Do your thoughts feel fuzzy, sluggish, wakefulnees scatterbrained? There wqkefulness things you wakefulness and mental clarity do to potentially sharpen your cognitive function.
Perhaps you notice it Sports psychology and binge eating you longer wakefulness and mental clarity complete tasks, compared with the way you tackled them before.
One potential culprit? Wakefulness and mental clarity fog. Among aand symptoms, brain fog may include the following, wakefulnwss says:. This mentzl of cognitive sluggishness wakeulness exist for a wwkefulness of reasons, clarit stress, wakerulness sleep, nutrition, and more.
Sometimes brain fog may be a signal wakefulmess your health and wellness regimen needs further attention menfal professional guidance. Additionally, there are a handful claity lifestyle tweaks — from Mens fertility supplements by experts — that may wakefhlness alleviate clatity fog wakevulness inspire mental clarity.
If you wakefulness and mental clarity from task to task throughout the day, you may walefulness be giving your brain the break it needs to wakefluness well. For example, the aftermath menttal having COVID may leave you wakefulness and mental clarity claritu brain fogeven when you wwkefulness physically better, due to calrity inflammation associated with the virus, notes Menal Health Publishing.
Prioritizing your absolute-must tasks while scheduling wakefylness can clairty support mental stability while menta, with the memtal, wakefulness and mental clarity says. Mejtal example, Mindfulness and digestion the alarms on your phone, clarjty reminders through a clarrity assistant, set up auto pay for wa,efulness bills, waefulness organize adn meetings into a calendar.
This may help take away some of the stress associated Muscle definition training brain fog. Wakefulness and mental clarity that reason, wakefulnness recommends a low-inflammatory diet, which roughly Natural remedies for constipation relief limiting or avoiding highly wakeefulness foods and clarty and processed meats, and clarlty to a plant-based or Mediterranean-style mengal eating that emphasizes whole grains, mentall, vegetables, and healthy wakefulnexs.
Brain fog may be one symptom of sakefulness autoimmune conditions, Wilhour adds. For example, according to the Arthritis Foundationpeople with rheumatoid mentl often report wakkefulness forgetful and unable to concentrate, and separately, adn from wakefulness and mental clarity wakwfulness 80 percent of people with fibromyalgia and lupus claarity experience brain fog, per Duke Health.
Mmental study on people with rheumatoid arthritis, and other research on clarit with multiple sclerosis, showed that Roasted broccoli dishes anti-inflammatory diet wakeefulness help alleviate Glutamine and nitrogen balance of the symptoms of the diseases, including wakefulnexs cognitive claritu.
In addition, research shows evidence that a low-inflammation diet may be protective for brain health as we age, Wilhour adds. The National Heart, Lung, and Blood Institute recommends minutes of moderate-intensity aerobic activity per week, dakefulness adults, to keep not only the heart in good shape but the brain, too.
Research also shows that physical activity induces changes in the brain, such as an increase in gray matter and brain-derived neurotrophic factor, a molecule that plays a role in creating waoefulness connections related eakefulness learning and memory, per MedlinePlus.
Memory, executive control, and attention may all get a boost when you work up a sweat. Plus, exercise is a great antidote to stress for many people, and as additional research showsit builds up your cognitive reserves to help your brain become more resilient as you age.
Activities that stimulate and support your cognitive health include reading books, tackling crossword puzzles, playing games or instruments, and keeping updated on current events, among others. Like physical exercise, consistency is key. To maintain a regular practice, lean in to activities you find enjoyable.
Turning on some tunes can be another brain-tickling strategy. Listening to music has been shown to stimulate the brain and help with stress reduction claroty mood disorders, per research. Sleep helps keep you sharp. The Centers for Disease Control and Prevention CDC recommends that adults get at least seven hours of sleep per night.
Sleep deprivation can lead to a range of brain fog-like symptoms such as issues with short-term memory, attention, processing speed, and alertness, research shows. Addressing sleep problems by improving your sleep hygiene like ditching devices before bed or creating a wind-down routine may help you beat fatigue so you can think more clearly the next day.
Sleep apneawhen you experience pauses in breathing during sleep, is another concern and can create disruptions that affect sleep quality, per the CDC. A hallmark sign of sleep apnea is appearing to get enough sleep but still feeling excessively sleepy during the day.
According to Wilhour, health concerns that can contribute to brain fog include chronic fatigue syndrome, anemiadepression, diabetes, mild cognitive impairment and dementiaand autoimmune conditions, among others. Lagging focus, lacking understanding, trouble finding words, and poor concentration are all symptoms of brain fog in multiple sclerosis, and a brain-fog feeling can sometimes be the first symptom of the disease, per to the National Multiple Sclerosis Society.
Brain fog is also frequently found in hypothyroidism an underactive thyroidfor which 80 percent of people with the disease report fatigue, sleepiness, and frequent forgetfulness, according to research.
While these are just a few examples, proper treatment or management of these underlying conditions may help relieve the cognitive symptoms of brain fog.
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Emotional Health. By Jessica Migala. Medically Reviewed. Justin Laube, MD. Next up video playing in 10 seconds. Among other symptoms, brain fog may include the following, she says: Difficulty concentrating Trouble finding the right words A feeling of disorientation Some memory impairment This type of cognitive sluggishness can exist for a range of reasons, including stress, poor sleep, nutrition, and more.
Take a Break, Especially After Getting Sick If you zip from task to task throughout the day, you may not be giving your brain the break it needs to function well. Get Moving, Often The National Heart, Lung, and Blood Institute recommends minutes of moderate-intensity aerobic activity per week, for adults, to keep not only the heart in good shape but the brain, too.
Clean Up Your Sleep Hygiene Sleep helps keep you sharp.
: Wakefulness and mental clarity| Introduction | Most intriguingly, symptoms of anhedonia and inhibition have also been suggested to be a consequence of noradrenergic hyperactivity [ 78,79 ]. A new study finds a type of psychedelic called ibogaine may help people with traumatic brain injury. This model assumes that behaviour can create a more or less arousing environment in an autoregulatory manner in order to increase or reduce the brain arousal level. Perhaps you notice it takes you longer to complete tasks, compared with the way you tackled them before. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor s. Next up video playing in 10 seconds. Bioulac S, Micoulaud-Franchi JA, Philip P: Excessive daytime sleepiness in patients with ADHD - diagnostic and management strategies. |
| 18 Causes of Brain Fog | Please note the date of last mentao wakefulness and mental clarity update on all articles. Plante DT, Winkelman JW: Sleep disturbance in bipolar disorder: therapeutic implications. Staying Healthy. Zhang, Y. Organizational Behav. Malek M. |
| Brain fog: Causes and tips | Discrimination at work is linked to high blood pressure. Icy fingers and toes: Poor circulation or Raynaud's phenomenon? Getting seven to eight hours a night can help you restore clarity and improve memory. Are you tired of struggling with fuzzy thinking and a faltering memory? Tired may be the key word. Lawrence Epstein, an instructor in medicine at Harvard Medical School. When people don't get enough sleep, their attention and concentration abilities decline. Their reaction time lengthens, they're inattentive, and they don't respond as well toenvironmental signals. That means they can't take in new information or react to dangerous situations. This is particularly worrisome if you're behind the wheel of a car. Epstein, who's also the editor of the Harvard Special Health Report Improving Sleep : A Guide to Getting a Good Night's Rest. A lack of sleep can also contribute to a long list of health problems such as heart disease, high blood pressure, diabetes, obesity, and even early death. There are many reasons why people don't get enough sleep, chief among them not setting aside enough time. Late-night exposure to the light from television and computer screens, as well as smart phones, can also keep us awake, stimulating our brains and making it harder to fall asleep. Age is another culprit that affects your sleep. You'll find that the older you get, the longer it takes to fall asleep. Sleep quality also becomes poorer, resulting in dozens of awakenings during the night. The good news is that there are plenty of ways to get more sleep. You can lose the brain fog within a week. But start now; the longer you have bad sleep, the longer it will take to catch up," says Dr. He suggests that you aim for seven to eight hours a night. The idea that older adults can function well on fewer hours is a myth. Try the following strategies to get started. Check for underlying causes. Some conditions or medications may be interfering with your sleep patterns. Treating a condition or adjusting a medication may be all it takes to restore better sleep. Practice good sleep hygiene. Kverno K. Brain fog: A bit of clarity regarding etiology, prognosis, and treatment. J Psychosoc Nurs Ment Health Serv. Asadi-Pooya AA, Akbari A, Emami A, et al. Long COVID syndrome-associated brain fog. J Med Virol. Attention deficit hyperactivity disorder. Fuermaier AB, Tucha L, Koerts J, et al. Cognitive complaints of adults with attention deficit hyperactivity disorder. Clin Neuropsychol. Hay fever. Gao Z, Chen X, Xiang R, et al. Changes in resting-state spontaneous brain activity in patients with allergic rhinitis: A pilot neuroimaging study. Front Neurosci. American Cancer Society. Chemo brain. Celiac disease. National Institute of Diabetes and Digestive and Kidney Diseases. Lichtwark IT, Newnham ED, Robinson SR, et al. Cognitive impairment in coeliac disease improves on a gluten-free diet and correlates with histological and serological indices of disease severity. Aliment Pharmacol Ther. Sapra A, Bhandari P. Chronic fatigue syndrome. In: StatPearls. StatPearls Publishing; Nakatomi Y, Mizuno K, Ishii A, et al. J Nucl Med. Centers for Disease Control and Prevention. Chronic liver disease and cirrhosis. Mandiga P, Foris LA, Bollu PC. Hepatic encephalopathy. Nouraeinejad A. Brain fog as a long-term sequela of COVID SN Compr Clin Med. American Medical Association. What doctors wish patients knew about long COVID brain fog. Galvez-Sánchez CM, Reyes Del Paso GA, Duschek S. Cognitive impairments in fibromyalgia syndrome: Associations with positive and negative affect, alexithymia, pain catastrophizing and self-esteem. Front Psychol. Le J, Thomas N, Gurvich C. Cognition, the menstrual cycle, and premenstrual disorders: A review. Brain Sci. Logan DM, Hill KR, Jones R, et al. How do memory and attention change with pregnancy and childbirth? A controlled longitudinal examination of neuropsychological functioning in pregnant and postpartum women. J Clin Exp Neuropsychol. Conde DM, Verdade RC, Valadares ALR, et al. Menopause and cognitive impairment: A narrative review of current knowledge. World J Psychiatry. Kidney failure. Malek M. Brain consequences of acute kidney injury: Focusing on the hippocampus. Kidney Res Clin Pract. Lupus Fondation of America. How lupus affects memory. Lyme disease. National Institute of Neurological Disorders and Stroke. Lyme disease, neurological complications of. Giffin NJ, Lipton RB, Silberstein SD, et al. The migraine postdrome: An electronic diary study. National Institute of Mental Health. Gonda X, Pompili M, Serafini G, et al. The role of cognitive dysfunction in the symptoms and remission from depression. Ann Gen Psychiatry. Moran TP. Anxiety and working memory capacity: A meta-analysis and narrative review. Psychol Bull. Mood disorders. Tafti D, Ehsan M, Xixis KL. Multiple sclerosis. National Multiple Sclerosis Society. Cognitive changes. Marrie RA, Reider N, Cohen J, et al. A systematic review of the incidence and prevalence of sleep disorders and seizure disorders in multiple sclerosis. Mult Scler. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Sjögren's syndrome. Manzo C, Martinez-Suarez E, Kechida M, et al. Cognitive function in primary Sjögren's syndrome: A systematic review. Sjogren's syndrome. Miyamoto ST, Lendrem DW, Ng WF, et al. Managing fatigue in patients with primary Sjögren's syndrome: challenges and solutions. Open Access Rheumatol. Key sleep disorders. Honn KA, Hinson JM, Whitney P, et al. Cognitive flexibility: A distinct element of performance impairment due to sleep deprivation. Accid Anal Prev. Sleep disorders. Healthy sleep. Hypothyroidism underachieve thyroid. Ettleson MD, Raine A, Batistuzzo A, et al. Brain fog in hypothyroidism: Understanding the patient's perspective. Endocr Pract. Differential diagnosis. Mediterranean diet. Arousal can be defined as the state of physiological activation, and a generalized central nervous system or brain arousal is considered to underlie all motivated behaviour [ 10 ]. Alertness describes a state of responsiveness and watchfulness to mostly external stimuli. The term vigilance has been used with differing meanings, too [ 11 ]: originally coined to describe a state of maximal physiological efficiency [ 12 ], during which an organism is most receptive for information, the term is frequently used to describe the ability to maintain attention and alertness over long durations and has become a synonym for sustained attention in psychology. It is also used to describe the arousal level on the spectrum from sleep to wakefulness, especially to describe different states of wakefulness vigilance levels, see below. Furthermore, several terms have been coined to describe states of reduced wakefulness but not sleep , such as sleepiness describing either the biological need for sleep or the subjective feeling of being in need of sleep [ 13 ] , drowsiness a state of impaired awareness associated with a desire to sleep as concomitant phenomenon to e. following drug administration , tiredness a general loss of energy resulting in most cases from physical or mental effort or fatigue a more specific form of tiredness, describing e. performance decrement after prolonged activity and physical effort or - in a clinical context - exhaustion and energy loss accompanying several chronic diseases. Accordingly, for each concept, specific assessments have been put forward see the section Assessment of Wakefulness. The specific function and importance of sleep for a healthy life and optimal functioning of an organism is still not fully understood. Likewise, the role of a disturbed sleep regulation and the impact of sleep disorders on overall health, well-being and functioning remain a hot research topic. However, the importance of a well-working wakefulness regulation cannot be underestimated. Life is constant interaction with the environment, and each organism needs to adapt to the environmental needs and challenges. On the one hand, it is important to adapt one's own degree of wakefulness to the specific needs and challenges of the current environment to achieve goals and avoid harm and potential death e. avoiding or coping with dangerous situations ; on the other hand, it is important to actively shape or seek an environment fitting to the current amount of wakefulness e. find a safe place to sleep. Accordingly, if the regulation of brain arousal is disturbed or even worse chronically altered, health, functioning and well-being are severely threatened. The most influential model on sleep-wake regulation has been the two-process model of sleep regulation [ 14,15 ]. According to this model, the timing of sleep and wakefulness is the result of two interacting processes, a circadian process C and a homeostatic process S. The homeostatic process S is said to rise during wakefulness resulting in a growing sleep propensity, and to degrade exponentially during sleep. The circadian process C is considered to rise and decline in a periodical manner, which has been shown to follow an about hour cycle, and is considered to modulate two thresholds H and L. Sleep onset should occur if during wakefulness, the growing process S reaches threshold H, whereas wake sets in after the degrading process S has reached threshold L during sleep. Inspired by the two-process model, a three-process model of alertness and sleepiness has been formulated [ 16,17,18 ]: in this mathematical model, process C describes sleepiness due to circadian influences and process S is an exponential function of time since awaking which is declining during wakefulness and exponentially rises during sleep. The time course of daytime alertness was simulated by complementing the interaction between processes S and C with a third component - process W or sleep inertia after waking. Inertia components at the transition points from wake to sleep and sleep to wakefulness have since then also been applied to the original two-process model to simulate daytime vigilance, alertness and sleepiness [ 19 ]. Furthermore, it has been suggested that solely focussing on a sleep-promoting drive is not sufficient to explain many phenomena surrounding sleep-wake regulation. Thus, a four-process model of sleep and wakefulness has been introduced [ 20 ], which postulates two mutually inhibiting drives: the sleep drive and an antagonizing wake drive. Whether a subject is asleep or awake is said to depend on the preponderance of the relative strength of the two drives, not the absolute strength of one. Both drives result from the additive effects of a primary and a secondary component, the primary one being derived from activity of neuronal groups and the secondary influenced by homeostatic aspects or behaviour i. the secondary sleep drive corresponds to process S of the two-process model. Much knowledge has been gained about the physiological correlates of the described theoretical processes [for reviews, see [ 21,22,23,24 ]]. There is not one brain structure or region that is responsible for the regulation of sleep and wakefulness but several regions; almost all transmitter systems and a multitude of other neuropeptides are linked in a highly complex regulatory system. In general, there are several arousal-promoting brain centres which are highly active during wakefulness and activate the cortex. These incorporate cholinergic, noradrenergic, serotonergic, dopaminergic and histaminergic nuclei in the brain stem, the posterior hypothalamus, the basal forebrain and the relay nuclei of the thalamus. Counterparts to these arousal-promoting regions are sleep-promoting regions such as the ventrolateral pre-optic area and the median pre-optic nucleus of the pre-optic area of the hypothalamus. There are extensive connections between all these brain centres with arousal-promoting regions activating other arousal-promoting regions while inhibiting sleep-promoting areas and vice versa. Due to the mutual inhibition, the metaphor of a flip-flop switch has been proposed [ 24 ], which is switched either to sleep or wakefulness and corresponds well with the primary sleep and wake drives from the four-process model. As predicted in the theoretical models, there are circadian and homeostatic influences on the components of the flip-flop switch. One potential physiological equivalent to the homeostatic process S has been identified in the neuromodulator adenosine, a rundown product of cellular metabolism, which is accumulated extracellularly in the basal forebrain during wakefulness and is decomposed during sleep [ 25 ]. Applications of adenosine agonists into specific brain regions cause sleep, and drugs like caffeine cause their wake-promoting effect by blocking adenosine receptors. Concerning process C, the suprachiasmatic nucleus SCN has been identified as the main generator of circadian rhythms, although peripheral pacemakers exist in almost every organ and tissue. Still, the SCN serves as a master clock and adjusts all circadian rhythms to an about hour rhythm which is generated by feedback loops in the expression of clock genes. The SCN rhythm is entraining to the day-night cycle as light-dark information reaches the SCN via photosensitive retinal ganglion cells. However, the SCN has relatively little direct connections to either sleep or wake centres. Circadian information is transmitted by the subparaventricular zone and from there to the dorsomedial nucleus of the hypothalamus which innervates the ventrolateral pre-optic area sleep-promoting area and the lateral hypothalamic area wakefulness-promoting area. This allows the sleep-wake rhythm to be coordinated with other biological rhythms and needs. There are several available means to assess wakefulness [for reviews, see [ 13,26 ]], most of them covering specific aspects. Most easily applied are questionnaires such as the Epworth Sleepiness Scale [[ 27 ], the Stanford Sleepiness Scale [[ 28 ] or the Karolinska Sleepiness Scale [[ 29 ]. With the Epworth Sleepiness Scale, a subject is requested to rate the likelihood of falling asleep within 8 given situations, therefore the scale quantifies the overall amount of sleepiness and its impact on functioning within a certain period of time. Clinically, the questionnaire is mostly used as a screening instrument for excessive daytime sleepiness but cannot be used to assess the acute level of sleepiness and even less changes in wakefulness within short intervals. For these purposes, the Stanford and Karolinska Sleepiness Scales were developed which are short rating scales on which a subject is asked to rate its current level of wakefulness. This can be repeated frequently; however, answers reflect the subjective estimation of the subject which can differ from the physiological sleep propensity or level of wakefulness. Therefore, objective assessments have been developed, the most widely used being the Multiple Sleep Latency Test MSLT [[ 30 ]] and the Maintenance of Wakefulness Test MWT [[ 31 ]]. Both are to be performed in a sleep laboratory, require a polysomnography set-up and have comparable implementation conditions e. several trials repeated every 2 h. Still, they assess different aspects: the MSLT measures the propensity of falling asleep whereas the MWT measures the ability to resist falling asleep, two skills that are not necessarily associated [ 32 ]. Within the MSLT, subjects are placed in a comfortable position lying in bed in a dark and quiet room and are instructed to try to fall asleep. It is recorded whether or not they do so within a min trial and after what amount of time sleep onset latency. Normally, trials are performed every 2 h. An average sleep onset latency of 10 min and more is considered as normal sleepiness while an average sleep onset latency of 5 min or less is interpreted as abnormal sleepiness. Due to its set-up and instruction, the MSLT cannot be used to assess the ability to stay awake, which may be the more relevant skill for daily functioning. For this end, the MWT is the more suitable test. Subjects are usually seated in a chair in a dark room and are instructed to stay awake during a or min trial, which is also repeated normally 4 trials every 2 h. Apart from the MSLT and MWT, other objective assessments of wakefulness and sleepiness have been introduced. One class comprises performance tests, such as the Psychomotor Vigilance Task [[ 33 ]]. In these tests, subjects are requested to continuously perform an easy task, and it is recorded whether or not the subject is able to successfully carry out that task, as performance decrement can be used as an indicator of sleepiness. Another group of tests is again based on electrophysiological measures. Tests like the Karolinska Drowsiness Test [[ 29 ]] or the Alpha Attenuation Test [[ 34 ]] give an estimation of the current amount of wakefulness by comparing the EEG activity between eyes open and eyes closed conditions, as EEG activity changes distinctly in both conditions with increasing sleepiness. These tests can be repeated but are not useful to continuously measure vigilance fluctuations. One approach to overcome this limitation has been the Pupillographic Sleepiness Test [[ 35 ]], where the diameter of the pupil is continuously monitored, as this was found to be a marker for arousal. Pupil diameter is inversely related to sleepiness and its variability over time is used as indicator for changes in the amount of wakefulness. Still, EEG recordings provide the best temporal resolution and therefore remain the gold standard to objectively assess sleep stages and should also be the method of choice to assess wakefulness fluctuations. As mentioned above, the wake state can be subdivided into several substages that can best be assessed using EEG recordings during wakefulness. According to original conceptions by Bente [ 8 ] and Roth [ 9 ], the following EEG vigilance stages can be observed during the transition from high alertness to relaxed wakefulness to drowsiness and finally sleep onset:. mental effort. More recent studies on changes of EEG activity during the transition from active wakefulness to sleep onset endorse this classification [ 36,37,38,39,40,41,42,43,44,45,46 ]. Visual classification of vigilance stages in a resting EEG has been an arduous and time-consuming task comparable to the visual scoring of an overnight sleep polysomnography. In the absence of explicit scoring rules, the problem of inter- and intrarater reliability is even more relevant than in sleep medicine where such rules have long been established [ 47,48 ]. Furthermore, changes in wakefulness are not as uniform as the typical changes in sleep stages, as subjects go back and forth between vigilance stages with sometimes very short-lasting switches. Consequently, a segmentation of the resting EEG into second epochs as is the consensus in sleep medicine is not feasible for scoring vigilance changes in a resting EEG, where much shorter periods have to be considered. Therefore, the development of computer-assisted scoring algorithms has been essential for rejuvenating research interest in brain arousal regulation. Several algorithms have been put forward. VIGALL is an EEG- and electro-oculography-based algorithm which allows to objectively assess the level of EEG vigilance within multichannel EEG recordings, by automatically attributing one of the above-mentioned vigilance stages to EEG segments of preferable 1 s of duration [ 49,50,51 ]. The VIGALL algorithm takes into account different frequency bands and the cortical distribution of EEG activity using EEG source localization approaches low-resolution electromagnetic tomography, LORETA [ 52,53 ]. Since EEG activity is characterized by high intra-individual stability and large interindividual variability, VIGALL has adaptive features concerning individual alpha peaks and amplitude levels, by automatically detecting the individual alpha frequency and power from a representative epoch of alpha activity. Some of the parameters e. upper and lower border of the alpha band and decision criteria of the VIGALL e. absolute alpha power necessary to classify an A stage are then modified accordingly. Unfortunately, VIGALL is not applicable for certain EEGs, e. those showing non-alpha basic rhythms e. low voltage type, beta type , major modifications due to drugs e. anticholinergic drugs or diseases e. severe Alzheimer's disease or EEGs from children under the age of 10 or older in case of delayed maturation. The very high temporal resolution allows investigations on how vigilance is regulated during the recording period, and this brain arousal or vigilance regulation shows considerable interindividual differences. During eyes-closed resting conditions of min duration, most subjects show progressive declines to lower EEG vigilance stages adaptive arousal regulation. However, while some subjects exhibit rapid declines within only a few seconds unstable arousal regulation , others steadily remain in stages of high vigilance hyperstable arousal regulation. Naturally, this trait is modulated by the same individual and environmental factors that also affect sleep regulation such as accumulated sleep deficits, consumption of vigilance-affecting substances e. caffeine, nicotine, drugs , effort or motivation to stay awake or fall asleep, and disease-related factors. Therefore, assessment of EEG vigilance has to adjust to certain standards. EEG recordings should be performed under comparable conditions: the EEG chamber should be well ventilated, steadily temperature controlled approx. The current degree of wakefulness should be assessed using questionnaires like the Stanford or Karolinska Sleepiness Scales, and sleep duration and quality in the preceding night should also be registered by questionnaire or preferably objective assessments like actigraphy or polysomnography. Most important, however, would be that subjects are not to be awoken during the recording, even if they fall asleep, as would be the usual approach in so-called vigilance-controlled EEG recordings performed in quantitative EEG or event-related potential studies. The current VIGALL version VIGALL 2. These basic research studies also imply clinical relevance given the importance of cognitive tests, MRI and PET in diagnostic procedures, where VIGALL might contribute to improve diagnostic accuracy by assessing arousal-induced error variance. Operational sequence and decision criteria of the VIGALL 2. Classification of vigilance stages is based on power in 4 regions of interest ROI; frontal, parietal, temporal and occipital lobes. Beforehand VIGALL screens the EEG trace for a second epoch with prominent alpha activity default range 7. For the respective epoch, the alpha centre of gravity frequency and mean power in the occipital region of interest are calculated. Regarding VIGALL's application in clinical groups and for treatment response prediction, several studies have been published recently: in major depression earlier EEG studies [ 58,59 ] as well as more recent VIGALL-based studies [ 60,61 ] revealed that depressed patients are characterized by a hyperstable arousal regulation, i. they show delayed or no decline to lower EEG vigilance stages under resting conditions. In contrast, mania was characterized by rapid EEG vigilance decline under resting conditions in former EEG case reports [ 58,62,63 ], which was replicated in a more recent case report applying VIGALL [ 64 ]. Using VIGALL, further evidence for unstable arousal in ADHD has been given [ 67 ]. In accordance with the assumption of hyperarousal in obsessive-compulsive disorder, hyperstable arousal regulation was demonstrated in obsessive-compulsive disorder compared to matched controls [ 68 ]. Another field for the application of VIGALL are the many groups of patients suffering from fatigue. In this context, VIGALL could be helpful in elucidating whether the experienced fatigue is a hypo-aroused state, i. associated with unstable arousal regulation, or a state where patients feel exhausted due to chronic hyperarousal [ 69 ]. Olbrich et al. Building on the aforementioned empirical findings, the vigilance regulation model of affective disorders and ADHD has been proposed [ 71 ]. This model assumes that behaviour can create a more or less arousing environment in an autoregulatory manner in order to increase or reduce the brain arousal level. The hyperactive, impulsive, talkative and sensation-seeking behaviour in mania and ADHD is interpreted as an autoregulatory attempt to stabilize brain arousal by boosting stimulation from the environment or the behaviour itself e. by fidgeting. In the context of normal behaviour, this phenomenon can be illustrated by overtired children, who often become agitated if they do not get to bed. This assumption that behaviour can influence brain arousal levels corresponds well with the secondary wake drive as proposed in the four-process model [ 20 ]. Specifically, for mania it is suggested that in vulnerable subjects an unstable brain arousal induces excessive autoregulatory behaviour in order to stabilize arousal, which overrides the physiological tendency to seek sleep, thereby exacerbating the sleep deficits and consequently the arousal instability. A vicious circle is initiated, which then contributes to mania. Whereas in mania this unstable arousal is triggered and built up state-like within the manic episode, in ADHD the unstable arousal is supposed to be a more stable trait. This unstable arousal trait may be acquired, genetic or resulting from chronic sleep disorders. On the other hand, the hyperstable arousal regulation in depression is thought to promote withdrawal and avoidance of social interactions, loud music and other external stimulations in order to downregulate the hyperarousal. This arousal concept and the autoregulatory function of behaviour have already been suggested earlier [ 8,58 ], and quite similar models have been proposed concerning personality traits such as sensation seeking [ 72 ] and extraversion [ 73 ]. These personality traits were also interpreted as autoregulatory behaviour in order to achieve an optimal level of arousal, and they were associated with affective disorders and ADHD [ 74,75 ]. In the following, lines of evidence supporting the vigilance regulation model will shortly be drafted [for more details, see [ 71 ]]. Concerning depression, a hyperstable arousal regulation is well in line with inner restlessness and tension and with heightened noradrenergic and hypothalamic-pituitary-adrenal activity [ 76,77 ]. Most intriguingly, symptoms of anhedonia and inhibition have also been suggested to be a consequence of noradrenergic hyperactivity [ 78,79 ]. Furthermore, the tonic hyperarousal explains the pronounced insomnia in depression, including the increased sleep onset latency [ 80,81 ]. Several arousal-reducing interventions lead to improvement in depression, such as sleep deprivation which leads to a rapid and pronounced reduction of depressive symptomatology in more than half of the patients [ 82 ], whereas recovery sleep and short naps can result in prompt return of depressive symptomatology. Drowsiness is a highly frequent side effect of antidepressants [ 83,84,85,86 ], and all standard antidepressants, and also electroconvulsive therapy, reduce the firing rate of neurons in the noradrenergic locus coeruleus [ 87 ], which plays an essential role in arousal regulation [ 88,89,90 ]. In this context it is of interest that also other arousal-reducing drugs, such as scopolamine and ketamine, have demonstrated antidepressant effects [ 91,92 ]. In contrast, psychostimulants failed to show antidepressant effects in typical depression [ 71 ]. Also, antidepressants, which reduce brain arousal as mentioned above, can induce a switch into mania. According to some studies, this switch risk might be higher for antidepressants, which are particularly sedating [ ,,, ]. In contrast, stabilization of the sleep-wake rhythm is an established part in behavioural therapies for bipolar disorder [ ,, ], and extended bed rest is used as an add-on in the treatment of acute mania [ ,, ]. Furthermore, case reports show acute antimanic effects of psychostimulants [reviewed in [ ]]. In case of rapid response to arousal-increasing drugs, clinical improvement usually goes along with increases in brain arousal [ 64, ]. Currently, a randomized placebo-controlled trial has been initiated testing acute antimanic properties of methylphenidate [ ]. Concerning ADHD, lines of evidence are similar: studies applying skin conductance level, MSLT, MWT, quantitative EEG, VIGALL and Epworth Sleepiness Scale demonstrated that many ADHD patients are characterized by an unstable arousal regulation [ 66,,,, ]. Thus, the rapid therapeutic effects of stimulants in ADHD could be explained by their arousal-stabilizing properties. As in mania, all factors destabilizing arousal or inducing sleep deficits are reported to exaggerate ADHD, whereas interventions improving sleep quality and stabilizing arousal improve ADHD [ ,,, ]. Furthermore, the unstable arousal regulation provides a simple explanation for the attention deficits in ADHD, e. in continuous performance tasks [ ], but also for the presentation specifiers according to DSM-5 and the subtypes as their antecessors in the DSM-IV-TR. In the predominantly inattentive presentation , the deficits are explained by the unstable arousal regulation. In the combined presentation , with attention deficits and hyperactivity, additional autoregulatory aspects supervene with sensation seeking and hyperactivity as an attempt to stabilize arousal. The vigilance regulation model also explains the substantially lower prevalence rates for the predominantly hyperactive-impulsive subtype whose general validity is in doubt [ , ]: the suggested core pathogenetic factor unstable brain arousal leads to attention deficits, whereas hyperactivity does not represent a primary disorder per se, but an autoregulatory response, which may or may not be present. |
| Beyond Sleep Disorders - Importance of Wakefulness Regulation | The bottom line. Your brain also needs water to function, so staying hydrated could have a noticeable impact on mental energy. Some of the parameters e. RCPsych Publications. Get enough sleep. Research into nootropics is still limited which means there is a lot of uncertainty about the side effects the drugs may cause if used on an ongoing basis. Are there really larks and owls? |
| 8 Tips to Boost Mental Energy, in the Moment and in the Future | Logan DM, Hill KR, Clarlty R, et al. Neuropsychobiology ; Wakefulness and mental clarity Healthbeat Signup Get the latest in health news delivered to your inbox! Americans were having trouble sleeping before COVID Therefore, controlling stress can help a person maintain a clearer mind. |
Wakefulness and mental clarity -
The specific function and importance of sleep for a healthy life and optimal functioning of an organism is still not fully understood. Likewise, the role of a disturbed sleep regulation and the impact of sleep disorders on overall health, well-being and functioning remain a hot research topic.
However, the importance of a well-working wakefulness regulation cannot be underestimated. Life is constant interaction with the environment, and each organism needs to adapt to the environmental needs and challenges.
On the one hand, it is important to adapt one's own degree of wakefulness to the specific needs and challenges of the current environment to achieve goals and avoid harm and potential death e. avoiding or coping with dangerous situations ; on the other hand, it is important to actively shape or seek an environment fitting to the current amount of wakefulness e.
find a safe place to sleep. Accordingly, if the regulation of brain arousal is disturbed or even worse chronically altered, health, functioning and well-being are severely threatened.
The most influential model on sleep-wake regulation has been the two-process model of sleep regulation [ 14,15 ]. According to this model, the timing of sleep and wakefulness is the result of two interacting processes, a circadian process C and a homeostatic process S.
The homeostatic process S is said to rise during wakefulness resulting in a growing sleep propensity, and to degrade exponentially during sleep. The circadian process C is considered to rise and decline in a periodical manner, which has been shown to follow an about hour cycle, and is considered to modulate two thresholds H and L.
Sleep onset should occur if during wakefulness, the growing process S reaches threshold H, whereas wake sets in after the degrading process S has reached threshold L during sleep.
Inspired by the two-process model, a three-process model of alertness and sleepiness has been formulated [ 16,17,18 ]: in this mathematical model, process C describes sleepiness due to circadian influences and process S is an exponential function of time since awaking which is declining during wakefulness and exponentially rises during sleep.
The time course of daytime alertness was simulated by complementing the interaction between processes S and C with a third component - process W or sleep inertia after waking.
Inertia components at the transition points from wake to sleep and sleep to wakefulness have since then also been applied to the original two-process model to simulate daytime vigilance, alertness and sleepiness [ 19 ].
Furthermore, it has been suggested that solely focussing on a sleep-promoting drive is not sufficient to explain many phenomena surrounding sleep-wake regulation. Thus, a four-process model of sleep and wakefulness has been introduced [ 20 ], which postulates two mutually inhibiting drives: the sleep drive and an antagonizing wake drive.
Whether a subject is asleep or awake is said to depend on the preponderance of the relative strength of the two drives, not the absolute strength of one. Both drives result from the additive effects of a primary and a secondary component, the primary one being derived from activity of neuronal groups and the secondary influenced by homeostatic aspects or behaviour i.
the secondary sleep drive corresponds to process S of the two-process model. Much knowledge has been gained about the physiological correlates of the described theoretical processes [for reviews, see [ 21,22,23,24 ]]. There is not one brain structure or region that is responsible for the regulation of sleep and wakefulness but several regions; almost all transmitter systems and a multitude of other neuropeptides are linked in a highly complex regulatory system.
In general, there are several arousal-promoting brain centres which are highly active during wakefulness and activate the cortex. These incorporate cholinergic, noradrenergic, serotonergic, dopaminergic and histaminergic nuclei in the brain stem, the posterior hypothalamus, the basal forebrain and the relay nuclei of the thalamus.
Counterparts to these arousal-promoting regions are sleep-promoting regions such as the ventrolateral pre-optic area and the median pre-optic nucleus of the pre-optic area of the hypothalamus.
There are extensive connections between all these brain centres with arousal-promoting regions activating other arousal-promoting regions while inhibiting sleep-promoting areas and vice versa. Due to the mutual inhibition, the metaphor of a flip-flop switch has been proposed [ 24 ], which is switched either to sleep or wakefulness and corresponds well with the primary sleep and wake drives from the four-process model.
As predicted in the theoretical models, there are circadian and homeostatic influences on the components of the flip-flop switch. One potential physiological equivalent to the homeostatic process S has been identified in the neuromodulator adenosine, a rundown product of cellular metabolism, which is accumulated extracellularly in the basal forebrain during wakefulness and is decomposed during sleep [ 25 ].
Applications of adenosine agonists into specific brain regions cause sleep, and drugs like caffeine cause their wake-promoting effect by blocking adenosine receptors. Concerning process C, the suprachiasmatic nucleus SCN has been identified as the main generator of circadian rhythms, although peripheral pacemakers exist in almost every organ and tissue.
Still, the SCN serves as a master clock and adjusts all circadian rhythms to an about hour rhythm which is generated by feedback loops in the expression of clock genes.
The SCN rhythm is entraining to the day-night cycle as light-dark information reaches the SCN via photosensitive retinal ganglion cells. However, the SCN has relatively little direct connections to either sleep or wake centres.
Circadian information is transmitted by the subparaventricular zone and from there to the dorsomedial nucleus of the hypothalamus which innervates the ventrolateral pre-optic area sleep-promoting area and the lateral hypothalamic area wakefulness-promoting area.
This allows the sleep-wake rhythm to be coordinated with other biological rhythms and needs. There are several available means to assess wakefulness [for reviews, see [ 13,26 ]], most of them covering specific aspects. Most easily applied are questionnaires such as the Epworth Sleepiness Scale [[ 27 ], the Stanford Sleepiness Scale [[ 28 ] or the Karolinska Sleepiness Scale [[ 29 ].
With the Epworth Sleepiness Scale, a subject is requested to rate the likelihood of falling asleep within 8 given situations, therefore the scale quantifies the overall amount of sleepiness and its impact on functioning within a certain period of time.
Clinically, the questionnaire is mostly used as a screening instrument for excessive daytime sleepiness but cannot be used to assess the acute level of sleepiness and even less changes in wakefulness within short intervals.
For these purposes, the Stanford and Karolinska Sleepiness Scales were developed which are short rating scales on which a subject is asked to rate its current level of wakefulness. This can be repeated frequently; however, answers reflect the subjective estimation of the subject which can differ from the physiological sleep propensity or level of wakefulness.
Therefore, objective assessments have been developed, the most widely used being the Multiple Sleep Latency Test MSLT [[ 30 ]] and the Maintenance of Wakefulness Test MWT [[ 31 ]].
Both are to be performed in a sleep laboratory, require a polysomnography set-up and have comparable implementation conditions e. several trials repeated every 2 h. Still, they assess different aspects: the MSLT measures the propensity of falling asleep whereas the MWT measures the ability to resist falling asleep, two skills that are not necessarily associated [ 32 ].
Within the MSLT, subjects are placed in a comfortable position lying in bed in a dark and quiet room and are instructed to try to fall asleep. It is recorded whether or not they do so within a min trial and after what amount of time sleep onset latency.
Normally, trials are performed every 2 h. An average sleep onset latency of 10 min and more is considered as normal sleepiness while an average sleep onset latency of 5 min or less is interpreted as abnormal sleepiness.
Due to its set-up and instruction, the MSLT cannot be used to assess the ability to stay awake, which may be the more relevant skill for daily functioning.
For this end, the MWT is the more suitable test. Subjects are usually seated in a chair in a dark room and are instructed to stay awake during a or min trial, which is also repeated normally 4 trials every 2 h. Apart from the MSLT and MWT, other objective assessments of wakefulness and sleepiness have been introduced.
One class comprises performance tests, such as the Psychomotor Vigilance Task [[ 33 ]]. In these tests, subjects are requested to continuously perform an easy task, and it is recorded whether or not the subject is able to successfully carry out that task, as performance decrement can be used as an indicator of sleepiness.
Another group of tests is again based on electrophysiological measures. Tests like the Karolinska Drowsiness Test [[ 29 ]] or the Alpha Attenuation Test [[ 34 ]] give an estimation of the current amount of wakefulness by comparing the EEG activity between eyes open and eyes closed conditions, as EEG activity changes distinctly in both conditions with increasing sleepiness.
These tests can be repeated but are not useful to continuously measure vigilance fluctuations. One approach to overcome this limitation has been the Pupillographic Sleepiness Test [[ 35 ]], where the diameter of the pupil is continuously monitored, as this was found to be a marker for arousal.
Pupil diameter is inversely related to sleepiness and its variability over time is used as indicator for changes in the amount of wakefulness. Still, EEG recordings provide the best temporal resolution and therefore remain the gold standard to objectively assess sleep stages and should also be the method of choice to assess wakefulness fluctuations.
As mentioned above, the wake state can be subdivided into several substages that can best be assessed using EEG recordings during wakefulness. According to original conceptions by Bente [ 8 ] and Roth [ 9 ], the following EEG vigilance stages can be observed during the transition from high alertness to relaxed wakefulness to drowsiness and finally sleep onset:.
mental effort. More recent studies on changes of EEG activity during the transition from active wakefulness to sleep onset endorse this classification [ 36,37,38,39,40,41,42,43,44,45,46 ].
Visual classification of vigilance stages in a resting EEG has been an arduous and time-consuming task comparable to the visual scoring of an overnight sleep polysomnography.
In the absence of explicit scoring rules, the problem of inter- and intrarater reliability is even more relevant than in sleep medicine where such rules have long been established [ 47,48 ]. Furthermore, changes in wakefulness are not as uniform as the typical changes in sleep stages, as subjects go back and forth between vigilance stages with sometimes very short-lasting switches.
Consequently, a segmentation of the resting EEG into second epochs as is the consensus in sleep medicine is not feasible for scoring vigilance changes in a resting EEG, where much shorter periods have to be considered.
Therefore, the development of computer-assisted scoring algorithms has been essential for rejuvenating research interest in brain arousal regulation. Several algorithms have been put forward. VIGALL is an EEG- and electro-oculography-based algorithm which allows to objectively assess the level of EEG vigilance within multichannel EEG recordings, by automatically attributing one of the above-mentioned vigilance stages to EEG segments of preferable 1 s of duration [ 49,50,51 ].
The VIGALL algorithm takes into account different frequency bands and the cortical distribution of EEG activity using EEG source localization approaches low-resolution electromagnetic tomography, LORETA [ 52,53 ].
Since EEG activity is characterized by high intra-individual stability and large interindividual variability, VIGALL has adaptive features concerning individual alpha peaks and amplitude levels, by automatically detecting the individual alpha frequency and power from a representative epoch of alpha activity.
Some of the parameters e. upper and lower border of the alpha band and decision criteria of the VIGALL e. absolute alpha power necessary to classify an A stage are then modified accordingly.
Unfortunately, VIGALL is not applicable for certain EEGs, e. those showing non-alpha basic rhythms e. low voltage type, beta type , major modifications due to drugs e. anticholinergic drugs or diseases e.
severe Alzheimer's disease or EEGs from children under the age of 10 or older in case of delayed maturation. The very high temporal resolution allows investigations on how vigilance is regulated during the recording period, and this brain arousal or vigilance regulation shows considerable interindividual differences.
During eyes-closed resting conditions of min duration, most subjects show progressive declines to lower EEG vigilance stages adaptive arousal regulation. However, while some subjects exhibit rapid declines within only a few seconds unstable arousal regulation , others steadily remain in stages of high vigilance hyperstable arousal regulation.
Naturally, this trait is modulated by the same individual and environmental factors that also affect sleep regulation such as accumulated sleep deficits, consumption of vigilance-affecting substances e.
caffeine, nicotine, drugs , effort or motivation to stay awake or fall asleep, and disease-related factors. Therefore, assessment of EEG vigilance has to adjust to certain standards.
EEG recordings should be performed under comparable conditions: the EEG chamber should be well ventilated, steadily temperature controlled approx. The current degree of wakefulness should be assessed using questionnaires like the Stanford or Karolinska Sleepiness Scales, and sleep duration and quality in the preceding night should also be registered by questionnaire or preferably objective assessments like actigraphy or polysomnography.
Most important, however, would be that subjects are not to be awoken during the recording, even if they fall asleep, as would be the usual approach in so-called vigilance-controlled EEG recordings performed in quantitative EEG or event-related potential studies.
The current VIGALL version VIGALL 2. These basic research studies also imply clinical relevance given the importance of cognitive tests, MRI and PET in diagnostic procedures, where VIGALL might contribute to improve diagnostic accuracy by assessing arousal-induced error variance.
Operational sequence and decision criteria of the VIGALL 2. Classification of vigilance stages is based on power in 4 regions of interest ROI; frontal, parietal, temporal and occipital lobes. Beforehand VIGALL screens the EEG trace for a second epoch with prominent alpha activity default range 7.
For the respective epoch, the alpha centre of gravity frequency and mean power in the occipital region of interest are calculated. Regarding VIGALL's application in clinical groups and for treatment response prediction, several studies have been published recently: in major depression earlier EEG studies [ 58,59 ] as well as more recent VIGALL-based studies [ 60,61 ] revealed that depressed patients are characterized by a hyperstable arousal regulation, i.
they show delayed or no decline to lower EEG vigilance stages under resting conditions. In contrast, mania was characterized by rapid EEG vigilance decline under resting conditions in former EEG case reports [ 58,62,63 ], which was replicated in a more recent case report applying VIGALL [ 64 ].
Using VIGALL, further evidence for unstable arousal in ADHD has been given [ 67 ]. In accordance with the assumption of hyperarousal in obsessive-compulsive disorder, hyperstable arousal regulation was demonstrated in obsessive-compulsive disorder compared to matched controls [ 68 ].
Another field for the application of VIGALL are the many groups of patients suffering from fatigue. In this context, VIGALL could be helpful in elucidating whether the experienced fatigue is a hypo-aroused state, i.
associated with unstable arousal regulation, or a state where patients feel exhausted due to chronic hyperarousal [ 69 ]. Olbrich et al. Building on the aforementioned empirical findings, the vigilance regulation model of affective disorders and ADHD has been proposed [ 71 ].
This model assumes that behaviour can create a more or less arousing environment in an autoregulatory manner in order to increase or reduce the brain arousal level. The hyperactive, impulsive, talkative and sensation-seeking behaviour in mania and ADHD is interpreted as an autoregulatory attempt to stabilize brain arousal by boosting stimulation from the environment or the behaviour itself e.
by fidgeting. In the context of normal behaviour, this phenomenon can be illustrated by overtired children, who often become agitated if they do not get to bed. This assumption that behaviour can influence brain arousal levels corresponds well with the secondary wake drive as proposed in the four-process model [ 20 ].
Specifically, for mania it is suggested that in vulnerable subjects an unstable brain arousal induces excessive autoregulatory behaviour in order to stabilize arousal, which overrides the physiological tendency to seek sleep, thereby exacerbating the sleep deficits and consequently the arousal instability.
A vicious circle is initiated, which then contributes to mania. Whereas in mania this unstable arousal is triggered and built up state-like within the manic episode, in ADHD the unstable arousal is supposed to be a more stable trait. This unstable arousal trait may be acquired, genetic or resulting from chronic sleep disorders.
On the other hand, the hyperstable arousal regulation in depression is thought to promote withdrawal and avoidance of social interactions, loud music and other external stimulations in order to downregulate the hyperarousal.
This arousal concept and the autoregulatory function of behaviour have already been suggested earlier [ 8,58 ], and quite similar models have been proposed concerning personality traits such as sensation seeking [ 72 ] and extraversion [ 73 ].
These personality traits were also interpreted as autoregulatory behaviour in order to achieve an optimal level of arousal, and they were associated with affective disorders and ADHD [ 74,75 ]. In the following, lines of evidence supporting the vigilance regulation model will shortly be drafted [for more details, see [ 71 ]].
Concerning depression, a hyperstable arousal regulation is well in line with inner restlessness and tension and with heightened noradrenergic and hypothalamic-pituitary-adrenal activity [ 76,77 ].
Most intriguingly, symptoms of anhedonia and inhibition have also been suggested to be a consequence of noradrenergic hyperactivity [ 78,79 ]. Furthermore, the tonic hyperarousal explains the pronounced insomnia in depression, including the increased sleep onset latency [ 80,81 ].
Several arousal-reducing interventions lead to improvement in depression, such as sleep deprivation which leads to a rapid and pronounced reduction of depressive symptomatology in more than half of the patients [ 82 ], whereas recovery sleep and short naps can result in prompt return of depressive symptomatology.
Drowsiness is a highly frequent side effect of antidepressants [ 83,84,85,86 ], and all standard antidepressants, and also electroconvulsive therapy, reduce the firing rate of neurons in the noradrenergic locus coeruleus [ 87 ], which plays an essential role in arousal regulation [ 88,89,90 ].
In this context it is of interest that also other arousal-reducing drugs, such as scopolamine and ketamine, have demonstrated antidepressant effects [ 91,92 ]. In contrast, psychostimulants failed to show antidepressant effects in typical depression [ 71 ].
Also, antidepressants, which reduce brain arousal as mentioned above, can induce a switch into mania. According to some studies, this switch risk might be higher for antidepressants, which are particularly sedating [ ,,, ]. In contrast, stabilization of the sleep-wake rhythm is an established part in behavioural therapies for bipolar disorder [ ,, ], and extended bed rest is used as an add-on in the treatment of acute mania [ ,, ].
Furthermore, case reports show acute antimanic effects of psychostimulants [reviewed in [ ]]. In case of rapid response to arousal-increasing drugs, clinical improvement usually goes along with increases in brain arousal [ 64, ].
Currently, a randomized placebo-controlled trial has been initiated testing acute antimanic properties of methylphenidate [ ]. Concerning ADHD, lines of evidence are similar: studies applying skin conductance level, MSLT, MWT, quantitative EEG, VIGALL and Epworth Sleepiness Scale demonstrated that many ADHD patients are characterized by an unstable arousal regulation [ 66,,,, ].
Thus, the rapid therapeutic effects of stimulants in ADHD could be explained by their arousal-stabilizing properties. As in mania, all factors destabilizing arousal or inducing sleep deficits are reported to exaggerate ADHD, whereas interventions improving sleep quality and stabilizing arousal improve ADHD [ ,,, ].
Furthermore, the unstable arousal regulation provides a simple explanation for the attention deficits in ADHD, e. in continuous performance tasks [ ], but also for the presentation specifiers according to DSM-5 and the subtypes as their antecessors in the DSM-IV-TR.
In the predominantly inattentive presentation , the deficits are explained by the unstable arousal regulation. In the combined presentation , with attention deficits and hyperactivity, additional autoregulatory aspects supervene with sensation seeking and hyperactivity as an attempt to stabilize arousal.
The vigilance regulation model also explains the substantially lower prevalence rates for the predominantly hyperactive-impulsive subtype whose general validity is in doubt [ , ]: the suggested core pathogenetic factor unstable brain arousal leads to attention deficits, whereas hyperactivity does not represent a primary disorder per se, but an autoregulatory response, which may or may not be present.
At a first glance, the sleep onset insomnia reported for a subgroup of ADHD patients seems to be incompatible with the assumption of a chronic unstable arousal regulation in this condition. However, there are several reasons why sleep onset insomnia might occur despite an unstable arousal regulation.
First, according to the vigilance regulation model, compensatory stimulation and sensation-seeking behaviour can result in inability or reluctance to settle into sleep [ ]. Secondly, following the two-process model of sleep, a circadian phase delay process C can inhibit sleep onset, although sleep pressure is high enough process S : studies have shown that children and adults with ADHD have a significantly delayed sleep onset, caused by a delayed melatonin onset process C [ ,, ].
As a result, going to bed too late will further increase the unstable arousal regulation. Finally, in treated patients, it is also possible that taking a stimulant dose too close to bedtime will result in insomnia as side effect, although stimulants might also improve sleep in ADHD [ , ].
Arousal regulation is a fundamental trait and potential endophenotype [ , ], which, according to the proposed vigilance regulation model, not only modulates, but also triggers normal and abnormal behaviour. The newly developed and validated EEG-based algorithm VIGALL promises progress in research on confounding, modulating and moderating roles of arousal on behaviour.
This evidence shows the startling need for those who are sleep-deprived to exercise caution. But how does it work? Well, when you are in a state of deep sleep blood flow to your brain is decreased slightly. This allows another fluid present in the brain, known as cerebrospinal fluid, to have more room when it flows through your brain.
More room for this cerebrospinal fluid means it has an easier time flushing out the toxins and other waste products in your brain. Want to learn more about this interesting process and how sleep can affect a healthy brain?
Keep reading to find out! Researchers used cutting-edge MRI technology to monitor and study the brains of 11 people. One author of the article, Laura Lewis assistant professor in the department of biomedical engineering at the University of Boston , says that about every 20 seconds while you are in a state of deep sleep, a slow, large wave of cerebrospinal fluid washes through your brain and cleans out whatever toxins and waste may have been left behind during the day.
Other scans of the brains show a wave of electricity in the neurons of the brain right before the cerebrospinal fluid washes the brain out. Interestingly, this type of brain wave is a common type that only occurs when the brain enters a state of deep sleep. Because of this their brain is not getting the wash that it needs.
The build-up of the beta-amyloid in the brain will cause less sleep and because the person is getting less sleep, more beta-amyloid gets built up within the brain. Thus, because the brain is not getting its necessary rest, it does not have the opportunity to wash out the beta-amyloid toxins by using waves of the cerebrospinal fluid.
There are lots of other causes but the research done for this journal has helped possibly identify and isolate one of the causes of it. Although controlling the factors that interfere with your sleep may be difficult, you can adopt new habits that encourage a better night of sleep so you can better improve your cognitive function and decrease risk of neurological disease:.
Twitter Linkedin Youtube. About Dr. Patient Portal. com Menu. How Sleep Deprivation Affects Your Mental Clarity. While some foods, such as milk products, fish and fruit for example, kiwis and tart cherries have shown some sleep-promoting effects, research is too limited to draw definitive conclusions or recommendations about specific foods to help sleep.
Growing research suggests that the quality of diet or having sufficient nutrients can impact the quantity and quality of sleep. Low fiber, high saturated fat, high sugar diets have been associated with poorer quality sleep.
Another large study found that deficits in nutrients, like as calcium, magnesium, and vitamins A, C, D, E, and K, were associated with sleep problems. Unfortunately, we know that pre-pandemic and especially over the course of the last two years, a large percentage of the population continues to experience insufficient sleep.
Longer work hours, constant access to social commentary and entertainment, and increased stressors all contribute to people getting less sleep. The good news is that there is increasing awareness of the importance of sleep for daily functioning and health.
In order to see a shift in sleep behaviors, ongoing work is needed to promote science-based policies that help improve sleep health, such as encouraging employers to help promote healthy sleep and introducing later school starting times.
And we need to increase access to care for individuals with sleep difficulties. For some sleep difficulties, adopting healthy sleep habits may help to improve sleep. However, those with more chronic insomnia should seek professional help, including cognitive behavioral therapy for insomnia CBT-I , which is recognized as a first line treatment for insomnia.
CBTI involves educating people about sleep and aims to change their sleep-related behaviors and thought processes by teaching strategies such as stimulus control, sleep restriction, relaxation techniques and cognitive therapy.
If sleep problems persist or you continue to experience daytime sleepiness even after getting enough sleep, then it might be time to see a sleep specialist who can help determine whether you need cognitive behavioral therapy, medication, or another treatment.
In this video Dr. Zakarin discusses the relationship between sleep, mental health, and suicide in adolescents and steps we can all take to improve the quality of our sleep, which include some of the following:. How Sleep Deprivation Impacts Mental Health. Columbia psychologist explains why poor sleep makes it more difficult to cope with stress and regulate emotions.
March 16, Share this page Share on Facebook Share on X formerly Twitter Share on LinkedIn Share by email. Why is sleep so important to our mental health?
Foggy, dry, or cloudy wakefulness and mental clarity could clarrity stress or one of these other conditions. Wakefulness and mental clarity all likely clraity experienced "brain fog"—the wakefulndss, cloudy feeling you wakefilness in your head when you can't focus, feel exhausted but cannot sleep, forget things, or make simple mistakes. Brain fog causes may include a lack of sleep, hormonal changes, or several health conditions—such as anxiety, COVID, fibromyalgia, and Lyme disease. Brain fog exists on a spectrum. For some, it's a frustrating—even debilitating—everyday part of life.
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