Summary of the mandatory literature for the course Evidence Based Cognitive Enhancement (ECE). This course is mandatory for all students following the Applied Cognitive Psychology (ACP) master at Leiden University (Universiteit Leiden). Through this summary, I passed the exam with a 7.5
1.Working on atypical schedules
Boivin, Tremblay & James
Shift work has been associated with a number of health problems including cardiovascular disease,
impaired glucose and lipid metabolism, gastrointestinal discomfort, reproductive difficulties, and breast
cancer. Individuals vary greatly in their capacity to adjust to atypical work schedules and their tolerance to
circadian misalignment. Predisposing individual and domestic factors have been identified, such as
increasing age, being a single woman in charge of children, and split sleep patterns, all of which can affect
the ability to adjust to atypical schedules.
Sleep–wake cycle disturbances
8 h of sleep and 16 h of wakefulness per day. When the sleep schedule is displaced, as is the case for shift
workers, the normal temporal relationship between the sleep–wake cycle and the endogenous circadian
pacemaker is perturbed, which can lead to reduced sleep duration. Which leads to a decrease in vigilance
and performance.
Circadian misalignment
Hormonal rhythms are influenced by an interaction of circadian and sleep–wake-dependent processes.
- Cortisol: In daytime workers, cortisol levels reach their minimal values early in the night and their
maximal values around the regular time of awakening. A misalignment in the cortisol rhythm
resulting in lower levels during the day.
- Melatonin: normally levels peak at night during the middle of the sleep episode and are
undetectable during the day.
It has been suggested that predisposing factors, including a morning-type chronotype, sleep disturbances,
medical and psychiatric conditions, and reduced
family support, may impair workers’ ability to adjust to shift work.
Countermeasures
- Stratetic napping: plan naps of 20–120 min in duration. Strategic napping can efficiently improve
alertness and performance
Prophylactic naps: planned in the evening prior to the shift to limit anticipated sleep
deprivation
Recuperative naps: taken at night to temporarily relieve sleepiness. Naps can negatively
affect the level of alertness and vigilance in the minutes immediately following the awakening
from sleep = sleep inertia, its duration varies according to time of day with a worsening for
naps planned at the end of a night shift.
- Bright light exposure: Exposure to bright light (1230– 12,000 lux), often in the first half of the night.
One major complaint of shift workers exposed to bright light is difficulty readjusting to a day-oriented
schedule on rest days. In addition to its phase shifting effect, bright light exposure can exert a direct
alerting effect leading to improved performance levels, reduced sleepiness scores, increased
vigilance levels as well as an increase in beta and reduction in alpha–theta EEG activity.
- Pharmalogical interventions: Use of pharmaceutical agents such as psychostimulants, hypnotics,
melatonin, or caffeine can be considered in these impaired workers to either enhance vigilance at
work or promote daytime sleep.
- Modafilnil: Modafinil is the only approved prescription stimulant drug for this disorder. It increases
glutamate release in thalamus and reduces GABA release in nucleus acumens. A reduction in the
risk of accidents while commuting back home in the morning was also reported. However, nighttime
improvements were modest since sleepiness remained high and the reported number of mistakes,
accidents, or near-accidents at work remained unchanged. Significant reduction of sleep onset on
nighttime MWT (maintenance of wakefulness) was reported. Daytime sleep disruption is also
observed when modafinil is given too late in the morning following a night shift.
- Caffeine: Caffeine administered just before night work can be used to counteract the drop of
vigilance and performance levels throughout the night. A total daily dosage of 600 mg of caffeine in
a slow-release formulation attenuates nighttime increases in microsleep duration and slows the
disintegration of attention. Caffeine administered in the 3 h preceding a nighttime sleep opportunity
is sufficient to increase time to fall asleep and reduce both total sleep time and sleep efficiency in
young and middle-aged subjects. Caffeine administration can effectively limit the decrease in
cognitive throughput, vigilance and reaction time observed towards the end of 28.57-h wake
, periods. However, caffeine administration results in a significant decrease in sleep efficiency
particularly when sleep occurs at inappropriate circadian phases.
- Hypnotics: Benzodiazepines (e.g., temazepam, triazolam) and non-benzodiazepines (e.g.,
zopiclone, zolpidem, zaleplon) have been approved for use in the treatment of insomnia. When
temazepan is administered before an afternoon sleep opportunity total sleep time is longer
compared to placebo, with an increase in stage 2 sleep.
- Melatonin: Melatonin phase shifting and sleep-promoting effects, are thought to come from
melatonin binding to MT1 and MT2 receptors. Melatonin increased sleep efficiency only when given
at times when endogenous melatonin was low. However, many studies in actual shift workers do
not show a significant effect of exogenous melatonin on daytime sleep quality and duration based
on sleep diary measures.
- Ramelteon, a high-affinity agonist of MT1 and/or MT2 receptors, is approved by the US FDA for the
treatment of transient and chronic primary insomnia characterized by trouble falling asleep.
However, night shift workers do not typically have trouble falling asleep.
Conclusion
Although each specific approach can lead to some reduction of fatigue in a given worker, no single one
represents a unique, comprehensive and sufficient solution to the complex problem of working on atypical
schedules.
1.The memory function of sleep. Nature reviews
Diekelman & Born
Sleep (loss of behavioural control and consciousness) is a state that optimizes the consolidation of
newly acquired information in memory, depending on the specific conditions of learning and the timing
of sleep. Consolidation during sleep promotes both quantitative and qualitative changes of memory
representations.
Sleep promotes primarily the consolidation of memory, whereas memory encoding (converting data
from one form to another, maps) and retrieval take place most effectively during waking.
Consolidation refers to a process that transforms new and initially labile memories encoded in the
awake state into more stable representations that become integrated into the network of pre-existing
long-term memories.
Sleep duration and timing
Significant sleep benefits on memory are observed after an 8-hour night of sleep,
but also after shorter naps of 1–2 hours even an ultra-short nap of 6 minutes can improve memory
retention. However, longer sleep durations yield greater
improvements, particularly for procedural memories. Sleep does not need to occur immediately but
should happen on the same day as initial training.
Explicit versus implicit encoding
whether memories gain acess to sleep-dependent consolidation depends on the conditions of encoding:
- Declarative memories (facts/events): explicit encoding (bewust)
- Procedural memories (knowing how): implicit & explicit
The benefit of sleep is greater for memories formed from explicitly encoded information that was more
difficult to encode or that was only weakly encoded and it is greater for memories that were
behaviorally relevant. Thus, sleep enhances the consolidation of memories for intended future actions
and plans.
Sleep changes memory representations quantitatively and qualitatively
Consolidation of memory during sleep can produce a strengthening of associations as well as
qualitative changes in memory representations. Sleep therefore provides stabilization and
enhancement of memory. Moreover, there is strong evidence for an active consolidation influence of
sleep which leads to qualitative changes.
Interacting or competing memory systems?
Two views: procedural and declarative memory systems interact during sleep-dependent consolidation.
Contrasting with this view of interacting is that memory systems compete and reciprocally interfere
during waking, but disengage during sleep. The two views might be reconciled by assuming a
sequential contribution of interaction and disengagement processes to consolidation, which might be
associated with different sleep stage.
,Influence of sleep stages on consolidation
Repeated awakenings cause stress, which itself influences memory function.
- SWS-rich, early sleep consistently benefits the consolidation of declarative memories.
- REM-rich sleep benefits nondeclarative types of memory (that is, procedural and emotional
aspects of memory).
These results are consistent with the dual-process hypothesis, which assumes
that SWS facilitates declarative, hippocampus-dependent memory and REM sleep supports non-
declarative, hippocampus-independent memory. Intermediate sleep stages can also contribute to
memory consolidation.
Synaptic consolidation
Consolidation involves the strengthening of memory representations at the synaptic level (synaptic
consolidation). Long-term potentiation (LTp) is considered a key mechanism of synaptic consolidation,
but it is unclear whether memory re-activation during sleep promotes the redistribution of memories
by inducing new lTp or whether re-activation merely enhances the maintenance of lTp that was
induced during encoding.
Synaptic homeostasis versus system consolidation
Two hypothesis for SWS
- Synaptic homeostasis: information encoding during wakefulness leads to a net increase in
synaptic strength in the brain. Sleep would serve to globally downscale synaptic strength to a
level that is suitable in term of energy and tissue volume demands and that allows for the reuse
of synapses for future encoding.
- Active system consolidation during sws: in the waking brain events are initially encoded in
parallel in neocortical networks and in the hippocampus. During subsequent periods of SWS the
newly acquired memory traces are repeatedly re-activated and thereby become gradually
redistributed such that connections within the neocortex are strengthened forming more
persistent representations. Reactivation of the new representations gradually adapt them to
pre-existing neocortical knowledge networks, thereby promoting the extraction of invariant
repeating features and qualitative changes in the memory representations.
The concept of active system consolidation during SWS integrates a central finding from behavioral
studies, namely that post-learning sleep not only strengthens memories but also induces qualitative
changes in their representations and so enables the extraction of invariant features from complex
stimulus materials, the forming of new associations and, eventually, insights into hidden rules.
A role for REM sleep in synaptic consolidation
The active system consolidation hypothesis leaves open one challenging issue: although it explains a
reactivation-dependent temporary enhancement and integration of newly encoded memories into the
network of pre-existing long-term memories, active system consolidation alone does not explain how
post-learning sleep strengthens memory traces and stabilizes underlying synaptic connections in the
long term. Hence, sleep presumably also supports a synaptic form of consolidation for stabilizing
memories and this could be the function of
REM sleep.
1.The sleep-deprived human brain
Impact of SD on the human brain across five functional domains:
1.Attention: serves ongoing goal-directed behavior. The prototypic impairments on such tasks are
known as ‘lapses’ or ‘microsleeps’, which involve response failures that reflect errors of omission.
Attentional maintenance becomes highly variable and resulting in unstable task performance.
Reductions in functional MRI (fMRI) signal in the dorsolateral prefrontal cortex (DLPFC) and
intraparietal sulcus while performing attentional tasks are a robust and reliable consequence of SD.
Indeed, sleep loss not only decreases task-related activity in these frontal and parietal regions but also
diminishes activity in, and connectivity with, the extrastriate visual cortex during visuospatial attention
tasks. Beyond attentional focus at any particular moment, sleep loss impairs the capacity to sustain
attention over time.
Default mode network
Instability of the default mode network (DMN) has been implicated in attentional impairments with SD.
Several reports describe an inability to fully disengage midline anterior and posterior cortical regions of
the DMN during both selective and sustained attentional task performance under SD conditions.
, Moreover, increased DMN activity during on-task performance for both sustained and selective
attention tests was predictive of slower and less accurate performance by the participant.
2.Working memory: the neural basis of which overlaps anatomically with the attention system — is
also impaired by SD. Deficits in both working- memory and attention tasks have been found to
correlate with reductions in DLPFC and posterior parietal activity.
3. Reward and processing in the sleep-deprived brain
Leading to alterations in motivated behaviours, such as risk taking, sensation seeking and impulsivity.
Rather, SD triggers a generalized increase in reward sensitivity that impairs reward discrimination
accuracy, such that the brain becomes less capable of accurately coding incremental increases in
reward value, from low to high. Inaccurate coding of reward and/or punishment valence in the PFC
following sleep loss may therefore prevent the ability to update changing incentive value (weights) of
reinforcing stimuli over time. This would further contribute to non-optimal reward-dependent decision
making and actions.Under conditions of sleep loss, low-effort rewards elicit even greater reward-
related brain activity than high-effort rewards, relative to sleep-rested conditions.
Sleep deprivation and dopamine function
SD significantly increases the tendency of reward sensitivity, risk taking and impulsivity, and disrupts
reward-value updating and integration. One reason could be altered dopamine signaling.
- First, dopamine is associated with arousal; innately higher levels of dopamine predict lower
sleep propensity.
- Second, rodent studies have established that wake-promoting stimulant drugs such as
amphetamine seem to operate in part by blocking dopamine metabolism, thereby increasing
dopamine transmission and thus arousal.
- Third, depleting catecholamines, including dopamine, reduces wake propensity, lowering
vigilance and inducing sleep.
SD downregulates the availability of dopamine D2 and D3 receptors in the striatum.
4. Aversive stimulus processing
Sleep loss reliably triggers changes in negative (aversive) emotional processing, including irritability,
emotional volatility, anxiety and aggression, as well as suicidal ideation, suicide attempts and suicide
completion.
- Aversive stimulus response: one night of SD was shown to result in a 60% increase in amygdala
reactivity to negative images, such as weapons.
- Emotion discrimination and expression: Sleep-deprived individuals therefore express a
generalized excess of emotional sensitivity, with impairment in emotional discriminatory
specificity. For example, sleep-deprived individuals are less accurate at rating facial expressions
within the moderate range of emotional strength and rate neutral images as more emotionally
negative. Promoting an overall bias towards increased (inaccurate) perception of negative
threat. SD compromises the faithful discrimination of emotional signals within higher-order
emotional brain regions by inducing network hypersensitivity and, in tandem, disrupts the
‘embodied’ reciprocity between viscerosensory central and peripheral autonomic processing of
complex social signals. As a result, there can be a loss of sensitivity in detecting, and accuracy
in recognizing, emotions.
5. Hippocampal memory processing
SD substantially decreases the ability to induce hippocampal long-term potentiation. Sleep loss reduces
hippocampal synthesis of proteins associated with neuroplasticity and impairs hippocampal
neurogenesis. In humans, SD impairs learning and encoding-related activity in the medial temporal
lobe
(hippocampus). Acetylcholinesterase inhibitors enhance attentional processes that support episodic
memory and directly affect sensory processing.
1.Light as a modulator of cognitive brain function
Vandewalle, Maquet, dijk
Light emerges as an important modulator of brain function and cognition. Light does not only provide
visual information but also constitutes a powerful modu-lator of non-visual functions including
improvement of alertness and performance on several cognitive tasks.
Circadian and non-visual effect of lights
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