects feel well rested immediately on waking. In sum, most people are not chronically sleep deprived but have the capacity to take more sleep, in the same way that we eat and drink in excess of physiological needs.

Humans↗

PubMed1989

A colony assay system that detects B cell progenitors in fresh and cultured bone marrow.

This report describes a colony assay system, based on methods used to grow myeloid precursors in semisolid medium, in which B cell progenitors can be grown. The formation of these B cell progenitor colonies is dependent upon soluble mediators from a stromal cell line known to support B lymphopoiesis. In initial experiments a double layer culture system was employed in which target cells in methylcellulose medium were separated from an adherent layer of S17 stromal cells by an agar interface. Target cells were harvested from Dexter type long-term bone marrow cultures at a time after transfer to the lymphoid Whitlock-Witte conditions, when myeloid progenitors were depleted and mature B cells had not yet appeared. On day 15 of culture a colony could be identified that contained several hundred tightly clustered lymphoid cells. There was a linear relationship between the number of cells plated and the number of colonies that developed. Identically appearing colonies were also observed in agar using fresh bone marrow cells as targets with either an underlayer of S17 cells or S17 conditioned medium to potentiate colony growth. Lymphoid colonies derived from fresh bone marrow appeared on days 6 and 14 of growth. A proportion of the cells from the fresh or cultured marrow derived colonies expressed the B220 antigen and cytoplasmic mu heavy chains, but surface IgM was never observed. Cell depletion experiments on antibody coated plates demonstrated the colony forming unit to be B220 antigen positive, surface IgM negative, and replating experiments indicated the colonies were lymphoid restricted in their differentiative potential.

Animals↗