Focus on Sleep Deprivation

¶ … Sleep Deprivation on the Brain

Studies on sleep deprivation continually display an inconsistent (negative) effect on mood, cognitive behaviour, and motor function as a result of a rising propensity for sleep as well as the destabilization of the wake condition. Unique neurocognitive domains such as executive attention, functioning memory, and conflicting higher cognitive behaviours are specifically apt to loss of sleep. In human beings, functional neurophysiological and metabolic studies prove that neural systems that are part of executive function (i.e., prefrontal cortex) are more prone to sleep deprivation in certain persons than in others. New persistent sleep deprivation studies, where sleep loss that are closely replicated in the society, show that deep neurocognitive shortfalls gather over time when faced with subjective adjustment to sleep sensation. All sleep deprivations that are related to any kind of disease-related disintegration like restless legs syndrome and sleep apnea equally lead to neurocognitive function reductions quite similar to those sleep restriction studies display. Function deficits related to sleep disorders are mostly seen as a mere function of severity of diseases; nevertheless, new experiments prove that the vulnerability of individuals to loss of sleep may play a more vital role than what was previously believed (Durmer & Dinges, 2005).

The Impact of Chronic Sleepiness

People suffering from sleep deprivation often talk about feeling foggy. Below are three reasons why this happens.

1. Thought processes are slowed down by sleepiness. According to scientists who study sleepiness, sleep deprivation leads to lower concentration and alertness. It is not easy to pay attention and focus, which means a person can get more confused easily. This hinders the ability of a person to carry out tasks that call for complex thoughts or logical reasoning. A person's sense of judgement can also be impaired by sleepiness. It becomes difficult to make decisions because an individual cannot carry out adequate assessment of situations and cannot also choose the right set of behaviours (Peri, n.d).

2. Memory is also impaired by sleepiness. According to researches, the nerve endings that are responsible for human memories are further strengthened during sleep. Sleep has a way of embedding what people have learned and the experiences they have had during the day into their short-term memory. It seems that every sleep phase plays a unique role in embedding new ideas and information into memories. If sleep is disrupted or cut short, these cycles are interfered with. When a person feels sleepy, he or she may easily forget or misplace important things most often. And the inability to concentrate and focus as a result of this sleepiness weakens a person's memory further (Peri, n.d).

3. Learning is made more difficult by poor sleeping habits. Sleep deprivation hinders the ability to learn in two distinct ways. Because an individual cannot pay attention when sleeping, picking up information is more difficult, so learning effectively becomes more difficult for the individual. Memory is also affected, despite being a very vital tool for learning. Sleepiness in children often leads to hyperactivity, also hindering learning. Teens easily lose their diligence, focus, and their memory capacity to do well in school works (Peri, n.d).

Sleep deprivation is closely linked to considerable financial, social, and costs related to health to a very large extent due to the fact that it leads to hampered cognitive behaviour as a result of rising sleeping instability and propensity of awakening neurobehavioral performances. Cognitive performances mostly affected by lack of sleep include cognitive speed and psychomotor, executive and vigilante attention, higher cognitive tendencies and working memory. Consistent sleep-restriction studies-which assesses the type of sleep deprivation individuals experience with premature sleep reduction and sleep fragmentation as a result of lifestyle and disorder-show that cognitive deficits build up to very severe levels over time, with the affected individual oblivious of the situation. Functioning neuroimaging has proved that constant and continuous prolonged cognitive lapses, which are known to be the main traits of sleep deprivation, involve circulated changes in the regions of the brain such as parietal and frontal control areas, thalamic and secondary sensory processing areas. There are vast disparities among persons in the level of their cognitive susceptibility to sleep deprivation, which may include disparities in parietal and prefrontal cortices, and that may possibly have a bed rock in the genes responsible for the regulation of circadian rhythms and homeostasis. Therefore, this cognitive deficit, which has always been known to be a product of the seriousness of clinical sleep lapses may be a function of some genetic traits associated with different cognitive susceptivity to sleep deprivation (Goel, Rao, Durmer & Dinges, 2009).

Cognitive Performance during Sleep Deprivation

It is a long established fact that sleep loss reduces aspects of neurocognitive function. The first ever published experimental research of cognitive behaviour impacts of sleep loss on people was given in an 1896 report and included 3 adults having 90 hours of complete wakefulness. Literarily, there are several hundreds of published works on the impacts of total sleep loss, but quite a few on the impacts of partial sleep loss, and only a few of the consistent partial sleep restraint. Additionally, neurocognitive techniques vary from study to study. Three aspects of measurements that are mostly used in sleep loss studies are cognitive behaviour, mood and motor function. Almost every form of sleep loss leads to higher mood states, mostly fatigue feelings, sleepiness, loss of vitality, and confusion. Though the feelings of anxiety, irritability, and depression are known to come from lack of sleep, evidence from the experimental study of the mood states as a result of sleep loss in a predictable and comfortable environment is missing. Conversely, these mood changes have been repeatedly observed whenever sleep deprivation happens with no regards for conditions. Sleep loss brings a wide range of cognitive function impairments in its wake, though there is a variation in the impacts of cognitive performances, though these variations in cognitive tasks sensitivity to sleep loss are quite considerable.

Generally, irrespective of the task, cognitive behaviour worsens progressively when there is an extension of time for the task in question; this is the main fatigue impact that is aggravated by sleep deprivation. Nevertheless, performance on the very minor cognitive tasks, which assess the cognitive throughput speed, working memory, and every other aspect of attention have been discovered to respond sensitively to sleep loss (Goel, Rao, Durmer & Dinges, 2009).

Attention and Working Memory

The two most commonly studied aspects of sleep deprivation (SD) studies are working memory and attention, which are known to be correlated. There are four subdivisions of working memory: visuospatial sketchpad, phonological loop, the central executive and episodic buffer. Acoustic and verbal information are believed to be temporarily stored by the phonological loop (echo memory); visuospatial information (iconic memory) is held by the sketchpad, while information from different sources, are integrated by the episodic buffer. They are all controlled by the central executive. Certain attentional roles may be played by the executive processes of working memory, like unrelenting concentration, which is referred to in this context as vigilance. Both working memory and attention are related to the functions of the frontal lobes. Since the frontal lobe is susceptible to SD, it is possible to come up with a hypothesis that both working memory and attention are hindered in times of prolonged wakefulness (Alhola & Polo-Kantola, 2007).

During the tasks of measuring working memory and attention, there are two important aspects of performance: accuracy and speed. Practically, people can easily switch their importance between the two, using attentional concentration. Most times, focusing on improving a particular aspect, results in the weakening of the other. This is known as the accuracy/speed trade-off phenomenon. According to some SD researches, impairments only exist in speed of performance, while accuracy remains impaired in others, the outcomes are quite opposites.

De Gennaro et al. (2001) recommended that in tasks that are self-paced, there will possibly be a stronger negative effect on speed, whereas accuracy remains unaffected. In tasks that are experimenter-paced, the outcomes would be quite opposites. Nevertheless, several studies have shown detrimental effects on both accuracy and speed (Chee and Choo 2004; Choo et al. 2005). The accuracy/speed trade-off phenomenon is partly affected by age, gender, and individual differences in terms of style and response (Karakorpi et al. 2006), which could explain the existence of several disparities in the SD outcomes.

There are arguments that reduced signal rates raise fatigue during performance in SD experiments and that topics can fall asleep while the test lasts. Thus, tasks that have varied signal loads can give rise to varied results with regards to speed of performance and accuracy (Alhola & Polo-Kantola, 2007).

Long-term Memory

Long-term memory can be shared between non-declarative and declarative (procedural) memory. Declarative memory is limited and explicit, while non-declarative memory implicit with a capacity that is practically unlimited. Declarative memory involves semantic memory, which is made up of understanding the world, and periodic memory, with lots of autographical data. The declarative memory content can be contained in verbal or visual forms and can be recalled voluntarily. Procedural or non-declarative memory involves the needed information in daily behaviour and functioning, e.g., perceptual and motor skills, priming and conditioned functions. In past studies, long-term memory has been assessed using different tasks, with very inconsistent results (Alhola & Polo-Kantola, 2007).

In episodic verbal memory, 35 hours of SD hindered free remembrance, but could not hinder recognition. One night of SD gave opposite results. Both free recall and recognition are episodic memory performances, which appear to be differently affected by SD. Temporal recall memory reduced during 36 hours of SD, though in the same research, face recognition was intact. Under verbal memory, same pattern was noted. Different neural bases may be one explanation, which lends support to the hypothesis of prefrontal vulnerability. There is a strong association between episodic memory and the medial temporal lobes functioning in times of free recall in a rested state, stronger activation of the brain is even found within the prefrontal cortex. It is not clear if this prefrontal activation mirrors the episodic memory performance, organizing the data in working memory, or controlling the memory and attention in an executive way. Instead, recognition is presumed to rely on the thalamus as an addition to the medial temporal lobes. Since the performance of the frontal brain regions is disturbed, especially by the SD, it is therefore not surprising that free recall is more easily affected than recognition (Alhola & Polo-Kantola, 2007).

In the field of SD research, prefrontal cortex susceptibility hypothesis has gotten very wide acceptance and support, despite this, every other brain area is equally involved. For example, the main role of the thalamus is still not known. The thalamic activation during SD has been noted by some studies assessing working memory and attention. This may be a reflection of an effort to recompense attentional function and phasic arousal in times of demanding low arousal condition as a result of SD.

In every other cognitive task, like logical reasoning or verbal memory, no rise in thalamic activation was discovered in spite of the deterioration behaviour that took place. This means that thalami activation in times of SD is mostly connected to some compensation and attentional function, which provides additional support for the theory that prefrontal dependent recall is more easily affected by SD than it is affected by thalamus dependent recognition. Nevertheless, it is quite possible that the patterns of brain activation adopted during SD are a reflection of something that is simply different from cognitive fields (Alhola & Polo-Kantola, 2007).

Other Cognitive Functions

The visuomotor performance is impaired by sleep deprivation, which is measured with digit symbol substitution of tasks, maze tracing, trail-making or letter cancellation. It is widely believed that most visual tasks would be mostly susceptible to sleep deprivation due to the fact that iconic memory has a very short duration as well as a limited capacity (Raidy and Scharff 2005). One other suggestion is the fact that SD hinders spatial attention engagement, which can be viewed as hindrances in saccadic eye motions (Bocca and Denise 2006). Reduced oculomotor performance is related to impaired visual function and sleepiness. Adding to the cognitive areas introduced already, several other cognitive processes are affected by SD. It raises critical thinking, errors in preservation, and difficulties with the utilization of new information in very complex tasks that require very innovative decision-making. Reduction in decision-making equally appears as a more variable function and applied approaches, atop being a riskier function (Killgore et al. 2006). Most other tasks have equally been used in studies on sleep deprivation. For instance, rhythm, motor function, repressive and expressive speech, and the memories measured using the Luria-Nebraska Neuropsychological Battery often deteriorated after just a single night of SD, while reading, writing, tactile function, intellectual and arithmetic processes remain unaffected. The negative effects of total SD experimental designs showed have been equally confirmed in real-life situations, mostly among health workers, military personnel and professional drivers. Residents' performance in routine activities and repeated tasks that require vigilance is more prone to error with prolonged wakefulness (Alhola & Polo-Kantola, 2007).

Memory Acquisition and Retention

Visual short-term memory is hindered by sleep deprivation. Its capacity is also limited by sleep deprivation. A new functional magnetic resonance imaging (fMRI) study (Chee & Chuah, 2007) adopted perceptual or memory load that is parametrically manipulated in two distinct visual tasks, and discovered that there is a decline in behavioural performance in both tasks as well as parietal and extrastriatal activation reduction after sleep deprivation.

On a more serious note, sleep deprivation minimized the linear link existing between parietal activation and memory load at rested wakefulness. However, cholinergic expansion using donepezil minimized the adverse impacts of sleep deprivation on behavioural function across the two tasks and raised parietooccipital activation in a way that is correlated with the function in persons who show vulnerability to sleep deprivation. Lapses in attention, following loss of sleep when compared to those following normal sleep were linked to minimized activation in the thalamus and visual sensory cortex (Goel, Rao, Durmer & Dinges, 2009).

Severe total sleep loss equally created an important deficit in hippocampal function throughout episodic memory encoding, which resulted in more severe consequent retention. Such discoveries mean that inadequate sleep compromises the behavioural and neural capacity for taking new experiences to heart, which is vital to learning processes. Analysis on functional connectivity proved that lack of sleep raised connectivity between the basic alertness networks and hippocampus of the thalamus and brainstem on a memory task consolidation. Like every other neuroimaging studies, these results support the belief that reduce areas of the brain involved in sensory/perceptual gating, arousal, and attentional functions make contributions to memory impairments, following loss of sleep. This conclusion was confirmed recently by a transcranial attractive stimulation research, which showed that simulation occurring in the left tangential occipital cortex enhanced memory performance after sleep deprivation (Goel, Rao, Durmer & Dinges, 2009).

Emotional Memories and Emotional Processing

The role sleep loss plays in consolidating emotional memories, whether positive or negative, and the role it plays in emotional processing has equally been monitored using FMRI. In one recent study, sleep loss reduced the recollection of both positive and neutral stimuli, and not negative stimuli. Successful recall of emotional stimuli brings out bigger responses in the indifferent cortical areas and hippocampus, which includes medial prefrontal cortex, in the group with adequate sleep than in the group with sleep deprivation. When large responses are elicited by sleep deprivation, recall of negative and not positive items within the amygdala and minimized functional correlation between the medial prefrontal cortex and amygdale result (Goel, Rao, Durmer & Dinges, 2009).

Verbal Learning

Employing novel multivariate procedures as against traditional group -- and voxel-wise assessments, two different studies pointed out reduced activation as an aftermath of sleep loss, which has connection with a decline in memory function in both verbal and nonverbal recognition tasks.

In contrast, all other fMRI studies discovered that increased sectional neural performance in the frontparietal network after sleep deprivation, which suggests that a neurobiologic mechanism for compensating cognitive and behavioural impairment results from loss of sleep. A good example, according to Drummond et al. (2000), enhanced activation in the parietal lobe and prefrontal cortex during a verbal learning task performance, following 35 hours of complete lack of sleep. Larger parietal activation was linked to increased memory function on the task. When there was a combination of arithmetic subtraction and verbal learning in a task that required divided attention, fMRI outcomes reflected higher activation in the prefrontal cortex, parietal regions, anterior cingulate cortex, and also showed a positive connection between memory performance and parietal activation, following sleep deprivation. According to Chee and choo (2004), better prefrontal cortex activation during a more complex verbal memory task performance and not during a simple working memory task performance after sleep deprivation. Prefrontal cortex and temporal activation were also increased by sleep deprivation during the performance of a very complex spatial routing task. In a similar way, Mander and co-researchers discovered better parietal activation while stealthy concentration lasted after sleep deprivation. Additionally, through the manipulation of verbal learning task using two-word difficulty levels, better activation was found in the parietal lobe and prefrontal cortex as a response to difficult words following a total of 36 hours lack of sleep. Furthermore, adopting a logic thinking task using parametrically manipulated task difficulty levels, better linear neural responses were discovered in the parietal lobe and prefrontal cortex connected with rising project demands, following sleep deprivation (Goel, Rao, Durmer & Dinges, 2009).